Endocrinology

÷ #All pituitary hormones are polypeptides

0 Patients with FHH have no clinical

findings and no treatment is
necessary.
362 SEC TION III ENDOCRINE ENDOCRINE—PHARMACOLOGY
` 

ENDOCRINE—PHARMACOLOGY
` 

Diabetes mellitus All patients with diabetes mellitus should receive education on diet, exercise, blood glucose
therapy monitoring, and complication management. Treatment differs based on the type of diabetes and
glycemic control:
ƒ Type 1 DM—insulin replacement
ƒ Type 2 DM—oral agents (metformin is first line), non-insulin injectables, insulin replacement;
weight loss particularly helpful in lowering blood glucose
ƒ Gestational DM—insulin replacement if nutrition therapy and exercise alone fail
Regular (short-acting) insulin is preferred for DKA (IV), hyperkalemia (+ glucose), stress
hyperglycemia.
These drugs help To normalize pancreatic function ( -glits, -glins, -glips, -glifs).

Biguanides,
thiazolidinediones

insulin sensitivity
Adipose tissue
Skeletal muscle
GLP-1 analogs, DPP-4
glucose production inhibitors, amylin analogs
Liver
glucagon release
SGLT2 inhibitors Pancreas (α cells)

glucose reabsorption gastric emptying

Kidney Stomach
Sulfonylureas, meglitinides,
GLP-1 analogs, DPP-4
α-Glucosidase inhibitors inhibitors

glucose absorbtion insulin secretion

Intestine Pancreas (β cells)

DRUG CLASS MECHANISM ADVERSE EFFECTS

Insulin preparations
Rapid acting (1-hr Bind insulin receptor (tyrosine kinase activity) Hypoglycemia, lipodystrophy, hypersensitivity
peak): Lispro, Aspart,
Glulisine (no LAG)
→
Liver:  glucose storage as glycogen
Muscle:  glycogen, protein synthesis
reactions (rare), weight gain

Short acting (2–3 hr Fat:  TG storage Lispro, aspart, glulisine

Plasma insulin level

peak): regular Cell membrane:  K+ uptake Regular

Intermediate acting NPH
(4–10 hr peak): NPH Detemir
Glargine
Long acting (no real
peak): detemir,
glargine 0 2 4 6 8 10 12 14 16 18
Hours
 ENDOCRINE ENDOCRINE—PHARMACOLOGY
`  SEC TION III 363

Diabetes mellitus therapy (continued)

DRUG CLASS MECHANISM ADVERSE EFFECTS

-
Increase insulin sensitivity
Biguanides Inhibit mGPD Ž inhibition of hepatic GI upset, lactic acidosis (use with caution in
Metformin gluconeogenesis and the action of glucagon. renal insufficiency), vitamin B12 deficiency.
 glycolysis, peripheral glucose uptake ( insulin Weight loss (often desired).
sensitivity).
Thiazolidinediones Activate PPAR-γ (a nuclear receptor) Ž  insulin Weight gain, edema, HF,  risk of fractures.
“-glits” sensitivity and levels of adiponectin Delayed onset of action (several weeks).
- Pioglitazone, Ž regulation of glucose metabolism and fatty Rosiglitazone:  risk of MI, cardiovascular
rosiglitazone acid storage. death.
Increase insulin secretion
Sulfonylureas (1st gen) Disulfiram-like reaction with first-generation
Chlorpropamide, sulfonylureas only (rarely used).
tolbutamide
Sulfonylureas (2nd gen) Close K+ channels in pancreatic B cell Hypoglycemia ( risk in renal insufficiency),
Glipizide, glyburide membrane Ž cell depolarizes Ž insulin weight gain.
Meglitinides release via  Ca2+ influx.
“-glins”
Nateglinide,
repaglinide

Increase glucose-induced insulin secretion

GLP-1 analogs  glucagon release,  gastric emptying, Nausea, vomiting, pancreatitis. Weight loss
Exenatide, liraglutide  glucose-dependent insulin release. (often desired).
 satiety (often desired).
DPP-4 inhibitors Inhibit DPP-4 enzyme that deactivates GLP-1 Respiratory and urinary infections, weight
“-glips” Ž  glucagon release,  gastric emptying. neutral.
Linagliptin, saxagliptin,  glucose-dependent insulin release.  satiety (often desired).
sitagliptin
Decrease glucose absorption
Sodium-glucose Block reabsorption of glucose in proximal Glucosuria (UTIs, vulvovaginal candidiasis),
co-transporter 2 convoluted tubule. dehydration (orthostatic hypotension), weight
inhibitors loss.
-

“-glifs” Use with caution in renal insufficiency

Canagliflozin, ( efficacy with  GFR).
dapagliflozin,
empagliflozin
α-glucosidase Inhibit intestinal brush-border α-glucosidases GI upset, bloating.
inhibitors Ž delayed carbohydrate hydrolysis and glucose Not recommended in renal insufficiency.
Acarbose, miglitol absorption Ž  postprandial hyperglycemia.
Others
Amylin analogs  glucagon release,  gastric emptying. Hypoglycemia, nausea.  satiety (often desired).
Pramlintide
 1) Postpartum thyroiditis is
similar to silent thyroiditis

*Difference:

6-
-But it is diagnosed within 12
months postpartum.
-After that it is stamped as
-

silent.

-Hashimoto thyroiditis ends

in hypothyroidism where is
the last two ends euThyroid

2) toxic adenoma
- autonomous production of thyroid hormones from the hyperplastic thyroid follicular
cells.
-radioactive iodine uptake scan reveals uptake only in the hyperactive nodule, with
suppression of uptake in the rest of the gland.

3) RAIU:
a) increase uptake:
-focal uptake :toxic adenoma,
-multinodular goiter :patchy distribution.
-Graves: diffuse
b) decrease uptake:
-exogenous Th: diffuse decrease
=]
-thyroiditis

4) Thyroid in pregnancy:
—> patients with baseline
hypothyroidism who become
pregnant should have their
replacement thyroxine dose
increased.

-patients with impaired thyroid

function (eg, chronic lymphocytic
[Hashimoto] thyroiditis) cannot
increase thyroid hormone production,
resulting in a relative hypothyroid
state
-
Wt loss supplement
 Approach to thyroid nodule:
-Once a thyroid nodule is found,
cancer RF (eg, family history,
←
-
- radiation exposure) should be
assessed by history.

. -Physical examination should

-
evaluate the size, mobility, and
firmness of the thyroid nodule and
check for the presence of enlarged
cervical lymph nodes.

it H —> Thyroid nodules >1 cm with

these high-risk sonographic
features—and all noncystic
thyroid nodules >2 cm—should
undergo fine-needle aspiration
-
(FNA).
-Certain sonographic features
(microcalcifications, irregular
margins, internal vascularity) :a
Cardiovascular effects of thyrotoxicosis much higher risk of malignancy
• Sinus tachycardia #CVS effects of thyroid:
Rhythm
• Premature atrial & ventricular -MOA: directly
-
through the effects of
complexes triiodothyronine (T3) on cardiac myocytes
• Atrial fibrillation/flutter
and blood vessels, +

z
• Systolic hypertension & ↑ PP
Hemodynamic • ↑ Contractility & cardiac output indirectly by increasing sensitivity to
circulating catecholamines.
effects •
•
↓ SVR
↑ Myocardial oxygen demand →
• High-output failure #Mechanism behind BP rise:
Heart failure • Exacerbation of preexisting low-
output failure
-Hyperthyroidism causes a decrease in
SVR, but BP (primarily systolic) rises due to
• Coronary vasospasm
Angina symptoms • Preexisting coronary positive inotropic and chronotropic
atheroscleros effects.
Vs
-In contrast, hypothyroidism causes diastolic hypertension due to an increase in SVR

-Thyrotoxicosis causes increased sensitivity to catecholamines due to increased

expression of beta-1 adrenergic receptors as well as changes in proteins controlling post
beta-1 adrenergic receptor activity.
5) Euthyroid sick syndrome
-Factors in acute illness that inhibit peripheral deiodination(T4-> T3) include high
endogenous cortisol levels, inflammatory cytokines (eg, TNF), starvation, and drugs
(eg, glucocorticoids, amiodarone), elevated FFA, caloric deprivation
-Common findings : low total and free T3 with a normal T4 and TSH (later dec)
-Mx: no Rx needed; just F/U of reports after baseline health

6) Hypopituitarism
- glucocorticoid deficiency, hypogonadism, and hypothyroidism.
-C/F: fatigue, cold intolerance, hypoglycemia, anorexia, and low libido.
-In contrast to primary adrenal insufficiency, aldosterone is normal in central
adrenal insufficiency due to hypopituitarism

7) eosinophilia: corticosteroid deficiency

Pt
8) preventing progress of DM nephropathy
-Strict blood pressure control, particularly using ACE I / ARBs, can reduce the progression
of diabetic nephropathy (DN).

-SGLT 2I: can only be used in patients with an estimated GFR of ≥30 mL/min/1.73 m2
and are limited in use due to cost and adverse effects (eg, urinary tract infections).

9) papillary thyroid cancer Mx:

-FNAC: large cells with ground glass cytoplasm, and pale nuclei containing inclusion
bodies and central grooving
a) Small tumors (<1-2 cm) without evidence of LN involvement / contralateral
thyroid abnormalities :partial thyroidectomy/lobectomy,

b) larger tumors: total thyroidectomy.

-In addition, regional lymph node or central compartment lymph node dissection is usually
performed for papillary cancer with lymph node metastasis or extrathyroidal invasion.

#Postoperative adjuvant therapies for patients at increased risk of recurrence :

radioiodine ablation and suppressive doses of thyroid hormone.

10) DM neuropathy
a)small nerve fibers :pain and paresthesia,
b) large fibers: sensory loss that can allow minor injuries to go unrecognized until the
development of an ulcer.
-Associated autonomic dysregulation can lead to decreased sweating and skin fissuring
and further increase the risk for ulceration.
Vs
#arterial ulcer: at the tips of the digits (least perfused areas); cool, pale skin with
dermal atrophy; and diminished pulses; typically painful unlike DM ulcer
#Venous ulcers: medial aspect of the leg above the malleolus with edema and stasis
dermatitis.
11) RAI
-MOA: causes radiation-induced destruction of thyroid follicular cells.
-As a result, these Rx are used for thyrotoxicosis due to thyroid hormone overproduction
but are not helpful for patients with excess release of preformed hormone.
12) Primary polydipsia
#Pathogenesis:
-increased water intake that surpasses
the kidney's ability to excrete it.

-The increased water leads to

hyponatremia (sodium <137 mEq/L), a
very dilute urine (osmolality <100
mOsm/kg), and urine osmolality < serum
osmolality.
Vs
13)Central DI
= - usually do not have an intact thirst

= mechanism and can have s. Na >150.

#Nephrogenic DI
- usually have an intact thirst
mechanism with lower s. Na (~145
mEq/L)
13) Proliferative diabetic retinopathy (PDR) and DM Nephropathy are chronic
microvascular complications of diabetes due to persistent hyperglycemia,
—> so their presence of PDR correlates with diabetic kidney disease

14) Milk alkali syndrome:

#C/F: Hypercalcemia; Metabolic alkalosis; Acute kidney injury; Suppressed PTH
#Rx: Discontinuation of causative agent; Isotonic saline followed by furosemide

15) causes of hypoglycemia in non-diabetic patients with elevated insulin levels:

1)insulinoma (beta cell tumor):Elevated Cpeptide levels +proinsulin levels >5 pmol/L

2) surreptitious use of insulin or sulfonylurea: proinsulin level is sometimes < 20%

of the total insulin immunoreactivity.
-diagnosis confirmed by measuring the plasma sulfonylurea level.

3) Non-beta cell tumors, typically large mesenchymal tumors,

-hypoglycemia independent of insulin.
-Such tumors produce IGF II which has an insulinomimetic action after binding
to insulin receptors
-suppressed insulin and c-peptide levels.
 16) PTH-independent
hypercalcemia in malignancy:

a) bony destruction by
osteolytic metastasis (eg,
breast, non-small cell lung
cancer, non-Hodgkin lymphoma,
multiple myeloma),

b)increased production of
1,25-dihydroxyvitamin D (eg,
lymphoma),
- -

c) increased IL-6 levels (eg,

multiple myeloma)
>14; rest all <12
Hypoglycemia in patients without diabetes
-
mellitus
• Drugs: quinolones, quinine, beta blockers
• Alcohol (usually with prolonged
starvation)
• Sepsis/critical illness
• Adrenal insufficiency
• Insulinoma
• Surreptitious insulin, sulfonylurea, or
17) Neuroblastoma meglitinide use
• Depleted glycogen stores (anorexia
-arises from neural crest cells, which are precursors nervosa)
to the sympathetic ganglia and adrenal medulla. • Severe hepatic failure
-Neuroblastoma arising in the cervical
paravertebral sympathetic chain can present as
isolated Horner syndrome (ie, ptosis, miosis,
anhidrosis
-Although sweating is often difficult to appreciate in young children, absent facial flushing
(ie, "harlequin" sign) can be observed in anhidrotic areas

#C/F:
• Abdominal mass; Periorbital ecchymoses (orbital metastases); Opsoclonus-myoclonus
syndrome

18) causes of acute hypocalcemia

-Neck surgery (parathyroidectomy); Pancreatitis

-Sepsis; Tumor lysis syndrome

-Acute alkalosis; Chelation: blood (citrate) transfusion, EDTA, foscarnet
 HypoCa in alcoholics
- MOA: Hypomagnesemia in
hospitalized alcoholics and
can cause hypocalcemia by
inducing resistance to
parathyroid hormone (PTH)
as well as by decreasing PTH
secretion.

-Mx: Hypocalcemia due to

hypomagnesemia is typically
refractory to treatment with
calcium unless magnesium
is replaced as well.

✓
#Calcium level changes based on Albumin concentrations :
- About 50% of circulating calcium is protein bound, predominantly to albumin.

- Consequently, serum total calcium varies with albumin concentration.

==>Interpretation of serum calcium levels requires correcting for the serum albumin level
(serum calcium concentration falls by 0.8 mg/dL for every 1 gm/L decrease in
albumin). #acid base pH and Ca:
-Ionized calcium competes with
Management of hypercalcemia
hydrogen ions to bind to albumin;
Short-term (immediate) treatment
• NS hydration + calcitonin
Severe
• Avoid loop diuretics unless volume -elevated pH —> dissociation of
(ca >14/ hydrogen ions from albumin,
overload (HF) exists
symptomatic allowing for increased calcium
Long-term treatment
• Bisphosphonate (zoledronic acid) binding —> a decrease in serum
• Usually no immediate treatment required ionized (free) calcium.
Moderate unless symptomatic
Ca 12-14 • Treatment is similar to that for severe
hypercalcemia
• No immediate treatment required
Asx / mild
• Avoid thiazide diuretics, lithium, volume
ca <12
depletion & prolonged bed rest
19) HypoCa after BT:
-Citrate in transfused blood binds ionized calcium
-Hypocalcemia is uncommon following BT in patients with normal liver function as citrate
is rapidly metabolized by the liver

-Other infused substances that can chelate calcium in the blood include lactate, foscarnet,
and sodium ethylenediaminetetraacetic acid (EDTA).

20) Approach to hypercortisolism:

1) 1st step:The initial step in the evaluation is to confirm hypercortisolism with
-a late-night salivary cortisol assay,
-24-hour urine free cortisol measurement, and/or
-overnight low-dose dexamethasone suppression test.

2) 2nd step:2 of these first-line tests should be abnormal to establish the diagnosis.
—>If hypercortisolism is confirmed, ACTH levels are measured to differentiate ACTH-
dependent (ie, Cushing disease, ectopic ACTH) from ACTH-independent (eg, adrenal
adenoma) causes

21) Somatic symptom disorder :> 6 mon

-involves excessive anxiety and behaviors related to ≥1 somatic symptoms. These patients
typically have high health care use and undergo multiple tests with negative results
-Rx: follow up to same doc; 2nd line: SSRI

22) type 2 DM In children:

-if children are obese (BMI >95th percentile); hyperglycaemia
Vs
#Glucokinase gene mutations —>maturity-onset diabetes of the young,
- decreased secretion of insulin at any given glucose level.
-patients are typically not obese and hyperglycemia is usually mild (<140 mg/dL).

23) #effect of thyroid on lipid:

-Hypothyroidism causes decreased LDL turnover, largely due to decreased expression

→
and activity of LDL receptors, leading to elevated circulating levels of total cholesterol and
LDL.

-decreased activity of LPL —> leading to hypertriglyceridemia

#evaluation:
—> TSH should also be checked prior to initiation of statin medications (eg, atorvastatin)
because untreated hypothyroidism can increase the risk of statin myopathy, and initiation of
statins can cause worsening of concurrent hypothyroid myopathy
 24) Adrenal crisis:
-refractory, acute-onset
hypotension following surgery
is due to adrenal crisis.

CRH -develop in the setting of an

acute stressor (eg, illness,
surgery) in patients with adrenal
insufficiency (AI) (eg, chronic
primary AI, secondary AI).

#Difference in adrenal crisis

= between 1o vs 2o:
-Adrenal crisis due to
secondary AI may present less
dramatically than that due to
= -
primary AI because only cortisol
is deficient and AT II-mediated
aldosterone production
remains intact
Vs (primary AI involves loss of
both cortisol and aldosterone)

25) primary hyperaldosteronism

-Plasma aldosterone : plasma renin
activity >20
-Adrenal suppression testing after
oral saline load confirms
diagnosis

-Abdominal imaging (eg, CT) & adrenal venous sampling to distinguish between U/L
adrenal adenoma vs B/L adrenal hyperplasia
#Mx: U/L-Sx; meds only if poor Sx candidate; B/L- aldosterone antagonist

#1) Spironolactone
-MOA: a progesterone and androgen receptor antagonist that can cause significant
side effects in both men (eg, decreased libido, gynecomastia) and women (eg, breast
tenderness, menstrual irregularities).

2) Eplerenone is a very selective mineralocorticoid antagonist with a very low

affinity for progesterone / androgen receptors.
- It has fewer endocrine side effects and is an alternate therapy.
 Thyrotoxicosis with
Thyrotoxicosis with ↓ RAIU
normal / ↑ RAIU
• Painless (silent) thyroiditis
• Subacute (de Quervain) thyroiditis
• Graves disease • Amiodarone-induced thyroiditis
• Toxic multinodular • Excessive dose (or surreptitious
goiter intake) of levothyroxine
• Toxic nodule • Struma ovarii
• Iodine-induced
• Extensive thyroid cancer metastasis

Syndrome of inappropriate antidiuretic hormone

• CNS disturbance (eg, stroke, hemorrhage, trauma)
• Medications (eg, carbamazepine, SSRIs, NSAIDs)
Etiologies • Lung disease (eg, pneumonia)
• Ectopic ADH secretion (eg, small cell lung cancer)
• Pain &/or nausea
• Mild/moderate hyponatremia: nausea, forgetfulness -Laboratory studies,
Clinical features
• Severe hyponatremia: seizures, coma including serum
• Euvolemia (eg, moist mucous membranes, no edema, no electrolytes, urine
JVD)
osmolality, and urine
• Hyponatremia
• Serum osmolality <275 mOsm/kg H2O (hypotonic)
sodium, are the 1st step
Laboratory findings • Urine osmolality >100 mOsm/kg H2O in establishing the
• Urine sodium >40 mEq/L diagnosis.

• Fluid restriction <800 ml ± salt tablets

Management
• Hypertonic (3%) saline for severe hyponatremia

27) Mx of nelson syndrome:

-Enlargement of pre-existing ACTH–secreting pituitary adenoma after bilateral adrenalectomy
for refractory Cushing disease—> increased ACTH (hyperpigmentation), mass effect
(headaches, bitemporal hemianopia).
Treatment: transsphenoidal resection, postoperative pituitary irradiation for residual tumor
 28) GH, fluctuates widely and has low
let sensitivity and specificity

→
2nd #Mx of acromegaly:
-skeletal and joint abnormalities are largely
irreversible.
-MCC of death: diastolic dysfunction
-Initial Rx :transsphenoidal resection of
the pituitary adenoma.
-For patients with residual or unresectable
tumors, medical therapy is indicated:

1) somatostatin analogues (eg,

octreotide)
2) growth hormone receptor antagonists
(eg, pegvisomant).
-

29) hyperosmolar hyperglycemic state (HHS

-elevated plasma osmolality (eg, >320 mOsm/kg); S. Glucose >1000 mostly
#Mx:
a) 1st step: In the 1st hour of treatment, NS should be used for resuscitation regardless
of sodium levels.
-The fluid can be changed to 0.45% NS after the second or third hour if the corrected serum
sodium is normal or high on repeat laboratory testing
2) 2nd line: IV regular insulin is preferred
#Metformin should not be given to
acutely ill patients with acute renal
failure, liver failure, or sepsis

-as these conditions increase the risk

of lactic acidosis.

#nephrotoxin like NSAIDs avoided in

renal failure

→
30)stress hyperglycemia
-Transient hyperglycemia without preexisting diabetes; Elevated glucose but normal
HBA1C
#Mx:
• Minimization of glucose in IV fluids
-severe elevations (>180-200 mg/dL) : Insulin to maintain blood glucose at 140-180
= -

-Goal:mildly elevated target glucose of 140-180 mg/dL (rather than normoglycemia) to

minimize the risk of insulin-induced hypoglycemia

Classification of multiple endocrine neoplasia 31) MEN 2A and 2B (usually due to RET
• Primary hyperparathyroidism (parathyroid proto-oncogene mutations) are also
adenomas or hyperplasia)
Type 1 associated with pheochromocytoma,

=
• Pituitary tumors (prolactin, visual defects)
• Pancreatic tumors (especially gastrinomas)
• Medullary thyroid cancer (calcitonin) -which can be asymptomatic at the time of
• Pheochromocytoma
Type 2A
• Primary hyperparathyroidism (parathyroid
diagnosis but cause life-threatening
hyperplasia) hypertensive crisis during surgical
• Medullary thyroid cancer (calcitonin) procedures (eg, thyroidectomy).
Type 2B • Pheochromocytoma
• Mucosal neuromas/marfanoid habitus

-so all MTC should undergo RET mutation testing and screening for pheochromocytoma
with a plasma fractionated metanephrine assay.
-If found, pheochromocytoma should be resected prior to thyroidectomy.

Differential diagnosis of myopathy

Muscle atrophy+ hypoTH signs
Disorder Clinical features ESR CK
are Classic for hypoTH myopathy
• Progressive proximal muscle
Glucocorticoid-
weakness & atrophy without pain / Norm Norm
Vs
induced
myopathy
tenderness al al Late/ not for inflammatory
•LE muscles are more involved
myopathy
• Muscle pain & stiffness in the
shoulder & pelvic girdle
Polymyalgia Norm
• Tenderness with decreased range ↑
rheumatica al
of motion at shoulder, neck & hip
• Responds rapidly to GC
• Muscle pain, tenderness &
Inflammatory proximal muscle weakness
↑ ↑
myopathies • Skin rash & inflammatory arthritis
may be present
• Prominent muscle pain/tenderness
Statin-induced Norm
with or without weakness ↑
myopathy al
• Rare rhabdomyolysis
• Muscle pain, cramps & weakness
involving the proximal muscles
• Delayed tendon reflexes &
Hypothyroid Norm
myoedema ↑
myopathy al
• Occasional rhabdomyolysis
• Features of hypothyroidism are
present
CK = creatine kinase; ESR = erythrocyte sedimentation rate.
 33) #Thyroid storm:
-fever must, mild HT, Pre existing thyrotoxicosis
Vs
#Pheochromocytoma: severe HT episodes
-Trigger: increases in intra-abdominal pressure (eg, tumor palpation, positional changes),
surgical procedures, anesthetic agents.,nonselective beta blockers

36) central precocious puberty:

Concentrated Hypothalamic glioma, pituitary
hamartoma, and idiopathic
precocious puberty
Dilute
-McCune-Albright
syndrome :peripheral precocious
puberty,
-

-Granulosa cell estrogen/

progesterone-secreting tumors:
premature breast development and
menses due to hyperestrogenism,
but not isolated acne and pubic hair.

#Precocious puberty: girls age <8; boys <9. -Mildly elevated DHEAS present in
children with premature adrenarche
is not sufficient to affect skeletal
(>2 SD above
chronological age) growth; therefore, bone age is
normal in these patients.
1st step
-

2nd step

3rd step

•
Non Classic adrenal insufficiency .

#Mx:
-Patients with central PP require MRI of the brain to evaluate for a hypothalamic or pituitary tumor
activating the HPG axis.
-If MRI is negative, the cause is most likely idiopathic precocious puberty, and GnRH therapy
can be initiated.
-GnRH desensitizes the pituitary and suppresses FSH and LH secretion to slow pubertal
progression and maximize height potential.
37) RF for diabetic Nephropathy:
• Long-standing diabetes (eg, 5-10 years)
• Evidence of other microvascular disease (eg, retinopathy suggested by decreased visual
acuity)
• Poor glycemic control (A1c >7.0%)
• Poorly controlled hypertension (>130/80 mm Hg)

—> the preferred screening test is the random urine albumin/creatinine ratio, which
detects excess albuminuria (>30 mg/g) earlier.

38) Patients with a diminished glucagon response, such as with pancreatogenic diabetes
(eg, chronic pancreatitis with fibrosis of the islets), can develop rapid and severe
hypoglycemia with little warning.

39) Electrolyte causes of nephrogenic DI: hyperkalaemia, hypercalcaemia

40) DKA resolution markers:

-The most accurate markers indicating resolution of DKA: serum anion gap and serum
beta-hydroxybutyrate levels.

41) pituitary apoplexy: H’age into prolactinoma

-sudden worsening in a K/C/O of large prolactinoma: sudden onset of severe headache
and visual disturbances+ loss of pituitary function

42) insulin dose in exercise:

-Exercise increases glucose uptake by skeletal muscle cells
-For training sessions within 3 hours of a meal, the premeal bolus insulin dose
preceding exercise should be reduced.

-For prolonged exercise (eg, distance running) the basal insulin will likely need
reduction as well.

—> Patients with diabetes who initiate a strenuous exercise regimen should also be
counseled to increase carbohydrate intake, particularly if training sessions are >60
minutes in duration.

43) Mx of 1o adrenal insufficiency:

-GC (eg, hydrocortisone, prednisone); MC (eg, fludrocortisone)
-Switching to dexamethasone would not correct this patient's mineralocorticoid deficiency
because this medication has only GC and no MC activity.

-#y hydrocortisone is preferred over dexamethasone??

because it has a shorter duration of action and can be given in divided doses to better
mimic the circadian rhythm of endogenous cortisol secretion.
 =

=
Hypercalcemia of malignancy
45)Pheochromocytoma Rx:
Cause Tumor type Mechanism Diagnostic
-patients should initiate
•
Squamou
preoperative alpha-adrenergic
s cell blockade (Phenoxybenzamine
• ↓ PTH
PTHrP* • Renal & • PTH mimic
• ↑ PTHrP irreversible and non selective
bladder blocker) 7-14 days prior to
• Breast &
ovarian surgery,
• ↓ PTH &
followed by beta-adrenergic
• Breast blockade 2-3 days prior to
Bone PTHrP
• Multiple • ↑ Osteolysis
metastases
myeloma
• ↓ Vitamin surgery.
D
1,25- • • ↓ PTH
• ↑ Calcium
dihydroxyvitami Lymphom • ↑ Vitamin
absorption
nD a D
 Stimuli for secretion of antidiuretic 47) Exercise-associated hyponatremia
hormone -occurs due to a combination of excessive fluid intake
Osmotic • Serum osmolality > ~285 and nonosmotically mediated release of
• Nausea inappropriately high levels of ADH
• Pain
• Physical or emotional
Nonosm stress
-severe cases: seizures, profound confusion, and
otic • Hypotension even death.
• Hypovolemia
• Hypoxia
• Hypoglycemia

48) CAH
-Males normal

#Signs of female virilization :

-clitoral enlargement-appear as
an underdeveloped phallus
-ectopic urethral meatus:
hypospadias

- Labioscrotal folds : partially /

completely fused.
-Gonads are nonpalpable as
female patients with CAH have
internal female organs and do
not have testes.

#evaluation:
-Initial evaluation of ambiguous genitalia : karyotype to confirm genotype and pelvic
ultrasound to assess for presence of female internal organs.
-Serum electrolytes should be obtained to screen for salt-wasting forms of CAH, which
can result in life-threatening adrenal crisis.

49) The tuning fork test is an easy and inexpensive way to assess for the loss of
vibratory sense in patients with diabetic neuropathy.
 50) PAC/ PRA:
-drugs that alter the PAC/PRA ratio (eg, spironolactone,
Early morning eplerenone, amiloride, triamterene) should be withdrawn
for 4 weeks before testing.

—> A PAC/PRA ratio >20 with plasma aldosterone >15

ng/dL suggests primary hyperaldosteronism and requires
further confirmatory adrenal suppression testing.

→ usually involves salt loading and documenting inability

a-
to suppress serum aldosterone.
-Hyperaldosteronism is

I
most commonly due to
bilateral adrenal
, hyperplasia (50%-60%)
-
or aldosterone-producing
adrenal adenoma
(40%-50%).
51) Factors increasing the risk for
osteomyelitis in DM foot
-positive probe-to-bone test, a
large ulcer (eg, >2 cm2), / an
ulcer lasting ≥1 week

⇐
 Effect of intensive glycemic control in type 2 52) FHH
diabetes Normally, high-normal calcium levels suppress
Macrovascular complications PTH secretion by the parathyroid glands, but in
No change (short-
(eg, acute myocardial
infarction, stroke)
term) FHH, higher calcium concentrations are required to
Microvascular complications
suppress PTH release.
Improve
(eg, nephropathy, retinopathy)
No change or -Concurrently, the defective CaSR leads to
Mortality
increased increased reabsorption of ca in renal tubules.
#D/D of PTH dependent hyperCa:
-In the evaluation of hypercalcemia, an elevated (or inappropriately normal) PTH level
suggests either primary hyperparathyroidism or FHH.

-However, patients with primary hyperparathyroidism have increased urinary calcium

excretion due to excessive mobilization of calcium from bones, whereas patients with
FHH usually have very low urinary calcium levels (typically <100 mg/24 hr).
-

#Urine calcium excretion can be more precisely assessed using the urine calcium/creatinine
clearance ratio (UCCR):
UCCR = (Ca urine/Ca serum)/(Creat urine/Creat serum)

* UCCR: usually <0.01 in FHH compared to >0.02 in primary hyperparathyroidism

53) PTU is usually not the

preferred drug due to a black box
warning of severe liver injury and
acute liver failure.

-But PTU is preferred during the

1st TM of pregnancy due to fetal
teratogenicity with MMI

-The MC S/E of ATDs: allergic

reaction (2% of patients).

-The most serious s/e :

agranulocytosis (0.3% of patients)
- all patients must be informed
about it.
54) Cradioprotective anti diabetic drugs:
-Sodium-glucose cotransporter 2 (SGLT-2) inhibitors (eg, canagliflozin, empagliflozin)
-Glucagon-like peptide-1 (GLP-1) receptor agonists (eg, semaglutide, liraglutide)

Both induce wt loss

55) ADR of SGLT 2I:
• Euglycemic ketoacidosis
• Increased risk of genitourinary infections
#C/I:
-Type 1 DM; H/O DKA; Impaired renal function (eGFR <30 mL/min/1.73 m2)

Glutides

Gliptins

By volume depletion

<
 Hyperthyroidism Mx

↳ by

⑧
1) ATD Rx : Patients with mild disease, small goiters, and low TSH receptor antibody titers can be
managed with an ATD alone and have a 50% likelihood of permanent remission. ATD therapy
alone is also used in pregnant women or older patients with limited life expectancy.

—> In patients who have significant symptoms and thyroid hormone levels >/=2-3 times
normal, an ATD with a beta blocker is initially recommended to stabilize the patient before
definitive treatment with RAI or thyroidectomy.

—> Pretreatment with ATDs is also recommended for patients at increased risk (eg, elderly,
significant comorbidities) for complications due to the transient worsening of
hyperthyroidism following RAI treatment.
—> ATD S/Es & what to do next ..??

- Agranulocytosis is the most feared side effect, and is seen in approximately 0.3% of patients

9
treated with antithyroid drugs.
- It is caused by immune destruction of granulocytes, and most cases occur within 90 days of
treatment.
- Routine monitoring of the granulocyte count is not cost effective and not advocated.
- Current recommendations state that once the patient complains of fever and sore throat, the
antithyroid drug should be discontinued promptly and the WBC count measured. A total
WBC count less than 1,000/cubic mm warrants permanent discontinuation of the drug. If
the total WBC count is more than 1,500 per cubic mm, antithyroid drug toxicity is unlikely to
be the cause of the sore throat and fever.

—> Rx of antithyroid drug-induced agranulocytosis includes

1. discontinuation of the offending drug and
2. intravenous administration of broad spectrum antibiotics (especially for Pseudomonas).
3. Granulocyte colony stimulating factors may be useful in increasing the WBC count.
4. Throat culture, oral penicillin and acetaminophen can be done/given as part of the evaluation/
management (along with CBC with differential count) of this patient.
 58) Mx of hypovolemic hyponatremia:
• Nonosmotic stimulation of antidiuretic hormone (ADH) occurs in response to
angiotensin II, hypovolemia (stimulates stretch receptors in the left atrium), and
hypotension (stimulates baroreceptors in the carotid arteries).

#Mx:
-normal saline is DOC as it replenishes the body's depleted salt stores, restores
euvolemia, and shuts off nonosmotic stimuli for ADH release.

59) Diabetes insididus cutoff limit:

-urine osmolality: < 300 (complete vs 300-600 in partial DI) ; S osmolality> 250
Vs
# urine specific gravity and urine osmolality (eg, typically >600 mOsm/kg H2O): DM.

Conditions that alter TBG concentration #Corrected calcium = (measured

Increased TBG Decreased TBG total calcium) + 0.8 × (4.0 g/dL −
• Androgenic hormones serum albumin in g/dL)
• High-dose -This patient's corrected serum
glucocorticoids/
• Estrogens (eg, pregnancy, OCs,
hypercortisolism calcium is 8.7 mg/dL (7.5 mg/dL +
HRT) & estrogenic medications (eg,
tamoxifen)
• Hypoproteinemia 0.8 [4.0 - 2.5]).
(eg, nephrotic -Because the normal calcium ranges
• Acute hepatitis
syndrome,
starvation) from 8.5-10.5 mg/dL, this patient
• Chronic liver disease requires no further intervention.

#MOA:
-RAI (131I) is taken up by the thyroid follicular cells in a manner similar to
that of natural iodine, and the subsequent beta emission induces slow
e-
necrosis of the thyroid follicular cells.
-This leads to clinical and biochemical resolution of hyperthyroidism
over the subsequent 6-18 weeks (not rapidly)—> permanent hypoTH
within months
60) DM foot ulcer:
a) Superficial diabetic foot infections may be monomicrobial,
b) deeper infections are almost always polymicrobial: Staphylococcus aureus,
Streptococcus pyogenes), gram-negative (eg, Pseudomonas aeruginosa), and
anaerobic organisms.
#C/Fs of Deep infection :
#C/Fs of Superficial infection : Suspected in those with ,
- Localized skin erythema, - long-standing wounds (>1-2 weeks),
- warmth, - systemic symptoms (fever, chills),
- tenderness, - large ulcer size (>2 cm),
- edema. - elevated ESR,
- presence / palpation of bone in the ulcer base.
—> Rx: Piptaz + vancomycin

Management of diabetic ketoacidosis

Management of type 2 diabetes in
• Rapid infusion of 0.9% normal saline patients with heart disease
IV
• Add dextrose 5% when serum • Smoking cessation
fluids Lifestyle • Regular exercise
glucose is ≤200 mg/dL
• Reduced fat intake
• Start continuous IV insulin infusion;
- • Metformin
hold if K <3.3 mEq/L Glycemic • GLP-1 agonists (eg,
• Switch to SQ (basal bolus) insulin managemen liraglutide)
for the following: able to eat, t • SGLT2 inhibitors (eg,
Insulin empagliflozin)
glucose <200 mg/dL, anion gap
Lipid-
<12 mEq/L & serum HCO3− ≥15 lowering • Statins
mEq/L therapy
• Overlap SQ & IV insulin by 1-2 hr • Goal BP <140/90 mm Hg
Blood
• Add IV K if serum K+ <5.3 mEq/L; (consider <130/80 mm
pressure
Hg)
Potass hold if ≥5.3 mEq/L control
• ACE inhibitors preferred
ium • Nearly all patients' K+ depleted,
Antiplatelet
even with hyperkalemia therapy
• Low-dose aspirin

Bicarb
• Consider for patients with pH ≤6.9
onate
• Consider for serum phosphate
Phosp <1.0 mg/dL, cardiac dysfunction, or
hate respiratory depression
• Monitor serum calcium frequently
 Distal sensory peripheral neuropathy in diabetes 63) previous hypoglycaemia:
mellitus
-Recurrent or severe hypoglycemia in
Large fiber Small fiber patients with long-standing diabetes
neuropathy* neuropathy*
reduces the glucose-raising effects
• Pressure, of epinephrine and suppresses the
Sensory • Pain &
proprioception & symptoms related to the
function temperature
balance
catecholamine surge,
Major • Numbness & poor • Burning & stabbing increasing the risk for progressively
symptoms balance pain
worsening hypoglycemic episodes.
• Diminished/
absent ankle • Reduced pinprick
Examinati reflexes sensation
on • Reduced/absent • Ankle reflexes
findings vibration, light possibly
touch & preserved
proprioception
*Patients can have mixed large & small fiber neuropathy.
-

Thyroid effects of amiodarone 66) SIADH in AI (both)

Disorder Features Treatment -because cortisol acts as an
• ↑ T4 None inhibitor of antidiuretic
Decreased T4-T3
conversion
• ↓ T3 needed hormone, AI often leads to the
• Normal/↑ TSH syndrome of inappropriate
Inhibition of thyroid • ↑ TSH Levothyroxi antidiuretic hormone release
hormone synthesis • ↓ T4 ne (SIADH) with hyponatremia.
• ↓ TSH Antithyroi
AIT type 1
• ↑ T3 & T4 d drugs - Hyperkalaemia differentiates
(iodine-induced
• ↓ RAIU
increase primary(raised) and secondary

t.ir
• Increased
in thyroid hormone (lowers)
vascularity on
synthesis)
ultrasound
• ↓ TSH Glucocorti 67) Mx of diabetic neuropathy:
• ↑ T3 & T4 coids 1st line:TCA but with caution at >65
AIT type 2 • Undetectable RAIU yrs

yo
(destructive thyroiditis) • Decreased
vascularity on
-2nd :SNRI duolexitine
ultrasound -3rd line: gabapentin
-4th: opioids
68) Diabetic screening:
-USPSTF: all Pt with > 135/80 BP
-ADA: all ppl >45 yrs or any age with RF
 67) post prandial hyperglycaemia
-elevated Hb A1c and elevated RBS despite normal
FBS levels(80-130) may have postprandial
hyperglycemia.

-A combined regimen including a long-acting basal

insulin-glargine (to control fasting glucose) + a rapid-
acting mealtime insulin aspart (to control postprandial
glucose) can improve glycemic control.

—> Very high A1c levels (>10%) suggest significant

hyperglycemia throughout the day, whereas lesser
abnormalities are often due to elevations in only
postprandial glucose levels.
-A1c is influenced by both fasting and postprandial glucose concentrations and is
useful for estimating overall glycemic control in patients with DM

68) Diabetic ketoacidosis

-causes osmotic diuresis and secondary hyperaldosteronism (Volume contraction)
leading to urinary potassium loss and a total body potassium deficit.

-However, laboratory potassium values are often normal or elevated.

-This finding is due to hyperosmolarity, which draws water and potassium into the
extracellular space, and insulin deficiency, which impairs cellular uptake of
potassium.

69) Non Classic CAH:

-C/F: early puberty
-Since the enzyme deficiency in nonclassic CAH is relatively mild, sufficient glucocorticoids
and mineralocorticoids are produced; therefore
-, patients do not have the salt-wasting seen in classic CAH, and electrolytes and blood
pressure remain normal.

-Diagnosis: confirmed by an exaggerated 17-OHP response on ACTH stimulation test.

-Rx:just GC (hydrocortisone) and not MC

70) Medullary thyroid CA:

-Serum calcitonin levels correlate with the risk of metastasis and recurrence, and are
measured serially following surgery.
Vs
# papillary/follicular thyroid cancer: elevated thyroglobulin; increased radiolabeled
iodine uptake
 ENDOCRINE ENDOCRINE—PHYSIOLOGY
`  SEC TION III 345

Signaling pathways of endocrine hormones

cAMP FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2- FLAT ChAMPs CHuGG
receptor), MSH, PTH, Calcitonin, Histamine
(H2-receptor), Glucagon, GHRH
cGMP BNP, ANP, EDRF (NO) BAD GraMPa
Think vasodilation and diuresis
IP3 GnRH, Oxytocin, ADH (V1-receptor), TRH, GOAT HAG
-
Histamine (H1-receptor), Angiotensin II,
Gastrin
Intracellular receptor Progesterone, Estrogen, Testosterone, Cortisol, PET CAT in TV All steroids except
Aldosterone, T3/T4, Vitamin D thyroid and & vit D
Receptor tyrosine IGF-1, FGF, PDGF, EGF, Insulin MAP kinase pathway
kinase Get Found In the MAP
Serine/threonine TGF-β
kinase receptor
Nonreceptor tyrosine G-CSF, Erythropoietin, Thrombopoietin JAK/STAT pathway
kinase Prolactin, Immunomodulators (eg, cytokines Think acidophils and cytokines
IL-2, IL-6, IFN), GH GET a JAKed PIG

Signaling pathways of steroid hormones

Binding to receptor Steroid hormones are lipophilic and therefore
located in nucleus
or in cytoplasm
H Hormone must circulate bound to specific binding
globulins, which  their solubility.

¥
In males,  sex hormone–binding
Transformation of R Receptor
receptor to expose globulin (SHBG) lowers free testosterone
DNA-binding protein Ž gynecomastia.
In females,  SHBG raises free testosterone
Binding to Ž hirsutism.
H

o
enhancer-like Cytoplasm
element in DNA R
Gene
 estrogen (eg, OCPs, pregnancy) Ž  SHBG.

Intron Exon
Pre-mRNA

mRNA Nucleus

Protein
Ribosome

Response
 ENDOCRINE ENDOCRINE—PATHOLOGY
`  SEC TION III 351

Thyroid cancer Typically diagnosed with fine needle aspiration; treated with thyroidectomy. Complications of
surgery include hypocalcemia
-
(due to removal of parathyroid glands), transection of -
recurrent
laryngeal nerve during ligation of inferior thyroid artery (leads to dysphagia and dysphonia
=
[hoarseness]), and injury to the external branch of the superior laryngeal nerve during ligation of
superior thyroid vascular pedicle (may lead to loss of tenor usually noticeable in professional voice
-
users).

=
Papillary carcinoma Most common. Empty-appearing nuclei with central clearing (“Orphan Annie” eyes) A ,
A
psamMoma bodies, nuclear grooves (Papi and Moma adopted Orphan Annie).  risk with RET/
PTC rearrangements and BRAF mutations, childhood irradiation.
Papillary carcinoma: most prevalent, palpable lymph nodes. Good prognosis.

Follicular carcinoma Good prognosis. Invades thyroid capsule and vasculature (unlike follicular adenoma), uniform
follicles; hematogenous spread is common. Associated with RAS mutation and PAX8-PPAR-γ

=
translocations. Fine needle aspiration cytology may not be able to distinguish between follicular
adenoma and carcinoma. So do biopsy
Medullary carcinoma From parafollicular “C cells”; produces calcitonin, sheets of polygonal cells in an amyloid stroma
B (stains with Congo red). Associated with MEN 2A and 2B (RET mutations). .
B

Undifferentiated/ Older patients; presents with rapidly enlarging neck mass Ž compressive symptoms (eg, dyspnea,
anaplastic carcinoma dysphagia, hoarseness); very poor prognosis. Associated with TP53 mutation.
-
-

#Treatment of chronic hypoparathyroidism after thyroidectomy:

- calcium and vitamin D supplements but Ca and phosphorus levels must be closely
monitored

—> A calcium-phosphorus product (serum calcium × serum phosphorus) >55

increases the risk of soft tissue calcification causing hypocalcemia and hyper
phosphatemia.

-Calcification in the basal ganglia can cause extrapyramidal manifestations, stones,

cataracts . UWSA2
71) unusual case of pancreatic CA:
-Depression, weight loss, and new-onset DM may occur as early manifestations of
pancreatic cancer.
-Next step. CT of the abdomen as part of the initial diagnostic evaluation.

72) exogenous steroid induced AI 3o

-On abrupt discontinuation of exogenous glucocorticoids, the pituitary gland may be
unable to increase ACTH secretion to meet metabolic demands for up to 6-12 months,
resulting in secondary AI.

-RF: who receives chronic glucocorticoids for ≥3 weeks / those who have cushingoid
features (eg, facial plethora, supraclavicular fat pad).

73) Gastrinoma approach:

-a level >1000 pg/mL is strongly suggestive, although gastric pH should also be
measured as gastrin may also be elevated due to failure of gastric acid secretion
(achlorhydria).

-A gastrin level of 110-1000 pg/mL is nondiagnostic and requires a follow-up

secretin stimulation test.

*Secretin stimulation test:

-Secretin inhibits gastrin release by normal gastric G cells but stimulates gastrin
release by gastrinoma cells; therefore, secretin administration should not cause a rise in
serum gastrin concentrations in patients with other causes of hypergastrinemia.

#Mx:
-Gastrinomas are managed with high-dose PPI
-surgery (eg, exploratory laparotomy and resection) considered in patients with sporadic
gastrinoma with no evidence of metastatic disease.
75) HHS
Common precipitating factors
include:
• Infection
1. • Medications impacting
-
carbohydrate metabolism
(eg, GC, thiazide diuretics,
atypical antipsychotics)

s ± • Interruption of insulin therapy

• Trauma or acute illness (eg,
myocardial infarction)
 #y CNS sx in HHS ??
-Neurologic symptoms ranging
from confusion to coma are due
primarily to high plasma
osmolality, usually >320

-In HHS, plasma osmolality is

elevated due to excess glucose,
drawing water out of cells,
which lowers plasma sodium
(dilution hyponatremia);

I
-however, cerebral edema does
not occur.

DKA HHS
• Glucose 250-500 • Glucose >600 mg/
mg/dL dL (33.3 mmol/L)
• (13.9-27.8 mmol/L) • Bicarbonate >18
-
• Bicarbonate <18
-
• Normal anion gap
• Elevated anion gap • Negative or small
• + s ketones serum ketones
• S osmolality < • Serum osmolality
320 mmol/kg >320 mOsm/kg
e- .

78) Indication for parathyroidectomy in primary hyperPTH:

•Age <50
• Symptomatic hypercalcemia
• Complications: Osteoporosis (T-score <−2.5, fragility fracture), nephrolithiasis/
calcinosis, CKD (GFR <60 mL/min)
• Elevated risk of complications: Calcium >1 mg/dL above normal
• urinary calcium excretion >400 mg/day

*Presurgical evaluation:
-Parathyroid imaging (eg, sestamibi scan, ultrasonography) helps optimize the surgical
approach by potentially determining the affected side and evaluating for the possibility of
a minimally invasive intervention.

79) Resolution of DKA is further supported by

- normalization of the venous pH and serum beta-hydroxybutyrate levels,rise in serum
bicarbonate, and tolerance of oral food intake.
79)Grades of graves ophthalmopathy
a) Mild Proptosis in Graves’ disease:
-Thyroid hormone increases sensitivity to catecholamines, and thyrotoxicosis of any
etiology may cause lid lag and retraction due to sympathetic activation and contraction of
the superior tarsal muscle —> Carries 2 mm of upper lid elevation

b) True exophthalmos that’s moderate to severe Proptosis with impaired

extraocular motion : seen only in Graves disease and is due to T cell activation and
stimulation of orbital fibroblasts and adipocytes by TRAB, resulting in orbital tissue
expansion and lymphocytic infiltration.

80) DI
1 Central DI causes : trauma, hemorrhage, infection, and tumors.

2 Nephrogenic DI results
-The sodium level may be in the high-normal range (intact thirst mechanism).
#Common causes :hypercalcemia, severe hypokalemia, tubulointerstitial renal
disease, and medications.
-drugs: lithium, demeclocycline, foscarnet, cidofovir, and amphotericin.

#Types of DI:
-Based on urine osmolality, DI may be complete (urine osmolality <300 mOsm/kg,
often <100 mOsm/kg) /
- partial (urine osmolality ranges from 300 to 600 mOsm/kg).

81)Moderately increased albuminuria (urine albumin-creatinine ratio of 30-300 mg/g)

—> an early sign of diabetic nephropathy
-Next step: should prompt therapy with ACE I / ARBs
Goals of health maintenance in diabetes mellitus
• Hemoglobin A1c: Every 3 months
Glycemic control
• Goal A1c: ≤7.0%
• Annual random urine albumin/
creatinine ratio*
Nephropathy prevention -

-
• Normal albumin excretion: <30
mg/g
• Regular screening & control of
lipids, blood pressure
Cardiovascular risk • Address lifestyle factors (eg, diet,
factor reduction exercise, smoking, weight)
• Daily aspirin if 10-year CVD risk →
>10%
• Ophthalmologic evaluation
Retinopathy screening
(every 1-3 years) 1 hr later

E-
• Annual comprehensive foot
Neuropathy screening
examination
*Begin at time of diagnosis for type 2 diabetes & 5 years after
diagnosis for type 1.
83) nonfunctioning (gonadotroph) adenoma
-Hypopituitarism with a mild to moderate increase in prolactin suggests a nonfunctioning
- -2
(gonadotroph) adenoma. .

-Patients may develop symptomatic hypogonadism or hypothyroidism but are frequently

asymptomatic until the adenoma becomes very large and causes a mass effect on
surrounding tissues.

- Production of most pituitary hormones (eg, TSH, LH) will be decreased due to
compression of the neighboring normal pituitary cells.

* mechanism of prolactin elevation:

==> By contrast, prolactin are often mildly to moderately elevated due to anatomic
disruption of the dopaminergic neural pathways that normally suppress prolactin
secretion.

Vs
#functional Adenoma:
(A more significant elevation of prolactin [eg, >200 ng/mL] would suggest a
prolactin-secreting adenoma (prolactinoma) rather than a nonfunctioning adenoma.)

84) RAI in ophthalmology:

-titers of TRAB increase significantly following RAI therapy
-
←
#Px:
-For this reason, administration of glucocorticoids with RAI is often advised to prevent
complications in patients with mild ophthalmopathy
-thyroidectomy is preferred over RAI :moderate or severe ophthalmopath

85) The diagnostic test of choice for osteomyelitis : MRI of the foot, which has a
sensitivity >90% and a high negative predictive value.

-Osteomyelitis-related bone changes are present on MRI <5 days after infection onset;
therefore, patients with symptoms for >1 week and a negative MRI are considered "ruled
out" for osteomyelitis.

86) Rx of euthyroid:
-occurs in patients with acute illness primarily due to decreased peripheral conversion of
T4 to T3.
-Rx: Treatment is not recommended unless abnormal thyroid function persists after
the patient has returned to baseline health.
Euthyroid sick syndrome
Early/mild Prolonged/severe
T3 ↓ ↓
T4 Normal ↓
TSH Normal ↓
 Diabetic Nephropathy Pathogenesis

Increased Osmotic Diuresis —>

Dehydration & RAAS activation—>
Increased GFR —>
Glomerular Changes

—>> ACEIs & ARBs have role in DN

by preventing Hyperfiltration &
increased GFR

- Initially, DN is characterized by hyperfiltration (ie,

increased glomerular filtration rate [GFR]);

- however, as the disease progresses, GFR falls,

manifesting as a rising serum creatinine level.

- Concurrently, glomerular protein losses lead to

moderately increased albuminuria (urine protein
excretion 30-300 mg/day; previously termed
microalbuminuria) and eventually severely
increased albuminuria (>300 mg/day).
Nephrotic syndrome
- advanced DN can present with frank proteinuria
and nephrotic syndrome.
 Endo Pedia obgy
1) TSH levels surge in healthy newborns immediately after delivery, leading to a rise
in free T4 and T3: upto 1 week
-This increase in TSH and T4 is physiologic and the basis for neonatal screening for
hypothyro idism.
—> Infants with thyrotoxicosis can have suppression of the normal TSH surge.

2) Neonatal thyrotoxicosis:
-Infants born to women with Graves' disease are at risk for thyrotoxicosis due to passage
of maternal TSH receptor antibodies across the placenta.
-C/F: Affected infants are irritable, tachycardic, and gain weight poorly.
-Rx: Methimazole + β blocker are given to symptomatic patients until the condition
self-resolves over a 3 months.

3) Congenital hypothyroidism:
-Although most neonates with congenital hypothyroidism are asymptomatic at
birth; a rare cause of delayed (>48 hr of life) passage of meconium.
#C/F :
-Supportive findings : constipation, a large fontanelle, hypotonia, and poor feeding and
growth; prolonged jaundice

=
#Dx: elevated TSH and low T4.
-intellectual defect if thyroid supplement not initiated within 2 weeks

4) suspected thyroid nodule in pregnancy:

-patient who has a >1-cm nodule with high-risk sonographic features, workup should
proceed with an FNA, which is safe during pregnancy.
-all pt with >2 cm unless cystic should undergo FNAC

Mx :
—> If a thyroidectomy is needed (due to CA), it can often be delayed until after delivery.
—> However, should the workup reveal a more aggressive or rapidly growing thyroid
cancer, the optimal timing of surgery would be during the second trimester.

5) Anti TPO and miscarriage:

-high titers of anti-TPO are associated with an increased risk of progression to overt
hypothyroidism in both euthyroid and hypothyroid women
 I
#short stature: height at the ≤2nd percentile for sex and age.
-Etio: due to constitutional growth delay / familial short stature.

7) Constitutional growth delay:

-Def: delayed bone age, with a normal linear growth velocity starting at age ≥3.

-They subsequently (eg, age ≥3) grow at a normal rate (ie, normal growth velocity), so their
growth curve remains below but parallel to the lowest percentile line (ie, linear growth
curve).
**Diff clues:
-Their puberty (including the adolescent growth spurt) is delayed,
- bone age (ie, skeletal maturation) is delayed compared to the chronological age.
—>Course: eventually have a normal growth spurt and reach a normal adult height.

-Mx : reassurance and monitoring of linear velocity.

Vs

8) familial short stature

*Similarity: Although these patients have normal linear growth velocity (eg, stable
percentile) similar to constitutional growth delay, one / both parents also have short stature
*Diff:
- have a bone age that correlates with chronologic age, and puberty is not delayed**
- An affected patient's adult height remains low.
 9) Reason for Sx in DKA:
-Without insulin, fatty acids break down to
ketones in the liver, which leads to acidosis
and the clinical manifestations of DKA (eg,
vomiting, abdominal pain).

10) Childrn with DKA are more prone to cerebral edema complication after Rx

11) HHS: acute vision loss can occur due to swelling of lens+ dehydration, polyuria
Vs
-DM retinopathy: gradual vision loss
12) A typical CF growth chart
- normal birth measurements with
subsequent failure to thrive,
characterized by weight deceleration
crossing ≥2 major percentiles (eg, 25th,
10th) followed by a deceleration in
linear growth velocity.

-In addition to malabsorption, recurrent

sinopulmonary infections impair growth
due to poor appetite and increased
metabolic needs during illness
Cardio

#Pain relievers in MI
Venodilation decreases the pain associated
with acute myocardial ischemia by reducing
preload, which leads to a reduction in
myocardial oxygen demand.

-This effect is most commonly caused by the

use of organic nitrates in the setting of
acute myocardial ischemia.
 312 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PATHOLOGY
``

Ischemic heart disease manifestations

Angina Chest pain due to ischemic myocardium 2° to coronary artery narrowing or spasm; no necrosis.
ƒ Stable—usually 2° to atherosclerosis (≥ 70% occlusion); exertional chest pain in classic
distribution (usually with ST depression on ECG), resolving with rest or nitroglycerin.

÷
ƒ Vasospastic (also called Prinzmetal or Variant)—occurs at rest 2° to coronary artery
spasm; transient ST elevation on ECG. Tobacco smoking is a risk factor; hypertension and
hypercholesterolemia are not. Triggers include cocaine, alcohol, and triptans. Treat with Ca2+
channel blockers, nitrates, and smoking cessation (if applicable).
ƒ Unstable—thrombosis with incomplete coronary artery occlusion; +/− ST depression and/or
T-wave inversion on ECG but no cardiac biomarker elevation (unlike NSTEMI);  in frequency
or intensity of chest pain or any chest pain at rest.
Coronary steal Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators
syndrome (eg, dipyridamole, regadenoson) dilates normal vessels Ž blood is shunted toward well-perfused
areas Ž ischemia in myocardium perfused by stenosed vessels. Principle behind pharmacologic
stress tests with coronary vasodilators.
Sudden cardiac death Death occurs within 1 hour of symptoms, most commonly due to lethal arrhythmia (eg, ventricular
fibrillation). Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated),
and hereditary ion channelopathies (eg, long QT syndrome, Brugada syndrome). Prevent with ICD.
Chronic ischemic Progressive onset of HF over many years due to chronic ischemic myocardial damage.
heart disease Myocardial hibernation—potentially reversible LV systolic dysfunction in the setting of chronic
ischemia. Contrast with myocardial stunning, a transient LV systolic dysfunction after a brief
episode of acute ischemia.
Myocardial infarction Most often due to rupture of coronary artery atherosclerotic plaque Ž acute thrombosis.  cardiac
biomarkers (CK-MB, troponins) are diagnostic.
Non–ST-segment elevation MI (NSTEMI) ST-segment elevation MI (STEMI)
Subendocardial infarcts Transmural infarcts
Subendocardium (inner 1/3) especially Full thickness of myocardial wall involved
vulnerable to ischemia
ST depression on ECG ST elevation, pathologic Q waves on ECG

LV RV LV RV LV RV
ST ST

ST

#Tenessey: S4
Kentucky: s3
#amboss: patient has suffered a gunshot wound
to the neck but presents with stable vital signs
and a normal physical examination.

-Stable patients with penetrating neck injuries

should be evaluated for possible injuries to the
trachea, larynx, and neck vessels.

-Multidetector CT angiography is the

recommended imaging modality for the
evaluation of these injuries.
# Normal changes to the aging heart include
-decreased resting and maximal cardiac output,
-decreased maximum heart rate,
-increased contraction and relaxation time of heart muscle,
-increased myocardial stiffness during diastole,
-decreased myocyte number, and pigment accumulation in myocardial cells.
->Increased ventricular wall stiffness contributes to the development of heart failure
with preserved ejection failure (diastolic dysfunction).

—> The adrenal medulla continues to release catecholamines in response to stress (fight
or flight) throughout life.

—> glomerular filtration rate (GFR) tends to decline with old age, a decreased GFR
would promote sodium retention and expansion of the intravascular volume.

—> Progressively decreasing baroreceptor sensitivity and defects in the myocardial

response to this reflex are the main reasons for the increased incidence of orthostatic
hypotension in the elderly.

#orthostatic hypotension in old age:

-In general, orthostatic hypotension results from insufficient constriction of blood vessels
in the lower extremities on standing, which may be due to a defect in autonomic
reflexes, decreased intravascular volume, or medications. 

-Some baroreceptor sensitivity is lost as a normal part of aging. 

-Arterial stiffness, decreased norepinephrine content of sympathetic nerve endings,

and reduced sensitivity of the myocardium to sympathetic stimulation all contribute
to a tendency toward orthostatic hypotension with age.

Type A dissection
Type B aortic dissection
 CARDIOVASCULAR CARDIOVASCULAR—PATHOLOGY
`` SEC TION III 305

Evolution of Commonly occluded coronary arteries: LAD > RCA > circumflex.
myocardial infarction Symptoms: diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw,
shortness of breath, fatigue.
TIME GROSS LIGHT MICROSCOPE COMPLICATIONS
0–24 hr Dark mottling Early coagulative necrosis
-
Ventricular arrhythmia, HF,
Ž cell content released into cardiogenic shock
blood; edema, hemorrhage,
wavy fibers
Occluded
artery
Reperfusion injury Ž free

¥
radicals and  Ca2+ influx
Ž hypercontraction of
Infarct myofibrils (dark eosinophilic
Dark mottling; stripes)
pale with
tetrazolium
stain

1–3 days Extensive coagulative necrosis Postinfarction fibrinous

-
Tissue surrounding infarct pericarditis
shows acute inflammation
with neutrophils
-

Hyperemia

3–14 days Macrophages, then granulation Free wall rupture Ž tamponade;

tissue at margins papillary muscle rupture
Ž mitral regurgitation;
Hyperemic border;
central yellow-brown
=
interventricular septal rupture
due to macrophage-mediated
softening structural degradation Ž left-
to-right shunt
LV pseudoaneurysm (risk of
rupture)
2 weeks to several
months
Contracted scar complete

=
Dressler syndrome, HF,
arrhythmias, true ventricular
aneurysm (risk of mural
thrombus)
Recanalized
artery

Gray-white
scar

#Patients with perioperative MI may lack chest pain and can develop cardiogenic shock
due to left ventricular systolic dysfunction.
-Pulmonary artery catheterization: low cardiac index and elevated PCWP
 306 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PATHOLOGY
``

Diagnosis of In the first 6 hours, ECG is the gold standard.

50

Multiples of upper limit of normal

myocardial infarction Cardiac troponin I rises after 4 hours (peaks Troponin I
at 24 hr) and is  for 7–10 days; more specific
than other protein markers. 10
CK-MB rises after 6–12 hours (peaks at
-
16–24 hr) and is predominantly found
-
5
in myocardium but can also be released CK-MB
Normal
from skeletal muscle. Useful in diagnosing 2
1
reinfarction following acute MI because levels
1 2 3 4 5 6 7 8
return to normal after 48 hours. Days after MI onset
-
Large MIs lead to greater elevations in troponin
I and CK-MB. Exact curves vary with testing
procedure.
ECG changes can include ST elevation
(STEMI, transmural infarct), ST depression
(NSTEMI, subendocardial infarct),
hyperacute (peaked) T waves, T-wave
inversion, new left bundle branch block, and
pathologic Q waves or poor R wave progression
(evolving or old transmural infarct).

ECG localization of INFARCT LOCATION LEADS WITH ST-SEGMENT ELEVATIONS OR Q WAVES

STEMI Anteroseptal (LAD) V1 –V2

E- I
Anteroapical (distal LAD) V3–V4
Anterolateral (LAD or LCX) V5–V6
Lateral (LCX) I, aVL
InFerior (RCA) II, III, aVF
Posterior (PDA) V7–V9, ST depression in V1 –V3 with tall R waves

V6

V5
I aVR V1 V4
Sternum
V4
V3
V1 V2
II aVL V2 V5

aVR aVL

I III aVF V3 V6

Post and inferior wall MI III

aVF
II II
 CARDIOVASCULAR CARDIOVASCULAR—ANATOMY
`` SEC TION III 283

CARDIOVASCULAR—ANATOMY
``

Anatomy of the heart

A LA is the most posterior part of the heart A ; enlargement of the LA (eg, in mitral stenosis) can lead
to compression of the esophagus (dysphagia) and/or the left recurrent laryngeal nerve, a branch of
RV
the vagus nerve, causing hoarseness (Ortner syndrome).
LV
RA
RV is the most anterior part of the heart and most commonly injured in trauma.
LA
pv
Ao

Pericardium Consists of 3 layers (from outer to inner): Pericarditis can cause referred pain to the neck,
ƒ Fibrous pericardium arms, or one or both shoulders (often left).
ƒ Parietal layer of serous pericardium
ƒ Visceral layer of serous pericardium
Pericardial cavity lies between parietal and
visceral layers.
Pericardium innervated by phrenic nerve.
Coronary blood LAD and its branches supply anterior 2/3 of Dominance:
supply interventricular septum, anterolateral papillary ƒ Right-dominant circulation (85%) = PDA
muscle, and anterior surface of LV. Most arises from RCA.
commonly occluded. ƒ Left-dominant circulation (8%) = PDA arises
PDA supplies AV node (dependent on from LCX.
dominance), posterior 1/3 of interventricular ƒ Codominant circulation (7%) = PDA arises
septum, posterior 2/3 walls of ventricles, and from both LCX and RCA.
posteromedial papillary muscle. Coronary blood flow peaks in early diastole.
RCA supplies SA node (blood supply
independent of dominance). Infarct may cause
nodal dysfunction (bradycardia or heart block).
Right (acute) marginal artery supplies RV.

PV
PV
LA LCA LA
LCX SVC
Aorta
SVC OMA
RCA RA
LAD IVC
PT
Key: RA
AMA = Acute marginal artery
LAD = Left anterior descending artery
LCA = Left coronary artery
LCX = Left circumflex artery
OMA = Obtuse marginal artery LV LV
PDA = Posterior descending artery
PT = Pulmonary trunk IVC RV RV
PV = Pulmonary vein
RCA = Right coronary artery AMA PDA
Anterior view Posterior view
290 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PHYSIOLOGY
``

Auscultation of the heart

Where to listen: APT M

Aortic root dilation

¥
Aortic area:
Systolic murmur AP
Aortic stenosis Pulmonic area:
Flow murmur Systolic ejection murmur
1
(eg, physiologic murmur) Pulmonic stenosis
Aortic valve sclerosis Atrial septal defect
2 Flow murmur
Left sternal border: A P
Diastolic murmur 3 Tricuspid area:
Aortic regurgitation Holosystolic murmur
(valvular)
Pulmonic regurgitation
4 Tricuspid regurgitation
Ventricular septal defect
VT
Systolic murmur T Diastolic murmur
5
Hypertrophic Tricuspid stenosis
cardiomyopathy M
Aortic 6
Mitral area (apex):
Pulmonic Holosystolic murmur
Tricuspid 7
Mitral regurgitation
Mitral
Systolic murmur
Mitral valve prolapse
Diastolic murmur
Mitral stenosis
MANEUVER CARDIOVASCULAR CHANGES MURMURS THAT INCREASE WITH MANEUVER MURMURS THAT DECREASE WITH MANEUVER
Standing Valsalva  preload ( LV volume) MVP ( LV volume) Most murmurs ( flow through
(strain phase) HCM ( LV volume) stenotic or regurgitant valve)
Passive leg raise  preload ( LV volume)
Most murmurs ( flow through MVP ( LV volume)
Squatting  preload,  afterload ( LV stenotic or regurgitant valve) HCM ( LV volume)
volume)
Hand grip  afterload Ž  reverse flow Most other left-sided murmurs AS ( transaortic valve pressure
-
across aortic valve ( LV (AR, MR, VSD) gradient)
volume) HCM ( LV volume)
Inspiration  venous return to right heart, Most right-sided murmurs Most left-sided murmurs
 venous return to left heart
 310 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PATHOLOGY
``

Atherosclerosis Very common. Disease of elastic arteries and large- and medium-sized muscular arteries; a form of
-
arteriosclerosis caused by buildup of cholesterol plaques in intima.
LOCATION Abdominal aorta > coronary artery > popliteal artery > carotid artery > circle of Willis.
A copy cat named Willis.
RISK FACTORS Modifiable: hypertension, tobacco smoking, dyslipidemia ( LDL,  HDL), diabetes.
Non-modifiable: age, male sex, postmenopausal status, family history.
SYMPTOMS Angina, claudication, but can be asymptomatic.
PROGRESSION Inflammation important in pathogenesis: endothelial cell dysfunction Ž macrophage and LDL
accumulation Ž foam cell formation Ž fatty streaks Ž smooth muscle cell migration (involves
PDGF and FGF), proliferation, and extracellular matrix deposition Ž fibrous plaque Ž complex
atheromas A Ž calcification (calcium content correlates with risk of complications).
COMPLICATIONS Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli.
Normal Endothelial Fatty streak Fibrous plaque
artery dysfunction formation formation
A

Lumen

LDL-laden Foam cell Smooth muscle Smooth

Endothelium Macrophage macrophage migration muscle
Smooth muscle Damaged endothelium Fatty streak
Fibrous plaque

Aortic aneurysm Localized pathologic dilation of the aorta. May cause abdominal and/or back pain, which is a sign
of leaking, dissection, or imminent rupture.

=
I
Abdominal aortic Usually associated with atherosclerosis. Risk factors include history of tobacco use,  age, male
aneurysm sex, family history. May -present as palpable pulsatile abdominal mass (arrows in A point to outer
A dilated calcified aortic wall, with partial crescent-shaped nonopacification of aorta due to flap/
clot). Most often infrarenal (distal to origin of renal arteries).

Liver
Sp

Thoracic aortic Associated with cystic

-
medial degeneration. Risk factors include hypertension, bicuspid aortic
aneurysm valve, connective tissue disease (eg, Marfan syndrome). Also associated with 3° syphilis
(obliterative endarteritis of the vasa vasorum). Aortic root dilatation may lead to aortic valve
-
regurgitation.

#Chronic systemic hypertension is the most important risk factor for aortic dissection,
especially in older patients (age >60). -

-Marfan syndrome is common in young patients (age <40) with aortic dissection, but it is rare
in older patients with dissection.
 Cardiac Surg obgy clue
1) pulmonary stenosis
-Systolic ejection click (high-pitch sound after S1 best heard during expiration)
followed by a crescendo-decrescendo systolic murmur over the left second
intercostal space (↑ on inspiration)

2) post CABG Acute mediastinitis :

-fever, chest pain, leukocytosis, and mediastinal widening on chest x-ray.
-Mx: drainage, surgical debridement, and prolonged antibiotic therapy.

3) post cardiac catheterization Cx:

# arteriovenous fistula
-mild localized pain and swelling ;continuous bruit +palpable thrill over the fistula site.
Vs
Femoral artery pseudoaneurysm: tender, pulsatile mass with an audible systolic
(rather than a continuous) bruit.
As soon as acute limb ischemia is clinically diagnosed,
4) 6 Ps of acute limb ischemia anticoagulation (eg, intravenous heparin infusion)
Pain; Pallor; Paresthesia should be initiated which prevents thrombus
Pulselessness; Poikilothermia propagation and distal thrombosis
(cool extremity); Paralysis
(late) • Immediate 1st line: Anticoagulation (eg, heparin)
• 2nd line: percutaneous thrombolysis (eg, alteplase) or
5) HOCM: surgical thrombectomy
-carotid pulse : dual upstroke due to midsystolic obstruction during cardiac
contraction. -systolic ejection murmur along the left sternal border with a strong apical
impulse.

6) MCC of SCD in adolescent : HOCM followed by long QT

Adults: CAD

7) VSD:
-Holosystolic murmur at lower left sternal border
-An apical diastolic rumble may also be heard from increased flow across the mitral valve
(from increased left-to-right shunting across the VSD).
—>As right ventricular pressure increases due to increased flow, the S2 will become more
prominent due to increased pressure closing the pulmonary valve.

8) TOF:
-PS harsh, systolic ejection murmur at the left upper sternal border is more prominent than
VSD murmur.
-tet spells (hypoxia, cyanotic episodes) while feeding

-Mx: improves with knee chest position and O2 as it increases the systemic resistance
9) Persistent pulmonary hypertension:
- ↓ Postductal relative to preductal oxygen saturation but NO BRACHIOFEMORAL
DELAY like coarctation of aorta

10) HOCM in DM mother infants: by fat and glycogen deposition

- LV septal Hypertrophy, mild RS distress but NO cyanosis; regress by 1 yr;
Vs

#Hypoplastic left heart syndrome (HLHS):

-Although left ventricular hypertrophy can occur in this condition, isolated hypertrophy of the
interventricular septum is not expected.
-although HLHS causes respiratory distress, cyanosis is always present
11) Benign murmur:
Early or midsystolic; Musical or vibratory; Grade 1-2 intensity; Decreases or
disappears with standing & Valsalva maneuver*
_

—>exception: Venous hum is a benign murmur exception that increases with

standing.
Vs
#Pathological murmur:
-holosystolic/ diastolic; harsh;grade >/=3; intensity persist with standing/ valsalva

12) Use of PDA patency in CHD

1) CoA: to provide Systemic blood flow via right-to-left ductal shunting
2) Tetralogy of Fallot : provide blood flow to the pulmonary circulation from the aorta
(ie, left-to-right shunt).
13) Vascular rings
PDA-dependent congenital heart - congenital malformations of the great vessels that
disease encircle and compress the trachea and/or
• Coarctation of the aorta esophagus.
• D-transposition of the great arteries
• Hypoplastic left heart syndrome
-RS symptoms : biphasic stridor that improves with
• Total anomalous pulmonary venous neck extension.
connection -Esophageal Sx: dysphagia, vomiting, and difficulty
• Tricuspid atresia
feeding
Vs
Infective Etiology: fever, pharyngitis, acute onset

14) Peripartum cardiomyopathy

-onset of SHF during last month of pregnancy/within 5 months following delivery
- absence of other causes of HF; absence of other heart disease prior to final month
-signs: S3; LVEF < 45%
-next best step: echo ; delivery if advanced HF and unstable

15) degree of LV dysfunction in alcoholic dilated cardiomyopathy directly proportional to

daily amount and overall duration of alcohol.
—> Abstinence normalises LV function.
14) Retroperitoneal hematoma: can even occur at supratherapeutic INR
-patient’s back pain + sigs of internal hemorrhage (dizziness, weakness, normal vitals) —
> put retroperitoneal hematoma high on the differential, and warrants an abdominal CT.

15) Acute aortic dissection:

• History of HTN*, Marfan syndrome, cocaine use
• Severe, sharp, tearing chest or back pain
• ± >20 mm Hg variation in SBP between arms

#Rx: IV beta blockers (eg, labetalol, esmolol) are the Rx of choice for the initial Mx
-MOA: lower heart rate and blood pressure and reduce left ventricular contractility.

16) Leriche syndrome: the triad of:

• Bilateral hip, thigh, and buttock claudication

• Absent / diminished femoral pulses: from the groin distally, often with symmetric
atrophy of the bilateral lower extremities due to chronic ischemia
• Impotence: almost always present in men with this condition; in the absence of
impotence, an alternate diagnosis

17) Cardiac Tamponade

- hypotension, tachycardia, distended jugular veins, and respiratory variation in systolic
blood pressure (ie, pulsus paradoxus)

18) Femoral artery aneurysm

- 2nd MC peripheral artery aneurysm after popliteal aneurysm
-C/F: pulsatile groin mass with continuous bruit below the inguinal ligament is characteristic;
anterior thigh pain is due to the compression of the femoral nerve that runs lateral to
the artery.

19) Ventricular aneurysm

-a late complication (ie, several months) following transmural myocardial infarction,
-ECG : persistent ST-segment elevation with deep Q waves.
-C/F: CHF; echo: dyskinetic wall motion leading to heart failure.

20) acquired ventricular septal defect :

-onset: complication of MI, typically 3-5 days post-infarction.
-C/F: sudden-onset hypotension and biventricular failure

21) Right ventricular infarction

-hypotension, elevated JVP, and clear lung fields,
- ECG : ST-segment elevation in the inferior leads (II, III, aVF).
-Evidence of pulmonary edema makes right ventricular infarction less likely.
 Mechanical complications of acute myocardial infarction
Involved
Complication
Time
coronary
Clinical Echocardiogram Valve replacement in aortic stenosis
course findings findings
artery • Aortic jet velocity ≥4.0
• m/sec, or
Hypotensio • Mean transvalvular
Right Severe AS criteria
n • Hypokinetic
ventricular Acute RCA pressure gradient ≥40
• Clear lungs RV
failure
• Kussmaul mm Hg
sign • Valve area usually ≤1.0
• Severe Severe AS & ≥1 of the
pulmonary • Severe mitral following:
Acute or
Papillary edema regurgitation
within RCA • Onset of symptoms (eg,
muscle rupture • New with flail
3-5 days
holosystoli leaflet Indications for angina, syncope)
c murmur valve replacement • Left ventricular ejection
fraction <50% -
• Chest pain -
LAD • New • Left-to-right • Undergoing other cardiac
(apical holosystoli ventricular surgery (eg, CABG)
Acute or shunt
Interventricular septal) or c murmur
within

for
septum rupture RCA • • ↑ O2 level
3-5 days
(basal Biventricul from RA to
septal) ar failure RV
• Shock
• Chest pain
Within 5 • Shock • Pericardial
Free wall
days* to LAD • Distant effusion with
rupture
2 weeks heart tamponade
sounds
• Subacute
• Thin &
Up to heart
Left ventricular dyskinetic
several LAD failure
aneurysm myocardial
months • Stable
wall
angina
*50% occur within 5 days.
LAD = left anterior descending; RA = right atrium; RCA = right coronary
artery; RV = right ventricle.

22) Sternal dehiscence

- a complication of cardiac surgery characterized by separation of the bony edges of the
sternum.
-C/F: report mild pain or sensation of chest wall instability , palpable rocking nd
clicking" with chest movement.
-Management : urgent surgical exploration and repair.

23) Abdominal aortic aneurysm:

-Other clues - pulsatile abdominal mass and prevertebral aortic calcification on
plain x-ray, consistent with extensive atherosclerosis.
-Proximal aneurysms : upper abdominal, flank, or back pain,
-whereas distal lesions :lower abdominal or groin pain.
—> In the event of rupture, hemorrhage usually occurs into the retroperitoneum/ anterior

* AAA rupture can present similarly to acute pyelonephritis but lacking fever,
urinary Sx
#Classic case: patient with RF for AAA comes with sudden-onset, severe abdominal
pain, hemodynamic instability (eg, symptomatic hypotension with weakness and
diaphoresis), and flank ecchymoses likely has a ruptured abdominal aortic aneurysm
24) Bowel ischemia Following AAA repair
-Bowel ischemia and infarction are possible early complications of operation on the
abdominal aorta, such as AAA repair.
-C/F: abdominal pain and bloody diarrhea.  Fever and leukocytosis may also be
present

25) hard signs of vascular injury:

• Observed pulsatile bleeding
• Presence of a bruit or thrill over the injury
• Expanding hematoma
• Signs of distal ischemia (eg, absent pulses, cool extremities)
-Mx: In the presence of a penetrating injury, such signs (with or without hemodynamic
instability) are almost universally predictive of the need for urgent surgical repair and
warrant immediate exploration

26) soft signs:

-If hard signs are absent, further evaluation for soft signs (eg, history of hemorrhage,
diminished pulses, bony injury, neurologic abnormality) should occur.
#Mx:
-If present, these signs indicate the need for additional testing such as
1)the injured extremity index (similar to ankle-brachial index)
2) If the index is abnormal (<0.9), patients should be considered for CT scan / conventional
arteriography and surgery in conjunction with management of other injuries (eg, bony
damage)

27) purulent pericarditis:

-C/F: fever, chills, leukocytosis with left shift, new arrhythmia, and a moderate pericardial
effusion on echocardiography.
Vs
Acute endocarditis: similar to above but murmurs +
Vs
Viral pericarditis: pleurisy, tachycardia, fever,small pericardial effusion
#venous hum is a common benign finding on Vasospastic angina
auscultation in childhood. The murmur is most • Hyperreactivity of coronary smooth
Pathogenesis
likely caused by turbulence in the internal jugular muscle

vein (e.g., when blood enters the thoracic inlet). • Young patients (age <50)
• Smoking (minimal other CAD risk
Although typically a continuous murmur that can Clinical
factors)
• Recurrent chest discomfort
occur on either side of the neck, it tends to be presentation
◦Occurs at rest or during sleep
louder during diastole and is more common on the ◦Spontaneous resolution <15
minutes
right. •Ambulatory ECG: ST elevation
Diagnosis
The murmur disappears or becomes softer when •Coronary angiography: No CAD
patients compress the internal jugular vein, in the Treatment
• CCB (preventive) diltiazem
• SL nitroglycerin (abortive)
supine position or flex their heads.This feature
helps differentiate it from the murmur in a patent
28) prosthetic valve dysfunction (PVD)
-A regurgitant murmur over a prosthetic valve suggests(PVD) in the form of a
paravalvular leak (> with mechanical valve) or transvalvular regurgitation (> with
bio prosthetic valve)
-C/F: serious complications (eg, heart failure) so should be promptly evaluated with
echocardiography.

—> To prevent PVT, patients with prosthetic valves are kept on antithrombotic therapy.
1) Mechanical prosthetic valves are more thrombogenic and require
anticoagulation.

2) Bioprosthetic valves are less thrombogenic and typically require only aspirin
therapy; however, PVT can still occur.

29) Venous graft failure following CABG surgery

-typically presents with a recurrence of symptoms of stable angina (eg, exertional
pressure-like chest pain).

30) Myocardial contusion :

- It has no specific chest x-ray findings, although sternal fracture should raise
suspicion.
- typically diagnosed by ECG (showing arrhythmia or new bundle branch block) or
echocardiography (showing wall motion abnormality or decreased contractility).

31) Pulmonary contusion :

- It causes parenchymal hemorrhage and edema that manifests as irregular,
nonlobular opacities.

33) When an infant with CHD has mixing oxygenated blood to deoxygenated blood
without MURMURS on examination then Dx is —>> through a patent foramen ovale.

34) Transposition of great vessel:

-cyanosis within 24 hours of life, a single S2 on auscultation (absent pulmonary
component of S2 because the aorta is anterior to the pulmonary artery), and a narrow
mediastinum ("egg on a string") on x-ray.

35) *Congenital contractural arachnodactyly is an autosomal dominant condition

resulting from mutations of the fibrillin-2 gene.

-C/F: tall stature, arachnodactyly, and multiple contractures involving large joints.

-Vs fibrillin 1 in marfan

34) source of DVT:
-Lower extremity deep vein thrombosis (DVT) is divided into 2 categories:
• Proximal/thigh (eg, iliac, femoral, popliteal): These are the source of >90% of
acute PEs, probably due to their large caliber and proximity to the lungs.

• Distal/calf: Although most DVTs occur in the calf vein, distal/calf DVTs are less likely
than proximal/thigh DVTs to embolize to the lungs and cause PE
-more likely to spontaneously resolve

#Thrombi originating from the renal veins : most common in patients with nephrotic
syndrome. The prevalence of PE in patients with nephrotic syndrome is 10%-30%.

35) Severe aortic coarctation,

- increases left ventricular afterload, can present in the neonatal period with
congestive heart failure (eg, respiratory distress, poor feeding) + cardiogenic
shock upon closure of the ductus arteriosus.

36) Mx of IE:
-Intravenous antibiotics decrease the risk of septic embolic events in patients with
native valve infective endocarditis.
#indications of valve Sx:
- stroke, significant valvular dysfunction, persistent/difficult to treat infection, or recurrent
embolism.
—> Mitral - 1st M/C involved in
IE, MVP and associated MR have
5-8 times higher risk of IE than
normal

—> Aortic - 2nd M/C involved in

IE, usually in congenital bicuspid
aortic valve with associated AS

- AR is less frequently seen in IE

Viral pleuritis (viral pleurisy)
• Viral prodrome (eg, cough,
rhinorrhea)
Clinical
• Pleuritic chest pain
presentati
• Shallow breathing & dyspnea
on
• Pleural friction rub
• Absence of pleural effusion
• Supportive care & analgesia
Treatment
with NSAIDs

Vs reflux esophagitis pain improves with sitting

 Infective endocarditis—modified Duke criteria 37) Post CABG pleural effusion:
Major criteria
• Blood culture positive for typical
1) small PE:
microorganism A] Post–cardiac surgery effusions that
• (eg, Staphylococcus aureus, Enterococcus,
viridans streptococci) meet the following criteria can be managed
• Echocardiogram showing valvular
vegetation
conservatively with observation only:
Minor criteria •Small to moderate in size and not
• Predisposing cardiac lesion
Diagnostic criteria • Intravenous drug use enlarging
for IE • Temperature >38 C (100.4 F)
• Embolic phenomena •Early onset (postop day 1 or 2)
• Immunologic phenomena (eg,
glomerulonephritis)
•Not associated with RS Sx
• Positive blood culture not meeting above
criteria
Definite IE B] Effusions that do not meet the above
• 2 major OR 1 major + 3 minor criteria
Possible IE
criteria should be actively investigated
• 1 major + 1 minor OR 3 minor criteria and treated
•
•
Fever (>90%)
Heart murmur (85%)
-because they may be due to serious post–
• Petechiae (≤50%) cardiac surgery complications, including
Clinical findings • Subungual splinter hemorrhages (<50%)
(frequency) • Osler nodes, Janeway lesions (<50%) hemothorax, central line erosion into the
•
•
Neurologic phenomena (embolic) (≤40%)
Splenomegaly (≤30%)
pleural space, mediastinitis, chylothorax,
• Roth spots (retinal hemorrhage) (<5%) and MI with HF
IE = infective endocarditis.

2) Large Pleural Effusion after CABG :

- Mx :
1) diagnostic thoracentesis and fluid
analysis.
2) Chest tube placement

38) unusual cardiac tamponade

-Patients with chest pain, signs of decreased
cardiac output, and pulsus paradoxus following a
viral infection most likely have cardiac
tamponade resulting from acute pericarditis.

-In this setting, right atrial filling is impaired,

which results in an increase in the systemic
venous pressure.
-However, the lungs remain clear to auscultation
because there is no backup of blood into the
pulmonary circulation.
 Surgical indications for severe chronic mitral
valve regurgitation
• Surgery if LVEF 30%-60%
(regardless of symptoms)
Primary • Consider surgery if successful
MR valve repair* is highly likely:
◦ Asymptomatic & LVEF >60%
◦ Symptomatic & LVEF <30%
Secondar • Medical management, valve
y MR surgery rarely indicated
*When possible, durable valve repair is favored over
replacement because replacement necessitates
lifelong anticoagulation & repeat replacement is
often needed after ~10 yr.

41) chest contusions with hypotension after trauma:

-Aortic rupture: flat veins ;hypovolemic shock
Vs
Cardiac tamponade: neck vein distended, obstructive
shock
42) Causes of pleuritic chest pain: costochondritis, pericarditis, malignancy, and infection
(pneumonia).

#postcardiac injury/ dressier: pleurisy+ diffuse ST elevation; Rx: NSAIDS+ colchicine

Vs
PE post MI Sx: pleurisy+ nonspecific ST changes+ U/L leg edema and pain

43) Renovascular hypertension

- suspected in all patients with resistant hypertension and diffuse atherosclerosis,
asymmetric kidney size, recurrent flash pulmonary edema, /

—> elevation in serum creatinine >30% from baseline after starting an ACEI/ ACRB
—> The presence of a continuous abdominal bruit has a high specificity for the presence
of renovascular hypertension.

==> systolic diastolic bruit is highly specific

-can have unequal BP on both arms but no pain like aortic dissection
44) Post Cardiac Sx Cxs :
1) Bacterial mediastinitis :
- fever, chest pain, and incisional purulence, dehiscence/crepitus within 2 wk of surgery.

2) Hemopericardium :
cardiac tamponade —> hypotension.

3) Venous graft failure following CABG surgery :

- recurrence of symptoms of stable angina (eg, exertional pressure-like chest pain).

45) Dual antiplatelet therapy:

-reduces the risk of stent thrombosis and is recommended in all patients for at least 12
months following drug-eluting stent placement.

46) Rx of long QT syndrome:

a) beta blockers (class II antiarrhythmics) dampen sympathetic activity and shorten the
QT interval at rapid heart rates to reduce the risk of syncope and death in congenital
LQTS; this benefit is most prominent withnonselective beta blockers,propranolol and
nadolol.

b) Implantable cardioverter-defibrillator placement or left cardiac sympathetic

denervation are also appropriate in some high-risk patients.

47) What if intolerant of one high-intensity statin??

-2nd line: switching to a different high-intensity or a moderate-intensity statin should
be considered
-3rd line: ezetimibe/ p2cki prevents intestinal brush enzymes
.

48) Acute limb ischemia after MI

-suggests embolization of a left ventricular (LV)
thrombus.
-Next step: Transthoracic echocardiography
should be performed to screen for LV aneurysm
and/or residual LV thrombus

49) Cardiac tamponade: pericardiocentesis

Vs
#constrictive pericarditis: pericardiectomy

-Sephanous Varix: venous hum

-without any RF for fistula, spontaneous continuous bruit with a mass: femoral artery
aneurysm amboss
50) malignant pericardial effusion
Lung cancer is the MC primary tumor implicated in malignant pericardial effusion (MPE).

#C/F:
-subacute (rather than rapid) accumulation of pericardial fluid accompanied by progressive
stretching of the pericardium.

-only nonspecific symptoms (eg, dyspnea, fatigue) until enough fluid accumulates
(typically 1-2 L) to increase intrapericardial pressure and compromise cardiac function (ie,
cardiac tamponade).
#Rx:
• Acute management: pericardiocentesis, cytologic fluid analysis
• Prevention of recurrence: prolonged drainage (eg, catheter, pericardial window)

51) secondary (functional) MR:

-Decompensated heart failure is a common cause of secondary (functional) mitral
regurgitation.
#Pathogenesis
-Increased (LVEDV) causes impaired valve closure due to dilation of the mitral valve
annulus and lateral papillary muscle displacement with restricted movement of the
chordae tendineae.

-Mx: MR resolves with reduction in LVEDV, resulting in disappearance of the associated

murmur.

52) MVP timings:

-manoeuver increasing LV cavity: midsystolic click occurs later in systole
- =
-manoeuver decreasing LV cavity: midsystolic click occurs earlier in systole
-Very enlarged LV cavity eg in HF: cusp never meet each other; so click disappear

53) D/D of HF after aortic dissection:

a) AR:
-Ascending aortic dissection can propagate proximally from the site of intimal tear to
involve the aortic valve—>causing acute AR and HF: pulm edema
Vs
b) Cardiac tamponade
-can be differentiated from acute AR by an absence of pulmonary edema.
54) Approach of blunt chest trauma:
-1st step: All patients with blunt chest trauma require a Cxray after primary trauma survey

# if blunt aortic injury suspected:

a) CT Angiography :for hemodynamically stable patients

b) Transesophageal echocardiography (likely in the operating room)

- For unstable, hypotensive patients

55) TR after Transvenous lead

-This complication should be suspected in patients presenting with RHF following
implantable pacemaker / cardioverter-defibrillator placement.

56) abdominal aortic aneurysm rupture:

May present with severe costovertebral tenderness mimicking Renal infarction
But
#Acute renal infarction :
- It presents with abdominal or flank pain accompanied by hypertension (rather than
hypotension) due to increased renin secretion.

57) Aortoenteric fistula

- an abnormal connection between the aortoiliac vessels and the GIT;
-C/F: abdominal pain, GIT bleeding, and hypotension.

59) Mx of shock:
-Patients with sepsis who do not achieve a mean arterial pressure (MAP) >60 mm Hg
after adequate fluid repletion (eg, septic shock) require a vasopressor to improve
MAP to goal range.
-The first-line vasopressor agent for septic shock : norepinephrine, which causes
significant peripheral vasoconstriction and moderate increase in cardiac output.

-Titration to achieve a MAP : 60-70 mm Hg and urine output : 0.5 mL/kg/hr is

indicated.
 Cardio ped

==> Systolic ejection murmur in the left sternal border consistent with pulmonic stenosis
(as seen in Tetralogy of Fallot) and history of becoming cyanotic while crying also
consistent with Tetralogy of Fallot
306 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PATHOLOGY
``

CARDIOVASCULAR—PATHOLOGY
``

Congenital heart diseases

RIGHT-TO-LEFT SHUNTS Early cyanosis—“blue babies.” Often diagnosed The 5 T’s:
prenatally or become evident immediately 1. Truncus arteriosus (1 vessel)
after birth. Usually require urgent surgical 2. Transposition (2 switched vessels)
treatment and/or maintenance of a PDA. 3. Tricuspid atresia (3 = Tri)
4. Tetralogy of Fallot (4 = Tetra)
5. TAPVR (5 letters in the name)
Persistent truncus Truncus arteriosus fails to divide into
arteriosus pulmonary trunk and aorta due to failure of
aorticopulmonary septum formation; most
patients have accompanying VSD.
D-transposition of Aorta leaves RV (anterior) and pulmonary trunk
Aorta
great vessels leaves LV (posterior) Ž separation of systemic Pulmonary
A and pulmonary circulations. Not compatible artery
with life unless a shunt is present to allow
mixing of blood (eg, VSD, PDA, or patent
foramen ovale).
Left
Due to failure of the aorticopulmonary septum to ventricle
spiral (“egg on a string” appearance on CXR) A .
Without surgical intervention, most infants die Right
within the first few months of life. ventricle

Tricuspid atresia Absence of tricuspid valve and hypoplastic RV;

requires both ASD and VSD for viability.
Tetralogy of Fallot Caused by anterosuperior displacement of the PROVe.
B
infundibular septum. Most common cause of Squatting:  SVR,  right-to-left shunt, improves
early childhood cyanosis. cyanosis.
Pulmonary infundibular stenosis (most Associated with 22q11 syndromes.
important determinant for prognosis)
Right ventricular hypertrophy (RVH)—
boot-shaped heart on CXR B
Overriding aorta S
VSD Q
Pulmonary stenosis forces right-to-left flow T
across VSD Ž RVH, “tet spells” (often
R
caused by crying, fever, and exercise due to
exacerbation of RV outflow obstruction).

Total anomalous Pulmonary veins drain into right heart

pulmonary venous circulation (SVC, coronary sinus, etc);
return associated with ASD and sometimes PDA to
allow for right-to-left shunting to maintain CO.
Ebstein anomaly Displacement of tricuspid valve leaflets Can be caused by lithium exposure in utero.
downward into RV, artificially “atrializing”
the ventricle. Associated with tricuspid
regurgitation, accessory conduction pathways,
right-sided HF.
 CARDIOVASCULAR CARDIOVASCULAR—PATHOLOGY
`` SEC TION III 307

Congenital heart diseases (continued)

LEFT-TO-RIGHT SHUNTS Acyanotic at presentation; cyanosis may occur Right-to-left shunts: early cyanosis.
years later. Frequency: VSD > ASD > PDA. Left-to-right shunts: “later” cyanosis.

÷
Ventricular septal Asymptomatic at birth, may manifest weeks O2 saturation  in RV and pulmonary artery.
defect later or remain asymptomatic throughout life.
C
Most self resolve; larger lesions C may lead to
LV overload and HF.

VSD LV
RV

Atrial septal defect Defect in interatrial septum D ; wide, fixed split O2 saturation  in RA, RV, and pulmonary
D
S2. Ostium secundum defects most common artery. May lead to paradoxical emboli
ASD
and usually an isolated finding; ostium (systemic venous emboli use ASD to bypass
primum defects rarer and usually occur lungs and become systemic arterial emboli).
with other cardiac anomalies. Symptoms Associated with Down syndrome.
range from none to HF. Distinct from patent
foramen ovale in that septa are missing tissue
rather than unfused.
Patent ductus In fetal period, shunt is right to left (normal). PDA is normal in utero and normally closes only
arteriosus In neonatal period,  pulmonary vascular after birth.
E
resistance Ž shunt becomes left to right
Ž progressive RVH and/or LVH and HF.
Associated with a continuous, “machine-like”
murmur. Patency is maintained by PGE
synthesis and low O2 tension. Uncorrected
PDA E can eventually result in late cyanosis

Ei
in the lower extremities (differential cyanosis).
Eisenmenger Uncorrected left-to-right shunt (VSD,
syndrome ASD, PDA) Ž  pulmonary blood flow
Ž pathologic remodeling of vasculature
Ž pulmonary arterial hypertension. RVH
occurs to compensate Ž shunt becomes right
to left. Causes late cyanosis, clubbing, and
polycythemia. Age of onset varies depending
on size and severity of initial left-to-right
shunt.

OTHER ANOMALIES
Coarctation of the Aortic narrowing F near insertion of ductus arteriosus (“juxtaductal”). Associated with bicuspid
aorta aortic valve, other heart defects, and Turner syndrome. Hypertension in upper extremities and

=
F
weak, delayed pulse in lower extremities (brachial-femoral delay). With age, intercostal arteries
Coarct
enlarge due to collateral circulation; arteries erode ribs Ž notched appearance on CXR.
Complications include HF,  risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and
possible endocarditis. -
Desc
Asc -
Ao
Ao
 308 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PATHOLOGY
``

Congenital cardiac ASSOCIATION DEFECT FAT .

defect associations Prenatal alcohol exposure (fetal alcohol VSD, PDA, ASD, tetralogy of Fallot
syndrome)
Congenital rubella IP PDA, pulmonary artery stenosis, septal defects
Down syndrome AV septal defect (endocardial cushion defect),
VSD, ASD
Infant of patient with diabetes during pregnancy →
Transposition of great vessels, VSD
Marfan syndrome MVP, thoracic aortic aneurysm and dissection,
aortic regurgitation
Prenatal lithium exposure Ebstein anomaly
Turner syndrome Bicuspid aortic valve, coarctation of aorta
Williams syndrome Supravalvular aortic stenosis
22q11 syndromes Truncus arteriosus, tetralogy of Fallot

Hypertension Persistent systolic BP ≥ 130 mm Hg and/or diastolic BP ≥ 80 mm Hg.

RISK FACTORS  age, obesity, diabetes, physical inactivity, high-sodium diet, excess alcohol intake, tobacco
smoking, family history; incidence greatest in Black > White > Asian populations.
FEATURES 90% of hypertension is 1° (essential) and related to  CO or  TPR. Remaining 10% mostly 2°
A to renal/renovascular diseases such as fibromuscular dysplasia (characteristic “string of beads”
appearance of renal artery A , usually seen in adult females) and atherosclerotic renal artery
stenosis or to 1° hyperaldosteronism.
Hypertensive urgency—severe (≥ 180/≥ 120 mm Hg) hypertension without acute end-organ
damage.
Hypertensive emergency—severe hypertension with evidence of acute end-organ damage (eg,
encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection,
kidney injury,- microangiopathic hemolytic anemia, eclampsia). .

PREDISPOSES TO CAD, LVH, HF, atrial fibrillation; aortic dissection, aortic aneurysm; stroke; CKD (hypertensive
nephropathy); retinopathy.

#Divine:
- VSD develops concentric hypertrophy in right heart due to pulm HT and eccentric
in left heart cz of increase overload from right Hrt (increase load so dilated ) —>
lungs (pulm Ht) —> left Hrt

- ASD is usually in septum Secundum; if it’s in septum primum then it’s associated
with down
1) viral Myocarditis
- most commonly caused, in children, by viral infection CXK, adeno
-C/F: typically presents following a viral prodrome with signs of heart failure (eg,
respiratory distress, murmur, cardiomegaly, hepatomegaly
-Onset: days-weeks vs few weeks In ARF

-Mx: Supportive (eg, diuretics, inotropes); IV immunoglobulin

2) PDA-dependent congenital heart disease

-1-day-old neonate has rapid onset of hypotension, cyanosis, and hypoxia that fails to
improve with 100% inspired oxygen (hyperoxia challenge).
Moderate or large ventricular septal defect
Antibiotic prophylaxis for secondary prevention
Timeline Pathophysiologic changes of rheumatic fever
• RV & LV pressures equal Severity
Duration of therapy
In utero • No significant hemodynamic following last attack
consequences Uncomplicated rheumatic
5 years / until 21*
fever
Postnatal • ↓ PVR, ↑ SVR
With carditis but no valvular
transition • Left-to-right shunting through VSD disease
10 years / until 21*

• RV volume overload/dilation
a With carditis & valvular

↳
Infancy 10 years / until 40*
• Pulmonary overcirculation disease
RHF Sx
• LA & LV volume overload/dilation *Whichever duration is longer.
-IM penicillin G benzathine every 3-4 weekly
• Pulmonary arterial vascular
thickening (↑ PVR)
Late childhood
• Right-to-left shunting through VSD
(ie, Eisenmenger syndrome)

2) Right atrial enlargement :

- can give the appearance of
As pulm is behind aorta
cardiomegaly.
-
- Infants age <1 year normally have a
transverse cardiothoracic ratio of
<60%.
- Children age >1 year and adults
should have a cardiothoracic ratio of

Do
<50%.

L
-
6) Syncope in children
-Most are benign cause (eg, reflex syncope, orthostatic hypotension), but some have a
cardiac etiology (eg, arrhythmia, Long QT; brugada) that may cause SCD if not dx.

**Clues in the history that suggest a cardiac cause

absence of prodromal symptoms, syncope with exertion) require further
investigation

The best next step in this patient is ECG

#Cx of cardiac syncope in kids:

-These syndromes increase the risk of life-threatening ventricular tachycardia.
-Acute arousal, as with a sudden auditory stimulus (eg, fire engine siren), can
trigger arrhythmia in long QT syndrome.

Vs
#Seizure activity (diagnosed on EEG)
-can cause LOC with jerking movements; other suggestive features (eg, prodromal
aura, tongue laceration, postictal period) are typically present.

==> Muscle jerks can occur in all types of syncope because sudden cerebral
hypoperfusion often causes brief myoclonus.

7) ASD:
1 Wide and fixed splitting of the second heart sound (S2):
-from delayed closure of the pulmonic valve due to RHF by LfT—> Rt shunt

2 Mid-systolic / ejection murmur over the left upper sternal border:

-Resulting from increased flow across the pulmonic valve.
-The low-velocity left-to-right shunt flow across the ASD itself does not produce any
audible murmur.
3 Mid-diastolic rumble: Resulting from increased flow across the tricuspid valve
 CVS medicine
1) AF:pulmonary vein ablation
-ECG: no distinct P waves; narrow QRS complex; atrial rate> 100
-Mx: rate control in stable pt: B blocker, CCB, digoxin
Rhythm control in unstable: amiodarone/ immediate synchronised cardioversion

#CHADSVASc: non-valvular AF score >2, Apixaban, rivaroxaban, dabigatran

Valvular AF: warfarin

2) Lone AF”:
-paroxysmal, persistent / permanent AF with no evidence of cardiopulmonary or
structural heart disease.
-Pts with lone AF are usually <60 and by definition, have CHA2-DS2-VASc scor of 0
-Rx: need no treatment with anticoagulants..

3)use Dependence action: more effect with with faster HR – class 1c (fleicanide,
propafenone)

4) CVS manifestations of Turner syndrome :

-bicuspid aortic valve, aortic root dilation, aortic coarctation, and hypertension;
-these changes increase the risk for aortic dissection.
-Therefore, all patients with TS require screening for cardiac disease with 4-extremity
BP and echocardiography.

5) Acute MR:
-LA size, LV size normal; LV EF: normal/ increased as no time for compensation

€
-C/F: so fluid accommodates in lungs causing pulmonary Edema.
Vs
Chronic MR:
-LA enlarge; LV undergoes eccentric hypertrophy; NO pulm edema
Hemodynamic changes in mitral regurgitation
Acute Compensated Decompensated
6) limb ischaemia: cool extremity
MR chronic MR chronic MR Vs
Preload ↑↑ ↑ ↑ -popliteal vein thrombosis: warm swelling
Afterload ↓ No change ↑

Contractile No
No change ↓ 7) limb ischaemia with PAD Vs other causes :
function change
1) without PAD:
Ejection
fraction
↑↑ ↑ ↓
-Cause: due to arterial embolus from AF
Forward stroke
volume
↓ No change ↓ =
-Onset of Sx: abrupt onset of 6 Ps of ALI
MR = mitral
regurgitation.

2) with PAD
-Cause: Patients with existing PAD who develop acute-on-chronic limb ischemia (eg,
due to thrombosis from plaque disruption)
→
-onset: often lack these classic features or develop them more slowly (over 1 day)
-
8) MR types:
1) Primary mitral regurgitation (MR) :
-defined as that caused by an intrinsic defect of the mitral valve apparatus (eg,
leaflets, chordae tendineae)
-Rx: surgery
2) secondary MR :
-results from other cardiac disease (eg, myocardial ischemia, dilated cardiomyopathy).
-Rx: ARB, BBs
-

9) Malignant pericardial effusions

- often large and prone to recurrence.
-acute management : pericardiocentesis
- prevention of reaccumulation: pericardial window / prolonged catheter drainage.

10) Ix of choice for aortic dissection:

A) CT angiography : Ix of choice in hemodynamically stable patients with no renal
dysfunction
—>> reveal : intimal flap separating the true and false lumens in the aorta.

B) Transesophageal (not transthoracic) echocardiography :

excellent sensitivity and specificity and is the preferred diagnostic study in patients
with hemodynamic instability or renal insufficiency

11)

12) valvulardisease.in pregnancy.

-AS, MS > risky in pregnancy so need prior surgery eg percutaneous valvutomy
intervention; AR and MR safer so need only medical Mx =

13) Permanent pacemaker placement

-Indication: Mobitz type II 2o AV block and 3o AV block

14) antihypertensives protocol:

-baseline BP <20 / <10 mm Hg above target: 1-drug antiHT therapy
-baseline BP ≥20/≥10 mm Hg above target: 2-drug therapy anti HT

15) Mx of AF:
-In patients with Afib for > 48 hours or if the time of onset is unknown, systemic
anticoagulation (e.g., low molecular heparin) is necessary for 3 weeks prior to electrical or
pharmacological cardioversion to reduce the thromboembolic risk.

- If onset is < 48 hours, rhythm control can be performed without prior TEE. Reversible
causes of Afib, such as hyperthyroidism and electrolyte imbalances, should be assessed
during initial evaluation. In hemodynamically unstable patients, rapid-acting anticoagulation
and electrical cardioversion should be performed immediately.
15)AAA screening:
-Because of the relationship between smoking and AAA, a one-time abdominal
ultrasound is recommended to screen for AAA in men ages 65 to 75 with any
smoking history.

16) Cardiac myxoma

-systemic embolization (eg, stroke, acute limb ischemia).
#C/F:
-obstructive symptoms may be transient and influenced by position (ie, mitral
obstruction is exacerbated by upright posture but is alleviated by lying down);

-tumor movement occasionally causes a characteristic "tumor plop" sound at the end of
diastole on auscultation.
-middiastolic murmur and sx of decreased cardiac output (eg, dyspnea, syncope).
-Constitutional symptoms: (eg, fever, weight loss)
-

17)

18) Atypical presentation of RVMI

-atypical epigastric pain rather than classic substernal chest pain.
-Nausea is also common, but when MI primarily affects the right ventricle, shortness of
breath is rarely present (due to absence of pulmonary edema).
-Bradyarrythmia+; hypotension

19) large anterolateral wall MI

-ECG shows ST-segment elevation in leads V1 through V6 (and possibly I and aVL)
indicative of a large anterolateral wall MI (left anterior descending artery occlusion).

E- 1st line

2nd line

3rd line
22) SVT:
A) Haemodynamically stable:
1st line: vagal manoeuvre
2nd line: IV adenosine
3rd line: B blocker, CCB, Digoxin ←
←

B) Haemodynamically unstable:
Immediate synchronised DC cardio version

23) Premature atrial contractions:

P waves gave atleast 3 different morphology; rhythm irregular
-pattern: singly/ bigemini

-MC association: COPD; tobacco, alcohol (healthy)

-

-Mx: Rx RF; B blockers if sx ←

-

24) Mx of Torsades:
A) unstable: defibrillator
B) stable: 1st line- MgSO4 then cure the causes
- if Quinine is the cause, Rx with sodium bicarbonate

25) Sick sinus syndrome:

-problem with P waves; either delayed (sinus pause) /absent (sinus arrest) P waves
-QRS normal
Vs
#AV block:
-P waves always present; delayed/dropped QRS.

26) 2 key indications for an exercise stress test include (1) History compatible with
coronary artery disease (angina, etc.) (2) Risk stratification prior to starting exercise
plan

#Localization of aortic regurgitation murmur can sometimes help to detemine the

location of the pathology, with loudest murmur at right sternal border most
consistent with aortic root disease and loudest murmur at left sternal border most
consistent with primary valvular disease
27) Cor pulmonale
- impaired function of the right ventricle due to pulmonary hypertension that usually
occurs due to chronic lung disease.
-Signs of right ventricular failure include:
• Elevated jugular venous pressure
• Right ventricular 3rd heart sound
• Tricuspid regurgitation murmur
• Hepatomegaly with pulsatile liver
• Lower-extremity edema, ascites, and/or pleural effusions

-Echocardiogram : signs of increased right heart pressures,

- right heart catheterization : pulmonary systolic pressure >25 mm Hg; lungs
unafffected
Reversible causes of asystole/pulseless
electrical activity
Only cpr and 5 Hs 5 Ts
epinephrine
Hypovolemia Tension pneumothorax
Hypoxia Tamponade, cardiac
.
Hydrogen ions Toxins (narcotics,
(acidosis) benzodiazepines)

= Thrombosis
Hypokalemia or
(pulmonary or
hyperkalemia
coronary)
2 shock Hypothermia Trauma
IV epinephrine
Shock

÷
28) Pulseless electrical activity
Amiodarone
(PEA)
-the presence of an organized
rhythm (AF) on cardiac monitoring
without a palpable pulse (or
. measurable blood pressure) in a
.
cardiac arrest patient.

29) MVP syndrome.

-Several nonspecific symptoms
(atypical chest pain, dyspnea,
palpitations, dizziness, anxiety, and
panic disorder) and nonspecific
electrocardiographic changes have
been attributed to MVP.

- patients should be reassured about

the benign nature of the symptoms.
 30) Normally functioning bicuspid aortic valves
-typically produce a prominent ejection click followed by a mid-systolic murmur best
heard over the right second intercostal space.
Comparison of left ventricular and right ventricular MI Management of ST-segment elevation myocardial
infarction
Left ventricular MI Right ventricular MI
• Caution with hypotension (eg, RV
• Clear lungs Nitrates
• Pulmonary edema infarction)
Clinical features • Marked
• S3 & S4
hypotension • Oral cardioselective (eg,
• Inferior ischemic Beta blockers metoprolol, atenolol)
changes • C/I in HF & bradycardia
• Ischemic changes in anterior,
ECG findings • ST-segment Antiplatelet • Aspirin & P2Y12 receptor blocker
lateral, or inferior leads
elevation in V4R therapy (eg, ticagrelor)
•Bradyarrhythmias
• Unfractionated heparin,
• ↑ RV preload, ↓ Anticoagulation
Hemodynamic • ↑ LV & RV preload
LV preload enoxaparin, or bivalirudin
findings •
=
↑ SVR
• ↑ SVR
=
• High potency (eg, atorvastatin,
Statin therapy
• Fluid rosuvastatin)
resuscitation • PCI ≤ 90 min from first medical
•Fluid restriction
• Avoid preload
Management •Preload & afterload reduction Coronary contact
reduction
•Reperfusion therapy reperfusion • Fibrinolytics (eg, alteplase) if
• Reperfusion
therapy PCI is unavailable
PCI = percutaneous coronary intervention; RV = right
ventricular.
31) Difference in Mx between RVMI vs LVMI:
a) RVMI:
-The failing RV becomes reliant on hydrostatic pressure to force blood through the
pulmonary circulation and is highly sensitive to a reduction in preload;

—>nitrates, diuretics, and opioids are best avoided because they reduce RV
preload and can profoundly worsen hypotension.

-Hypotension in the setting of RVMI is best initially treated with intravenous normal
saline to further increase RV preload and provide additional hydrostatic pressure to
assist blood flow through the pulmonary circulation.
Vs
b) LV contractile dysfunction resulting from LVMI
-which is often recognized by pulmonary edema
—> worsens with increased preload, and intravenous fluids should be avoided.

==>BOTH: standard management of an acute STEMI with dual antiplatelet therapy,

statins, anticoagulation, and urgent revascularization (eg, percutaneous intervention).
 CHA2DS2-VASc score
Risk criteria Score
C Congestive heart failure 1
H Hypertension 1
A2 Age ≥75* 2
D Diabetes mellitus 1
S2 Stroke/TIA/thromboembolism 2

V
Vascular disease (prior myocardial infarction,
peripheral artery disease, or aortic plaque)
1 =
A Age 65-74* 1
Sc Sex category (ie, female) 1 Classification of angina
• Typical location (eg, substernal),
Maximum score 9
quality & duration
*Patients are assigned to 1 of the 2 categories. Classic • Provoked by exercise or emotional
TIA = transient ischemic attack. stress
• Relieved by rest or nitroglycerin
• 2/ 3 characteristics of classic
Atypical
angina
• <2 /3 characteristics of classic
Nonanginal
angina

→ ¥
34) When to suspect drug induced HT??
—> an early age of onset (ie, age <30 in the absence of family history),
—> severe / malignant HT,
—> resistant HT despite an appropriate 3-drug treatment regimen, and
—> a sudden rise in BP in a patient with previously well-controlled hypertension.

In light of this patient's clinical presentation, a urine drug screen should be obtained to
evaluate for illicit drug use.
Vs
#Pheochromocytoma is a rare disorder that typically manifests with intermittent severe
hypertension associated with paroxysms of diaphoresis, headache, and tachycardia.
Chronic, mild hypertension is less typical. ( 150 is mild)
#illicit drugs associated with hypertension: stimulants (eg, amphetamines, 3,4-
methylenedioxymethamphetamine [MDMA or Ecstasy]), phencyclidine (PCP), and
marijuana; cocaine

35) Supraventricular tachycardia SVT:

#Def: SVT refers to any tachycardia originating above the His-bundle and includes
sinus tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation,
atrioventricular (AV) nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia
(AVRT), and junctional tachycardia.

-ECG: regular and narrow complex tachycardia (QRS duration < 120 ms) at a rate of
approximately 160 beats per minute.

#How to identify causes of SVT?.

-vagal maneuvers/ IV adenosine temporarily slow conduction via the AV node and can aid in
diagnosis by unmasking "hidden" P waves in patients with atrial flutter or atrial tachycardia.

—> They can also cause a transient AV nodal block and terminate AV node-dependent
arrhythmias, including AVNRT and orthodromic AVRT.

36) arrhythmic syncope:

-arrhythmic cause of syncope usually have underlying structural heart disease
- may not have any prodromal symptoms prior to the syncopal episode
Vs
#vasovagal / neurocardiogenic syncope:
-frequently experience a prodrome with nausea, pallor, diaphoresis, and generalized sense
of warmth prior to the syncopal episode.

37) Post MI VF:

-—> Ventricular fibrillation is the most frequent underlying arrhythmia responsible for
sudden cardiac arrest in the setting of acute MI;
—> more than 50% occur within the first hour of symptom onset.

—> Reentry is the predominant mechanism responsible for ventricular arrhythmias in the
immediate post-infarction period.

#underlying mechanism :
1) "immediate" or phase 1a ventricular arrhythmias:
-onset: Arrhythmias occurring within 10 minutes of coronary occlusion
-Acute ischemia causes heterogeneity of conduction with areas of marked conduction
slowing and delayed activation, which in turn predisposes to reentrant arrhythmias.

2)"delayed" or phase 1b arrhythmias

-Onset: 10-60 minutes after acute infarction
-Pathogenesis: result from abnormal automaticity.
38) Isolated systolic hypertension
-an important cause of hypertension in elderly patients,
-Pathogenesis: increased stiffness or decreased compliance of the arterial wall.
-It is associated with an increase in cardiovascular morbidity and mortality

39) Lifestyle interventions for hypertension

-Lifestyle modification should be
Approximate ↓ the 1st-line intervention for newly
Modification Recommended plan systolic BP
(mm Hg) diagnosed stage I hypertension.
Diet high in fruits & vegetables & low in
DASH diet 11
saturated & total fats -The most effective lifestyle
Weight loss Reduction of BMI to <25 kg/m2
6 per 10-kg intervention for reducing blood
loss
pressure is weight loss in obese
Aerobic
exercise
30 minutes/day for 5+ days/week 7 patients.
Dietary <1.5-2.3 g/day (response varies)
5-8
sodium Dont tick that first
Alcohol ≤2 drinks/day in men, ≤1 drink/day in
5
limitation women
DASH = Dietary Approaches to Stop Hypertension.

40) Aortic stenosis (AS)

-C/F: angina,syncope, HF
-but such Sx do not typically occur until -0
the stenosis becomes severe, indicated
by valve area <1 cm2.

-if valve area >1; most likely due to

obstructive CAD not AS

Second-degree atrioventricular block:

distinguishing features of Mobitz types I & II
Mobitz type I Mobitz type II
Below AV node
Level of block AV node
(eg, His bundle)
Progressive
Constant PR interval
prolongation of
ECG findings with randomly dropped
PR interval followed by
QRS complexes
dropped QRS complex
QRS complexes Narrow Narrow or wide
Decreased vagal
tone
Block improves Block worsens
(eg, exercise,
atropine)
Increased vagal tone
(eg, carotid Block worsens Block improves
massage)
Risk of complete High (indication for
Low
block PPM)
AV = atrioventricular; PPM = permanent pacemaker.
41) IE by drug abuse:
-No murmur; less HF; septic pulm emboli; few peripheral IE manifestation

Heart failure with preserved left ventricular ejection 42) WPW:

fraction • Hemodynamically unstable :
• LV diastolic dysfunction: hypertension with immediate electrical
concentric LVH, restrictive cardiomyopathy, cardioversion
hypertrophic cardiomyopathy • For stable patient: anti-
• Valvular heart disease: aortic stenosis/ arrhythmic drugs3 ibutilide /
regurgitation, mitral stenosis/regurgitation
Causes
• Pericardial disease: constrictive pericarditis,
procainamide
cardiac tamponade
• Systemic disorders (high-output failure): #Avoid:
thyrotoxicosis, severe anemia, large AV nodal blockers such as BB,
arteriovenous fistula CCBs, digoxin, and adenosine
• Control blood pressure & heart rate avoided as they can cause
Manageme • Address concurrent conditions: AF & MI increased conduction through
nt • Treat volume overload with diuretics the accessory pathway.
• Exercise training/cardiac rehabilitation

43) (S3) is a low frequency diastolic sound heard just after S2 that is associated with left
ventricular failure.
-IV diuretics provide symptomatic benefits to patients with decompensated heart failure.

44) JVP:
-TR: Prominent v waves
(Specific); absent x
descent due to
continuous atrial filling

-TS: prominent A waves

due to obstructed RV
filling; flattened y
descent

-cardiac tamponade:
flattened y decent due to
restriction of passive RV
filling

-cannon A waves(surge in
JVP intermittently):
arrhythmia involving AV
block; PVC
#Jugular venous pulse (JVP):
-a wave—atrial contraction. Absent in AF
-c wave—RV contraction (closed tricuspid valve bulging into atrium).
-
-
-x descent—downward displacement of closed tricuspid valve during rapid ventricular
ejection phase. Reduced or absent in tricuspid regurgitation and right HF because pressure
gradients are reduced.
-v wave—right atrial pressure due to filling (“villing”) against closed tricuspid valve.
-y descent—RA emptying into RV. Prominent in constrictive pericarditis, absent in cardiac
tamponade.

46) peripheral edema of CCB : by precapillary vessels (arteriolar dilation)

-ACEI cause post-capillary venodilation and can normalize the increased capillary
hydrostatic pressure.

- In clinical studies, the combination of CCB and ACE inhibitors was associated with a
significantly lower risk of CCB-associated peripheral edema

47) Loop diuretics cause hypokalemia and hypomagnesemia.

-These cause ventricular tachycardia, and also potentiate the side effects of digoxin.

48) Tc 99 scan for coronary perfusion:

• Patients with normal tracer uptake at both rest and exercise :low likelihood of ischemia
with an excellent prognosis and <1% annual risk of(CAD).

• A decreased tracer uptake both at rest and with exercise (fixed defect) :
likely scar tissue with decreased perfusion and CAD.

• A decreased tracer uptake with stress but normal uptake at rest (reversible defect) :
inducible ischemia and likely CAD.
They benefit by aspirin

49) examination findings are consistent with severe AS:

• A soft, single second heart sound (S2)
• A delayed and diminished carotid pulse ("parvus et tardus")
• Loud and late-peaking systolic murmur
 49) Types of obstructive shock
A) pre pulmonary: PCWP low/ normal as blood does not pass to left
1) Obstructive shock due to acute pulmonary embolism :
- increased RAP (proximal to the obstruction) and decreased PCWP and CI (distal to the
obstruction).
- SVR is increased in response to low CI.

2) Tamponade
-represents aunique scenario in which PCWP is elevated despite decreased blood flow to
the left atrium. (Exception to above rule of PCWp)

B) post pulm: PCWP elevated : cardiogenic shock

-obstruction of left side of heart: AS/ aortic dissection
Hemodynamic measurements in shock
Hypovolemi 50) Mx of hypertensive emergencies:
Cardiogenic Obstructive Distributive
Parameter c
shock shock shock -MAP should be lowered by 10%-20%
shock
in the 1st hour and by another
CVP
(right-sided ↓ ↑ ↑ ↓ 5%-15% over the next 23 hours.
preload)
PCWP -An excessive drop in blood pressure
(left-sided ↓ ↑ ↓* ↓
preload) can lead to cerebral ischemia, with
Cardiac altered mental status and/or generalized
index ↓ ↓ ↓ ↑** seizures.
(LV output)
SVR
↑ ↑ ↑ ↓
(afterload)
SvO2 ↓ ↓ ↓ ↑**
*In tamponade, left-sided preload (CO) is decreased, but
measured PCWP and RAP is paradoxically increased due to
external compression by pericardial fluid.
**Cardiac index & SvO2 are usually decreased in neurogenic
shock due to impaired sympathetic reflexes.

=
-
52) Fibromuscular dysplasia: > F
#C/F:
• Internal carotid artery stenosis: Recurrent headache; Pulsatile tinnitus; TIA; Stroke
• Renal artery stenosis: Secondary hypertension; Flank pain
#Mx:
• 1st line: ACE inhibitors or ARBs
• 2nd line: PTA; Surgery (if PTA unsuccessful)

53) High-output heart failure : eccentric

-It involves hyperdynamic circulation (evidenced by widened pulse pressure and brisk
carotid upstroke) and increased cardiac venous return leading to peripheral and
pulmonary edema.
-laterally displaced point of max impulse; systolic murmur by high BF

54) screening For DM in HT:

-Patients with HT should be screened for DM with either FBS / HbA1c
—> Even in the absence of hypertension, screening for diabetes is advised for
patients age 40-70 with a BMI ≥25.

55) Supravalvular aortic stenosis (AS)

-the 2nd MC type of AS, usually refers to congenital left ventricular outflow tract
obstruction due to discrete or diffuse narrowing of the ascending aorta.

#murmur of supravalvular AS vs AS
-systolic murmur similar to valvular AS; at the 1st rt intercostal space,
Vs
valvular AS murmur : 2nd right intercostal space

#C/F:
-unequal carotid pulses, differential BP in the upper extremities (high-pressure jet in
-
ascending aorta), and a palpable thrill in the suprasternal notch.
#MI:

=
—> Patients with significant supravalvular AS develop left ventricular hypertrophy
over time and can also have coronary artery stenosis as an associated anomaly.

—> These changes, along with the increase in myocardial oxygen demand during
exercise, can lead to subendocardial or myocardial ischemia, which is likely responsible
for this patient's anginal symptoms during exercise.
 56) CN poisoning
#Etio: combustion of carbon- and
nitrogen-containing compounds (eg,
wool, silk), industrial exposure
(eg, metal extraction in mining),
and medications (eg, sodium
nitroprusside)., fire in plastic factory,
vehicular fire

#toxicity dose:
-Prolonged infusion (>24 hours)
at high rates (5-10 µg/kg/min) can
lead to cyanide toxicity, especially in
#Mx: patients with CKD
-As a result, low infusion rates (<2 µg/kg/min), short-term use, and close monitoring are
recommended. Rx: sodium thiosulfate.
#Management of new-onset AF
57) - assessing for rate vs rhythm control strategy
and preventing systemic embolization.

a)Hemodynamically unstable patients:

require emergency cardioversion.

b) Stable patients/asx/ mild Sx like fatigue :

receive medical therapy (eg, beta blockers,
diltiazem, digoxin) to control the ventricular rate.
#Indication for rhythm control:
-considered in patients unable to achieve adequate heart rate control or in those with
recurrent symptomatic episodes (eg, palpitations, lightheadedness, dyspnea,
angina) /
-HF Sx in the setting of underlying left ventricular systolic dysfunction.

58) Hypovolemic shock hemodynamics: .

- an initial decrease in preload and cardiac output followed by a compensatory increase

in SVR, HR, and EF

59) CHF due to left ventricular systolic dysfunction

-decreased cardiac output/index, increased(SVR), and an increase in(LVEDV)- last 2 by
RAAS +
 Chemotherapy-induced cardiotoxicity 61) atypical symptoms in diabetic MI:
#Associated with anthracyclines -Diagnosing acute coronary syndrome (ACS) is
challenging in elderly patients because they often have
• Myocyte necrosis &
destruction (fibrosis)
atypical symptoms (eg, dyspnea, nausea, diaphoresis),
Type I
• Progression to overt
°
clinical particularly if they have comorbid diabetes mellitus.
heart
→ failure
• Less likely to be reversible
-An ECG should be obtained early to avoid diagnostic
• Associated with trastuzumab
delay.
• Myocardial stunning/ -Dx: STEMI criteria include new ST-segment elevation
Type hibernation without myocyte in 2 contiguous leads.
II destruction
• Asymptomatic left ventricular
systolic dysfunction
• More likely to be reversible

63) Prosthetic valve -

thrombosis:
-left sided: systemic emboli
-Rt sided: pulm emboli

É
#Mx :
-To prevent PVT, patients with
prosthetic valves are kept on
antithrombotic therapy.

1) Mechanical prosthetic valves

are more thrombogenic :
-
- -
-

require anticoagulation.

2) Bioprosthetic valves are less

thrombogenic : typically require
only aspirin therapy; however,
PVT can still occur.

÷
# Mx of small to moderately sized (ie, 3 cm to 5.5 cm) (AAAs) : lifestyle modification,
with smoking cessation as the best intervention to minimize AAA progression.
66) Rupture of AAA :
-> with large aneurysmal size (>5.5 cm) / rapid rate of expansion (eg, >1 cm/year), and
preemptive surgical repair is the definitive treatment.

- Why Non- Surgical Mx is more important?.

As surgery carries a relatively high risk of complication, with the risk of repair
typically greater than the risk of rupture until the aneurysm reaches a large size.

-Therefore, Mx of small to moderately sized AAA involves surveillance with serial

abdominal ultrasound and lifestyle modification to limit AAA progression.

67) Long QT syndrome (LQTS)

- QTc >450 msec in M or >470 msec in F
- Etiology: congenital / acquired

-Cx: increased risk of sudden cardiac death

due to torsades de pointes / polymorphic
ventricular tachycardia.

T
A
←7

g o

68) tachycardia-mediated cardiomyopathy

-Mechanism: Chronic tachycardia causes structural changes in
the heart including LV dilatation and myocardial dysfunction.

-lead to tachycardia-mediated cardiomyopathy; : AF, atrial flutter,

ventricular tachycardia, incessant atrial/junctional tachycardia, and
atrioventricular nodal reentrant tachycardia: all are supravalvular

#Rx:
-aggressive rate control / restoration of normal sinus rhythm
due to potential reversibility of tachycardia-mediated
cardiomyopathy and normalization of LV systolic function.

-Therapeutic options : AV nodal blocking agents, antiarrhythmic

drugs, and catheter ablation of arrhythmia.
Indications for statin therapy in prevention of ASCVD
• Established ASCVD
◦ Acute coronary syndrome
Secondary ◦ Stable angina
prevention ◦ Arterial revascularization (eg,
CABG)
◦ Stroke, TIA, PAD
• LDL ≥190 mg/dL
Primary • Age ≥40 with diabetes mellitus
prevention • Estimated 10-year risk of ASCVD
>7.5%-10%

Éi-=
72) MS: Left atrial dilation is typical and may be recognized by elevation of the left main
stem bronchus on chest x-ray.
-Atrial fibrillation is a common complication and can precipitate acute decompensated heart
failure in previously well-compensated patients.

73) Rx of decompensated HF: #The initial therapy of patients

with pulmonary edema and
hypoxemia due to acute
- -

decompensated heart failure :

-÷
aggressive intravenous
diuresis, oxygen
supplementation, and
possibly assisted ventilation.

74) MOA of nitrates:

-systemic vasodilation with a decrease in left ventricular EDV and wall stress resulting in
decreased myocardial oxygen demand.

75) Amyloid cardiomyopathy

-should be suspected in patients with unexplained congestive heart failure, proteinuria,
and left ventricular hypertrophy in the absence of a history of hypertension.

#Restrictive cardiomyopathy: idiopathic or due to infiltrative diseases (eg, sarcoidosis,

amyloidosis), storage diseases (eg, hemochromatosis), or endomyocardial fibrosis.

76) Stress-induced (takotsubo) cardiomyopathy

• Postmenopausal woman
77) Primary hyperPTH causes 2o HT by:
Risk factors
-
• Recent physical or emotional -increased renin secretion, sympathetic
stressor hyperresponsiveness, and peripheral
• Chest pain mimicking myocardial artery vasoconstriction.
infarction
Clinical • Decompensated heart failure -Other CVS manifestations of
features • Moderate troponin elevation hyperparathyroidism : left ventricular
• ECG: ischemic changes in
precordial leads hypertrophy, arrhythmias, and vascular
and valvular calcification.
• Catheterization: no obstructive
CAD clue
Diagnosis -Rx of PHPT usually results in normalization
• Echo: LV apical hypokinesis,
basilar hyperkinesis of blood pressure.
• Resolves in several weeks with
Treatment
supportive care

Vs no ECG change in diffuse esophageal

-
spasm
-
78) Positive pressure mechanical ventilation induced cardiac arrest
-causes an acute increase in intrathoracic pressure.
—> In the setting of decreased CVP (eg, hypovolemic shock), initiation of
mechanical ventilation can cause acute loss of RV preload, loss of CO, and cardiac
arrest.

79) Choice of antihypertensive drug for comorbid conditions 80) BNP:

• Angina pectoris: beta blocker, CCB -Elevated plasma brain natriuretic
Coronary • Post–myocardial infarction: ACE inhibitor peptide levels have high Sn for
atherosclerosis or ARB, the diagnosis of CHF
• beta blocker
Heart failure with
reduced ejection
• ACE inhibitor or ARB, beta blocker, -In contrast, clinical signs of CHF
diuretic, aldosterone antagonist (eg, B/L lung crackles, elevated
fraction
Atrial fibrillation JVP, lower extremity edema, S3)
• Beta blocker, nondihydropyridine CCB
or flutter have high sp but low Sn
- -
Chronic kidney
• ACE inhibitor or ARB
disease -BNP levels >400 pg/mL:CHF
Gout
• Losartan, other ARB, CCB (avoid whereas <100 pg/mL had a high
diuretics)
NPV for CHF as a cause of
Osteoporosis • Thiazide diuretic dyspnea.
Migraine • Beta blocker, CCB

81) ADR of High dose niacin

-role of PG is confirmed by the fact that low-dose aspirin can greatly reduce or prevent
cutaneous flushing and pruritus if taken 30 minutes before niacin.

-Flushing and pruritus usually improve after 2-4 weeks of therapy.

82) Digoxin cardiac arrhythmia:

—> atrial tachycardia ( 200/min) slower than AFL (300) + atrioventricular (AV) block (MC
2o Mobitz type I) is specific for digoxin overdose

-others: VT; sinus bradycardia;; NEVER 2o Mobitz II

83) Mx of carotid artery stenosis

-Initial interventions for all patients with carotid artery stenosis : intensive medical
management (ie, aspirin, statin, blood pressure control)

#indications of carotid endarterectomy:

Symptomatic (TIA / ischemic stroke in the distribution of the affected vessel) with
stenosis (70%-99%)/ ASx with >80% stenosis
-
-
84) Uremic pericarditis (UP)
-BUN >60 can lead to inflammation of the visceral and parietal layers of the pericardium.
-Most UP patients do not present with the classic ECG changes of pericarditis as
myocardium is spared

#Mx: Hemodialysis leads to rapid resolution of chest pain and reduces the size of any
associated pericardial effusion.

-Systemic anticoagulation (eg, heparin) can cause hemorrhage into the pericardial space
and should be avoided during hemodialysis.

85) Low-grade atrioventricular block

-including 1o degree and Mobitz type I 2o are common on resting ECG in highly trained
endurance athletes because of high levels of resting vagal tone.

-Mx: These findings are benign and require no intervention.

86) 1st line medicine In RAS:

-ACEI/ARBS are indicated for initial therapy in patients with renovascular hypertension
(due to renal artery stenosis): U/L and B/L until S creat <30%.

-sx indication: Renal artery stenting or surgical revascularization is reserved for patients

I
with resistant hypertension

87) Medical therapy shown to improve morbidity and mortality in patients with known
coronary heart disease includes:

1 Dual antiplatelet therapy (DAPT) : aspirin + P2y12 receptor blockers (eg, clopidogrel,
prasugrel, ticagrelor)
2 Beta blockers
3 ACEI / ARBS
4 HMG-CoA reductase inhibitors (statins)
5 Aldosterone antagonists (eg, spironolactone, eplerenone) in patients with left
ventricular ejection fraction ≤40% who have heart failure symptoms or diabetes
mellitus

-Isosorbide mononitrate, a long-acting nitrate providing rapid, symptomatic relief in

patients with recurrent angina, has no mortality benefit in patients with coronary heart
disease
88) constrictive pericarditis: JVP elevated; RHF signs;
presence of hepatojugular reflux, Kussmaul's sign (lack of decrease in JVP on
inspiration), and a pericardial knock (mid-diastolic sound);
→
-Dx: Echocardiography -increased pericardial thickness, abnormal septal motion, and
biatrial enlargement.
-Rx: Diuretics can provide temporary relief,
pericardiectomy is the definitive treatment for patients with refractory symptoms
and not pericardiocentesis

Vs
portal vein thrombosis/ compression: JVP normal

89) S3: HF; restrictive cardiomyopathy; high output state; > 40 yrs
S4: younger adults; ventricular hypertrophy; acute MI

90) Calciphylaxis (calcific uremic arteriolopathy)

-systemic arteriolar calcification and soft-tissue calcium deposition with local ischemia and
necrosis. It is primarily seen in patients with longstanding end-stage renal disease.

-RF: hyperparathyroidism, hyperphosphatemia, and hypercalcemia, although serum

calcium is often normal.
-Unlike atherosclerosis, here pulse is normal

91) Patients with septic shock first require aggressive volume resuscitation with
intravenous 0.9% saline prior to the initiation of vasopressors to restore adequate tissue
perfusion.

92) Ischemia-reperfusion syndrome

- a form of compartment syndrome that occurs following reperfusion of an acutely ischemic
limb.
-C/F: severe pain that is worsened on passive range of motion, paresthesias, and sensory
and motor deficits.
-Rx: fasciotomy

93) How to differentiate cardiac vs liver causes of LE edema:

Hepatojugular reflux is a useful clinical tool

-peripheral edema due to heart failure : elevated JVP and positive hepatojugular reflux.
Vs
-peripheral edema from primary hepatic disease and cirrhosis : reduced / normal JVP
and negative hepatojugular reflux.
 Type of stress Mechanism Best for Not for 95) MCC of + hepatojugular
Exercise ECG test • ↑ HR • Patients able • LBBB reflux.
• ↑ BP to reach tHR • Pacemaker
(tHR = 85% • Patients
-Constrictive pericarditis, right
of 220 − age) unable to ventricular infarction, and restrictive
reach tHR
cardiomyopathy
Pharmacologic • Nonselective • LBBB • Reactive
stress test with adenosine • Pacemaker airway
adenosine or agonist • Patients disease 96) Congenital bicuspid aortic
dipyridamole • Dilates unable to • Patients on
coronary reach tHR dipyridamole
valve: sporadic/AD
arteries or - the MCC of(AR) in developed
without ↑ HR theophylline
or BP
countries, with patients typically
Dobutamine • Β-1 agonist • Reactive Tachyarrhythmia
diagnosed in their 30s or 40s.
stress • ↑ HR ± BP airway
echocardiography disease
• Patients
The AR is usually valvular but can
unable to also be due to aortic root dilation.
reach tHR

97) Mx of PAD of LE:

* 1st step) started appropriately on low-dose aspirin and statin therapy.

*2nd step) The next step is to enroll the patient in a supervised exercise program.
-Exercise therapy for a minimum of 12 weeks, with 30-45 minutes of exercise at least
3 times a week, is recommended for all patients with claudication.

-The goal : to reproduce the claudication symptoms during each session.

-Supervised exercise programs have been shown in multiple clinical trials to reduce
symptoms and improve the maximum walking distance in these patients.

*3rd line) Percutaneous or surgical revascularization is generally reserved for patients

who have persistent symptoms despite initial exercise and/or pharmacologic therapy.

98) Carotid sinus hypersensitivity

- involves an exaggerated vagal response that is often triggered by tactile stimulation
(shaving, rubbing of a shirt collar while dressing or turning the head) .

-The exaggerated response causes a >3 second ventricular pause and >50 mm Hg
drop in SBP, —> transient reduction in cerebral perfusion that manifests as syncope
or presyncope.

#RF: In some individuals, especially elderly men with atherosclerotic disease, the
carotid sinus baroreceptors become overly sensitive, triggering an exaggerated vagal
response.

#Mx: The diagnosis is made by carotid massage producing an exaggerated vagal

response; this maneuver is often aided by a tilt table to ensure the patient is secured and
does not fall.
#Rx: placement of a permanent pacemaker.
 Clues to etiology of syncope
100) First-line antihypertensive
• Trigger (eg, emotional stress, prolonged
standing)
therapy in nonpregnant patients
Vasovagal
• Prodrome (eg, nausea, sweating,
warmth) - thiazide diuretics, TCA
Reflex
syncope Situational
• Occurs with micturition, defecation, - calcium channel blockers,
swallow,
→ or cough - ACE inhibitors (or angiotensin II
Carotid • Tactile stimulation of carotid sinus while receptor blockers).
hypersensitivi standing
ty • Advanced age, carotid atherosclerosis
• Vasodilators (eg, alpha-1 blockers,
- Beta blockers not recommended :
antihypertensives) because they are associated with
Medications
• Inotropic/chronotropic blockade less reduction in risk of stroke and
Orthosta (eg, beta blockers)
tic mortality compared to other agents.
Hypovolemi
syncope • History consistent with volume loss
a
101) 1st drug given in ACS:
Autonomic • Advanced aged
dysfunction • Predisposing (eg, DM, Parkinson) -suspected acute coronary syndrome
LV outflow • Syncope with exertion
(ACS) should be administered
obstruction • Systolic ejection murmur aspirin as soon as possible.

{
• No warning symptoms
Cardiac
Ventricular • Cardiomyopathy or ischemic HD —> Early antiplatelet therapy with
tachycardia (monomorphic)
syncope
• QT-interval prolongation (polymorphic)
aspirin reduces the rate of
myocardial infarction and overall
• Preceding fatigue or light-headedness
Conduction
• ECG abnormalities (eg, sinus pauses, mortality in patients with ACS.
impairment*
dropped QRS) Followed by other drugs

102) Exertional syncope

-Etio: cardiac causes including
ventricular arrhythmias (due to MI) and
outflow tract obstruction (eg, aortic
stenosis [AS], hypertrophic
cardiomyopathy).
=.-Patients with fixed outflow obstruction
(eg, severe AS) cannot increase cardiac
output in response to exercise-induced
vasodilation, leading to hypotension,
transient cerebral hypoperfusion, and
decreased exercise tolerance,
presyncope, or syncope.
103) Mx of pulm HT according to causes:
-idiopathic : endothelin receptor blocker
-associated with LVF: loop diuretics; ACEI
-COPD: O2: bronchodilator

104) MR after RVMI :

-a) Immediate Acute MR: developing within hours of MI is most likely due to papillary
muscle displacement as a result of hypokinesis of the underlying (LV) wall

=
Vs
b) late acute MR:
-acute MR can also develop several days after MI due to papillary muscle rupture, rather
than displacement).

*PM mitral papillary muscle is MC affected due to singular blood supply from the
RCA along the inferior myocardial wall.

#Hemodynamic changes:
-acute MR: leads to abrupt elevation of left atrial and ventricular filling pressures and
consequent acute pulmonary edema.
-
Vs
-Unlike chronic MR, acute MR does not cause any significant change in left atrial or
ventricular size or compliance.

106) DCM by viral myocarditis:

#Pathogenesis:
-Most cases of viral myocarditis likely remain clinically undetectable, but some may have a
genetic predisposition that allows viral infection (eg, coxsackievirus, adenovirus,
parvo B19) to persist within cardiomyocytes, causing disruption of myocardial
contractility.

-With progressive biventricular contractile failure, there is compensatory eccentric

hypertrophy and the eventual development of(DCM).

#echo: DCM is recognized by dilated ventricular chambers and diffuse hypokinesis of

the ventricular walls.

#Rx:
-Treatment of DCM due to viral myocarditis : mostly supportive and involves medical
management of heart failure with reduced ejection fraction (eg, diuretics, beta blocker, ACE
inhibitor),
with some patients experiencing eventual recovery of cardiac function.
107) Situational syncope
- a form of vasovagal (neurally mediated) syncope associated with specific triggers (eg,
c-
micturition, defecation, cough).
-These triggers cause an alteration in the autonomic response and can precipitate a
predominant cardioinhibitory, vasodepressor, or mixed response.

#Pathogenesis:
• Increased parasympathetic stimulation can manifest as profound bradycardia, varying
degrees of atrioventricular block, or asystole.

• Decreased sympathetic output can lead to vasodilation, hypotension, or syncope.

In addition, this patient's likely prostatic hyperplasia (difficulty initiating voiding, nocturia)
may have caused increased strain while voiding, thereby exacerbating the cardioinhibitory
syncopal response.

108) BNP
- natriuretic hormone released from ventricular myocytes in response to high ventricular
filling pressures and wall stress in patients with CHF.
-It is derived from the cleavage of the prohormone proBNP= biologically active BNP
+ inert N-terminal proBNP (NT-proBNP).

109) Hypertrophic cardiomyopathy (HCM)

-an AD genetic disorder caused by mutation in one of the several genes encoding the
myocardial contractile proteins of the cardiac sarcomere.

-Mutations in the cardiac myosin binding protein C gene and cardiac beta-myosin
heavy chain gene are responsible for about 70% of identifiable mutations in patients with
HCM.

110) Hyperdynamic state in sepsis:

-Early septic shock is associated with a hyperdynamic cardiovascular state that occurs in
response to peripheral vasodilation with capillary leak and intravascular hypovolemia.

→
-This leads to an increase in stroke volume, heart rate, and pulse pressure, which results in
-
bounding peripheral pulses. -

VD .

111) Approach to mild HT:

a) severe >180/ 120/ or evidence of end-organ damage
-should be prescribed antihypertensive therapy immediately.

b)mild blood pressure elevations,

-the diagnosis should first be confirmed outside of a health care setting with ambulatory
blood pressure monitoring or home measurement.
112) Diastolic and continuous murmurs
-usually due to an underlying pathologic cause, and their presence should prompt further
evaluation with a transthoracic echocardiogram.
Vs
#Midsystolic murmurs in otherwise young, asymptomatic adults
-usually benign and do not require further evaluation.

113) AR:
-high-pitched, blowing quality, and, when it is due to valvular (rather than aortic root)
abnormalities, is best heard along the left sternal border at the 3rd/4th intercostal
spaces
-Exacerbating factor: patient sitting up and leaning forward while holding the breath in full
expiration.

114) Cardiac monitoring immediately preceding the vasovagal syncope :sinus

bradycardia and asystole due to sinus arrest.
Vs
Normal BP rules out orthostatic syncope
115) Obesity
-particularly central or visceral, is the
single greatest lifestyle RF for HT, with an
attributable risk of approximately 60%-70%

-In patients with obesity, each kilogram (2.2

lb) of weight loss can lower the blood
pressure up to 2 mm Hg;

—> therefore, weight loss is the most

effective nonpharmacologic intervention
for lowering blood pressure.

-However, additional lifestyle

modifications, including dietary changes,
and exercise, are typically implemented
concurrently.
117) HT and alcohol:
-Excessive alcohol intake (ie, >2 drinks/day) and binge drinking (ie, ≥5 drinks in a single
sitting) are associated with increased incidence of hypertension, and failure to respond to
appropriate antihypertensive therapy.

-In contrast, moderate alcohol intake is associated with lower blood pressure.

118) Causes for persistent HT despite taking antiHT:

-medication nonadherence, dietary indiscretion (eg, excessive sodium intake), and
concurrent medications (eg, NSAIDs, decongestants, GC) that raise BP.

119) HT increases the risk of stroke more than any other risk factor including
hypercholesterolemia, diabetes mellitus, smoking, and sedentary lifestyle.

120) digoxin interaction:

-Amiodarone (or verapamil, quinidine, and propafenone) increases the serum levels
of digoxin (by interfering with digoxin metabolism) and can lead to toxicity in a patient who
has previously been on a stable digoxin regimen.

-It is recommended that the digoxin dose be decreased by 25%-50% when initiating
amiodarone therapy,
—> close monitoring of digoxin levels once weekly for the next several weeks.

121) Mx of pericarditis:-
• 1st-line therapy for viral/idiopathic pericarditis: NSAIDs + Colchicine
• 2nd-line therapy for viral/idiopathic pericarditis: Corticosteroids
-

• Key idea: Uremic pericarditis should be treated with hemodialysis (AEIOU mnemonic to
remember indications for hemodialysis)

• Key idea: Peri-infarction pericarditis (several days after MI) should receive supportive
management and NOT be treated with NSAIDS due to concern for impaired wound
healing and possible increased risk of post-MI mechanical complications (free wall
rupture, etc.)

121) • Femoropopliteal artery plaque –> Calf claudication

• External iliac artery plaque –> Thigh and calf claudication
• Aortoiliac plaque –> Gluteal, thigh and calf claudication + impotence (in a man)
121) AS:
-The 3 MCC of aortic stenosi: senile calcific AS, bicuspid aortic valve, and RHD
—>A bicuspid aortic valve is the cause of AS in the majority of patients age <70.

122) Pulsus bisferiens (or biphasic pulse)

-refers to 2 strong systolic peaks of the aortic pulse from left ventricular ejection separated
by a midsystolic dip.

#Etiology :
1) significant aortic regurgitation (with or without aortic stenosis),
2) HOCM
3) occasionally, large PDA

123) Exercise stress ECG

recommended as an initial test for
diagnosis and risk stratification in
most patients with suspected
stable ischemic heart disease.

—> The presence of epigastric

discomfort on exertion that is not -.
relieved by antacids is concerning for
cardiac pathology.

—>Evaluation for possible

gastrointestinal etiology (eg, peptic
ulcer disease, esophageal motility
disorders) should be considered in
patients with no evidence of MI on
initial evaluation.
 Treatment of chronic stable angina 125) Use dependence
• First-line therapy -Def: enhanced pharmacologic effects of a
Beta blockers • ↓ Myocardial contractility & drug during faster heart rates and is seen
heart rate with class I (especially IC) and class IV
Nondihydropyridine
• Alternative to beta blocker (CCB)
• ↓ Myocardial contractility &
CCBs
heart rate
a) Class IC agents:flecainide; propefenone
• Added to beta blocker
when needed
-cause a progressive decrease in impulse
Dihydropyridine • Coronary artery conduction with faster heart rates—>
CCBs vasodilation increase in the QRS complex duration.
• ↓ Afterload by systemic
vasodilation
b) Calcium channel blockers (CCBs)
• Long-acting added for
persistent angina
(verapamil and diltiazem)
Nitrates -MOA: increase in calcium channel blockade
• ↓ Preload by dilation of
capacitance veins with increasing ventricular activation.
• Alternative therapy for -cause a prolongation of the refractory
Ranolazine refractory angina period of the AV node—> increased PR
• ↓ Myocardial calcium influx interval; no change in the QRS complex
duration.
126) Rx after MI :
1) medical therapy
-Following MI, patients should be placed on optimal medical therapy with a beta blocker ,
ACE I / ARB and possibly a mineralocorticoid antagonist (eg, spironolactone).

—> In many patients, any systolic dysfunction following MI will normalize or significantly
improve with medical therapy, lowering the risk of SCD.

2) However, in patients with persistent LV ejection fraction ≤30% despite optimal

medical therapy, the risk of SCD remains high
- primary prevention with placement of an implantable cardioverter-defibrillator (ICD)
is indicated.

127) Rx of dressler syndrome

-High-dose (NSAIDs) (eg, aspirin 1000 mg / ibuprofen 800 mg every 6-8 hours);

XxAnticoagulation should be avoided to prevent hemorrhagic pericardial effusion.

Vs
128) Intravenous alteplase (tissue plasminogen activator)
- a fibrinolytic agent indicated for the treatment of ACS due to STEMI when timely
primary percutaneous revascularization is unavailable.

==> Fibrinolytic therapy is not indicated in ACS due to UA or NSTEMI.

Management of unstable angina & Common complications of IE
non–ST-segment elevation myocardial infarction
• Heart failure
• Caution with hypotension (eg, right • Perivalvular
Nitrates
ventricular infarction) Local (cardiac) abscess
• Cardioselective (eg, metoprolol, • Pericarditis
atenolol) • Intracardiac fistula
Beta blockers • Contraindicated in heart failure & • Septic embolism
bradycardia • Metastatic
• Intravenous for hypertensive patients Distant (embolic) abscess
• Aspirin & P2Y12 receptor blocker • Mycotic aneurysm
Antiplatelet therapy • Organ infarction
(eg, clopidogrel)
• Unfractionated heparin, enoxaparin,
Anticoagulation
bivalirudin, or fondaparinux
• High intensity (eg, atorvastatin,
Statin therapy
rosuvastatin)
• Percutaneous coronary intervention
Coronary reperfusion
within 24 hr
X
130) Perivalvular abscess
-MC valve: 30%-40% of patients with aortic valve IE and is MC in bicuspid valve.
*CLUE:
-It is generally suspected when patients with IE have persistent bacteremia or develop
cardiac conduction abnormalities (eg, heart block) on ECG+ fever+ leucocytosis

#Pathogenesis behind AV block :

-Conduction abnormalities are common because the aortic valve ring between the right
cusp and the noncoronary cusp overlies the intraventricular septum, which harbors
the proximal ventricular conduction system.
Vs
#lyme Ds : valves spared

131) arrhythmic syncope:

-Patients with syncope not clearly attributable to a benign etiology (eg, reflex or
orthostatic syncope)
-Next step: should undergo further cardiac workup (eg, ambulatory ECG)

-Clue: Syncope that occurs while supine or sitting, at rest, and without warning
symptoms suggests an arrhythmic etiology.
 132) hyponatremia in CHF
-In CHF, low CO, along with
decreased perfusion pressure at the
baroreceptors and renal afferent
arterioles —>leads to neurohumoral
activation with the release of renin,
NE and(ADH).

-ADH (vasopressin) binds to V2

receptors in the renal CD and
promotes water reabsorption,

-while renin and NE increase

proximal sodium and water
reabsorption and limit water
delivery to the distal tubules
—> These actions promote free
water retention and lead to
dilutional hyponatremia.

133) Approach to HT
-The initial evaluation of hypertension focuses on identifying complications or comorbid
conditions that might influence management.

-Assessment :serum chemistry panel, hemoglobin/hematocrit, and urinalysis.

-screen for major atherosclerotic risk factors with a lipid panel ; FBS / Hb A1c.
Laboratory evaluation of hypertension Common mechanisms of high-output heart failure
• S electrolytes (Na, K, Ca) Increased quantity • Morbid obesity
• S creatinine of peripheral vessels • Paget disease
Renal function
• Urinalysis
tests • Acquired AV fistula (eg,
• Urine albumin/creatinine
ratio (optional) Bypass of systemic trauma, HD)
arteriolar resistance • Congenital AV
• FBS / Hb A1c malformation
Endocrine tests • Lipid profile
• TSH Vasodilation due to • Hyperthyroidism
unmet • Severe anemia
• ECG
Cardiac tests metabolic demand in • Thiamine deficiency
• Echocardiography (optional)
tissues (wet beribe
• Complete blood count
Other tests
• Uric acid (optional)
 Bacterial endocarditis prophylaxis
136) Antibiotic prophylaxis for
• Prosthetic heart valve infective endocarditis (IE)

{
• Previous infective endocarditis

-
• Structural valve abnormality in transplanted heart - recommended only in patients with
High-risk
cardiac
• Certain CHD subtypes very high risk of adverse outcomes
◦ Unrepaired cyanotic CHD from IE (eg, prosthetic heart valve,
conditions
◦ Repaired CHD with residual defect
◦ Repaired CHD with use of prosthetic material in previous IE).
preceding 6 months
• Gingival manipulation or respiratory tract incision -It is not recommended in
◦ Viridans group Streptococcus coverage patients with mitral valve
(eg, amoxicillin 60 min prior
Indicated
• GU or GI tract procedure in setting of active prolapse, other acquired valvular
procedures
&
infection dysfunction (eg, rheumatic
◦ Enterococcus coverage (eg, ampicillin) fever), and relatively low-risk
appropriate
• Surgery on infected skin or muscle
coverage
◦ Staphylococcus coverage (eg, vancomycin) congenital heart disease (eg,
• Surgical placement of prosthetic cardiac material atrial septal defect, bicuspid
◦ Staphylococcus coverage (eg, vancomycin) aortic valve). Uwsa1
137) Doppler echocardiography is useful for detecting the presence and severity of
valvular regurgitation or stenosis. The ultrasound beam records blood flow and
velocity across the heart valves:
• Blood flow toward the transducer is recorded above the baseline.
• Blood flow away from the transducer is recorded below the baseline.

-Using the apical window (with the transducer placed at the cardiac apex), aortic flow
appears as a shift below the baseline and mitral flow appears above the baseline.

-In patients with valvular stenosis (ie, smaller cross-sectional valve area), obstruction to
blood flow causes flow velocity to increase in order to maintain overall forward blood flow
across the valve.
-This increased flow velocity, detected as a murmur on auscultation, can be measured
during Doppler echocardiography.
 138) Oxygen saturation and heart pressures in VSD : RV o2> RA
-blood in RA: 65% oxygenation vs blood in RV: 79% saturation (raised)
whereas in normal circumstances these readings should be similar.

-This gradient in oxygen saturation suggests that there is oxygenated blood from
the left heart flowing into the right heart at the ventricular level like VSD.

-The increased right-sided heart pressures are due to increased blood flow from the left-
to-right shunt. The low cardiac output also stems from this new defect.

-Pulmonary capillary wedge pressure (reflecting left atrial pressures) may be

elevated.
Vs

139) heart pressures in PE:

*similarity with VSD:
-The soft holosystolic murmur at the left sternal border in PE is most likely due to TR from
elevated right-sided heart pressures. (Confusing with VSD)

*Difference with VSD

The cardiac catheterization : low CO, elevated RA pressure, elevated RV pressure equally
unlike VSD (RVP> RAP O2)
- elevated pulmonary artery pressure.
vmr
-However, the (PCWP), which reflects left atrial pressure is normal vs abnormal in VSD

-ECG abnormalities generally proceed in a stepwise

manner as follows: tall, peaked T waves →
progressive lengthening of the PR interval →
absent/flattened (ie, low amplitude) P waves →
QRS complex widening → sine wave pattern.
÷
142) PE
-Pregnancy increases the risk of venous thromboembolism.
—> Ventilation/perfusion (V/Q) scan is preferred over CT angiogram in initial
evaluation for pulmonary embolism (PE) in pregnant women with a normal chest x-
ray.
—> In any patient (pregnant, nonpregnant) with high pretest probability of PE, only a
normal V/Q scan rules out PE, and low- or moderate-probability V/Q scan results
require further testing.

143) Certain beta-blockers (metoprolol succinate, carvedilol, bisoprolol) have been shown
to improve symptoms and overall long-term survival in stable patients with heart failure and
left ventricular (LV) systolic dysfunction (LV ejection fraction <40%)

Joint National Committee 8 recommendations for treating 144) RAS Ix:

hypertension -noninvasive assessment with
Initiate Rx Goal blood pressure renal duplex Doppler
>150 mm Hg systolic ultrasonography / CT / MR
Age >60
BP or
<150/90 mm Hg angiography (MRA) for the
>90 mm Hg diastolic diagnosis of RAS.
BP
Age <60, >140 mm Hg systolic
chronic kidney BP or
-Renal Doppler ultrasound is the
<140/90 mm Hg initial preferred modality in patients
disease, >90 mm Hg diastolic
diabetes BP with renal insufficiency due to risk
Thiazide diuretic or CCB, of contrast-induced nephropathy
Black CT alone or in combination (with CT angiography) and
(ACEI/ARB, not first-line)
nephrogenic systemic fibrosis (with
Thiazide diuretic, ACEI, gadolinium-enhanced MRA).
Initial treatment Other ethnicities ARB, or CCB,
choice alone or in combination
145) RF for DM:
ACEI or ARB,
All ethnicities with alone or in combination -obesity, high calorie diet,
chronic kidney disease with sedentary lifestyle
other drug classes

Mechanical prosthetic valve thrombosis (aortic & mitral valve)

• Aspirin 75-100 mg/day
Prevention • Mitral valve: warfarin with target INR 2.5-3.5
• Aortic valve: warfarin with target INR 2.0-3.0
• Inadequate anticoagulation
• Mitral valve risk > aortic valve risk
Clinical features • Obstructive thrombus mimics valvular stenosis
• Heart failure, cardiogenic shock
• Systemic thromboembolic events (eg, stroke)
• Echocardiogram visualizes thrombus
• Anticoagulation (eg, heparin)
Diagnosis & • Fibrinolytic therapy (typically avoided if
treatment possible)
• Immediate surgery for severe heart failure or
large thrombus
 Hypertension stages
Category &
Management Comments
definition
Elevated BP
Weight loss, exercise, dietary
(SBP
Lifestyle changes changes (reduced salt, alcohol
120-129;
in moderation, DASH diet)
DBP <80)
An antihypertensive drug is
needed if:
Stage 1 HTN
Lifestyle changes • Comorbid DM, CKD, or
(SBP
± 1 antihypertensive ASCVD
130-139;
drug • OR
DBP 80-89)
• 10-year risk of ASCVD
>10%
Stage 2 HTN Lifestyle changes A 2-drug combination is
(SBP ≥140; AND 1-2 recommended if BP is ≥20/10
DBP ≥90) antihypertensive drugs mm Hg above target

Causes of acquired long QT syndrome

• Diuretics (due to electrolyte imbalances)
• Antiemetics (eg, ondansetron)
• Antipsychotics (eg, haloperidol, quetiapine,
risperidone)
• Tricyclic antidepressants
• Selective serotonin reuptake inhibitors
Medications
(eg, citalopram)
• Antiarrhythmics (eg, amiodarone, sotalol,
flecainide)
• Antianginal drugs (eg, ranolazine)
• Anti-infective drugs (eg, macrolides,
fluoroquinolones, antifungals)
• Electrolyte imbalances (↓ potassium,
Metabolic ↓ magnesium, ↓ calcium)
disorders • Starvation
• Hypothyroidism
Bradyarrhythmi • Sinus node dysfunction
as • Atrioventricular block (2nd or 3rd degree)
• Hypothermia
• Myocardial ischemia/infarction
Others
• Intracranial disease
• HIV infection
#Surgery for AAA:
-Without immediate repair, acutely ruptured AAA is fatal, usually within hours.
-An alternative to open surgery is endovascular aneurysm repair (EVAR), which is
becoming more feasible and widely accepted when it is anatomically and clinically
appropriate
 Acute thrombotic
Heparin if
occlusion dit PAD
Old
Age

}
H - HTM

I Itlypenlipidemin
Smokes

L Limb threatening Cxg Non healing Ulcers

preserved
Daily living activity limitation
for failure to respond to previous
DVT Mx Protocols

e-

E O .

O
 PE Mx Approach

.
=

€ 74

0 .
-

f - .
328 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PHARMACOLOGY
``

Lipid-lowering agents
DRUG LDL HDL TRIGLYCERIDES MECHANISMS OF ACTION ADVERSE EFFECTS/PROBLEMS
HMG-CoA reductase    Inhibit conversion of HMG- Hepatotoxicity ( LFTs),
inhibitors CoA to mevalonate, a myopathy (esp when

30
Atorvastatin, cholesterol precursor; used with fibrates or
simvastatin Ž  intrahepatic cholesterol niacin) -

Ž  LDL receptor recycling →

Ž  LDL catabolism
 in mortality in patients
with CAD
Bile acid resins   slightly  slightly Prevent intestinal GI upset,  absorption of
other drugs and fat-
Cholestyramine, -
reabsorption of bile acids;
soluble vitamins
colestipol, liver must use cholesterol to
colesevelam make more
Ezetimibe  /— /— Prevents cholesterol Rare  LFTs, diarrhea

=
absorption at small intestine
brush border
Fibrates    Activate PPAR-α Myopathy ( risk with
Gemfibrozil, Ž upregulate LPL Ž  TG statins), cholesterol
bezafibrate, clearance gallstones (via
fenofibrate Activate PPAR-α Ž induce inhibition of cholesterol
HDL synthesis 7α-hydroxylase)
Niacin    Inhibits lipolysis (hormone- Flushed face

F- for
sensitive lipase) in adipose (prostaglandin mediated;
tissue; reduces hepatic  by NSAIDs or long-
VLDL synthesis term use)
Hyperglycemia
Hyperuricemia
PCSK9 inhibitors    Inactivation of LDL-receptor Myalgias, delirium,
Alirocumab, degradation Ž  removal of dementia, other
evolocumab LDL from bloodstream neurocognitive effects
Fish oil and marine  slightly  slightly  at high Believed to decrease FFA Nausea, fish-like taste
omega-3 fatty acids doses delivery to liver and decrease
activity of TG-synthesizing
enzymes

Clinical clues to renovascular disease

• Resistant HTN (uncontrolled despite 3-drug
regimen)
• Malignant HTN (with end-organ damage)
HTN-related • Onset of severe HTN (>180/120 mm Hg) after
symptoms age 55
• Severe HTN with diffuse atherosclerosis
• Recurrent flash pulmonary edema with severe
HTN
Physical examination
• Asymmetric renal size (>1.5 cm)
• Abdominal bruit
Supportive Laboratory results
evidence • Unexplained rise in serum creatinine (>30%) after
starting ACE inhibitors or ARBs
Imaging results
• Unexplained atrophic kidney
 CARDIOVASCULAR CARDIOVASCULAR—PHARMACOLOGY
`` SEC TION III 329

Lipid-lowering agents (continued)

Liver Blood Enterocyte Intestinal lumen

Acetyl-CoA

ApoE Lymphatics CHOLESTEROL

HMG-CoA ABSORPTION
receptor CHY CHY
HMG-CoA CHY
reductase rem Ezetimibe
Triacylglyceride LPL
Mevalonate
HDL FFA
pool
Cholesterol Cholesterol
Cholesterol VLDL VLDL FFA FFA
Bile acids Bile acids
MEVALONATE

o
SYNTHESIS Niacin
BILE ACID
LPL REABSORPTION
Statins HDL LPL-
Lovastatin receptor FFA
Pravastatin UPREGULATION
Simvastatin HDL HDL Bile acid resins
Atorvastatin Lipolysis Fibrates Cholestyramine
Rosuvastatin FFA Colestipol
Gemfibrozil
Bezafibrate Colesevelam
Adipose tissue
LDL Fenofibrate
LDL
LDL
receptor
ADIPOSE LIPOLYSIS

PCSK9
LDL-RECEPTOR
DEGRADATION
E Niacin

PCSK9 inhibitors
Alirocumab
Evolocumab

Cardiac glycosides Digoxin.

MECHANISM Direct inhibition of Na+/K+ ATPase Digoxin
Na+/Ca2+ Na+/K+
Ž indirect inhibition of Na+/Ca2+ exchanger. exchanger ATPase
 [Ca2+]i Ž positive inotropy. Stimulates vagus
nerve Ž  HR.
Ca2+
Na+ K+

↑TnC Ca 2+ ↑ cardiac
SR ↑↑Ca2+ binding contraction

CLINICAL USE HF ( contractility); atrial fibrillation ( conduction at AV node and depression of SA node).
ADVERSE EFFECTS Cholinergic effects (nausea, vomiting, diarrhea), blurry yellow vision (think van Glow),
arrhythmias, AV block.
Can lead to hyperkalemia, which indicates poor prognosis.
Factors predisposing to toxicity: renal failure ( excretion), hypokalemia (permissive for digoxin
binding at K+-binding site on Na+/K+ ATPase), drugs that displace digoxin from tissue-binding
sites, and  clearance (eg, verapamil, amiodarone, quinidine).
ANTIDOTE Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+.
330 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PHARMACOLOGY
``

Antiarrhythmics— Slow or block conduction (especially in depolarized cells).  slope of phase 0 depolarization.
sodium channel  action at faster HR. State dependent  HR Ž shorter diastole, Na+ channels spend less time in
blockers (class I) resting state (drugs dissociate during this state) Ž less time for drug to dissociate from receptor.
Effect most pronounced in IC>IA>IB due to relative binding strength. Fast taxi CAB.
Class IA Quinidine, procainamide, disopyramide.
0 mV
“The queen proclaims Diso’s pyramid.” 0 mV
Slope of
MECHANISM Moderate Na+ channel blockade. phaseof0
Slope
 AP duration,  effective refractory period 0 mV INa 0
phase

=
INa
(ERP) in ventricular action potential,  QT Slope of
interval, some potassium channel blocking phase 0
INa
effects.
CLINICAL USE Both atrial and ventricular arrhythmias,
especially re-entrant and ectopic SVT and VT.
ADVERSE EFFECTS Cinchonism (headache, tinnitus with
quinidine), reversible SLE-like syndrome
(procainamide), HF (disopyramide),
thrombocytopenia, torsades de pointes due to 0 mV
 QT interval. Slope of
0 mV
phaseof
Slope 0
Class IB Lidocaine, phenytoin, mexiletine. INa 0
phase
0 mV I
“I’d Buy Liddy’s phine Mexican tacos.” Na
Slope of
phase 0
MECHANISM Weak Na+ channel blockade. INa
 AP duration. Preferentially affect ischemic or
depolarized Purkinje and ventricular tissue.
CLINICAL USE Acute ventricular arrhythmias (especially post-
MI), digitalis-induced arrhythmias.
IB is Best post-MI.
ADVERSE EFFECTS CNS stimulation/depression, cardiovascular
depression.
Class IC Flecainide, propafenone. 0 mV
0 mV
“Can I have fries, please?” Slope of
MECHANISM Strong Na+ channel blockade. phaseof
Slope
0 mV 0
INa 0
phase
Significantly prolongs ERP in AV node and INa
Slope of
accessory bypass tracts. No effect on ERP in phase 0
Purkinje and ventricular tissue. INa
Minimal effect on AP duration.
CLINICAL USE SVTs, including atrial fibrillation. Only as a last
resort in refractory VT.
ADVERSE EFFECTS Proarrhythmic, especially post-MI
(contraindicated). IC is Contraindicated in
structural and ischemic heart disease.
 CARDIOVASCULAR CARDIOVASCULAR—PHARMACOLOGY
`` SEC TION III 331

Antiarrhythmics— Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol.

β-blockers (class II)
MECHANISM Decrease SA and AV nodal activity by  cAMP,  Ca2+ currents. Suppress abnormal pacemakers by
-
 slope of phase 4.
AV node particularly sensitive— PR interval. Esmolol very short acting.

=
CLINICAL USE SVT, ventricular rate control for atrial fibrillation and atrial flutter.
ADVERSE EFFECTS Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF),
CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.
Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in vasospastic angina.
β-blockers (except the nonselective α- and β-antagonists carvedilol and labetalol) cause unopposed
α1-agonism if given alone for pheochromocytoma or for cocaine toxicity (unsubstantiated). Treat
β-blocker overdose with saline, atropine, glucagon.
60 Decrease slope Prolonged
of phase 4 repolarization
Membrane potential (mv) 30 depolarization (at AV node)

0
–30 Threshold
potential
–60
–90
0 100 200 300 400 500 600 700 800
Time (ms)
Pacemaker cell action potential

Antiarrhythmics— Amiodarone, Ibutilide, Dofetilide, Sotalol. AIDS.

potassium channel
blockers (class III)
MECHANISM  AP duration,  ERP,  QT interval.
CLINICAL USE Atrial fibrillation, atrial flutter; ventricular
tachycardia (amiodarone, sotalol).
ADVERSE EFFECTS Sotalol—torsades de pointes, excessive β Remember to check PFTs, LFTs, and TFTs when
blockade. using amiodarone.
Ibutilide—torsades de pointes. Amiodarone is lipophilic and has class I, II, III,
Amiodarone—pulmonary fibrosis, and IV effects.
hepatotoxicity, hypothyroidism or
hyperthyroidism (amiodarone is 40%
iodine by weight), acts as hapten (corneal
deposits, blue/gray skin deposits resulting
in photodermatitis), neurologic effects,
constipation, cardiovascular effects
(bradycardia, heart block, HF).

0 mV
Markedly prolonged
repolarization (IK)

−85 mV
Cell action potential
332 SEC TION III CARDIOVASCULAR CARDIOVASCULAR—PHARMACOLOGY
``

Antiarrhythmics— Diltiazem, verapamil.

calcium channel
blockers (class IV)
MECHANISM Decrease conduction velocity,  ERP,  PR interval. -3
CLINICAL USE Prevention of nodal arrhythmias (eg, SVT), rate control in atrial fibrillation.
ADVERSE EFFECTS Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression).

60

Membrane potential (mv)

Slow rise of
30 action potential Prolonged
repolarization
0 (at AV node)
Threshold
–30 potential
–60
–90
0 100 200 300 400 500 600 700 800
Time (ms)

Other antiarrhythmics
Adenosine  K+ out of cells Ž hyperpolarizing the cell and  I-
Ca, decreasing AV node conduction. Drug of

=
choice in diagnosing/terminating certain forms of SVT. Very short acting (~ 15 sec). Effects
blunted by theophylline and caffeine (both are adenosine receptor antagonists). Adverse effects
include flushing, hypotension, chest pain, sense of impending doom, bronchospasm.
Magnesium Effective in torsades de pointes and digoxin toxicity.

Ivabradine
MECHANISM IVabradine prolongs slow depolarization (phase “IV”) by selectively inhibiting “funny” sodium
channels (If ).
CLINICAL USE Chronic stable angina in patients who cannot take β-blockers. Chronic HFrEF.
ADVERSE EFFECTS Luminous phenomena/visual brightness, hypertension, bradycardia.
 Infection

#pneumococcal bacteremia; asplenic patients with pneumococcal infections are also more
likely to develop purpura fulminans (characterized by DIC, tissue thrombosis, and skin
hemorrhage and necrosis), reflecting infection severity.

• Infections that need to be treated with immunoglobulin: Dangerous infections To Be

Healed Very Rapidly (Diphtheria, Tetanus, Botulism, Hepatitis B, Varicella, Rabies
 Antibiotics of choice
1) Pertussusis: Macrolides
2) otitis media: Amoxycillin- mild; Augmentin: severe
3) Influenza : Oseltamivir

4) Otitis media: oral Ab vs topical in otitis externa

• Initial: amoxicillin
• 2nd-line: amoxicillin-clavulanate
• Penicillin-allergic: clindamycin or azithromycin
Vs
OE: topical FQ;
Malignant OE: IV FQ

5) Infective endocarditis:
- in absence of culture: Vancomycin
- if penicillin sensitive str. Viridans: Aqueous penicillin G
- if Rt sided IE by IV drug: MC Staph so Vancomycin

6) Cat scratch Ds: Azithromycin ( henselae)

Cat bite ( P. Multimodal, Anaerobes): Augmentin

7) pinworm: Pyrantel pamoate/ albendazole to pt+household contact

8) Acute rhinosinusitis: capsule Augmentin only if bacterial

9) unilateral cervical lymphadenitis: Clindamycin (covers both Staph+ str.
Pyogenes)+Augmentin

10)Typical lobar/ focal pneumonia: Amoxicillin (str. pneumonia)

11) Atypical pneumonia: Macrolides ( Mycoplasma, chlamydia, virus)

12) Osteomyelitis : Vancomycin

13) typhoid. Ceftriaxone

14) Lymphangitis: Cephalexin (covers str. Pyogenes + MSSA)

-
15) Catheter related blood stream infection: Vancomycin + ceftazidime ( staph + CONS)

16) SSSS: Vancomycin + clindamycin

17) Clostridium difficle: Oral vancomycin/ Fidaxomycin

18) PID. Outpatient: Ceftriaxone + doxycycline

19) Human fist bite: Augmentin (covers Staph, strep, eikinella, H
. influenza, anaerobes

20) post splenectomy fever: 1st line:Augmentin; 2nd line: levofloxacin

21) Hot tub folliculitis : FQ effective if pseudomonas

. TMP SMX if Staph aureus

22) invasive burn wound infection: Piptaz/ carbapenems(pseudomonas)+ vancomycin

(MRSA)

¥
Noninvasive burn wound infection: Cefazolin/ clindamycin

23) Vibrio Vulnificus: IV Ceftriaxone+ doxycycline

24) Deep diabetic foot ulcer: IV Piptaz+ vancomycin

25) Epiglottitis: Ceftriaxone( H influenza, str Pneum)+ vancomycin (MRSA)

26) Cystic fibrosis: Piperacillin-tazobactam and tobramycin adults

Vanco children

27) Actinomycetes: mild without fistula- oral penicillin

Severe case- IV penicillin with concomitant surgery

28) cervicitis:
• Empiric: ceftriaxone + doxycycline*
• Confirmed chlamydia: doxycycline*/azithro in Pregnancy
• Confirmed gonorrhea: ceftriaxone

Virus DOC
1) Croup/ Laryngotracheitis:
Mild(stridor only on agitation: corticosteroids
Mod- severe (Stridor even at rest): racemic epinephrine + CS

Parasite
1) Ivermectin :strongyloidiasis; onchocerciasis
2) Praziquantel :schistosomiasis
 Diagnosis of choice
1) ventilator associated pneumonia: Lower RS tract ET sample

2) Diabetic foot with bone felt: Bone biopsy / culture

If debridement of deep ulcer: Ulcer base scrapping

3) pyogenic liver abscess: CT abd

4) Amoebic liver abscess: Serology

5) Hydatid cyst: USG

. Egg shell calcification with internal
septation on CT

Tetanus prophylaxis
Clean or minor wound Dirty or severe wound
• Tetanus toxoid- • Tetanus toxoid-
containing containing
vaccine* only if vaccine* only if
>3 tetanus toxoid doses
last dose >10 last dose >5 years
years ago ago
• No TIG • No TIG
• Tetanus toxoid-
• Tetanus toxoid-
Unimmunized, uncertain, containing
containing
or <3 tetanus toxoid vaccine*
vaccine* only
doses +
• No TIG
• TIG
*Booster given as tetanus/diphtheria (Td) toxoids adsorbed or tetanus
toxoid/reduced diphtheria toxoid/acellular pertussis (Tdap)

Allergic bronchopulmonary aspergillosis

(ABPA)
• Asthma
History
• Cystic fibrosis
Chest • Recurrent fleeting infiltrates
imaging • Bronchiectasis
• Positive Aspergillus skin test
&/or IgE
Diagnosis
• Elevated serum IgE
• Eosinophilia

#Areas with moderate to high prevalence of hepatitis A include most parts of South America,
Africa, Asia, Eastern Europe, Mexico, and Central America, respectively. Travelers to
countries of these areas should get vaccinated against the hepatitis A virus
1) Croup Case clue
-organism: Parainfluenza
-subglottic edema and narrowing, presents with a seal like barky cough and inspiratory
stridor vs stridor+ Ill child with fever, sore throat, drooling in epiglotiitis
-Rx: • Mild (no stridor at rest): humidified air ± corticosteroids
• Moderate/severe (stridor at rest): corticosteroids + nebulized epinephrine
Vs
2) bronchiolitis :<2 yrs
-small airway inflammation with RSV
-cough and wheezing, not stridor

3) Haemophilus influenzae type b Epiglottitis

-often have stridor and respiratory distress, they typically appear ill and have a high fever,
difficulty swallowing, and drooling

4) watery diarrhoea/vomiting within 1–6 hours: Staph aureus, B cerious

5) Spontaneous onset gas gangrene without prior trauma in patient of colo rectal
cancer: C.septicum

6) bloody diarrhoea with beef eating: E HEC

Bloody diarrhoea by contact with reptiles: S.non-typhi

7) Central venous catheters are the most common cause of nosocomial bloodstream
infections as they create a direct pathway for colonized skin organisms to access the
circulatory system. MCC: Staph; Eg: Candidemia

8) Catheter-related bloodstream infection (CRBSI):

-Because tunneled dialysis catheters have a cuff that prevents bacterial migration along
the exterior of the catheter, so they usually lack infection around the external catheter
site (eg, erythema, purulence).

—> systemic signs of infection (eg, fever, chills, malaise) +Progressive s/o: shock (eg,
lactic acidosis, confusion, hypotension)

9) Lymphangitis:
-Tender, erythematous streaks proximal to wound in 1-3 days after injury at hike
• Regional tender lymphadenopathy (lymphadenitis)
• Systemic symptoms (eg, fever, tachycardia)
Vs
Sporotrichosis: nodular swelling along proximal lymphatics develops over weeks not
days
CDC guidelines for prevention of CVC related infections
(Central Venous Catheter- related) :

1) HAND HYGIENE

2) maximal barrier precautions including sterile sheet

drape,Gloves, masks, long sleeved gown

3) preparation of injection site with chlorhexidine

4) Prompt removal of catheter when no longer needed

5) Femoral access has the highest chances of infection so

always Use IJV or SUBCLAVIAN VEINS
10) Catheter-associated urinary tract infection (CA-UTI)
-prevented by avoiding unnecessary catheter use and minimizing the duration of
catheterization.

-clean intermittent catheterization (CIC), which involves periodic insertion and

removal (eg, every 4-6 hours) of a clean urinary catheter and can often be performed
by the patient, is usually the initial treatment.

11) Osteomyelitis in children

# Children: Staph aureus is MCC
# Infant: E. coli and (group B Streptococcus)
# Puncture wound, IV drug abuser: P. Aeruginosa
# sickle Ds: Salmonella (capsulated)

✓
i

12) Lemierre syndrome (LS) fusobacterium

prior H/O of tonsillitis +Lateral neck swelling and tenderness at SCM muscle +internal
jugular venous thrombosis
-septic thromboemboli can seed other organs, particularly the lungs, causing
respiratory symptoms and leading to nodules on chest x-ray

# Management:
-In addition to supportive (eg, airway) management,
-Rx with IV antibiotics
- possibly, surgery (eg, incision and drainage, vein excision) in patients with no response
to antibiotics.

13) Shigella complication

-In children, seizures in the setting of an acute bacterial gastroenteritis should raise
concern for Shigella infection.
-- rectal prolapse; bacteremia ; (HUS)
180 SEC TION II MICROBIOLOGY MICROBIOLOGY—SYSTEMS
` 

Common causes of meningitis

NEWBORN (0–6 MO) CHILDREN (6 MO–6 YR) 6–60 YR 60 YR +
Group B Streptococcus S pneumoniae S pneumoniae S pneumoniae

{
E coli N meningitidis N meningitidis N meningitidis
Listeria H influenzae type b Enteroviruses H influenzae type b
.
Group B Streptococcus HSV Group B Streptococcus
Enteroviruses Listeria
Give ceftriaxone and vancomycin empirically (add ampicillin if Listeria is suspected).
Viral causes of meningitis: enteroviruses (especially coxsackievirus), HSV-2 (HSV-1 = encephalitis), HIV, West Nile virus (also
causes encephalitis), VZV.
In HIV: Cryptococcus spp.
Note: Incidence of Group B streptococcal meningitis in neonates has  greatly due to screening and antibiotic prophylaxis in
pregnancy. Incidence of H influenzae meningitis has  greatly due to conjugate H influenzae vaccinations. Today, cases are
usually seen in unimmunized children.

Cerebrospinal fluid findings in meningitis

OPENING PRESSURE CELL TYPE PROTEIN GLUCOSE
Bacterial   PMNs  
Fungal/TB   lymphocytes  
Viral Normal/  lymphocytes Normal/ Normal

Infections causing Most commonly viridans streptococci and Staphylococcus aureus. If dental infection or extraction
brain abscess precedes abscess, oral anaerobes commonly involved.
Multiple abscesses are usually from bacteremia; single lesions from contiguous sites: otitis media
and mastoiditis Ž temporal lobe and cerebellum; sinusitis or dental infection Ž frontal lobe.
Toxoplasma reactivation in AIDS.

Osteomyelitis RISK FACTOR ASSOCIATED INFECTION

A Assume if no other information is available S aureus (most common overall)

Sexually active Neisseria gonorrhoeae (rare), septic arthritis more
common
Sickle cell disease Salmonella and S aureus
Prosthetic joint replacement S aureus and S epidermidis
Vertebral involvement S aureus, M tuberculosis (Pott disease)
Cat and dog bites Pasteurella multocida
IV drug use S aureus; also Pseudomonas, Candida
Elevated ESR and CRP sensitive but not specific.
Radiographs are insensitive early but can be useful in chronic osteomyelitis ( A , left). MRI is best
for detecting acute infection and detailing anatomic involvement ( A , right). Biopsy or aspiration
with culture necessary to identify organism.
14) Non-typhoid; non-invasive; common in USA; self-limiting
Vs
Typhoid: severe, bacteremia, fatal , needs Ab; > Developing country

15) Lobar pneumonia:

• Abrupt onset of fever, cough, chest pain; Increased work of breathing
• O/E: Focal crackles
Vs
#Interstitial pneumonia:
• Prolonged, gradually worsening cough but less severe
• No: Chest pain, hypoxia, and RS distress are unusual
• walking pneumonia: patients not appear ill
• O/E: Bilateral crackles, wheezing /rhonchi

16) Bacterial meningitis in children (age >1 month)

-Age <1: bulging fontanelle, irritability, poor feeding as Fontanelle acts as pop off valve
-Age >1: signs of increased ICP (eg, headache, vomiting), meningeal signs (eg, nuchal
rigidity)
#Cx: Intellectual/behavioral disabilities; Hearing loss; Cerebral palsy; Epilepsy

17) Herpangina
-caused by Coxsackie A virus
-Common site of ulcer: posterior soft palate, anterior palatine pillars, tonsils, and
uvula
Vs
Herpetic gingivostomatitis
-caused by HSV
-Common sites: (buccal mucosa, tongue, gingiva, hard palate) and lips

18) Rabies:
• Incubation: 1-3 months after exposure
• nonspecific prodrome x few days;
• pain, tingling, and/or numbness of the bite wound,(highly suggestive)
• Hydrophobia ( spitting saliva and water) & aerophobia (fear of drafts of air) due
to pharyngeal spasm)
• Autonomic instability (hypersalivation), vitals unstable; fluctuating Agitation &
altered mental status; muscle contractions (eg, facial grimacing, opisthotonos)
Vs
3 week incubation in tetanus+ trismus (inability to open mouth)
19) sickle cell disease (SCD) sepsis:
-MCC: Str. pneumoniae, H. influenzae, and N. meningitidis.
-incidence of bacteremia has decreased by improved vaccination
-Prevention: should receive prophylactic penicillin until at least age 5.

20) Pertussis
-In infants, the initial phase may be short/mild or absent, whereas
- paroxysmal phase is severe with gagging, gasping, cyanosis, and life-threatening
apnea.

21) Early onset neonatal sepsis (age <7 days):

-Vertical transmission in utero or during vaginal delivery by colonised vaginal wall
-maternal intrapartum Ab Px: Reduced transmission
Typically presents within 24 hours

Vs
#Late onset neonatal sepsis (age ≥7 days)
-Horizontal transmission from colonized household
-Maternal intrapartum Ab Px: does not reduce the incidence of late-onset disease.
Typically presents age 4-5 weeks

22) meningitis PEP:

-Antibiotics (rifampin/ ciprofloxacin/ ceftriaxone) should be administered as soon as
possible after exposure, ideally within a day of diagnosis but up to 2 weeks
Regardless of vaccination status.

23) neonatal sepsis:

-1st step: CBC with differential, urinalysis, cerebrospinal fluid (CSF) analysis, and
cultures of all 3 fluids (blood, urine, CSF) taken before administering antibiotics

24) meningitis: full fontanelles and apnea; lethargy

25) Viral upper respiratory syndrome: Rhinorrhea, coryza, sneezing, mild pharyngitis;
systemic Sx mild
#Influenza: Prominent with possible high fever, myalgias, headache
#Streptococcal pharyngitis: Pharyngeal erythema, tonsillar hypertrophy & exudates,
tender cervical lymph nodes

26) Ecthyma gangrenosum (EG): pseudomonas

-C/F: begin as painless red macules and become indurated pustules/bullae, often with
"punched-out" gangrenous ulcers +fever ; MC in immunodeficient sepsis pt
Vs
#PG: in IBD with violaceous border but without fever
27) 1o Influenza pneumoniae
-acute worsening of symptoms (dyspnea, cough)
-leukocytosis (although <15,000/mm3)
-hypoxia, and bilateral, diffuse interstitial infiltrates on chest x-ray.
Vs

28) 2o bacterial pneumonia

-Streptococcus pneumoniae, Staphylococcus aureus, and (less commonly) Pseudomonas
- high fever, significant leukocytosis (>15,000/mm3), and lobar infiltrates on CXR

29) Rash + Diarrhea with Mononucleosis like C/Fs —> S/O Acute HIV Infection
-Viral load is markedly elevated (>100,000 copies/mL) —> only significant lab finding

30) Systemic Septic emboli —> If Left sided Valves involved

-Pulmonary Septic Emboli —> If Right sided Valves involved especially in IV Drug
abusers
#Rx:
• Acute: Empiric treatment with vancomycin
• Subacute: Treatment based on culture results

31) sporotrichosis:
-papule forms at the site of entry,soon ulcerates, draining an odorless, nonpurulent fluid.
-Several proximal lesions may develop along lines of lymphatic drainage (NOTE NOT
LN)
Vs
#Cat scratch fever: cutaneous lesion (vesicular, erythematous, or papular) with
prominent, tender, regional lymphadenopathy and possible systemic spread.

32) septicemia caused by Neisseria meningitidis:

-young adult has an abrupt onset of fever, vomiting, and severe myalgias with findings of
mottled skin, cool extremities, and confusion.
-This rapid progression of symptoms over 4 hours
—> -severe myalgias (eg, marked leg pain), which are often more painful than those
in viral illnesses s/o early meningitis

33) erysipelas:
-Superficial dermis and lymphatics; raised sharply demarcated edges; rapid spread;
fever early course
Vs
#Non-Purulenf cellulitis:
-deep dermis and SC fat; flat edges with poor demarcation; indolent course; fever later
in course
 2) Erysipelas
a warm, tender, erythematous rash notable for
raised, sharply demarcated borders
—> Involvement of the external ear is
particularly suggestive of erysipelas as this skin
lacks a lower dermis level (making cellulitis, a
deeper skin infection, unlikely).
#

—> Dx of erysipelas is usually based on clinical findings, but blood cultures are useful in
patients with extensive rash, systemic toxicity, or underlying comorbidities (eg, diabetes).

Rx of Erysipelas :
1) Most patients receive intravenous antibiotics (eg, ceftriaxone, cefazolin),

2) For without systemic symptoms —> with oral medication (eg, amoxicillin).

3) If possible, the underlying source of skin breach should be addressed to help prevent
recurrence.

D/D :

1) Clostridium perfringens causes gas gangrene and manifests with severe pain, bullae, soft
tissue crepitus, and signs of systemic toxicity (including shock and multiorgan failure).

2) Enterococcus, Haemophilus influenzae, Pseudomonas aeruginosa, and Staphylococcus

aureus usually cause cellulitis, a deeper skin infection of the lower dermis and subcutaneous
fat.
—> Cellulitis tends to have a slower onset (over days), indistinct/flat borders, and fewer initial
systemic symptoms (eg, fever).

—> S aureus in particular is associated with purulent skin and soft tissue infections (eg, pus
drainage, furuncle/carbuncle/abscess formation).

—> Pseudomonas can also cause external otitis, which is often accompanied by ear pain and
discharge, an edematous ear canal, and hearing loss (not seen in this patient).
34) Rocky Mountain spotted fever
-constitutional symptoms, confusion, signs of septic shock, petechial rash starting
from ankles wrist, thrombocytopenia, hyponatraemia and minimal
leukocytosis(<100) on lumbar puncture
-trip to North Carolina.

#Pathogenesis: This bacterium attacks vascular endothelial cells, which causes

progressive capillary permeability, fluid extravasation, hypovolemia, and poor tissue
perfusion.

35) Mycobacterium avium complex

-subacute) Fever & weight loss

-Abdominal pain & diarrhea —> GIT C/Fs; LAD & (often) hepatosplenomegaly

36) How to Dx Viral Esophagitis from Candida??

viral esophagitis is more likely than candidal esophagitis in patients
who have:
• Severe odynophagia (pain with swallowing) as the
predominant symptom
• No dysphagia (difficulty swallowing)
• No thrush; last 2 + in Candida esophagitis
37) Major criteria for Duke IE
Major criteria
• Blood culture positive for typical
microorganism
• (eg, Staphylococcus aureus,
Enterococcus, viridansstreptococci) oh
• Echocardiogram showing valvular
vegetation

==> best next step: 3 blood cultures from 3 different venepuncture sites sent (over 1
hr in acute illness and several hrs in stable pt) before Ab and echo
-in stable pt, ab administered after culture

38)Post exposure Prophylaxis schedule for hepatitis A: especially given in Mexico

- within 2 weeks of exposure; close contacts of Hep A infected
-younger patients (age <40) :should receive Hep A vaccine,
-older patients (age >41) :should receive Hep A Ig.

39) children with suspected bacterial pharyngitis should not be treated without culture cz it’s
useless to start Ab in viral pharyngitis
41) U/L cervical adenitis: Staph aureus, Str. Pyogenes, anaerob, MAC
B/L adenitis: adenovirus, EBV/CMV
# MAC LNopathy: underlying skin is violet and thin

43) prophylaxis for Lyme Ds: doxycycline stat especially if tick is attached >36 hours

44) TB Rx in Pregnancy: HRE x 2 mon followed by HR x 7 mon

45) IE by UTI/ cystoscopy: enterococcus.

IE with colon CA/ IBD: str. Bovis, S gallolyticus..
IE with viridans: dental procedure

46) splenic abscess: triad of fever, leucocytosis and left upper quadrant abd pain
-Dx: CT; -Rx: Ab + splenectomy must (as microabscess can be missed in aspiration)
-RF: bacteremia from a distant infection (eg, infective endocarditis MC, cholecystitis).
-> in: immunocompromise from HIV, hematologic malignancy, or diabetes mellitus.

47) Ehrlichiosis: by lone star tick

-RMSF but without rash; intracytoplasmic morula in monocytes; leukopenia; MEGA
berry

48) syphilis treatment follow-up:

-repeat non treponemal serology 4 fold titre fall at 6-12 months confirms adequate Rx

49) CMV: periventricular calcification

Toxoplasmosis: diffuse intracerebral calcification

50) Features specific for congenital Syphillis:

-copious clear, purulent/ serosanguineous rhinorrhoea (snuffles)
-diffuse maculopapular rash on palm and sole; desquamating /bullous
-Abnormal long bone radiographs (metaphyseal lucency)

51) Disseminated gonococcal infection: IV ceftriazone+ azithro

-Purulent monoarthritis without skin lesion
Or
-Triad:
1) Tenosynovitis
2) Dermatitis: polymorphic : mostly vesiculo pustular and not maculopapular
3) Migratory asymmetric polyarthralgia (think something else if static
symmetric )without Purulent arthritis
Vs
#Chikunguniya: malaise, symmetric polyarthralgia, maculopapular rash, leukopenia and
thrombocytopenia after visit to puerto rica

52) Gonococcal pharyngitis with PID:

-non exudative Pharyngitis with fever and lower abdominal pain in a young, sexually
active patient +/- non tender LNopathy

54) uncomplicated pyelonephritis:

-Does not require imaging except if persistent Sx despite 48-72 hrs of therapy, unusual
urinalysis (hematuria); H/O nephrolithiasis
-urine culture sent before starting empiric Ab
Vs
Complicated: needs imaging for complications and prompt therapy

55) Ventilator associated pneumonia: >/= 48 hrs after intubation

-1st step: CXray; if negative exclude VAP
-2nd step: lower Resp. Tract sampling prior to Antibiotics
—> if VAP fails to improve after Ab, CT chest for complications/ think for other causes

57) Legionella pneumoniae:

-Bradycardia relative to High grade fever (>102F); GIT Sx, CNS (confusion),
RS,hepatitis
#Lab: hyponatremia; Gm stain: many N but no organism; Legionella U. Ag test
specific
#Rx: Macrolides/ FQ

58) West Nile virus (WNV) is the most common cause of arboviral-acquired disease in the
US. Although WNV infection is asymptomatic in the majority of patients (approx. 80%), it
can lead to West Nile fever, a self-limiting disease that typically lasts 3–10 days and
manifests with fever, headaches, and a transient maculopapular rash on the trunks and
extremities, as seen here.

-In up to 1% of patients, WNV infection can lead to a neuroinvasive disease that

manifests with fever and meningitis, encephalitis, or acute flaccid paralysis.

-Risk factors for neuroinvasive disease : age > 60 years, immunosuppression, or other
comorbidities (e.g., hypertension, diabetes mellitus). Because the condition is usually self-
limited, treatment is supportive.
59) Dx of mucormycosis: sinus endoscopy with biopsy and culture

60) Rx of Lyme disease AV block: IV Ceftriaxone

61) Indication for acyclovir in chickenpox <12 yrs

-Antiviral therapy with acyclovir for chickenpox in children ≤ 12 years of age is only
indicated if the child is at a high risk of developing complications; for example,
-those taking intermittent/chronic glucocorticoids (risk of disseminated varicella
infection and complications like pneumonia), those taking long-term salicylates
(risk of Reye's syndrome), and in those who have a pre-existing skin/pulmonary
disease (risk of secondary bacterial infection)

62) Cutaneous leishmaniasis (CL)

-manifests as an ulcerating skin lesion at the site of a sandfly bite; the lesion gradually
resolves without treatment.
#mucosal leishmania:
-However, certain species of Leishmania (L. braziliensis, L. guyanensis, L. panamensis)
can cause mucosal leishmaniasis (MLs) months to years after CL resolves. The
nasopharynx is typically affected in ML, which can result in nasal blockage, mucosal
bleeding, and/or septal destruction. Cervical lymphadenopathy can also occur.

-South America (especially Bolivia, Peru, and Brazil): endemic for ML

59) Cervical actinomycosis:
-slowly growing non painful, non tender Indurated mass —> may cause abscess, fistula
-MC site: Mandible; NO fever
-Rx: 1st line: High dose penicillin; alternative: clindamycin; IV penicillin + surgical
resection if severe recalcitrant case

60) a) Cat scratch Ds:papule at bite site followed by regional LNnopathy after 1-2
wks
Vs
b)Pasteurella multicida: cellulitis and other soft tissue infection within 1 to 2 days of
cat bite

—>cat scratch Rx: no need of Ab in immunocompetent; azithRomycin in immuno

suppressed

61)Bite wounds with high risk of infection: should be left open to heal by secondary
intention
-Crush injuries, bite on hands or feet, wound on body >12 hours or face >24 hours,cat
bites except face, human bites except face, bites in immunocompromised.

62) neutropenia: ANC = 690 leukocytes × 20% neutrophils = 138 neutrophils/mm3)

-ANC < 1500, neutropenia < 500
-MC organism: pseudomonas
-Mx: blood and urine culture followed by IV anti-pseudoMonal antibiotics: Piptaz,
Meropenem, cefepime

63) Diagnosis of Cl. Difficle diarrhoea requires:

1) watery diarrhoea (>/=3 loose stools/24 hrs) with/without lower abdominal pain, low
grade fever and leukocytosis
+
2) +stool testing for Cl. Difficle toxin/ enzyme immunoassay
-Rx: oral vancomycin/ fidoxamycin x 10 days

64) Latent TB
- DeF: reactive TST / IGRA with a negative chest x-ray and absence of symptoms.
-Therefore, the optimal next step in management is to obtain a screening chest x-ray. To
exclude TB as Rx differs
-Rx: -If no signs or symptoms of active TB are present, treatment with :
1)daily isoniazid and pyridoxine x 9 months
2) weekly rifapentine, high-dose isoniazid, and pyridoxine x 12 weeks is generally
curative.

65) urinary Sx with HSV:

-Dysuria: due to urine contact on the open ulcers and a sterile pyuria
-viral infection within the lumbosacral plexus —> ANS dysfunction —> resultant
acute urinary retention.
66) HUS
#Pathogenesis: The Shiga toxin induces endothelial damage in renal glomeruli—> to
platelet activation, microthrombi formation, and microangiopathic hemolytic
anemia.
The mechanical intravascular shearing of red blood cells (RBCs)

#C/F: Preceding bloody diarrhea; Fatigue, pallor; Bruising, petechiae; Oliguria, edema
#Lab:
• Hemolytic anemia (schistocytes, ↑ bilirubin); Thrombocytopenia; AKI (↑ BUN, ↑ creat)
#Mx: Fluid & electrolyte management; BT if Hb<6 ; Dialysis if AKI

67) ETEC:
-onset: during international travel; watery; duration: <5 days
Vs
68) Giardia duodenalis
-Mechanism: disrupts the epithelial tight junctions between small intestinal enterocytes,
leading to acute malabsorption
-Duration: lasting up to a month.
-Cx: if Left untreated, severe weight loss and vitamin deficiencies.
-Onset: after 1-2 weeks

69) gonococcal proctitis

-patient with new sexual partners has developed tenesmus (eg, straining with minimal stool
production) and mucopurulent rectal discharge

70) #Annual Chlamydia trachomatis screening

- indicated for all sexually active women age <25 due to the increased incidence of
infection in this patient population.

-For this reason, dual contraception with condoms plus another contraceptive method is
recommended for adolescents

71) HPV vaccine

-Individuals age ≥15 require 3 doses of the(HPV) vaccine to achieve immunity: 0,2,6
-In contrast, individuals age <15, such, require only 2 doses administered 6 months
apart to achieve equivalent immunity.
 Syphilis treatment
72) Posttransplantation
Stage First-line Alternate lymphoproliferative disorder
Primary (chancre)
Doxycycline × 14
Secondary (diffuse Penicillin G IM × 1 -RF: occurs in those on high-dose
days
rash) immunosuppressive medications
Latent following transplantation.
(asymptomatic) Doxycycline × 28
Penicillin G IM × 3 -Etiology: (EBV)
Tertiary (eg, CV, days
-C/F: reticuloendothelial
gummas)
manifestations (eg,
Neurosyphilis lymphadenopathy,
Penicillin G IV × 10-14 Ceftriaxone IV × 14
(eg, meningitis,
ocular)
days days* hepatosplenomegaly, cytopenias)
*Penicillin desensitization followed by IV penicillin is preferred for
those with penicillin allergy who have neurosyphilis, but ceftriaxone -Lab: elevated EBV titers.
can be used in those unable to be desensitized.

73) IM:
-Avoid sports for ≥3 weeks (contact sports ≥4 weeks) due to the risk of splenic rupture

74) Despite vaccination, S pneumoniae remains by far the most common cause of
sepsis in patients with SCD, usually from non-vaccine serotypes.
- Prevention: should receive prophylactic penicillin until at least age 5.

75) Vaccine-strain measles

- considerably less infectious and does not require airborne precautions.
-but they should stay away from immunocompromised as it’s live attenuated

76) Indications of steroids in PCP include:

-Hypoxia often worsens with the initiation of antimicrobial treatment due to the release of
pro-inflammatory intracellular macromolecules during lysis of the organism.

• a PaO2 ≤70 mm Hg
• an alveolar-arterial (A-a) gradient ≥35 mm Hg, or
• pulse oximetry <92% on room air.

77) Alternate oral regimens for mild/moderate PCP :

- dapsone-TMP, primaquine with clindamycin, / atovaquone suspension.

=
#Alternate regimens for moderate/severe disease : intravenous (IV) pentamidine /
primaquine + IV clindamycin.

78) PCP clue:

-AIDS pt developing ARDS; B/L diffuse interstitial infiltrates; elevated LDH
 Stage Lyme disease 78) Role of dexamethasone in meningitis??
Early localized • Erythema migrans 1) In children,
(days to 1 • Fatigue, headache -reduce the risk of SNHL when Haemophilus
month) • Myalgias, arthralgias influenzae type b is the causative organism;
• Multiple erythema migrans
Early • Unilateral/bilateral CN
disseminated palsy (eg, CN VII)
2) in adults,
(weeks to • Meningitis It is recommended in S pneumoniae meningitis
months) • Carditis (eg, AV block) as it is lowers risk of unfavorable outcomes and
• Migratory arthralgias
death.
Late • Arthritis
(months to • Encephalitis Cerebrospinal fluid analysis
years) • Peripheral neuropathy
WBC count Glucose Protein
Diagnosis
(cells/mm3) (mg/dL) (mg/dL)
Vaccine-strain versus wild-type varicella Normal 0-5 40-70 <40
# incubation period of 1-3 weeks (both) Bacterial
>1,000 <40 >250
Vaccine strain Wild type meningitis

• <10 lesions Tuberculous

100-500 <45 100-500
meningitis
• Maculopapular &/or
• >100 lesions
vesicular Viral meningitis 10-500 40-70 <150
• Vesicular in
• Mildly contagious Guillain-Barré
successive crops 0-5 40-70 45-1,000
• Mild fever -/+ syndrome
• Highly contagious
• not a C/I to future VZV
WBC = white blood cell.
vaccine.

79) Histoplasmosis:
-lab: pancytopenia; transaminitis; raised LDH and ferritin; urine/S.histoplasma Ag
#Rx: mild/maintenance: itraconazol; mod-severe: amphotericin
-After 1-2 weeks of clinical improvement after IV ampho, most patients are switched to
oral itraconazole (fungistatic) for ≥1 year of maintenance

-Clue: bird droppings; HIV CD 4<100; CXray: reticulonodular infiltrates

80) meningitis by RMSF vs N. meningitis

A) meningococcal meningitis, which also causes petechial rash, fever, and sepsis.

-LP:dramatic leukocytosis (eg, >1000/mm3), high protein, and Low glucose

Vs
B)LP of RMSF :mild leukocyte elevation (<100/mm3),minimal protein
elevation,normal glucose.

81) Miliary tuberculosis

-C/F: presents with subacute or chronic fevers, weight loss, fatigue, and pulmonary
symptoms in immunodeficient or infants—> so false neg TB test; needs culture for dx
-Chest x-ray :diffuse reticulonodular pattern (millet seed).

-Extrapulmonary disease may occur in the lymph nodes, liver, bones, and central
nervous system.
Vs
-Mycoplasma: not long H/O; typically H/O 2-3 weeks
-HL: mediastinal mass

82) heterophile antibody (Monospot) test,

-a specific test that detects EBV antibodies that agglutinate to horse red blood cells.

-timing: Heterophile antibodies arise within a week of symptoms (25% false-negative rate
during the first week of illness) and persist for up to a year.
-children: heterophile antibody test is not accurate in children age <4, for whom
serum anti-EBV antibody testing is recommended instead.

83) B/L pneumonia : Mycoplasma;Chlamydia;Viruses (rare) vs lobar in bact

84) Mx of NAAT based STI:

-if no result: empiric azithro + Ceftriaxone
-confirmed chlamydia: azithro
-confirmed gonorrhoea: Ceftriaxone

—> Both azithromycin and ceftriaxone are active against gonococcal infections.
Ceftriaxone monotherapy was previously used in the treatment of gonococcal
infections, but due to increasing cephalosporin resistance, current guidelines
recommend the combination of ceftriaxone and azithromycin.

85) D/D of vaginitis:

a) BV: thin off white discharge with fishy order;no inflammation; pH:>4.5
Vs
b) TV: thin yellow green malodorous frothy discharge; vaginal inflammation
Clinical features of toxic shock syndrome Culture-positive infective endocarditis
• Prosthetic valves
• Fever usually >38.9 C (102 F) • Intravascular catheters
• Hypotension with systolic BP ≤90 mm Hg Staphylococcus
• Implanted devices (eg,
aureus
• Diffuse macular erythroderma pacemaker/defibrillator)
• Skin desquamation, including palms & soles, 1-2 • Intravenous drug users
weeks after illness onset Viridans :
• Gingival manipulation
• Multisystem involvement (3 or more systems) • Respiratory tract incision or
sanguine, mitis
biopsy
◦ Gastrointestinal (vomiting &/or diarrhea)
◦ Muscular (severe myalgias or elevated • Prosthetic valves
Staphylococcus
• Intravascular catheters
creatine kinase) epidermidis
• Implanted devices
◦ Mucous membrane hyperemia
• Nosocomial urinary tract
◦ Renal (BUN or serum creatinine >1-2x Enterococci
infections
upper limit of normal)
Streptococcus • Colon carcinoma
◦ Hematologic (platelets <100,000/mm3) gallolyticus • Inflammatory bowel
◦ Liver (ALT, AST & total bilirubin >2x upper limit (formerly S bovis) disease
of normal) • Immunocompromised
Fungi
◦ Central nervous system (altered mentation host
(eg, Candida)
without focal neurological signs) • Intravascular catheters
86) antibiotics causing Clostridioides :
fluoroquinolones, penicillins, cephalosporins, and clindamycin).

87) cervical lymphadenitis:

-C/F: Enlarged (3-6 cm), erythematous, markedly tender cervical node;± Fever; ±
Suppurations, Abscess formation
-Rx: 1st line:clindamycin; 2nd line: Augmentin

#Bacterial: U/L vs viral: B/L

88) rubella vs high febrile and Coryza,
conjunctivitis in measles
• Congenital:
◦SNHL
◦ Cataracts
◦ PDA
• Children:
◦ Fever
◦ Cephalocaudal spread of
maculopapular rash
Post auricular LN specific
• Adolescents/Adults:
◦ Same as children +
arthralgias/arthritis
Classification of herpes zoster pain
Pain Timeframe Treatment
Acute Persists ≤30
NSAIDs,
herpetic days from rash
neuralgia onset
analgesics Congenital toxoplasmosis vs congenital cytomegalovirus

Persists >30 Toxoplasmosis CMV

Subacute days but • Maternal consumption of • Maternal contact
NSAIDs,
herpetic resolves within Pathogene undercooked meat or with infected
analgesics
neuralgia 4 months of
sis inadvertent ingestion of cat bodily fluids (eg,
rash onset
feces saliva)
Tricyclic
Persists >4 • Chorioretinitis
Postherpetic antidepressant • Chorioretinitis
months from • Diffuse intracranial
neuralgia s, gabapentin, • Periventricular
rash onset calcifications
pregabalin intracranial
Classic • Macrocephaly (ie,
calcifications
#Perinatal Hep B: features* hydrocephalus) or
• Microcephaly
-if untreated, 90% risk for future microcephaly
• Sensorineural
• Seizures
chronic hep B Majority are asx
hearing loss
-newborns of all mothers with active • Toxoplasma serology or • Urine or saliva
hepatitis B infection should be Diagnosis
PCR CMV PCR
passively immunized at birth • Pyrimethamine, • Ganciclovir or
with HBIG followed —> active Treatment sulfadiazine, folinic acid valganciclovir if
for 1 yr symptomatic
immunization with recombinant
HBV vaccine. *Nonspecific features of congenital infections include jaundice,
hepatosplenomegaly, rash & growth restriction.
• Schedule: within 12 hours of
birth, regardless of the infant's
birth weight or clinical condition.
 90) Hep B serology:
#In the recovery phase,
-all 3 Ab

- #The lone presence of IgM HBcAb

} (and occasionally IgG HBcAb) is
usually suggestive of the window
period,
-
-which occurs after the disappearance
-
of HBsAg but before the appearance of
HBsAb.

91) Rx of syphilis in pregnancy:

-Patients with penicillin allergy should
-
receive skin testing to confirm an
IgE-mediated reaction.

IgM IgG
Anti- Anti- HBV
-If the test is positive,
HBsAg HBeAg anti-
HBc
anti-
HBc
HBs HBe DNA patients are desensitized
Acute HBV
to penicillin prior to
Early phase + + + +++
receiving treatment with
Window phase + +
intramuscular penicillin G
Recovery phase + + + Likely +
benzathine.
Chronic HBV carrier + +
Acute flare of chronic HBV + Likely + + + +
Vaccinated for HBV +
Immune due to natural HBV
+ +
infection

92) Babesiosis:
• Onset: approximately 48-72
- J
hours after attachment. -

• RF: severe illness: immunocompromise, age >50, or a H/O splenectomy

• Fever, fatigue, myalgias, headache (flu-like symptoms)
• If severe: ARDS, CHF, DIC, splenic rupture
• Anemia, thrombocytopenia, increased bilirubin/LDH/LFTs
• mild hepatosplenomegaly ; leucocytosis
**HBsAg and anti-HBc : the
#Mx:
most appropriate diagnostic
•Atovaquone + azithromycin
tests for acute hepatitis B
• Quinine + clindamycin (if severe) infection as they are both
• Resolution: Sx may take up to 3 months to fully resolve. elevated during initial
Vs infection and anti-HBc will
#RMSF: rash predominant; no anemia remain elevated during the
window period
93) Bacterial gastroenteritis
- suspected in a patient with fever, abdominal cramping, and bloody or mucoid
diarrhea. #Lab: Positive stool culture is diagnostic,

#Mx: treatment is generally supportive care and close follow-up in well-appearing

children.
-Empiric antibiotics not recommended due to increased risk of HUS with E. coli O157:H7.

94) Aspergillus: stain shows mold

Vs
Other fungi: yeast

95) The only cause of bloody small volume watery diarrhoea in HIV: CMV colitis (<50)
Rest all: watery diarrhoea

96) Mx of nocardiosis:
-pulm nocardiosis: TMP SMX
-Brain involvement: carbapenems
-if possible, drain abscess surgically; duration of Rx: 6-12 months
Treatment of Clostridioides difficile infection
• Vancomycin PO
Initial
OR
episode
• Fidaxomicin
• First recurrence
◦ Vancomycin PO in a prolonged pulse/
taper course
◦ OR
◦ Fidaxomicin if vancomycin was used in
Recurrence
initial episode
• Multiple recurrences
◦ Vancomycin PO followed by rifaximin
(or above regimens)
◦ Fecal microbiota transplant
Fulminant
(eg,
• Metronidazole IV plus high-dose
hypotension/
vancomycin PO (or PR if ileus is present)
shock,
• Surgical evaluation
ileus,
megacolon)

97) Mx of Brain abscess

-Diagnosis requires CT-guided aspiration or surgical biopsy to obtain tissue for Gram stain
and culture (bacterial, fungal, mycobacterial).
*Rx:
-Most patients are treated with empiric, intravenous antibiotics (eg, metronidazole,
ceftriaxone, and vancomycin) and aspiration of the lesion.
134 SEC TION II MICROBIOLOGY MICROBIOLOGY—CLINICAL BACTERIOLOGY
` 

MICROBIOLOGY—CLINICAL BACTERIOLOGY
` 

Gram-positive lab algorithm

Gram (purple/blue)

Branching
Bacilli Cocci
filaments

Aerobic Anaerobic Aerobic Anaerobic

Listeria Clostridium Nocardia Actinomyces

Bacillus Cutibacterium (weakly acid fast) (not acid fast)
Corynebacterium
(formerly
Propionibacterium)
Catalase

(Pairs or Streptococcus (Clusters) Staphylococcus

chains)
Hemolysis Coagulase

α γ
(Partial (Complete
hemolysis,
green)
β hemolysis,
clear)
(No hemolysis,
grows in bile)
S aureus
Novobiocin
Optochin sensitivity Bacitracin sensitivity Growth in 6.5% NaCl sensitivity
and bile solubility and PYR status and PYR Status NE

OP Group B Group A S saprophyticus S epidermidis

S agalactiae S pyogenes

Viridans streptococci
(no capsule) Enterococcus
S pneumoniae Nonenterococcus E faecium
S mutans (encapsulated) S bovis
S mitis E faecalis

Important tests are in bold. Important pathogens are in bold italics.

Note: Enterococcus is either α- or γ-hemolytic.

Gram-positive cocci antibiotic tests

Staphylococci Novobiocin—Saprophyticus is resistant; Sapro is a no-go on Novo
epidermidis is sensitive
Streptococci Optochin—Viridans is Resistant; Pneumoniae is OVRPS (overpass)
Sensitive
Bacitracin—group B strep are Resistant; group B-BRAS
A strep are Sensitive
 Bacterial meningitis 97) Indications of head CT scan
Risk group Common organisms Empiric antibiotics prior to LP : but after Ab
Streptococcus Vancomycin + 3rd- -to rule out intracranial mass in
pneumoniae, Neisseria generation patients with certain risk factors (eg,
Age 2-50
meningitidis cephalosporin immunocompromised state,
Vancomycin + previous central nervous system
S pneumoniae, N ampicillin + 3rd- disease, new-onset seizures,
Age >50
meningitidis, Listeria generation
cephalosporin papilledema, altered mental
S pneumoniae, N Vancomycin +
status, focal neurologic deficits).
Immunocompromise meningitidis, Listeria, ampicillin +
d gram-negative rods cefepime #Spectrum of Ab:
Gram-negative rods, -Cefepime :covers most of the
Neurosurgery/
penetrating skull
MRSA, coagulase- Vancomycin + major organisms of bacterial
negative cefepime meningitis (eg, Streptococcus
trauma
staphylococci
pneumoniae, Neisseria
• 3rd-generation cephalosporins: ceftriaxone or cefotaxime
• Alternatives to cefepime: ceftazidime or meropenem
meningitidis, group B streptococci,
• Alternative to ampicillin: trimethoprim-sulfamethoxazole for Haemophilus influenzae) as well as
Listeria Pseudomonas aeruginosa.

-Vancomycin : cephalosporin-resistant pneumococci,

- ampicillin : Listeria monocytogenes

98) PEP VZV in newborn:

-indication: for newborns born to mothers with varicella developing 5 days before to 2
days after delivery.
-Prophylaxis :VZV Ig
-infant has not had time to make his own IgG, and because IgG takes 2-3 weeks to
develop after illness, the mother will not have transferred any varicella-specific IgG to the
infant via the placenta. Therefore, this infant lacks protective antibody.

99)Difference in RSV bronchiolitis between old child and <2 yrs child??
1) older children:
-RSV infection is generally a self-limiting, mild
-upper respiratory tract infection (eg, nasal congestion, rhinorrhea).

2) children age <2 years

-tend to have lower respiratory tract involvement.
- wheezing and/or crackles and respiratory distress can have a waxing/waning course
that peaks on days 5-7 of illness

#Complications:
-Infants age <2 months are at high risk of developing apnea and respiratory failure
from bronchiolitis.
-In addition, they tend to develop recurrent wheezing throughout childhood.
100) indication of Palivizumab prophylaxis in selected infants of RSV :
• <29 weeks gestation
• Chronic lung disease of prematurity
• Hemodynamically significant congenital heart disease
101) Candida vaginitis
—>> vulvovaginal erythema +
vaginal discharge + Normal
Vaginal pH of 4

102) Rx of HIV neuropathy

> in California, Utah Gabapentine

103) Hydatid cyst

-Source: dog ; sheep in rural area
-CT: large smooth cyst with eggshell calcification and internal septation
-Mx: Albendazole x 6 months and cbc fortnightly for leukopenia ; percutaneous therapy
If >5cm/ septation; risk of rupture

104) whipple Ds:

-MC presents with weight loss.
a) GIT sx: abdominal pain, diarrhea, and malabsorption, flatulence, and steatorrhea.

b) Extraintestinal manifestations: migratory polyarthropathy, chronic cough, and

myocardial or valvular involvement leading to congestive failure or valvular
regurgitation.: joints, CVS and RS

-Later stages CNS: dementia supranuclear ophthalmoplegia and myoclonus.

- Intermittent low-grade fever, pigmentation, and lymphadenopathy occasionally
#Rx: amboss
-IV ceftriaxone for 2 weeks
-Maintenance treatment : oral TMP SMX xa year.
Whipple disease is lethal if left untreated.

105) parvovirus B19:

• Acute infection
◦ B19 IgM antibodies in immunocompetent patients
◦ NAAT for B19 DNA in immunocompromised patients
• Previous infection: B19 IgG antibodies
-• Reactivation of previous infection: NAAT for B19 DNA
106) Condylomata acuminata (anogenital warts) in pregnancy
-may worsen during pregnancy due to physiologic immunosuppression.
#Rx:
-Topical trichloroacetic acid is first-line therapy in pregnancy,
although no treatment modality prevents vertical transmission.

107) Meningococcal meningitis

- a potentially fatal infection that presents
with rapidly progressive symptoms (eg,
=
fever, headache, nuchal ridigity, = .

petechiae) over 12-24 hours.

-If clinical suspicion is high, empiric
vancomycin and ceftriaxone should be - -

administered as soon as possible;

—> lumbar puncture should not delay - o

treatmen
#when not to terminate Pap
test in >65 yrs??
-If a patient has a history of CIN
2 / higher on histology,

g
-
screening continues for
another 20 years after detection
-
(past age 65 if indicated).
.

-Terminating Pap tests at age 65

Normal may not be appropriate for
women with cervical cancer
risk factors (eg,
←
immunosuppression, high-risk
sexual activity, tobacco use,
diethylstilbestrol exposure).

109) Acute rhinosinusitis:

• Viral: Rx with supportive
◦ No fever or early resolution of fever( <3 days)
◦ Mild symptoms (eg, well-appearing, mild facial pain)
◦ Improvement & resolution by day 5-10
• Bacterial: Rx with Ab
◦ High Fever ≥3 days OR
◦ New/recurrent fever after initial improvement (biphasic )OR
◦ Persistent symptoms ≥10 days without improvement
# bacterial rhinosinusitis: non typeable H influenza (MC); str Pneumoniae; moraxella
-2 MC RF : viral upper respiratory infections and allergic rhinitis
-Rx: amoxy: Augmentin

110) Hot tub folliculitis: TMP SMX umresponsive rash as it’s not Staph aureus
#Mx: The eruption is usually self-limited and does not require treatment. However,
patients should be advised to avoid the contaminated water
—>If lesions persist, an oral fluoroquinolone may be considered
Differential diagnosis of travel-associated diarrhea
112) Secondary bacterial
Short-term illness Characteristics
pneumonia
Rotavirus & • Brief illness - the MC influenza complication
norovirus • Vomiting common
#Clue:
Enterotoxigenic
Escherichia coli - should be suspected when fever
• Contaminated food & drinking water
Enteropathogenic E and pulmonary sx worsen after
coli initial improvement.
• Prominent abdominal pain
Campylobacter • Pseudoappendicitis
• Bloody diarrhea
#Age group:
-Most cases occur in patients age
Salmonella • Frequent fever
>65,
Shigella • Fever, bloody diarrhea & abdominal pain
-but community-acquired MRSA
Long-term illness
(>2 weeks)
has a predilection for young
patients with recent influenza.
Entamoeba
• Prolonged bloody diarrhea
histolytica
• Prolonged watery diarrhea #C/F: rapidly progressive,
Giardia
• Fat malabsorption, bloating common necrotizing pneumonia with high
• Asymptomatic patients may continue to fever, productive cough (often with
shed organism for months
hemoptysis), leukopenia, and
Cryptosporidium
Cystoisospora • Chronic watery diarrhea in
multilobar cavitary infiltrates.
(formerly Isospora) immunosuppressed patients -MC: str pneumonia
Microsporidia species -if > severe then Staph
Cyclospora • May cause prolonged, relapsing infection

-Diarrhea lasting >2 weeks is typically parasitic rather than bacterial or viral.

113) cryptococcal meningitis

-Patients with HIV who have subacute-onset of low-grade fever, headache, and signs of
increased ICP + nothing on neuroimaging
-Dx: detection of the cryptococcal antigen or isolation of the organism in CSF

#Mx: IV amphotericin B (AmB) + flucytosine induction therapy x 2 weeks/ until Sx

resolve/ CSF clear
-followed by high dose fluconazole x consolidation (8 weeks) : prevents relapse
-maintenance low dose fluco therapy x indefinitely / until CD4 counts rise to >100/mm3
for >3 months on antiretroviral therapy (ART).

-Intrathecal AmB : last option

 115) organisms associated with colon CA:
-clostridium septicum; strep. Bovis
-so do colonoscopy in bacteremia caused by them

-Pathogenesis: tumor cells frequently undergo

anaerobic glycolysis, which creates an adequate
environment for the germination of C septicum spores;

and tumors damage the colonic mucosa, which allows sporulated bacteria to translocate
into the bloodstream.

116) neurocysticercosis
-Source: Taenia solium is a pork tapeworm whose eggs cause neurocysticercosis.
These eggs hatch—> larvae—> penetrates intestinal wall—> Brain

#C/F:
-Most infections are asymptomatic, but patients can develop seizure (without other
symptoms) or signs of increased ICP (vomiting, headaches, papilledema) months or years
after inoculation.

#Diagnosis:(>1 cyst often with enhancement/edema; calcified nodule on brain MRI

#Rx: anti epileptic; albendazole; steroid

117) malaria chemoprophylaxis:

a) CQ resistant area: Africa, Asia (including India), and Oceania
-atovaquone-proguanil, doxycycline, or mefloquine.

#Mefloquine treatment : begin >2 weeks prior to travel, continued during the stay, and
discontinued 4 weeks after returning.

-Neuropsychiatric side effects (eg, anxiety, depression, restlessness) occur in

approximately 5% of patients and should prompt a change to an alternate medication.

b) CQ sensitive area: parts of Central America, Caribbean

-CQ chemoprophylaxis

#Phases of malaria C/F:

-The typical cycle (uncommon) consists of a cold phase (chills, shivering), then a hot
phase (high-grade fevers), then a sweating stage (diaphoresis, fever resolution).
Vs
#Babesiosis,
- has a similar presentation to malaria but is more commonly seen in the northeastern and
midwestern United States not Africa
 160 SEC TION II MICROBIOLOGY MICROBIOLOGY—PARASITOLOGY
` 

Cestodes (tapeworms)
ORGANISM DISEASE TRANSMISSION TREATMENT
Taenia solium A Intestinal tapeworm Ingestion of larvae encysted in Praziquantel
undercooked pork
Cysticercosis, Ingestion of eggs in food Praziquantel; albendazole for
neurocysticercosis (cystic contaminated with human neurocysticercosis
CNS lesions, seizures) B feces
Diphyllobothrium Vitamin B12 deficiency Ingestion of larvae in raw Praziquantel, niclosamide
latum (tapeworm competes for B12 freshwater fish
in intestine) Ž megaloblastic
anemia
Echinococcus Hydatid cysts D (“eggshell Ingestion of eggs in food Albendazole; surgery for
granulosus C calcification”) in liver E ; cyst contaminated with dog feces complicated cysts
rupture can cause anaphylaxis Sheep are an intermediate host

A B C D E
Liver

St

Trematodes (flukes)
ORGANISM DISEASE TRANSMISSION TREATMENT
Schistosoma Liver and spleen enlargement Snails are intermediate host; Praziquantel
A
( A shows S mansoni egg cercariae penetrate skin of
with lateral spine), fibrosis, humans in contact with
inflammation, portal contaminated fresh water (eg,
hypertension swimming or bathing)
Chronic infection with
B
S haematobium (egg with
terminal spine B ) can lead
to squamous cell carcinoma
of the bladder (painless
hematuria) and pulmonary
hypertension
Clonorchis sinensis Biliary tract inflammation Undercooked fish Praziquantel
Ž pigmented gallstones
Associated with
cholangiocarcinoma

#Thick blood smears are used as initial tests to detect the parasites, while thin blood
smears confirm the diagnosis and determine the type of Plasmodium species.
118) Ascariasis
-RF: recent travel from endemic regions (eg, Asia, Africa, South America).
-C/F: often asymptomatic but may cause pulmonary / intestinal manifestations.
-Complications : obstruction of the small bowel or hepatobiliary tree (eg, cholangitis,
pancreatitis).
119) ==> If the HIV status of the
-Treatment : albendazole or mebendazole. source patient is unknown but the
Occupational HIV postexposure prophylaxis
patient has risk factors for HIV,
prophylactic therapy should be
Exposure of
• Mucous membrane, nonintact skin, or initiated while awaiting results of
percutaneous exposure HIV testing.
High-risk contact Exposure to
(prophylaxis • Blood, semen, vaginal secretions, or any
#Testing schedule:
recommended) body fluid with visible blood (uncertain
risk: cerebrospinal fluid, pleural/ -HIV testing immediately to
pericardial fluid, synovial fluid, peritoneal establish baseline serologic status;
fluid, amniotic fluid) -repeated : 6 weeks, 3 months,
Low-risk contact Exposure to and 6 months
(prophylaxis not • Urine, feces, nasal secretions, saliva,
recommended) sweat, tears (with no visible blood)
• Initiate urgently, preferably in the first
Timing few hours
• Continue for 28 days
>3-drug regimen recommended:
• Two nucleotide/nucleoside reverse

RE
transcriptase inhibitors (eg, tenofovir,
emtricitabine) +
Regimen
+
• Integrase strand transfer inhibitor (eg,
raltegravir), protease inhibitor, or non-
nucleoside reverse transcriptase inhibitor
Salmonella
121) Viral gastroenteritis: Nontyphoidal Typhoidal
• Fecal-oral transmission • Major cause of
• Most common in
developing countries
gastroenteritis
with poor sanitation
• 1) Norovirus: MCC among all Epidemiolo
worldwide (including
(eg, unvaccinated
US)
ages; vaccinated child gy
• Associated with
travelers)
• Associated with
undercooked poultry/
contaminated food or
eggs
• 2) Rotavirus: common in water
unvaccinated, age ≤2; • Fever & bacteremia
• Abdominal pain &
• Vomiting
rose spots
• Rota in adolescents and adults • Diarrhea ± blood
Clinical • Late findings:
• Fever
is typically mild or • Invasive disease rare
hepatosplenomegaly
, intestinal
asymptomatic due to the perforation
presence of Ab from prior Diagnosis • Stool culture • Blood culture
exposure or vaccination. • Potentially fatal
• Usually self-limited • Antibiotics (eg,
Outcome &
• Antibiotics rarely ceftriaxone)
treatment
needed • Drug resistance
122) HCV screening steps:
-1st step: Screening for (HCV) begins with antibody testing.
-2nd step:Those with + Ab screens require HCV RNA PCR testing for confirmation of
chronic infection.
-3rd step: Those with + HCV RNA have chronic HCV infection—> Rx
-Negative HCV RNA indicates no current infection;

#Neg HCV RNA and + Ab:

-resolved infection / false-positive HCV antibody testing.
-False + excluded by repeated + test

123) stop INH only if severe hepatotoxicity (>10 times)

Key respiratory tract infections in children

Classic Causes of meningitis in children
Diagnosis Presentation
pathogen • Group B Streptococcus
• E. coli & other gram-negative
• Age 6 months to 3 <1 mo
bacteria
Laryngotrache •Parainfluenza years nth
• Listeria monocytogenes
itis (croup) virus • Barking cough, stridor, HSV
hoarseness
≥1 • Strep. pneumoniae
• Unvaccinated children month • N. meningitidis
• Sore throat, dysphagia,
Epiglottitis •H. influenzae
drooling, tripod
position
• Age <2
Bronchiolitis • RSV
• Wheezing, coughing

125) Cx of IM:
• Acute airway obstruction: Rx with steroids
• Autoimmune hemolytic anemia & thrombocytopenia
• Splenic rupture

126) Trichinellosis
#C/F: typically presents with GIT complaints (eg, abdominal pain, nausea, vomiting)
followed by the characteristic triad of periorbital edema, myositis, and eosinophilia
-Other findings : fever, subungual splinter h’ages, and conjunctival / retinal h’ages.

#Lab: eosinophilia (usually >20%): hallmark of the disease.

-Other findings : possible elevated CK and WBC.

#Mx: Mild infections : typically self-limited;

-severe infections : antiparasitic therapy (eg, mebendazole, albendazole) with steroids.

#Source: typically acquired via ingestion of raw or undercooked meat from infected animals
(e.g., bears), which contains encysted larvae. Cooking meat to 71°C (160°F) kills any
potential larvae in contaminated meat, preventing infection with Trichinella spiralis.
127) Dx of HIV in infancy :
-Because maternal antibodies may be present in HIV-negative children age <18 months,
DNA PCR testing of blood can confirm the diagnosis.
-After age 18 months, persistence of HIV antibody is confirmatory of infection

128) Tuberculous meningitis

-C/F: subacute symptoms of meningeal irritation (eg, vomiting, headache, nuchal rigidity)
- imaging : basilar meningeal enhancement (Clue), hydrocephalus, and stroke due to
vasculitis.

129) MC CAP In HIV: CD4< 200

-Patients with HIV are at increased risk of community-acquired pneumonia:
-Strp pneumoniae MC in both HIV and non HIV: rusty sputum specific

130) invasive aspergillosis:

nodular halo sign
Vs
- CMV and PCP: B/L patchy
infiltrates
I -

-
-

Mortality >50%

131) urgent airway Mx in Epiglottitis:

-Swelling of these structures often leads to rapid airway deterioration; therefore, airway
management is the main priority.

-signs: Patients with epiglottitis who develop rapid-onset respiratory failure (eg, tripod
position, hypoxia, drooling, tachypnea) require urgent airway management.

* steps:
1st line) In patients unable to maintain adequate oxygen saturations,
bag-valve-mask ventilation (BVM) with 100% oxygen (to keep oxygen saturation
≥~88%)

2nd line ) If BVM does not result in adequate oxygenation (ie, oxygen saturation remains
low) —> endotracheal intubation using a video laryngoscope (to facilitate direct
visualization of the epiglottis).
3rd line) Due to risk of rapid respiratory deterioration, failure of a single attempt at
endotracheal intubation with a video laryngoscope —> Immediately surgical
cricothyrotomy —> establishes an airway below the epiglottal swelling and potential
obstruction.

#Mx of underlying cause of Epiglottitis 2nd : then start Ab.

132) septic arthritis non responsive:

-patients occasionally have continued symptoms despite a few days of vancomycin
treatment, which usually indicates infection with an organism not covered by vancomycin
(eg, gram-negative Kingella kingae.).
-add Ceftriaxone

133) TB source in USA

-Most cases of active tuberculosis in the United States occur in foreign-born individuals
who have recently emigrated from endemic areas (especially Mexico, the Philippines,
China, Vietnam, India, Dominican Republic, and Haiti), with the highest rates for
those arriving in the last 5 years.
—> an extremely high case rate in the first year after entry into the US. Even after 5
years, the rates are still up to 10 times higher than US-born individuals.

134) HIV-associated nephropathy

-caused by direct infection of the renal epithelial cells by HIV
-C/F: heavy proteinuria, rapidly progressive renal failure, and edema; increased
creatinine -MC in patients of sub-Saharan African descent with advanced HIV infection.
Vs

#Primary membranous nephropathy

-causes nephrotic syndrome with proteinuria;
-it typically causes a slowly progressive CKD; mostly normal creat initialLy
-Secondary membranous nephropathy typically occurs with Hepatitis B and C, not
HIV.
Vs

#BK virus–induced nephropathy

-causes progressive renal failure but is characterized by an interstitial nephritis with
hematuria, pyuria, and white blood cell casts, not marked proteinuria.
-It occurs more commonly in patients who have received renal transplants
135) Histoplasmosis
-closely mimics the presentation of sarcoidosis and should be considered when a patient
with suspected sarcoidosis deteriorates after immunosuppressive therapy.

—> In endemic regions, dimorphic fungi (eg, Histoplasma, Blastomyces, Coccidioides)

should be excluded before immunosuppression is initiated.

136) Ab of choice in neutropenia:

-Rx: Empiric monotherapy with an anti-pseudomonal agent (eg, cefepime, meropenem,
piperacillin-tazobactam) is recommended for initial management.

137) Infection in solid organ transplant :

-MC 2 organism: Pneumocystis pneumonia and cytomegalovirus (CMV).

-In the absence of prophylaxis, patients who present with a systemic illness involving
multiple organ systems (eg, pneumonitis, hepatitis, gastroenteritis- bloody stool vs
nonbloody in legionella ) should be tested for CMV.
Vs
No systemic involvement in PCP

#Dx: Viremia can be detected in the blood using polymerase chain reaction (PCR) but may
not always be present; tissue biopsy is the gold standard as it is tissue invasive CMV

#Rx: discontinuing antimetabolite immunosuppression (eg, mycophenolate) and initiating

antiviral therapy.
-Oral antiviral: minimal Sx ; IV antiviral: severe Ds

138) necrotising surgical site infection:

-pain, edema or erythema spreading beyond surgical site,
-systemic signs: fever, tachycardia, hypotension
- Paraesthesia and Anaesthesia at wound edge;
- Purulent, cloudy grey discharge (Dish water drainage)
- subcutaneous gas/ crepitus
==> next step: surgical exploration before anything

139) Rx of KAposi
-HAART and chemotherapy (advanced cases)
-alpha interferon alpha

#Kaposi: lymphocytes, plasma vs neutrophils in bartonella hensle

 PPD/TST
Patients to treat 140) screening for latent TB in HIV:
induration
• HIV-positive patients -Although patients with LTBI who are

E-
• Recent contacts of known TB case not immunocompromised have a low
• Nodular or fibrotic changes on chest x-
lifetime risk (~5-10%) of TB
≥5 mm ray consistent with previously healed
TB
reactivation,
• Organ transplant recipients & other
immunosuppressed patients -those with HIV are significantly
• Recent immigrants (<5 years) from TB-
more likely (30- to 100-fold) to
endemic areas develop active disease.
• Injection drug users *screening
-Therefore, LTBI testing is

=
• Residents & employees of high-risk
settings (eg, prisons, nursing homes, recommended for all patients with
hospitals, homeless shelters) newly diagnosed HIV.
≥10 mm
• Mycobacteriology laboratory personnel
• Higher risk for TB reactivation (eg, -Test: (TST) /(IGRA)
diabetes, leukemia, end-stage renal
disease, chronic malabsorption syndromes)
- but the IGRA is generally preferred
• Children age <4, or those exposed to adults due to higher Sn/sp and lower risk for
in high-risk categories anergy (FN result) at low CD4 counts.
≥15 mm • All of the above plus healthy individuals

115) Hep C course:

-Hepatitis C has a high mutation rate, and lifelong immunity does not occur. Patients
who have experienced spontaneous hepatitis C viral clearance, as well as those
successfully treated with antiviral therapy, remain at risk for reinfection.

116) Ab in Epiglottitis:
# MC organisms: H influenza is MC:
-But, due to widespread vaccination against Hib, the incidence has diminished.
-proportion of epiglottitis caused by other pathogens, such as other strains of H
influenzae, Strepto (S pneumoniae, S pyogenes), and Staphy aureus has increased.

#Mx: After securing the airway in patients with epiglottitis, initial treatment consists of
broad-spectrum antibiotic therapy with
ceftriaxone (targeting Haemophilus influenzae and Streptococcus species) +
vancomycin (targeting Staphylococcus aureus).
 >> →

High sp

High sn

118) Initial evaluation is typically with rapid

antigen detection testing (RADT), which is
Adults
quick and highly specific but has limited
sensitivity.
-Because the risk of acute rheumatic fever is
much higher in children with untreated
streptococcal pharyngitis than in adults, a
negative RADT in a child should be
confirmed with a throat culture, which has
greater sensitivity

-In contrast, confirmatory culture is not

typically required in adults.

119) organisms causing brain abscess:

• Staphylococcus aureus
• Viridans streptococci
• Anaerobes

120) coccidiodes: > in desert area

 121Source:
-hematogenous spread of recent UTI
-Staphylococcus aureus accounts for about
50% of cases of pyogenic spinal osteomyelitis.
As it’s from
distant foci -However, other pathogens, including Gram-
a negative bacilli can also cause osteomyelitis.

122) dx of PCP:
-Diagnosis requires the identification of
Pneumocystis jirovecii organisms in respiratory
secretions using microscopy with specialized
stains.
-Samples : induced sputum /if this is
unrevealing, bronchoscopy with
bronchoalveolar lavage.
Osteomyelitis in children
Most common
Vanco+ Ceftriaxone Patient population
organisms
Empiric antibiotic therapy

• Low likelihood of MRSA

•Staphylococcus ◦ Nafcillin/oxacillin OR cefazolin
Healthy children
aureus • High likelihood of MRSA
◦ Clindamycin OR vancomycin
• Salmonella • As above
Children with sickle spp PLUS
cell disease •Staphylococcus • 3o cephalosporin (ceftriaxone,
aureus cefotaxime)
Plain x-rays can be normal in the first 2-3 weeks of infection. Magnetic resonance imaging
(MRI) is the modality of choice for patients with suspected vertebral osteomyelitis. It can
also detect epidural abscess and cord compression. Radionuclide bone scanning using
gallium is an alternate for patients who cannot undergo MRI

124) Differentiating botulism from Myasthenia gravis:

-myasthenia gravis: pupillary function is generally spared: as CN spared and ptosis by
muscle
-autonomic dysfunction is less prominent,
-symptom progression is typically less rapid than in botulism.
Diagnostic tests for pulmonary tuberculosis
AFB • Low cost & rapid (minutes to hours)
smear • Low sensitivity because high burden (>10,000/mL)
microscop of organisms required in sample
y • Cannot differentiate TB from non-TB mycobacteria
Nucleic
• Higher cost & slightly less rapid (1-2 days)
acid
• Higher sensitivity (only ~10 bacilli/mL required for
amplificati
positive test)
on
• Can differentiate TB from non-TB mycobacteria
testing
• Gold standard, quantitative & allows for drug
Sputum
sensitivity testing
culture
• Slow: takes 3-8 weeks
Infection Control Isolation Precautions

-
-.
126) Mx of influenza
• Those with no risk factors for influenza complications: do not require diagnostic testing
and are generally treated symptomatically.

• Those with risk factors (eg, age ≥65, chronic medical problems, pregnancy) for
influenza complications :
-should receive antiviral therapy (eg, oseltamivir), regardless of symptom duration.

-Timing: Antivirals can also be considered in those without risk factors who come to the
office within 48 hours (not 4 days) of symptom onset as treatment may reduce
symptom duration

127) congenital syphilis:

• Copious clear, purulent, or serosanguineous rhinorrhea (snuffles)
• A diffuse maculopapular or bullous rash that often involves the buttocks, legs, and
soles and may desquamate
• Long bone abnormalities on x-ray (eg, metaphyseal lucencies, tibial destruction)
#Mx:
-Affected infants, typically of undiagnosed or inadequately treated mothers, warrant
penicillin therapy to prevent late manifestations of disease (eg, saddle nose,
Hutchinson teeth, and saber shins).

128) The combination of dysuria + sterile pyuria is a common presentation for

Chlamydia trachomatis urethritis in sexually active women.
-Next step: require nucleic acid amplification testing for chlamydia and gonorrhea.

129) Antimicrobial chemoprophylaxis against Neisseria meningitidis

- indicated for close contacts (regardless of vaccination status) who have had exposure
during the 7 days before symptom onset until 24 hours after appropriate
antibiotic initiation.
-Medication regimens : rifampin, ciprofloxacin, or ceftriaxone asap

130) Toxic shock syndrome

-caused by Staphylococcus aureus bacteremia and associated exotoxin release,
#C/F fever, hypotension, tachycardia, and a diffuse, red, macular rash;Diarrhoea,
AMS without FND
#Rx : fluid replacement and Ab therapy with clindamycin + vancomycin.

131) Staphylococcus aureus : the MCC of bacterial pneumonia in young children

with cystic fibrosis, especially in those with coexisting influenza infection.

-Px: CF with severe pneumonia, frequent hospitalizations, or recurrent skin infections, IV

vancomycin should be included for empiric therapy against MRSA
 134) key features distinguishing
Opportunistic infections in HIV
meningococcal disease from more
Infection CD4 cell count Prophylaxis
benign illnesses include:
Trimethoprim-
• <200/mm3 OR
sulfamethoxazole
Pneumocy • Oropharyngeal
Alternate therapies: • Severe myalgias (eg, diffuse leg
stis candidiasis OR pain)
• Dapsone
jirovecii • History of PCP
infection
• Atovaquone • Cold hands/feet
• Pentamidine
• Mottled skin or pallor
TMP SMX
Alternate therapies: **Early meningococcal infection
• Dapsone + - often nonspecific (eg, fever,
Toxoplas <100/mm3 & positive pyrimethamine +
ma gondii IgG antibody leucovorin pharyngitis) but should be suspected
• Atovaquone ± in a patient with rapidly progressive
pyrimethamine plus illness, severe myalgias (eg, leg
leucovorin
pain), and poor perfusion (eg,
Histoplas <150/mm3 & endemic mottled skin, cold hands/feet).
Itraconazole
ma area
Close contact with
person with VariZIG or IVIG
-Positive CSF culture obtained via
VZV chickenpox / shingles & administered within 4 lumbar puncture is diagnostic.
no H/O prior disease / days of exposure
negative Ab to VZV 135) Current guidelines recommend
cefazolin or cefuroxime
administered within 60 minutes of
Sexually transmitted infection screening*
skin incision as prophylaxis
• Neisseria gonorrhoeae (eg, NAAT) during hip or knee arthroplasty
• Chlamydia trachomatis (eg, NAAT) and should be discontinued
All patients/
• Syphilis (eg, RPR)
diagnosed with within 24 hours: NBME 8
• HIV (eg, 4th-generation antigen/
any 1 STI
antibody)
X HPV unless RF +
• Women only: Trichomonas vaginalis
Additional testing (eg, wet mount)
for certain • Herpes simplex virus screening (eg,
populations serology) only when history of
characteristic lesions

137) Rx of neonatal sepsis vs maternal endometritis:

• Key idea: All neonates with concern for sepsis should be empirically treated with
ampicillin and gentamicin
• Key idea: Mothers with postpartum endometritis are treated with ampicillin +
gentamicin + clindamycin (only difference between the two)
138) tunneled Catheter related infection:
-Initial workup includes 2 sets of blood cultures, ideally one from a peripheral site and one
from the central catheter.
-Empiric antibiotic therapy : vancomycin + cefepime (or gentamicin).

—> Catheter removal is indicated if any of the following are present:

• Severe sepsis
• Hemodynamic instability
• Evidence of metastatic infection (eg, endocarditis)
• Pus at the exit site of the catheter
• Continued symptoms after 72 hours of empiric antibiotics

-Long-term catheters (in place >14 days) should be removed if there is blood culture
evidence of S aureus, Pseudomonas aeruginosa, or fungi (eg, Candida).

139) divine podcast:

● M with lower abdominal pain + urinary incontinence + new parter 2 weeks ago →
cystitis
○ Tx? TMP-SMX or cipro
■ Nitrofurantoin never used in men

● Fever + flank pain + urinary sxs → pyelo

○ Dx? CT abdomen with contrast
○ Tx?
■ Ceftriaxone
■ Cipro
■ TMP-SMX

○ What if pt is diabetic & not improving on abx?

■ NBS? Another CT scan to r/o complication (e.g. emphysematous pyelo, perinephric
abscess)

● UTI in pregnant woman

○ Tx for cystitis? Nitrofurantoin
○ Tx for pyelo? ceftriaxone

● UTIs associated with sexual activity?

○ Ppx abx prior to intercourse
○ Urinate after sex
 Features of necrotizing fasciitis 140) Ab of choice for necrotising fasciitis:
• Streptococcus pyogenes (group A Streptococcus) -When the etiology of the necrotizing fasciitis
Microbiology
•
•
Staphylococcus aureus
Clostridium perfringens
is unknown, broad-spectrum therapy should
• Polymicrobial be started. This includes:
• Bacteria spread rapidly through subcutaneous
tissue & deep fascia, undermining the skin
Pathogenesis
• Most commonly involves the extremities & perineal 1 Piperacillin/tazobactam / carbapenem will
region
cover Group A Streptococcus and
• Often antecedent history of minor trauma
Clinical • Erythema of overlying skin anaerobes
manifestation
s
•
•
Swelling & edema
Pain out of proportion to examination findings
2 Vancomycin :MRSA
• Systemic symptoms (eg, fever & hypotension) 3 Clindamycin : inhibit toxin formation by
Treatment
• Requires surgical debridement & broad-spectrum streptococci/staphylococci
antibiotics

141) UTI with alkaline urine (pH >

7), and an indwelling urinary
catheter :
-Proteus mirabilis.
Vs E. coli doesn’t cause alkaline pH
 SEPSIS Evaluation & Mx in ER :
#Sepsis
- is an acute life-threatening condition characterized by organ dysfunction due to a
dysregulated immune response to infection. The previously widely used term
“systemic inflammatory response syndrome” (SIRS) is now considered outdated because
its criteria were too simplified
—>Organ dysfunction is determined using a sequential organ failure assessment
(SOFA) score that considers multiple parameters, but may be quickly evaluated

#qSOFA score, a calculation that assigns 1 point each for ,

1) respiratory rate >22/min,
2) confusion,
3) SBP ≤100 mm Hg.

-qSOFA scores ≥2 —>> septic.

#Sepsis Mx :
-Patients with sepsis require the following early interventions to reduce complications and
risk of death
-As investigation (eg, foot imaging) and Rx (eg, foot debridement) of the source of
infection often take several hours, empiric Ab should be initiated first .
-Fluid resuscitation and antibiotics should be given prior to consideration of
additional testing.

I) Aggressive fluid resuscitation within first 3 hours :

-Rapid administration of relatively large volumes (eg, 30 mL/kg) of IV crystalloid fluids x
within first 3 hours;
-500 mL boluses are typically given with an assessment for pulmonary edema (eg,
worsened hypoxia) between doses.

#Indicators of an adequate response include:

- achieving a MAP of 60 -70 mm Hg and urine output of >0.5 mL/kg/hour.
-As tissue perfusion improves, acidosis (eg, lactic acidosis) usually improves.

II) Broad-spectrum antibiotics within 1 hour:

- Empiric treatment with a beta-lactam/beta-lactamase inhibitor (eg, piperacillin-
tazobactam), a carbapenem (eg, meropenem), or a 4th-generation cephalosporin
(eg, cefepime) is typically administered +
vancomycin is often added to cover MRSA.

-Blood cultures should be drawn prior to antibiotic initiation to help identify the
causative pathogen.
 CNS

• Key idea: Best test to CONFIRM diagnosis of pseudoseizure is Video EEG

monitoring because you can look at whether the patient’s seizure-like symptoms
correlate with EEG changes seen during a true seizure
 NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PATHOLOGY
`  SEC TION III 511

NEUROLOGY—PATHOLOGY
` 

Common brain lesions

AREA OF LESION CONSEQUENCE EXAMPLES/COMMENTS
Frontal lobe Disinhibition and deficits in concentration, #Nondominant frontal lobe
orientation, judgment; may have reemergence lesions :typically affect the way a
of primitive reflexes
person conveys emotion through
Frontal eye fields Destructive lesions (eg, MCA stroke): eyes look

E
toward brain lesion (ie, away from side of
speech (motor aprosodia)+ C/L
hemiplegia) weakness, and apraxia.
Paramedian pontine Eyes look away from brain lesion (ie, toward side
reticular formation of hemiplegia)
Medial longitudinal Internuclear ophthalmoplegia (impaired Multiple sclerosis
fasciculus adduction of ipsilateral eye; nystagmus of
contralateral eye with abduction)
Dominant parietal Agraphia, acalculia, finger agnosia, left-right Gerstmann syndrome
cortex disorientation Normal fn: C/L sensory loss
Nondominant parietal Agnosia of the contralateral side of the world Hemispatial neglect syndrome
cortex
Hippocampus Anterograde amnesia—inability to make new
(bilateral) memories
Basal ganglia May result in tremor at rest, chorea, athetosis Parkinson disease, Huntington disease, Wilson
disease
Subthalamic nucleus Contralateral hemiballismus
Mammillary bodies Wernicke-Korsakoff syndrome—Confusion, Wernicke problems come in a CAN O’ beer
(bilateral) Ataxia, Nystagmus, Ophthalmoplegia, and other conditions associated with thiamine
memory loss (anterograde and retrograde deficiency
amnesia), confabulation, personality changes
Amygdala (bilateral) Klüver-Bucy syndrome—disinhibited behavior
(eg, hyperphagia, hypersexuality, hyperorality) -
HSV-1 encephalitis

Dorsal midbrain Parinaud syndrome—vertical gaze palsy, Stroke, hydrocephalus, pinealoma

pupillary light-near dissociation, lid retraction,
convergence-retraction nystagmus
Reticular activating Reduced levels of arousal and wakefulness Coma
system (midbrain)
Cerebellar Intention tremor, limb ataxia, loss of balance; Cerebellar hemispheres are laterally located—
hemisphere damage to cerebellum Ž ipsilateral deficits; affect lateral limbs
fall toward side of lesion
Cerebellar vermis Truncal ataxia (wide-based, “drunken sailor” Vermis is centrally located—affects central body
gait), nystagmus Degeneration associated with chronic alcohol use
Red nucleus Decorticate (flexor) posturing—lesion above Worse prognosis with decerebrate posturing
(midbrain) red nucleus, presents with flexion of upper In decorticate posturing, your hands are near the
extremities and extension of lower extremities cor (heart)
Decerebrate (extensor) posturing—lesion at or
below red nucleus, presents with extension of
upper and lower extremities
#Nondominant temporal lobe lesions : impair ability to comprehend emotional gestures
(sensory aprosodia). + C/L homonymous quadrantanopsia due to the inferior optic
radiations involvement.
506 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—EMBRYOLOGY
` 

Posterior fossa malformations

Chiari I malformation Ectopia of cerebellar tonsils inferior to foramen magnum (1 structure) A . Congenital, usually

=
asymptomatic in childhood, manifests in adulthood with headaches and cerebellar symptoms.
Associated with spinal cavitations (eg, syringomyelia).
Chiari II malformation Herniation of cerebellum (vermis and tonsils) and medulla (2 structures) through foramen
magnum Ž noncommunicating hydrocephalus. Usually associated with aqueductal stenosis,
lumbosacral myelomeningocele (may present as paralysis/sensory loss at and below the level of the
lesion). More severe than Chiari I, usually presents early in life.
Dandy-Walker Agenesis of cerebellar vermis Ž cystic enlargement of 4th ventricle (arrow in B ) that fills the
malformation enlarged posterior fossa. Associated with noncommunicating hydrocephalus, spina bifida.
A B

Chiari I
malformation
Syrinx

Syringomyelia Cystic cavity (syrinx) within central canal of spinal cord (yellow arrows in A ). Fibers crossing in
A
anterior white commissure (spinothalamic tract) are typically damaged first. Results in a “cape-
like,” bilateral, symmetrical loss of pain and temperature sensation in upper extremities (fine
-
touch
- sensation is preserved).
Associated with Chiari I malformation (red arrow in A shows low-lying cerebellar tonsils), scoliosis
and other congenital malformations; acquired causes include trauma and tumors. Most common
location cervical > thoracic >> lumbar. Syrinx = tube, as in “syringe.”

Dorsal root
ganglion
Loss of pain
and temperature
sensation at affected
dermatomes C5-T4
shown here

Expanding syrinx
can affect multiple
dermatomes

Afferent
Lateral spinothalamic tract
pain, temperature

Anterior white commissure

compressed by syrinx
518 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PATHOLOGY
` 

Headaches Pain due to irritation of structures such as the dura, cranial nerves, or extracranial structures. More
common in females, except cluster headaches.
CLASSIFICATION LOCALIZATION DURATION DESCRIPTION TREATMENT
Cluster a
Unilateral 15 min–3 hr; Excruciating periorbital pain Acute: sumatriptan, 100% O2.
repetitive (“suicide headache”) with Prophylaxis: verapamil.
lacrimation and rhinorrhea.

⇐
-

May present with Horner

syndrome. More common in
males.

Migraine Unilateral 4–72 hr Pulsating pain with Acute: NSAIDs, triptans,

nausea, photophobia, or dihydroergotamine.
phonophobia. May have Prophylaxis: lifestyle changes
“aura.” Due to irritation of (eg, sleep, exercise, diet),
CN V, meninges, or blood β-blockers, amitriptyline,
Virat BBAT
vessels (release of vasoactive topiramate, valproate,
neuropeptides [eg, substance botulinum toxin, anti-CGRP
P, calcitonin gene-related monoclonal antibodies.
peptide]). POUND–Pulsatile, One-day
duration, Unilateral, Nausea,
Disabling.
Tension
-
Bilateral > 30 min Steady, “band-like” pain. No Acute: analgesics, NSAIDs,
(typically 4–6 photophobia or phonophobia. acetaminophen.
hr); constant No aura. Prophylaxis: TCAs (eg,
-

amitriptyline), behavioral
therapy.

Other causes of headache include subarachnoid hemorrhage (“worst headache of my life”), meningitis, hydrocephalus,
neoplasia, giant cell (temporal) arteritis.
a
Compare with trigeminal neuralgia, which produces repetitive, unilateral, shooting/shock-like pain in the distribution of
CN V. Triggered by chewing, talking, touching certain parts of the face. Lasts (typically) for seconds to minutes, but episodes
often increase in intensity and frequency over time. First-line therapy: carbamazepine.

Migraine therapy
# prophylactic medication should be considered
• Triptans
Abortiv • NSAIDs, acetaminophen
in patients who:
e • Antiemetics • Have frequent (eg, >4/month) or long-lasting (eg,
• Ergotamine >12 hours) episodes
• Anticonvulsants • Experience disabling symptoms that prevent
(topiramate or valproate) regular activities despite abortive treatment
Prevent • Beta blockers
ive (pregnancy), Verapamil
• Antidepressants (tricyclic • Are unable to take or have had no relief with
or venlafaxine) abortive medications

• Overuse abortive medication (eg, nonsteroidal

anti-inflammatory drugs [NSAIDs]) and have
rebound headache
1)Brain death: Case clue
-coma, absent cranial nerve reflexes and brain-originating motor responses, and apnea.
-Movements originating in the spinal cord (eg, deep tendon reflexes) +

2) Subarachnoid haemorrhage:
-thunderclap headache( severe within 1 min) + Sx of meningeal irritation (eg, nuchal
rigidity, photophobia, nausea).
-Noncontrast CT scan: acute bleeding around the brainstem and basal cisterns.

3) Lacunar stroke/ subcortical stroke:

-HT pt with pure motor(MC) / pure sensory deficits and absent cortical signs ( aphasia,
agnosia, neglect, apraxia, hemianopia), seizure, or mental status changes)
Vs

4) stroke by cardiac thrombi in AF/ large artery atherosclerosis:

-stroke in cortical regions due to occlusion of major cerebral arteries.
-deep penetrating vessels involved in a lacunar stroke are rarely affected by
cardioembolism.

5) West Nile encephalitis is characterized by fever, headache, and confusion.

#Neuroinvasive West Nile infection

- myelitis, resulting in an acute paralysis syndrome characterized by asymmetric flaccid
weakness in the limbs.

7) Foodborne botulism
-sudden onset of bilaterally symmetric weakness starting with the face/cranial nerves
and descending to the trunk, the upper extremities, and then the lower extremities.

-preceded by a prodrome of gastrointestinal symptoms and may lead to respiratory failure if

respiratory muscles are affected.

8) Guillain-Barré syndrome
- characterized by ascending symmetric paralysis associated with weak/absent deep
tendon reflexes and autonomic dysfunction.

-after an antecedent respiratory tract / GIT (eg, Campylobacter jejuni) infection and can
require respiratory support if it progresses to involve the respiratory muscles.
9) Transverse myelitis:
-Motor weakness, sensory dysfunction, +/- ANS dysfunction below a distinct spinal
level following any infection GIT/URTI
-MRI : increased T2 signal in the cervical spinal cord without any mass lesions /
compression.
#Rx: 1st line: High-dose IV glucocorticoids; 2nd line Plasmapheresis:

10) Hemisection /Brown-Séquard syndrome,

• Ipsilateral hemiparesis and diminished proprioception, vibratory sensation, and light
touch at the level of the spinal cord injury and below
• Contralateral diminished pain and temperature sensation 1-2 levels distal to the
cord injury and below

11) Complete spinal transection at T8 or T10

- bilateral paralysis and complete loss of sensation below the level of injury.

12) anterior spinal artery injury at T8 or T10 /anterior cord syndrome;

-distal paralysis (LCT) and decreased pain and temperature sensation (LST) bilaterally,
with preserved distal proprioception, vibratory sensation, and light touch due to
sparing of the dorsal columns.

13) Brain tumor headache:

-The most common symptom is a dull headache associated with >1 of the following:
• Nausea and vomiting (due to increased ICP)
• Focal neurologic manifestations (due to tumor invasion or compression)
• Symptoms worsening during the night or with positions that raise ICP (eg,
bending, coughing)
#Funduscopic: papilledema, a sign of elevated ICP, supports the diagnosis.

14) Shy-Drager syndrome

1 Parkinsonism
2 Autonomic dysfunction (postural hypotension, abnormal sweating, disturbance of bowel
or bladder control, abnormal salivation or lacrimation, impotence, gastroparesis, etc)

I
3 Widespread neurological signs (cerebellar, pyramidal or lower motor neuron)
#Mx:
-Anti-Parkinsonism drugs are generally ineffective,
-
- treatment is aimed at intravascular volume expansion with fludrocortisone, salt .

supplementation, alpha-adrenergic agonists; constrictive garments to the lower body.

15) acute spinal cord compression (SCC)

Neoplastic epidural spinal cord compression causes worsening focal back pain, B/L LE
weakness, sensory loss, and gait ataxia. LMN signs in same side, UMN in LE
-Bowel/bladder disturbances are late findings. In the acute phase of spinal cord injury,
patients can develop spinal shock with absence of reflexes and flaccid paraplegia as a
result. # Rx: IV GC and Surg
19) Diffuse axonal injury (DAI) :GCS<8
- causes severe neurologic impairment in the absence of major CT scan findings.
-MRI is more sensitive :minute punctate hemorrhages in the white matter and blurring
of the gray-white interface.

19) (Todd) paralysis: Transient limb weakness following partial seizure activity

20) Normal-pressure hydrocephalus : disproportional ventriculomegaly

-progressive gait difficulties (ataxia), cognitive disturbances, and urinary incontinence.
-Brain imaging : ventricular enlargement that is out of proportion to sulci enlargement.

-Pathogenesis: NPH can be idiopathic or occur secondary to neurologic insults (eg,

subarachnoid hemorrhage, trauma, meningitis) that result in scarring of the arachnoid
granulations responsible for cerebrospinal fluid resorption.

21) Toxic-metabolic encephalopathy

-Etiology: infection, toxins, or metabolic derangements (eg, electrolytes disturbance, uremia,
hyperammonemia).
-C/F: confusion, lethargy, and neuromuscular findings (eg, bradykinesia, asterixis) due to
global cerebral dysfunction.
-Focal neurologic deficits are not characteristic.

22) Chronic subdural hematoma

-RF: Elderly patients due to increased fall risk and cerebral atrophy.
-C/F: presents insidiously weeks after the initial injury with headache, somnolence,
confusion, and focal neurologic deficits.
Vs
Acute subdural: onset-1-2 days after insult; coma; headache; raised ICT

23) Mx of TN:
-TN is most often caused by vascular compression of the trigeminal nerve root as it enters
the pons.
-Because of the risks associated with neurosurgical microvascular decompression, control
of symptoms with medication is preferred; surgery is reserved for patients who fail medical
management.
#Rx:
-1st line: carbamazepine / oxcarbazepine, inhibit AP by modulating Na channels.
-Oxcarbazepine is often better tolerated (eg, less nausea/vomiting, less risk for leukopenia),
but patients are at risk for hyponatremia due to increased sensitivity to antidiuretic hormone.
-2nd line: baclofen
#Evaluation:
• MRI/MRA of the brain with contrast
• Nerve conduction (eg, trigeminal reflex) testing if unable to obtain MRI
 18) Subclavian steal syndrome (> on left)
-Subclavian steal syndrome occurs
atherosclerosis of the left subclavian artery
proximal to the origin of the vertebral artery.

-Significant stenosis or occlusion leads to

decreased pressure in the distal subclavian
artery and reversal ("steal") of blood flow in
the ipsilateral vertebral artery

-C/F: often asymptomatic but may have

symptoms of UE ischemia (eg, pain, fatigue,
paresthesias) /

vertebrobasilar insufficiency (eg, dizziness,

ataxia, dysequilibrium) that are worsened by
upper extremity exercise.
##Diagnosis :
- typically made by Doppler ultrasound or magnetic resonance angiography.

#Treatment : lifestyle management (eg, lipid-lowering interventions, smoking cessation)

and sometimes stent placement.

32) Cauda equina syndrome:

-by compression of ≥2 spinal nerve roots in the lumbar cistern
-severe, radicular lower back pain plus impaired motor/sensory/reflex activity in the lower
extremities,
-bowel/bladder/sexual dysfunction late , and/or saddle anesthesia (Like LMN)
#next best step: -Surgical decompression within 24-48 hours is generally required to
prevent irreversible neurologic sequelae.

Vs Conus medullary/Brain/ spinal cord : UMN+ perianal anaesthesia can occur

31) Isolated cranial nerve palsies can be suggestive of a ruptured or enlarging

saccular aneurysm with active or impending subarachnoid hemorrhage.
-Isolated oculomotor nerve palsy can indicate an aneurysm of the posterior communicating
artery.

32) UWSA 1: New-onset seizures are a common presentation of brain tumors, the most
common of which in adults are astrocytomas.
—>> The prognosis of astrocytomas is most affected by tumor grade, with increased
atypia, mitoses, neovascularity, or necrosis conveying a worse prognosis.
23) Thromboembolic stroke converting to H’agic stroke:
-This condition usually occurs within 48 hours of the thrombotic stroke and often manifests
with deteriorating mental status.
-Diagnosis : emergent noncontrast CT scan of the head.

24) chronic inflammatory demyelinating polyneuropathy (CIDP): >8 wk vs acute

onset in GBS
not length dependent.
-Therefore, it classically causes both proximal (eg, hip girdle) and distal (eg, hand)
muscle weakness+ LMNs (eg, hyporeflexia, muscle atrophy) + distal sensory loss
(vibration and position sense are often preferentially affected )

25) Cluster headache:

-> in M; peaks at midnight; with ANS sx; Rx: 100% Oxygen

27) Tick-borne paralysis

-rapidly (in hours vs weeks to days in GBS) progressive ascending paralysis (which
may be asymmetrical/U/L ), absence of fever and sensory abnormalities, and normal
CSF examination (unlike abnormal CSF in GBS)

- Removal of the tick results in spontaneous improvement in most patients.

29) Cerebral amyloid angiopathy

MCC of spontaneous lobar (eg, parietal, occipital) hemorrhage, particularly in the elderly.

30) Miller Fisher syndrome (MFS): variant of Guillain-Barré syndrome

#Pathogenesis:
-Antibodies directed at GQ1b, a ganglioside found in peripheral nerves, contribute to the
rapid-onset ophthalmoplegia (possibly due to the high levels of GQ1b in CN 3,4,6).

#C/F:
-ophthalmoplegia, lower-extremity weakness, ataxia and areflexia that developed 3-4 days
after a gastrointestinal illness.
-Extremity weakness may occur,unlike classic GBS, paralysis is less common.
Vs
#botulism
- symmetric descending weakness (as opposed to the lower-extremity weakness in this
patient), and even though ophthalmoplegia may occur, facial weakness, dysphagia, and
dysarthria are typical.

31) Stroke patients, particularly those with symptoms of dysarthria, are often at risk for
oropharyngeal dysphagia.
-In the setting of acute stroke, such patients should be given nothing (eg, food, drink,
medications) by mouth until a swallow evaluation can be performed.
33) Intracranial hypertension
- headache (worse at night, leaning/ valsalva), nausea/vomiting, and mental status
changes.
-O/E: Papilledema and focal neurologic deficits

**Sx can worsen with maneuvers that further increase intracranial pressure (eg,
leaning forward, Valsalva, cough). SPECIFIC

-Cushing reflex (hypertension, bradycardia, respiratory depression) is a worrisome

finding suggestive of brainstem compression.

34)cavernous sinus thrombosis:

-severe headache; B/L periorbital edema; and cranial nerve III, IV, V, and VI deficits, B/L
mid face tenderness
Vs
Periorbital cellulitis: U/L ophthalmoplegia and periorbital edema

35) Internal carotid artery dissection

- common cause of stroke in young patients and can occur spontaneously or after mild
trauma or illness.
-partial Horner syndrome (ptosis and miosis without anhidrosis), U/L headache and
neck pain, and cerebral ischemia (transient ischemic attack, stroke
#Rx: as other strokes

37) Myotonic dystrophy

- AD disorder caused by the expansion of CTG trinucleotides.
-Myotonia (delayed muscle relaxation); Progressive muscle weakness and atrophy (eg,
face, hands)
-inability to quickly release the hand grip clue
-CTG: cataract, toupee baldness, gonadal atrophy

-Childhood form:By 10 yrs of age —> cognitive (eg, intellectual impairment) and
behavioral manifestations (eg, ADHD, mood disorder), Sleep disturbances ( excessive
daytime sleepiness )

38) #Cervical radiculopathy:

-neck pain that radiates to the shoulder/arm and unilateral upper extremity sensory, motor,
and/or reflex abnormalities in a dermatomal distribution.
-Spine imaging :abnormal facet joints, sclerosis and osteophytes
39) Concussion
-patient who developed disorientation after a head injury but does not have sustained
neurologic deficits likely has a concussion, a form of mild traumatic brain injury.
-Typical Sx : headache, disorientation, dizziness, and/or amnesia associated with
abnormalities in coordination, speech, attention, or emotions.
-Rest >24 hours resolves it.
Vs

40) Postconcussion syndrome

- characterized by prolonged (>4 weeks) concussion symptoms (eg, headache, sleep
disturbance, amnesia, vertigo) if pt resumes physical activity soon

--MC symptom of PCS is headache, which may resemble a tension (ie, bandlike
pressure) or migraine (eg, unilateral throbbing) headache; is often triggered by
cognitive exertion; and can have associated phonophobia,

-Management is symptomatic care because most patients improve within 3 months.

41)Simple febrile seizures

O
-typically benign and occur in children age 6 months to 5 years.
-generalized, last <15 minutes, and do not recur within 24 hours.
-Diagnostic testing is unnecessary, and management is with supportive care (eg,
antipyretics) and reassurance.
44) carotid artery injury
-Posterior oropharyngeal trauma fall with object in mouth), or neck strain/manipulation (eg,
yoga, sports). can result in internal carotid artery dissection or thrombus formation,
-C/F: hemiplegia, facial droop, and aphasia.

45) Intraventricular hemorrhage

-common complication of prematurity
-C/F: acute neurologic changes (eg, seizure, apnea), a bulging fontanelle, and a
rapidly increasing head circumference.

46) Breath-holding spells

-occur in children age 6 months to 2 years (exclude out of this age)
-C/F: present with either cyanosis or pallor (ie, pallid breath-holding spell) following
physical or emotional distress.

47) Central cord syndrome

- common after whiplash-type injuries in older adults with underlying cervical
spondylosis. -Damage to the central cervical spinal cord : U/E motor, sensory, and reflex
abnormalities;
-sacral (eg, bowel/bladder) and lower extremity function is generally preserved

48) Thoracic aortic aneurysm repair

-cause spinal cord ischemia, especially of the anterior cord.
-Anterior cord syndrome :distal, bilateral flaccid paralysis; loss of pain/temperature and
crude touch sensation; and urinary retention.

49) cocaine induced stroke

• Young age:
-
• Absence of typical risk factors: Chronic hypertension -

• Sympathetic activation: acute hypertension, tachycardia, mydriasis, and hyperthermia

• Location: subcortical locations (eg, thalamus) and has a higher risk of associated
intraventricular hemorrhage.

50) Differentiating homocystinuria from Marfan syndrome:

-homocystinuria also have intellectual disability, downward lens dislocation, and
hypercoagulability so increased risk of stroke

51) Lesch-Nyhan syndrome

-developmental delay and hypotonia in infancy and progress to (extrapyramidal)
chorea, dystonia, and spasticity(pyramidal) in early childhood.
-Cardinal findings : self-mutilation and gouty arthritis.

52) Todd paralysis:

-patient's transient hemiplegia following an episode of loss of consciousness with gradual
return to baseline and normal imaging
53) spinal epidural abscess (SEA).
-Most patients have fever, malaise, and neurologic symptoms
- typically progress in the following fashion (due to worsening spinal cord
compression):
1 Focal back pain →
2 Nerve root pain (eg, shooting, electric-shock sensation) →
3 Motor weakness, sensory changes, bowel/bladder dysregulation →
4 Paralysis

#Dx: MRI of the affected spinal area

#Mx: Ab(vancomycin +Ceftriaxone/FQ covering pseudo ); aspiration as MC organism:
Staph aureus

54) 1) Classic early vitamin K deficiency bleeding VKDB:

- onset: presents in the first week of life
-C/F: easy bruising and mucosal and gastrointestinal bleeding.

2) Late-onset VKDB
-Onset: occurs between age 2 weeks and 6 months
-C/F: more commonly associated with intracranial hemorrhage

55) Subfalcine herniation: pupil spared; consciousness iintzct

-Uncal: Ipsilateral dilated & fixed pupil

-Central: Bilateral midposition & fixed pupils (loss of sympathetic & parasympathetic
innervation); Decorticate (flexor) → decerebrate (extensor) posturing

-Tonsillar: Coma, loss of CN reflexes, flaccid paralysis, respiratory arrest (brainstem

compression)

56) A patient with a traumatic epidural hematoma who developed somnolence and left
lower extremity weakness while awaiting surgery which is acute deterioration , concerning
for brain herniation

57) paroxysmal sympathetic hyperactivity

-disrupted inhibition by damage to cortical areas may result in paroxysmal sympathetic
hyperactivity, a syndrome characterized by rapid-onset episodes of
tachycardia, hypertension, and tachypnea often accompanied by fever and
diaphoresis.

-These episodes, which can last up to 20-30 minutes, are usually triggered by external
stimuli (eg, bathing, repositioning) but may occur spontaneously.
#Rx: avoid triggers; opioids, GABA agonist, a 2 agonist
58) RA are at risk for atlantoaxial instability;
-RF: neck extension during intubation can result in subluxation with cord compression
and cervical myelopathy.
-C/F: slowly progressive, spastic paraparesis involving the upper and lower extremities,
hyperreflexia, sensory changes, and a positive Babinski sign; Neck pain radiating to
occipital region
-Hoffman sign : positive (flexion and adduction of the thumb when flicking the nail of the
middle finger)

59) copper deficiency= B12 def

-C/F: pt with distal extremity paresthesia, loss of proprioception and vibration sense, and
ataxia has peripheral neuropathy.
-In association with anemia, skin depigmentation, and edema

60) physiologic tremor

-An enhanced physiologic tremor is typically a fine, fast, symmetric action tremor of the
hands that increases with sympathetic activity.
-Certain medications (eg, selective serotonin reuptake inhibitors, beta agonists) can cause
enhanced physiologic tremor, which generally improves with dose reduction or
medication cessation.
Vs

#psychogenic tremor: high amplitude, low f

- • Abrupt onset and static course that results in functional disability out of proportion to
tremor magnitude
• Increased severity with attention(eg examination) and decreased with distraction
• Complex features or clinical inconsistencies with known tremor syndromes (eg, can
write words but not draw spirals); fingers are often spared.
• Changeable features including shifting tremor frequency
Vs
61) essential tremor
-most prominently in the hands and can be worsened by anxiety,
-it most often presents in older adults as a tremor of the hands that is suppressed at rest,
exacerbated by outstretched arms, and more pronounced at the end of goal-directed
movements.

#Rx: •Beta blockers: propranolol. •Anticonvulsants: primidone

62) Local anesthetic systemic toxicity:

-if epidural analgesia injected into vasculature
-CNS overactivity (eg, perioral numbness, metallic taste, tinnitus) and generalized
tonic-clonic seizures by blocking inhibitory neural pathways .
 -

63)Absent seizure:
• staring spells; Preserved muscle tone vs lost in narcolepsy; Unresponsive to tactile/
verbal stimulation
vs responsive in inattentive ADHD
• Short duration (<20 sec) vs >1 min in non epileptic staring spells
classic 3-Hz spike on EEG.
• Simple automatisms frequently present: oral (eg, lip smacking, chewing) or eyelid (eg,
blinking, fluttering) movements.
-Hyperventilation can trigger episode; Normal CNS exam

64) CSF findings of GBS:

-elevated protein, normal cell count and glucose
-Dx of choice: nerve conduction

# rare case: GBS can also be triggered by HIV

64) Progressive supranuclear palsy
-a rare syndrome that presents with falls, impaired vertical gaze, and parkinsonism.
Vs
#Multiple system atrophy: motor abnormalities (tremor and rigidity), autonomic
dysfunction (orthostatic hypotension and incontinence), and cerebellar symptoms
(dysdiadochokinesia, gait disturbances, dysarthria
-ineffective to anti Parkinson’s drugs

65) Dementia with Lewy bodies :

- dementia + ≥2 of the following: visual hallucinations (not required for dx) ,
parkinsonism, fluctuating cognition (good and bad days), and REM sleep behavior
disorder (enacting dreams )
-Cognitive impairment would develop in this condition before or at the same time as
parkinsonism, not years later, as seen in PD

66) Friedreich ataxia

-CNS: Cerebellar ataxia, Dysarthria; Loss of vibration and/or position sense; Absent deep
tendon reflexes unique from B12
-others: Hypertrophic cardiomyopathy; scoliosis; DM

67) **Findings used to diagnose coma :

-impaired brainstem activity (e.g., disruption of the pupillary light, extraocular, and
corneal reflexes),
-motor dysfunction (e.g., decorticate or decerebrate posturing), and
-impaired level of consciousness

Vs
#locked-in syndrome,
-Exaggerated deep tendon reflexes can be seen in locked-in syndrome, which mimics
coma but is due to an ischemic or hemorrhagic stroke of the brainstem area.
-Patients have total paralysis of the limbs and an inability to speak, retain cognition and
alertness, and can only communicate with their eyes.

68) Anti-NMDA receptor encephalitis

- an autoimmune encephalitis syndrome characterized by psychiatric symptoms (eg,
anxiety, psychosis), cognitive dysfunction (eg, memory impairment), seizure,
autonomic instability, dystonia, and rigidity.
-MC in F; > in young women (median age of 21)

- associated with ovarian teratoma in >50% of cases;

#Rx: Tumor removal; immunosuppressant
 Common etiologies of Cognitive impairment in elderly patients
pediatric stroke • Slight decrease in fluid intelligence (ability to process new information
quickly)
• Sickle cell disease: • Normal functioning in all activities of daily living
MCC • normal scores on objective measures of cognition (eg, Montreal
• Prothrombotic disorders Normal aging Cognitive Assessment [MoCA] score ≥26/30)
• Congenital cardiac • occasional word-finding difficulty (expressive aphasia)
disease • mild memory loss but are able to provide details about incidents of
forgetfulness
• Bacterial meningitis • Changes in sleep pattern
• Vasculitis
• Focal cerebral • Mild decline( modest but notable) in ≥1 cognitive domains
Mild neurocognitive
• objective evidence of impairment (eg, MoCA score <26/30)
arteriopathy disorder
• Normal functioning in all activities of daily living with compensation
• Head/neck trauma /mild cognitive
• I.e. Although independence is generally preserved, ADLs take
impairment/ MCI
greater effort, time, and/or compensatory strategies.
• Significant decline in ≥1 cognitive domains
• Irreversible global cognitive impairment
Major neurocognitive
• Marked functional impairment
disorder /dementia
• Chronic & progressive, months to years
• Eg: Alzheimers Ds, vascular dementia
• Reversible mild-moderate cognitive impairment
Major depression/
• Features of depression (mood, interest, energy)
Pseudodementia
• Episodic, weeks to months
Types of headache
Migraine Cluster Tension -Vs B/L headache in migraine of
Sex
Female > male Male > female Female > male children
predilection
Family
Often present No No
history
Onset Variable During sleep Under stress
Band-like pattern
Location Often unilateral Behind one eye around the head
(bilateral)
Pulsatile & Dull, tight &
Character Excruciating, sharp & steady
throbbing persistent
30 minutes to 7
Duration 4-72 hours 15-90 minutes
days
Auras-
scintillating
Sweating, facial flushing, Muscle tenderness
Associated flash
symptoms photophobia,
nasal congestion, lacrimation in the head, neck, or #if no response to therapy:
phonophobia &
& pupillary changes shoulders
-Following such a therapy,
nausea
patients with GCSE typically
regain responsiveness in 10-20
minutes.

-Persistent unresponsive
state,may be due to either:
• Sedation due to persistent
Levetiracetam effects of BZD/
• nonconvulsive status
epilepticus).

—>Therefore, to differentiate
between these 2 states, EEG
e-
.

should be performed.
-
73) traumatic spinal cord injury
-disruption of the autonomic tracts involved in bladder control can lead to urinary
retention. Therefore, catheterization should be performed

74) Sturge-Weber syndrome

- (port-wine stain) along the trigeminal nerve distribution
- leptomeningeal capillary-venous malformations affecting the brain and eye.
-C/F: Seizures, intellectual disability, and visual field defects, glaucoma

75) Any 1 of the following is an indication for cervical spine imaging:(with CT spine)
• Neurologic deficit
• Spinal tenderness The presence of a single vertebral fracture (especially cervical)
• Altered mental status in a patient with blunt trauma is an indication to image the
• Intoxication entire spine because the risk of a second, noncontiguous
• Distracting injury vertebral fracture is as high as 20%.

76) Amyotrophic lateral sclerosis -bulbar symptoms (eg, dysphagia, dysarthria) +

both UMN (eg, pathologic jaw jerk reflex) + LMN (eg, tongue fasciculations and
atrophy).

#Dx:
-Clinical evaluation; EMG 0 .

-MRI(to exclude other causes)

#Mx: —>> Universally Fatal so Rx is based on slowing the progression & symptom control
• Riluzole - glutamate inhibitor, a 1st-line therapy improve survival by reducing
glutamate-mediated excitotoxicity.
• Edaravone , an antioxidant, which likely slows disease progression, often used in
combination with Riluzole,
• Respiratory support (eg, NIPPV)
• Nutritional support (eg, PEG tube)
• Multidisciplinary Symptoms control

77) ICH in young patients

- commonly due to arteriovenous malformation,
-C/F: recurrent headache, seizure, or focal neurologic deficits.

78) Pronator drift:

-UMNL cause more weakness in the supinator muscles compared to the pronator
muscles of the upper limb.
-As a result, the affected arm drifts downward and the palm turns (pronates) toward
the floor (opposite to the lesion side )

Vs
#Cerebellar lesions result in an upward drift (rather than the downward drift seen in
pyramidal tract lesions) due to hypotonia.
568 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PHARMACOLOGY
` 

Parkinson disease The most effective treatments are non-ergot dopamine agonists which are usually started in
therapy younger patients, and Levodopa (with carbidopa) which is usually started in older patients. Deep

I
brain stimulation of the STN or GPi may be helpful in advanced disease.
STRATEGY AGENTS
Dopamine agonists Non-ergot (preferred)—pramipexole, ropinirole; toxicity includes nausea, impulse control disorder
(eg, gambling), postural hypotension, hallucinations, confusion.
Ergot—bromocriptine rarely used due to toxicity.
 dopamine availability Amantadine ( dopamine release and  dopamine reuptake); toxicity = peripheral edema, livedo
reticularis, ataxia.
 L-DOPA availability Agents prevent peripheral (pre-BBB) l-DOPA degradation Ž  l-DOPA entering CNS Ž  central
l-DOPA available for conversion to dopamine.
ƒ Levodopa (l-DOPA)/carbidopa—carbidopa blocks peripheral conversion of l-DOPA to
dopamine by inhibiting DOPA decarboxylase. Also reduces side effects of peripheral l-DOPA
conversion into dopamine (eg, nausea, vomiting).
ƒ Entacapone and tolcapone prevent peripheral l-DOPA degradation to 3-O-methyldopa
(3-OMD) by inhibiting COMT. Used in conjunction with levodopa.
Prevent dopamine Agents act centrally (post-BBB) to inhibit breakdown of dopamine.
breakdown ƒ Selegiline, rasagiline—block conversion of dopamine into DOPAC by selectively inhibiting MAO-B.
ƒ Tolcapone—crosses BBB and blocks conversion of dopamine to 3-methoxytyramine (3-MT) in
the brain by inhibiting central COMT.
Curb excess Benztropine, trihexyphenidyl (Antimuscarinic; improves tremor and rigidity but has little effect on
cholinergic activity bradykinesia in Parkinson disease). Tri Parking my Mercedes-Benz.
DOPA
DECARBOXYLASE CIRCULATION
Dopamine 3-OMD
INHIBITOR
– L-DOPA
COMT INHIBITORS
Carbidopa DDC COMT – (peripheral)

÷
BLOOD-
BRAIN Entacapone
BARRIER Tolcapone

L-DOPA

DDC COMT INHIBITOR

(central)
PRESYNAPTIC
Dopamine –
TERMINAL FROM THE Tolcapone
SUBSTANTIA NIGRA COMT
3-MT
DOPAC

–
Autoregulatory MAO TYPE B
receptor INHIBITORS
Reuptake
Selegiline
Rasagiline

DOPAMINE +
AVAILABILITY

Amantadine

Dopamine receptors + DOPAMINE AGONISTS

POSTSYNAPTIC
TERMINAL IN
THE STRIATUM Pramipexole (non-ergot)
Ropinirole (non-ergot)
-
Bromocriptine (ergot)
79)PD psychosis (hallucinations, delusions, paranoia) in PD is common; Etio:
1) the underlying disease process,
2) medication, or
3) a combination of the two.

#Culprit drugs for psychosis:

- dopamine precursors (eg, levodopa) and
-dopamine agonists (eg, pramipexole).

#Management:
-1st step :reviewing the patient's medication and considering a cautious dose reduction

-2nd line: Patients who do not improve with a reduction or who cannot tolerate a dose
reduction due to resurgent motor symptoms can be treated with a low-potency, second-
generation antipsychotic (eg, quetiapine, pimavanserin).

80) Mastoiditis causing brain abscess:

-source: Direct spread of bacteria from otitis media or mastoiditis can cause a temporal
brain abscess.
-C/F: nocturnal headache, morning vomiting, fever, and focal neurologic deficits.
-Dx: visualization of a ring-enhancing lesion on CT scan or MRI of the brain
-Rx: IV vancomycin+ ceftazidime/ Piptaz

81) Focal seizures

-originate in a single cerebral hemisphere and can spread to involve both hemispheres,
causing impairment of awareness (with or without automatisms) and inability to respond to
external stimuli.
Vs

#absence seizures:
-lasting only 10-20 seconds.
-easily provoked by hyperventilation and not associated with a postictal period.
Vs
#Juvenile myoclonic epilepsy
-presents in adolescents with myoclonic jerks immediately on wakening.
-Absence and generalized tonic-clonic seizures may also be seen.
Vs

#Lennox-Gastaut syndrome:
-typically presents by age 5 with intellectual disability and severe seizures of varying types
-Interictal EEG demonstrates a slow spike-and-wave pattern.
82) Alzheimer’s Ds:
-early memory loss is prominent
Vs
#Vascular dementia: executive function loss is earlier

83) RS exam in GBS:

-Once GBS is suspected in a hemodynamically stable patient, the next step in
-

management is to assess pulmonary function with spirometry.

- Forced vital capacity (FVC) and negative inspiratory force monitor respiratory
muscle strength, and serial pulmonary function testing should be performed given the
potential for rapid progression of disease.

- A decline in FVC (≤20 mL/kg) indicates impending respiratory failure warranting

endotracheal intubation.

#indications for elective or emergency intubation :

1) respiratory distress (eg, tachypnea, accessory muscle use),
2) severe dysautonomia (eg, heart rate and blood pressure instability), or
3) widened pulse pressure.

84) # Onset & Progression of different stroke

1) intraparenchymal brain hemorrhage
-Onset: sudden focal neurologic deficits that gradually worsen over minutes to hours.
-As the hemorrhage expands, headache, vomiting, seizures (if lobar), and altered mental
status can develop.

2) subarachnoid hemorrhage and embolic stroke

- symptom severity is maximal at onset

3)Ischemic stroke
-symptoms classically progress in a stuttering fashion.
Management of traumatic brain injury
Antipsychotic medication effects (dopamine
Goal Interventions
antagonism) in dopamine pathways
• Maintain MAP: isotonic fluids, vasopressor therapy
Maintain CPP • Reduce ICP: head elevation, sedation, osmotic therapy (eg, Pathway Effect
(= MAP − ICP) hypertonic saline, mannitol), decompressive interventions
(eg, CSF removal, craniectomy) Mesolimbic Antipsychotic efficacy

Prevent ICH
• Antifibrinolytic therapy( tranexamic acid) within 1st 3 hr Extrapyramidal symptoms:
• Reversal of preexisting anticoagulation Nigrostriatal Acute dystonia, akathisia,
• Prevent seizures (eg, levetiracetam, phenytoin) parkinsonism
• Control blood glucose (eg, insulin to target 140-180 mg/dL
Other
glucose) Tuberoinfundi
measures
• Maintain normothermia (eg, antipyretics, surface-cooling Hyperprolactinemia
bular
devices)

Acute traumatic coagulopathy, a state of hypocoagulability and

hyperfibrinolysis, can complicate traumatic brain injury (TBI)
 87) Mx of idiopathic intracranial
HT:
Before drugs, do LP after normal
imagining
1) 1st line:Acetazolamide.
→ 2) 2nd line: Furosemide can be
added for patients with continued
symptoms on acetazolamide.

3) 3rd line:
-For patients with symptoms
Vs away in refractory to medical therapy or
putamen H’age those with progressive vision
loss,
—>surgical intervention : optic
nerve sheath decompression /
lumboperitoneal shunting is
recommended
 #Occlusion of the internal
carotid artery, which
If ant limb—> pure sensory supplies the anterior
circulation, generally
results in extensive
neurologic deficits as
both the MCA and ACA
territories are affected.
Frontal eye field
-Symptoms include
dense, contralateral
hemiplegia (face, arm,
and leg equally affected)
with contralateral
sensory, visual, language,
or spatial impairments.

58) Neurogenic shock after spinal tract injury:

-Acute spinal cord injury often manifests with loss of spinal cord function (eg, areflexia,
anesthesia, paralysis, distended bladder) below the level of the lesion.

-Lesions that arise above T1 also often cause neurogenic shock due to interruption of
the descending sympathetic fibers, which results in unopposed parasympathetic
stimulation of the vessels (hypotension) and heart (bradycardia).
-above is preceded by massive SANS stimulation transiently

—> Hypothermia is also common due to a lack of peripheral vasoconstriction.

16) Vascular dementia

-following stroke presents as sudden or stepwise decline in executive function that
interferes with activities of daily living.
*FNd
-Patients often have focal neurologic findings on examination (eg, hemiparesis,
pronator drift, Romberg sign) due to prior (potentially unrecognized) strokes.

- neuroimaging classically :cerebral infarction and/or deep white matter changes from
chronic ischemia
Vs
• early personality and behavioral changes (eg, disinhibition, apathy).
• compulsive behaviors (eg, hoarding, hyperorality).
• executive dysfunction.
Memory deficits tend to appear later in the disease course in fronto temporal dementia
 I

The oculocephalic reflex is a component of the neurological

exam that is usually performed prior to declaring brain
death. However, oculocephalic reflex testing requires quickly
turning the patient's head to one side and it should not be
performed in patients with C-spine injuries. Amboss

87) NPH: disproportional rise in ventricular volume compared to normal sulci

Vs
Proportionate rise with respect to sulci in ex vacuo ventriculomegaly

88) Descending aortic dissection type B: anterior spinal artery ischaemia-anterior

cord syndrome in mid thoracic region; U/E intact
Vs
Ascending aortic dissection type A: vertebral artery dissected- neck pain, ischemic
stroke; headache; posterior cord ischaemia i.e. DCML Lost
90) Medication overuse headache
-chronic, milder near-daily headache in the setting of regular use of acute headache
medications in patients with a preexisting headache disorder but pattern changes from
previous one .
-C/F :headache that is present upon awakening and brief symptom relief followed by
rebound pain.
-Management : cessation of the culprit medication.
Vs
Severe, thunderclap headache in >50 yrs- CA

91) initial workup of suspected dementia:

-before a definitive diagnosis is made, all patients should undergo a workup for potentially
reversible causes of cognitive impairment.

-include neuropsychological testing (eg, Montreal Cognitive Assessment), selected

laboratory testing (CBC, complete metabolic panel, TSH, vitamin B12), vit D, syphilis,
CSF for meningitis if RF +;
neuroimaging (eg, MRI).

92) Alcoholic neuropathy

-a toxic neuropathy that typically results in a symmetric distal polyneuropathy (ie,
stocking and glove pattern) characterized by paresthesia, burning pain, and ataxia.
-Loss of distal DTR (eg, ankle) and light touch and vibratory sense are common.

93) MCC Of H’agic stroke in children:

• Vascular malformations
◦ AVM (isolated or associated with HHT); Aneurysm
• Hematologic abnormalities (eg, hemophilia, sickle cell disease)

Pediatric traumatic brain injury (PECARN rule)

• Altered mental status (fussy behavior)
• Loss of consciousness
High-risk
• Severe mechanism of injury (fall >0.9 m [3
features
ft], high impact, MVC)
age <2
• Nonfrontal scalp hematoma
• Palpable skull fracture
• Altered mental status (eg, somnolence,
agitation)
• Loss of consciousness
High-risk
• Severe mechanism of injury (fall >1.5 m [5
features
ft], high impact, MVC)
age ≥2-18
• Vomiting, severe headache
• Basilar skull fracture signs (eg, CSF
rhinorrhea)
Management • Head CT scan without contrast
Observation for 4-6 hours may be an alternative option if mental
status is normal and there are no signs of a basilar skull fracture.
95) Spinal epidural hematoma
-Etiology: a potential complication of neuraxial anesthesia (eg, epidural block), lumbar
puncture, or spinal surgery and is more common in older adults taking antithrombotic
medications.

#C/F; Bleeding within the spinal canal results in cord compression, leading to progressive
motor and sensory dysfunction in the distribution of the affected nerve root;
-bowel and bladder dysfunction; localised back pain/ tenderness

#Mx: urgent MRI and neurosurgical decompression.

96) Creutzfeldt-Jakob disease

#C/F: Rapidly progressive dementia
• ≥2 out of 4 clinical features:
◦ Myoclonus: BZD as supportive rx
◦ Akinetic mutism
◦ Cerebellar or visual disturbance
◦ Pyramidal/extrapyramidal dysfunction (eg, hypokinesia)
#Dx:
• MRI: widespread atrophy (cerebrum & cerebellum), cortical enhancement (ie, cortical
ribboning), enhancement of putamen & caudate head (ie, hockey stick sign)
• CSF: normal routine analysis, positive 14-3-3 protein titers, positive RT-QuIC test
• EEG: sharp, triphasic, synchronous discharges
• Neuropath: spongiform degeneration without inflammation

97) Sydenham chorea

- an autoimmune complication of group A Streptococcus infection
-MOA: molecular mimicry, in which antistreptococcal antibodies cross-react with
neuronal antigens in the basal ganglia.

#Neuropsychiatric manifestations :
chorea (jerky irregular involuntary contraction of limb and face) , milkmaid grip (hand
grip loosens by intermittent chorea) , hypotonia, emotional lability (laughter), and
OCD
+ May have associated enlarged tonsils

98) Management of ischaemic stroke:

-Once hemorrhage is excluded, thrombolytic therapy should be considered as long as no
absolute contraindications exist.
.
# Thrombolytic DOC:
-Intravenous alteplase (tissue plasminogen activator) within 4.5 hours of sx onset.

- aspirin and heparin can increase the risk of intracranial H’age.

 100) Lhermitte sign
-occurs when neck flexion compresses
and activates the ascending
spinothalamic pain tracts but is
nonspecific
- seen in multiple CNS diseases
-
MS, transverse myelitis; cervical
spondylosis/ myelopathy 3 M

101) cervical myelopathy:

-Spinal cord compression by
degenerative vertebra: UMN signs in
L/E
-compression of cervical spinal roots
at the same level: LMN in U/E
+
Lhermite sign( absent in AMLS) diff

102) Relationship of Antipsychotics with Lewy body dementia :

- Severe sensitivity to antipsychotics (dopamine antagonists) is commonly seen in
patients with DLB and is considered a supportive clinical feature.

- Antipsychotic ADRs : worsening of parkinsonian symptoms, confusion, and autonomic

dysfunction

103) Huntington Ds
• Motor: chorea, delayed saccades
• Psychiatric: depression, irritability, psychosis, obsessive-compulsive symptoms
• Cognitive: executive dysfunction

104) Suspect a MS when B/L trigeminal neuralgia

105) myasthenia crisis: severe respiratory distress in MG

-triggers: Infection or surgery; Pregnancy or childbirth; Tapering of immunosuppressive
drugs; Medications (eg, aminoglycosides, beta blockers; Macrolides; FQs)
#Rx
Avoid pyridostigmine as it increases secretion
• Intubation for deteriorating respiratory status
• Plasmapheresis / IVIG +corticosteroids
 106) Diagnostic steps in SAH
-1st line:CT sensitive within 2-6
hrs
-2nd Line:LP even >6 hrs;
Rx: alteplase if CT nondiagnostic and high
suspicion
Rx: steroid
107) what if DM neuropathy pt
develops motor Sx and
+babinski??
—>> Peripheral neuropathy strictly
affects the lower motor neurons.

—>> unlikely to cause weakness that

is present throughout the legs and is
of relatively rapid onset (eg, months)
#Next step:
Evaluation of Nerve C/Fs d/t Spine pathology :
- patient should be questioned about recent fevers (concerning for epidural abscess)
or weight loss (concerning for malignancy).

- Dx: MRI of the spine should be performed to evaluate for cord compression.
- It’s an emergency as Presence of UMn because delay in diagnosis would likely lead to
worsening neurologic deficits.

108) Alzheimer’s Ds +F/H/O:

-Patients with a family history of Alzheimer disease are at increased risk of developing the
disease but can mitigate risk by addressing modifiable risk factors.

—> Aggressive treatment of cardiovascular risk factors (eg, hypertension, diabetes,

obesity/physical inactivity), especially in mid-life, can help reduce risk.

109) Changing headaches:

-Headaches that are new or differ in character from prior, that are present on
awakening, and that are associated with frequent nausea and vomiting as well as blurry
vision are concerning for a pathological cause.
-Dx: evaluated early with an MRI of the brain.

110) INH induced neuropathy:

-numbness and tingling in a "stocking-glove" distribution. Physical examination usually
reveals deficits in proprioception and vibration; over time, touch, pain, and temperature
sensation may be affected.

-Vulnerable: DM; malnourished with limited store

111) Phenytoin toxicity: cerebellar dysfunction
-Trigger: liver Ds; CYP inhibitors

112) Distal symmetric polyneuropathy

• Diabetes mellitus —> M/C Cause
• Long-standing HIV infection
• Uremia
• Medications (eg,metronidazole, Amiodarone, Dapsone, fluoroquinolones, Digoxin
—>> MAD FD) ACUTE
• Chemotherapy (eg, cisplatin, paclitaxel)
• Toxicity (eg, alcohol abuse, heavy metal exposure)
• Multiple Myeloma in Elderly

114) epidural Hematoma: lucid interval;

Subdural headache: unconscious/ drowsy at start

115) SAH complications:

a) Vasospasm : after 3days
-Prevention: initiation of nimodipine.

b) Subacute hydrocephalus
-C/F: headaches. Patients tend to develop progressive mental decline and multiple
-

neurologic deficits due to compression of the cranial nerves, brainstem, and/or

cerebral cortex.

c) rebleeding -first 24 hrs

risk can be high in untreated SAH, surgical repair of the aneurysm (eg, endovascular
coiling in this patient) practically eliminates the rebleeding risk.

116) Postictal lactic acidosis

-commonly occurs following a tonic-clonic seizure.
-Prognosis: It is a transient anion gap metabolic acidosis that resolves without
treatment within 90 minutes following resolution of seizure activity.

#Next best step: observation and a repeat chemistry panel after approximately 2 hours.
—> If the metabolic acidosis has not resolved, other potential causes of anion gap
metabolic acidosis (eg, intoxication, sepsis) should be investigated.
 Antiplatelet/antithrombotic therapy for ischemic stroke 117) CSF rhinorrhea:
Clinical presentation Therapy -Clear,U/L rhinorrhea that increases
Presentation within 3-4.5 hours
at times of relatively increased
Intravenous alteplase ICP (eg, bending over, bowel
of symptom onset
Stroke with no prior antiplatelet
movements) is suspicious for CSF
Aspirin rhinorrhea
therapy
Aspirin +
Stroke on aspirin therapy -Etiology:caused by head trauma;
dipyridamole OR clopidogrel
Long-term anticoagulation Non traumatic raised ICP
Stroke with evidence of atrial
(eg, warfarin, dabigatran,
fibrillation -

- rivaroxaban) -Test: CSF-specific proteins (β-2

Stroke with large anterior transferrin, β-trace protein
Mechanical thrombectomy
circulation artery occlusion
(regardless if patient received
within 24 hours of symptom
alteplase), then aspirin
onset
Patient with intracranial large- Aspirin + clopidogrel for 90
artery atherosclerosis days, then aspirin

118) Empiric Rx of lung abscess:

-1st line: Ampicillin-sulbactam, imipenem, meropenem
-2nd Alternate: clindamycin

-never Metro as it doesn’t cover everything

119) Mx of restless leg syndrome:

-iron supplementation if S.ferritin<75 Ug/L, conservative measures,

- pharmacotherapy with dopamine agonists (eg, pramipexole) / alpha-2-delta calcium

channel ligands (eg, gabapentin).

120) complication of status epilepticus:

-increased risk of developing permanent injury due to excitatory cytotoxicity.

—> Cortical laminar necrosis is the hallmark of prolonged seizures and can lead to
persistent neurologic deficits and recurrent seizures.

121) Cerebral venous sinus thrombosis

typically presents in prothrombotic conditions (eg, postpartum) with headache,
increased ICP, seizures, and stroke.

-Diagnosis: visualizing a flow void on MR venography of the brain.

-Rx: heparin acutely; x thrombolytics due to risk for H’age
Broca's aphasia often represents a broken speech system.

i .

123) RF for MS:

-MC in Caucasian women age <50.
-RF: vit D deficiency, geographic location, genetic (HLA-DRB1), & smoking.

124) Vascular dementia types:

• Single, strategic infarction: One infarction may be large enough to cause poststroke
vascular cognitive impairment if it affects key brain areas (ie, frontal lobes,
thalamus).; onset: soon at a time after stroke

• Multiple infarctions: Multi-infarct dementia occurs when small infarcts combine to

cause enough cumulative damage to the brain, resulting in noticeable cognitive
deficits.
- Patients may not have a history of overt stroke but rather have a stepwise decline in
cognitive function: slower onset
Vs
# In contrast, Alzheimer disease typically experience insidious onset of memory
impairment over many months to years with personality and behavioral changes
occurring relatively later in the disease course
125) Alcoholic cerebellar degeneration :> 10 yrs of alcohol
- caused by damage to the Purkinje cells of the cerebellar vermis.
-C/F: slowly progressive onset of ambulation difficulties, including wide-based gait and
postural instability. Truncal coordination (eg, tandem gait) is impaired,
—> but limb coordination (eg, finger-nose test) is relatively intact.

126) Brain Mets: MC lung CA

-C/F headache, focal neurologic dysfunction, cognitive change, or seizure.
-MRI : multiple, well-circumscribed lesions with vasogenic edema at the gray and
white matter junction.
127) 1st step in intracerebral H’age
with herniation:
-Patients with intracerebral
hemorrhage can have rapid clinical
deterioration, especially when brain
herniation is present.

—> When a change in clinical status

occurs, the ABCs (Airway, Breathing,
Circulation) should be reassessed
because intubation and mechanical
ventilation may be necessary (eg,
airway protection).

-later other measures

128) -Whiplash most commonly causes cervical strain without associated cervical spine
fracture. So doesn’t need imaging

129) Evaluation of 1st seizures:

-1st line: )excluding metabolic (eg, hypoglycemia, electrolyte disturbances) and toxic
(eg, amphetamine use, benzodiazepine/alcohol withdrawal) causes.

-#Basic laboratory tests :

serum electrolytes, glucose, calcium, magnesium, complete blood count, renal function
tests, liver function tests, and a toxicology screen.

-2nd line) Routine EEG

-is useful for risk-stratifying patients after a first-time seizure once metabolic and toxic
etiologies have been excluded.

-The presence of epileptiform activity on an EEG indicates a higher risk of seizure

recurrence and therefore may justify the need to start anti-epileptic therapy.
3rd line) Neuroimaging:
-(CT) scan of the brain without contrast is the initial imaging study of choice in patients
with unprovoked first seizure to exclude acute neurologic problems (eg, intracranial or
subarachnoid bleed) that might require urgent intervention. 

-MRI is more sensitive than CT in identifying most structural causes of epilepsy and is
the neuroimaging modality of choice in elective situations.

130) Rx of parkinson Ds dementia PDD:

A) Rx for cognitive impairment of PDD : symptomatically with cholinesterase inhibitors
(eg, donepezil).
B) Rx for Psychotic symptoms of PDD : dose reduction of antiparkinsonian agents
and/or low-potency antipsychotics (eg, pimavanserin, quetiapine).

131) Mx of PD tremor:
1) younger patients (eg, age ≤65) with tremor-dominant PD: Trihexyphenidyl.

2) older patients with mild, tremor-dominant disease:

amantadine is sometimes used to avoid the anticholinergic effects of trihexyphenidyl.
132) Hydrocephalus in infants:
-USG: before closure of Fontanelle vs MRI after closure
-don’t confuse it’s developmental hault with that of rette syndrome

133) Cerebellar H’age:

- • Unlike other forms of stroke, hemiparesis and sensory loss are rare
#Mx:
• Reversal of anticoagulation; BP management
• ICP management (eg, head of bed elevation, mannitol)
• Surgical decompression indicated with:
◦ Hemorrhage >3 cm
◦ Neurologic deterioration (eg, impaired consciousness)
◦ Brainstem compression, obstructive hydrocephalus

134) Mx of acute attack of MS:

a) Acute exacerbations of MS with disabling neurologic symptoms :
-GC (eg, intravenous methylprednisolone).
-Plasmapheresis in refractory to corticosteroids.

b) Maintenance Rx: Interferon beta or glatiramer acetate can be used as chronic

maintenance therapy in patients with relapsing-remitting or secondary, progressive
forms of multiple sclerosis.
135) Tabes dorsalis:
• Sensory ataxia: DCML
• Lancinating pains: brief periods of shooting/
burning pain in the face, back, or extremities.
• Neurogenic urinary incontinence
• Argyll Robertson pupils: normal pupillary
constriction with accommodation but not
with light.

#Rx:10-14 days of IV penicillin G

Vs
136) Mechanism behind Cushing triad
-Elevated ICP has led to a decrease in
cerebral perfusion pressure (CPP).

-The sympathetic nervous system is activated

in this situation to increase mean arterial
pressure to maintain CPP, which explains
patient's hypertension.
 NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PATHOLOGY
`  SEC TION III 547

Herniation syndromes Cingulate (subfalcine) herniation under Can compress anterior cerebral artery.
Falx cerebri falx cerebri
Lateral Central/downward transtentorial Caudal displacement of brain stem Ž rupture of
ventricles
herniation paramedian basilar artery branches Ž Duret
Supratentorial
mass hemorrhages. Usually fatal.
Uncus
Tentorium Uncal transtentorial herniation Uncus = medial temporal lobe. Early herniation
cerebelli Ž ipsilateral blown pupil (unilateral CN III
Kernohan compression), contralateral hemiparesis. Late
Duret notch
hemorrhage herniation Ž coma, Kernohan phenomenon
(misleading contralateral blown pupil and
ipsilateral hemiparesis due to contralateral
compression against Kernohan notch).
Cerebellar tonsillar herniation into the Coma and death result when these herniations
foramen magnum compress the brain stem.

Motor neuron signs

SIGN UMN LESION LMN LESION COMMENTS
Weakness + + Lower motor neuron (LMN) = everything
Atrophy − + lowered (less muscle mass,  muscle tone, 
reflexes, downgoing toes)
Fasciculations − +
Upper motor neuron (UMN) = everything up
Reflexes   (tone, DTRs, toes)
Tone   Fasciculations = muscle twitching
Babinski + − Positive Babinski is normal in infants
Spastic paresis + −
Flaccid paralysis − +
Clinical features of brain herniation
Clasp knife spasticity + −
Herniation
Common features
type
• Herniation of cingulate gyrus underneath falx cerebri
• No pupillary involvement, consciousness often
Subfalcine preserved
• Contralateral leg weakness (ipsilateral ACA
compression)
• Herniation of uncus (medial temporal lobe) under
tentorium cerebelli
• Ipsilateral dilated & fixed pupil (ipsilateral oculomotor
e-
nerve [CN III] compression)
Uncal
• Early: contralateral hemiparesis (ipsilateral cerebral
peduncle compression)
• Late: ipsilateral hemiparesis (contralateral cerebral
peduncle compression)
• Caudal displacement of diencephalon & brainstem
• Rupture of paramedian basilar artery branches
Central • Bilateral
-
midposition & fixed pupils (loss of sympathetic

I
& parasympathetic innervation)
• Decorticate (flexor) → decerebrate (extensor) posturing
-
• Herniation of cerebellar tonsils through foramen
magnum
Tonsillar
• Coma, loss of CN reflexes, flaccid paralysis, respiratory
arrest (brainstem compression)
ACA = anterior cerebral artery; CN = cranial nerve.
137) Idiopathic intracranial hypertension
- MC in obese women of childbearing age and can present with positional headaches,
pulsatile tinnitus, and papilledema.
-Diagnosis :MRI of the brain followed by lumbar puncture.
138) SAH
Isolated oculomotor nerve palsy can indicate an aneurysm of the posterior
communicating artery.
Vs
#Carotid artery dissection
- typically presents with unilateral headache and ipsilateral Horner syndrome. Generalized
headache is not typical, and pupillary dilation is not expected (Horner syndrome
causes pupillary constriction).
139) Internuclear ophthalmoplegia
- The affected eye (ipsilateral to the
lesion) is unable to adduct and the
contralateral eye abducts with
nystagmus.

-Unilateral MLF lesions : lacunar stroke

in the pontine artery distribution;

-bilateral lesions: multiple sclerosis.

140) autonomic dysreflexia:

-Spinal cord injury above T6 can be
complicated by autonomic dysreflexia

- noxious stimuli below the injury level

trigger an unregulated SANS
response, leading to severe HT.

-A compensatory PANS response above the

lesion typically causes bradycardia.
Management includes removing noxious
stimuli and treating the hypertension

141) Brain mets Mx:

a) solitary brain metastasis in patients with good performance status and stable extracranial
disease: Surgical resection

-This is typically followed by stereotactic radiosurgery (SRS) / whole brain radiation therapy
(WBRT) to the tumor bed.
#Stereotactic radiosurgery (SRS): for small tumor (<3 cm )
-It can deliver precisely-targeted radiation in fewer high-dose treatments than traditional
therapy, which can help preserve healthy tissue.

b) multiple brain metastases: whole brain radiation therapy

Vs
#Chemotherapy
-might be used in case of brain metastasis from chemosensitive tumors (eg, small cell
lung cancer, lymphoma, choriocarcinoma).
-However, it has not shown benefit in the management of brain metastasis from NSCLC.

143) Diagnosing Alzheimer disease in HIV :

-Because HIV infection is being successfully managed with ART and patients are living
longer with lower morbidity,
-common forms of dementia such as Alzheimer disease (also show diffuse cortical
atrophy ) have become much MC than HIV-associated dementia in these patients.
Vs
#HIV-associated dementia :severe form of subcortical dementia found almost
exclusively in untreated HIV-infected patients.(CD <200)

—> In contrast to the characteristic cortical dysfunction seen in AD (ie, amnestic

symptoms),
-HAD is predominantly a subcortical dementia characterized by apathy, early
impairments in attention, and subcortical motor symptoms.

144) embolic to H’agic stroke:

-Patients with large or embolic ischemic strokes and those treated with thrombolytics are at
high risk for hemorrhagic transformation.

-Onset: usually occurs within 48 hours of the stroke and often manifests with
deteriorating mental status.
-Diagnosis : emergent repeat noncontrast CT scan of the head.

145) disorders causing dysphagia:

-If the bedside swallowing test is positive, a formal swallowing study, such as a
videofluoroscopic swallowing examination, is required to confirm the diagnosis.
#Next best step:
-Patients with ALS and swallowing difficulties may need specialized nutritional support
(e.g., pureed food, thickened liquids, nasogastric tube, percutaneous endoscopic
gastrostomy).
 Interventions to reduce intracranial pressure 146) AMLS:
↓ Brain -can cause respiratory insufficiency
• Osmotic therapy (eg, hypertonic due to respiratory muscle
parenchymal
saline, mannitol) to extract water
volume weakness.
• Head elevation to ↑ venous outflow
↓ Cerebral #Mx:
• Sedation to ↓ metabolic demand
blood
• Hyperventilation to ↓ PaCO2, -NPPV prolongs survival and
volume
resulting in vasoconstriction improves quality of life.
• CSF removal (eg, external ventricular -Tracheostomy and invasive
↓ CSF volume
drain) mechanical ventilation: for patients
↑ Cranial with C/I to NIPPV (eg, inability to
• Decompressive craniectomy clear secretions, severe bulbar
volume
dysfunction) or those with
progressive respiratory failure
despite NIPPV.
148) Alzheimer’s RF:
• Key idea: 2 most important risk factors for Alzheimer’s is (1) Increased age (2) Family
history of early-onset dementia (often due to mutation in Amyloid precursor protein or
presinilin-1/2)
• Key idea: Early-onset Alzheimer’s defined by symptoms appearing age 65 or
younger

149) Astrocytomas are the most common brain tumors in adults, and represent a
subcategory of gliomas, which include all brain tumors of glial cell origin.
-Other gliomas : oligodendrogliomas and ependymomas.
-The most important prognostic factors for astrocytomas : patient age, functional
status, and tumor grade.

# Classification:
a) Low-grade astrocytomas : grade I / II.
-They typically have increased cellular proliferation and atypia, but lack necrosis, mitoses,
and neovascularity.
b) Grade III astrocytomas / anaplastic astrocytomas,
- increased number of mitoses.
c) Glioblastoma multiforme (GBM):is a grade IV astrocytoma
-the worst prognosis of all.
-Neovascularity or necrosis is characteristically present in GBMs.
 Restless leg syndrome
• Iron deficiency anemia 151) Acute postinfectious cerebellar ataxia
Associated
•
•
Uremia (ESRD, CKD)
Diabetes mellitus
- the most common etiology of ataxia in children
secondary • Multiple sclerosis, Parkinson disease and often follows viral illness (CSX, HHV )
causes • Pregnancy
• Drugs (eg, antidepressants, -It is a diagnosis of exclusion.
metoclopramide)
• Supplement iron when serum ferritin ≤75
µg/L
Mild/intermittent symptoms:
• Use supportive measures (eg, leg
massage, heating pads, exercise)
Treatment • Avoid aggravating factors (eg, sleep
deprivation, medications)
Persistent/moderate to severe symptoms:
• Dopamine agonists (eg, pramipexole)
• α2δ calcium channel ligands (eg,
gabapentin)

152) Head CT imaging in infants meningitis

CSF analysis and administration of antibiotics are the priorities when meningitis is
suspected. Herniation is extremely rare in infants as their fontanelles are open and can
accommodate some brain swelling.

#Therefore, head CT imaging should be reserved for patients:

- who are comatose,
- have focal neurologic findings, or
-a history of neurosurgical procedure ie, ventriculoperitoneal shunt,
In the absence of such findings, a head CT scan will only delay appropriate testing and
treatment

153) #Mx of trigeminal neuralgia

-TN is usually treated with medications first (eg, carbamazepine, oxcarbazepine).
-If treatment is unsuccessful, surgery (eg, nerve decompression, radiosurgery) can be
considered.

#ADR of Carbamazepine:
-nausea and vomiting.
- leukopenia and aplastic anemia; therefore, CBC is included in monitoring.

—>> When this medication fails or causes adverse effects, other agents :
- oxcarbazepine,
- baclofen can be considered.

—>> Oxycodone is a narcotic used for many painful disorders and has been used in TN to
provide temporary relief while waiting for carbamazepine to reach full effect;
however, very high doses are often needed, which can cause sedation and risk of
overdose.
156) Rx of mild mod Alzheimer’s: done riva
Mod severe: memantine
Vs
#Rx of fronto temporal dementia : SSRI, trazodone

157) Pathophysiology of TN
-compression of the trigeminal nerve root as it enters the pons, leading to demyelination
and atrophy of the nerve.
-causes: Compression most commonly occurs due to a vascular loop, neoplastic growth,
or multiple sclerosis plaque.
158) aqueduct of Sylvius stenosis: dilation of 1st 3 ventricles except 4th.
-Rx: aqueductoplasty
Vs
# non communicating hydrocephalus: All 4 chambers dilated
-Rx: VP shunt

159) Diffuse axonal injury can occur in child abuse shaken baby

160) Mx of locked in syndrome:

-physiotherapy, which consists of passive stretching exercises and frequent repositioning to
avoid decubitus ulcers.
-Patients learn to communicate using blinking, vertical eye movements, eye-gaze sensor-
controlled computer communication programs, and speech synthesizers.
-Some patients may recover some motor control, breathing, swallowing, and/or speaking
ability.
 D/D MRI brain lesions
1) Cerebral toxoplasmosis :multiple ring-enhancing lesions with edema

2) HIV-associated dementia
-RF: occurs almost exclusively in untreated HIV-infected patients with advanced
disease (eg, CD4+ <200)
-C/F: characterized by apathy, attention impairment, and subcortical motor symptoms
(eg, impaired psychomotor speed).

-MRI brain: diffuse brain atrophy, ventricular enlargement, and reduced

attenuation of white matter structures diffusely

3) Primary CNS lymphoma :a single, well-defined, ring-enhancing lesion with

surrounding edema: periventricular

4) Progressive multifocal leukoencephalopathy (PML): CD4 count <200/mm3).

- imaging :multiple focal nonenhancing brain lesions with no mass effect (edema)

5) Multiple sclerosis (MS) : inflammatory white matter lesions (not well-

circumscribed lesions at the gray and white matter junction).

6) Subacute sclerosing panencephalitis (SSPE): brain scarring and atrophy.

7) HSV encephalitis: typically reveals U/L temporal lobe–enhancing lesions with mass
effect.
 Psychiatry

#Key idea: Polysomnography is the gold-standard for virtually all sleep conditions
(obstructive sleep apnea, Narcolepsy, REM sleep behavior disorder, etc.)

#Optimal acute pain control for patients with substance use disorder on chronic
methadone maintenance therapy includes continuing their baseline methadone dose
and adding additional non-opioid and opioid medications on a flexible schedule,
such as patient-controlled analgesia.
554 SEC TION III PSYCHIATRY PSYCHIATRY—PSYCHOLOGY
` 

PSYCHIATRY—PSYCHOLOGY
` 

Classical conditioning Learning in which a natural response Usually elicits involuntary responses.
(salivation) is elicited by a conditioned, Pavlov’s classical experiments with dogs—
or learned, stimulus (bell) that previously ringing the bell provoked salivation.
was presented in conjunction with an
unconditioned stimulus (food).

Operant conditioning Learning in which a particular action is elicited because it produces a punishment or reward.
Usually elicits voluntary responses.
Reinforcement Target behavior (response) is followed by desired Skinner operant conditioning quadrants:
reward (positive reinforcement) or removal of
Increase behavior Decrease behavior
aversive stimulus (negative reinforcement).
Punishment Repeated application of aversive stimulus

stimulus stimulus
Positive Positive

Remove a Add a
(positive punishment) or removal of desired reinforcement punishment
reward (negative punishment) to extinguish
unwanted behavior. Negative Negative
reinforcement punishment
Extinction Discontinuation of reinforcement (positive or
negative) eventually eliminates behavior. Can
occur in operant or classical conditioning.

Transference and countertransference

Transference Patient projects feelings about formative or other important persons onto physician (eg, psychiatrist
is seen as parent).
Countertransference Doctor projects feelings about formative or other important persons onto patient (eg, patient
reminds physician of younger sibling).

Ego defenses Thoughts and behaviors (voluntary or involuntary) used to resolve conflict and prevent undesirable
feelings (eg, anxiety, depression).
IMMATURE DEFENSES DESCRIPTION EXAMPLE
Acting out Subconsciously coping with stressors or A patient skips therapy appointments after deep
emotional conflict using actions rather than discomfort from dealing with his past.

Denial
reflections or feelings.
Avoiding the awareness of some painful reality.
⇐
A patient with cancer plans a full-time work
schedule despite being warned of significant
fatigue during chemotherapy.
Displacement Redirection of emotions or impulses to a neutral After being reprimanded by her principal, a
person or object (vs projection). frustrated teacher returns home and criticizes
her husband's cooking instead of confronting
the principal directly.
Dissociation Temporary, drastic change in personality, A victim of sexual abuse suddenly appears numb
memory, consciousness, or motor behavior to and detached when she is exposed to her
avoid emotional stress. Patient has incomplete abuser.
or no memory of traumatic event.
 PSYCHIATRY PSYCHIATRY—PSYCHOLOGY
`  SEC TION III 555

Ego defenses (continued)

IMMATURE DEFENSES DESCRIPTION EXAMPLE
Fixation Partially remaining at a more childish level of A surgeon throws a tantrum in the operating
=
development (vs regression). room because the last case ran very late.
Idealization Expressing extremely positive thoughts of self A patient boasts about his physician and his
and others while ignoring negative thoughts. accomplishments while ignoring any flaws.
Identification Largely unconscious assumption of the A resident starts putting his stethoscope in his
characteristics, qualities, or traits of another pocket like his favorite attending, instead of
person or group. wearing it around his neck like before.
Intellectualization Using facts and logic to emotionally distance A patient diagnosed with cancer discusses the
oneself from a stressful situation. pathophysiology of the disease.
Isolation (of affect) Separating feelings from ideas and events. Describing murder in graphic detail with no
emotional response.
Passive aggression Demonstrating hostile feelings in a A disgruntled employee is repeatedly late to
nonconfrontational manner; showing indirect work, but won’t admit it is a way to get back at
opposition. the manager.
Projection Attributing an unacceptable internal impulse to A man who wants to cheat on his wife accuses
an external source (vs displacement). his wife of being unfaithful.
Rationalization Asserting plausible explanations for events that A man who was recently fired claims that the
actually occurred for other reasons, usually to job was not important anyway.
avoid self-blame.
Reaction formation Replacing a warded-off idea or feeling with an A stepmother treats a child she resents with
emphasis on its opposite (vs sublimation). excessive nurturing and overprotection.
Regression Involuntarily turning back the maturational A previously toilet-trained child begins
clock to behaviors previously demonstrated bedwetting again following the birth of a
under stress (vs fixation). sibling.
Repression Involuntarily withholding an idea or feeling A 20-year-old does not remember going to
from conscious awareness (vs suppression). counseling during his parents’ divorce 10 years
earlier.
Splitting Believing that people are either all good or all A patient says that all the nurses are cold and
bad at different times due to intolerance of insensitive, but the doctors are warm and
ambiguity. Common in borderline personality friendly.
disorder.
MATURE DEFENSES
Sublimation Replacing an unacceptable wish with a course A teenager’s aggression toward his parents
of action that is similar to the wish but socially because of their high expectations is channeled
acceptable (vs reaction formation). into excelling in sports.
Altruism Alleviating negative feelings via unsolicited A mafia boss makes a large donation to charity.
generosity, which provides gratification (vs
reaction formation).
Suppression Intentionally withholding an idea or feeling from An athlete focuses on other tasks to prevent
conscious awareness (vs repression); temporary. worrying about an important upcoming match.
Humor Lightheartedly expressing uncomfortable feelings A nervous medical student jokes about the
to shift the internal focus away from the distress. boards.
Mature adults wear a SASH.
 Lines of treatment
1) PTSD: 1st line - trauma focussed CBT
2nd line- SSRI/SNRI; 3rd line: prazosin for bad dreams

2) Borderline personality: 1st line-psychotherapy(dialectical behavioural therapy

Adjuvant for mood stabilise: 2o antipsychotics, mood stabilisers

3) Social anxiety disorder: CBT; SSRI/SNRI

4) performance anxiety: B blockers

5) alcohol withdrawal: BZD

6) Alcohol abuse : 1st line: Acambrosate Naltrexone ( x Naloxone)

2nd line: Disulfiram ( after self motivation and abstinence)

7) Insomnia related to shift work: Melatonin

8) Panic: acute Rx: BZD

-Long term / those with abusive potential: SSRI/SNRI

9) Generalised anxiety disorder:

1st line: SSRI/SNRI
2nd line: BZD
3rd line: Buspirone

10) adjustment disorder: psychotherapy that focuses on improving coping skills and promoting
a return to functioning.

#MOA of antipsychiatry drugs:

1) 2o antipsychotics:
-MOA: mixed serotonin-dopamine antagonist activity with binding at both 5HT 2A +
D2 receptors.

1) 1o antipsychotics block
-dopamine D2 -/x: responsible for their antipsychotic effect.
-may x/- a 1 adrenergic and dopamine D1 receptors

3) venlafaxine : -/x of 5HT + NE reuptake inhibition

4) Amantadine: increase dopamine availability +weak -/x of NMDA glutamate receptor;

5) Trazodone: mild serotonin reuptake inhibitor with additional activity at the 5-

HT2A and 5-HT2C receptors. -Indication: insomnia in the setting of depression.
 Depression Rx protocols
1) 1st line in MDD:
bupropion/fluoxetine/mirtazapine/ venlafaxine /Valozodone( 5HT modulator)

A) Bupropion: NE and DA reuptake inhibitor

-favorable side effect profile for a patient with DM, Metabolic syndrome, smoker &
excessive sleepiness.
-It has mild stimulant effects and therefore can increase wakefulness, energy, and
concentration.

Adv: not causing sexual side effects , Wt loss,

Disadv: can be activating and worsen insomnia.
C/I :history of seizures and those with eating disorders.

B) mirtazapine
- an option when switching, with effects of sedation and weight gain
- preferred choice for insomnia & thin patients with loss of appetite.

C) serotonin modulators (eg, vortioxetine) —> for insomniacs as it’s extremely sedative

# COMBINATION Rx In special situation :

2) 2nd line after failure with 1st line monotherapy in nonpsychotic depression :
2 antidepressants (SSRI, escitalopram
+ dopamine-norepinephrine reuptake inhibitor/bupropion

3) treatment-resistant, nonpsychotic depression and bipolar disorder:

antidepressant (eg, fluoxetine) +lithium

4)1st line treatment of major depressive disorder with psychotic features is

-antidepressant + antipsychotic(eg Resperidone) /ECT.

-Indications of ECT: typically reserved for patients who require rapid response due to
severe suicidality or refusal to eat or drink.

Xx : Antipsychotic monotherapy (eg, aripiprazole, quetiapine) / antidepressant

monotherapy (eg, mirtazapine, venlafaxine) is not as effective as combination therapy.

## MDD failure to response:

-failure to respond to an adequate trial (≥6 weeks) of the therapeutic dose of SSRI
#Ix for maintenance ADD( 1-3 yrs):
-patients with ≥2 episodes
-early age of onset (≤18),
-persistent residual depressive symptoms, and
-comorbid psychiatric disorders. Maintenance therapy can be continued for ~1-3 years.

#Ix for indefinite Rx:

-highly recurrent illness (eg, ≥3 lifetime depressive episodes),
-chronic episodes (≥2 years), severe ongoing psychosocial stressors,
-severe episodes (eg, suicide attempts)

-Recurrent major depression may be conceptualized as a chronic illness similar to other

chronic medical diseases (eg, hypertension, diabetes) that often require long-term
medications.

#Patients with a single episode of MDD:

-should continue antidepressants for an additional 6 months following acute response
to reduce the risk of relapse.

#antidepressant of choice for MI: sertaline

X citalopram as it increases risk for QT prolongation

-DOC in childhood depression: fluoxetine

5) Rx of Tourette syndrome:
-1st-o antipsychotics haloperidol and pimozide are approved by the FDA
- However, 2nd -o antipsychotics (eg, risperidone, aripiprazole) are well studied and
increasingly preferred in children due to their favorable side effect profile.

-Other treatments for Tourette syndrome: alpha-2 adrenergic agonists, tetrabenazine, and
habit reversal therapy.

6) acute attack of panic and specific phobia: urgent termination by BZD

-no role of SSRI/ SNRI
 PSYCHIATRY PSYCHIATRY—PATHOLOGY
`  SEC TION III 593

Psychiatric emergencies
CAUSE MANIFESTATION TREATMENT
Serotonin syndrome Any drug that  5-HT. 3 A’s:  activity (neuromuscular; Cyproheptadine (5-HT2
Psychiatric drugs: MAOIs, eg, clonus, hyperreflexia, receptor antagonist)
SSRIs, SNRIs, TCAs, hypertonia, tremor, seizure), Prevention: avoid simultaneous
vilazodone, vortioxetine, autonomic instability (eg, serotonergic drugs, and allow
buspirone hyperthermia, diaphoresis, a washout period between
Nonpsychiatric drugs: diarrhea), altered mental status them
tramadol, ondansetron,
triptans, linezolid, MDMA,
dextromethorphan,
meperidine, St. John’s wort
Hypertensive crisis Eating tyramine-rich foods (eg, Hypertensive crisis Phentolamine
aged cheeses, cured meats, (tyramine displaces other
wine, chocolate) while taking neurotransmitters [eg,
MAOIs NE] in the synaptic cleft
Ž  sympathetic stimulation)
Neuroleptic malignant Antipsychotics (typical Malignant FEVER: Dantrolene, dopaminergics (eg,
syndrome > atypical) + genetic Myoglobinuria, Fever, bromocriptine, amantadine),
predisposition Encephalopathy, Vitals benzodiazepines; discontinue
unstable,  Enzymes (eg, causative agent
CK), muscle Rigidity (“lead
pipe”)
Delirium tremens Alcohol withdrawal; occurs 2–4 Altered mental status, Longer-acting benzodiazepines
days after last drink hallucinations, autonomic
Classically seen in hospital hyperactivity, anxiety,
setting when inpatient cannot seizures, tremors,
drink psychomotor agitation,
insomnia, nausea
Acute dystonia Typical antipsychotics, Sudden onset of muscle Benztropine or
anticonvulsants (eg, spasms, stiffness, and/or diphenhydramine
carbamazepine), oculogyric crisis occurring
metoclopramide hours to days after medication
use; can lead to laryngospasm
requiring intubation
Lithium toxicity  lithium dosage,  renal Nausea, vomiting, slurred Discontinue lithium, hydrate
elimination (eg, acute kidney speech, hyperreflexia, aggressively with isotonic
injury), medications affecting seizures, ataxia, nephrogenic sodium chloride, consider
clearance (eg, ACE inhibitors, diabetes insipidus hemodialysis
thiazide diuretics, NSAIDs).
Narrow therapeutic window.
Tricyclic TCA overdose Respiratory depression, Supportive treatment, monitor
antidepressant hyperpyrexia, prolonged QT ECG, NaHCO3 (prevents
toxicity Tricyclic’s: convulsions, coma, arrhythmia), activated
cardiotoxicity (arrhythmia due charcoal
to Na+ channel inhibition)
 Case clue Pedia psyc
1) Paradoxical agitation
-increased agitation, confusion, aggression, and disinhibition, typically within an hour of
administration of BZD especially in elderly

2) Mx of serotonin syndrome:
• Discontinuation of all serotonergic medications
• Supportive care, sedation with benzodiazepines: 1st line
• Serotonin antagonist (cyproheptadine) if supportive measures fail:2nd line
• Immediate sedation, paralysis & tracheal intubation if temperature >41.1 C (106 F)

5) ADHD Rx:
A) Medical Rx only in school going children (>6 yrs)
-1st line: methylphenidate, amphetamines
-2nd line: Nonstimulant like NE reuptake inhibitor atomoxetine and alpha-2 adrenergic
agonists. Atomoxetine is appropriate for patients with a
h/O illicit substance use / when there is a strong family preference against stimulant
medication.

B) Behavioural Rx in preschool children (4-5 yrs)

6) Mild neurocognitive disorder

(mild cognitive impairment)
• Mild decline in ≥1 cognitive domains
• Normal functioning in all activities of daily living
with compensation
Major • Significant decline in ≥1 cognitive domains
neurocognitive • Irreversible global cognitive impairment
disorder • Marked functional impairment
(dementia) • Chronic & progressive, months to years

7) Reactive attachment disorder:

-Early childhood abuse or neglect can result in disrupted attachment to caregivers and
difficulty forming healthy relationships.
-a pattern of emotional and social withdrawal as well as a lack of positive response
to attempts to comfort
8) Early onset Psychosis in a child :
—> hallucinations, delusions, confused speech, and/or behavior and negative symptoms
(eg, lack of motivation, social withdrawal).
- Children with psychosis would be expected to have marked changes in functioning
across multiple domains, including a decline in social interaction and academic
performance.
Vs
→
-imaginary friend : MC in children age 3-6 but can be seen throughout school-age years.

9) pseudocyesis
-patient presents symptoms of early pregnancy and believes she is pregnant.
-However, her office examination (thin endometrial stripe, negative urine pregnancy
test) excludes pregnancy.

10) separation anxiety: occurs only when separating from the parent (normal by 9 mon)
Vs
- stranger anxiety distress: occurs when the primary attachment figure is still present
eg: child cries when nurse picks child from moms lap..(normal by 6 mon)

11) Early Vs Late Autism :

1) early/ severe:
-In cases of severe autism, where language and intellectual development are affected,
children are typically diagnosed by age 5.

2) late/ milder:
-However, in high functioning autism, where language and intellectual development
may be normal, patients come to attention only later when social demands reveal the
child's social-emotional deficits.

12) The recommended washout

Prognostic factors in schizophrenia UWSA2
period for most antidepressants
Good Poor prior to beginning treatment with a
• Onset in childhood or MAOI is 14 days.
• Later onset adolescence
• Female sex • Male sex
• Acute onset with • Gradual onset (prodrome), no -However, due to fluoxetine's long
precipitant precipitant half-life, it is recommended that at
• Predominantly positive • Predominantly negative
symptoms symptoms least 5 weeks elapse between
• No family history • Family history of psychotic stopping fluoxetine and starting
• Short duration of active illness MAOI treatment;
symptoms • Long duration of untreated
psychosis
# other characteristics features of autism:
- Lack of interest in shared social play and impaired joint attention (eg, lack of pointing
or bringing objects to others)
-Odd repetitive behaviors (eg, lining up toys) and rigid adherence to routines (eg,
distress over small changes) are also common.
-Intense fixated interests: only 1 toy; extra interest in horse
-Adverse responses to sensory input: doesn’t like typical odour/ taste
-Nonverbal communication: eye contact; looking when called by name
Vs

12) Language disorder

-presents in early childhood and can be difficult to diagnose due to considerable variability
in language acquisition before age 4.
-Differentiating clue:, nonverbal communication (eg, eye contact)/ gazing at toy when
pointed out should be normal.
-NO lack of social interaction and restricted interests are more consistent with ASD.

=>Language delay without an attempt to compensate through nonverbal means of

communication is characteristic of ASD.

13) Lesch-Nyhan syndrome:

-self-mutilating behaviors like biting his fingers and tongue, dystonia, writhing
movements, delayed motor development, nephrolithiasis, gout

14) Mania in Pregnancy

-switching to lamotrigine, a mood stabilizer with a favorable pregnancy safety profile,
is appropriate for euthymic patients
—> In patients who switch to another medication, pregnancy should be delayed for 3-6
months to assess the efficacy of the medication. .

15) OCD in pregnancy:

-patient's new onset of time-consuming, intrusive obsessions (ie, excessive
preoccupation about contamination of breast milk, obsessional fears of harming the
baby) and associated compulsive behaviors (excessive washing and showering) are
consistent with (OCD).

—> Pregnancy and the postpartum period are associated with increased risk for new
onset, recurrence, or exacerbation of OCD.
16) benzodiazepine withdrawal
-onset: within 24-48 hours of discontinuation
-C/F: patient's tremulousness, hallucinations, and elevated vital signs (eg,
hypertension, tachycardia) in the context of a prescription of benzodiazepines (eg,
anxiety, insomnia) are suggestive of delirium due to benzodiazepine withdrawal.
Vs
Sedation, vitally stable in BZD toxicity

17) Prenatal exposure to cocaine

- result in jitteriness, excessive sucking, and a hyperactive Moro reflex (due to the
toxic effects of cocaine);
-Long-term effects on behavior, attention level, and intelligence may be seen.

18) Neonatal abstinence syndrome

- caused by infant withdrawal to opiates and usually presents in the first few days of life.
-C/F: irritability, a high-pitched cry, poor sleeping, tremors, seizures, sweating,
sneezing, tachypnea, poor feeding, vomiting, and diarrhea

-Rx: symptomatic care; 2nd line: morphine, methadone, buprenorphine MMB

19) fetal hydantoin syndrome:

-by Prenatal exposure to phenytoin
-C/F: nail and digit hypoplasia, dysmorphic facies, and intellectual disability. Growth
deficiency can also be seen

20) disruptive mood dysregulation disorder

-irritable mood, accompanied by repetitive temper outbursts (verbal or physical) that are
out of proportion to the stimulus and inconsistent with developmental level.
-Onset: manifest prior to age
#Rx: Treatment: CBT, stimulants, antipsychotics.

21) Pediatric depression

-symptoms of irritability, annoyance, and argumentative behavior rather than
depressed mood;
-withdrawal from academic and social activities(peers) so together with poor sleep,
poor appetite, impaired concentration, and psychomotor agitation (restlessness, fidgeting)

#Rx; DOC: fluoxetine; 2nd line: venlafaxine

22) Genetic predisposition is the strongest predisposing factor for bipolar disorder. While
the lifetime risk of developing bipolar disorder is ∼ 2% in the general population, a first-
degree relative of an individual with bipolar disorder has a lifetime risk up to 10%, and
monozygotic twins have up to a 70% lifetime risk of developing the disorder.
22) Rett syndrome
-occurs mainly in girls ; 6-18 months
-characterized by neurodevelopmental regression (ie, loss of speech and purposeful
hand movements, gait disturbance) after a period of normal development.
-Seizures are also common, breathing abnormal: hyper then hypo;
-Diagnosis: MECP2 mutation on DNA analysis confirms the diagnosis.
Vs
→
#lysosomal storage disease manifest before 6 months

23) antidepressant causing HT:

Venlafaxine, serotonin-norepinephrine reuptake inhibitor class, has been associated
with dose-dependent hypertension.

1) At lower doses, it primarily inhibits the reuptake of serotonin.

2) As the dose increases, however, the drug also inhibits norepinephrine reuptake,
potentially causing increased systolic and diastolic blood pressure
—> hypertensive effect is especially significant at doses >300 mg daily

24) Selective mutism: onset <5 yrs

-diagnosis requires consistent (≥1 month) failure to talk in situations in which it is
expected (eg, school) despite the patient's speaking in other situations.
#Mx: -CBT with graded exposure to social situations, family therapy, SSRIs.

25) Wilson Ds
• Hepatic (acute liver failure, chronic hepatitis, cirrhosis)
• Neurologic (parkinsonism, gait disturbance, dysarthria)
• Psychiatric (depression, personality changes, psychosis)

==> New-onset psychosis in an adolescent with neurologic dysfunction (eg,

tremor, parkinsonism) raises concern for Wilson disease.

26) Substance-induced mood disorder

-occurs when mood symptoms are produced as a direct result of substance intoxication
or withdrawal.
—>> Cocaine can produce manic-type symptoms during intoxication and
depression during withdrawa
26) psychosis in pediatrics:
-The sudden onset of psychosis in a child or adolescent is rare, and it is important to
search for potentially reversible conditions such as medical disorders / substance use

#Common medical conditions : SLE, thyroiditis, metabolic or electrolyte disorders,

CNS infection, and epilepsy.

27) post Partum depression screening:

-Because of the high incidence of postpartum depression and underreporting of
symptoms, all women require screening (regardless of prior psychiatric history) with a
standardized, validated tool such as the Edinburgh Postnatal Depression Scale (EPDS).
- EPDS has a high sensitivity (90%);

28) early-onset schizophrenia

Onset of psychotic symptoms prior to age 18 is referred to as early-onset schizophrenia
and is associated with a more severe course of illness.

2) Adolescents commonly have a prodromal phase marked by social withdrawal and

academic decline, which can last for weeks to years prior to the onset of active psychotic
symptoms.

28) Oppositional defiant disorder

-pervasive pattern of argumentative and defiant behavior toward authority figures.
Vs
#It does not involve the more severe violations of basic rights of others in conduct
disorder.

29) Co administration of triptan+ ergots

-Patients who have already received a triptan / an ergot derivative (also a 5-HT agonist)
within the past 24 hours should not receive another triptan as this combination can cause
—> severe, prolonged VC due to the overactivation of serotonin receptors, resulting in
elevated blood pressure, myocardial infarction, or stroke.

30) social communication disorder:

-Children with social communication disorder present at an early age with difficulties in
both verbal and nonverbal communication, such as adapting to social settings (e.g.,
being quiet during a performance) and using communication methods adequately (e.g.,
body language, eye contact)
580 SEC TION III PSYCHIATRY PSYCHIATRY—PATHOLOGY
` 

Childhood and early-onset disorders

Attention-deficit Onset before age 12. ≥ 6 months of limited attention span and/or poor impulse control.
hyperactivity Characterized by hyperactivity, impulsivity, and/or inattention in ≥ 2 settings (eg, school, home,
disorder places of worship). Normal intelligence, but commonly coexists with difficulties in school. Often
persists into adulthood. Commonly coexists with oppositional defiant disorder. Treatment:
stimulants (eg, methylphenidate) +/– behavioral therapy; alternatives include atomoxetine and
α2-agonists (eg, clonidine, guanfacine).
Autism spectrum Onset in early childhood. Social and communication deficits, repetitive/ritualized behaviors,
disorder restricted interests. May be accompanied by intellectual disability and/or above average abilities in
specific skills (eg, music). More common in males. Associated with  head and/or brain size.
Conduct disorder Repetitive, pervasive behavior violating societal norms or the basic rights of others (eg, aggression
toward people and animals, destruction of property, theft). After age 18, often reclassified as
antisocial personality disorder. Treatment: psychotherapy (eg, cognitive behavioral therapy
[CBT]).
Disruptive mood Onset before age 10. Severe, recurrent temper outbursts out of proportion to situation. Child is
dysregulation constantly angry and irritable between outbursts. Treatment: CBT, stimulants, antipsychotics.
disorder
Intellectual disability Global cognitive deficits (vs specific learning disorder) that affect reasoning, memory, abstract
thinking, judgment, language, learning. Adaptive functioning is impaired, leading to major
difficulties with education, employment, communication, socialization, independence.
Treatment: psychotherapy, occupational therapy, special education.
Intermittent explosive Onset after age 6. Recurrent verbal or physical outbursts representing a failure to control aggressive
disorder impulses. Outbursts are out of proportion to provocation and may lead to legal, financial, or social
consequences. Episodes are not premeditated and last < 30 minutes. Treatment: psychotherapy,
SSRIs.
Oppositional defiant Pattern of anger and irritability with argumentative, vindictive, and defiant behavior toward
disorder authority figures lasting ≥ 6 months. Treatment: psychotherapy (eg, CBT).
Selective mutism Onset before age 5. Anxiety disorder lasting ≥ 1 month involving refraining from speech in certain
situations despite speaking in other, usually more comfortable situations. Development (eg, speech and
language) not typically impaired. Interferes with social, academic, and occupational tasks. Commonly
coexists with social anxiety disorder. Treatment: behavioral, family, and play therapy; SSRIs.
Separation anxiety Overwhelming fear of separation from home or attachment figure lasting ≥ 4 weeks. Can be
disorder normal behavior up to age 3–4. May lead to factitious physical complaints to avoid school.
Treatment: CBT, play therapy, family therapy.
Specific learning Onset during school-age years. Inability to acquire or use information from a specific subject
disorder (eg, math, reading, writing) near age-expected proficiency for ≥ 6 months despite focused
intervention. General functioning and intelligence are normal (vs intellectual disability).
Treatment: academic support, counseling, extracurricular activities.
Tourette syndrome Onset before age 18. Sudden, recurrent, nonrhythmic, stereotyped motor and vocal tics that
persist for > 1 year. Coprolalia (involuntary obscene speech) found in some patients. Associated
with OCD and ADHD. Treatment: psychoeducation, behavioral therapy. For intractable and
distressing tics: tetrabenazine, antipsychotics, α2-agonists.
 PSYCHIATRY PSYCHIATRY—PATHOLOGY
`  SEC TION III 583

Schizophrenia
spectrum disorders
Schizophrenia Chronic illness causing profound functional Associated with altered dopaminergic activity,
impairment. Symptom categories include:  serotonergic activity, and  dendritic
ƒ Positive—excessive or distorted functioning = -
branching. Ventriculomegaly on brain
(eg, hallucinations, delusions, unusual imaging. Lifetime prevalence—1.5% (males
thought processes, disorganized speech, > females). Presents earlier in males (late teens
bizarre behavior) to early 20s) than in females (late 20s to early
ƒ Negative—diminished functioning (eg, flat 30s).  suicide risk.
or blunted affect, apathy. anhedonia, alogia, Heavy cannabis use in adolescence is associated
social withdrawal) with  incidence and worsened course of
ƒ Cognitive—reduced ability to understand or psychotic, mood, and anxiety disorders.
make plans, diminished working memory, Treatment: atypical antipsychotics (eg,
inattention risperidone) are first line.
Diagnosis requires ≥ 2 of the following active Negative symptoms often persist after treatment,
symptoms, including ≥ 1 from symptoms #1–3: despite resolution of positive symptoms.
1. Delusions
2. Hallucinations, often auditory
3. Disorganized speech
4. Disorganized or catatonic behavior
5. Negative symptoms
Symptom onset ≥ 6 months prior to diagnosis;
requires ≥ 1 month of active symptoms over
the past 6 months.
Brief psychotic disorder—≥ 1 positive symptom(s) lasting < 1 month, usually stress-related.
Schizophreniform disorder—≥ 2 symptoms lasting 1–6 months.
Schizoaffective Shares symptoms with both schizophrenia and mood disorders (major depressive or bipolar
disorder disorder). To differentiate from a mood disorder with psychotic features, patient must have > 2
weeks of psychotic symptoms without a manic or depressive episode.
Delusional disorder ≥ 1 delusion(s) lasting > 1 month, but without a mood disorder or other psychotic symptoms. Daily
functioning, including socialization, may be impacted by the pathological, fixed belief but is otherwise
unaffected. Can be shared by individuals in close relationships (folie à deux).
Schizotypal personality Cluster A personality disorder that also falls on the schizophrenia spectrum. May include brief
disorder psychotic episodes (eg, delusions) that are less frequent and severe than in schizophrenia.

Manic episode Distinct period of abnormally and persistently elevated, expansive, or irritable mood and  activity
or energy lasting ≥ 1 week. Diagnosis requires hospitalization or marked functional impairment
with ≥ 3 of the following (manics DIG FAST):
ƒ Distractibility ƒ Flight of ideas—racing thoughts
ƒ Impulsivity/Indiscretion—seeks pleasure ƒ  goal-directed Activity/psychomotor
without regard to consequences (hedonistic) Agitation O
ƒ Grandiosity—inflated self-esteem ƒ  need for Sleep
ƒ Talkativeness or pressured speech
584 SEC TION III PSYCHIATRY PSYCHIATRY—PATHOLOGY
` 

Hypomanic episode Similar to a manic episode except mood disturbance is not severe enough to cause marked
impairment in social and/or occupational functioning or to necessitate hospitalization.
Abnormally  activity or energy usually present. No psychotic features. Lasts ≥ 4 consecutive days.

Bipolar disorder Bipolar I—≥ 1 manic episode +/− a hypomanic or depressive episode (may be separated by any
length of time).
Bipolar II—a hypomanic and a depressive episode (no history of manic episodes).
Patient’s mood and functioning usually normalize between episodes. Use of antidepressants can
destabilize mood. High suicide risk. Treatment: mood stabilizers (eg, lithium, valproic acid,
carbamazepine, lamotrigine), atypical antipsychotics.
Cyclothymic disorder—milder form of bipolar disorder fluctuating between mild depressive and
hypomanic symptoms. Must last ≥ 2 years with symptoms present at least half of the time, with
any remission lasting ≤ 2 months.

Major depressive Recurrent episodes lasting ≥ 2 weeks characterized by ≥ 5 of 9 diagnostic symptoms including
disorder depressed mood or anhedonia (or irritability in children). SIG E CAPS:
ƒ Sleep disturbances
ƒ  Interest in pleasurable activities (anhedonia)
ƒ Guilt or feelings of worthlessness
ƒ  Energy
ƒ  Concentration
ƒ Appetite/weight changes
ƒ Psychomotor retardation or agitation
ƒ Suicidal ideation
Screen for previous manic or hypomanic episodes to rule out bipolar disorder.
Treatment: CBT and SSRIs are first line; alternatives include SNRIs, mirtazapine, bupropion,
electroconvulsive therapy (ECT), ketamine.
Responses to a significant loss (eg, bereavement, natural disaster, disability) may resemble a
depressive episode. Diagnosis of MDD is made if criteria are met.
MDD with psychotic MDD + hallucinations or delusions. Psychotic features are typically mood congruent (eg,
features depressive themes of inadequacy, guilt, punishment, nihilism, disease, or death) and occur only
in the context of major depressive episode (vs schizoaffective disorder). Treatment: antidepressant
with atypical antipsychotic, ECT.
Persistent depressive Also called dysthymia. Often milder than MDD; ≥ 2 depressive symptoms lasting ≥ 2 years (≥ 1
disorder year in children), with any remission lasting ≤ 2 months.
-
MDD with seasonal Formerly called seasonal affective disorder. Major depressive episodes occurring only during a
pattern particular season (usually winter) in ≥ 2 consecutive years and in most years across a lifetime.
Atypical symptoms common. Treatment: standard MDD therapies + light therapy.

Depression with Characterized by mood reactivity (transient improvement in response to a positive event),
atypical features hypersomnia, hyperphagia, leaden paralysis (heavy feeling in arms and legs), long-standing
interpersonal rejection sensitivity. Most common subtype of depression. Treatment: CBT and
SSRIs are first line. MAO inhibitors (MAOIs) are effective but not first line because of their risk
profile.
Vs inability to respond to positive Sx in melancholic depression
D/D b/w 4 Anxiety related Disorders :
Panic : 1 month Duration & rest all 6 months duration
1) GAD :
Constant, Chronic, Excessive worry for Multiple Daily issues >=6 months
— >= 3 of RF-CIMS for Adults GAD Dx
— Only 1 additional of RF-CIMS for Pediatric GAD Dx :d/t >Perfectionism & Irritability is predominant
Rx : CBT, SSRI / SNRIs —> 2nd line : BZDs, Buspirone

2) Specific Phobia : COMMON

Anxiety related to a particular situation or exposure eg., Height >6 months
- 10% of Population have this
Rx : CBT (most important), BZDs [ No role of SSRI/ SNRIs ]

3) Social Phobia :
- Anxiety related to Social situation with fear of embarrassment & criticism for >6 months with
Good Performance
- D/D : Performance Anxiety — Anxiety related to Performance only not for Social Gatherings,
Poor Performance
Rx : CBT, SSRI / SNRIs —> Beta- Blockers for Performance Subtype,
Avoid BZDs as much as possible

4) Panic :
- Isolated Panic has a nature of being Unprovoked, Recurrent attacks with multiple body features with for
>=1 month of Avoiding a situation + Constant worry for future attacks
- Panic is also common with other Psychiatric disorders
- Associations : Depression (60%), Agoraphobia (40%), Suicidal risk, substance abuse, Mania
— Agoraphobia : Avoiding situations where escape in not possible, +/- Panic associations
Rx : BZD for acute Management, CBT, SSRI / SNRIs

==> Same Rx for GAD & Social Phobia : CBT, SSRI / SNRI f/by BZDs
==> Same Rx for Panic & Specific phobia : Urgent termination of anxiety by BZD fby CBT,SSRI
1) Antidepressants induced mania: Psych medicine
**patient's atypically rapid improvement in depression after 2 days of
antidepressant treatment (typical time to onset of effect is 2 weeks) is an additional
clue that she may be in the bipolar spectrum.

#Mx:
1) 1st line most appropriate initial step: to discontinue the antidepressant to prevent
further worsening of mania.
2) 2nd line: If manic symptoms persist despite discontinuing the antidepressant,
treatment with a mood stabilizer (eg, lithium, valproate) / an antipsychotic (eg,
quetiapine) should be considered

2) Panic disorder:
- Diagnosis requires that at least some of these panic attacks are untriggered or
unexpected (eg, at home, relaxing with friends) +
-≥1 months of worry about future attacks or change in behavior (eg, avoidance).

3) Generalized anxiety disorder

- ≥6 months of persistent worry about multiple issues of daily life
**Diff:
- panic disorder may exhibit some degree of chronic anxiety, but this is due to fears of
having additional attacks, not excessive anxiety about everyday issues.

4) Hoarding disorder
-difficulty discarding possessions regardless of their actual value.
-Rx: best treated with cognitive-behavioral therapy, SSRI

5) Li toxicity:
-C/F: Neurologic (eg, altered mental status, seizure, fasciculations, tremor) and
gastrointestinal (eg, vomiting, diarrhea)
#Mx:
-mild overdoses :hydration and monitoring
#hemodialysis:
a) lithium levels >2.5 mEq/L + signs of toxicity.
b) levels >4 mEq/L and creatinine >2.0 mg/dL regardless of symptoms.

-RF: NSAIDS, ACE I, ARBS ; dehydration by any cause (eg, diuretics, gastrointestinal
illness); Intentional overdose, metronidazole,tetracycline , antiepiletpics, SSRI

#Predrug Ix:BUN and creatinine), Ca, URM, UPT, and TFT

- ECG due to risk for CAD because lithium may cause dysrhythmias

#Longterm effects: hyperparathyroidism causing hyperCa, nephrogenic DI, CKD, and

hypothyroidism)
 " Lithium—> Tremors
④ 2 different types of Tremors by Lithium :
—> Tremor is a common adverse effect of lithium, possibly due to
increased iron accumulation in the substantia nigra.

1) Lithium-induced enhanced physiologic tremor is typically

symmetric, limited to the hands and upper limbs, and occurs when the
medication is started or the dose is increased (eg, after a manic
episode).
- It is nonprogressive and often decreases over time, even with no
dosage reduction.
Lithium-enhanced physiologic tremor must be distinguished from
tremor due to lithium toxicity.

2) Lithium induced tremors due to its toxicity:

It typically causes an irregular, coarse tremor involving multiple parts
of the body (not just the hands) accompanied by gastrointestinal or
additional neurologic symptoms.

Rx of lithium induced Tremors:

—> Lithium toxicity requires treatment (eg, hydration, hemodialysis);

in contrast, lithium-enhanced physiologic tremor is often managed
with watchful waiting and modification of aggravating factors.
2

④ Lithium —> Hyperparathyroidism —> Hypercalcemia

 7) long-acting injectable (LAI) (depot)
6) Acute stress disorder
antipsychotic:
• Duration ≥3 days & ≤1 month -Both 1o-generation (haloperidol, fluphenazine)
• Exposure to actual or
threatened trauma and 2nd-generation (risperidone, paliperidone,
• Symptoms from following olanzapine, aripiprazole) antipsychotics are
categories: available in LAI formulations.
◦ Avoidance of internal
memories or external
Clinical #Indication:
reminders
features
◦ Intrusion (eg, nightmares, -unstable illness who live alone and have poor social
flashbacks) support systems, poor insight, and
◦ Dissociation (eg, amnesia
for event, derealization) —> frequent medication nonadherence but good
-
◦ Arousal (eg, insomnia, response
-
are good candidates for LAI
hypervigilance, startle) antipsychotics.
◦ Negative mood
Vs
• Trauma-focused, brief CBT Don’t mix this with treatment resistant
1st line
Managem • Consider medication for schizophrenia which needs clozapine
ent insomnia, intense anxiety
• Monitor for PTSD (symptom
duration >1 month)

8) Mx of suicidability: Narcolepsy •
• Recurrent lapses into sleep or
High imminent risk (ideation, intent & plan) naps (≥3 times/week for 3 months)

=
• Ensure safety: hospitalize immediately (involuntarily if necessary) • ≥1 of the following:
-
• Remove personal belongings & objects in room that may present ◦ Cataplexy: Brief loss of muscle
DSM-5
self-harm risk diagnosti
tone precipitated by strong
• Constant observation & security may be required to hold against will c criteria emotion (eg, laughter,
excitement)
High nonimminent risk (ideation, intent, but no plan to act in near,
◦ Low cerebrospinal fluid levels
future) of hypocretin-1
• Ensure close
-
follow-up ◦ Shortened REM sleep latency
• Treat modifiable risk factors (underlying depression, psychosis,
• Hypnagogic or hypnopompic
substance abuse, pain) Associated
hallucinations
• Recruit family or friends to support patient features
• Sleep paralysis
• Reduce access to potential means (secure firearms, medications)

9) Mx of Body dysmorphic (eg: over reacting to slight acne)

-1st line-SSRI; CBT; cosmetic Rx won’t help

10) Indications of Clozapine

- treatment-resistant psychosis; schizoaffective disorder with multiple hospitalizations ;
limited functional independence (ie, living in a group home)

#ADR:
-neutropenia/agranulocytosis, seizures, and myocarditis.
-
-
-Compared with other antipsychotics, clozapine carries the greatest risk of dose
dependent seizure.
512 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—ANATOMY AND PHYSIOLOGY
` 

Sleep physiology Sleep cycle is regulated by the circadian rhythm, which is driven by suprachiasmatic nucleus (SCN)
of the hypothalamus. Circadian rhythm controls nocturnal release of ACTH, prolactin, melatonin,
norepinephrine: SCN Ž norepinephrine release Ž pineal gland Ž  melatonin. SCN is regulated
by environment (eg, light).
Two stages: rapid-eye movement (REM) and non-REM.
- "
Alcohol, benzodiazepines, and barbiturates are associated with  REM sleep and N3 sleep;

E
norepinephrine also  REM sleep.
Benzodiazepines are useful for night terrors and sleepwalking by  N3 and REM sleep.
SLEEP STAGE (% OF TOTAL SLEEP DESCRIPTION EEG WAVEFORM AND NOTES
TIME IN YOUNG ADULTS) murmur
Awake (eyes open) Alert, active mental concentration. Beta (highest frequency, lowest amplitude).
Awake (eyes closed) Alpha.
Non-REM sleep
Stage N1 (5%) Light sleep. Theta.
Stage N2 (45%) Deeper sleep; when bruxism (“twoth” [tooth] Sleep spindles and K complexes.
grinding) occurs.
Stage N3 (25%) Deepest non-REM sleep (slow-wave sleep); Delta (lowest frequency, highest amplitude),

m
-
Terror in three sleepwalking, night terrors, and bedwetting deepest sleep stage.
occur (wee and flee in N3).
REM sleep (25%) Loss of motor tone,  brain O2 use, variable Beta.
pulse/BP,  ACh. REM is when dreaming, Changes in elderly:  REM,  N3,  sleep latency,
nightmares, and penile/clitoral tumescence  early awakenings.
occur; may serve memory processing function. Changes in depression:  REM sleep time,
Extraocular movements due to activity of PPRF  REM latency,  N3, repeated nighttime
(paramedian pontine reticular formation/ awakenings, early morning awakening (terminal
conjugate gaze center). insomnia).
Occurs every 90 minutes, and duration Change in narcolepsy:  REM latency.
 through the night. At night, BATS Drink Blood.

Depression and narcolepsy sleep

more in REM
 11) Gambling Disorder
—> diagnosis requires ≥4 of following:
1) preoccupation with gambling,
2) frequent return to gambling to attempt to recover past losses,
3) tendency to damage relationships or jeopardize employment, and
4) reliance on others to make up for financial losses.
#Rx: CBT

12) PTSD: >1 month vs < 1 month in acute stress disorder

13) Delusional disorder:
Borderline personality disorder
-1/>1 delusion maybe towards 1-2
• Pervasive pattern of marked impulsivity, with unstable matters x > 1 month
relationships, self-image & affects, plus ≥5 of the
following features: Vs
◦ Frantic efforts to avoid abandonment 14) Paranoid personality disorder
◦ Unstable & intense interpersonal - lifelong pattern of distrust and
relationships
Diagnos ◦ Markedly & persistently unstable self-image
suspicion of others, beginning in
tic ◦ Impulsivity in ≥2 areas that are potentially early adulthood.
criteria self-damaging
◦ Recurrent suicidal behaviors or threats of -The paranoid beliefs are generally
self-mutilation (eg, cutting)
◦ Affective instability (marked mood reactivity) pervasive (not simply directly at
◦ Chronic feelings of emptiness one person) and not of delusional
◦ Inappropriate & intense anger intensity.
◦ Transient stress-related paranoia or dissociation
- -

15) bupropion
- lower seizure threshold.
-C/I: BN, anorexia nervosa, or epilepsy.

16) Risperidone
- high frequency of prolactin elevation.
Vs
-In comparison to antipsychotics, prolactinomas capable of producing very high levels of
prolactin (>200 ng/mL).

17) mania in ADHD:

-Mania: short H/O with DIGFAST
Vs
ADHD: long H/O and no DIGFAST

18) opioid withdrawal: last 3-5 days vs amphetamine: wanes in short time
19) antisocial personality disorder: no guilt; blames other, P/H/O conduct +
Vs
# intermittent explosive disorder: guilt present after episode

20) Borderline personality :

-mood instability that is typically reactive to interpersonal stressors; long H/O from
teenage, No delusion of grandiose
Vs
Cyclothymic/ bipolar: whose moods do not appear reactive to situations; short H/O

21) ECT: bipolar depression, bipolar mania , catatonia

-Rx resistance depression ; Psychotic features with depression
-Emergency conditions:Pregnancy;Refusal to eat or drink; Imminent risk for suicide
-Procedure: 1 min seizure weekly 3 timesx 6-12 Rx
22) Mx of bipolar:
Antipsychotic extrapyramidal effects Pharmacotherapy*
-Most patients require maintenance
• Sudden, sustained for many years,
Acute contraction of the • Benztropine
dystonia neck, mouth, tongue • Diphenhydramine
& eye muscles #Indications of lifelong
• Beta blocker maintenance :
• Subjective (propranolol) - severe course (eg, frequent
Akathisia restlessness, inability • Benzodiazepine episodes, suicide attempts, severe
to sit still (lorazepam)
• Benztropine symptoms, hospitalization)
Parkinsoni • Gradual-onset tremor, • Benztropine
sm rigidity & bradykinesia • Amantadine #If this patient insists on
• Gradual onset after stopping lithium,
prolonged therapy -1st step: try to cross-taper to
Tardive (>6 months): • Valbenazine another antimanic agent (eg,
dyskinesia dyskinesia of the • Deutetrabenazine
mouth, face, trunk &
valproate, lamotrigine, quetiapine).
extremities
*Management may include reducing the dose or switching to
another antipsychotic, depending on the clinical scenario.
—>If the patient refuses all pharmacotherapy, lithium should be slowly tapered over weeks
to months and frequently monitored to identify early signs and symptoms of recurrence.

23) 2o antipsychotic
1) Obesity, MetS S/E: Clozapine; Olanzapine
2) prolong QT interval: ziprasidone
3) EPS: Resperidone

24) Nightmare disorder: REM disorder

-On awakening, the child is fully alert, remembers the dream, and can usually be
consoled.
- Although frightening, nightmares are typically transient and developmentally normal for
most children.
Vs
25) Sleep terror disorder,
-non-REM arousal disorder
-incomplete awakenings, unresponsiveness to comfort, and no recall of dream
content.

- marked autonomic arousal and amnesia for the episode in the morning.

26) SSRI ADR:

-patient's worsening anxiety, with jitteriness, insomnia, and new-onset anxiety after
starting SSRI reflects the stimulating effects of fluoxetine.

- most appropriate next step :temporary dose reduction with the goal of improving
tolerability; dose increases may subsequently be reattempted.

27) dysthymia: rule of 2

-Chronic depressed mood ≥2 years (1 year in children/adolescents); No symptom-
free period for >2 months; needs only >2 Sx of depression
Vs
MDD: >5/9 Sx of SIGCAPS x >2 weeks

28) Mx of conversion disorder:

DSM-5 personality disorders
• Education about the disorder
• Paranoid: suspicious, distrustful,
hypervigilant • Cognitive-behavioral therapy
Cluster A
Odd/
• Schizoid: prefers to be a • Physical therapy for motor symptoms
loner, detached, unemotional
eccentric
• Schizotypal: unusual thoughts,
perceptions & behavior 29) dopamine agonist–induced impulse control
• Antisocial: disregard & violation of disorder
the rights of others
• Borderline: chaotic relationships, Ropinirole and other dopamine agonists can induce
Cluster B
abandonment fears, labile mood, impulse control disorders that may present with a
impulsivity, inner emptiness, self-
Dramatic/
harm manic-like syndrome.
erratic
• Histrionic: superficial, theatrical, #C/F: pathological gambling, compulsive shopping
attention-seeking
• Narcissistic: grandiosity, lack of and eating, and hypersexuality; impulsive
empathy overspending, abruptly quitting job, elevated mood,
• Avoidant: avoidance due to insomnia, pressured speech).
fears of criticism & rejection
Cluster C
• Dependent: submissive, clingy,
Anxious/
fearful
needs to be taken care of #Rx: discontinuation of the offending agent
• Obsessive-compulsive: rigid,
controlling, perfectionistic
ECT

Antidepressants typically take up to

6-8 weeks for response and must be
combined with an antipsychotic
medication to effectively treat major
depression with psychotic features.

"

of
—>> Why ECT ..?

Because ECT is generally faster

than pharmacotherapy, it is used to
achieve a rapid response in
- depressed elderly patients who are
unable to eat and drink,
- psychotic, or
- actively suicidal.

typically
administered 3
times a week
for a course of
6-12 treatments
—> inducing a 30- to 60-second GTCS
30) Normal stress reactions
- lower severity and absence of marked distress/ significant functional impairment.

Dissociative disorders 31) Peutz-Jeghers syndrome

-Persistent or recurrent experiences of 1
•macules (eg, lips, buccal mucosa,
or both: palms/soles)
◦ Depersonalization (feelings of • ≥2 GIT hamartomatous polyps
Depersonalization/ detachment from, or being an
derealization disorder outside observer of, one's self) ◦ Abdominal pain due to
◦ Derealization (experiencing obstruction or intussusception
surroundings as unreal) ◦ Anemia due to acute/chronic
• Intact reality testing
bleeding
• isolated impairment in
autobiographical memory. If the
◦ Rectal prolapse
amnesia is accompanied by travel or • ↑ Cancer risk (GIT, breast,
Dissociative amnesia
wandering, the specifier is "with genital tract)
dissociative fugue" • Positive family history
• Not explained by another disorder
(eg, substance use, post-traumatic #Mx:
stress disorder) •Annual anemia screening
• Marked discontinuity in identity & loss • Cancer screening (eg, upper/
Dissociative identity
of personal agency with lower endoscopy)
fragmentation into ≥2 distinct
disorder
personality states
• Associated with severe trauma/abuse

32) Antipsychotic medication should be maintained indefinitely in patients with

schizophrenia, including those with a first episode of psychosis to prevent relapse

33) OCPD: insight absent; justifies oneself

Vs
OCD: insight +; frustrated with oneself

34) Patients who experience sexual assault are at high risk for developing post-
traumatic stress disorder, depression, and suicidality.

35) Rx of anorexia nervosa: olanzepine, CBT NO SSRI

Bulimia nervosa: CBT, SSRI ;
Binge eating disorder: CBT, SSRI, lisdexamfetamine , topiramate

36) # Candidates for augmentation in MDD

-partial response (generally defined as 25%-50% improvement) to 1st-line treatment and
are tolerating their current medication

#major augmentation strategies:

-adding an antidepressant with a different mechanism of action (eg: Bupropion after
SSRI) / 2-o antipsychotic (eg, aripiprazole)/ lithium/ T3/ psychotherapy.
37) Mania in adolescence
-may be confused with normal adolescent moodiness, defiance, overconfidence, and risk
taking.
-However, an abrupt change from baseline, together with decreased need for sleep,
distractibility, excessive goal-directed activity, and grandiosity, should raise
suspicion for a manic episode.

38) brief psychotic disorder after death of a loved one:

-bizzare behaviour, hallucination (not necessarily of deceased)
Vs
#Acute stress disorder: startled/ hypervigilant behaviour of the traumatic event

39)normal grief: upto 1 yr

Complex brief: >1 yr

40) Agoraphobia —> Panic

-Patients with panic attacks frequently develop agoraphobia, which is anxiety and
avoidance of ≥2 situations in which it may be difficult to escape or get help (eg,
being outside the home or in enclosed spaces, using transportation)
-Mx: CBT

41) Major depressive disorder is associated with hyperactivity of the hypothalamic-

pituitary-adrenal axis, resulting in increased cortisol levels.

=
42) adjustment disorder with depressed and anxious mood
#Case clue: patient's 5-week history of mild mood symptoms in response to psychosocial
stressors (eg, relationship, work) that has resulted in distress and her seeking help is
most consistent with an adjustment disorder with depressed and anxious mood.
Vs
-Her symptoms are insufficient in number and severity to meet diagnostic criteria
for a major depressive episode

-Mx: A nonpharmacological approach (ie, psychotherapy as opposed to

pharmacotherapy) is the most appropriate intervention for this patient.

43) Valproate toxicity:

-Among the psychotropic medications listed, hepatotoxicity is most commonly
associated with the anticonvulsant mood stabilizer valproate
-Additionally, tremor, GIT Sx , thrombocytopenia, and alopecia occurs
Vs
-Lithium is not metabolized and is excreted almost exclusively through the kidneys. It
is associated with effects on renal and thyroid function.
44) lithium can enhance a physiologic tremor, which is typically a fine, symmetric action
tremor of the hands that increases with sympathetic activity.

45) somatic symptomatic disorder:

-A history of childhood sexual abuse and/or adult sexual trauma has been consistently
associated with the development of lifetime somatic symptom disorders (SSDs).

-Other significant risk factors for SSD : female sex, low educational level, chronic illness
as a child, or childhood exposure to a family member with a chronic illness.

46) Mx of delirium in elderly: vit H (haloperidol)

. Typical and atypical antipsychotics ; avoid BZD as it may worsen delirium

47) Posttraumatic stress disorder in children

-C/F:may present with distressing dreams with vague content and reenactment of traumatic
themes in play, rather than clearly formulated memories.

-often accompanied by emotional dysregulation and behavioral difficulties.

48) Childhood trauma is associated with BPD

49) short acting BZD withdrawal eg: alprazolam:

-appear as early as 24 hours after cessation
-C/F: seizures, tremors, anxiety, perceptual disturbances, and psychosis.

50) Rapid eye movement (REM) sleep behavior disorder

- dream enactment that occurs during REM sleep due to absence of muscle atonia. If
awakened, patients become fully alert and recall their dreams. In older patients, these
behaviors may be a sign of neurodegeneration.
Vs

#Nightmare disorder :
- vivid recall of disturbing dream content. However, unlike RBD, it is not associated with
motor activity or sleep-related injury.
Vs
#Sleep terrors and sleepwalking
-non-REM sleep arousal disorders that typically occur in younger patients during slow-wave
(N3), non-REM sleep.
51) Narcissistic personality disorder
-an exaggerated sense of self-importance, need for admiration, sense of entitlement, and
lack of empathy

↳
52) oculogyric crisis: results in a forced upward gaze deviation.

53) SSRI discontinuation syndrome

- mnemonic FINISH: Flu-like symptoms, Insomnia, Nausea, Instability, Sensory
disturbances, and Hyperarousal. BUT NO FEVER following abrupt discontinuation of
paroxetine
-# Culprit drugs:
→antidepressants with a shorter elimination half-life (eg, paroxetine,
-Serotonergic
venlafaxine), higher doses, and longer duration of treatment are associated with
more severe ADS symptoms.

54) Cognitive deficits

-Cognitive deficits that interfere with independence in everyday activities are a key
feature that distinguishes dementia (major neurocognitive disorder) from normal age-
related changes.
-Patients with dementia have functional impairments that necessitate assistance.
Pharmacotherapy of psychosis
• Second-generation antipsychotics (eg,
55) bullemia nervosa: extreme
risperidone, aripiprazole, quetiapine, olanzapine, compensation
Medications
ziprasidone) Vs
• First-generation antipsychotics (eg,
haloperidol) Binge eating: no/ Mild healthy
• Adjunctive benzodiazepines for agitation compensation
• Chronic nonadherence: consider long-acting
Special injectable
populations • Treatment resistance (2 failed trials):
consider clozapine

56) Abrupt discontinuation of antidepressants

- withdrawal syndrome that includes anxious and depressive exacerbations; symptoms
are more severe in antidepressants with a short half-life (eg, paroxetine).

* which antidepressant causes withdrawal??

-Fluoxetine's long half-life (ie, 4-6 days with chronic use) makes it unlikely to cause
clinically significant withdrawal after only 2 missed doses,
Vs
-whereas lorazepam may produce withdrawal symptoms within 1-2 days (t1/2 of 12 hr).
 57) Anorexia nervosa : BMI <18.5/ < 10th percentile
- Medical complications due to malnutrition : bradycardia, hypotension, edema,
gastroparesis, cardiac atrophy, and decreased bone mineral density.

58) Mechanism behind TD:

-prolonged exposure to dopamine-blocking agents, which is thought to result in the
upregulation and supersensitivity of dopamine receptors.
Causes of delirium 59) CT of schizophrenia
• Dementia -Enlargement of the lateral cerebral
Predisposi • Parkinson disease ventricles
ng risk • Prior stroke
factors • Advanced age
-Decreased volume of the
• Sensory impairment hippocampus and amygdala
• Drugs (eg, narcotics, sedatives, antihistamines, 60) Indication for hospitalisation in
muscle relaxers, polypharmacy) Anorexia nervosa
• Infections (eg, pneumonia, urinary tract infection,
meningitis)
• Bradycardia (<40/min), dysrhythmia
• Electrolyte disturbances (eg, hyponatremia, • Hypotension (<80/60 mm Hg),
Precipitating hypercalcemia) orthostasis
factors • Metabolic derangements (eg, volume depletion, • Hypothermia (<35 C)
vitamin B12 deficiency, hyperglycemia)
• Systemic illnesses (eg, congestive heart failure, • Electrolyte disturbance, marked
hepatic failure, malignancy) dehydration
• Central nervous system conditions (eg, seizure, • Organ compromise (renal, hepatic,
stroke, head injury, subdural hematoma)
cardiac)
• <70% expected weight (BMI <15
61) NMS vs serotonin syndrome. kg/m2)
-gradual onset, Lead-pipe rigidity and absence of hyperreflexia: NMS
-SS: within 24 hrs; hyperreflxia ; exclude If 2 week washout period

62) Korsakoff syndrome

- a potential complication of WE that is characterized by retrograde and anterograde
amnesia with preserved long-term memory, confabulation, lack of insight and apathy.
Vs
#Dissociative amnesia
- develops in the context of psychologic trauma, affects traumatic autobiographical
memory, and is frequently reversible.
-There is no evidence of trauma in korsakoff, whose memory deficits involve widespread
memory systems.

63) Nonsuicidal self-injury / self mutilation/ Parasuicide

-a nonspecific psychiatric symptom commonly seen in adolescents that is used as a
temporary means to relieve distressing, negative emotions.
-Initial management :suicide risk assessment and comprehensive psychiatric evaluation.
63) Differentiating panic from pheochromocytoma:
-Patients with generalized anxiety disorder and panic disorder may have similar psychiatric
and sympathetically driven somatic symptoms (eg, palpitations, diaphoresis) as those
found in pheochromocytoma;

#Clue for pheochromocytoma:

-however, severe, drug-resistant hypertension, hyperglycemia, and episodic
pounding headache are not associated with either condition.

64) Major depressive disorder with seasonal pattern (seasonal affective disorder)
-C/F: characterized by seasonal onset and remission (MC fall-winter onset and spring-
summer remission).

#Rx: bright light therapy alone / with an antidepressant; always start with SSRI

-Bright light therapy: administered with a 10,000-lux light box shortly after awakening.
- Most patients experience clinical improvement in 1-4 weeks and continue treatment
through the fall or winter until spontaneous remission in the spring or summer.

65) Mx of agitated Pt:

-Efforts to calm the patient with verbal techniques are unsuccessful and he has a history of
assaultive behavior (ie, recent fight), and he has been physically aggressive with the
physician and security guards.
#Next step:
-To maintain safety, he requires immediate emergency intervention, which should
include both physical restraints and medications to calm him (typically an
intramuscular antipsychotic, a benzodiazepine, or a combination of the two)

66) Rx of agitated Pt :
-Medication options for acute psychotic agitation : antipsychotics , benzodiazepines/
combo .
Benzodiazepines are preferred for the management of acute agitation in patients who have
a QTc ≥500 ms due to the risk of QTc prolongation associated with antipsychotics
(ziprasedone)

67) Counselling the druggist

-Even though the patient was unsuccessful, his effort at sobriety indicates that he had
moved into the action phase of change, taking concrete steps to alter his behavior.

-The physician should validate that the week of sobriety was a major step in the right
direction, explaining that relapse is a common part of the cycle and reinforcing the patient's
intrinsic motivation to take further action.
 69) speech in psychiatry pt:
amboss
a) Circumstantial speech
-a person expresses a
thought in a complicated,
long-winded manner that
deviates from the topic
several times before
ultimately explaining the
central idea.

b) Thought-blocking
-affected person suddenly
stops talking for no apparent
reason and either continues
the sentence after a delay or
changes the topic.

c) Loose associations
- commonly associated with schizophrenia, Affected individuals suffer from incoherent
thinking that is expressed in sudden, illogical, and frequent changes in topic.

-Whereas individual sentences in themselves are grammatically correct, often no logical

connection can be established within or between sentences.

d) Flight of ideas : mania

-quick succession of ideas, abrupt changes in topic, and rapid speech.

-Although the topics change rapidly, the logical sequence of ideas or sentences is not
altered and is typically based on understandable associations

e) Clang associations
- words are used based on rhyme patterns instead of their meaning.
 Pharmacotherapy for smoking cessation 70) Cyclothymic disorder :
Treatment Indications
Adverse effects/ characterized by short
contraindications
hypomanic and mild depressive
Long-acting NRT • ↓ Cravings & daytime • No significant effects, episodes over at least 2 years.
(nicotine patch) withdrawal symptoms safe in almost all
• Long-acting may be patients
Short-acting NRT
combined with short- —> To diagnose the condition,
(nasal spray,
acting NRT (“patch
gum, the hypomanic episode must be
plus”)
lozenge, inhaler)
• ↓ Post-cessation • Contraindicated in
shorter than 1 week and the
weight gain patients with seizure depressive episodes must be
Bupropion • Good choice for
patients with unipolar
or eating disorders shorter than 2 weeks.
depression -means both are incomplete
• More effective than • Possible ↑ risk of
Varenicline
bupropion or NRT cardiovascular events

71) Rx of conversion disorder:

-Patient education is the first step of care in patients with conversion disorder as
symptoms may resolve after explanation of the diagnosis and its causes.

-Strategies for presenting the diagnosis to patients include asking about their perspective
of the problem, taking their symptoms seriously, explaining clinical features that are
inconsistent with neurologic disease, and emphasizing that symptoms are potentially
reversible.

72) Narcolepsy Rx:

-1st line: modafinil; 2nd line: stimulants methylphenidate, amphetamine

73) anatomy involved in:

-wernicke: Mamillary body, dorsomedial thalami
- korsakoff: corpus callosum

74) Brain autopsy findings in Depression : Vs - decreased hippocampal and frontal lobe
volume

75) Mania Rx in Pregnancy: haloperidol, 2o antipsychotics, ECT

Psychotherapy :

==> Family therapy : Useful in

Schizophrenia,
Adolescent violent behaviour

==> Exposure therapy :

- goal is to decrease the patient's reactivity through repetitive exposures to a stimulus.
- phobic and other anxiety disorders.

—> Exposure and response therapy :

-ERP therapy involves repeated exposure to thoughts, images, and situations that
provoke obsessional fears followed by prevention of the accompanying compulsion.
 Hemat

# Vit B2 def: pancytopenia with hypersegmented N vs

Myelodysplastic syndrome: pancytopenia but with hyposegmented granulocytes UWSA1
-Similarity: both may have macroovalocyte

# Malignancy can cause disseminated intravascular coagulopathy,

- the anemia seen in patients with DIC is often due to microangiopathic hemolysis.UWSA1
 434 SEC TION III HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
` 

Heme synthesis, The porphyrias are hereditary or acquired conditions of defective heme synthesis that lead to the
porphyrias, and lead accumulation of heme precursors. Lead inhibits specific enzymes needed in heme synthesis,
poisoning leading to a similar condition.
CONDITION AFFECTED ENZYME ACCUMULATED SUBSTRATE PRESENTING SYMPTOMS
Lead poisoning Ferrochelatase and Protoporphyrin, ALA Microcytic anemia (basophilic stippling in
A ALA dehydratase (blood) peripheral smear A , ringed sideroblasts in
bone marrow), GI and kidney disease.
Children—exposure to lead paint Ž mental
deterioration.
Adults—environmental exposure (eg, batteries,
ammunition) Ž headache, memory loss,
demyelination (peripheral neuropathy).
Acute intermittent Porphobilinogen Porphobilinogen, ALA Symptoms (5 P’s):
porphyria deaminase, ƒ Painful abdomen

AFI
previously called ƒ Port wine–colored Pee
uroporphyrinogen I ƒ Polyneuropathy
synthase (autosomal ƒ Psychological disturbances

€
dominant mutation) ƒ Precipitated by factors that  ALA synthase
(eg, drugs [CYP450 inducers], alcohol, -
starvation)
Treatment: hemin and glucose.
Porphyria cutanea Uroporphyrinogen Uroporphyrin (tea- Blistering cutaneous photosensitivity and
tarda decarboxylase colored urine) hyperpigmentation B .
B
- . Most common porphyria. Exacerbated with
alcohol
-
consumption.
Causes: familial, hepatitis C.
Treatment: phlebotomy, sun avoidance,
antimalarials (eg, hydroxychloroquine).

MITOCHONDRIA Glucose, hemin CYTOPLASM

Sideroblastic anemia (X-linked) Lead poisoning

Succinyl CoA + glycine

B₆
Aminolevulinic
acid
ALA dehydrogenase
Porphobilinogen p
ALA synthase Porphobilinogen
(rate-limiting step) deaminase
Acute
intermittent
Hydroxymethylbilane porphyria
Mitochondrial
membrane H
v Uroporphyrinogen III
Heme Uroporphyrinogen
decarboxylase
Ferrochelatase Porphyria cutanea tarda
Lead C
poisoning Fe2+
Protoporphyrin Coproporphyrinogen III

#Acute intermittent porphyria

- discrete attacks of abdominal pain, peripheral neuropathy (> in U/E) with proximal
muscle weakness, autonomic dysfunction, and neuropsychiatric manifestations;No jaundice
f.

-Dx: Urobilinogen levels are typically elevated, and elevated urinary porphyrin levels
confirm the diagnosis.
430 SEC TION III HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
` 

Non-Hodgkin lymphoma
TYPE OCCURS IN GENETICS COMMENTS
Neoplasms of mature B cells
Burkitt lymphoma Adolescents or young t(8;14)—translocation “Starry sky” appearance, sheets of lymphocytes
adults of c-myc (8) and with interspersed “tingible body” macrophages
heavy-chain Ig (14) (arrows in A ). Associated with EBV.
Jaw lesion B in endemic form in Africa; pelvis
or abdomen in sporadic form.
Diffuse large B-cell Usually older adults, Mutations in BCL-2, Most common type of non-Hodgkin lymphoma
lymphoma but 20% in children BCL-6 in adults.
Follicular lymphoma Adults t(14;18)—translocation Indolent course with painless “waxing and
of heavy-chain Ig (14) waning” lymphadenopathy. Bcl-2 normally
and BCL-2 (18) inhibits apoptosis. -

Mantle cell lymphoma Adult males >> adult t(11;14)—translocation Very aggressive, patients typically present with
females of cyclin D1 (11) and late-stage disease.
heavy-chain Ig (14),
CD5+
Marginal zone Adults t(11;18) Associated with chronic inflammation (eg,
lymphoma Sjögren syndrome, chronic gastritis [MALT
lymphoma]).
Primary central Adults EBV related; Considered an AIDS-defining illness. Variable
nervous system associated with HIV/ presentation: confusion, memory loss, seizures.
lymphoma AIDS CNS mass (often single, ring-enhancing lesion
-
on MRI) in immunocompromised patients C ,
needs to be distinguished from toxoplasmosis
via CSF analysis or other lab tests.
Neoplasms of mature T cells
Adult T-cell lymphoma Adults Caused by HTLV Adults present with cutaneous lesions; common

JIMI
(associated with IV in Japan (T-cell in Tokyo), West Africa, and the
drug abuse) Caribbean.
Lytic bone lesions, hypercalcemia.
.
Mycosis fungoides/ Adults Mycosis fungoides: skin patches and plaques D
Sézary syndrome (cutaneous T-cell lymphoma), characterized by
atypical CD4+ cells with “cerebriform” nuclei
and intraepidermal neoplastic cell aggregates
(Pautrier microabscess). May progress to Sézary
syndrome (T-cell leukemia).
A B C D
432 SEC TION III HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
` 

Myelodysplastic Stem cell disorders involving ineffective Pseudo-Pelger-Huet anomaly—neutrophils

syndromes hematopoiesis Ž defects in cell maturation with bilobed (“duet”) nuclei A . Typically seen
A
of nonlymphoid lineages. Caused by de novo after chemotherapy.
mutations or environmental exposure (eg, • Dysplastic red & white blood cells*
radiation, benzene, chemotherapy). Risk of on peripheral smear
• Bone marrow biopsy (hypercellular
transformation to AML.
marrow)
-
• Transfusions for symptomatic
cytopenias
Treatment
• Chemotherapy
• Hematopoietic stem cell transplantation
*Dysplastic changes include ovalomacrocytosis & neutrophil
hyposegmentation/hypogranulation.
Leukemias Unregulated growth and differentiation of WBCs in bone marrow Ž marrow failure Ž anemia
( RBCs), infections ( mature WBCs), and hemorrhage ( platelets). Usually presents with
 circulating WBCs (malignant leukocytes in blood); rare cases present with normal/ WBCs.
Leukemic cell infiltration of liver, spleen, lymph nodes, and skin (leukemia cutis) possible.
TYPE NOTES
Lymphoid neoplasms
Acute lymphoblastic Most frequently occurs in children; less common in adults (worse prognosis). T-cell ALL can

I
leukemia/lymphoma present as mediastinal mass (presenting as SVC-like syndrome). Associated with Down syndrome.
Peripheral blood and bone marrow have  lymphoblasts A . -.
TdT+ (marker of pre-T and pre-B cells), CD10+ (marker of pre-B cells).
Most responsive to therapy.
May spread to CNS and testes.
i t(12;21) Ž better prognosis.
Chronic lymphocytic Age > 60 years. Most common adult leukemia. CD20+, CD23+, CD5+ B-cell neoplasm. Often
-
leukemia/small asymptomatic, progresses slowly; smudge cells B in peripheral blood smear; autoimmune
lymphocytic hemolytic anemia. CLL = Crushed Little Lymphocytes (smudge cells).
lymphoma Richter transformation—CLL/SLL transformation into an aggressive lymphoma, most commonly
diffuse large B-cell lymphoma (DLBCL).
Hairy cell leukemia Adult males. Mature B-cell tumor. Cells have filamentous, hair-like projections
(fuzzy appearing on LM C ). Peripheral lymphadenopathy is uncommon.
I
Causes marrow fibrosis Ž dry tap on aspiration. Patients usually present with massive splenomegaly
and pancytopenia.
-

Stains TRAP (tartrate-resistant acid phosphatase) ⊕ (trapped in a hairy situation). TRAP stain
=
largely replaced with flow cytometry. Associated with BRAF mutations.
-
Treatment: cladribine, pentostatin.
Myeloid neoplasms
Acute myelogenous Median onset 65 years. Auer rods D ; myeloperoxidase ⊕ cytoplasmic inclusions seen mostly in
leukemia
-

APL (formerly M3 AML);  circulating myeloblasts on peripheral smear.

Risk factors: prior
- =
exposure to alkylating chemotherapy, radiation, myeloproliferative disorders,
Down syndrome. APL: t(15;17), responds to all-trans retinoic acid (vitamin A) and arsenic, which
-
induce differentiation of promyelocytes; DIC is a common presentation. -

#Acute: > blast #Acute myeloid leukemia (AML) : the MC acute leukemia in
Chronic: > cytes, long adults and is typically associated with fatigue and symptoms
H/O so mild Sx related to >1 cytopenias (Including WBC)
- CML : low LAP -Acute promyelocytic leukemia is a unique form of AML that often
score presents with life-threatening coagulopathy due to DIC
 HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
`  SEC TION III 433

Leukemias (continued)
Chronic myelogenous Peak incidence: 45—85 years; median age: 64 years. Defined by the Philadelphia chromosome
leukemia (t[9;22], BCR-ABL) and myeloid stem cell proliferation. Presents with dysregulated production of
mature and maturing granulocytes (eg, neutrophils, metamyelocytes, myelocytes, basophils E )
and splenomegaly. May accelerate and transform to AML or ALL (“blast crisis”).
Very low leukocyte alkaline phosphatase (LAP) as a result of low activity in malignant neutrophils,
vs benign neutrophilia (leukemoid reaction) in which LAP is  due to  leukocyte count with
neutrophilia in response to stressors (eg, infections, medications, severe hemorrhage).
Responds to bcr-abl tyrosine kinase inhibitors (eg, imatinib).
A B C D E

Chronic Malignant hematopoietic neoplasms with varying impacts on WBCs and myeloid cell lines.
myeloproliferative
disorders
Polycythemia vera Primary polycythemia. Disorder of  RBCs, usually due to acquired JAK2 mutation. May present
as intense itching after shower (aquagenic pruritus). Rare but classic symptom is erythromelalgia
-hypertension, transient vision disturbances,
aquagenic pruritus, or thrombosis. (severe, burning pain and red-blue coloration) due to episodic blood clots in vessels of the

I
-Facial plethora and splenomegaly are extremities A .

F-
common on physical examination.  EPO (vs 2° polycythemia, which presents with endogenous or artificially  EPO).
Treatment: phlebotomy, hydroxyurea, ruxolitinib (JAK1/2 inhibitor).
Essential Characterized by massive proliferation of megakaryocytes and platelets. Symptoms include
thrombocythemia bleeding and thrombosis. Blood smear shows markedly increased number of platelets, which may
be large or otherwise abnormally formed B . Erythromelalgia may occur.
Myelofibrosis Obliteration of bone marrow with fibrosis C due to  fibroblast activity. Associated with massive
splenomegaly and “teardrop” RBCs D . “Bone marrow cries because it’s fibrosed and is a dry tap.”
RBCs WBCs PLATELETS PHILADELPHIA CHROMOSOME JAK2 MUTATIONS
Polycythemia vera    ⊝ ⊕

Essential − −  ⊝ ⊕ (30–50%)
thrombocythemia
Myelofibrosis  Variable Variable ⊝ ⊕ (30–50%)

CML    ⊕ ⊝

A B C D
446 SEC TION III HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PHARMACOLOGY
` 

Warfarin
MECHANISM Inhibits vitamin K epoxide reductase by competing with vitamin K Ž inhibition of vitamin K–
dependent γ-carboxylation of clotting factors II, VII, IX, and X and proteins C and S. Metabolism
affected by polymorphisms in the gene for vitamin K epoxide reductase complex (VKORC1). In
laboratory assay, has effect on extrinsic pathway and  PT. Long half-life.
“The ex-PresidenT went to war(farin).”
CLINICAL USE Chronic anticoagulation (eg, venous thromboembolism prophylaxis and prevention of stroke
in atrial fibrillation). Not used in pregnant patients (because warfarin, unlike heparin, crosses
placenta). Monitor PT/INR.
ADVERSE EFFECTS Bleeding, teratogenic effects, skin/tissue necrosis A , drug-drug interactions (metabolized by
A
cytochrome P-450 [CYP2C9]).
Initial risk of hypercoagulation: protein C has shorter half-life than factors II and X. Existing
protein C depletes before existing factors II and X deplete, and before warfarin can reduce factors
II and X production Ž hypercoagulation. Skin/tissue necrosis within first few days of large doses
believed to be due to small vessel microthrombosis.
Heparin “bridging”: heparin frequently used when starting warfarin. Heparin’s activation of
antithrombin enables anticoagulation during initial, transient hypercoagulable state caused by
warfarin. Initial heparin therapy reduces risk of recurrent venous thromboembolism and skin/
tissue necrosis.
For reversal of warfarin, give vitamin K. For rapid reversal, give FFP or PCC.

Heparin vs warfarin
Heparin Warfarin
ROUTE OF ADMINISTRATION Parenteral (IV, SC) Oral
SITE OF ACTION Blood Liver
ONSET OF ACTION Rapid (seconds) Slow, limited by half-lives of normal clotting
factors
DURATION OF ACTION Hours Days
MONITORING PTT (intrinsic pathway) PT/INR (extrinsic pathway)
CROSSES PLACENTA No Yes (teratogenic)

Direct coagulation factor inhibitors

DRUG MECHANISM CLINICAL USE ADVERSE EFFECTS
Bivalirudin, Directly inhibit thrombin Venous thromboembolism, Bleeding (reverse dabigatran
argatroban, (factor IIa) atrial fibrillation. Can be used with idarucizumab)
-
dabigatran in HIT, when heparin is BAD Dabigatran is the only oral
for the patient agent in class
Do not require lab monitoring
Apixaban, edoxaban, Directly inhibit factor Xa Treatment and prophylaxis Bleeding (reverse with
rivaroxaban for DVT and PE; stroke andexanet alfa)
-
prophylaxis in patients with Oral agents that do not usually
atrial fibrillation require lab monitoring
 HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PHARMACOLOGY
`  SEC TION III 447

Anticoagulation reversal
ANTICOAGULANT REVERSAL AGENT NOTES
Heparin Protamine sulfate ⊕ charged peptide that binds ⊝ charged
heparin
Warfarin Vitamin K (slow) +/– FFP or PCC (rapid)
Dabigatran Idarucizumab Monoclonal antibody Fab fragments
Direct factor Xa Andexanet alfa Recombinant modified factor Xa (inactive)
inhibitors

Antiplatelets All work by  platelet aggregation.

DRUG MECHANISM CLINICAL USE ADVERSE EFFECTS
Aspirin Irreversibly blocks COX Acute coronary syndrome; Gastric ulcers, tinnitus, allergic
Ž  TXA2 release coronary stenting.  incidence reactions, renal injury
or recurrence of thrombotic
stroke
Clopidogrel, Block ADP (P2Y12) receptor Same as aspirin; dual Neutropenia (ticlopidine); TTP
prasugrel, ticagrelor, Ž  ADP-induced expression antiplatelet therapy may be seen
ticlopidine of GpIIb/IIIa
Abciximab, Block GpIIb/IIIa (fibrinogen Unstable angina, percutaneous Bleeding, thrombocytopenia
eptifibatide, tirofiban receptor) on activated coronary intervention
platelets. Abciximab is made
from monoclonal antibody
Fab fragments
Cilostazol, Block phosphodiesterase Intermittent claudication, Nausea, headache, facial
dipyridamole Ž  cAMP in platelets stroke prevention, cardiac flushing, hypotension,
stress testing, prevention of abdominal pain
coronary stent restenosis

Thrombolytics Alteplase (tPA), reteplase (rPA), streptokinase, tenecteplase (TNK-tPA).

MECHANISM Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin
clots.  PT,  PTT, no change in platelet count.
CLINICAL USE Early MI, early ischemic stroke, direct thrombolysis of severe PE.
ADVERSE EFFECTS Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding,
recent surgery, known bleeding diatheses, or severe hypertension. Nonspecific reversal with
antifibrinolytics (eg, aminocaproic acid, tranexamic acid), platelet transfusions, and factor
corrections (eg, cryoprecipitate, FFP, PCC).
1) hereditary spherocytosis
infant of north European descent has jaundice, hemolytic anemia, and elevated (MCHC)
- #Lab: ↑ MCHC; Negative Coombs test; Spherocytes on PS; ↑ Osmotic fragility on
acidified glycerol lysis test; Abnormal eosin-5-maleimide binding test
Vs

2) physiological jaundice:
-expected in the 1st week of life due to increased RBC turnover (shorter fetal RBC
lifespan) and decreased bilirubin clearance

==> severe or prolonged neonatal jaundice (>1 week) raises suspicion for inherited
hemolytic anemia.

-
/ <1.5 lac in non pregnant
F, < 1 lac in Pregnancy

.
Pregnancy
X warfarin
3) differentiating iron deficiency vs thalassemia minor:
-The 2 MCC of microcytic anemia: iron deficiency and thalassemia minor

*Similarity:
similar laboratory (eg, low [MCV], low [MCHC]) and PS target cells, hypochromia) findings.
* Differentiation requires iron studies, but empiric iron supplementation is
sometimes prescribed.
==> Lack of improvement in hemoglobin levels within 4 weeks makes T minor likely
Iron deficiency anemia & thalassemias
Iron Alpha- Beta-
Parameter deficiency thalassemia thalassemia
anemia minor minor #TM
MCV ↓ ↓ ↓
-normal red cell distribution width (RDW)
RDW ↑ Normal Normal
and normal-to-elevated total RBCs
RBCs ↓ Normal Normal
typically result in a Mentzer index (MCV/
RBC) <13.
Peripheral Microcytosis,
smear hypochromia
Target cells Target cells -Reticulocyte count may be slightly
↓ Iron &
Normal/↑ Normal/↑ elevated due to a compensatory bone
Serum iron
studies
ferritin
iron & ferritin
(RBC
iron & ferritin
(RBC
marrow response to anemia.
↑ TIBC
turnover) turnover)
Response to iron ↑ No No
supplementation Hemoglobin improvement improvement
Hemoglobin
electrophoresis
Normal Normal Abnormal
 HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
`  SEC TION III 429

Microcytic, hypochromic anemias (continued)

Lead poisoning Lead inhibits ferrochelatase and ALA dehydratase Ž  heme synthesis and  RBC protoporphyrin.
Also inhibits rRNA degradation Ž RBCs retain aggregates of rRNA (basophilic stippling).
Symptoms of LEAD poisoning:
ƒ Lead Lines on gingivae (Burton lines) and on metaphyses of long bones D on x-ray.
ƒ Encephalopathy and Erythrocyte basophilic stippling.
ƒ Abdominal colic and sideroblastic Anemia.
ƒ Drops—wrist and foot drop.
Treatment: chelation with succimer, EDTA, dimercaprol.
Exposure risk  in old houses with chipped paint (children) and workplace (adults).
Sideroblastic anemia Causes: genetic (eg, X-linked defect in ALA synthase gene), acquired (myelodysplastic syndromes),
and reversible (alcohol is most common; also lead poisoning, vitamin B6 deficiency, copper
deficiency, drugs [eg, isoniazid, linezolid]).
Lab findings:  iron, normal/ TIBC,  ferritin. Ringed sideroblasts (with iron-laden, Prussian blue–
stained mitochondria) seen in bone marrow E . Peripheral blood smear: basophilic stippling of
RBCs. Some acquired variants may be normocytic or macrocytic.
Treatment: pyridoxine (B6, cofactor for ALA synthase).
A B C D E

Interpretation of iron studies

Iron Chronic Pregnancy/
deficiency disease Hemochromatosis OCP use
Serum iron    —

IE
Transferrin or TIBC  a  
Ferritin    —
% transferrin saturation  —/  
(serum iron/TIBC)
 = 1° disturbance.
Transferrin—transports iron in blood.
TIBC—indirectly measures transferrin.
Ferritin—1° iron storage protein of body.
a
Evolutionary reasoning—pathogens use circulating iron to thrive. The body has adapted a system in which iron is stored
within the cells of the body and prevents pathogens from acquiring circulating iron.

#Dx of MM:
-(SPEP) is a common screening test for MM
-Bone marrow biopsy, a more invasive procedure, can then confirm diagnosis (>10% clonal
plasma cells).
 4) One of the most common coagulation inhibitors :
lupus anticoagulant (LA), a type of an antiphospholipid
antibody.
-LA binds to the phospholipids used in most PTT tests and
prevents them from inducing coagulation (prolonging PTT).

==> This laboratory artifact is resolved with the addition of

phospholipids (which eventually overwhelm all the antibody
binding sites).
Multiple myeloma
• Plasma cell neoplasm produces
Pathophysiolog
monoclonal paraprotein
y
(immunoglobulin)
• Bone pain, fractures
5) Anemia of chronic Ds: • Constitutional symptoms (weight
Manifestations
#Etiology: loss, fatigue)
• Recurrent infections
-Malignancy (including Hodgkins lymphoma);
• Normocytic anemia
Chronic infection; Rheumatic disease; • Renal insufficiency
Obesity; DM; CHF Laboratory
• Hypercalcemia (constipation,
muscle weakness)
• Monoclonal paraproteinemia (M-
spike)
#Lab: Normocytic/slightly microcytic
• Osteolytic lesions/osteopenia
anemia↓ S. iron, iron-binding capacity, ↑ Radiology
(osteoclast activation)
bone marrow iron, ↑ ferritin; Lower than
expected erythropoietin for degree of
anemia

#Mx:
1st line: Treat underlying condition
• 2nd line: EPO if not responsive to
underlying Ds Rx
• 3rd line: packed RBC
6) Hydrops fetalis in
hemoglobin Barts Alpha-thalassemia
-it has an extreme affinity for Genotype Disorder Clinical features
oxygen (>10 times more than 1 gene loss Alpha-thalassemia
Asymptomatic, silent carrier
hemoglobin A) and does not (αα/α-) minima

release oxygen to the tissues. 2 gene loss

(αα/- -) or
Alpha-thalassemia
Mild microcytic anemia
minor
(α-/α-)
-This results in severe fetal 3 gene loss
Hemoglobin H disease Chronic hemolytic anemia
hypoxemia, development of (α-/- -)

high-output cardiac failure, and 4 gene loss Hydrops fetalis, High-output cardiac failure, anasarca,
(- -/- -) hemoglobin Barts death in utero
subsequent hydrops fetalis and
intrauterine fetal demise.
 HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
`  SEC TION III 431

Normocytic, Normocytic, normochromic anemias are classified as nonhemolytic or hemolytic. The hemolytic
normochromic anemias are further classified according to the cause of the hemolysis (intrinsic vs extrinsic to the
anemias RBC) and by the location of the hemolysis (intravascular vs extravascular). Hemolysis can lead to
increases in LDH, reticulocytes, unconjugated bilirubin, pigmented gallstones, and urobilinogen
in urine.
Intravascular Findings:  haptoglobin,  schistocytes on blood smear. Characteristic hemoglobinuria,
hemolysis hemosiderinuria, and urobilinogen in urine. Notable causes are mechanical hemolysis (eg,
prosthetic valve), paroxysmal nocturnal hemoglobinuria, microangiopathic hemolytic anemias.
Extravascular Mechanism: macrophages in spleen clear RBCs. Findings: spherocytes in peripheral smear
hemolysis (most commonly due to hereditary spherocytosis and autoimmune hemolytic anemia), no
hemoglobinuria/hemosiderinuria. Can present with urobilinogen in urine.

Nonhemolytic, normocytic anemias

DESCRIPTION FINDINGS
Anemia of chronic Inflammation (eg,  IL-6) Ž  hepcidin  iron,  TIBC,  ferritin.
disease (released by liver, binds ferroportin on Normocytic, but can become microcytic.
intestinal mucosal cells and macrophages, Treatment: address underlying cause of
thus inhibiting iron transport) Ž  release of inflammation, judicious use of blood
iron from macrophages and  iron absorption transfusion, consider erythropoiesis-
from gut. Associated with conditions such stimulating agents such as EPO (eg, in chronic
as chronic infections, neoplastic disorders, kidney disease).
chronic kidney disease, and autoimmune
diseases (eg, SLE, rheumatoid arthritis).
Aplastic anemia Failure or destruction of hematopoietic stem  reticulocyte
-
count,  EPO.
A
cells. Causes (reducing volume from inside Pancytopenia characterized by anemia,
diaphysis): leukopenia, and thrombocytopenia (not to be
ƒ Radiation confused with aplastic crisis, which causes
ƒ Viral agents (eg, EBV, HIV, hepatitis viruses) =
anemia only). Normal cell morphology,
ƒ Fanconi anemia (autosomal recessive DNA but hypocellular bone marrow with fatty
repair defect Ž bone marrow failure); infiltration A (dry bone marrow tap).
normocytosis or macrocytosis on CBC Symptoms: fatigue, malaise, pallor, purpura,
ƒ Idiopathic
-
(immune mediated, 1° stem cell mucosal bleeding, petechiae, infection.
defect); may follow acute hepatitis Treatment: withdrawal of offending
ƒ Drugs (eg, benzene, chloramphenicol, agent, immunosuppressive regimens (eg,
alkylating agents, antimetabolites) antithymocyte globulin, cyclosporine), bone

⇐ marrow allograft, RBC/platelet transfusion,

bone marrow stimulation (eg, GM-CSF).
6) complications of HL Rx: >5 years after Rx.
• Secondary solid organ malignancy: breast, lung, git, thyroid)
• hematologic malignancy : ALL, NHL
• Secondary malignancies are the leading cause of death in those who have been
cured of HL.
• Cardiovascular disease: Risk of coronary artery disease, valve damage, peripheral
vascular disease, and cardiomyopathy are increased in those who have been treated
for HL.
-CVS disease is the leading nonmalignant cause of death in long-term HL survivors.

#Other common treatment-related complications : pulmonary disease (eg, fibrosis,

bronchiectasis) and hypothyroidism from chest radiation and neuropathy from
chemotherapy.

7) TTP:
#Pentad:
• Hemolytic anemia (↑ LDH, ↓ haptoglobin) with schistocytes
• Thrombocytopenia (↑ bleeding time, normal PT/PTT)
• Renal failure; Neurologic manifestations; Fever
#RF: HIV, infection, drugs

#Mx: Plasma exchange; Glucocorticoids; Rituximab

8) ALL:
-Bone marrow biopsy with >25% lymphoblasts
-Multidrug chemotherapy e-

9) ALL vs aplastic anemia:

1) similarity: pancytopenia; fever
2) difference:
- ALL: Bone pain due to hypercellular marrow, LNopathy
-

-Aplastic anemia: No=

B
BONE Pain due to hypocellular marrow; No LNopathy.
-

10) aplastic anaemia:

• Autoimmune
• Infections (eg, HIV, Epstein-Barr virus)
• Drugs (eg, carbamazepine, chloramphenicol,
-
sulfonamides)
• Exposure to radiation or toxins (eg, benzene, solvents)
11) #Similarity between Vit K deficiency and DIC: Iron deficiency anemia in young children
-RF: acutely ill • Prematurity
-Bleeding from IV site • Lead exposure
- Lab: raised PT, aPTT • Age <1
-Delayed introduction of solids
Risk
(ie, exclusive BF after 6 months)
#Difference: factors
-Cow's, soy, or goat's milk
1) Vit K deficiency: • Age >1
RF: liver Ds, Antibiotics, malnutrition ->24 oz/day cow's milk
-<3 servings/day iron-rich foods
Vitals: hemodynamically stable;
NO SHOCK • Screening hemoglobin at age 1
Diagnosi
• Hemoglobin <11 g/dL, ↓ MCV,
NO Multiorgan failure s
↑ RDW e-

Treatme • Empiric trial of Fe

2) DIC nt supplementation
RF: different #Mx:
Vitals: SHOCK -Hb should be rechecked in 4 weeks;
MODS -if the Hb level has risen 1 g/dL, the oral iron therapy should be
continued for 2-3 months after the hemoglobin normalizes to
replete iron stores.
13) Afibrinogenemia : AR
-C/F: Severe bleeding classically develops at the site of the umbilical cord after birth.
-Lab: Like PT and PTT, thrombin time is prolonged

14) Infantile Vit K deficiency: onset 2-7 days of life

15) Bleeding from angiodysplasias

- triggered by underlying aortic stenosis, which is associated with low levels of von
Willebrand factor multimers;
-this glycoprotein is often destroyed when it passes through the damaged valve at high
velocity.

16) Hemophilic arthropathy

- a consequence of recurrent hemarthroses
-Pathogenesis:hemosiderin deposition leading to synovitis and fibrosis within the joint.
-
-
-Mx: The risk reduced by prophylactic treatment with factor concentrates.

17) Bleeding characteristics :

1) Hemophilia :
Hemarthrosis ; skeletal muscle hematoma after minor trauma is also common.
-
-Onset: typically begin during toddlerhood when the child is ambulatory.

2) Platelets disorders : Petechiae; mucosal bleeding

3) vWF deficiency : Heavy menstrual bleeding ; prolonged mucosal bleeding (eg, oropharyngeal, gastrointestinal,
=
uterine), but bleeding into deep tissue is not seen.
Acute vs chronic disseminated intravascular coagulation (DIC) 18) differentiate sideroblastic vs iron
Acute DIC Chronic DIC deficiency anemia??
Sepsis *Diff:

%
Severe trauma Malignancy (eg,
Common etiologies
Obstetric pancreatic) a) Sideroblastic:
complications -increased S. iron concentration
Coagulation studies Prolonged Often normal - normal / decreased TIBC due to heme
Platelets Low Often normal deficit so Fe stored in mitochondria
Fibrinogen Low Often normal Vs
D-dimer High High b) iron deficiency anemia
Bleeding risk Very high Mildly increased - decreased S. Fe concentration
Thromboembolism
Mildly increased Very high
- high TIBC
risk
t *Similarity: microcytic hypochromic anemi

✓ 19) Hydroxyurea in sickle cell:

-MOA: increasing the amount of HbF in
circulation, which dilutes the number
of sickled cells in circulation and

⑤
reduces vaso-occlusive episodes,
° the need for transfusions, and
-
episodes of acute chest syndrome.

—> although SCD typically have HbF concentration 5%-15%, those with SCD on
hydroxyurea will often have HbF >15%.
O
-ADR: myelosuprresion

20) Mx of SCD stroke:

• Exchange transfusion
• Simple transfusion if exchange transfusion is unavailable
#Primary prevention:
• Transcranial doppler screening during childhood
• Hydroxyurea
• ± Chronic transfusions

21) Splenic sequestration

- a potentially life-threatening complication of SCD in which sickled red blood cells (RBCs)
become trapped in the splenic sinuses, a large volume of blood pools in the spleen.

-C/F: The spleen rapidly enlarges (ie, tender splenomegaly), and hemoglobin drops
acutely from baseline, resulting in fatigue, pallor, tachycardia, and even shock (eg,
hypotension, weak pulses).
-Lab: thrombocytopenia; haemolytic anemia; reticulocytosis
Vs
#HF: can present with shock, anaemia but hepatomegaly present; not splenomegaly
 -

o
#Pulm HT in SCD:
-Pathogenesis: Intravascular hemolysis, leading to chronic inflammation and endothelial
dysfunction, causes hyperplasia and hypertrophy of small pulmonary vessels (ie,
vascular remodeling) and increased pulmonary vascular resistance (PVR).

-C/F: exertional dyspnea and signs of RHF (eg, hepatomegaly, edema).

22) Folate deficiency in SCD

-SCD: normally causes normocytic, hemolytic anemia with compensatory reticulocytosis.
-Chronic hemolysis without adequate folic acid intake:
increases the risk for folate deficiency, a macrocytic anemia with an inappropriately low
reticulocyte count.

23) Splenic infarction

-Etiology: usually occurs in the setting of splenic artery (or subbranch) occlusion due to
hypercoagulable states, embolic disease, or hemoglobinopathy (eg, sickle cell disease or
trait).
—> Although patients with sickle cell trait are generally asymptomatic, they occasionally
develop splenic infarction and intravascular hemolysis in the setting of certain stressors
such as air travel or dehydration
436 SEC TION III HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
` 

Platelet disorders All platelet disorders have  bleeding time (BT), mucous membrane bleeding, and
microhemorrhages (eg, petechiae, epistaxis). Platelet count (PC) is usually low, but may be
normal in qualitative disorders.
DISORDER PC BT NOTES
Bernard-Soulier –/  Autosomal recessive defect in adhesion.  GpIb Ž  platelet-to-vWF adhesion.
syndrome Labs: abnormal ristocetin test, large platelets.
Glanzmann –  Autosomal recessive defect in aggregation.  GpIIb/IIIa ( integrin αIIbβ3) Ž 
thrombasthenia platelet-to-platelet aggregation and defective platelet plug formation.
Labs: blood smear shows no platelet clumping.
Immune   Destruction of platelets in spleen. Anti-GpIIb/IIIa antibodies Ž splenic
thrombocytopenia macrophages phagocytose platelets. May be idiopathic or 2° to autoimmune
disorders (eg, SLE), viral illness (eg, HIV, HCV), malignancy (eg, CLL), or
drug reactions.
Labs:  megakaryocytes on bone marrow biopsy,  platelet count.
Treatment: steroids, IVIG, rituximab, TPO receptor agonists (eg, eltrombopag,
romiplostim), or splenectomy for refractory ITP.

Thrombotic Disorders overlap significantly in symptomatology.

microangiopathies
Thrombotic thrombocytopenic purpura Hemolytic-uremic syndrome
EPIDEMIOLOGY Typically females Typically children
PATHOPHYSIOLOGY Inhibition or deficiency of ADAMTS13 (a Commonly caused by Shiga toxin-producing
vWF metalloprotease) Ž  degradation of Escherichia coli (STEC) infection (serotype
vWF multimers Ž  large vWF multimers O157:H7)
Ž  platelet adhesion and aggregation
(microthrombi formation)
PRESENTATION Triad of thrombocytopenia ( platelets), microangiopathic hemolytic anemia ( Hb, schistocytes,
 LDH), acute kidney injury ( Cr)

✓
DIFFERENTIATING SYMPTOMS

LABS
Triad + fever + neurologic symptoms Triad + bloody diarrhea
Normal PT and PTT helps distinguish TTP and HUS (coagulation pathway is not activated) from
DIC (coagulation pathway is activated)
TREATMENT Plasma exchange, steroids, rituximab Supportive care
21) Idiopathic thrombocytopenia purpura
- usually diagnosed after excluding other possible causes of thrombocytopenia.
-All patients with ITP should be tested for hepatitis C and HIV as thrombocytopenia
may be the initial presentation of HIV infection (up to 5%-10% of patients).

#Lab:
• Isolated thrombocytopenia- <1lac; Few platelets (size normal to large) on PS
#Mx:
• Children
◦ Observe if cutaneous symptoms only
◦ Glucocorticoids, IVIG, or anti-D (if Rh + and Coombs -) if bleeding
• Adults -

◦ Observation if cutaneous symptoms AND platelets ≥30,000/mm3

◦ Glucocorticoids, IVIG, or anti-D if bleeding or platelets <30,000/mm3

21) Alcohol causes all types of anemia:

-Macrocytic: Alcohol also directly hastens folate deficiency by reducing folate absorption
in the small intestine
-microcytic anemia : gastritis / bleeding varices (iron deficiency anemia)
- normocytic anemia :direct toxic effects on the bone marrow.

22) Rx of an acute bleed in a patient

with inhibitor development
-bypassing products (eg, recombinant
activated factor 7, activated PCC);

-Adv: such agents work downstream in the

coagulation cascade to promote clotting
- -
without the need for factor VIII.

23) Iron def anemia in elderly taking aspirin:

-NSAIDS are a common cause of iron deficiency anemia, often through chronic blood loss
from the gastrointestinal tract- gastritis, gastric ulcer.
-Iron deficiency anemia should prompt a thorough evaluation for the cause as early low-
grade bleeding can herald later catastrophic hemorrhage.

-Elderly patients often have a low-grade chronic anemia at baseline and may not
tolerate additional blood loss
24) PNH:
-Hemolysis leading to hemoglobinuria
-Cytopenias - fatigue and dyspnea from anemia
-Hypercoagulable state (eg, portal vein thrombosis) - acute abdominal pain that may be
due to severe hemolysis or portal vein thrombosis

25) conjugated capsular Pneumococcal vaccination + penicillin prophylaxis BD until

5 yrs can prevent almost all cases of pneumococcal sepsis in patients with SCD

Common causes of macrocytic 26) Factor V Leiden

anemia* - the MC inherited hypercoagulable disorder in the
• Folate deficiency
Caucasian population—>increased risk of thrombosis.
• Vitamin B12 deficiency
• Myelodysplastic syndromes —> suspect when unprovoked first-time thrombus in
• Acute myeloid leukemias young (age <45) patients or those with an unusual
• Drug-induced (eg, site of thrombus (mesenteric, portal, cerebral vein)
hydroxyurea, zidovudine,
chemotherapy agents)
• Liver disease #Increased prothrombin biosynthesis is from a
• Alcohol abuse
• Hypothyroidism i prothrombin gene mutation, AD—> 2nd-MC inherited
thrombophil
*Mean corpuscular volume >100
µm3.

27) Chronic ITP:

-Most cases of ITP self-resolve within 3 months;
-

-Criteria: however, some patients continue to have platelets <100,000/mm3 for >1 year,
-

#Evaluation:
Chronic ITP evaluation includes bone marrow examination +
- blood tests for infection (eg, HIV, hepatitis C, cytomegalovirus) and autoimmune disorders
(eg, systemic lupus erythematosus, thyroid disease).
#Mx: If laboratory evaluation is negative, management is similar to acute ITP.

28) uremic platelet dysfunction:

-Platelet dysfunction is the MCC of abnormal hemostasis in patients with chronic kidney
disease.
#Dx: PT, PTT, and platelet count are normal. BT: prolonged.
#Rx:
-DDAVP :DOC, *MOA: DDAVP/ vasopressin increases the release of factor VIII:von

-
-

Willebrand factor multimers from endothelial storage sites.

-Platelet transfusion is not indicated because the transfused platelets quickly become
inactive.

-other Rx: cryoppt; conjugated estrogen

.
438 SEC TION III HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PATHOLOGY
` 

Blood transfusion therapy

COMPONENT DOSAGE EFFECT CLINICAL USE
Packed RBCs  Hb and O2 carrying capacity Acute blood loss, severe anemia
Platelets  platelet count ( ∼ 5000/mm3/unit) Stop significant bleeding (thrombocytopenia,
qualitative platelet defects)
Fresh frozen plasma/  coagulation factor levels; FFP contains all Cirrhosis, immediate anticoagulation reversal
prothrombin coagulation factors and plasma proteins; PCC
complex concentrate generally contains factors II, VII, IX, and X, as PCC=VIt K -.
..

well as protein C and S FPP= all

Cryoprecipitate Contains fibrinogen, factor VIII, factor XIII, Coagulation factor deficiencies involving
vWF, and fibronectin fibrinogen and factor VIII
Blood transfusion risks include infection transmission (low), transfusion reactions, iron overload (may lead to 2°
hemochromatosis), hypocalcemia (citrate is a Ca2+ chelator), and hyperkalemia (RBCs may lyse in old blood units).

Leukemia vs lymphoma
Leukemia Lymphoid or myeloid neoplasm with widespread involvement of bone marrow. Tumor cells are
usually found in peripheral blood.
Lymphoma Discrete tumor mass arising from lymph nodes. Variable clinical presentation (eg, arising in
atypical sites, leukemic presentation).

Hodgkin vs Hodgkin Non-Hodgkin

non-Hodgkin Both may present with constitutional (“B”) signs/symptoms: low-grade fever, night sweats, weight
lymphoma loss.
Localized, single group of nodes with Multiple lymph nodes involved; extranodal
contiguous spread (stage is strongest predictor involvement common; noncontiguous spread.
of prognosis). Better prognosis. Worse prognosis.
Characterized by Reed-Sternberg cells. Majority involve B cells; a few are of T-cell
lineage.
Bimodal distribution: young adulthood and Can occur in children and adults.
> 55 years; more common in males except for
nodular sclerosing type.
Associated with EBV. May be associated with autoimmune diseases
and viral infections (eg, HIV, EBV, HTLV).

Hodgkin lymphoma Contains Reed-Sternberg cells: distinctive tumor giant cells; binucleate or bilobed with the 2 halves as
A
mirror images (“owl eyes” A ). RS cells are CD15+ and CD30+ B-cell origin. 2 owl eyes × 15 = 30.
SUBTYPE NOTES

Nodular sclerosis Most common

Lymphocyte rich Best prognosis (the rich have better bank accounts)
Mixed cellularity Eosinophilia; seen in immunocompromised
patients
Lymphocyte depleted Worst prognosis (the poor have worse bank
accounts); seen in immunocompromised patients
 Diamond-Blackfan anemia Vs transient
Pathogenesis • Congenital erythroid aplasia erythrocytopenia of
childhood:

I
• Craniofacial abnormalities
• Triphalangeal thumbs -acquired; onset: 6
Clinical findings • Increased risk of
malignancy mon- 5 yrs
<1 yr -mostly after 1 yr
• Macrocytic anemia
Laboratory • Reticulocytopenia
findings • Normal platelets, white
blood cells
• Corticosteroids
Treatment • Red blood cell
transfusions
30) Pseudothrombocytopenia
- a laboratory error caused by platelet aggregation in vitro. 9
#Mechanism: due to incompletely mixed blood samples / the presence of serum antibodies to
ethylenediaminetetraacetic acid (EDTA), an anticoagulant

#alternative option:
-Drawing blood samples in tubes with a non-EDTA anticoagulant (eg, heparin, sodium citrate)
normalizes the automated platelet count and confirms the diagnosis
.
#Mx: cz it’s not true thrombocytopenia, they do not require intervention / monitoring.

31) Drug-induced hemolytic anemia

# triggered: by penicillin and cephalosporin medications.

#C/F: extravascular hemolytic anemia such as fatigue, weakness, splenomegaly, dark

urine, and jaundice.
#Mx: Discontinuation of the offending drug usually results in complete resolution of
symptoms within days. No additional workup is generally required.

Hemoglobin electrophoresis patterns in sickle cell & beta-thalassemia 32) Thalassemia vs sickle Ds
Condition
Hemoglobi Hemoglobin Hemoglobi Hemoglobi -similarity: HbF rises
nA A2 nF nS
Normal 95%-98% ~2.5% <1% Absent
Beta-thalassemia
-Diff: HbA2 rises in TM
↓ ↑ Near normal Absent
minor HbS rises in SCD
Beta-thalassemia
Absent ↑↑ ↑↑ Absent
major
Sickle cell trait ↓↓ Near normal Near normal ↑
-Drug improving survival:
Sickle cell disease Absent Near normal ↑↑ ↑↑
Hydroxyurea in SCD
Iron chelation in TM
33) CLL
-In an elderly patient, severe lymphocytosis combined with hepatosplenomegaly,
lymphadenopathy, and bicytopenia (anemia, thrombocytopenia) strongly suggests
underlying chronic lymphocytic leukemia (CLL).
Vs
No cytopenia; just LNopathy in lymphomas

#Dx: CLL is diagnosed by flow cytometry (clonality of mature B cells).

Vs
LN biopsy in lymphoma

34) Methemoglobinemia:
-large oxygen saturation gap: pulse oximetry(low original value) -ABG O2 (high false
value)
-blood gas analysis frequently returns a falsely elevated result for oxygen
saturation (eg, 99% in this patient) as it provides an estimate based only on the PaO2 not
effective Hb O2 binding.

-At levels >50%: risk of severe symptoms (eg, altered mental status, seizures, respiratory
depression) and death.

35) Warfarin-induced skin necrosis

-Onset: typically occurs within the first few days of warfarin therapy.
-Pathogenesis: It is caused by a rapid decline in protein C levels, usually in patients with
underlying hereditary protein C deficiency.
-Rx: immediate warfarin cessation and administration of protein C concentrate.
-7
36) autoimmune haemolytic
anemia in leukemia:
IM
-anemia with reticulocytosis
37) NHL In SLE :
-Patients with chronic autoimmune diseases are at increased risk for lymphoproliferative
disorders such as non-Hodgkin lymphoma (NHL) due to
-Pathogenesis:chronic B-cell stimulation,immune dysregulation,immunosuppressant
-C/F: painless lymphadenopathy and B symptoms.

Microcytic/
hypochromic Findings in Iron Studies Management of sickle cell anemia
anemias • Vaccination
Typically depressed serum iron level, • Penicillin (until age 5)
1. Iron-deficiency Mainten • Folic acid supplementation
increased total iron binding capacity
anemia
(TIBC), and decreased serum ferritin level ance • Hydroxyurea (for patients
with recurrent vaso-
Normal to high serum iron and ferritin
2. Thalassemias
levels occlusive crises)
Acute • Hydration
3. Anemia of Below normal TIBC; Normal or increased
chronic disease serum ferritin level pain • Analgesia: opiods, Nsaids
crises • +/- Transfusion
4. Sideroblastic Normal to high serum iron and ferritin
anemia values

40) Fanconi anemia: Rx marrow transplant

• Short stature
• Hypo-/hyperpigmented macules
• Abnormal thumbs
• Genitourinary malformations

5
41) protein gap (difference between total protein and albumin >4 g/dL).
-A protein gap indicates elevated nonalbumin protein in the serum;
-Etiology: polyclonal gammopathies (infection, connective tissue disease) / excessive
monoclonal protein (MM, Waldenström macroglobulinemia).

-Next step:(SPEP) can determine if a protein gap is caused by a monoclonal or polyclonal

source.

42) basophilic stippling:

-Precipitation of ribosomal ribonucleic acid :lead poisoning; sideroblastic anemia
-appears as multiple, scattered, blue granules within the RBC cytoplasm
Vs
#Howell-Jolly bodies :
-nuclear remnants within RBC typically removed by the spleen.
-Their presence strongly suggests asplenia or functional hyposplenism.
 Causes of hemolysis
45) Splenic sequestration crisis
• Microangiopathic hemolytic anemia
Intravasc (eg, disseminated intravascular coagulation)
ular • Transfusion reactions
-C/F: anemia, splenomegaly, and
hemolysi • Infections (eg, clostridial sepsis) hypovolemic shock.
s • Paroxysmal nocturnal hemoglobinuria
• Intravenous Rho(D) immunoglobulin infusion -Rx: focuses on the restoration of
• Intrinsic RBC enzyme deficiencies (eg, G6PD) circulatory volume with IV fluids
• Hemoglobinopathies (eg, sickle cell, and packed RBC transfusion.
thalassemia)
-Splenectomy not 1st line
Extravasc • Membrane defects (eg, hereditary
ular spherocytosis)
hemolysi • Hypersplenism, intravenous immunoglobulin 47) Rx of spherocytosis:
s infusion -FA supplementation
• Warm- or cold-agglutinin autoimmune hemolytic -BT -splenectomy
anemia (most cases)
• Infections (eg, Bartonella, malaria)

48) Nasopharyngeal CA:

• Obstruction: Nasal congestion,
recurrent epistaxis, headache > 3
mon

=
• Mass effect: Cranial nerve palsy,
recurrent serous OM d/t
eustachian tube blockade

• Spread: Neck mass d/t early mets

(cervical LN)
Vs
No Adjacent structure involvement in
nasal polyps

49) The normal BT : 2-7 minutes.

-The normal CT: 8-15 minutes

50) Hodgkin lymphoma

-C/F: common cause of a mediastinal mass that often presents with compressive

-50
symptoms (eg, cough, shortness of breath, retrosternal pain).

-Peripheral lymphadenopathy, B symptoms, pruritus, and alcohol-associated pain

=
- Laboratory : elevated serum LDH and eosinophilia.

-alcohol-induced vasodilation within the lymph nodes, causing capsular distension

 51) inadequate response to EPO in CKD:
-advanced ESRD CKD :a hypoproliferative
(normochromic, normocytic) anemia due to
decreased EPO production by the failing
kidneys.
-goal of erythropoiesis-stimulating agents
(ESAs), such as erythropoietin or
darbepoetin, :Hb 10-11.5 g/dL.

#Case: so if CKD anemia pt develops

hypochromic (low mean corpuscular
hemoglobin concentration) and microcytic
(low mean corpuscular volume) anemia that
has not responded to ESA therapy; suggests
concurrent iron deficiency,
which is the most common cause of inadequate
response to ESAs in patients on dialysis.

#Mechanism behind Fe def:

-Iron stores can be rapidly depleted during hematopoiesis after ESA administration,
especially in chronically ill patients whose iron stores may already be low.

#prevention:
-Iron stores should therefore be evaluated prior to starting ESAs and frequently
thereafter. -Rx of choice for iron deficiency in patients on dialysis : IV iron.

52) Malaria Cx in SCD:

-Nonimmune children are at highest risk of death, but the sickle cell trait confers some
protection from severe complications (does not prevent malaria)

53) Renal involvement in SCD

-Hyposthenuria is the inability of the kidneys to concentrate urine and can occur in
patients with sickle cell disease and sickle cell trait.
- polyuria, low urine specific gravity, and normal serum sodium.

#Pathogenesis
-In response to hypoxic, hyperosmolar conditions of the renal medulla, RBC sickle in the
vasa recta, impairing free water reabsorption and countercurrent exchange. Patients
typically have polyuria and nocturia despite fluid restriction
-Urinary diluting capacity is also intact as it is a function of the superficial loop of
Henle, which is not supplied by the vasa recta.
#Rx:
-Typically, mild hyposthenuria due to SCT requires no treatment.
-In patients with SCD, red blood cell transfusions often improve urine-concentrating
ability and provide relief of symptoms.
54) Most patients with sickle cell trait lead normal, healthy lives.
-Painless hematuria is the most common complication.

55) Acute intermittent porphyria

-should be suspected in patients with sudden-onset abdominal pain, neuropsychiatric
symptoms (eg, neuropathies, anxiety, mood changes, psychosis), and a family history of
similar episodes.

56) Gaucher disease

-cytopenias, bone pain, failure to thrive, and hepatosplenomegaly.
-Presentation ranges from mild to severe, and diagnosis can occur at any age.
Vs
#Acute lymphocytic leukemia
-anemia, thrombocytopenia, bone pain, and hepatosplenomegaly.
*diff:
-However, leukocyte count would be abnormal, lymphadenopathy or fevers are frequently
present, and age at onset is typically younger.

57) Waldenstrom macroglobulinemia (WM)

-hyperviscosity syndrome (diplopia, tinnitus, headache, dilated/segmented funduscopic
findings), neuropathy (electric sensation), evidence of infiltrative disease
(hepatosplenomegaly, anemia, thrombocytopenia), suggesting WM.

-M spike; IgM ab +;; Rx:plasma exchange

58) post splenectomy thrombocytosis

-Because the spleen removes senescent platelets, patients often have dramatic
thrombocytosis (as high as 1,000,000/mm3) following splenectomy.
*Course:
-In most patients, platelet elevations resolve within weeks or months.
-However, a minority will have persistent thrombocytosis for years.
Vs

#Reactive (secondary) thrombocytosis:

caused by cytokines that promote platelet production, is usually driven by an inflammatory
state (eg, infection, recent surgery, malignancy);
*Course:
-once the inflammatory response quells, reactive thrombocytosis should resolve.

59) Iron therapy increases reticulocyte production followed by an increase in hematocrit

and hemoglobin in approximately 1 month.
60) myelodyspLastic syndrome:
-Macrocytic anemia, BM- sideroblastic anemia; but normal B12 and folate

61) hemophilia A: BT normal; just PTT prolonged

Vs
#vwf deficiency: BT and PTT prolonged

62) Polycythymia Vera:

-1st line: Phlebotomy
-2nd line: hydroxyurea

63) extramedullary hematopoesis: erythroid colonies in epidural space and widening of

diploid space on skull

64) Thrombocytopenia in cirrhosis is by hypersplenism as a result of portal hypertension

 Hemat pedia and OBGY
Neonatal polycythemia 1) gestational thrombocytopenia: never <1 lac
• Hematocrit >65% in term -generally mild and does not cause maternal / fetal
Definition
infants
morbidity.

I
• Increased erythropoiesis
from intrauterine hypoxia:
maternal diabetes, -onset: usually arises in the 2nd half of the

I
hypertension, or smoking; pregnancy (not at 10 weeks),
IUGR -

• Erythrocyte transfusion:
-PS: paucity of platelets
Causes
delayed cord clamping; twin-
twin transfusion
• Genetic/metabolic disease: Onset:2-3 month
hypothyroidism or
hyperthyroidism; genetic
trisomy (13, 18, 21)
• Asymptomatic (most
common)
• Ruddy skin
#Below due to reduced organ
Clinical perfusion by viscosity
presentati • Hypoglycemia,

tie
on hyperbilirubinemia
• Respiratory distress,
cyanosis, apnea
• Irritability, jitteriness
• Abdominal distension
• Intravenous fluids
Treatment • Glucose
• Partial exchange transfusion

-After delivery, circulating erythropoietin (EPO) normally decreases due to increased

oxygen concentration in tissue

4) physiological neonatal jaundice:

-Almost all newborns on days 2-4 of life have physiologic jaundice due to indirect
hyperbilirubinemia. -
e
#Pathogenesis
1 At birth, fetal red blood cells (RBCs) are increased (hematocrit 50%-60%) with a
shortened life span (90 days), resulting in high RBC turnover and increased bilirubin
production.

2 Hepatic bilirubin clearance is decreased because uridine diphosphogluconurate

glucuronosyltransferase (UGT) activity does not reach adult levels until age 2 weeks.
This hepatic enzyme conjugates bilirubin, making it soluble (ie, excretable).
-Eastern Asian newborns have decreased UGT compared to that of other ethnicities.

3 Enterohepatic recycling is increased because the low bacterial load in the newborn gut
-
results in slower conversion of bilirubin to urobilinogen for fecal excretion.
 →
-Prognosis: Physiologic jaundice of the newborn is benign and resolves by age 1-2 weeks
.
-Px: Frequent feeding promotes gut colonization and fecal excretion. Phototherapy may be
indicated for rapidly rising levels of bilirubin to prevent kernicterus.

5) Rh incompatibility:
- doesn’t affect Rh neg child

Differential diagnosis of polycythemia

Primary (↓ EPO) Secondary (normal/↑ EPO)
• Polycythemia vera (JAK2 • Hypoxemia
mutation) ◦ Cardiopulmonary disease
• EPO receptor mutations ◦ Obstructive sleep apnea
◦ High altitude
• EPO-producing tumors (renal,
hepatic)
• Congenital (high-affinity
hemoglobin)
• Following renal transplantation
• Androgen supplementation
 Approach to Pancytopenia
Step —1 :
- Reticulocyte count : The major clue is the minimal reticulocyte response despite significant anemia.

Step — 2 :
- Kidney Function : Pancytopenia can be seen in advanced renal disease due to impaired production of
erythropoietin, Serum creatinine makes the diagnosis —> Impaired kidney function will have Elevated
Serum Creatinine.
- With normal kidney function —> reticulocytopenia most likely reflects bone marrow failure due to
hematologic stem cell damage (eg, aplastic anemia) or infiltrative disease (eg, leukemia).

Step — 3 :
E-
- A peripheral blood smear and bone marrow evaluation ,
i) Aplastic anemia : peripheral smear shows a paucity of normal-appearing cells, and bone marrow
evaluation reveals a profoundly hypocellular marrow with an abundance of fat.
ii) Leukemia : blast cells on peripheral smear and bone marrow biopsy

IE
 GIT

Rt shoulder pain : think GB; LfT shoulder pain: spleen, MI

Key idea: Surgical resection is the treatment of choice for virtually all stages of
colorectal cancer, regardless of side (left vs right)

—> Screening colonoscopy is recommended for high-risk patients at age 40 / 10

years before the age of diagnosis in the relative (whichever comes first). Step 3
 GASTROINTESTINAL GASTROINTESTINAL—ANATOMY
`  SEC TION III 367

Liver tissue The functional unit of the liver is made up of Zone I—periportal zone:
architecture hexagonally arranged lobules surrounding the ƒ Affected 1st by viral hepatitis
central vein with portal triads on the edges ƒ Best oxygenated, most resistant to circulatory

=
A
(consisting of a portal vein, hepatic artery, bile compromise
ducts, as well as lymphatics) A . ƒ Ingested toxins (eg, cocaine)
Apical surface of hepatocytes faces bile Zone II—intermediate zone:
canaliculi. Basolateral surface faces sinusoids. ƒ Yellow fever
Kupffer cells (specialized macrophages) located Zone III—pericentral vein (centrilobular) zone:
in sinusoids (black arrows in B ; yellow arrows ƒ Affected 1st by ischemia (least oxygenated)
show hepatic venule) clear bacteria and ƒ High concentration of cytochrome P-450
B damaged or senescent RBCs. ƒ Most sensitive to metabolic toxins (eg,
Hepatic stellate (Ito) cells in space of Disse ethanol, CCl4, halothane, rifampin,
store vitamin A (when quiescent) and produce acetaminophen)
extracellular matrix (when activated). ƒ Site of alcoholic hepatitis
Responsible for hepatic fibrosis.

Blood flow Bile flow

Sinusoids Hepatic vein

Hepatic
vein Endothelial
cells

Stellate cell
Zone 3
Zone 2
Space of Disse
Zone 1

Zone 1

Zone 2 Kupffer cell

Zone 3

Branch of
hepatic artery
Branch of
portal vein
Bile ductule

Portal triad

#Fecal elastase
-a noninvasive test with high Sn and Sp for severe pancreatic exocrine insufficiency.
-Elastase is a proenzyme (zymogen) produced in pancreatic acinar cells and activated by
trypsin in the duodenal lumen;

# —>> In ALF due to acetaminophen toxicity, liver transplantation is firmly indicated in

patients with grade III or IV hepatic encephalopathy, PT >100 seconds, and serum
creatinine >3.4 mg/dL.
 GASTROINTESTINAL GASTROINTESTINAL—PATHOLOGY
`  SEC TION III 395

Wilson disease Also called hepatolenticular degeneration. Autosomal recessive mutations in hepatocyte
A
copper-transporting ATPase (ATP7B gene; chromosome 13) Ž  copper incorporation into
apoceruloplasmin and excretion into bile Ž  serum ceruloplasmin. Copper accumulates,
especially in liver, brain, cornea, kidneys;  urine copper.
Presents before age 40 with liver disease (eg, hepatitis, acute liver failure, cirrhosis), neurologic
disease (eg, dysarthria, dystonia, tremor, parkinsonism), psychiatric disease, Kayser-Fleischer rings
(deposits in Descemet membrane of cornea) A , hemolytic anemia, renal disease (eg, Fanconi
syndrome).
Treatment: chelation with penicillamine or trientine, oral zinc. Liver transplant in acute liver
failure related to Wilson disease.

Hemochromatosis Autosomal recessive. On HFE gene, located on chromosome 6; associated with HLA-A3. Leads
A
to abnormal iron sensing and  intestinal absorption ( ferritin,  iron,  TIBC Ž  transferrin
"

saturation). Iron overload can also be 2° to chronic transfusion therapy (eg, β-thalassemia major).
Iron accumulates, especially in liver, pancreas, skin, heart, pituitary, joints. Hemosiderin (iron)
can be identified on liver MRI or biopsy with Prussian blue stain A .
Presents after age 40 when total body iron > 20 g; iron loss through menstruation slows progression
in women. Classic triad of cirrhosis, diabetes mellitus, skin pigmentation (“bronze diabetes”). Also
causes restrictive cardiomyopathy (classic) or dilated cardiomyopathy (reversible), hypogonadism,
arthropathy (calcium pyrophosphate deposition; especially metacarpophalangeal joints). HCC is
common cause of death.
Treatment: repeated phlebotomy, iron (Fe) chelation with deferasirox, deferoxamine, deferiprone.

Biliary tract disease May present with pruritus, jaundice, dark urine, light-colored stool, hepatosplenomegaly. Typically
with cholestatic pattern of LFTs ( conjugated bilirubin,  cholesterol,  ALP,  GGT).
PATHOLOGY EPIDEMIOLOGY ADDITIONAL FEATURES
Primary sclerosing Unknown cause of concentric Classically in middle-aged men Associated with ulcerative
cholangitis “onion skin” bile duct with ulcerative colitis. colitis. p-ANCA ⊕.  IgM.
fibrosis Ž alternating Can lead to 2° biliary
strictures and dilation with cholangitis.  risk of
“beading” of intra- and cholangiocarcinoma and

÷
extrahepatic bile ducts on gallbladder cancer.
ERCP, magnetic resonance
cholangiopancreatography
(MRCP).
Primary biliary Autoimmune reaction Classically in middle-aged Anti-mitochondrial antibody ⊕,
cholangitis Ž lymphocytic infiltrate #Cx: women.  IgM. Associated with other
+/–  granulomas • Malabsorption, fat-soluble vitamin autoimmune conditions
Ž destruction of lobular bile deficiencies (eg, Hashimoto thyroiditis,
ducts. • Metabolic bone disease rheumatoid arthritis, celiac
(osteoporosis, osteomalacia)
• Cirrhosis disease).
• Hepatocellular carcinoma Treatment: ursodiol.
-

Secondary biliary Extrahepatic biliary obstruction Patients with known May be complicated by
cirrhosis Ž  pressure in intrahepatic obstructive lesions (gallstones, ascending cholangitis.
ducts Ž injury/ fibrosis and biliary strictures, pancreatic
bile stasis. carcinoma).
 GASTROINTESTINAL GASTROINTESTINAL—PATHOLOGY
`  SEC TION III 387

Colonic polyps Growths of tissue within the colon A . Grossly characterized as flat, sessile, or pedunculated on the
basis of protrusion into colonic lumen. Generally classified by histologic type.
HISTOLOGIC TYPE CHARACTERISTICS
Generally non-neoplastic

€ #
Hamartomatous Solitary lesions do not have significant risk of transformation. Growths of normal colonic tissue
polyps with distorted architecture. Associated with Peutz-Jeghers syndrome and juvenile polyposis.
Hyperplastic polyps Most common; generally smaller and predominantly located in rectosigmoid region. Occasionally

Inflammatory
evolves into serrated polyps and more advanced lesions.
Due to mucosal erosion in inflammatory bowel disease.
ca
pseudopolyps
Mucosal polyps Small, usually < 5 mm. Look similar to normal mucosa. Clinically insignificant.
Submucosal polyps May include lipomas, leiomyomas, fibromas, and other lesions.
Malignant potential
Adenomatous polyps Neoplastic, via chromosomal instability pathway with mutations in APC and KRAS. Tubular
B histology has less malignant potential than villous C (“villous histology is villainous”);
tubulovillous has intermediate malignant potential. Usually asymptomatic; may present with
occult bleeding.
Serrated polyps Neoplastic. Characterized by CpG island methylator phenotype (CIMP; cytosine base followed
by guanine, linked by a phosphodiester bond). Defect may silence MMR gene (DNA mismatch

-
-
repair) expression. Mutations lead to microsatellite instability and mutations in BRAF. “Saw-
tooth” pattern of crypts on biopsy. Up.to 20% of cases of sporadic CRC.
A B C

Polyp

Polyp

Cancer

Sessile Pedunculated

Polyposis syndromes
Familial adenomatous Autosomal dominant mutation of APC tumor suppressor gene on chromosome 5q22. 2-hit
polyposis
→
hypothesis. Thousands of polyps arise starting after puberty; pancolonic; always involves rectum.
Prophylactic colectomy or else 100% progress to CRC. -

Gardner syndrome FAP + osseous and soft tissue tumors (eg, osteomas of skull or mandible), congenital hypertrophy of
- =
retinal pigment epithelium, impacted/supernumerary teeth.
Turcot syndrome FAP or Lynch syndrome + malignant CNS tumor (eg, medulloblastoma, glioma). Turcot = Turban.
Peutz-Jeghers Autosomal dominant syndrome featuring numerous hamartomas throughout GI tract, along with

=⇐
syndrome hyperpigmented macules on mouth, lips, hands, genitalia. Associated with  risk of breast and GI
cancers (eg, colorectal, stomach, small bowel, pancreatic).
Juvenile polyposis Autosomal dominant syndrome in children (typically < 5 years old) featuring numerous
syndrome hamartomatous polyps in the colon, stomach, small bowel. Associated with  risk of CRC.
 # approach to cirrhosis:

-MCC of cirrhosis in the

United States:
Viral hepatitis, chronic
alcohol abuse, nonalcoholic
fatty liver disease, and
hemochromatosis

-The initial evaluation :

consists of obtaining a
medical history, including
Rx: ursodiol inquiring about medications,
social habits (eg, alcohol
use, drug use, high-risk
sexual activity), and family
history (eg, to exclude
hemochromatosis).

#Pathogenesis of Cirrhosis :
- characterized by progressive liver fibrosis, which results in the formation of a high-
resistance system (ie, portal hypertension). This results in the following alterations:

1 Nitric oxide and other vasodilatory factors are formed, possibly from bacterial
products (eg, endotoxin) that accumulate due to the reduced host defenses (eg,
impaired reticuloendothelial function) and increased portosystemic shunting (eg,
decreased toxin clearance) seen with cirrhosis.

2 Splanchnic vasodilation occurs as a result, leading to significantly decreased

systemic vascular resistance (SVR) and a compensatory increase in heart rate and
cardiac output (hyperdynamic circulation).

3 The (RAAS) is activated and antidiuretic hormone is released to maintain renal

perfusion, leading to retention of sodium and water.

**Somatostatin analogs such as octreotide are a mainstay in management of

variceal bleeding only not other causes
 AST and ALT —> distributed widely throughout the body,
1) AST present and very active in the liver, heart, kidney, and skeletal
muscle.
2) ALT is also present in reduced quantities in the kidney, heart, and
skeletal muscle, it is predominantly found in the liver and is therefore more
specific for hepatocyte injury.

Pt with mild (< 250 U/L) & asymptomatic elevation of AST & ALT

1st step :
- screening for all hepatitis risk factors,
AST / ALT 1) drug and alcohol intake,
Elevation 2) travel outside the United States,
3) blood transfusions, or
Evaluation 4) high-risk sexual practices.

provide insight as to whether transaminase elevation could be caused by

1) alcohol,

2) medications (eg, NSAIDs, antibiotics, HMG-CoA reductase inhibitors, antiepileptic drugs,

antituberculous drugs, herbal preparations),

3) viral agents.

2nd Step ,
- After thoroughly questioning the patient about his history and
- having him discontinue all alcohol and drug use —>
repeat the liver function tests.

—> If the transaminases elevated > 6 minths — chronic

Testing for viral hepatitis B and C, hemochromatosis, and fatty

liver should then be undertaken to further evaluate chronically
elevated transaminases.

3rd Step ,
If these tests prove unremarkable, Ix for
1) muscle disorders (eg, polymyositis) and
2) thyroid disease
 382 SEC TION III GASTROINTESTINAL GASTROINTESTINAL—PATHOLOGY
` 

Inflammatory bowel diseases

Crohn disease Ulcerative colitis
LOCATION Any portion of the GI tract, usually the terminal Colitis = colon inflammation. Continuous
ileum and colon. Skip lesions, rectal sparing. colonic lesions, always with rectal involvement.
GROSS MORPHOLOGY Transmural inflammation Ž fistulas. Mucosal and submucosal inflammation only.
Cobblestone mucosa, creeping fat, bowel wall Friable mucosa with superficial and/or
thickening (“string sign” on barium swallow deep ulcerations (compare normal B with
x-ray A ), linear ulcers, fissures. diseased C ). Loss of haustra Ž “lead pipe”
appearance on imaging.
MICROSCOPIC MORPHOLOGY Noncaseating granulomas and lymphoid Crypt abscesses and ulcers, bleeding, no
aggregates. Th1 mediated. granulomas. Th2 mediated.
COMPLICATIONS Malabsorption/malnutrition, colorectal cancer ( risk with pancolitis).
Fistulas (eg, enterovesical fistulae, which can
cause recurrent UTI and pneumaturia),
-
Fulminant colitis, toxic megacolon, perforation.

=
phlegmon/abscess, strictures (causing
obstruction), perianal disease.
INTESTINAL MANIFESTATION Diarrhea that may or may not be bloody. Bloody diarrhea.
EXTRAINTESTINAL MANIFESTATIONS Rash (pyoderma gangrenosum, erythema nodosum), eye inflammation (episcleritis, uveitis), oral
ulcerations (aphthous stomatitis), arthritis (peripheral, spondylitis).
Kidney stones (usually calcium oxalate), 1° sclerosing cholangitis. Associated with
gallstones. May be ⊕ for anti-Saccharomyces p-ANCA.
cerevisiae antibodies (ASCA).
TREATMENT Corticosteroids, azathioprine, antibiotics (eg, 5-aminosalicylic preparations (eg, mesalamine),
-
ciprofloxacin, metronidazole), biologics (eg, 6-mercaptopurine, infliximab, colectomy.
-
infliximab, adalimumab).
For Crohn, think of a fat granny and an old Ulcerative colitis causes ULCCCERS:
crone skipping down a cobblestone road away Ulcers
from the wreck (rectal sparing). Large intestine
Stones are more common in Crohns. Continuous, Colorectal carcinoma, Crypt
abscesses
Extends proximally
Red diarrhea
Sclerosing cholangitis
A B C
Normal

#Mx:
-Dx: Endoscopic evaluation (eg, colonoscopy) distinguishing them from each other.
#Initial management of both CD and UC :5-aminosalicylic acids+ corticosteroids.
-Maintenance therapy for : azathioprine / antitumor necrosis factors.
 GIT diagnosis of choice
1) Acute diverticulitis: CT scan with contrast ( high Sn and Sp)

Diverticular bleeding: colonoscopy/ tagged RBC scan

-Avoid: Barium, sigmoido/ colonoscopy in diverticulitis due to the risk for perforation

2) Small bowel follow-through

-is performed by giving oral contrast to the patient and using fluoroscopy to follow the contrast into the
small bowel.

- indication: diagnosing small bowel pathology

(eg, stricture, obstruction, masses)

3) Esophageal dysphagia and excluding CA: upper endoscopy

Staging: PET/ CT

4) Esophageal motility disorder: Esophageal manometry

5) GERD with red flag signs: upper endoscopy

6) Psoas abscess: CT scan;

USG less sensitive as abscess is deep in pelvis

7) Acute appendicitis:
-Healthy, non pregnant adult: CT scan even if alvarado>4 to reduce the NaR rates
(nothing on pathology)

- pregnancy, Children. USG/ MRI

8) Gastroparesis: Nuclear gastric emptying scan

9) Acute Cholangitis: USG

10) Cholecystitis: USG 1st choice
-HIDA scan 2nd choice if
. . usg findings are equivocal

29) malrotation: NG tube displaced—> upper GIT series with barium swallow

30) Pyloric stenosis: USG: elongated thickened pylorus

31) Meckels diverticulum: Meckle scan

32) Malignant biliary obstruction: 1st line- USG/CT

. 2nd line- MR cholangiopancreatogram/
. ER cholangiopancreatogram

33) Pyogenic liver abscess: CT scan

34) splenic abscess: CT scan
#Emphysematous cholecystitis: 1st line: CT ( high sn in delineating air fluid structures)
. USG poor sn in differentiating airfluid

-5=3
11) Pancreatic Cancer Head(Jaundice): USG: 1st line
CT scan: 2nd line
ERCP: 3rd line
Percutaneous transhepatic cholangiogram: 4th line

*Tail and body (no juandice): CT scan

12) Gastric cancer: Initial: Esophagoduodenoscopy

. Later stage for Mets: CT scan

13) Mesenteric ischaemia: CT /MR angiogram 1st line

. Mesenteric angiography 2nd line
=
14) Hiatus hernia. Barium swallow (high Sn)

Ear
15) Achalasia . Barium swallow (initial)
. Manometry (definitive)

16) zenkers diverticulum. Swallow with contrast esophagography

17) H pylori. Endoscopy (gold standard)

.
18) Ischaemic colitis. Urgent CT scan

19) Esophageal rupture. Esophagography with water soluble contrast

20) Duodenal hematoma.

- O
CT scan

21) Biliary colic. USG for GB stones; vitals, LFT, WBC- normal

22) acute pancreatitis: CT scan

GB stone pancreatitis: USG; 2nd line: ERCP
Chronic Pancreatitis: CT scan

23) Biliary atresia. Intraoperative cholangiogram (gold standard)

Liver biopsy

#Biliary cyst: 1st line: USG

. ERCP if obstruction suspected

24) HCC.
⇐ Triple phase CT scan

25) Mallory weiss: Endoscopy: tear/ gastritits -

26) borhaeve/ Esophageal rupture: CT/ esophagography with water contrast

27) Intussusception: USG: target sign and immediate air enema to reduce bowel ow
28) meconium ileus nd hirshprung: abd Xray —> contrast enema
 Case clue. GIT surg
1) For patients with PAT, any of the following is
an indication for immediate exploratory
laparotomy:

• Evidence of ongoing hemorrhage:

hemodynamic instability (systolic blood
pressure <90 mm Hg) or frank blood in the
nasogastric tube or rectum
• Peritonitis (eg, rigidity, rebound
tenderness)
• Evisceration (ie, externally exposed
CT, local wound exploration, FAST intestines)
• Impalement (ie, penetrating object still in
situ)

= -

2) factitious diarrhea:
-Diarrhea that is not explained after extensive evaluation suggests possible factitious
diarrhea.
-Dx:
a) stool osmolality (hypoosmolality suggests addition of water or dilute fluid;
hyperosmolality suggests addition of concentrated fluid [eg, urine]),
b) stool electrolytes (elevated magnesium or phosphate suggests use of saline
osmotic laxatives), and
c)stool osmotic gap: Osmotic laxatives (eg, lactulose, polyethylene glycol) cause a high
osmotic gap diarrhea, whereas senna and bisacodyl produce a low osmotic gap secretory
diarrhea.
3) Splenic Infarction :
-C/F: pain and tenderness LUQ; fever, nausea, splenomegaly,leukocytosis

#Etio: Thrombosis :cancer,[SLE], [APLAS]);

-Embolism due to atrial fibrillation, endocarditis, or atheroma;
-Hemoglobinopathy (eg, sickle cell disease)
IgE- & non–IgE-mediated food allergies
Clinical
Example Age Symptom onset
features
• Urticaria
Immediate
IgE mediated Anaphylaxis Any • Vomiting, wheezing
(<1 hr)
• Angioedema, hypotension
Food protein–
• Painless, bloody stools
induced allergic <6 months Insidious
• Well appearing
proctocolitis
Non–IgE
mediated Food protein–
• Profuse vomiting,
induced
<12 months Within hours diarrhea (± blood),
enterocolitis
dehydration
syndrome

4) malrotation with midgut volvulus:

• Abdominal x-ray: ± dilated bowel, air-fluid levels, pneumoperitoneum
• Upper gastrointestinal series (gold standard): ligament of Treitz on right; corkscrew,
or bird's-beak, duodenum

#C/F:
-Presentation in infants is typically acute and includes signs of small bowel obstruction,
such as bilious emesis, absent bowel sounds, and abdominal distension and
tenderness.
-Hypovolemic and/or septic shock can also occur

5) Hirschsprung disease
-Classic rectal examination: an expulsion of stool or gas ("squirt sign") due to
temporary relief of the distal obstruction.
-Additional findings : abdominal distension and tenderness and thin caliber stools due to
failure of the distal colon to relax, refractory constipation

-Dx:Rectal suction biopsy (gold standard); Anorectal manometry, contrast enema

(adjuncts)

6) Toxic megacolon: diffuse dilation of colon in its normal anatomic position

Vs Volvulus: only a loop of bowel dilated and twisted away from its normal position

7) Bilary cyst:
#Classic triad* in children/adults: Abdominal pain; RUQ mass; Jaundice
#Mx: cyst resection to dec risk of malignancy (cholangiocarcinoma)
8) Rectus sheath hematomas
-C/F: acute abdominal pain with a palpable abdominal wall mass lateral to umblicus,
associated with anemia by blood loss and leukocytosis.

-RF:due to rupture of the inferior epigastric artery from blunt trauma or forceful
abdominal contractions (eg, severe coughing), particularly in those receiving
anticoagulation therapy.

#Mx:
a) Hemodynamically stable: serial monitoring of CBC, reverse anticoagulation and
transfuse blood products when appropriate
b) Unstable: angiography with embolization, surgical ligation

9) esophageal perforation:
-Etiology: Instrumentation (eg, endoscopy), trauma; Effort rupture (Boerhaave syndrome);
Esophagitis (infectious/pills/caustic)
-C/F: Chest/back &/or epigastric pain, systemic signs (eg, fever); Crepitus, Hamman
sign (crunching sound on auscultation);
-Pleural effusion with atypical (eg, green) fluid
-Dx: esophagography/ CT with water contrast

Vs
Pancreatitis: foll ERCP; amylase rich ; epigastric pain; x chest pain

10) Types of perforation:

1) acutely:during rapid compression of the GI tract that causes high intraluminal pressure)
or
2)delayed fashion (eg, several hours to days following trauma):
• Bowel contusion (eg, thickened [edematous] proximal small bowel on initial CT scan)
In
progressing to full-thickness injury
.

• Injured mesenteric vasculature (eg, mesenteric hematoma on initial CT scan)

=
progressing to ischemia and necrosis .

* Mx of delayed perforation:
-However, an extended period of observation should be considered due to the risk of
progression to perforation—> immediate Sx
11) Retroperitoneal tear:
- delayed presentation(1 day after trauma) as retroperitoneum GIT spillage is
sequestered by peritoneum
-classic back/ flank pain
#organs causing retroperitoneal tear:
1)Duodenum perforation: free air in retroperitoneum
Vs
2) kidney, pancreas perforation : by fluid spillage- free fluid in retroperitoneum

Vs
Peritoneal perforation: air in peritoneum; immediate Sx
Retroperitoneal abdominal organs
12) hiatus hernia : retrocardiac air-fluid level
• Suprarenal (adrenal) glands Mx of Sliding hernia:
• Aorta & inferior vena cava

=
• Duodenum* (except 1st part)
-asymptomatic patients: no further evaluation beyond
• Pancreas* (head & body) observation.
• Ureters -reflux Sx :should be medically managed (eg, PPI).
• Colon* (ascending & descending) -refractory GERD symptoms :can be considered for antireflux
• Kidneys surgery (eg, Nissen fundoplication)
• Esophagus
• Rectum (mid-distal)
Mnemonic: SAD PUCKER
a) symptomatic sliding hernias : medical
treatment of reflux symptoms,
*Secondarily retroperitoneal (developed
intraperitoneal & migrated retroperitoneal). b) PEHs : require surgical repair.
13) sequence of Mx in variceal bleeding: :
1) Catheters
-2 large-bore catheters, crystalloid solution has been administered for volume resuscitation,
-packed red blood cell transfusion (which is indicated, despite a hemoglobin >7 g/dL, due to
ongoing hemodynamic instability)

2) Intubation in upper gastrointestinal bleeding who have a depressed level of consciousness +

ongoing hematemesis to protect the airway as part of initial stabilization and resuscitation prior to 3

3) Prompt endoscopic(<12 hrs) treatment with ligation / sclerotherapy should then be

performed to stop the bleeding.
-Nasogastric tube placement may help decompress the stomach and facilitate in the removal of
blood for improved visualization prior to endoscopy.

4) For SBP:
-receive prophylactic antibiotics to prevent spontaneous bacterial peritonitis.
-Diagnostic paracentesis could be considered at a later point to evaluate for spontaneous bacterial
peritonitis, which can be a complicating factor in patients with cirrhosis and gastrointestinal
hemorrhage.

5) somatostatin analog (eg, octreotide) to reduce variceal hemorrhage and improve hemostasis.
14) SBO:
-C/F: nausea, vomiting, abdominal bloating, and dilated loops of bowel on abdominal x-
ray.
-Etiology:Adhesions, typically postoperative, are the MCC
Incarceration is MCC in Pre existing femoral hernia

it

6 monthly
-

Radiation proctitis exclude if later than 1 yr

Acute radiation
Chronic radiation proctitis
proctitis
Postradiation
• ≤8 weeks • >3 months to years
onset
• Obliterative endarteritis &
• Direct mucosal
Pathogenesis chronic mucosal ischemia
damage
• Submucosal fibrosis
• Diarrhea, mucus • Severe bleeding
Manifestations discharge, tenesmus • ± Strictures with
• Minimal bleeding constipation & rectal pain
Endoscopic • Severe erythema • Multiple telangiectasias
appearance • Edema, ulcerations • Mucosal pallor & friability
26) D/D liver abscess
• Endoscopic thermal
• Antidiarrheals (eg,
coagulation 1) Pyogenic liver abscess: fever,
Management loperamide)
• Butyrate enemas
• Sucralfate or WBC raise, RUQ pain, sterile
glucocorticoid enemas
pleural effusion, jaundice +
2) amoebic liver abscess: H/O: biliary tree, DM, pancreatic
- fever, RUQ pain, jaundice rare Ds.
-Travel to developing country, H/O prior diarrhoea
-No eosinophilia; cyst> on right side due to greater portal blood supply to right

#Diagnosis : CT , Mx: blood cultures, Ab, aspiration, and drainage.

Vs
-Echinococcus granulosus: Cysts on a CT scan - thin-walled, septated lesions,
occasionally with calcification.
18) pilonidal sinus:
-fluctuant mass 4-5 cm cephalad to the anus in the intergluteal region with associated
mucoid, purulent, or bloody drainage.
-Trigger: worsened by activities that stretch the overlying skin (eg, bending down).
Vs
#perianal abscess : fever, malaise, anal pain, and a tender, erythematous bulge at the
anal verge.

19) Gastric outlet obstruction

-C/F: intractable nausea and vomiting, early satiety, and weight loss, succusion splash
#Etio: peptic ulcer disease, bezoar, gastric polyps),
-up to 80% of cases occur due to malignancy, MC pancreatic adenocarcinoma with
gastric or duodenal invasion; bezoars; post acid ingestion stricture;

20) Abdominal malignancies (eg, stomach, pancreas, colon, ovaries)

can spread via the thoracic duct to the left supraclavicular lymph nodes (Virchow node)
—an ominous sign.

21) Postcholecystectomy syndrome

-C/F: persistent abdominal pain or dyspepsia either postoperatively (early) / months
to years (late) after cholecystectomy.

-Etiologies : biliary (eg, retained common bile duct, cystic duct stone) /
extra-biliary (eg, pancreatitis, peptic ulcer disease) /sod causes.

-Ix: Abdominal imaging (eg, ultrasound) followed by direct visualization (eg, ERCP,
MRCP) can establish the diagnosis and guide therapy toward the causative factor.

-elevated ALP, mildly abnormal serum aminotransferases, and dilated common bile
duct on abdominal ultrasound
#Rx: ERCP with sphincterotomy

22) differentiate abdominal compartment vs shock/Cardiac cause:

1) abdominal compartment:
-compression of IVC by abdomen increases pressure ( CVP) but restricts vena cava
blood flow and decreases venous return to the heart (ie, cardiac preload).

2) hypovolemic Shock:
-reduced cardiac preload is typically reflected in a low CVP
-but CVP and Preload moves in opposite direction in compartment.
23) Abdominal compartment syndrome
#RF:Massive fluid resuscitation (eg, trauma, sepsis)
◦ Major intraabdominal surgery or pathology (eg, pancreatitis)
◦ Intraabdominal fluid collections (eg, bleeding, ascites)

#C/F: -Tense, distended abdomen

• ↑ ventilatory requirements
• ↑ CVP (venous compression but ↓ venous return & cardiac preload)
• Hypotension, tachycardia; ↓ urine output (↓ intraabdominal organ perfusion)

24) pancreatic cysts:

-Most pancreatic cysts are benign and can be managed conservatively (eg, surveillance
imaging);

#cyst with high risk for malignancy:

• Large size (≥3 cm)
-

• Solid components or calcifications

• Main pancreatic duct involvement (ie, ductal dilation) we
• Thickened or irregular cyst wall

-requires further evaluation to rule out malignancy. Endoscopic ultrasound (EUS)–

guided biopsy is a minimally invasive approach to tissue sampling;
-Rx: surgical resection (without prior biopsy) may be considered for very high-risk
lesions.

25) Post-ERCP complications

- postprocedural abdominal pain is relatively common and may be due to infection (eg,
ascending cholangitis), perforation, or pancreatitis.
-The m/c complication is post-ERCP pancreatitis, which occurs in up to 10% of
patients and is particularly prevalent in those with SOD.

26) small intestinal bacterial overgrowth (SIBO).

-abdominal bloating, steatorrhea (elevated fecal fat), and macrocytic anemia In the
setting of a Roux-en-Y gastric bypass

27) Roux-en-Y gastric bypass Stomal stenosis Cx:

-results from a narrowing of the gastrojejunal anastomosis GJ

-C/F: nausea, postprandial vomiting, gastroesophageal reflux, and dysphagia.

-Mx: Esophagogastroduodenoscopy is used for both diagnosis and treatment.
 Dumping Syndrome Vs SIBO
- Both are complication of gastric bypass

1) Dumping syndrome (DS)

# Pathogenesis:
-when high-carbohydrate foods are rapidly emptied into the small bowel, leading
to osmotically driven fluid shifts from the plasma to the intestine.
#C/F:
- Although patients have abdominal pain and diarrhea soon (<30 min) after meals,
the fluid shifts result in sympathetic activation, leading to tachycardia,
diaphoresis, and flushing. Hypoglycemia may also occur.

—> DS is not associated with steatorrhea or vitamin B12 deficiency (ie,

macrocytic anemia).

2) Small intestinal bacterial overgrowth (SIBO)

# Pathogenesis: The proximal small intestine normally contains minimal bacterial

colonization due to gastric acidity and peristalsis;
-however, gastric bypass procedures result in a blind loop of intestine that
allows for excessive bacterial growth.

#C/F: bloating, flatulence, and watery diarrhea; malabsorption and nutritional

deficiencies may also occur.
 #Case: SIBO by non surgical case
-K/C/O DM and on opioids 66-year-old woman comes to the office due to bloating,
flatulence, and abdominal discomfort for the past 6 months. The patient has mild,
intermittent, crampy abdominal pain that is unrelated to eating and does not improve after
defecation.
-She also has 2 or 3 loose, watery bowel movements daily.
-rest all negative H/O.
#Case discussion:
-This patient with uncontrolled diabetes and opiate use has bloating, abdominal pain,
loose stools, and a positive glucose breath test; this presentation suggests small
intestinal bacterial overgrowth (SIBO).

#Pathogenesis:
-SIBO results when bacteria originating from the colon grow in excess in the small bowel
.
#Etiology:
*Surgical cause:
-surgery involving the ileocecal valve.

*Nonsurgical cause:
- It can develop in patients with altered small bowel motility (eg, uncontrolled diabetes
mellitus, chronic opiate use, scleroderma)
-Other predisposing conditions : small intestinal diverticula, chronic pancreatitis, and
gastric hypochlorhydria (eg, chronic proton pump inhibitor use).

#C/F:
-Patients typically have mild abdominal pain, bloating, flatulence, and watery diarrhea.

IT
may be elevated due to bacterial production of the nutrient. .
C
-Vitamin B12 deficiency is common due to bacterial consumption; however, folate levels

#Dx: The gold standard for diagnosis is a jejunal aspiration demonstrating a high bacterial
concentration (eg, >103 colony-forming units/mL); however, this test is invasive and not
easily performed.

**Clue:
-SIBO is more commonly diagnosed by a carbohydrate breath test using either glucose
or lactulose.
-Patients with SIBO have an earlier peak in breath hydrogen/methane (due to
carbohydrate
-
metabolism by bacteria in the small intestine) compared to those without
SIBO (in whom carbohydrate metabolism primarily occurs in the colon).
-

wa
#Rx: oral antibiotics (eg, rifaximin, neomycin) to reduce bacterial load.
28) Angiodysplasia:
-episodes of maroon colored painless bleed; often missed on colonoscopy as AV
_
malformation is behind haustral fold
-association: AS, VwF deficiency ,CKD
#Mx: Asymptomatic patients do not require treatment.
-Those with anemia or bleeding can be treated with cautery.
29) complicated SBO
- increased risk of impending
ischemia, strangulation, and
necrosis
—>warranting emergency
abdominal exploration.

/proctoscopy #Signs:
-changes in the character of the pain,
fever, hemodynamic instability
1st (hypotension, tachycardia), guarding,
Unless normal leukocytosis, and significant
colonoscopy before 2-3 yrs
metabolic acidosis (low bicarbonate).

29) Approach to blood PR:

-Minimal rectal bleeding is usually due to hemorrhoids or other benign conditions.
Evaluation depends on the patient's presentation and risk factors.
-Patients >50 or with features suggesting malignancy should undergo colonoscopy.
-younger patients (age <40) and no other RF, office-based anoscopy first.

30) Pernicious anemia

-Over time, the atrophic gastric mucosa undergoes intestinal-type metaplasia, which
dramatically increases the risk of gastric cancer.
-Therefore, patients with pernicious anemia require esophagogastroduodenoscopy at
initial diagnosis and with any suspicious symptoms (eg, positive fecal occult blood
test, mid-epigastric abdominal pain).

31) appendiceal abscess:

-Patients who present with appendicitis >5 days after the onset of symptoms have a
high incidence of perforation with abscess formation. /contained abscess.
#Mx:
-If the patients are otherwise stable, they may be treated with IV hydration, antibiotics,
bowel rest, and interval appendectomy-return in 6-8 weeks on an elective basis

32) pathologies with eggshell calcification:

-Hydatid cyst, porcelain GB
33) New IDA in elderly patients
- should be considered to be from (GI) blood loss (eg, polyps, cancer, angiodysplasia)
until proven otherwise
-The next step in evaluation would be colonoscopy and endoscopy.
-A single negative occult blood test does not exclude the possibility of GIT bleeding.

34) normal liver span (eg, 6-12 cm at midclavicular line)

35) Duodenal Hematoma:

-delayed presentation after BAT
-C/F: upper GIT obstruction with bilious emesiss
-CT: homogenous density (ie, coagulated blood) within the C-shaped duodenum.
- Xray: gastric dilation with scant distal gas

36) Intussusception
#C/F:
- presents in children age 6-36 months has episodes of inconsolable crying, with legs
drawn to the abdomen due to pain, followed by asymptomatic periods.

-Emesis may follow episodes of abdominal pain and is initially nonbilious but may
become bilious as the obstruction persists.
-palpable as a sausage-shaped abdominal mass.

-Cx: Ongoing obstruction can also compromise circulation, causing mucosal ischemia,
occult bleeding, and, if untreated, grossly bloody currant jelly stools.

#Mx:
-A target sign on ultrasound should prompt reduction with air or water-soluble contrast
enema.
* Indication of Laparotomy
-if enema reduction is ineffective/ if a pathological lead point is identified/ if the patient has
signs of perforation (eg, free air on x-ray, rigid abdomen)

37) Rx of bacterial pyogenic liver abscess: IV Ab+ percutaneous aspiration / drainage

Vs
Amoebic liver abscess: tissue agent (metronidazole, tinidazole) followed by paromomycin
to eradicate intestinal colonization.

Dx: E histolytica serology (liver abscess)

Vs Stool ova & parasites, stool antigen testing (colitis)
38) post op ileus:
-Some degree of ileus occurs following most abdominal procedures; however, persistence
of the signs and symptoms (>3-5 days postoperatively) is termed prolonged (or

=
"pathologic") postoperative ileus (PPI).

#Pathogenesis:
-increased splanchnic nerve sympathetic tone. following peritoneal instrumentation, local
release of inflammatory mediators, and postoperative opiate analgesic use (which
causes decreased gastrointestinal motility and disordered peristalsis).

#Prevention:
-epidural anesthesia, minimally invasive surgery, and judicious perioperative use of
intravenous fluids (to minimize gastrointestinal edema).

-PPI onset: continuation of post op normal ileus; hours to days after OT

Vs
Mechanical bowel obstruction by adhesions: Sx develop after normal return of bowel
function following OT
39) free perforation of the GIT in the
setting of ongoing inflammation (eg,
diverticulitis) often have a classic pain
sequence:
• Moment of perforation: sudden, severe
pain (± vomiting, lightheadedness or
syncope)
• After perforation to 2 hours: temporary
relief or decreased pain as the inflamed
organ decompresses

L .
• >2 hours after perforation: generalized,
constant pain due to peritonitis (± sepsis/
septic shock)
40) Rx of acute cholangitis
-Aggressive IV volume resuscitation should be administered, and blood cultures
should be collected, followed immediately by empiric antibiotic offering broad coverage
of enteric organisms (eg, piperacillin/tazobactam, ciprofloxacin with metronidazole).

-Definitive treatment : biliary drainage (eg, gallstone removal, stent placement),

which is best accomplished by (ERCP) within 24-48 hours or more urgently in
severe cases.

-Eventual cholecystectomy :indicated with acute cholangitis due to gallstone disease.

-However, cholecystectomy is not a priority at this time and does not address the acute
infection in the biliary tract.
 41) Colonic ischaemia:
-trigger: follows an episode of
hypotension

-Sites: arterial watershed areas at

the splenic flexure and rectosigmoid
junction.
#Ix:
-CT scan: Colonic wall thickening, fat
stranding
-Endoscopy: Edematous & friable
mucosa
#Mx:
• Intravenous fluids & bowel rest
• Antibiotics with enteric coverage
• Colonic resection if necrosis
develops

Eradication of H pylori causes remission in some patients with gastric MALT lymphoma, but it
is not curative for adenocarcinoma.

42) Mx of diverticulitis:
-Diverticulitis can be classified as uncomplicated (75%) or complicated (25%).
1) Uncomplicated diverticulitis in stable patients
-managed in the outpatient setting with bowel rest, oral antibiotics, and observation

#indication of hospitalization and IV antibiotics : for patients with uncomplicated

diverticulitis who are elderly, immunosuppressed, have high fever or significant
leukocytosis, or have significant comorbidities

2) Complicated diverticulitis :
-diverticulitis associated with an abscess, perforation, obstruction, or fistula formation.

For management of diverticulitis complicated by abscess:

a) A fluid collection <3 cm: intravenous antibiotics and observation, with surgery
reserved for patients with worsening symptoms.

b)A fluid collection ≥3 cm: antibiotics and have CT-guided percutaneous drainage.
-If the symptoms are not controlled (eg, within a few days), surgical drainage and
debridement are recommended

—> Sigmoid resection is generally reserved for patients with fistulas, perforation with
peritonitis, obstruction, or recurrent attacks of diverticulitis
 I
43) emphysematous cholecystitis vs simple cholecystitis:
-unlike simple cholecystitis this neeeds emergency cholecystectomy.
-

-USG less sensitive in delineating air fluid levels so CT scan its first line.
-unlike other cholecystitis this has indirect hyperbilirubinaemia due to bacterial exotoxin
induced haemolysis

-causative organism: E. coli and clostridium; so Rx with Piptaz

- = .

44) Mx of Achalasia:
-1st line: Laparoscopic myotomy and pneumatic balloon dilation
-2nd line: Options for patients at high surgical risk : botulinum toxin injection, nitrates, CCB

45) Gallstone ileus

- As the stone advances it may cause "tumbling" obstruction (stuttering Sx) before
ultimately causing complete obstruction (SBO signs) .
#most imp RF: cholecystitis
#Treatment : surgical removal of the stone and cholecystectomy.
—>> Emphysematous Cholecystitis : More of Liver , GB & Systemic fxs; Ileus
—>> Gallstone ileus : More of SBO fxs
46) Mx of hemorrhoids:
-Initial management of uncomplicated hemorrhoids : increased intake of fluid and fiber,
reduction of fat and alcohol intake, and regular exercise.

-Additional measures : phlebotonics, topical hydrocortisone, astringents, and local

anesthetics.
-Sx: Rubber band ligation and surgical hemorrhoidectomy : only for patients with
refractory symptoms or prolapsed hemorrhoids that cannot be reduced manually.

47) atraumatic splenic rupture:

-C/F: acute abdominal pain, shock, and anemia (big clue)
-Peritonitis and left shoulder pain may also be present.
#Etio:
• Hematologic malignancy (eg, leukemia, lymphoma)
• Infection (eg, CMV, EBV, malaria)

I
• Inflammatory disease (eg, SLE, pancreatitis)
• Splenic congestion (eg, cirrhosis, pregnancy)
• Medications (eg, anticoagulation, G-CSF)

48) CT of pseudomembranous colitis: thickened colon with contrast trapped between

haustral folds.
48) ALF :
-defined as severe acute liver injury without underlying liver disease and is characterized
by elevated aminotransferases (often >1,000 U/L), hepatic encephalopathy, and
synthetic liver dysfunction (defined as prolonged prothrombin time [PT] with INR
>1.5).

#Prognostic indicators :
-rising serum bilirubin and PT.
-degree of hepatic encephalopathy as grade III hepatic encephalopathy (characterized
by marked confusion and incoherence) is associated with an only 40%-50% chance of
spontaneous recovery.

#MCC of death: Cerebral edema

-Rx: liver transplantation

49) Anastomotic leak

-C/F: a serious postoperative complication that can present with fever, abdominal pain,
tachypnea, and tachycardia, usually within the first week after bariatric surgery.

#diagnosis : oral contrast–enhanced imaging abdominal CT scan/upper GIT series); Rx:

urgent surgical repair.

50) Infected pancreatic necrosis

- suspected in patients who develop worsening abdominal pain, unstable vital signs, or
signs (eg, fever, leukocytosis) of infection 7-10 days after onset of acute necrotizing
pancreatitis.
-CT abdomen : gas within the pancreatic necrotic collection is diagnostic.

-Mx: IV ab; Débridement (eg, endoscopic, surgical) is often required but is ideally delayed
until the patient has stabilized on antibiotic therapy and the necrotic collection has become
encapsulated (ie, walled off), which facilitates débridement.

51) Pancreatic pseudocyst

- Diagnosis: CT
#Mx:
-Expectant management : minimal / no symptoms and without complications.
-Endoscopic drainage: patients with significant symptoms (eg, abdominal pain, vomiting),
infected pseudocyst, or evidence of pseudoaneurysm.
#Cx:
-spontaneous infection, duodenal or biliary obstruction, pseudoaneurysm (due to digestion
of adjacent vessels), pancreatic ascites, and pleural effusion
52) Role of Ab in anal crypt gland abscess:
-Systemic antibiotic therapy, which may decrease recurrence and anorectal fistula
formation, should be given to patients with high-risk features (eg, systemic illness,
diabetes) and considered for all patients.

53) Succusion splash:

-Retained gastric material >3 hours after a meal will generate a splash sound and indicates
-

the presence of a hollow viscus filled with both fluid and gas.

54) D/D of chronic GERD with new onset dysphagia and disappearance of reflux:
a) Strictures
-typically cause slowly progressive dysphagia to solid foods without anorexia or weight
loss.
-As they progress, they can actually block reflux, leading to improvement of heartburn
symptom

**Strictures tend to appear as symmetric, circumferential narrowing : barium swallow.

-Mx: Nonetheless, in any case of stricture in the setting of Barrett's esophagus, biopsy is
necessary to rule out adenocarcinoma

Vs
b) Adenocarcinoma
-typically occurs in patients who have had GERD symptoms for >20 years.

** Barium swallow :asymmetric narrowing of the esophageal lumen.

55) when to suspect pathological lead point in intusussception

• Recurrent intussusception
• Atypical age for intussusception (not between 6-36 month)
• Atypical location of intussusception (eg, small bowel into small bowel)
• Persistent rectal bleeding despite reduction of intussusception

#Mx:
-The next step :a Meckel scan, a study using 99m technetium pertechnetate to detect
gastric mucosa, which is often present in a Meckel diverticulum.

-CT scan of the abdomen may also be considered if there is high suspicion for a lead point
not detected by other imaging modalities (eg, ultrasound).
56) autoimmune metaplastic atrophic gastritis (AMAG)
-Because AMAG is associated with an increased risk for gastric adenocarcinoma and
neuroendocrine tumors==> routine surveillance endoscopy is indicated.

÷
57) Thrombosed external hemorrhoids
-purple or blue anal bulges below the dentate line and may cause severe pain.
#Mx:
-Although conservative management (eg, fiber, stool softeners, topical anti-inflammatories
and antispasmodics) is usually indicated,
-patients with severe pain should undergo hemorrhoidectomy under local anesthesia.

58) acalculous cholecystitis

-RF: This condition is most often seen in severely ill patients in the ICU with multiorgan
failure, severe trauma, surgery, burns, sepsis, or prolonged parenteral nutrition.

#Pathogenesis
-Acalculous cholecystitis is likely due to cholestasis and gallbladder ischemia leading
to secondary infection by enteric organisms —> resultant edema and necrosis of GB.
-Most patients affected by this condition have no prior history of gallbladder disease.

#Dx:
-Radiologic signs : GB wall thickening and distension and the presence of pericholecystic
fluid.
#Mx:
-antibiotics followed by percutaneous cholecystostomy under radiologic guidance
followed by Cholecystectomy with drainage once the patient's condition improves.

60) Key idea: Indications for surgery in setting of acute diverticulitis

(1) Emergency operation (peritonitis, abscess, etc.) (2) Any patient who has survived 2
episodes of acute diverticulitis should have elective removal of affected area to prevent
recurrence

61) Mx of Fetal impaction causing fecal incontinence:

-managed with manual rectal disimpaction followed by enemas to clear the bowels.
-Once complete emptying has been achieved, the patient should increase fiber and fluid
intake as well as start an aggressive bowel regimen to prevent recurrence.

62) Mx of unresectable pancreatic cancer:

-Endoscopic stent placement: can effectively relieve CBD obstruction in most patients
and is less invasive and less risky than surgery.
-Surgical bypass (eg, anastomosis between the gallbladder or CBD and jejunum): is
sometimes considered as a second-line option in patients in whom stent placement would
be technically challenges
#Mx of SBO: Old free 120:
• Key idea: Most patients with small bowel obstruction can be managed conservatively with nasogastric decompression + fluids +
NPO
• Common causes of SBO: Adhesions, hernias, malignancy, IBD (Crohn’s), gallstone ileus
• Key idea: If a patient with an SBO has changes in character of pain, fever, hemodynamic instability, peritoneal signs or
leukocytosis/acidosis, those are signs that they may have a complicated SBO –> Urgent surgical laparotomy

63) Mx of FNH
-FNH is more common in women than men. It may
be estrogen sensitive, and patients on oral
contraceptives tend to have larger and more vascular
lesions.
-FNH is generally stable and does not normally result
in complications.
-Management : conservative; some providers advise
women to discontinue use of oral contraceptives and
offer serial examinations for patients with larger
masses (>8 cm).
MRI FNH

64) Hemobilia Cms

-A liver injury from penetrating trauma can disrupt normal hepatic parenchyma and stroma,
including bile ducts, hepatic arteries and veins, and the portal veins.
-If a drain is not placed into the liver during repair, hematomas can accumulate or drain into
the biliary system, and ongoing bleeding may not be immediately detected.

—>Blood in the duodenum without a clear source in the setting of a liver injury is
consistent with a diagnosis of hematobilia, in which blood from a hepatic source drains into
the biliary tree and through the sphincter of Oddi into the duodenum.

65) Amboss: H/P of GERD

-hyperemia of the distal third of the esophagus and the biopsy showing nonkeratinized
stratified squamous epithelium with hyperplasia of the basal cell layer and
neutrophilic inflammatory infiltrates, is consistent with GERD.

66) acute postoperative hepatitis is highly suggestive of halothane hepatitis.

-Halothane hepatitis commonly leads to elevated serum aminotransferases, elevated
bilirubin, eosinophilia, and slightly elevated alkaline phosphatase
-onset:(2 days to 3 weeks) post op

-Liver biopsy: not necessary for diagnosis but typically shows massive centrilobular hepatic
necrosis.
 GIT Pedia /obs
1) Biliary atresia
- fibrotic obliteration of extrahepatic bile duct, intrahepatic bile duct proliferation
-C/F: presents at age 2-8 weeks with direct hyperbilirubinemia (eg, jaundice, acholic
stools, dark urine).

#Liver biopsy should be performed in all patients because a delay (beyond age 8 weeks)
-

in diagnosis and surgical intervention for BA is associated with a higher risk of liver
transplantation and mortality

#Rx:Surgical hepatoportoenterostomy (Kasai procedure); Liver transplant

2) #D/D of hepatocellular pattern of LFT in pregnancy?

-The differential for abnormal liver enzymes in pregnant patients is broad and includes
1) diseases specific to pregnancy (eg, preeclampsia, acute fatty liver of pregnancy)
2) those that affect the general population (eg, viral hepatitis, autoimmune hepatitis).

3) Mx of cyclic vomiting syndrome:

-Rx : abortive (eg, triptans) and/or supportive (eg, antiemetics, rehydration)
# Prognosis: most children have gradual resolution of sx during adolescence.
#Key historical features: H/O identifiable triggers (eg, stress, infection) or a personal/
family history of migraines.

4) High levels of progesterone during pregnancy typically cause slowed colonic motility,
resulting in constipation.
-The presence of diarrhea should prompt consideration of other etiologies such as IBS.

-2 .

ng

-
5) Intrahepatic cholestasis of pregnancy
-C/F: pruritus that is worse on the hands and feet in 3rd TM
-Fetal Cx: IUFD,preterm,NRDS; meconium aspiration

=
-Lab: elevated total bile acids (≥10 µmol/L),
—> The risk of (IUFD) is high when s.BA ≥100 µmol/L.
#Rx: Ursodeoxycholic acid; Antihistamines; Delivery at 37 weeks gestation
.

6) Food protein–induced allergic proctocolitis

- a common, benign reaction to proteins (eg, cow's milk casein;whey; soy) in breast milk or
formula.
-C/F: a well-appearing infant with painless, bloody stools+/- eczema after 1-4 wks
-Pathogenesis: Non–IgE-mediated reaction; Eosinophilic inflammation of rectosigmoid
colon
-Mx: hydrolysed formula

7) Symptomatic cholelithiasis in pregnancy

#Mx:
• Conservative because most cases resolve with supportive care (eg, pain control).
• Cholecystectomy is usually delayed until the postpartum period.
• Cholecystectomy (for complicated, recurrent cases)

8) Gastric cancer
- common in those from Eastern Asia, Eastern Europe, and South America.
-C/F: progressive epigastric pain and weight loss. Friable tumor vessels can bleed into the
stomach lumen, leading to iron deficiency anemia.
-Metastasis to the liver : hepatomegaly and elevated transaminases and ALP

9) gastroschisis
-Elevated maternal serum(AFP) because AFP passes through the exposed bowel wall into
the amniotic fluid+ free-floating intestines on prenatal ultrasound
#Consequences:
-continued exposure of the intestines to amniotic fluid causes chronic inflammation and
edema, resulting in intestinal thickening—> increases the risk of necrotizing enterocolitis
and bowel obstruction, —> lead to short bowel syndrome.

-Nutrients are also lost across the exposed bowel, which can result in FGR and
oligohydramnios

#Mx: sterile saline dressings and plastic wrap immediately after delivery to minimize
insensible heat and fluid losses
-defect is repaired surgically.
10) Duodenal atresia,
-fetal ultrasound as a fluid-filled stomach and duodenum (ie, double bubble sign) with
associated polyhydramnios.
**Mx: surgical repair is urgent not Karyotype to diagnose Down

#Association:
-Because it is commonly seen in Down syndrome and VACTERL (Vertebral, Anal atresia,
Cardiac, Tracheoesophageal fistula, Esophageal atresia, Renal, Limb) association, the
presence of duodenal atresia requires evaluation for other fetal malformations (eg,
ventricular septal defects).

11) Pyloric stenosis:

-hydration and electrolyte before pylorotomy

12 Mx of congenital umbilical hernia:

-Association: hypothyroidism and Ehlers-Danlos, Beckwith-Wiedemann, and Down
syndromes/ normal
#Mx:
a) Small umbilical hernias
-typically close spontaneously as the rectus abdominis muscles grow together and fascial
layers fuse.

b) large (>1.5
-
cm diameter) hernias or in patients with underlying medical problems:
-Spontaneous closure is less likely

-Indication of Surgery : recommended around age 5 for persistent hernias, / sooner if

complications occur.
Vs
# Acquired hernia: Abdominal ultrasound is often performed in an older child or adult when
an acquired umbilical hernia is suspected.

13) Gastroschisis vs omphalocele:

-gastroschisis: an naked intestinal protrusion lateral to the umbilicus
vs omphalocele: a covered protrusion of abdominal contents.
#Mx: Immediate surgery is performed for both unlike congenital umbilical hernia

14) umbilical granuloma

-presents in newborns after the umbilical cord has separated with a moist, red,
pedunculated, friable umbilical mass. #Rx :silver nitrate.
15) jejunal atresia:
#Pathogenesis:
-Atresia of the jejunum or ileum is thought to occur due to a vascular accident in utero

=
that causes necrosis and resorption of the fetal intestine, leaving behind blind proximal and
distal ends of intestine.

#RF: poor fetal gut perfusion from maternal use of vasoconstrictive medications or
substances such as cocaine and tobacco.
Vs
In contrast to duodenal atresia, jejunal and ileal atresia are not associated with
chromosomal abnormalities.

#Dx: A triple bubble sign and gasless colon on abdominal x-ray (above) reflects gas
trapping in the stomach, duodenum, and jejunum.

#Rx: resuscitation and stabilization of the patient, followed by surgical correction.

#Prognosis: depends on the length of affected bowel as well as the patient's gestational
age and birth weight.

In esophagus: u do Xray Non Ig E

But not in trachea mediated
# not beyond
1 yrs

-
-

-
→
18) Approach to painless blood streaked stool in well kid <6 mon :
-2 MCC: anal fissure / food protein–induced allergic proctocolitis (FPIAP).
-Next step:
a normal rectal examination, history of loose stools (as opposed to constipation), and
presence of mucus in the stool make FPIAP the most likely diagnosis.
Vs

# Meckles diverticulum:
-Although painless, bloody stools are classic in older children, symptoms at age <6 months
are exceedingly rare ; mostly at 2
-usually are related to associated complications, such as intestinal obstruction causing
ill appearance, vomiting, and abdominal distension.

19) Acute appendicitis in pregnancy

-may have an atypical presentation (eg, right mid-to-upper quadrant or flank pain) due to
displacement of the appendix by the uterus.
-Cx: This can result in delayed diagnosis and increased risk for complications (eg,
appendiceal rupture, fetal demise).

#Mx: immediate surgery.

20)Necrotizing enterocolitis:
-Intestinal inflammation and necrosis cause feeding intolerance (eg, gastric residuals,
bilious emesis), a tender and distended abdomen, and gastrointestinal (GI) bleeding (eg,
hematochezia, hematemesis)
#Mx:
-Discontinuation of enteral feeds; Nasogastric decompression; Blood cultures & empiric
antibiotics; IV fluid repletion
21) diaphragmatic hernia.
-Cxray : chest tubes (shown in
green) are in place;
-confirm by CT
-however, the nasogastric tube
(shown in blue), correctly
positioned along the greater
curvature of the stomach, is
located abnormally in the left
hemithorax. CLUE

-1st step in Mx of congenital diaphragmatic hernia : endotracheal intubation &

mechanical ventilation
-A gastric tube should also be placed immediately to decompress the stomach and bowel.
-Bag-and-mask ventilation can exacerbate respiratory decline and should be avoided.
22) Screening in TEF
-Because TEF with EA often occurs with VACTERL association (Vertebral, Anal, Cardiac,
TracheoEsophageal fistula, Renal, and/or Limb anomalies),
—> all patients who have TEF with EA should undergo screening echocardiography
and renal ultrasonography.
Gastrointestinal obstruction in the neonate
Key features Imaging
• Delayed passage of
Contrast enema: transition
meconium, abdominal
zone between distal
Hirschsprung distension
narrow aganglionic
disease • Forceful expulsion of
segment & proximal
gas/stool on rectal
dilated bowel
examination
• Delayed passage of
meconium, abdominal
Meconium Contrast enema:
distension
ileus microcolon
• Associated with cystic
fibrosis
• Bilious emesis &
Intestinal • X-ray: double bubble
abdominal distension
atresia sign (duodenal atresia)
within days of birth
• Bilious emesis & • Upper GI: right-sided
Malrotation abdominal distension ligament of Treitz,
with volvulus (any age, usually age <4 corkscrew-shaped
weeks) duodenum
• Age 3-5 weeks
Pyloric
• Nonbilious projectile • Ultrasound: hypertrophy
stenosis
vomiting after feeds

Infant constipation
Functional Pathologic causes
• Introduction of solid • Down syndrome
foods • Abnormal physical findings
Risk factors
• ↓ Water intake (eg, displaced anus, tuft at
• ↓ Fiber diet gluteal cleft)
• Delayed passage of
• Infrequent defecation meconium
• Hard, painful stools • Fever or vomiting
Clinical
• Large-caliber or • Ribbon stools
features
pellet-like stools • Poor growth
• ± Anal fissure • Severe abdominal
distension
• Workup for serious organic
• Add undigestable, cause
osmotically active • Hirschsprung disease
Management carbohydrate (eg, (barium enema)
prune or apple juice/ • Cystic fibrosis (sweat
puree) chloride test)
• Spinal dysraphism (MRI)
 GIT medicine
1) screening guidelines in FAP
*Starting age:
-annual screening sigmoidoscopies for children starting at age 10-12, —>
followed by annual colonoscopies once colorectal adenomas are detected / if the
patient is age >50.

*Attenuated FAP:
-delayed start of screening (age 25) and longer screening intervals (1-2 years).

# Indication for Proctocolectomy:

-who initially present with CRC or adenomas with high-grade dysplasia.
-severe symptoms from colonic neoplasia (eg, hemorrhage)
- significant increase in polyp number during the screening interval.

-In patients with classic FAP who do not have any of the above findings, surgery does not
need to be performed urgently and may be delayed until early twenties

2) UC:
#extracolonic manifestations: erythema nodosum and pyoderma gangrenosum,
episcleritis, spondyloarthritis, and 1o sclerosing cholangitis (elevated ALP raises
suspicion; no need of routine Surveillance)
-Colonic Cx: Toxic megacolon; CRC

4) Pancreatic cancer
-The most common symptom of pancreatic cancer is insidious, continuous midepigastric
pain that often radiates to the flanks or back and is sometimes worse with eating and lying
down.
-CT scan : first-line test for suspected pancreatic cancer.

5)) chronic mesenteric ischemia

#C/F: usually presents with severe pain with eating (intestinal angina) and food
aversion, wt loss
-However, the pain is generally intermittent.
-H/O : atherosclerosis +
#Diagnosis :CT angiography (which is noninvasive) rather than mesenteric angiography
(an invasive procedure).
6) Pancreatic cancer: Head vs tail CA presentation
1) tumors in the head of the pancreas: associated with obstructive jaundice (CBD
obstruction), steatorrhea, and epigastric pain; non tender distended GB Dx: USG
-CT: double duct sign dilation of both the intra- and extrahepatic bile ducts as well as the
=
-
pancreatic duct (ie, double duct sign).

2) tumors in the body or tail of the pancreas

-progressive, constant back pain that is worse at night when lying supine.
-normal spine and neural exam; next step:CT

7) Celiac Ds:
#Extra intestinal features: can be solely +
•General: failure to thrive/weight loss, short stature,* delayed puberty/menarche*
• Oral: enamel hypoplasia, atrophic glossitis
• Dermatologic: dermatitis herpetiformis
• Hematologic: iron deficiency anemia (due to malabsorption)
• Neuropsychiatric: peripheral neuropathy, mood disorders (eg, anxiety, depression)
• Musculoskeletal: arthritis, osteomalacia/rickets* (due to vitamin D malabsorption),

#Dx: •Screening Test : ↑ Tissue transglutaminase IgA antibody

I
• Dx confirmation test : Proximal intestinal biopsy (villous atrophy, crypt hyperplasia,
intraepithelial lymphocytosis)

8) IgA negative celiac Ds:

-due to an associated selective IgA deficiency, which is common in celiac disease.
*how to confirm in that case?
-If IgA serology is negative but the suspicion for celiac disease is high, total IgA should
be measured (or IgG-based serologic testing should be done).

11) Mx of ascites:
• 1st line: Spironolactone
• 2nd line: furosemide usually avoided in cirrhosis because it is less effective in this
population and predisposes to electrolyte wasting.
 -

• #NONPHARMAC ADVISE:
• Alcohol abstinence: cessation improves portal hypertension and decreases ascites.
• sodium restriction: fluid restriction is not indicated in patients with normal sodium
levels
• Avoid ACE inhibitors, angiotensin receptor blockers, NSAIDs

# Refractory ascites:
-• Large-volume paracentesis
• Transjugular intrahepatic portosystemic shunt: refractory ascites or esophageal varices
who have failed endoscopic or medical management.
# Y ACEI avoided in cirrhosis.??
-Patients with cirrhosis have low mean arterial pressure due to splanchnic vasodilation
and are dependent on the renin-angiotensin-aldosterone system to help normalize blood
pressure and renal perfusion.
- ACE inhibitors blunt this critical response and promote organ hypoperfusion

12) cirrhosis Ascitic fluid characteristic:

-yellowish or straw-colored; low total protein (<2.5 g/dL)
-high serum-ascites albumin gradient (≥1.1).
-Cell count and differential should be obtained to rule out spontaneous bacterial
peritonitis (ie, neutrophil count ≥250/mm3) so done in all Pt
13) Management of gallstones 14) Ascites fluid characteristics
• No treatment • Bloody: trauma, malignancy, TB (rarely)
Gallstones without
required in most • Milky: chylous
symptoms Color
patients • Turbid: possible infection
• Elective laparoscopic • Straw color: likely more benign causes
-
cholecystectomy Neutrop • ≥250/mm3: peritonitis (secondary or
Gallstones with
• Possible hils spontaneous bacterial)
typical biliary colic
symptoms MD
ursodeoxycholic acid
in poor surgical
.
• ≥2.5 g/dL (high-protein ascites)
candidates ◦ CHF, constrictive pericarditis, peritoneal
Total carcinomatosis, TB, Budd-Chiari syndrome,
Complicated • Cholecystectomy protein fungal
gallstone disease* within
-
72 hr • <2.5 g/dL (low-protein ascites)
*Acute cholecystitis, choledocholithiasis, ◦ Cirrhosis, nephrotic syndrome
= -
gallstone pancreatitis.
. • ≥1.1 g/dL (indicates portal hypertension)
-
◦ Cardiac ascites, cirrhosis, Budd-Chiari
-Symptoms often subside within a few syndrome -
SAAG
days with volume resuscitation, • <1.1 g/dL (absence of portal hypertension)
antibiotics, and pain medications. ◦ TB, peritoneal carcinomatosis, pancreatic
ascites, nephrotic syndrome

-early cholecystectomy (within 72 #Pathophysiology in portal hypertension

hours) reduces disease duration, (cirrhosis):
duration of hospitalization, and with increased hydrostatic pressure within
mortality when compared to delayed hepatic capillary beds.
cholecystectomy (>7 days after
hospitalization)
==> Cell count and differential are also performed in all patients to rule out spontaneous
bacterial peritonitis, a life-threatening infection of the ascitic fluid.
-Peritonitis symptoms usually include fever, abdominal pain, and mental status changes;
however, findings may be subtle in early infection.

Miscellaneous ascitic fluid tests

(perform when clinically indicated) KIT pla
• ↑ In biliary or bowel
Bilirubin
perforation
• ↓ In infection, malignancy,
Glucose
bowel perforation
Lactate • ↑ In infection, malignancy,

⇐=
dehydrogenase bowel perforation
Amylase • ↑ In pancreatic ascites

Triglycerides • ↑ In chylous ascites

Cytology • Suspected malignant ascites
Gram stain and
• Suspected bacterial peritonitis
culture

Pneumobilia with gallstone ileus

 Modified Alvarado score
Points
15) appendicitis evaluation:
(each)
Clinical feature
-The evaluation of patients with suspected appendicitis (eg,
• Migratory RLQ pain modified Alvarado score ≥4) now includes imaging, which can
• Anorexia
• Nausea or vomiting visualize the appendix (eg, normal vs nonperforated or
1
• Fever >37.5 C (>99.5 F) perforated appendicitis) before OT.
• RLQ rebound
tenderness
• RLQ tenderness —> CT scan of the abdomen and pelvis is the recommended
2 • Leukocytes >10,000/
mm3 imaging study in nonpregnant adults.
9 Total possible score -USG/MRI for children/ pregnancy
0-3: Appendicitis unlikely.
≥4: Evaluate for appendicitis.
RLQ = right lower quadrant.

Risk factors

17) GB stone site difference:

a) CBC obstruction with stone / CA :
- normally cause obstructive jaundice +
very high alkaline phosphatase
levels.
Vs
b) stone in cystic duct:
-Acute cholecystitis usually presents
IV PPI with sudden onset of RUQ pain,
fever, vomiting, and leukocytosis.

18) Alarm features of IBS:

• Older age of onset (≥50)
• Gastrointestinal bleeding
• Nocturnal diarrhea
• Worsening pain
• Unintended weight loss

=
• Iron deficiency anemia
• Elevated CRP
• + fecal lactoferrin or calprotectin
• F/H/O: early colon cancer or IBD

19) Hereditary hemochromatosis

-extreme hyperferritinemia (eg, serum ferritin >1000 ng/mL) must not wait for
genetic testing results before receiving urgent phlebotomy

-because they are at exceptionally high risk for immediate and irreversible end-organ
damage (eg, cardiomyopathy, cirrhosis, arthritis, diabetes).
 20) Dyspepsia
#Rome III criteria:> 1 required
- post prandial fullness
-early satiety
-epigastric pain/ burning
#Mx:
= -Dx:Biopsy of the gastric
☐ antrum during
endoscopy
• Age ≥60: Upper
endoscopy
- • Age <60:
◦Testing and
treatment for H
pylori
- ◦Upper endoscopy
in high-risk
patients (eg, overt
= GI bleeding,
significant weight
loss, >1 alarm
symptom)
21) Dumping syndrome
- a common postgastrectomy complication characterized by GIT (eg, nausea, diarrhea,
abdominal cramps) + vasomotor (eg, palpitations, diaphoresis) symptoms.
#Timing: 15-30 minutes after meals
#Rx: Replace simple sugars with complex carbohydrates; Incorporate high-fiber &
protein-rich foods

22) acute pancreatitis:

-Pancreatic enzymes are more specific > CT imaging

# which pancreatic enzyme is > specific ???

-Amylase rises within 6-12 hours of Sx onset and may remain elevated for 3-5 days.
-Lipase rises within 4-8 hours of Sx onset but remains elevated longer than amylase (8-14
days).
— > As a result, lipase is more useful and sensitive than amylase for diagnosis

23) Hemobilia (bleeding into the biliary tract):

-Etiology: usually occurs as a complication of hepatic or biliopancreatic interventions (eg,
liver biopsy, cholecystectomy, ERCP
-C/F: presents with RUQ pain, jaundice, and upper GIT bleeding post procedure
#Types:
a) early: Massive hemobilia results in hemodynamic instability and occurs immediately after
the procedure;
b) intraductal hematoma :delayed UGIB until after dissolution of the clot (usually ~5 days
post-procedure).
24) Chemotherapy-related diarrhea
-C/F: voluminous, watery, brown stool that persists despite periods of fasting (eg,
nocturnal diarrhea).
-Evaluation : CBC, serum chemistry, and stool studies (eg, Clostridioides difficile, fecal
occult blood) to rule out other etiologies.
-Rx: oral hydration and antidiarrheal medications (eg, loperamide).

25) clostridium difficle in UC:

-CDI is typically marked by watery stools (≥3 episodes in 24 hours) with no frank
blood or melena
Vs
#ulcerative colitis: small-volume bloody stools

= -

- -

26) porcelain GB:

Caused by calcification from GB stones associated with adenoca
Vs
Echinococcus cyst: cyst within liver associated with anaphylaxis

27) Gallstone pancreatitis

- most likely if pt does not use alcohol, takes no medications, has normal triglyceride and
calcium levels, and has had no recent major illness.

-Other clues: high BMI, alanine aminotransferase >150 U/L, and elevated alkaline
phosphatase also suggest gallstone pancreatitis.

#Dx:
-1st line: USG: most accurate
-2nd line: If the USG nondiagnostic, (ERCP) may be performed to better visualize the
biliary tree.
28) colorectal CA RF:
a) type 2 diabetes
- risk for CRC, especially early-onset (ie, age <50) cancer,
- Hyperinsulinemia results in increased circulating levels of insulin-like growth factor-1,
which inhibits colorectal epithelial cell apoptosis and promotes neoplastic progression.
b) obesity
- associated with increased expression of inflammatory cytokines (eg, tumor necrosis
factor-alpha), which may promote development

C) exposure to a abdominopelvic radiation: associated with a significant risk of developing

colon adenocarcinoma- estimated risk >4 times higher than that of the general population.

29) D/D of GIT conditions causing Pallor +microcytic, hypochromic anemia:

1) colon (eg, malignancy, polyps): Colonoscopy
2) upper GI tract (eg, peptic ulcer): upper endoscopy
3) less commonly, the small bowel (eg, angiodysplasia).
4) small bowel evaluation (eg, video capsule endoscopy, deep enteroscopy) may be
required if initial tests are unrevealing.
Next step: FOBT; if + colonoscopy; else endoscopy; if both -; then 3

30)Biliary colic:
-Mechanism: when the gallbladder contracts against a gallstone (or sludge) that is
temporarily blocking the cystic duct.

-C/F: dull postprandial right upper quadrant (RUQ) or epigastric pain that worsens over an
hour after meal and subsides with gallbladder relaxation.
-Nausea, vomiting, and diaphoresis may occur;

—> however, vital signs, white blood cell count, and liver function tests (LFTs)
should remain normal.(diff clue)
Vs

31) Acute cholecystitis:

-a common complication of gallstone disease, can occur with complete obstruction of the
cystic duct.
#Diff point:
-In contrast to biliary colic, acute cholecystitis typically presents with severe, unremitting
RUQ pain and signs of systemic illness (eg, fever, tachycardia, leukocytosis).
-LFTs typically remain normal,
Vs

LFT elevations should raise suspicion for biliary obstruction (eg,

choledocholithiasis, cholangitis).

#Characteristic USG of cholecystitis:GB wall thickening, edema & pericholecystic fluid.

 Severe acute pancreatitis 32) IBD surveillance
Definitio
• Acute pancreatitis with >/1organ failure (eg, -Diagnosing IBD and distinguishing
respiratory, cardiovascular, renal) persisting >48
n
hr
between CD and UC requires
colonoscopy with biopsies.
• Patient factors:
◦ Older age (eg, age >55)
◦ Comorbidities, including obesity (BMI >30 kg/m2) -An elevated fecal calprotectin
• Clinical findings: would not distinguish between CD
◦ Altered mental status
◦ SIRS (eg, leukocytes >12,000/mm3, temperature
and UC
Predicto >38 C [100.4 F])
rs • Laboratory findings of intravascular volume depletion:
◦ ↑ BUN (>20 mg/dL) and/or ↑ creatinine (>1.8 mg/
dL)
◦ ↑ HCT (>44%)
• Radiologic findings:
◦ CXR: pulmonary infiltrates, pleural effusions
◦ Abdominal CT scan: severe pancreatic necrosis

33) Management of MALT :

-All patients with MALT lymphomas should be tested for H pylori infection
1) patients with a positive result who have earlystage MALT lymphoma
-should undergo H pylori eradication therapy (eg, quadruple therapy).
-The majority of patients achieve complete remission with antibiotic treatment.

2) more advanced malignancies or with H pylori-negative tumors

-should be considered for radiation therapy, immunotherapy (eg, rituximab), or single-agent
chemotherapy.
34) Management of chronic liver disease
-involves both treatment of the underlying

E-
cause and strategies to prevent further liver
damage (eg, alcohol avoidance, hepatitis
A and hepatitis B vaccination).

e. 35) Parinaud syndrome

-occurs in pinealomas
-C/F: limitation of upward gaze, bilateral
eyelid retraction, and light-near
dissociation, ataxia , nystagmus

-Pineal gland tumors can also cause

persistent headache and vomiting due to
obstructive hydrocephalus.
36) Acute colonic pseudoobstruction (Ogilvie syndrome)
#C/F: Abdominal distension, pain, obstipation, vomiting
#Dx: X-ray: colonic dilation (predominantly affecting the proximal colon), normal
haustra, nondilated small bowel without anatomic obstruction

#Mx: -NPO, nasogastric/rectal tube for colonic decompression

• Neostigmine if no improvement within 48 hr/ or if the cecal diameter on imaging
exceeds 12 cm (which is a strong predictor of impending perforation)

38) Diverticulosis and lower GIT bleeds

- the MCC of gross lower gastrointestinal bleeding in adults.
-C/F: Bleeding is typically painless but may be associated with lightheadedness and
hemodynamic instability.

#Mx: Diverticular hemorrhage usually resolves spontaneously but occasionally requires

endoscopic or surgical intervention.
—>Diverticulosis is most common in the sigmoid colon, but diverticular bleeding is
more common in the right colon.
Vs
#bleeding due to angiodysplasia is usually venous, it is typically low-volume, whereas
diverticulosis can cause large-volume arterial hemorrhage.
Vs -
#it would be unusual for hemorrhoids to cause massive lower GI bleeding (eg,
hypotension, lightheadedness).

39) Acute cholangitis :

-RUQ pain, fever, jaundice, hypotension, and altered mental status: Reynolds pentad
Vs no jaundice and no abnormal LfT in cholecystitis

-Pathogenesis: an infection of the extrahepatic biliary system that usually occurs due to
biliary obstruction (eg, bile stone, malignancy, stricture), which predisposes patients to
bacterial invasion of the normally sterile biliary tree

-ultrasound or CT scan : dilation of the intrahepatic and common bile duct.

-Lab: direct hyperbilirubinemia, elevated ALP, and elevated GGT

-
O
-Mx: Antibiotic coverage of enteric bacteria; Biliary drainage by ERCP within 24-48 hr
-
40) primary sclerosing cholangitis (PSC).
-In a young adult male with a H/O hematochezia (IBD)+ recurrent acute cholangitis
#Dx:
-may have normal USG because intrahepatic bile ducts are not easily visible.
-MRCP overcomes this limitation and is the preferred test to confirm the diagnosis

41) Role of alcohol abstinence in cirrhosis:

-In patients with alcoholic cirrhosis, cessation of alcohol use can reduce liver
inflammation, fibrogenesis, and portal pressure, which can lead to the resolution of
ascites and, ultimately, improved survival.

42) hypotension in pancreatitis:

-Acute pancreatitis complicated by hypotension is thought to arise from intravascular
volume loss secondary to local and systemic vascular endothelial injury.
-This causes vasodilation, increased vascular permeability, and plasma leak into the
retroperitoneum, resulting in systemic hypotension.
43) elevated conjugated (direct)
hyperbilirubinemia +elevated ALP:

-cholestasis pattern in the setting of

extrahepatic / intrahepatic biliary
obstruction.
—>a) The next appropriate step in
management for patients with
predominantly cholestatic pattern is to
obtain an abdominal ultrasound to
assess hepatic parenchyma and
biliary ducts.
=
—> biliary dilatation :extrahepatic
cholestasis;

the absence of biliary dilatation :

intrahepatic cholestasis.
b) 2nd step: Then do anti mitochondrial
ab test
 44) NAFLD:
#Dx: ± Steatohepatitis (AST/ALT ratio <1); Hyperechoic texture on USG; macrovesicular
steatosis
#Pathogenesis:
-due to increased transport of free fatty acids (FFA) from adipose tissue to the liver,
decreased oxidation of FFA in the liver, or decreased clearance of FFA from the liver (due to
decreased VLDL production

45) malignant potential of polyps:

• Predominance of villous features (long glands on histologic examination), particularly in
the presence of high-grade dysplasia
• Large size (eg, >1 cm)

-sessile polyps
-
• High number (eg, >3 concurrent adenomas)

46) Stool osmotic gap Stool is normally nearly isoosmolar with the serum (usually ~290
290 mOsm/kg − 2 x (stool mOsm/kg).
Na + stool K)
<50 Secretory diarrhea —> Therefore, the stool osmotic gap (SOG), which is normally
50-125 Indeterminate between 50 and 125 mOsm/kg, can help determine the etiology
of watery diarrhea.
>125 Osmotic diarrhea

1) Osmotic diarrhea
-Pathogenesis: occurs due to the presence of a nonabsorbed, osmotically active solute
(eg, polyethylene glycol, sorbitol, lactose intolerance) which inhibits water resorption
- does not occur during fasting .

2) Secretory diarrhea
- toxins (eg, produced by Vibrio cholerae),
-hormones (eg, produced by VIPomas),
-congenital disorders of ion transport (eg, cystic fibrosis), or
-bile acids (in postsurgical patients).

47) Spontaneous bacterial peritonitis

#Dx:PMNs >250/mm3
• Positive culture, often gram-negative organisms (eg, Escherichia coli, Klebsiella)
• Protein <1 g/dL; SAAG >1.1 g/dL
#Rx:

%:
• Empiric antibiotics - 3o cephalosporins (eg, cefotaxime)
• Fluoroquinolones for SBP prophylaxis
48) Bloody ascites:
-peritoneal RBC is >50,000 mm3 Is required for bloody ascites
#Etio:
1) Trauma:
-Most cases occur due to localized trauma from a paracentesis;
-however, these bleeds usually resolve without intervention.

2) malignancy
Persistently bloody ascites found on multiple paracenteses suggests an underlying
malignancy.
-HCC MC; ovary, prostate
—> so next step: abd imaging; AFP; cytological analysis of ascitic fluid

49) Autoimmune hepatitis:

-hepatocellular pattern of liver injury; large gamma gap >4; anti smooth Ab
-

50) common drugs associated with pancreatitis include:

1 Diuretics (furosemide, thiazides)
2 Drugs for inflammatory bowel disease (sulfasalazine, 5-ASA)
3 Immunosuppressive agents (azathioprine)
4 HIV-related medications (didanosine, pentamidine)
5 Antibiotics (metronidazole, tetracycline)

51) RF for sigmoid volvulus:

-Chronic constipation
-Colonic hypomotility (eg, neurogenic bowel in neurologic disorders, diabetic
enteropathy) can contribute to constipation

52) MOA of lactulose lactitol in hepatic encephalopathy:

#MOA: Colonic bacteria metabolize lactulose to short-chain fatty acids (eg, lactic acid,
acetic acid).
-This acidifies the colon to stimulate conversion of the absorbable ammonia to the
nonabsorbable ammonium (an ammonia trap) and causes bowel movements
(which facilitates fecal nitrogen excretion).

#end point: The medication is titrated to produce 2 or 3 semiformed stools daily.

53) Screening of HCC:

-in any patient with cirrhosis, screening abdominal ultrasound is recommended every 6
months to evaluate for new-onset HCC.
54) IBD induced TM:
-IBD patients are at the highest risk of developing TM early in the disease, usually within 3
-
years of diagnosis and sometimes at initial presentation

=
#Mx:
-intravenous corticosteroids.
-Other management : supportive care (eg, IV fluids, electrolyte repletion), bowel rest and
decompression (eg, nasogastric tube), and broad-spectrum antibiotics.

-surgical intervention (eg, subtotal colectomy with end-ileostomy) may be required if

symptoms fail to improve.

Not hep C 55) Painless jaundice with

conjugated hyperbilirubinemia
and markedly elevated ALP:

-Shock liver needs hypotension ;

-Etiology: biliary obstruction
-Budd chiari needs severe RUQ pain due to pancreatic or biliary
cancer. choledocholithiasis
and benign biliary strictures.

Triad

57) Duodenal ulcer (DU)

MCC in USA: alcoholic; -2 MC Etiology: H pylori / NSAIDS
NASH; Hep C in IV drug
-Mx of H pylori-associated ulcer : acid
suppression + antibiotic eradication
(clarithromycin+ Amoy+ MTZ +
bismuth )
Not alone PPI

-
58) Hepatic adenoma: benign epithelial tumor
-RF: besides OCP, pregnancy, androgenic steroids
-CT: well demarcated hyperechoeic lesion with peripheral enhancement vs central scar
-
in FNH; USG: solid mass vs cystic mass in H cyst -

-Cx: progressive growth, rupture, and malignant transformation.

-Mx: Asymptomatic & <5 cm – stop oral contraception
• Symptomatic or >5 cm – surgical resection

59) although toxic megacolon is clinically diagnosed; it requires radiographic evidence

abdominal CT (>6 cm) + systemic toxicity signs before jumping to Rx

#y best next step is CT before Rx??

==> C/I :-instillation of contrast (eg, enema) or air (eg, colonoscopy) into a dilated,
inflamed colon can cause perforation —> C/I until diagnosis of TM has been excluded
(eg, abdominal CT scan).

60) Etiology of SIBO:

*Surgical cause:
-surgery involving the ileocecal valve.

*Nonsurgical cause:
- altered small bowel motility (eg, uncontrolled diabetes mellitus, chronic opiate use,
scleroderma)
-Other : small intestinal diverticula, chronic pancreatitis, and gastric hypochlorhydria (eg,
chronic proton pump inhibitor use).

#Dx: gold standard for diagnosis :jejunal aspiration demonstrating a high bacterial
concentration (eg, >103 colony-forming units/mL);

**Clue:
-SIBO is more commonly diagnosed by an abnormal carbohydrate breath test using
either glucose or lactulose.
#Rx: oral antibiotics (eg, rifaximin, neomycin) to reduce bacterial load.

61) UC in Pregnancy
-Pregnancy is a high-risk period for patients with ulcerative colitis (UC) as there is often
worsening disease activity that can lead to fetal complications, : preterm delivery and
-
small for gestational age.
-
-

-Mx: Remission should ideally be achieved before conception. Most medications used to
control UC are considered safe for continuation throughout pregnancy.
62) chronic pancreatitis imaging: pancreatic atrophy and calcifications

63) colon cancer screening:

• High-sensitivity stool-based testing (eg, fecal occult blood testing [FOBT] or fecal
immunochemical testing [FIT] annually)
• Direct visualization techniques (eg, colonoscopy every 10 years, flexible
sigmoidoscopy every 5 years),
• A combination (eg, flexible sigmoidoscopy every 10 years with FIT annually).

64)MC drugs causing pancreatitis:

-Diuretics, thiazides (eg, hydrochlorothiazide) and most loop diuretics (eg,
furosemide), are among the most common offenders.

-Mechanism: These drugs may trigger pancreatitis via hypersensitivity to the sulfonamide
molecule (a structural component of thiazides and most loop diuretics),
pancreatic ischemia due to reduced blood volume, and/or increased viscosity of
pancreatic secretions.
Colon cancer screening in patients at increased risk 66) Gilbert syndrome
10 yearly in normal person - intermittent jaundice and indirect
Indication Colonoscopy recommendations (unconjugated) hyperbilirubinemia in
Family history of the absence of other laboratory
adenomatous polyps or abnormalities
CRC • Age 40 OR 10 years before the age

E-
• 1 first-degree relative of diagnosis in affected relative*
age <60 • Repeat every 5 years -Trigger: Jaundice is often triggered
• ≥2 first-degree relatives by periods of stress, such as febrile
at any age
illness, dehydration, fasting,
Inflammatory bowel disease
• Ulcerative colitis • Begin 8 years after disease onset vigorous exercise, menses, and
• Crohn disease with • Repeat every 1-3 years surgery.
colonic involvement
Classic familial • Age 10-12
adenomatous polyposis • Repeat annually
• Age 20-25
HNPCC (Lynch syndrome)
• Repeat every 1-2 years
67) Stress ulceration
-common in patients in the ICU and can cause occult or gross GIT bleeding.
-RF: shock, sepsis, coagulopathy, mechanical ventilation, traumatic spinal cord/brain
injury, burns, and high-dose corticosteroids.
-Rx: PPI prophylactic and therapeutic

68) Hyperplastic polyps : non-neoplastic abnormality commonly found on screening

colonoscopy.
-Small (<1cm) hyperplastic polyps do not increase the risk for colon cancer, and
patients may continue colorectal screening at the usual intervals (eg, repeat colonoscopy
in 10 years for individuals at otherwise average risk).
68) Triglyceride-induced pancreatitis 70) Sphincter of Oddi dysfunction
Triglyceride levels (mg/dL) -functional biliary disorder due to
• <500: minimal risk dyskinesia or stenosis of the SOD
• 500-999: mild risk
Risk • 1,000-1,999: moderate risk
• ≥2,000: high risk -C/F: recurrent, episodic pain in the
Other risk factors: pregnancy, alcoholism, obesity, RUQ / epigastric region, with
uncontrolled diabetes
corresponding elevations in
• Intravenous fluid hydration, pain control
• Glucose ≥500 mg/dL: consider insulin infusion aminotransferases and ALP.
Manageme
nt
• Glucose <500 mg/dL or severe pancreatitis (eg, lactic -Opioid may worsen
acidosis, hypocalcemia): consider apheresis
(therapeutic plasma exchange)
-Dx: manometry; Rx: sphincterotomy
71) D/D of large AST ALT elevation (> 1000)
-acute viral hepatitis: significant hyperbilirubinemia, nausea, and vomiting.

=
Vs
#Ischemic hepatic injury
-occurs in the setting of hypotension with milder increases in the total bil and ALP.
-In patients who survive the inciting condition (eg, hypotension), liver enzymes typically
return to normal within a few weeks.

72) Budd chiari syndrome: Dx

• Hepatic venous outflow obstruction
• Usually due to:
• Abdominal Doppler ultrasound – ↓ .

I
hepatic vein flow
◦ Myeloproliferative disorder (eg, PV) • Investigation for underlying
◦ Malignancy (eg, hepatocellular carcinoma) disorders (eg, JAK2 testing for PV)
◦ Oral contraception use/pregnancy
Vs
HCC: polycythemia but the presence of aquagenic
-
pruritis, severe polycythemia
(HCT > 60%), and facial plethora make PV far more likely.
-

73) false-positive D-xylose test (ie, low urinary D-xylose level despite normal mucosal
absorption) can be seen in the following:

• Delayed gastric emptying

• Impaired glomerular filtration
• Small intestinal bacterial overgrowth (SIBO), characterized by alterations in small
intestinal flora (due to abnormal intestinal anatomy or motility), leading to bacterial
fermentation of the D-xylose before it can be absorbed. SIBO is treated with rifaximin
74) Chronic radiation proctopathy
-onset: often causes bloody stools, but usually presents for the first time within 1st year.
-Colonoscopy : pale mucosa with ulcers, strictures, telangiectasias, and focal
hemorrhage.
Vs
#Ischemic colitis
- a common complication of vascular surgery, as patients are often older and have
extensive underlying atherosclerosis.
-CT imaging : thickening of the bowel wall.
-Colonoscopy : cyanotic , edematous friable mucosa and hemorrhagic ulcerations.

Medication-induced esophagitis 76) Bile acid diarrhea

Drug class Drug - a common complication of cholecystectomy and occurs
Antibiotics Tetracyclines due to the overly rapid release of bile into the intestines,
where it overwhelms the resorptive capacity of the
Anti- Aspirin & many
inflammator nonsteroidal anti- terminal ileum and spills into the colon,
y agents inflammatory drugs
Bisphospho Alendronate, -C/F: resulting in secretory (fasting) diarrhea.
nates risedronate
Potassium chloride, -Rx: Bile-acid binding resins (eg, cholestyramine,
Others colestipol, colesevelam) are first-line therapy
iron

79) Psoas abscess Vs appendicitis:

#Similarity: Psoas sign +; fever,
leucocytosis, RLQ tenderness
—> next step in both: CT

#Difference:
-psoas abscess: subacite; lil long course;
normal rectal exam
-RF; H/O prior soft tissue infection/CD/
intrabdominal exam

Vs
Appendicitis: acute short H/O;
Pain on rectal Exam

-Proximal aneurysms : upper abdominal, flank/ back

pain,
-distal lesions :lower abdominal / groin pain
-clue : Paravertebral calcification
 Microscopic colitis: autoimmune 80) Triggers of hepatic
• Watery, nocturnal, nonbloody diarrhea; encephalopathy:
Clinical fecal urgency & incontinence
findings • Abdominal pain, fatigue, weight loss, • Drugs (eg, sedatives, narcotics)
arthralgias • Hypovolemia (eg, diarrhea)
• Smoking, medications (eg, NSAIDs, • Electrolyte changes (eg,
Triggers hypokalemia)
PPIs, SSRIs, ranitidine)
• ↑ Nitrogen load (bleeding)
• Colonoscopic biopsy with lymphocytic • Infection (eg, pneumonia, UTI,
infiltration of lamina propria SBP)
Diagnosi ◦ Collagenous: thickened
• Portosystemic shunting (eg,
s subepithelial collagen band
TIPS)
◦ Lymphocytic: high levels of
intraepithelial lymphocytes
Manage • Remove possible triggers
ment • Antidiarrheal medications & budesonide

81) #Pathogenesis of HypoK exacerbating HE:

• Hypokalemia, which can exacerbate HE as the resultant intracellular acidosis (excreted
intracellular potassium replaced by hydrogen ions to maintain electroneutrality) causes
increased NH3 production (glutamine conversion) in renal tubular cells

• Metabolic alkalosis (elevated bicarbonate), which can also exacerbate HE as it

promotes conversion of ammonium (NH4+), which cannot enter the CNS, to NH3,
which can enter the CNS
#Mx:
-As a result, patients with HE and hypokalemia require prompt potassium repletion in
addition to intravascular volume repletion.
-Disaccharides (eg, lactulose, lactitol) are also administered to lower NH3 levels.

82) Mx of eosinophilic esophagitis:

-In patients in whom eosinophilic esophagitis is suspected, a 2-month trial of PPI therapy
is considered part of the diagnostic evaluation;

—> if there is no symptom improvement following this trial, endoscopy with esophageal
biopsy is performed.
*Dx;
-Circular rings and esophageal furrows are nonspecific findings that may be present on
endoscopy; diagnosis is confirmed by ≥15 eosinophils per high-power field
#Rx;
-1st-line treatment : dietary modification to avoid potential food triggers.
-Pharmacologic management :topical (eg, swallowed) fluticasone.
83) Mx of UC based on severity :
a) Mild ulcerative colitis (UC)
-Def: <4 bowel movements a day, intermittent hematochezia, normal inflammatory
markers, and no anemia.
*Rx:
-1st-line :5-aminosalicylic acid medications; suppositories or enemas are preferred in
patients with UC limited to the rectosigmoid/ steroid enema
-vs oral therapy is used for more extensive disease.

b) Mx for Moderate to Severe UC :

-Def: >6 bowel movements a day, with frequent hematochezia as well as anemia and
elevated inflammatory markers.
*Rx;
-TNF-alpha I (eg, infliximab, adalimumab, golimumab) induction and maintenance therapy

c) Mx for Refractory UC :
—> A total proctocolectomy with ileoanal anastomosis

84) HCC: raised ALP; AFP; LFT normal/not

Vs
#Cholangiocarcinoma: raised ALP/ CEA/ CA 199; but NOT AFP

85) First-line treatment for an obstructing Schatzki ring/

esophageal ring :
- mechanical dilation using bougie or balloon dilators.
-This would improve this patient's symptoms immediately.
However, recurrence of strictures is possible and subsequent
dilatations may be needed.

#Dx:endoscopy shows ring (full circle vs half circle in webs) like

obstruction but normal mucosa

86) colon CA: mc site rectosigmoid> ascending >descending

86) Pseudocyst:
- does not cause jaundice and wt loss like adenoCA

87) Smoking is strongly associated with increased severity and progression of Crohn
disease and should be avoided in these patients.

87) esophageal varices prophylaxis: amboss

-small <5 mm:nonselective B blocker (avoided in active bleeding as it blunts HR
increase
-if large >5mm: ligation
 MESENTERIC ISCHEMIA
ACUTE MESENTERIC ISCHEMIA

Urge to defecate

A.fib., cardiovascular aneurysm,

shock, vasoconstriction, acute
thrombosis due to peripheral
arterial disease or low cardiac
output states

Elevated Hb
(hemoconcentration)

Or low bicarb

- Most common in elderly

- May result from cardiac embolus (a. fib), arterial thrombus (atherosclerosis) or other etiology (as in
shock or vasoconstriction)
- Periumbilical abdominal pain can be associated with N/V—out of proportion to PE findings if
prolonged more focal abdominal tenderness (due to local inflammation/infarction, perforation or
peritonitis) or peritoneal signs (eg guarding, rebound tenderness)
- CT: focal or segmental bowel wall thickening, pneumatosis intestinalis, small bowel dilation, mesenteric
stranding and mesenteric thrombi
- Management: Patients with evidence of bowel infarction undergo immediate operative evaluation;
otherwise, diagnosis can be confirmed radiologically by CT angiography. Treatment includes open
embolectomy with vascular bypass or endovascular thrombolysis. In addition, patients should be
started on broad-spectrum antibiotics and, in the absence of active bleeding, anticoagulation to
reduce the risk of clot expansion

(vs appendicitis) = (Acute appendicitis is uncommon in

elderly patients; if it occurs, the presentation Is less
acute. In addition, In the absence of perforation and
significant hypotension, patients with appendicitis rarely
develop metabolic acidosis.)
25
Page
CHRONIC MESENTERIC ISCHEMIA

May also complain of nausea,

early satiety and diarrhea. Pain
starts within first hour of eating
and resolves within next 2 hours
(~50%)
The pathophysiology of the pain is most
likely related to shunting of blood away
may also be helpful from the small intestine to meet the
increased demand of the stomach. In
patients with atherosclerosis, the celiac
or the superior mesenteric arteries may
be narrowed and unable to dilate
appropriately to maintain adequate
blood now to the intestines.

- Abdominal x-ray and CT may show calcified vessels—diagnosis require better calcification

ISCHEMIC COLITIS
The pain of IC is usually moderate and
lateralizes to the affected side. Repair of an
abdominal aortic aneurysm Is a common
precipitating event as patients are often older
and have extensive atherosclerotic vascular
disease. Contributing factors may include
loss of collateral circulation, manipulation of
vessels with surgical instruments, prolonged
aortic clamping and impaired blood flow
through the Inferior mesenteric artery.

Fever, nausea, leukocytosis

CT scan with IV contrast is

(edema) performed urgently to
assess immediate need for
surgery i.e. extensive
bowel damage,
, hemorrhagic ulceration with a sharp perforation, gangrene if
transition from affected to unaffected mucosa.
surgery not needed
colonoscopy to confirm Dx

Unless the patient has perforation or

bowel gangrene, most cases are
managed conservatively with
intravenous fluids, bowel rest, and
antibiotics.
26

- Commonly involved sites: splenic flexure at watershed line btw territory of superior and inferior
Page

mesenteric artery and rectosigmoid junction at watershed btw sigmoid artery and superior rectal artery
 Diverticular disease
• Diverticulosis: ↑ intraluminal pressure causing
herniation
• through points of weakness (vasa recta
penetration)
Etiology • Diverticular bleeding: injury to exposed vasa
recta
• Diverticulitis: trapped food particles & ↑
intraluminal pressure
• causing microperforation
• Diverticulosis: none
Symptom • Diverticular bleeding: painless hematochezia
s • Diverticulitis: left lower quadrant pain, nausea,
vomiting, fever
Risk • Diet high in red meat & fat & low in fiber
factors • Obesity, physical inactivity, smoking
 Respiratory

==> Key idea: Risk factors for asthma include (1) Family
history of atopy (2) Environmental exposures (second-hand
smoke, pollution, etc.) NBME 8
 Loud P2
crackles are typical (particularly if significant enough to cause PH)

1) Pathogenesis of PH in SCD :
- multifactorial

- Intravascular hemolysis, leading to chronic inflammation and endothelial

dysfunction, —> hyperplasia and hypertrophy of small pulmonary vessels (ie,
vascular remodeling) and increased pulmonary vascular resistance (PVR).

- Increased PVR leads to decreased right ventricular (RV) output and left ventricular
filling.
—> As a result, cardiac output is unable to sufficiently increase during exercise.

2) Pathogenesis of Pulmonary fibrosis

-It is a potential complication of SCD (eg, following recurrent episodes of acute chest
syndrome and pulmonary infarction) characterized by restrictive lung disease due to
parenchymal scarring.
Case :
—> A 6-yrs old child has URTI with
severe chest pain,
On examination, it shows crepitus,
Case :
—>>H/O Anxiety disorder & Depression.
—>> On examination, BP : 90/56 mm Hg,
P: 68/min, RR : 8/min
- no response to painful stimuli
- Pupils are normal in size
- Breath sounds are normal.
—>> patient is given a dose of naloxone
but remains unresponsive.

ABG as follows:
Arterial blood
gases
pH 7.2
64 mm
PaO2 Hg
74 mm
PaCO2 Hg
29 mEq/
HCO3− L
 #y MTZ not preferred??
-Metronidazole has
excellent efficacy against
obligate anaerobes but
minimal efficiency
against facultative
anaerobes.

-Because lung
abscesses are often a
mixture of obligate and
facultative anaerobes,
metronidazole is not
recommended (failure
rates >50%).

pneumonectomy
lobectomy
 RESPIRATORY RESPIRATORY—PATHOLOGY
`  SEC TION III 677

Pneumoconioses Asbestos is from the roof (was common in insulation), but affects the base (lower lobes).
-
Silica and coal are from the base (earth), but affect the roof (upper lobes).
Asbestosis Associated with shipbuilding, roofing, Affects lower lobes.
plumbing. “Ivory white,” calcified, Asbestos (ferruginous) bodies are golden-brown
-
supradiaphragmatic A and pleural B plaques fusiform rods resembling dumbbells C ,
are pathognomonic of asbestosis. found in alveolar sputum sample, visualized
Risk of bronchogenic carcinoma > risk of using Prussian blue stain, often obtained by
mesothelioma.  risk of Caplan syndrome bronchoalveolar lavage.
(rheumatoid arthritis and pneumoconioses  risk of pleural effusions.
with intrapulmonary nodules).
Berylliosis Associated with exposure to beryllium in Affects upper lobes.
aerospace and manufacturing industries.
sa
←
Granulomatous (noncaseating) D on histology
and therefore occasionally responsive to
steroids.  risk of cancer and cor pulmonale.
Coal workers’ Prolonged coal dust exposure Ž macrophages Affects upper lobes.
pneumoconiosis laden with carbon Ž inflammation and Small, rounded nodular opacities seen on

II
fibrosis. imaging.
Also known as black lung disease.  risk of Anthracosis—asymptomatic condition found in
Caplan syndrome. many urban dwellers exposed to sooty air.

→
Silicosis Associated with sandblasting, foundries, Affects upper lobes.
mines. Macrophages respond to silica “Eggshell” calcification of hilar lymph nodes on
and release fibrogenic factors, leading to CXR.
fibrosis. It is thought that silica may disrupt The silly egg sandwich I found is mine!
phagolysosomes and impair macrophages,
increasing susceptibility to TB.  risk of
.
cancer, cor pulmonale, and Caplan syndrome.
A B C D

#Rx of idiopathic interstitial fibrosis:

-Antifibrolytics: pirfenidone; nintedanib
-o2; pulm rehabilitation
-smoking cessation and GERD Rx: RF control
-lung transplantation
 →

# How to detect hypercapnia??

-Altered mental status in the setting of an acute exacerbation of COPD) raises suspicion for
symptomatic hypercapnia and should be promptly investigated with arterial blood gas
analysis.

-C/F of symptomatic hypercapnia are predominantly neurologic.

-mild to moderate degrees of hypercapnia: may have headaches or hypersomnolence,
-higher blood CO2 levels (eg, >75-80 mm Hg) : cause delirium, confusion, lethargy,
and eventually coma (CO2 narcosis) or seizures.
#COPD induced V/Q Mismatch & its Compensation :
- In advanced COPD, destruction of the terminal bronchioles and alveoli causes
areas of physiologic dead space to develop.
- affected regions have limited surface area available for gas exchange, which
leads to ventilation/perfusion (V/Q) mismatch causing local hypoxia and
hypercapnia.

- Pulmonary circuit VC d/t Hypoxia —> Hypoxia induces selective

vasoconstriction in these areas of the lung and redirects blood flow to better
ventilated alveoli, reducing V/Q mismatch.

#How supplemental O2 worsens already compensated V/Q mismatch of COPD :

Supplemental oxygen improves hypoxia at the cost of CO2 retention,
by the following mechanisms:

• Loss of compensatory vasoconstriction in areas of ineffective gas exchange

worsens V/Q mismatch
• Increase in oxyhemoglobin reduces the uptake of CO2 from the tissues by the
Haldane effect
• Decreased respiratory drive and slowing of the respiratory rate causes
reduced minute ventilation

#Pathogenesis of Hypercapnia causes alterations in CNS functions :

1) Consciousness alterations :
acidosis caused by an acute increase in CO2 ,
increases brain GABA and glutamine
&
decreases brain glutamate and aspartate, causing a change in level of
consciousness.

2) Hypercapnia also causes reflex cerebral vasodilation and may induce seizures.

#How to use O2 in COPD patients & what to be done if Hypercapnia occurs..?

-Oxygen should be used cautiously with a goal SaO2 of 90%-93% or PaO2 60-70
mm Hg.
- Patients who develop significant acidosis or have severely reduced level of
consciousness require mechanical ventilation.
 Lung volumes & Pressures

Extra alveoli / proximal Lung alveoli are

airway pathology damaged

-
Resistive P increases I
-Measurement of airway pressures can be useful in mechanically ventilated patients.

#peak airway pressure :

- (the maximum pressure measured as the tidal volume is being delivered) equals the sum of the
resistive pressure (flow x resistance) and the plateau pressure.
Peak airway pressure = resistive pressure + plateau pressure

#plateau pressure :
- the pressure measured during an inspiratory hold maneuver, when pulmonary airflow and thus resistive
pressure are both 0.
-It represents the sum of the elastic pressure and positive end-expiratory pressure (PEEP).
0
Plateau pressure = elastic pressure + PEEP

#Elastic pressure :
-is the product of the lung's elastance and the volume of gas delivered.
-Because elastic recoil is inversely related to lung compliance, the elastic pressure can be calculated as
tidal volume/compliance.
—>Decreased compliance (eg, pulmonary fibrosis) —> stiffer lungs and higher elastic pressure.

# EtioPathogenesis of altered peak pressure:

-Increased peak pressure associated with an unchanged plateau pressure suggests a pathological process
causing increased airway resistance, such as bronchospasm, mucus plug, or endotracheal tube obstruction

-Elevation of both peak and plateau pressures indicates a process causing decreased pulmonary
compliance, such as pulmonary edema, atelectasis, pneumonia, or right mainstem intubation. I I
 RS case clue
1) COPD: smoking H/O must; scant sputum; Dx: Cxray
Exacerbation: change in sputum colour; increased cough; dyspnea

2) Bronchiectasis: RF like recurrent infection and others +;large amount of sputum >100ml
Diagnosis: CT of choice
In CF: Bronchiectasis is in Rt upper lobe

3) Acute Bronchitis: chronic cough > 5 days-3 mon after viral URTI; no fever; B/L
wheeze that clears on coughing..: post infectious ;Rx: supportive

4) Tension pneumothorax:
Vitals unstable; U/L breath sound absent; sudden onset of breathlessness

5) Acute massive pulmonary embolism :

→
- abrupt increases in RAP to >10 mm Hg and PA pressure to >40 mm Hg; intact PCWP
(elevated in LHF)

6) Pneumomia: fever; yellow sputum; lung consolidation

-No consolidation visible on Xray in immunodeficient so do CT chest in suspected
-PCP pneumoniae can exacerbate SIADH and hyponatremia

7) Solitary pulmonary nodule: upto 3 cm surrounded by pulm parenchyma

-Nodules <0.8 cm with smooth margins : less likely to be malignant;
- nodules ≥2 cm with irregular or spiculated margins : likely to be malignant.
-malignant double in months or 1-2 yrs.

9) Acute hypersensitivity pneumonitis

-classically presents with recurrent episodes of abrupt-onset fever, dyspnea,
nonproductive cough, and fatigue that coincide with intermittent exposure to an inhaled
antigen.

-often mistaken for bacterial pneumonia and given Ab but self-resolves within a few days
after removal of antigen exposure.
-Xray: micronodular infiltrates B/L

10) Occupational asthma (OA)

- induced by workplace antigen exposure (eg, animal proteins, flours, isocyanates).
-Chronic OA may result in persistent airway inflammation that abates only after prolonged
absence( 1-2 weeks)

-diagnosed by workplace-specific declines in peak expiratory flow rate >20%

10) Pulmonary contusion:
-After blunt chest trauma, pt has dyspnea, tachypnea, and hypoxemia after sometime
-CT scan: ground-glass opacities in the lung adjacent to the affected chest wall
(anterior, peripheral lung)/ nonlobar infiltrates ; Xray may be neg initially
-Dx of choice: CT
-It is frequently associated with rib fractures but may occur in their absence,
especially in children (whose more elastic chest walls can transmit more kinetic energy
without fracturing).
Vs
Diffuse infiltrates with pulm edema of myocardial contusion/CHF
-Mx: supportive care

11) Ventilator-associated pneumonia

- is a hospital-acquired pneumonia that develops ≥48 hours after ET

12) Phrenic N injury:

-After CABG, exertional dyspnea, orthopnea, and paradoxical movement of the
abdomen during inspiration, findings suspicious for diaphragmatic weakness.

13) flail chest.

patient with tachypnea, hypoxia, and a segment of the chest wall that moves inward
during inspiration and out in expiration.
-Mx: mechanical positive pressure ventilation

14) venous air embolism (>50 ml air)

-sudden-onset respiratory distress following removal of a central venous catheter/
barotrauma; sx
-Mx:
-left lateral decubitus position : trap air on the lateral right ventricular wall and help
prevent RVOT obstruction and embolization of air into the pulmonary circulation—>
hypoxemia, obstructive shock, cardiac arrest

-High-flow oxygen :encourage absorption of the N2 in air embolus.

15) Amniotic fluid embolism syndrome

-rapid onset of respiratory failure, severe hypotension, and DIC during labor or the
immediate postpartum period.

16) Foreign body aspiration

-persistent cough/localised wheezing/dec breath sound (focal area) following a
choking episode.
-X-ray : U/L lung hyperinflation/ hyper resonance and mediastinal shift to normal
side; atelactasis if complete
-x-ray may be normal. #Next step: rigid bronchoscopy if suspicion high.
20) Exudative & transudative pleural effusions
Exudate Transudate
Pleural protein/serum protein >0.5
OR
Pleural LDH/serum LDH >0.6
Light criteria Exudate criteria not met
OR
Pleural LDH >2/3 upper limit of normal of
serum LDH
Pathophysiology Inflammation MRI Hydrostatic or oncotic pressure
• Infection (eg, TB, pneumonia)
• Malignancy
• Cirrhosis (hepatic hydrothorax)
• Connective tissue disease; RA
Common causes • Nephrotic syndrom
• Pulmonary embolism
HF
• Pancreatitis
• Post-CABG

# pancreaticopleural fistula
-resulting in an amylase-rich exudative pleural effusion occurs most commonly as a result
of acute or chronic pancreatitis.
-Management : bowel rest to promote fistula closure; ERCP/stent for drainage

21) DVT evaluation:

-RF:
a) inherited (eg, Factor V Leiden, prothrombin gene mutation, protein C deficiency)
b) acquired (eg, immobilization, surgery, malignancy, medications).

# when to suspect CA??

-In the absence of any clear provoking factors (eg, recent procedure, immobilization),
patients with a first episode of VTE should be referred for age-appropriate cancer
screening (eg, colonoscopy) to evaluate for malignancy

—> In addition, if the patient has specific symptoms of malignancy, such as weight loss or
pain, more extensive cancer screening (eg, CT scan of the chest, abdomen, pelvis) can be
considered

#when to suspect inherited cause??

-Extensive testing for an underlying inherited cause (eg, deficiency of protein C, protein S,
or antithrombin III) is generally only performed when the patient's history is suggestive (eg,
age <45, recurrent DVT, multiple or unusual sites of thrombosis, F/H/O- VTE).

—> Protein C, protein S, and antithrombin III levels are also affected by anticoagulant
therapy
19) Aspiration pneumonitis :
acute lung injury secondary to a chemical burn from aspirated sterile gastric contents;
CXray: B/L infiltrates; onset: hours after aspiration event; Rx: supportive
Vs
#aspiration pneumonia:an infectious disease caused by aspiration of infected
oropharyngeal secretions;CXray: infiltrates in dependent lung segment;onset:days after
-Rx: Ab
22) Asthma and PaO2:
-Severe hypoxemia (eg, PaO2 <60 mm Hg on room air) is relatively rare in an acute
asthma exacerbation and suggests a very severe exacerbation or the presence of
comorbid pathology (eg, pneumonia).

- PaO2 of 65 mm Hg : an expected level of hypoxemia and is not as concerning as the

normal PaCO2.

0
23) impending respiratory failure in asthma
-Patients with an acute asthma exacerbation usually have respiratory alkalosis with a low
PaCO2 due to hyperventilation.
-
—>A normal or elevated PaCO2 is an alarming and extremely important finding that
suggests impending respiratory failure.

24) obesity hypo ventilation syndrome

• Obesity with BMI ≥30 kg/m2
•Awake daytime hypercapnia (PaCO2 >45 mmHg);No alternate cause of hypoventilation
-Mx: 1st line NPPV

25) chronic cough(>8 weeks)

-MCC: upper airway cough syndrome (postnasal drip), GERD, and asthma.

-Other causes : drugs (ACE I), airway disease (eg, nonasthmatic eosinophilic bronchitis,
chronic bronchitis, bronchiectasis, malignancy), and pulmonary parenchymal disease
(eg, lung abscess, interstitial lung disease).
26) Lung malignancy is a
potential cause of localized
airway obstruction and may
present with episodes of
= recurrent pneumonia.

-CT scan chest:next step

18) localized intrapulmonary shunting (eg, lobar pneumonia, atelectasis, basilar

pulmonary edema) typically does correct with increased FiO2
Vs
Diffuse shunt doesn’t correct with O2 as > 50% alveoli involved
# Next step of Pt do not respond after 2-3 weeks ??
-may require further investigation (eg, sinus imaging, pulmonary function tests, high-
resolution CT scan of the chest) /
empiric sequential therapy for GERD, cough-variant asthma, chronic sinusitis, and non-
asthmatic eosinophilic bronchitis.
27)y increased breath sound nd fremitus in pneumoniae??
-In general, sound and vibration travel faster and more efficiently in solids or liquids
than in air, which results in increased intensity of breath sounds and increased tactile
fremitus in patients with a consolidative process inside the lung (eg, bacterial pneumonia).
Vs
-However, if fluid (pleural effusion) or air (pneumothorax) are present just outside the
lung in the thoracic cavity, they can act to insulate sound and vibration originating
from the lung, which leads to decreased breath sounds and decreased tactile fremitus.

-egophony (sounds like the letter

"A" when the patient says the
letter "E"): pneumonia
- -

Shallow breathing
—>> Excess of PEEP : Barotrauma
—>> Excess of FiO2 : O2 Toxicity
-
I
29) Postoperative measures used to decrease the risk of pneumonia :

1) incentive spirometry — most effective so is thus the first line preventive measure
2) deep breathing exercises,
3) continuous positive airway pressure (CPAP) —
4) intermittent positive pressure breathing.

30) massive PE increases pulmonary vascular resistance and right ventricular pressure,
causing right ventricular hypokinesis and dilation and hypotension-RHF

31) Acute nitrofurantoin-induced pulmonary injury

-MOA: due to a hypersensitivity that can present with fevers, shortness of breath, dry
cough, and erythematous rash.
-Onset:Sx usually begin 3-9 days from medication initiation.

-Dx: Bilateral basilar opacities and pleural effusions are common.

-Rx: cessation of nitrofurantoin
Vs
Chronic drug use: interstitial lung Ds

32) pulm Cx of RA:

-Rheumatoid arthritis can cause exudative pleural effusions characterized by low
glucose, very high lactate dehydrogenase, and (often) low pH and is associated with
interstitial lung disease.
-pulm nodules; ILD

17] ILD:
-Inspiratory "Velcro" (eg, fine, dry) crackles are sensitive for interstitial fibrosis, which
is present in many forms of ILD.

-typically audible long before abnormalities on chest x-ray (CXR) or PFT emerge,
underscoring the value of careful auscultation.
-So preferred initial test: HRCT thin slice method preferred > spiral CT

Solitary pulmonary nodules

• Large size*
• Advanced patient age
• Female sex
Factors
• Active or previous smoking
increasing
• Family or personal history of
malignant
lung cancer
probability
• Upper lobe location
• Spiculated radiographic
appearance
*Size >2 cm independently correlates with >50%
malignant probability.
 34) Ventilatory setting in ARDS:
-LTVV (6 mL/kg of ideal body
weight) decreases the likelihood of
overdistending alveoli and
provoking barotrauma due to high
plateau pressures (pressure applied
to small airways and alveoli).

• Increasing the fraction of inspired

oxygen (FiO2) administered by the
ventilator improves oxygenation;

-Increasing positive end-expiratory pressure (PEEP) also improves oxygenation by

preventing alveolar collapse at the end of expiration, thereby decreasing shunting
and the work of breathing.

#Ideal levels:
-Given the severe hypoxemia seen in ARDS, PEEP levels up to 15-20 cm H2O may be
necessary to maintain oxygenation.

-goal: arterial(PaO2) at 55-80 mm Hg / peripheral (SpO2) at 88%-95% (ie, preventing

SpO2 <88%, not <92%)

#Avoid:
-In contrast, higher TV in ARDS result in elevated pulmonary pressures due to the work of
forcing larger volumes into stiff lungs (decreased compliance), leading to increased
alveolar distension.
-prolonged FiO2 levels >0.6 : associated with oxygen toxicity.

35) AAT deficiency should be considered in a number of situations,

1) COPD at a young age (<45 years);
2) COPD with minimal or no smoking history;
3) basilar-predominant COPD; or
4) a history of unexplained liver disease.

36) Asthma clue:

-Intermittent episodes; wheezes on forceful expiration (induced for test)

#Mx of asthma exacerbation:

-Endotracheal intubation and mechanical ventilation are indicated in patients with
severe asthma unresponsive to maximal medical therapy and who have signs of
impending respiratory arrest.
-Signs:AMS, minimal aeration, hypercarbia, and worsening hypoxemia.
-
 ⇐ r -

Causes of hypoxemia 38) diffuse pulm edema:

A-a Corrects with -In contrast to hypoxemia due to
Examples gradie supplemental
nt O2?
diffuse pulmonary edema,
hypoxemia due to localized
Reduced PiO2 High altitude Normal Yes
intrapulmonary shunting (eg, lobar
CNS depression,
Hypoventilation
morbid obesity
Normal Yes pneumonia, atelectasis, basilar
pulmonary edema)
Diffusion Increas
limitation
Emphysema, ILD
ed
Yes typically does correct with
Small PE, lobar Increas increased FiO2 because only a
V/Q mismatch* Yes
pneumonia ed portion of the lungs is affected
Large and the normally ventilated
Diffuse pulmonary Increas
intrapulmonary
edema ed
No alveoli compensate via
shunt
increased O2 transfer.
Massive PE, right-to-
Large dead-space Increas
left intracardiac No
ventilation ed
shunt
*Caused by localized dead-space ventilation and/or
intrapulmonary shunting.

#Large-scale dead-space ventilation (eg, massive pulmonary embolism)

-the other major cause of hypoxemia that does not correct with supplemental O2.
-Although alveolar ventilation is normal, there is no perfusion of large portions of the
lung (extreme V/Q mismatch), resulting in minimal gas exchange.
39) asthma exacerbation can be complicated by mucus plugging and large-volume
atelectasis.

42) D/D b/w only OSA & OSA + OHS :

1) Only OSA : hypoventilation only at night with transient hypoxia and hypercapnia that
resolve while awake
—> OSA: just backfilling of tongue irrespective of obesity
.
2) OSA + OHS : Physical restriction of the thoracic cavity caused by excess thoracic tissue
continues throughout the day, resulting in chronic hypoxia and hypercapnia.

Pulmonary function test

43) Diff idiopathic pulm Arterial HT from
Restrictive lung
Normal
Obstructive lung
disease
other causes of PAH:
disease -Absence of alveolar airspace disease and
(including obesity)
>80% normal FEV1 and FEV1/FVC ratio help
FEV1 (of Decreased Decreased differentiate PAH from pulmonary
predicted)
hypertension due to lung disease
FEV1/ Normal to
>70% Decreased
FVC increased
>80%
-cz only arterial intimal hyperplasia in
FVC (of
Normal to
Decreased former
decreased
predicted)
 Pulmonary function tests in chronic lung disease
45) community acquired
Pulmonary Restrictiv
Interstitial
arterial e chest
pneumoniae:
Asthma COPD lung -even though, in practice, patients
hypertensi wall
diseases
on disease are sometimes diagnosed clinically,
TLC Normal/↑
00
↑ ↓ Normal ↓ guidelines specifiy that the
FEV1/
↓* ↓ Normal Normal Normal
diagnosis of CAP requires the
FVC presence of a lobar, interstitial, or
DLCO Normal/↑ ↓† ↓ ↓ Normal cavitary infiltrate on chest imaging
(usually chest x-ray).
*With positive bronchodilator response.
†Normal in early COPD.

#when to suspect CAP??

-patient with a sick contact, cough, and no upper respiratory symptoms (eg, rhinorrhea,
sore throat) has right lower lobe crackles.
—>These focal findings raise concern for a pulmonary consolidation consistent with CAP
(rather than bronchitis).

-Symptomatic treatment alone in the setting of consolidation is insufficient due to the risk of
secondary bacterial pneumonia

46) hypertrophic osteoarthropathy:

-The development of clubbing and sudden-onset joint arthropathy in a chronic smoker
is suggestive of hypertrophic osteoarthropathy.

#Association: often associated with lung cancer, and therefore a chest x-ray is indicated
to rule out malignancy and/or other lung pathology.

-
 Large, free/ loculated effusion

:
Sterile

WBC < 50k

LDH < 1k WBC>50k; LDH > 1k

Oral Ab IV ab+ drainage

47) RF for pneumonia complications such as empyema: immunocompromised (eg,

HIV, post-transplant).

#Mx: All empyemas (and many complicated parapneumonic effusions) require prolonged
antibiotics (2-4 weeks) and drainage (usually with a chest tube).

48) The MC type. of lung cancer in never-smokers is adenocarcinoma, which typically

arises in the lung periphery

Major risk factors for ventilator-

associated pneumonia
• Acid suppression (eg, PPI, H2R
blocker, antacid)
• Supine position
• Pooled subglottic secretions
• Paralysis & excessive sedation
• Excessive patient movement while
intubated
• Frequent ventilator circuit changes

51) indications of long-term home oxygen therapy (LTOT) in COPD:

1 Resting arterial oxygen tension (PaO2) <55 mm Hg / pulse oxygen saturation
(SaO2) <88% on room air
2 PaO2 <59 mm Hg or SaO2 <89% in patients with cor pulmonale/ hematocrit >55%

-The dose of supplemental oxygen should be titrated so that SaO2 is maintained at >90%
during sleep, normal walking, and at rest.
-Survival benefits of home oxygen therapy are significant when it is used for >15 hours a
day.
 ÷
So on opposite
side

Characteristics of high-altitude pulmonary edema versus multifocal

pneumonia

#Similarity: both have fever, leukocytosis, hypoxemia, B/L lung crackles

High-altitude pulmonary edema (HAPE) Multifocal pneumonia (infection)
• Recent arrival at high altitude (<1
week) as it almost never occurs
• Persistent stay at high
#blood goes wherever gravity after >1 week at the same altitude.
altitude
takes it (irrespective of damaged • Absent or mild leukocytosis
• WBC >15,000 mm3 with
• Procalcitonin normal
lungs) but air goes only to good • Marked early improvement with O2
bands s/o bacterial
• Procalcitonin elevated
lungs • #Mechanism: O2 alleviates the
• Minimal early improvement
hypoxic vasoconstriction in HAPE
with O2 (due to widespread
• O2 reduce alveolar-capillary
#Disease with decreased NO level?? perfusion pressure and rapidly
intrapulmonary shunting)
improve the edema and hypoxemia.
- CF (low) and kartagener (very low)
 SAbA: acute is albuterol
LABA: salmeterol (serial so long ); formeterol

#Treatment of an acute asthma exacerbation

-short-acting beta agonist (eg, albuterol) : manage immediate bronchoconstriction
-glucocorticoid (eg, prednisone) : control late-phase inflammation and prevent
symptom relapse.

56) lung exam in asthma:

-hyperresonant due to air trapping, and tactile fremitus is decreased, wheezing
57) Segmental PE Vs massive PE:
-Although dyspnea and pleuritic chest pain are common symptoms of segmental PE
Vs
-syncope tends to occur only in massive PE.

-Dx: Although echocardio has poor sensitivity for segmental PE, massive PE often has
visible echocardiographic abnormalities that allow for rapid bedside diagnosis.

58) measures reducing COPD

mortality:

-smoking cessation

=
-Long-term supplemental oxygen
therapy (LTOT)
- lung reduction surgery

59) CPAP-associated epistaxis.

-Mechanism: because of its drying
. effect on the nasal mucosa.

—> Humidification is often effective

in preventing CPAP-associated
ET with epistaxis.
mechanical
ventilation is
considered if
NPPV fails

60) pneumothorax by venti:

-Positive pressure ventilation (eg, mechanical ventilation) poses the risk of pulmonary
barotrauma, leading to alveolar rupture and pneumothorax formation.

-RF: COPD are at higher risk due to preexisting pulmonary hyperinflation and the
presence of bullae or blebs

-# change in ventilation settings in pneumothorax:

-The collapsed lung, receiving a relatively stable volume of air from the ventilator, results
in increased peak pressure (a measure of increased resistance to air flow from the
ventilator) and increased plateau pressure (a measure of the lung's decreased
ability to expand [compliance]).

Vs hazy lungs in ARDS

61) Glucose changes in Pleural fluid :
1) Glucose level <60 mg/dL or pleural fluid/serum glucose ratio <0.5 is usually seen in :
due to rheumatoid pleurisy, complicated parapneumonic effusion or empyema,
malignant effusion, tuberculous pleurisy, lupus pleuritis, or esophageal rupture

2) Pleural glucose <30 mg/dL

-in particular suggests an empyema or rheumatic effusion.

# Why glucose reduced in pleural fluid :

-due to the high metabolic activity of leukocytes (and/or bacteria) in the fluid.

- Transudates and all other exudative effusions usually have pleural fluid glucose similar to
blood glucose concentration.

62) AAT deficiency

#Mx:
-IV human AAT + bronchodilators and corticosteroids as needed.
-severe lung disease are candidates for lung transplantation, whereas hepatic failure
treated with liver transplantation.

Community-acquired pneumonia
Setting Recommended therapy
• Healthy patients
◦ Amoxicillin / doxycycline
Outpati • Comorbid conditions (eg,
ent diabetes, malignancy)
◦ Fluoroquinolone / beta-
lactam + macrolide
Inpatie
nt • Fluoroquinolone/
I
(non- • Beta-lactam + macrolide
ICU)
Inpatie
• Beta-lactam + Macrolides;/
nt
• Beta-lactam + fluoroquinolone
(ICU)

Covers Strp, H influ, legionella,

mycoplasma
 66) Treatment of acute
bronchitis
- a) primarily supportive and
may include throat lozenges and
over-the-counter cough
suppressants (eg,
dextromethorphan/guaifenesin).

-b) Patients with associated

wheezing in the setting of
underlying pulmonary disease
(eg, asthma)
may benefit from inhaled
bronchodilators (eg, albuterol);
otherwise, these medications are
not generally recommended.

Acute bronchitis
• Preceding respiratory illness (90%
Etiology
viral)
68) Role of pH in Pleural fluid :
• Cough for >5 days to 3 weeks (± - Normal pleural fluid pH : ~ 7.60.
purulent sputum)
Clinical • Absent systemic findings (eg, fever,
presentation chills) 1) Transudative fluid pH : 7.4 - 7.55
• Wheezing or rhonchi, chest wall
tenderness 2) Exudate pH : 7.30 - 7.45
• Clinical diagnosis, CXR only when
pneumonia suspected
Diagnosis &
• Symptomatic treatment (eg, NSAIDs
treatment
&/or bronchodilators)
• Antibiotics not recommended

3) Pleural fluid pH < 7.30 (with normal arterial pH and low pleural glucose) :

- usually due to increased acid production by pleural fluid cells and bacteria (eg,
empyema)/

- decreased hydrogen ion efflux from the pleural space (eg, pleuritis, tumor,
pleural fibrosis).
71) Myoclonus
-sudden, involuntary muscle contraction or relaxation that results in movement of limbs/
joints.

-Etiology: cardiac arrest

#Types:
1) the acute form (myoclonus status epilepticus [MSE])
-occurs while patients are still unconscious and is characterized by generalized (often
symmetric) myoclonus that involves the axial, limb, and facial muscles.
-Prolonged MSE is a marker of poor prognosis.

2) Lance-Adams syndrome,
-the chronic form of PHM, presents days to weeks after the initial insult once the patient has
regained consciousness.
-It is typically focal in nature and exacerbated by action;
-negative (relaxation) myoclonus also occurs, leading patients to drop objects or fall.

72) Pneumomia in immunodeficient:

-Patients with community-acquired pneumonia usually have a pulmonary infiltrate on initial
chest x-ray. However, those who are immunosuppressed may have normal pulmonary
imaging despite signs and symptoms that localize the infection to the lungs.

-These patients should undergo high-resolution CT scan of the chest to identify pulmonary
infiltrate.

73) #How to differ CHF from COPD exacerbation??

1) CHF:
-crackles on lung examination;
-Xray: white out lungs at site of edema
- ABG :hypoxia + hypocapnia + respiratory alkalosis;

2) COPD exacerbation
- less likely to cause bilateral crackles and more likely to cause significant (rather than
occasional) wheezing
-ABG: respiratory acidosis (acute or acute-on-chronic) due to CO2 retention.
-Xray: black lungs like emphysema

74) OSA unusual case:

-Not all patients have obvious respiratory symptoms (eg, snoring, gasping for air); the
sequelae of OSA (eg, erectile dysfunction, arterial hypertension) may be what prompts
the initial evaluation
 • Cx-ray in chronic bronchitis:
prominent bronchovascular
markings(due to inflammation)
and a mildly flattened diaphragm.

• In contrast, the Cxray in

emphysema : decreased
vascular markings and
hyperinflated lungs.

• predominant chronic bronchitis

may demonstrate more
pronounced hypoxemia(due to
infammation) than emphysema.

E-
74) Laryngomalacia: inspiratory stridor
- tracheomalacia: expiratory stridor
- subglottic stenosis: biphasic stridor as cricoid cartilage stays stiff throughout

75) Methemoglobinemia
-triggers: oxidizing agent (eg, dapsone, nitrites, anesthetics).
-Pulse oximetry saturation is typically low and does not improve with the administration of
oxygen;clue
#Dx:
• Saturation gap (>5% difference between oxygen saturation on pulse oximetry &
ABG)
=
• Normal PaO2
#Rx:
-1st line: - Methylene blue acts as an electron acceptor for NADPH and is reduced to
leucomethylene blue, which in turn reduces methemoglobin to hemoglobin.

-2nd line: High-dose ascorbic acid (vitamin C) when methylene blue is unavailable or C/
I (eg, G6PD deficiency).

77) complications of positive pressure ventilation: Alveolar damage, pneumothorax, and

hypotension. Pneumothorax presents with sudden-onset shortness of breath,
hypotension, tachycardia, tracheal deviation, and unilateral absence of breath
sounds.
Vs
#ET in 1 bronchus: no hemodynamic instability

Common types of hypersensitivity pneumonitis

Condition Causative agent
Moldy hay
Farmer's lung (thermophilic actinomycetes, Aspergillus
spp)
Bird fancier's
Proteins in avian droppings or feathers
lung
Mycobacterium avium complex,
Hot tub lung
Cladosporium spp
Mushroom worker's
lung
Thermophilic actinomycetes
Potato riddler's
lung
Wine maker's
Botrytis spp
lung
Cheese maker's
Penicillium spp, Aspergillus spp
lung
Chemical worker's
Spray paints, dyes, varnishes
lung
78) GERD as a trigger of asthma:
-Comorbid gastroesophageal reflux disease (GERD) is common in patients with asthma
*Pathogenesis:
- can exacerbate asthma symptoms through microaspiration of gastric contents,
leading to an increase in vagal tone and bronchial reactivity.

*Clues to GERD in asthma:

-patient with asthma has several clues in her history suggesting comorbid GERD,
including sore throat, morning hoarseness, worsening cough only at night, and
increased need for her albuterol inhaler following meals

#Mx:
-Proton-pump inhibitor (PPI) therapy has been shown to improve both asthma
symptoms and peak expiratory flow rate in asthma patients with evidence of comorbid
GERD

79) Indication of Tracheostomy :

Because an endotracheal tube can cause damage to the larynx and upper trachea over
time (eg, tracheal stenosis),
**tracheostomy is indicated when prolonged intubation (eg, >7-10 days) is required.

# Disadvantage of endotracheal tube:

- inflated cuff of ET tube can cause ischaemia, necrosis and stenosis of upper airway..
- whereas tracheal tube has cartilage so less chance of stenosis..

80) #Extubation criteria :

—> The initial criteria for extubation readiness include:
• pH >7.25
• Adequate oxygenation
—>>> PaO2 ≥60 mm Hg on minimal support (ie, fraction of inspired oxygen [FiO2]
≤40% and positive end-expiratory pressure [PEEP] ≤5 cm H2O
• Intact inspiratory effort and sufficient mental alertness to protect the airway

#Role of Spontaneous Breathing Trial (SBT) Before Extubation :

—> As there is short-term risk of recurrent respiratory failure requiring reintubation, most
patients who meet the above criteria should undergo a spontaneous breathing trial (SBT)
to help confirm readiness for extubation.

—> During an SBT, patients remain intubated but ventilatory support is turned off,
allowing patients to breathe on their own for a short period of time (eg, 1-2 hours).
#Role of RSBI in Extubation :
Candidacy for successful extubation may be further assessed during an SBT using the
rapid shallow breathing index (RSBI): RR/ TV

—>> Patients with a high RSBI (eg, >105) are breathing fast and shallow and are
unlikely to do well without continued ventilatory support.

Unloading

81) Hyperventilation syndrome

-presents with acute onset of deep breathing and/or tachypnea often accompanied by
neurologic symptoms (some tingling sensation) due to hypoCa by alkalosis
—> Lung examination is normal.

# Mx:
-Education and reassurance are key components of treatment.

-1st line: Patients should be taught abdominal (diaphragmatic) breathing, a

retraining maneuver that involves trying to keep the chest still;

-2nd line: If the episode does not improve with breathing retraining, a small dose (not a
high dose) of a short-acting benzodiazepine (eg, lorazepam)

-Breathing into a paper bag was previously recommended to improve hypocarbia by

rebreathing CO2; however, this can also result in hypoxia and therefore should not be
done.
 Differential diagnosis based on DLCO 82) Bronchial carcinoid tumors
Restrictive pattern - the MC central lung CA in young
Obstructive
(FEV1/FVC >70%
pattern
predicted,
Normal nonsmokers.
(FEV1/FVC <70% spirometry *C/F
FVC <80%
predicted)
predicted) -They typically arise in the proximal
• Interstitial lung
• Anemia airway and cause airway
• Pulmonary obstruction (dyspnea, wheezing,
diseases
Low embolism
DLCO
• Emphysema • Sarcoidosis
• Pulmonary
postobstructive pneumonia)/
• Asbestosis hemoptysis.
hypertensi
• Heart failure
on
• Musculoskeletal #Dx:
• Chronic
Normal
bronchitis
deformity -CT scan with contrast : reveals an
DLCO • Neuromuscular
• Asthma
disease
avidly enhancing (ie,
hypervascular) mass with an
• Pulmonary
hemorrha endobronchial component.
Increas
ge
ed • Asthma • Morbid obesity
•
DLCO
Polycythe
mia

83) small cell lung CA Mx:

• Patient with small cell lung cancer (uniform, small
round cells with dark nuclei), which is often initially
treated with chemotherapy followed by radiation
and/or surgery
• Patient is young and has no signs of metastasis so
palliative care isn’t appropriate

—>surgical resection is NOT used in small cell

lung cancer specifically (“the cells are too small
This is mucus plus as same side for the surgeon to see!”)
deviation not pleural effusion

84) Bronchiectasis Mx.

• Potential etiologies of bronchiectasis: (1) Congenital: Cystic fibrosis, Kartagener’s (2)
Chronic/prior infection: Aspergillosis, mycobacteria (3) Rheumatic disease:
Rheumatoid arthritis, Sjogren’s (4) Immunodeficiency: Hypogammaglobulinemia (5)
Airway obstruction: Cancer

• Key idea: Bronchiectasis should be worked up with CF testing, PFTs, sputum

culture, immunoglobulin levels and high-resolution CT of the chest
85) Mx of asthma
-#Rx:
1) Immediate phase:
-Initial treatment with inhaled short-acting beta agonist (eg, albuterol), improves
symptoms by relaxing airway smooth muscle and reversing bronchoconstriction.

2) late-phase reaction:
In addition to bronchodilators, systemic glucocorticoid (eg, prednisone, dexamethasone)
to reduce ongoing bronchial inflammation and severity of the late-phase reaction.

86) # Indication for antibiotics in COPD

- All patients with acute COPD exacerbation should receive bronchodilators and systemic
glucocorticoids.
In addition, antibiotics are indicated for patients with the following:

• Moderate to severe COPD exacerbation (defined as >2 cardinal symptoms),

especially with increased sputum purulence or
• Mechanical ventilation requirement (endotracheal intubation or noninvasive
positive pressure)

# Advantage of antibiotics in COPD:

-In such patients, antibiotic therapy has demonstrated increased likelihood of clinical
improvement, reduced risk of subsequent exacerbation, and decreased in-hospital
mortality in cases requiring mechanical ventilation.

empiric antibiotic therapy is directed at common upper respiratory bacterial

pathogens (Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus
pneumoniae) and

-Ab: macrolides (eg, azithromycin)+ respiratory FQs (eg, levofloxacin,

moxifloxacin)/ penicillin/beta-lactamase inhibitors (eg, amoxicillin-clavulanate).
-Typical duration of antibiotic therapy : 3-7 days.

87) Mx of hemoptysis
-The greatest danger in massive hemoptysis is not exsanguination but asphyxiation due to
the airway flooding with blood.
-Initial management in hemoptysis involves establishing adequate patent airway,
maintaining adequate ventilation and gas exchange, and ensuring hemodynamic stability.
-Patients should be placed with the bleeding lung in dependent position (lateral position).
-Bronchoscopy is the procedure of choice to identify the site and attempt early therapeutic
intervention.
88) Mx of exercise induced asthma:
- Beta agonists and mast cell stabilizers are important in the management of EIB.
1) Short-acting beta-adrenergic agonists such as albuterol, used 10-20 minutes prior to exercise, are
typically sufficient to prevent symptoms.
- SABA is considered first-line therapy if used only intermittently (less than daily).

2) An antileukotriene agent can be used 15-20 minutes prior to exercise for those unable to tolerate beta
agonists.
- Montelukast can be used as an alternative to daily inhaled corticosteroids in patients who exercise daily
and require daily albuterol pre-treatment.

3) A combination of beta agonists and antileukotriene agents may also be used in high-performance
athletes.

4) Steroid inhalers may be appropriate for athletes who exercise daily and would require daily pre-
treatment with albuterol. These are also the preferred treatment for persistent asthma.
89) Differentiate COPD versus Bronchiectasis??
-Bronchiectasis is a disease of abnormal bronchial widening in the setting of recurrent
infection and inflammation.

⇐
1) Its presentation can be similar to that of chronic bronchitis, but in bronchiectasis,
sputum production is more prominent (> 100 ml/day)
Vs scant sputum in chronic bronchitis

2) the chest x-ray of bronchiectasis:dilated conducting airways vs

prominent bronchovascular marking in chronic bronchitis

.
3) FVC is often low (<80% of predicted) due to airway destruction vs
normal FVC in bronchitis

4) in bronchiectasis, and exacerbations are typically bacterial

(usually viral in chronic bronchitis)

5) smoking is the most important risk factor for chronic bronchitis,

a causal relationship with bronchiectasis has not been established.

90) Which Cxs occur in COPD patients post operatively :

—>> At increased risk for postoperative pulmonary complications :
- pneumonia
- respiratory failure requiring mechanical ventilation.

#How to reduce Post Op Cxs in COPD patients :

—>> Medical optimization of COPD symptoms (eg, dyspnea, wheezing) prior to surgery
helps reduce this risk.

#role of smoking :
- Active smoking is also an independent risk factor for postoperative pulmonary
complications, and this effect is amplified in patients with underlying lung disease. So
we stop it 4-6 wk before
Predictors of 30-day mortality in PE
• Hypotension SBP <90 mm
• Tachycardia, >110/min
• Tachypnea, >30/min
• Hypothermia, <30 C (<86 F)
Clinical
• Hypoxemia, <90%
• Altered mental status
• History of cancer
• Age >80
Radiological • Right ventricular dysfunction
• Troponin
Laboratory
• Brain natriuretic peptide
 Management options for pulmonary embolism 92) Key idea: On NBME exam, crackles often
• All patients unless specific mean (1) Pulmonary edema (heart failure
Anticoagulation contraindications to
anticoagulation
exacerbation, etc.) (2) Interstitial lung disease
• Anticoagulation contraindicated or (IPF, sarcoidosis)
Inferior vena
ineffective
cava filter
• Low cardiopulmonary reserve
• Pulmonary embolism with
• Key idea: Normal CT better for detecting
hypotension (systolic blood cancer, whereas high-resolution CT needed
Thrombolysis pressure <90 mm Hg)
AND to have enough resolution to see the
• Low bleeding risk
fibrotic lung disease
• Shock likely to cause death within
hours
• Key idea: IPF exclusively seen in older
Embolectomy
(percutaneous
OR patients and much higher risk of IPF in
• Failed thrombolysis (or
or surgical) patients with significant smoking history
thrombolysis contraindicated) with
persistent hypotension

#Key idea: Bladder cancer, kidney cancer, and pancreatic cancer will almost always be
seen in smokers on the NBME!
#Remember NG tube/ ET tube worsens aspiration pneumonia not relieving it
-Head elevation relieves it

93) pulmonary cachexia

-Severe chronic obstructive pulmonary disease commonly accompanied by pulmonary
cachexia, which is characterized by loss of lean muscle mass due to energy imbalance
and systemic inflammation.

Vs

Although most cases occur in the central portion of the lung

(proximal tracheobronchial tree), up to 40% arise in the periphery.

# granuloma with acellular content: cassation so TB

If wid cellular content: sarcoidosis
95) pH changes in OSA: amboss
-Borderline low pH, normal O2, elevated pCO2, elevated serum bicarbonate concentration,
and decreased s Cl are consistent with compensated respiratory acidosis.

-Respiratory acidosis develops in patients with OSA during sleep due to upper airway
obstruction that causes alveolar hypoventilation and subsequent retention of CO2.
Prolonged periods of respiratory acidosis are eventually compensated by renal retention of
bicarbonate and decreased chloride reabsorption.

-While awake, patients with OSA do not have upper airway obstruction, so arterial pCO2
typically returns to normal level

96) Pathogenesis of ARDS

1) Gas exchange is impaired due to ventilation-perfusion mismatch

2) Lung compliance (ability to expand) is decreased (stiff lungs) due to

• -both loss of surfactant and
• -increased elastic recoil of edematous lungs

3) Pulmonary arterial pressure is increased (pulmonary hypertension) due to

• -hypoxic vasoconstriction,
• -destruction of lung parenchyma, and
• -compression of vascular structures from positive airway pressure in mechanically
ventilated patients
Empyema
• Bacterial invasion of pleural space resulting in
fibrinopurulent consolidation
Etiology
• Usually due to progression of a complicated
parapneumonic effusion
Common • Oral anaerobic bacteria (likely most common)
organisms • Streptococcus pneumoniae, Staphylococcus aureus
• Symptoms of pneumonia (eg, fever, dyspnea, pleuritic
chest pain)
Clinical • Insidious presentation (eg, 1-2 weeks or more), weight
features loss
• Laboratory evidence of inflammation (eg, leukocytosis,
thrombocytosis)
• Chest tube drainage when possible (ie, empyema is free
flowing)
Manageme • Intrapleural fibrinolytic drugs (eg, tPA/DNase) may assist
nt* drainage
• Surgical decortication for highly fibrotic, loculated
effusions
*In addition to antibiotics.
 RS paediatric
1) Transient tachypnea of the newborn: self-limited condition
-caused by delayed resorption and clearance of pulmonary fluid; > with C/S
-C/F: present shortly after birth with respiratory distress and fluid in the interlobar
fissures on chest x-ray.
2) D-transposition of the great arteries
-C/F: tachypnea and cyanosis without retractions or grunting.
-Clue: As most of the systemic blood flow bypasses the pulmonary vasculature,
supplemental oxygen does not significantly improve oxygenation.

3) Severe aortic coarctation

- shock due to poor distal perfusion on closure of the DA.
-Onset: DA begins to constrict as early as 12 hours (not immediately) after birth.

-Clue: a lower postductal (eg, left lower extremity) than preductal (eg, right upper
extremity) oxygen saturation would be expected.

4) Persistent pulmonary hypertension of the newborn

-high pulmonary vascular resistance, causing right-to-left shunting across the DA.
-C/F:Cyanosis and respiratory distress occur, but chest x-ray is often normal, and
preductal oxygen saturation is typically higher than postductal saturation.

5) Respiratory distress syndrome

-C/F: preterm infants with grunting, flaring, retractions, and cyanosis immediately
after birth.
-Cxray:diffuse, ground-glass opacities and air bronchograms.

6) Congenital diaphragmatic hernia

- respiratory distress at birth with absent breath sounds on the affected side, a barrel-
shaped (round chest, and a scaphoid (flat) abdomen.

-cxr:intrathoracic bowel loops and a displaced cardiac silhouette

-Ix of choice: CT chest and abd: > sensitive

8) Allergic bronchopulmonary aspergillosis (ABPA)

must be suspected when lung function declines without explanation, or persistent
lower respiratory infection symptoms occur despite adequate antibiotic therapy;
IgE > 1000 especially in Pt wid underlying structural Ds like asthma and CF
D/D for Respiratory Distress in a Neonate

•
-
9) Apnea of prematurity: due to immature central respiratory centers in the pons
and medulla
• Intermittent apnea (cessation of respiration for >20 seconds)
• Often associated with bradycardia & desaturation
• Well-appearing between episodes
*Rx: Caffeine till 34-36 weeks post maturation age ; Noninvasive ventilation ; Resolves
with time

Vs
#Indications for Apnea Evaluation in newborns :
—>> Evaluation for other causes of apnea is reserved for the following situations:

• New, sudden-onset apnea after first few days of life

• Severe manifestations of apnea (eg, requiring resuscitation)
• Ill-appearing with abnormal physical examination findings between episodes
• Symptoms persist longer than expected (ie, beyond term)

10)pneumothorax in children:
-RF: premature neonates, particularly with RDS receiving mechanical ventilation.
#Dx: Transillumination reveals increased brightness on the affected side.
#Mx: Hemodynamic instability / signs of tension pneumothorax (eg, mediastinal shift)
warrant emergency needle thoracostomy.

11) RF increasing RDS:

-prematurity;male sex, perinatal asphyxia, maternal diabetes, and CS without labor

-High levels of circulating insulin antagonize cortisol and block the maturation of
sphingomyelin, a vital component of surfactant.

#Factors decreasing RDS:

-Intrauterine growth restriction, maternal hypertension, and chronic intrauterine
stress from prolonged rupture of membranes decrease the risk of RDS.
-Intrauterine stress is thought to stimulate early fetal lung maturity.

12) Pediatric OSA:

-MCC: adenotonsillar hypertrophy
-Cx: Poor growth (ie, failure to thrive); Poor school performance; Cardiopulmonary (eg,
hypertension, structural heart changes); enuresis due to raised BNP

-Rx: Tonsillectomy & adenoidectomy

Amniotic fluid embolism 13) Normal RS physiologic changes in pregnancy
• Advanced maternal *Pathophysiology: progesterone-induced sensation of
age dyspnea and an increase in minute ventilation that is
• Gravida >5 (live
driven mostly by increased tidal volume, RR same
births or stillbirths)
• Cesarean or
Risk factors -Basilar lung compression by the gravid uterus
instrumental
delivery decreases residual volume and FRC
• Placenta previa or -Vital capacity and FEV1 : unchanged
abruption
• Preeclampsia
14) FEV1 and (DLCO) are the best predictors of
• Cardiogenic shock
Clinical • Hypoxemic postoperative outcomes following lung resection
presentatio respiratory failure (Should be >40%)
n • DIc
• Coma or seizures 15) Coarctation of aorta different murmurs:
• Respiratory & a) systolic murmur (due to blood flow through a
Treatment hemodynamic support constricted aorta) heard at the left infraclavicular area
• ± Transfusion
anteriorly and left interscapular area posteriorly
(sometimes difficult to auscultate in the supine position);
b) continuous at multiple areas on thorax (collateral vessels )
-H4 (left ventricular hypertrophy)

17) Empiric Ab in CF:

-Empiric antistaphylococcal antibiotics should be administered immediately and intravenously in
patients with severe pneumonia.

1) Cefepime, a 4o cephalosporin, provides coverage for both (MSSA) and Pseudomonas

2) IV vancomycin is therefore the most empiric antibiotic choice as it covers MRSA

-Ciprofloxacin: P aeruginosa in adults with CF

 RESPIRATORY RESPIRATORY—PATHOLOGY
`  SEC TION III 709

Lung cancer Leading cause of cancer death. SPHERE of complications: Superior vena cava/
Presentation: cough, hemoptysis, bronchial thoracic outlet syndromes, Pancoast tumor, Horner
obstruction, wheezing, pneumonic “coin” syndrome, Endocrine (paraneoplastic), Recurrent
• Key idea: Lung lesion on CXR or noncalcified nodule on CT. laryngeal nerve compression (hoarseness),
cancer classically Sites of metastases from lung cancer: liver Effusions (pleural or pericardial).
metastasizes to (jaundice, hepatomegaly), adrenals, bone Risk factors include tobacco smoking, secondhand
(pathologic fracture), brain; “Lung ‘mets’ smoke, radiation, environmental exposures (eg,
the adrenal gland Love affective boneheads and brainiacs.” radon, asbestos), pulmonary fibrosis, family history.
In the lung, metastases (usually multiple Squamous and small cell carcinomas are sentral
lesions) are more common than 1° (central) and often caused by smoking.
neoplasms. Most often from breast, colon,
prostate, and bladder cancer.
TYPE LOCATION CHARACTERISTICS HISTOLOGY
Small cell
Small cell (oat cell) Central Undifferentiated Ž very aggressive. Neoplasm of
carcinoma May produce ACTH (Cushing syndrome), ADH neuroendocrine
(SIADH), or Antibodies against presynaptic Ca2+ Kulchitsky cells Ž small
channels (Lambert-Eaton myasthenic syndrome) dark blue cells A .
or neurons (paraneoplastic myelitis, encephalitis, Chromogranin A ⊕,
subacute cerebellar degeneration). Amplification of myc neuron-specific
oncogenes common. Managed with chemotherapy +/– enolase ⊕,
radiation. synaptophysin ⊕.
Non-small cell
Adenocarcinoma Peripheral Most common 1° lung cancer. Most common subtype Glandular pattern, often
in people who do not smoke. More common in females stains mucin ⊕ B .
than males. Activating mutations include KRAS, EGFR, Bronchioloalveolar subtype:
and ALK. Associated with hypertrophic osteoarthropathy grows along alveolar septa
-
(clubbing). Ž apparent “thickening”
Bronchioloalveolar subtype (adenocarcinoma in situ): of alveolar walls. Tall,
CXR often shows hazy infiltrates similar to pneumonia; columnar cells containing
better prognosis. mucus.
Squamous cell Central Hilar mass C arising from bronchus; cavitation; cigarettes; Keratin pearls D and
carcinoma hypercalcemia (produces PTHrP). intercellular bridges
(desmosomes).
Large cell Peripheral Highly anaplastic undifferentiated tumor. Strong Pleomorphic giant
carcinoma association with tobacco smoking. May produce hCG cells E .
Ž gynecomastia. Less responsive to chemotherapy;
removed surgically. Poor prognosis.
Bronchial carcinoid Central or Excellent prognosis; metastasis rare. Symptoms due to mass Nests of neuroendocrine
tumor peripheral effect or carcinoid syndrome (flushing, diarrhea, wheezing). cells; chromogranin A ⊕.
A B C D E
 710 SEC TION III RESPIRATORY RESPIRATORY—PHARMACOLOGY
` 

Pancoast tumor Also known as superior sulcus tumor. Carcinoma that occurs in the apex of lung A may cause
A
Pancoast syndrome by invading/compressing local structures.
Compression of locoregional structures may cause array of findings:
ƒ Recurrent laryngeal nerve Ž hoarseness
ƒ Stellate ganglion Ž Horner syndrome (ipsilateral ptosis, miosis, anhidrosis)
1st rib
ƒ Superior vena cava Ž SVC syndrome
Mass ƒ Brachiocephalic vein Ž brachiocephalic syndrome (unilateral symptoms)
ƒ Brachial plexus Ž shoulder pain, sensorimotor deficits (eg, atrophy of intrinsic muscles of the
hand)
ƒ Phrenic nerve Ž hemidiaphragm paralysis (hemidiaphragm elevation on CXR)

Superior vena cava An obstruction of the SVC that impairs blood B

syndrome drainage from the head (“facial plethora”;
A
note blanching after fingertip pressure in A ),
SVC
neck (jugular venous distention), and upper
Ao
extremities (edema). Commonly caused by
malignancy (eg, mediastinal mass, Pancoast clot
tumor) and thrombosis from indwelling
catheters B . Medical emergency. Can raise RA
LV
intracranial pressure (if obstruction is severe)
-

-
Ž headaches, dizziness,  risk of aneurysm/
rupture of intracranial arteries.

RESPIRATORY—PHARMACOLOGY
` 

H1-blockers Also called antihistamines. Reversible inhibitors

of H1 histamine receptors. May function as
neutral antagonists or inverse agonists.
First generation Diphenhydramine, dimenhydrinate, Names usually contain “-en/-ine” or “-en/-ate.”
chlorpheniramine, doxylamine.
CLINICAL USE Allergy, motion sickness, vomiting in pregnancy,
sleep aid.
ADVERSE EFFECTS Sedation, antimuscarinic, anti-α-adrenergic.
Second generation Loratadine, fexofenadine, desloratadine, Names usually end in “-adine.” Setirizine
cetirizine. (cetirizine) is second-generation agent.
CLINICAL USE Allergy.

Superior vena cavaFar

ADVERSE EFFECTS less sedating than 1st generation because of
syndrome
 entry into CNS.
: potential complication of lung malignancy,
-C/F: headache, facial swelling, and jugular venous engorgement without peripheral
edema vs edema + in HF
#Mx:
-The primary treatment is radiation therapy as a palliative measure.
-Malignancy-related SVC syndrome, especially when it causes respiratory compromise,
may require endovenous stenting followed by radiation therapy, although this
treatment is primarily palliative.
-Depending on the type of malignancy and prior treatment course, some patients may
benefit from chemotherapy.
 RS surgery
1) Tracheobronchial injury
-Persistent pneumothorax and large air leak despite tube thoracostomy in the setting
of blunt chest trauma suggest tracheobronchial rupture.

-next best step: Bronchoscopy can confirm the diagnosis prior to operative repair.

2) Bronchiolitis obliterans
- chronic lung transplant rejection and is common >5 years posttransplant.
-gradually progressive dyspnea and nonproductive cough)
- PFT: obstructive pattern.

3) Nonseminomatous germ cell tumors

-typically produce both alpha fetoprotein and human chorionic gonadotropin tumor markers.
-anterior mediastinal mass

4) blunt thoracic aortic injury (BTAI): MC site isthmus

-Widened mediastinum on chest x-ray and left-sided pleural effusion (hemothorax) may be
present from hemorrhage preceding containment (eg, hematoma).

-next step: CT angio (DONT TICK TTE )

5) Displaced fractures of ribs 9-12 can injure intraabdominal organs, including the spleen.
Bleeding that irritates the diaphragm may cause referred pain (eg, to the left shoulder).

6) Atelectasis
-common postoperative complication that results from shallow breathing and weak
cough due to pain.
-Time: postoperative days 2 and 3 following abdominal / thoracoabdominal surgery.
-prevention: Adequate pain control, deep-breathing exercises, directed coughing, early
mobilization, and incentive spirometry
Vs

-GA related: aspiration and residual anesthetic effects usually appear within the first few
hours after surgery, often before the patient leaves the perioperative unit.

7) 1) FB in upper airway (eg, larynx) : stridor +/- life-threatening, ARD

Vs
2) chronic FB in the lower airways (eg, bronchi) :
NO stridor but can present with recurrent pneumonia that improves symptomatically but
still has persistent radiographic changes.
8) hereditary hemorrhagic telangiectasia (HHT)/ Osler-Weber-Rendu disease:
-patient's constellation of hemoptysis, chronic recurrent epistaxis, pulmonary bruit,
nodular lung lesions, and anemia

9) lung transplant:
a) acute: <6 months; Rx: High dose GC
Vs
b) chronic/ bronchiolitis obliteran: months-yrs after transplant; Rx: repeat transplant

10) intercostal vessel tear:

#Classic case: Hypovolemic shock in the setting of blunt chest trauma is concerning for
intrathoracic hemorrhage. Rib fractures (with intercostal vessel injury) are a common
cause of hemothorax.
#Mx:
-Hemothorax is treated with tube thoracostomy, which is sufficient to resolve many
cases, although if immediate chest tube output is >1,500 mL /of blood, Persistent
hemorrhage: >200 mL/hr for >2 hours, / continuous need for blood transfusion to
maintain hemodynamic stability emergent surgical thoracotomy is indicated.
Vs
#ascending aorta tear:
-typically occurs after a more severe mechanism of rapid deceleration (eg, fall >3 m [10
ft], motor vehicle collision), and the aortic isthmus (rather than the ascending aorta) is
the most commonly affected site.

-Ascending aortic involvement would likely have additional findings :acute coronary
syndrome, cardiac tamponade, or focal neurologic deficits (from cerebrovascular
ischemia).

11) Superior pulmonary sulcus (Pancoast) tumors : lung Apex tumour

-location: arise in the apical pleuropulmonary groove

12) #Danger box: even small external wound injury suggest serious underlying injury

-Central penetrating wounds inside "the box"—delineated superiorly by the clavicles,

inferiorly by the costal margins, and laterally by the nipples—are particularly
dangerous because of the underlying heart and mediastinal structures.

Clavicle

☐ Nipple

Costal margin
#Case : Bronchiolitis obliterans :
—> After 5 years of Lung transplant, patient is
experiencing breathlessness with following PFT :

76% of #Case clue : A lung transplant recipient with progressive

Forced vital dyspnea, an obstructive pattern (ie, FEV1/FVC <70%) on
expect
capacity (FVC) pulmonary function testing (PFT), and no evidence of
ed
infection (eg, no fever, chest x-ray abnormalities, or
Forced
60% of organisms on bronchoalveolar lavage) likely has
expiratory
expect bronchiolitis obliterans, the major manifestation of chronic
volume in 1
ed lung transplant rejection.
second (FEV1)
FEV1/FVC —>> Despite immunosuppressive therapy, nearly 50%
68%
ratio
of lung transplant recipients develop evidence of
chronic rejection by 5 years posttransplant.
13)Indications for Emergent thoracotomy:
- some patients (up to 15%) require emergent thoracotomy for extreme bleeding,
including those with:

• Initial bloody output >1,500 mL

• Persistent hemorrhage: >200 mL/hr for >2 hours, or continuous need for blood
transfusion to maintain hemodynamic stability

14) SVC:
*Etio:
-CA: small cell lung cancer) and NHL
-Other: fibrosing mediastinitis (secondary to histoplasmosis or Tb infection) or
thrombosis secondary to indwelling central venous devices.

-When the history and physical examination are suggestive, chest x-ray is warranted.

15) #Mx of spontaneous pneumothorax:

-depends on the size of the lesion and the clinical status of the patient.
*Types:
-Radiographically, pneumothoraces are categorized as small (≤2 cm) or large.
1) Small pneumothoraces in clinically stable patients
-observation and supplemental oxygen (regardless of oxygen saturation), which
enhances the speed of resorption.

2) large pneumothoraces
a) Stable patients with large pneumothoraces:
-should undergo decompression with a large-bore needle (eg, 14- to 18-gauge)
inserted in the 2nd / 3rd intercostal space in the midclavicular line / at the 5th intercostal
space in the mid or anterior axillary

b) hemodynamically unstable
-should undergo emergent placement of a tube thoracostomy

## what if no response by above measures??

If the lung fails to adequately re-expand (eg, <90% expansion) and a persistent air leak
is present,

-placement of a one-way valve,

-creation of a blood patch, or
-video-assisted thoracoscopic surgery (VATS) can be used.
—> For patients with recurrence, VATS pleurodesis or chemical (eg, tetracycline
derivative, talc) pleurodesis can be performed
 Acute respiratory distress syndrome: management & prognosis 16) Fluid balance
-def: net sum of all fluid intake and
• Lung protection: limit alveolar distending
volume (VT 6 mL/kg) & pressure (Pplat ≤30 output from the time of admission
cm H2O) .
Mechanical • Ventilation: tolerate permissive hypercapnia -Patients with ARDS often have an
ventilation by LVTV(ie, ↑ PaCO2 & ↓ pH acceptable) to
avoid excessive VT
initial positive fluid balance (eg,
• Oxygenation: set lowest feasible FiO2 (goal volume resuscitation for sepsis,
SpO2 92%-96%) to avoid O2 toxicity blood transfusion for trauma).
• Treat underlying etiology: source control (eg,
sepsis) -During hospitalization, a
• Prevent iatrogenic harm: negative fluid
Supportive care balance, timely extubation (eg, minimize
conservative fluid strategy aimed at
sedation) achieving a neutral or negative fluid
• ± Corticosteroids: select patients with balance accelerates recovery from
moderate-to-severe early ARDS ARDS, with a trend toward
• Mortality rate: 40% in hospital, death mostly improved survival rate ("dry lungs =
due to multiorgan failure
• Morbidity rate: 50% with chronic cognitive
happy lungs").
Prognosis
impairment & physical debility, 25% with
chronic pulmonary dysfunction (restriction & ↓
DLCO)

-This goal is accomplished by:

• Minimizing intake: avoiding unnecessary fluid boluses, concentrating intravenous drips
• Promoting removal: diuretics, renal replacement therapy

17) deep sulcus sign: deep costophrenic angle- pneumothorax

Vs
Blunted sulcus sign: pleural effusion

18) simple Pneumothorax: chest tube at 4th ICS, mid auxiliary

Vs
Tension : needle decompression at 2nd ICS mid Cavicular

19) Mechanism behind atelactasis: amboss

-In patients with bibasilar atelectasis, collapsed alveoli are unable to participate in gas
exchange, allowing venous blood to pass into the arterial circulation without becoming
oxygenated, which results in a right-to-left
-
shunt.
-The alveolar-arterial gradient is increased because of the VP mismatch.

20) don’t treat asymptomatic sarcoidosis just monitor

21) ways to check the location of ET: amboss

-chest x-ray, end tidal CO2 measurement via capnography, and epigastric
auscultation (gurgling suggests ET tube is in the GI tract).
-if ET in 1 bronchus: just pull it out
-if in esophagus (gurgling sound): remove ET and reintubate

21) Mx of rib fracture at single site:

-Analgesia and conservative fracture management are the treatment of choice for
uncomplicated rib fractures involving < 3 ribs, in which neither hemothorax,
pneumothorax, nor any other associated injuries are seen on FAST scan.

-NSAIDs are typically prescribed, and they may be given in conjunction with opioids or
intercostal nerve blocks if necessary.
-Adequate pain control is important in preventing splinting and atelectasis and their
sequelae (e.g., pneumonia).

22) Laryngotracheal stenosis

-should be suspected in individuals who develop subacute or progressively worsening
dyspnea, stridor, and signs of respiratory distress (tachypnea, accessory muscle use)
in the weeks or months following extubation, particularly in patients with prolonged
intubation (> 7 days).

#Mechanism:
-Pressure from the endotracheal tube causes local tissue ischemia, inflammation,
necrosis, and fibrosis, leading to laryngeal stenosis, while an overinflated cuff will
cause tracheal stenosis through a similar mechanism.
-PFT: fixed upper airway obstruction, but definitive diagnosis requires laryngoscopy
 Obs

# RDS in Infants of diabetic mothers

-Infants of diabetic mothers, regardless whether pre-gestational or gestational, are
at increased risk of respiratory distress syndrome (RDS), preterm delivery, and fetal
macrosomia.
#Pathogenesis
-Maternal hyperglycemia, with resultant fetal hyperinsulinemia, delays cellular
maturation. Consequently, immature pneumocytes in the fetal lungs are unable to
produce surfactant, resulting in RDS.
 Secondary aka Late PPH

I :

—> Case Discussion:

In a patient who has Gestational Diabetes with delivery of macrosomic infant & had intraamniotic
infection, the most likely cause of secondary PPH is retained products of conception from her prior
intraamniotic infection and prolonged induction of labor.

secondary (late) postpartum hemorrhage (PPH) :

—> Risk factors for secondary PPH are similar to immediate-onset PPH and include :
- prolonged labor,
- fetal macrosomia,
- intraamniotic infection Common causes are retained products of conception, postpartum endometritis,
and inadequate placental site involution (ie, subinvolution).

Intraamniotic Infection & Late PPH :

—> Pathogenesis :
- Patients with an intraamniotic infection are at risk for retained products of conception, even if the
infection is adequately treated, because the intrauterine inflammation allows for adherence of the
placental membranes to the uterine wall.
—> Uterine Tonicity :
- In contrast to a retained placenta, which causes immediate PPH with uterine atony (eg, boggy, enlarged
uterus), retained products of conception typically cause late PPH with either a boggy or firm uterus.
—> Evaluation :
Evaluation is with pelvic ultrasound (which can identify the location of the retained products),
—> Rx:
- dilation and curettage.
 Fates of Labor

1) Normal Vaginal Delivery :

- If above mentioned progress happens that is consistent with normal labor progression.
- With associated normal fetal station progression seen on the labor curve (from −2 to +1 station).
- With this normal labor progression, stable vital signs, and a category I fetal heart rate tracing (ie,
reassuring status), continue expectant management of NORMAL VAGINAL DELIVERY.

2) Cesarean Section Delivery

- Cesarean delivery is indicated for active phase labor arrest , defined as,
— no cervical change for ≥4 hours with adequate contractions or
-
— ≥6 hours with inadequate contractions
OR
— a category III fetal heart rate tracing.

3) Intra Uterine Pressure Catheter & Oxytocin augmentation :

- When labor has not completely arrested but cervical change slows to <1 cm/2 hr (labor protraction), an
intrauterine pressure catheter is placed to measure contraction frequency and force (via Montevideo units).
- If contractions are inadequate (<200 Montevideo units), labor is augmented with oxytocin in order to
increase contraction frequency and force.

4) Operative - Vacuum/ Forcep assisted Delivery :

- An operative vaginal delivery (eg, forceps-assisted vaginal delivery) is performed to expedite delivery
for
— category III tracings
or
— maternal exhaustion during the second stage of labor (10 cm dilation until fetal delivery).
# subchorionic hematoma
- an abnormal collection of blood between the uterus and the gestational sac. It can present
with first-trimester bleeding or as an incidental finding on routine ultrasonography.

-Management : expectant; serial ultrasounds can be performed to provide reassurance.

First Phase
Complications

÷
Normal Rate is
>=1 cm/2 hour

:
<1 cm/ 2 hours :
Protracted Labor

No Change :
Arrested Labor

Not to be mistaken :

==> An operative vaginal delivery (eg, vacuum-assisted vaginal delivery) is performed during the second stage of
labor (10 cm dilation until fetal delivery) to expedite delivery for category III tracings or maternal exhaustion. 
 Obs case clue
1) External anal sphincter insufficiency after delivery
a) Benign cause (eg, pelvic floor stretching by delivery:
-normal anal sphincter tone ; Sx resolves as the pelvic muscle regains tone

b) anal sphincter muscle defect

-weakened anal sphincter tone and asymmetric contraction / a palpable defect
-Requires endoanal ultrasonography before surgical repair

2) Metabolic complications of infants of diabetic mothers :

- hypoglycemia, hypocalcemia (decreased PTH by hypoMg) , and hypomagnesemia (by
osmotic diuresis)
-Serum calcium level should be obtained for symptomatic neonates (eg, jitteriness),
particularly if serum glucose is normal (>40)
-Rx:1st solve hypomagnesemia then hypoCa; Mostly Ca resolves on own

3) Abdominal x-ray : indicated for delayed passage of meconium (age >48 hr),

4) Placenta accreta:
-2nd-trimester ultrasound : a low-
lying placenta, myometrial thinning,
and numerous placental lacunae.

-Cx: increased risk of PPH not AP

-Rx: don’t try to remove placenta; CS
-
hysterectomy with placenta in situ
-

5) Preeclampsia
-due to insufficient trophoblast
invasion and resultant low
uteroplacental perfusion.
Fetal growth restriction
Vs
Symmetric Asymmetric
-placenta accreta:
• Estimated fetal weight <10th
Definition percentile or=birth weight <3rd . have excessive trophoblast invasion
percentile for gestational age =
and placental hyperperfusion (eg,
Onset • 1st trimester
• 2nd/3rd numerous lacunae).
trimester
• Chromosomal • Uteroplacental
abnormalities insufficiency
Etiology
• Congenital • Maternal
infection malnutrition
• "Head-
Clinical • Global growth
sparing"
features lag
growth lag
• Monitor/treat complications (eg,
Management hypoglycemia, hypothermia,
-3
polycythemia)
6) Eclampsia: sometime may present with only postictal state
• Hypertension, typically severe (ie, SBP ≥160 or DBP ≥110 mm Hg) vs hypotension
by epidural systemic absorption
• Seizure, typically tonic-clonic with postictal phase
• Severe headache
• Visual disturbances (ie, scotoma)
• Hyperreflexia dont mix with Malignant hyperthermia
• Proteinuria
CT head :B/L frontal or occipital edema
-

7) #retained placenta: causes immediate PPH with uterine atony (eg, boggy, enlarged
uterus)
Vs
#retained products of conception: typically cause late PPH with either a boggy or firm
uterus

8) secondary (late) postpartum hemorrhage (PPH). heavy vaginal bleeding (eg,

saturating ≥1 pad/hr, passage of large clots) >24 hours after delivery

*Risk factors for secondary PPH are similar to immediate-onset PPH :prolonged labor,
fetal macrosomia, and intraamniotic infection

9) Cervical laceration
*RF: trauma associated with operative vaginal delivery or fetal macrosomia (ie, >4 kg),
typically causes an immediate, not late, PPH.
-patient's bleeding is from the cervix itself not os

11) acid base balance in pregnancy:

Respiratory alkalosis as progesterone activated respiratory centres

#5 cm uterine size discrepancy is abnormal

12) obs causes of DIC: PPH, AP

13) Labor: painful, regular contractions that cause cervical
change. 10) Short interpregnancy interval
#False labor : mild, irregular contractions that cause no cervical
• <6-18 months
change and ultimately resolve without intervention. Definition from delivery to
next pregnancy
-Mx; Patients in false labor can be discharged home with labor • Maternal
anemia
precautions Complication • PPROM
s • Preterm delivery
'

#Etio of false labour: benign conditions (eg, mild dehydration) / • Low birth
I weight
serious etiologies (eg, PPROM, AP); .
- PPROM = preterm prelabor rupture
—> therefore, all patients with contractions (regardless of of membranes.
gestational age) require evaluation.
12)vaginal fluid leakage in pregnancy:
1) continuous: Vesicovaginal fistula

2) Intermittent:

→
a) PPROM: fern test+; nitrazine blue test+; gush of fluid by valsalva (coughing)
b) bacterial vaginosis: malodorous vaginal discharge
c) stress urine incontinence: leakage on raised intra abdominal pressure (standing
from sitting, laughing) ; pooling of urine In posterior vaginal wall.
-
-

13) Normal pregnancy follow up:

- monthly till 2 TM; 2 weekly till term( 36 week) ; weekly till delivery

14) Fetal head position:

-MC and safe: occipitoanterior as it has the smallest diameter.
-occipitotransverse: cause cephalopelvic disproportion and 2nd stage labour arrest

15) labour stage:

a) first stage of labor: begins with the onset of regular contractions and lasts until
complete (10 cm) cervical dilation.
• the latent phase (0-6 cm), when the cervix dilates slowly and has no defined
expected rate of cervical change
• the active phase (≥6-10 cm), when the cervix dilates rapidly with a normal
progression of ≥1 cm / 2 hours
b) second stage of labor: from cervix 10 cm dilated to fetal delivery; prolonged by
or
epidural

#Arrest of 2nd stage: no progress in spite of Pushimg for

a) primi: >3 hrs (without epidural)/ >4 hrs (with epi)
b) multiparty: >2 hrs(without epidural)/ >3 hrs (with epi)
-Etiology: Fetal malposition (eg, nonocciput anterior) contributes to cephalopelvic
disproportion, the most common cause of second stage arrest.
#3rd stage labour: upto placenta delivery

16) Tachysystole: >5 contractions/ 10 min;

Mx: left lateral position; stop uterotonic drugs,tocolytics

17) ADR of excessive oxytocin given for prolonged labour/ PPH:

-Hypotension; tachysystole; hyponatremic seizure ( oxytocin similar to vasopressin)
-hypoNa Rx with cessation and 3% NS in seizures.

18) Magnesium toxicity :

-High levels of Mg inhibit presynaptic Ach release—> NM inhibition.
-so, the 1st sign of magnesium sulfate toxicity : often hyporeflexia.

19) Classical C/S scar (upward vertical)

-> risk for uterine rupture ; other RF for rupture: mother>35 yrs;
 21) MCC of PPH
after C/S and
absent uterine

II
atony : rupture of

=
uterine artery into
retroperitoneum;

-Hemodynamically
unstable

Prolonged BT/CT —> VWD

22) Postpartum urinary retention:
-inability to void by 6hours after vaginal
delivery / 6 hours after removal of indwelling
catheter after C. sec.
-Dx: Bladder catheterization more accurate than
bladder USG >/=150 mL of urine confirms
diagnosis

÷
#Mx: usually self resolves in <1 wk; else
intermittent catheterisation

23) postpartum endometritis:

-fever 38C (100.4F) outside the 1st 24 hours
postpartum (known as postpartum fever); uterine
tenderness and malodorous discharge

- MCC of puerperal fever on 2nd & 3rd day

postpartum
- Causative organism: polymicrobial

—> Temp. of 37.9°C (100.2°F) after delivery is considered normal

24) Pubic symphysis diastasis:

#C/F:
-suprapubic pain that radiates to the back, hips, thighs, or legs ;Intact CNS exam
-O/E: point tenderness to palpation over the pubic symphysis and sometimes
-
have a
waddling gait.
-

#Management: conservative with supportive care (eg, pelvic support, physical therapy)
#Prognosis: most patients recover within the first 4 weeks postpartum.
-

20) Transverse lie: MC presentation: shoulder

25) Perineal laceration:
-1o: vaginal mucosa, perineal skin; 2o: muscle (bulbocavernosa); perineal body
-3o:sphincters anal (both ); 4o: rectal mucosa

#Mx: 1o, 2o: heal quickly; so supportive care

3o, 4o: anal incontinence, RV fistula ; so surgical repair

26) rectovaginal fistula (RVF):

-malodorous, tan-brown vaginal discharge +posterior vaginal dark red, velvety lesion
(rectal mucosa)
-MCC: obs injury; timing: within 1st 2 weeks postpartum
Vs

27) Vesicovaginal fistulas

-C/F: clear, watery vaginal discharge (ie, urine) and a fistulous tract on the anterior,
rather than the posterior, vaginal wall.

28) Fetal fibronectin (fFN),

•
— Timing: high until 20 weeks, low during 2nd & 3rd trimester & High again at term

ii.
#Mechanism: an extracellular matrix protein located between the maternal decidua and
fetal chorion, is secreted whenever this interface is disrupted (ie, labor).

#Indication: fFN testing helps distinguish preterm and false labor.

29) Abruptio:
#C/F:
-painful Vaginal bleeding; tender uterus;
-Fetus: loss of FHR variability
-uterus contraction: high frequency, low
amplitude

#Rx:
1st line: IV fluids with crystalloids
2nd line: left lateral position
3rd line: BT if no response to fluids;

#Rx: all APH with emergency CS except AP

*Concealed AP: focal pain then progressing to

diffuse abd pain/ back pain ; fundal Ht> expected
30) Placenta accreta:
#Antenatal USG: an irregular / absent myometrial-placental interface (retroplacental
hypoechoic zone) + intraplacental villous lakes —> planned C/S
-if Undiagnosed: difficulty with placenta delivery necessitates manual extraction —>
placental adherence and massive hemorrhage

31) Placenta previa:

-may resolve by lengthening of uterus towards fundus. So routine obs care and follow up
-Avoid digital cervical exam and vaginal delivery, intercourse; speculum and TVUS
safe.
-Only maternal blood affected so FHR normal initially

32) breast abscess in lactational mastitis:

-when pt with lactational mastitis on antibioticsx week, improved in pain, erythema but
worsening fever, malaise with tender nodularity/ fluctuate mass in breast, suspect
breast abscess.
—> lactational mastitis should improve with antibiotics in 1-2 days
0
—>next best Ix: USG

33) uterine rupture:

-loss of Fetal station; palpable abd Fetal parts; FHR decceleration: staircase sign

34) Ectopic pregnancy:

-Triad: abdominal pain, vagina bleeding, Amenorrhea;
#normal viable intrauterine pregnancy BHCG
-Next step: B HCG +; 2nd step: TVUS to confirm pregnancy location
level: rises every 2 days; ectopic rises at slower
rate.
35) vasa previa:
-Painless vaginal bleeding with ROM or contractions
-FHR abnormalities (eg, bradycardia, sinusoidal
pattern)
-Fetal exsanguination & demise
#Rx: urgent C/S at 34-35 weeks; no need of
MgSO4/ betamethasone MTX : <3.5 cm sac size,
No Fetal cardiac activity
36) Post LP headache: Not >5k HCG
-Headache occurs in occipital region and worsens by
sitting due to leakage of CSF
Normally HCG shud
-no associated hypertension/FND
double in 4 days
-Rx: epidural patch

37) Pre eclampsia :

-usually >20 weeks gestation; but occurs at <20 weeks in H mole
-Dx: urine protein/creatinine ratio >0.3 /24 hr U. > 300 mg/24hr / dipstic>+1
 #Risk factors for pre eclampsia:
-maternal age <18 or >40, multiple gestation,
nulliparity, preexisting DM, CKD and prior
preeclampsia, Obesity, Chronic HTN, SLE

Severe features of pre-eclampsia

=

38) Mx of pre eclampsia:

- goal : to stabilize mother by administering anti-hypertensive meds

i
• Without severe features: delivery at ≥37 weeks (after maternal stabilisation)
• With severe features: delivery at ≥34 weeks
• Magnesium sulfate (seizure prophylaxis); Antihypertensives: IV labetelol,
hydralazine

#AntiHT of choice:
-Labetalol: x β- in ↓ HR as it can further ↓ causing dizziness or lightheadedness
- Hydralazine: SAFE in bradycardia as it causes tachy
-Oral nifedipine: x in emesis
- furosemide: DOC in preeclampsia with pulmonary edema

##Methyldopa: DOC for Chronic HT of pregnancy

Preeclampsia prevention
• Prior preeclampsia
40) Choice of anti HT: • Chronic kidney disease
1) Non pregnant: • Chronic hypertension
High risk
- thiazide diuretics, • Diabetes mellitus
• Multiple gestation
- calcium channel blockers, • Autoimmune disease
- ACE inhibitors (or angiotensin II receptor blockers).
• Obesity
- Beta blockers not recommended Moderate
• Advanced maternal age
risk
Vs • Nulliparity
2) pregnancy: extended release Nifedipine Prevention
• Low-dose aspirin (81 mg) at 12
weeks gestation
 #In patients with vaginal
bleeding and unknown
placental location (even though
u r suspecting PP) ,
the best next step is
transabdominal ultrasound.

-Transabdominal ultrasound
has a high false-positive rate for
detecting placenta previa;

therefore, if transabdominal
imaging reveals a possible
previa, transvaginal
ultrasound is performed.

-Transvaginal ultrasound is safe in patients with suspected placenta previa as

visualization is optimal 2-3 cm away from the cervix, and the angle of the vagina prevents
the ultrasound probe from entering the cervical canal.

- Because most of the bleeding is maternal in origin (rather than fetal), reactive
tracings are initially seen..it’s not an indication for C/S

←#Mx of threatened abortion:

-Course: Patients with a threatened
abortion frequently have uncomplicated
pregnancies with normal outcomes.

-Therefore, management of a threatened

abortion is expectant with outpatient
observation.
-Serial ultrasounds can be performed until either the symptoms resolve or there is
progression to a complete abortion.

# Choriocarcinoma unusual case

-patient presents with abnormal uterine bleeding, pelvic pressure, a symmetrically
enlarged uterus, and a friable (vascular) vaginal nodules (it’s not kaposi) after
spontaneous abortion, a presentation concerning for choriocarcinoma, a type of
gestational trophoblastic neoplasia (GTN).
51) Choriocarcinoma:
-< 6 months after pregnancy/ abortion
-Mets sign : lungs; -staging: Cxray not CT scan; Rx:chemotherapy
41) type 1 diabetes mellitus (T1DM) are at risk for pre eclampsia
—> diabetic nephropathy (eg, proteinuria) and
—> vascular disease (eg, hypertension),
-so they are started on aspirin Px

42) 24 hr Urine protein in high risk at baseline decides the delivery plan:
• it helps determine whether blood pressure elevations later in pregnancy are due to
gestational hypertension or preeclampsia, which affects antepartum management and
delivery timing:

a) gestational hypertension : BP elevations with no significant changes in proteinuria.

-Mx:typically managed as outpatients and delivered at 37-39 weeks gestation.
Vs
b) preeclampsia: BP elevations and worsening proteinuria.
-Mx:require inpatient care and possible preterm delivery (<37 weeks gestation).

c)nephrotic-range proteinuria (>3.5 g/day) :at risk for thromboembolism and require
anticoagulation during pregnancy and postpartum.
43) Mg C/I in myasthenia gravis
as drug - release of Ach at NM.
-Rx of eclampsia: valproate
-

44) Acute fatty liver of

pregnancy (AFLP)
*Similarity: C/F overlap with
H those of HELLP syndrome,

*Difference:
-AFLP has > extrahepatic complications eg: leukocytosis, hypoglycemia, and AKI.
-Severe hypertension < in AFLP than in HELLP syndrome.
Vs
#HELLP: HT; low PC; Hematoma in liver capsule; MAHA
#Cx of hellp: Abruptio placentae; Subcapsular liver hematoma; ARF; Pulmonary edema;
DIC -

45) ovarian hyper stimulation syndrome:

-Pathogenesis: infertility treatment HCG injection —> over stimulation of ovarian
vascularity + multiple maturation of ovarian follicles

-C/F: Hemoconcentration, e- imbalance, 3rd space fluid loss; MODS, DIC, RF, Death
-USG: bilateral enlarged, cystic ovaries with multiple follicles; normal uterus
46)Fibroids in Pregnancy
-discrepancy between the uterine size and gestational age + H/O heavier, longer
menses with pelvic pressure prior +; O /E: enlarged uterus with an irregular contour

47) degenerating fibroids:

-Pathogenesis: as myometrial blood flow shifts toward the developing fetus and placenta during
pregnancy, leading to fibroid infarction and necrosis.
-C/F: degenerating fibroids cause uterine contractions (due to PG release) and fundal tenderness,
a tender mass, and leukocytosis (due to inflammatory cytokine release).

-Mx: conservatively managed : indomethacin for patients <32 weeks gestation)

-

=
48) uterine inversion:
-excessive traction causes the fundus to collapse into the endometrial cavity and prolapse through
the cervix
-O/E: fundus is no longer palpable transabdominally; firm, rounded mass protruding through
the vagina.

49) Vaginal hematoma

- firm, rounded bluish vaginal mass; -hypovolemic shock;
-blood loss is typically hidden in the paravaginal space (ie, occult bleeding with no passage of
large clots), and the uterine fundus remains palpable transabdominally.
RF: operative delivery, big baby
#Mx: non expanding- observe; expanding- embolisation/ Sx

50) meralgia paresthetica (MP):

-localized pain and paresthesia in the lateral thigh; no motor weakness as it’s sensory N.
-common in 3rd TM due to compression
-Mx: conservative; avoid tight clothing; Gabapentine ; no role of physical therapy

52) Mx of CL removal in pregnancy:

-patients with CL removal prior to 10 weeks gestation(eg:ovary removal in torsion) require
postop progesterone supplementation (eg, vaginal progesterone) to prevent pregnancy loss.
- Supplementation can be discontinued after 10 weeks gestation.

53) GBS Rx:

1) 1st line: Intrapartum IV penicillin/ ampicillin

2) if allergic to penicillin:
a) P/H/O of mild anaphylaxis: Cephalexin as cephalosporin has less cross reactivity
b) P/H/O of severe anaphylaxis:
- test for sensitivity to clindamycin and erythromycin: give clindamycin if both sensitive
- if resistant: give vancomycin; it’s less effective so observe baby after birth
 Prevention of complications:

POSTPARTUM HEMORRHAGE
UTERINE INVERSION

Se
Traction
AlsoNeurogenic Shock die
effect on surrounding peritoneum
rescuing in Paradoxical Bradycardi

potentially fatal
Risk factors:
Immediate manual replacement of uterus:

Uterine atony
after replacement
assisi

I
D/D of Uterine Inversion :
1. Prolapsing Fibroid : appear as a firm, rounded mass
protruding into the vagina; however, it is not typically
associated with severe abdominal pain or hypotension. In
addition, the uterine fundus would remain palpable
transabdominally.
47

2. Vaginal hematoma : a cause of postpartum hemorrhage that

can appear as a firm, rounded bluish vaginal mass. However,
Page

blood loss is typically hidden in the paravaginal space (ie,

occult bleeding with no passage of large clots), and the
uterine fundus remains palpable transabdominally.
54) Listeria monocytogens:
a) Infection 1st and 2nd TM: typically results in granulomatosis infantiseptica (ie,
disseminated abscesses/granulomas) and possiblee- IUFD.

b) Infection in 3rd TM :less severe and present as fetal distress, preterm delivery, or
early-onset neonatal sepsis.

55) ART during pregnancy:

a) Intrapartum
Viral load ≤1,000 copies/mL: ART + vaginal delivery
Viral load >1,000 copies/mL: ART + zidovudine + cesarean delivery
-
b) Postpartum
• Mother: continue ART —>
• Infant (maternal viral load ≤1,000 copies/mL): zidovudine
• Infant (maternal viral load >1,000 copies/mL): multidrug ART →
56) Alloimmunisation: rh- mom, rh + 2nd baby
-To prevent the maternal immune system from developing anti-D antibodies, anti-D
immune globulin is given
Dose: 1st administered at 28 wk gestation and repeated within 72 hrs of delivery.

-A standard dose of 300 µg at 28 weeks gestation can usually prevent

alloimmunization. However, ~50% of Rh-negative women will need a higher dose
after delivery, placental abruption, or procedures.
—> The Kleihauer-Betke (KB) test is commonly used to determine the dose.
Breastfeeding jaundice vs breast milk jaundice

Diagnosis Timing Pathophysiology

Clinical 57) Normal BF:
features
-On average, exclusively breastfed
Insufficient intake of breast milk
resulting in: Suboptimal BF newborns should feed for ≥10-20
First
Breastfeeding
week
• Decreased bilirubin S/o minutes per breast every 2-3 hours.
jaundice elimination dehydratio
of life
• Increased enterohepatic n
I
circulation -During the first week of life, the
Starts
at age
• Adequate number of wet diapers a day should
High levels of β-glucuronidase in breastfeed
Breast milk
3-5
breast milk deconjugate intestinal ing
equal at least the infant's age in days
days;
jaundice
peaks
bilirubin & increase enterohepatic • Normal (eg, a 4-day-old infant should have ≥4
circulation examinati
at 2
on wet diapers a day).
weeks

58) Mx of BF jaundice:
1) 1st line: If bilirubin levels are below the phototherapy threshold, breastfeeding jaundice
can be managed by optimizing lactation and increasing breastfeeding frequency.
2) 2nd line: If the mother's milk supply is inadequate, supplementation with cow's milk-
based formula can be considered, but breastfeeding should not be discontinued.
3) if dehydrated: IV fluids during hospitalisation
59) #indications for phototherapy??
-The threshold for phototherapy in a full-term, healthy, 4-day-old infant :total bilirubin ≥20 mg
-Exchange transfusion : levels ≥25 mg/dL/ those with bilirubin-induced neurologic
dysfunction.

60) Perimenopausal pregnancy

-Pregnancy can present in a perimenopausal woman with insomnia, fatigue, weight gain,
-
-should be evaluated with an hCG level. →
amenorrhea, and an enlarged uterus Vs atrophied uterus in menopause

62) Approach to Acute abdomen pain in F:

-Ixs based on Pregnancy test :
1) If the pregnancy test is +, pelvic USGto evaluate for an intrauterine or ectopic pregnancy
- helpful for evaluating ovarian pathology.
2) If the pregnancy test is -, abdominal CT can be considered to evaluate possible
appendicitis or kidney stones

3) Abdominal x-ray may also then be considered to rule out intestinal obstruction or
perforation (free air under the diaphragm).

Nonstress test 63) Initial maternal awareness of fetal

• Baseline of 110-160/min movement typically occurs at 16-20 weeks
Reactiv
• Moderate variability (6-25/min) gestation, and
• ≥2 accelerations in 20 minutes, each peaking
e
≥15/min above baseline & lasting ≥15 - maternal monitoring of fetal movement
seconds (eg, kick counts) begins in the third
Nonrea
• Does not meet criteria for reactivity
trimester (≥28 weeks gestation).
ctive

-normal fetal activity: ≥10 movements in 2 hours) typically indicates a normal fetal
acid-base status and low risk of fetal demise.

62) Signs of placental separation : a gush of blood, umbilical cord lengthening, increased
uterine tone, and rising of the fundus in the abdomen.
-Following placental separation, uterine contractions typically cause placental expulsion.

63) Retained placenta:

-The third stage of labor (ie, fetal delivery until placental delivery) typically lasts <30
minutes. In contrast, delayed placental delivery occurs when the placenta does not deliver
within 30 minutes
*Mx:
-Initial management includes gentle downward cord traction and oxytocin
administration to promote placental separation and expulsion.
-If the placenta does not deliver with these measures, manual placental extraction or
dilation and curettage are indicated.
64) PPROM:
-Membrane rupture at <37 weeks prior to labor onset
#Mx: <34 weeks (reassuring): latency antibiotics, corticosteroids
• <34 weeks (nonreassuring): delivery
I
• ≥34 weeks: delivery
#Cx:
-Preterm labor; Intraamniotic infection; Placental abruption; Umbilical
-
cord prolapse

65) Underweight (BMI <18.5 kg/m2) patients are advised to gain 12.7-18.1 kg (28-40 lb)
during pregnancy.

66) Risk factors for fetal anemia ←

- fetomaternal hemorrhage, maternal alloimmunization, and in utero infection (eg,
parvovirus), but not poor weight gain in pregnancy

67) Septic pelvic thrombophlebitis

- a postoperative / postpartum infected thrombosis of the deep pelvic or ovarian veins.
#Clue: -

treated empirically with antibiotics.

I
-Because the MC etiology for postpartum fever is endometritis, patients are initially

—> Persistent fever unresponsive to broad-spectrum antibiotic therapy and a negative

infectious evaluation (eg, blood and urine cultures, urinalysis) suggest SPT, which is a
-

diagnosis of exclusion.

#Mx: anticoagulation and broad-spectrum antibiotics.

68) complications of preeclampsia:

a) Maternal: abruptio placentae, DIC, and eclampsia
b) Fetus: FGR/LBW (ie, small for gestational age infant) even if the neonate is delivered at
term.

69) Erb-Duchenne palsy: The MC type of brachial plexus injury by shoulder dystocia
-involves cervical nerves (C5-7) upper trunk in brachial plexus
-Weakness of the deltoid and infraspinatus muscles (innervated by C5),
-biceps (innervated by C6), and
-wrist/finger extensors (innervated by C7) —> predominance of the opposing muscles.

#C/F:"waiter's tip":adducted, pronated, extended elbow, wrist and fingers flexed

#Management
- observation and physical therapy: because up to 80% of patients have spontaneous
recovery within 3 months.
-Surgical intervention (nerve graft, reconstruction, decompression) :
for infants with no improvement by age 3-9 months but is not necessarily curative
70) Superficial surgical site infection (ie, cellulitis)
-C/F: can occur after cesarean delivery and present with postpartum fever (≥38 C
more than 24 hours after delivery) as well as incisional induration and erythema.

-RF: obesity and emergency surgery (eg, inadequate skin antisepsis or antibiotic
prophylaxis).

71) Menopause like Sx after BF:

-Elevated prolactin levels associated with BF suppress GnRH release and induce a
hypoestrogenic postpartum state.
-C/F: experience dyspareunia due to atrophic vaginal changes (eg, dryness, loss of
rugation).
→
-Rx: supportive with nonhormonal lubricants and moisturizers.
-

72) Stretching of the round ligament

-caused by the enlarging gravid uterus can cause pain due to irritation of local nerve
fibers.
#C/F: the pain is typically located in the lower abdomen and ipsilateral labia and is not
associated with sensory changes
Vs
Sensory Sx in outer upper thigh : meralgia paresthetica

73) External cephalic version (ECV),

#Timing: performed in patients with malpresentation at ≥37 weeks gestation but not
in preterm patients as most fetuses will spontaneously rotate.
#Cx:
-risk of prelabor rupture of membranes and abruptio placentae, which require delivery
(and possible prematurity complications if delivered at <37 weeks gestation).
-ECV is not recommended during active labor due to its low success rate at that time.

74) Mx of migraine in pregnancy:

• 1st-line :Acetaminophen

←
• 2nd line: a low-potency opioid (eg, acetaminophen-codeine), antiemetics (eg,
promethazine), / caffeine/butalbital

• 3rd line: More potent opioids (eg, oxycodone) are typically not used due to their
tendency to worsen gastrointestinal symptoms (eg, constipation, nausea) during
pregnancy; however, they can be considered if all other options fail to improve
symptoms

#Preventive: propranolol
75) Screening during pregnancy: -

a) Anti D Ig:
-schedule: administered at 28-32 weeks gestation and again within 72 hours of
delivery if the baby is found to be Rh (D) positive.

—>The initial timing of 28-32 weeks is selected because the half-life of anti-D immune
globulin is about 6 weeks, which would cover any potential future exposure to fetal
red blood cells through most of the third trimester.

b) Routine Group B Streptococcus (GBS) rectovaginal screening

-timing:should be performed at 36-38 weeks gestation as the results are valid for 5 wks
-GBS colonization may be transient; for example, a patient who is negative at 28
weeks can become positive at 37 weeks.

—> Testing at 28 weeks is too early because there is no reason to assume the patient will
deliver prematurely.

c) HIV:
-Pregnant women should be screened for HIV infection at the first prenatal visit as early
initiation of anti-retroviral medications can significantly decrease disease transmission to the
fetus.
-Rescreening in the 3rd trimester : recommended for high-risk individuals

76) Intra-amniotic infection (chorioamnionitis)

-C/F: maternal fever + >/1 maternal and fetal tachycardia, uterine fundal tenderness, and
maternal leukocytosis.
#Mx: broad-spectrum IV Ab (eg, ampicillin, gentamicin, clindamycin) + immediate
delivery via augmentation of labor (to remove the source of infection) NOT C/S unless
indicated

77) IVH screening:

-Because IVH can be asymptomatic, all preterm neonates born at <32 weeks gestation
require screening head ultrasound.
Causes of hyperandrogenism in pregnancy
78) uterine atony
Diagnosis Clinical features
- a soft, boggy, enlarged uterus with the
Placental • No ovarian mass
fundus palpable above the umbilicus
aromatase • High maternal & fetal virilization risk because of decreased uterine tone.
deficiency • Resolution of maternal symptoms after delivery
• Solid, unilateral/bilateral ovarian masses

'
• Moderate maternal virilization risk; high fetal
Luteoma
virilization risk
• Spontaneous regression of masses after delivery
• Cystic, bilateral ovarian masses
Theca lutein • Moderate maternal virilization risk; low fetal
cyst virilization risk
• Spontaneous regression of masses after delivery
• Solid unilateral complex ovarian mass
Sertoli-
• High maternal & fetal virilization risk
Leydig
• Surgery required (2nd trimester or
tumor
postpartum)
 80) PPH: >500 mL after vaginal delivery; >1,000 mL after cesarean delivery
#immediate PPH: within 60 min

Amniotic fluid index (AFI)

Oligohydramnios Polyhydramnios (AFI ≥24
(AFI <5 cm) cm)
• Preeclampsia • Esophageal/duodenal
• Abruptio atresia
placentae • Anencephaly
Causes • Uteroplacental • Multiple gestation

I
insufficiency • Congenital infection
-
.

• Renal anomalies • Diabetes mellitus

• NSAIDs
• Meconium • Fetal malposition
aspiration • Umbilical cord prolapse
Complicatio
• Preterm delivery • Preterm labor
ns
• Umbilical cord • Preterm premature rupture
compression of membranes

-Amniotic fluid volume is maintained via

amniotic fluid production (ie, fetal urination) and
removal (ie, fetal swallowing); a normal volume
is required for fetal development (eg, lung
maturity).
Antepartum fetal surveillance Biophysical profile*
Test Description Normal result Abnormal result
Component Normal finding
• Nonreactive:
• Reactive: • <2 Nonstress Reactive fetal heart rate
Nonstress External fetal heart rate
• ≥2 accelerations test monitoring
accelerati • Recurrent
test monitoring for 20-40 minutes
ons variable or late Amniotic Single fluid pocket ≥2 × 1 cm or
• 2 points decelerations fluid volume amniotic fluid index >5
• 0 points
Fetal
• Nonstress test plus ≥3 General body movements
ultrasound assessment of movements
the following:
◦ Amniotic fluid volume
• Equivocal: 6 ≥1 Episodes of flexion/
points Fetal tone extension of fetal limbs or
◦ Fetal breathing
• Abnormal: 0,
Biophysical movement
8 or 10 points 2, or 4 points spine
profile ◦ Fetal movement
• Fetal
◦ Fetal tone
Oligohydramni ≥1 Breathing episode for
• 2 points per category if
os breathing
normal ≥30 seconds
movements
• 0 points if abnormal
• (maximum 10/10) Maximum score = 10: 0 = abnormal,
External fetal heart rate No late or 2 = normal for each component.
Late decelerations
Contraction monitoring during spontaneous or recurrent
with >50% of *Performed continuous observation for
stress test induced (eg, oxytocin, nipple variable ≥30 minutes.
- contractions
stimulation) uterine contractions decelerations

=
-
Doppler
High-velocity
#next step if abnormal BPP score (eg, 4/10) is
sonography Evaluation of umbilical artery flow consistent with fetal hypoxia.
diastolic flow Decreased, absent,
of the in fetal intrauterine growth
umbilical restriction only
in umbilical or reversed end- -Prompt delivery is indicated due to the high
artery probability of fetal demise.
artery

#Next step if nonreactive NST: requires further evaluation with a (BPP) / contraction stress test (CST). These

=
tests are equivalent in assessing fetal status and are selected based on available resources and relevant
contraindications.
-Contraindications to CST include contraindications to labor (eg, placenta previa, prior myomectomy).
 #Goal of Intrapartum electronic fetal
heart rate (FHR) monitoring
-to assess fetal brain oxygenation
status because a well-oxygenated
brain provides autonomic control of the
heart.

#Head compression does not result in

→ hypoxemia
-so doesn’t cause an abnormal BPP.
#Post term pregnancy
- (BPP) is performed in patients at
risk for uteroplacental insufficiency
(eg, ≥41 weeks gestation).

-Chronic hypoxemia causes an

abnormal BPP (<4) and suggests
imminent risk of fetal demise;

-Mx: delivery is typically indicated.

-Nuchal cords do not cause

oligohydramnios or decreased
fetal breathing movements

- -

FMx: amnioinfusion
Fetal heart rate tracing patterns #Mx of cat 3:
Requires all the following criteria: -maternal repositioning
• Baseline 110-160/min
• Moderate variability (6-25/min) - other intrauterine resuscitative interventions
Category I
• No late/variable decelerations (eg, oxygen administration, intravenous fluids,
• ± Early decelerations
-
• ± Accelerations
K discontinuing uterotonics)
Category • Not category I or III (indeterminate
II pattern) - Patients remote from delivery (not completely
≥1 of the following characteristics: [10 cm] dilated) who do not improve with
• Absent
-
variability + recurrent late initial resuscitative measures require an
g
decelerations
Category
• Absent variability + recurrent variable immediate cesarean delivery.
III
decelerations
• Absent variability + bradycardia
-
• Sinusoidal pattern
-
 VARIABLE DECELERATIONS
- Abrupt fetal heart rate (FHR) ↓ to a nadir followed by rapid return to baseline
- Duration and depth of each deceleration can be quite variable

Cord compression:
- Amniotomy (artificial rupture of membranes) release of amniotic fluid mechanical compression
and occlusion of umbilical artery, particularly during contractions ↑ in fetal systemic vascular
resistance and BP fetal baroreceptor activation ↓ fetal pulse ↓ BP
- Cord compression can impede fetal blood flow
- Intermittent variable decelerations (associated with <50% of contractions)— well tolerated by the
fetus— do not typically cause fetal hypoxia require close observation without intervention
- Recurrent variable decelerations occur with >50% of contractions— require treatment, as fetal acidosis
can develop with increasing frequency and severity of decelerations.
Maternal repositioning (e.g. left lateral position)—1st line—may ↓ cord compression and improve
blood flow to placenta
Amnioinfusion—2nd line if above fails—as cord compression may result from amniotomy and loss of
amniotic fluid, hence, instillation of saline into amniotic sac may ↓ cord compression and variable
decelerations
Instrumental vaginal delivery (eg, forceps, vacuum) would be indicated to expedite delivery if the

I
patient is fully (10 cm) dilated
o
: DO NOT use oxytocin as it can ↑ contraction strength and frequency and worsen variable
decelerations

Nuchal cord
- Cord around neck
- Associated with recurrent variable decelerations (abrupt decreases in FHR below the baseline of varying

=
depth and duration) but not adverse fetal outcomes. It is a common finding on ultrasound and at
delivery

Fetal baseline Hr >160/min, moderate variability, fetal tachy

Maternal fever
causes: intra amniotic infection (chorioamnionitis)
other causes : maternal Hyperthyroidism, meds (terbutaline), abruptio
placentae

VEAL CHOP
Variable: Cord compression
Early: Head compression
Accelerations: OK
Late: Placental
insufficiency
21
Page
83) Exercise should be avoided in pregnancy with the following features:
• At risk for preterm delivery due to
◦ cervical insufficiency
◦ preterm labor during current pregnancy
◦ preterm premature rupture of membranes

• At risk for antepartum bleeding due to

◦ placenta previa
◦ persistent second- or third-trimester bleeding

• With underlying conditions that could be exacerbated by exercise, such as

◦ severe anemia
◦ hypertensive disorders of pregnancy (eg, preeclampsia)
◦ restrictive lung disease
◦ severe heart disease

84) complete abortion

-a type of spontaneous abortion,
typically presents as lower
abdominal pain and heavy vaginal
bleeding with the passage of clots at
<20 weeks gestation.

-C/F: sx worsen until the products of

conception, often described as a
solid or sack-like bloody, white
Only mass, are expelled and the
symptoms lessen and resolve.

#Lab.
-+ β-hCG as it can take up to 6
weeks for β-hCG levels to become
undetectable.
#RF: tobacco, alcohol, and cocaine
use.
85) testing for Chlamydia trachomatis and Neisseria gonorrhoea is unnecessary in this
patient who is asymptomatic and who is not currently sexually active.

86) Gestational age estimation:

-Ultrasound dating with fetal crown-rump measurement in the first trimester is the most
accurate way to determine estimated gestational age (EGA). EGA should not be changed
based on measurement discrepancies on a second or third trimester ultrasound.

—> If the EGA varies by >7 days in the first trimester and >10 days in the second
trimester, then ultrasound EGA is used rather than LMP.

87) Endometrial ablation involves the resection and destruction of the endometrial lining
of the uterus for patients who have heavy menstrual bleeding and are unable to take
combination oral contraceptives, do not desire future pregnancy, or fail medical
management.

Gestational diabetes mellitus 87) Cx of shoulder dystocia:

• Human placental lactogen -Fetal complications : brachial plexus injuries,
Pathophysiology
secretion clavicular or humeral fractures, and hypoxic
• 24-28 weeks gestation encephalopathy.
Screening • 1-hr 50 g GCT
• 3-hr 100 g GTT
-Maternal complications : 4th-o (ie, rectal
• 1st-line: diet
Management • 2nd-line: insulin, glyburide, mucosa) perineal lacerations and PPH
metformin
• Fasting: <95 mg/dL #Next best step: Elevate legs & flex hips,
• 1-hr postprandial: ≤140 mg/ thighs against abdomen (McRoberts)
Target blood glucose
dL
goals
• 2-hr postprandial: ≤120 mg/
dL 88) Inadequate contractions
Postpartum
• Fasting glucose at 24-72 hr -defined as occurring less than 3/4 times in a
• 2-hr 75-g GTT at 6- to 12-
management
week visit 10-minute period with a strength less than
GCT = glucose challenge test; GTT = glucose tolerance
200 Montevideo units.
test.

-Montevideo units are calculated by summing the strength of each uterine contraction
(uterine peak pressure minus baseline pressure) over a 10- minute interval.

—> eg a patient has contractions every 5 minutes that are 30 mm Hg in pressure (60
Montevideo units). This indicates that the inadequate, hypotonic contractions are the
most likely cause of this patient's protraction of active labor.
Turtle sign: retraction of fetal head into perineum after delivery

E E -

both

×
43
Page
88) H mole:
-first-trimester vaginal bleeding, a uterine size–date discrepancy, and markedly elevated
β-hCG levels (eg, >100,000 mIU/mL).

89) An anembryonic gestation,

-a pregnancy with no embryonic development, can present
with vaginal spotting. However, it typically does not cause a
uterine size-date discrepancy.

-Ultrasound : an empty hypoechoic gestational sac (ie,

gestational sac ≥25 mm with no embryo or yolk sac).

HIV management during pregnancy 90) Preterm labour:

• HIV RNA viral load at initial visit, every 2-4 weeks after #RF: prior spontaneous preterm
initiation or change of therapy, monthly until undetectable, delivery, short interpregnancy
then every 3 months
Antepartu
• CD4 cell count every 3-6 months interval (eg, <6-18 months), and
m
• Resistance testing if not previously performed genitourinary tract infection (eg,
• ART initiation as early as possible
• Avoid amniocentesis unless viral load ≤1,000 copies/mL
group B Streptococcus [GBS],
• Avoid artificial ROM, fetal scalp electrode, operative
Chlamydia trachomatis).
vaginal delivery
Intrapartu
m
• Viral load ≤1,000 copies/mL: ART + vaginal delivery - In <34 weeks gestation, Mx
• Viral load >1,000 copies/mL: ART + zidovudine +
cesarean delivery includes attempts to delay
• Mother: continue ART delivery and minimize neonatal
Postpartu • Infant (maternal viral load ≤1,000 copies/mL): zidovudine morbidity and mortality
m • Infant (maternal viral load >1,000 copies/mL): multidrug
ART
associated with preterm delivery

# role of Mg:
-decreases the risk of cerebral
palsy in very preterm neonates
<32 wks.

*y not at ≥32 weeks ??

- potential maternal risks (eg,
respiratory depression, cardiac
arrest) associated with
magnesium toxicity

- → O -
91) Low back pain during pregnancy:
- common in the third trimester of pregnancy due to postural changes, weakened
abdominal muscles, and joint/ligament laxity.
#Mx: Conservative management - behavioral modifications, exercise, heating pads, and
massage.
-Pregnancy-related back pain usually resolves after delivery.

92) Inadequate contractions (<200 Montevideo units averaged over 10 minutes)

commonly lead to labor arrest

93) Inevitable abortion management :

1) Hemodynamically UNSTABLE pts .-
—> Surgical management via suction curettage as it removes the retained products of
conception, which stops the bleeding so solves the hemodynamic unstability

2) Hemodynamically STABLE pts .-

—> Expectant or medical (eg, misoprostol) management avoids the risk of surgical
complications (eg, uterine perforation, intrauterine adhesions)

94) Twins
-chorionicity (number of placentas)
-amnionicity (number of amniotic sacs) of the gestation
-monochorionic diamniotic twins (1 placenta, 2 amniotic sacs): T sign ; twin twin
transfusion syndrome
-Dichorionic diamniotic: lambda sign -MC and least Cx
-monochorionic monoamniotic :cord entanglement.

#Mx of twin twin transfusion:

-Mild TTTS : expectantly managed with serial ultrasounds to evaluate for worsening
clinical features.
-Moderate-to-severe : treated with laser coagulation of the placental anastomoses.
95) Breech presentation:
• Frank: hips flexed & knees extended (buttock presenting)
• Complete: hips & knees flexed
• Incomplete: 1 or both hips not flexed (feet presenting)

# breech presentation with no contraindications to vaginal delivery (eg, placenta

previa, prior classical cesarean delivery)
-can be offered an external cephalic version (manual rotation of the fetus to cephalic
presentation) at ≥36 weeks gestation.

96) ADR of epidural block:

-Hypotension is a common S/E of epidural anesthesia.
-Pathogenesis: blood redistribution to the lower extremities and venous pooling from
sympathetic blockade.
#Rx: left lateral position, IVF, vasopressors
Vs
#Wet tap: postural headaches that are worse with sitting up and improved with lying down
after delivery. Hypotension is not characteristic.
Vs
# "high spinal" or "total spinal,"
-Depression of cervical spinal cord and brainstem activity occurs when local anesthesia
ascends toward the head,

- It may happen with intrathecal injection or overdose of the anesthetic.

-C/F:1st signs- hypotension, bradycardia, and respiratory difficulty, and later,
diaphragmatic paralysis and possibly cardiopulmonary arrest.
 Postdural Puncture Headache

Remember:
= Positional Headache is the clue

Pathogenesis behind Post-Dural Puncture Headache :

==>> During placement of neuraxial anesthesia, unintentional dural puncture may occur, causing
cerebrospinal fluid leakage, low cerebrospinal fluid pressure, and resultant slight herniation of the brain
and brainstem.

- Therefore, patients can develop a positional headache (ie, headache worsens when sitting or standing
and improves with lying down), which correlates with the increased and decreased herniation/pressure on
the brain, within 72 hours of the procedure.

- Other associated symptoms may include nausea, vomiting, and neck stiffness.

Mx :
==> Most postdural puncture headaches are self-limited;
- If severe symptoms that interfere with activities of daily living : Rx epidural blood patch.

D/D :

==> Bacterial meningitis can occur as a complication of epidural placement and present with headache
and neck stiffness; this diagnosis is unlikely in a patient with no fever or altered mental status.

==> BPPV presents with positional nausea and vomiting (and occasionally headache) + Dizziness.

==> Migraine headaches can be associated with nausea, vomiting, and neck stiffness; they are often
improved with sleep and being in a dark room. However, headache is not positional.

==> Preeclampsia with severe features can develop postpartum, particularly in patients with gestational
hypertension, and present with headache and edema. However, headaches due to preeclampsia are not
positional.
 Women 3,35 yrs are at sed risk of fetal Aneuploidy
2. Prenatal Testing
PRENATAL forFETAL
TESTING FOR Fetal Aneuploidy
ANEUPLOIDY

£ :

- 0
Down 72 Up
SECOND TRIMESTER QUADRUPLE SCREENING Syndrome 9hcg
Inhibin A
rprate si

13
Page
97) BOTH painless vs painful in AP bleeding
placenta previa: maximum maternal bleeding; so mom hemodynamically unstable
Vs
Vasa previa: minimum bleeding; mom hemodynamically stable

98) GBS sepsis in neonate:

-early onset sepsis (<7 days): vertical transmission; so prevented by intrapatum Ab
Vs
-late onset sepsis(>7 days): horizontal transmission(hands) ; not prevented by Ab

99) Hyperemesis gravidarum

- results in a weight loss of >5% of prepregnancy weight, hypochloremic met alkalosis, and
ketonuria. -

—> HG can be differentiated from typical nausea and vomiting of pregnancy by the
presence of ketones on urinalysis, laboratory abnormalities and changes in volume status

100) Acute cervicitis in pregnancy:

-exclude abortion; yellow mucus discharge; Vaginal spotting;
-Cx: abortion; PPROM; neonatal conjunctivitis
101) Gestational DM
Routine prenatal laboratory tests - screening with a 1-hour 50-g
• Rh (D) type, antibody screen GCT, followed by confirmation
• Hemoglobin/hematocrit, MCV with a 3-hour 100-g glucose
• HIV, VDRL/RPR, HBsAg tolerance test:
• Rubella & varicella immunity -schedule: 24-28 wk

I
-
Initial prenatal visit • Pap test (if screening -Mx: • 1st-line: diet
indicated) • 2nd-line: insulin, glyburide,
• Chlamydia PCR metformin
• Urine culture
• Urine protein -Postpartum: FBS at 24-72hr
• Hemoglobin/hematocrit Followed by 2 hr GGT at 6-12 week
• Antibody screen if Rh (D)
24-28 weeks
negative 102) If fetal presentation is
• 50-g 1-hour GCT uncertain on digital cervical
• Group B Streptococcus examination
35-37 weeks —> a transabdominal ultrasound
culture
should be performed to confirm
fetal presentation and determine
the safest route of delivery.
103) Mx of BV in Pregnancy:
-Rx of symptomatic BV is metronidazole (500 mg twice daily for 7 days) or
clindamycin, regardless of pregnancy status.
-studies have shown no increased risk of congenital anomalies. Therefore, treatment does
not need to be delayed until the second trimester
 104) PPROM:
-rupture of membranes at
<37 weeks gestation prior to
the onset of labor (irregular
contractions and a closed
cervix).

OI
-

Vs
#Preterm: labour signs
started like cervical
.
effacement; dilation

105) non-lactating women

. typically resume menses
within 10 weeks of birth

See
105) IUFD should be suspected when fetal Doppler sonography fails to detect a fetal
.

heart rate in patients with decreased or absent fetal movement. (>20 wks)
-trans abdominal
-
Ultrasound is necessary to confirm the diagnosis.
.

To BF

;
-

Not Hep unless cracked nipples

108)absent or minimal variability (ie, ≤5/min):
-Pathogenesis: can indicate fetal metabolic acidosis and impending fetal compromise.
-
#Drug induced: -
-However, certain medications can cause transient absent or minimal variability unrelated
to fetal acid-base status.

-Opioids (eg, morphine) may decrease fetal heart rate variability due to fetal CNS
depression; exposed fetuses also typically have decreased frequency of accelerations.

-Mx: These changes are temporary and normalize as the medication effect
diminishes; therefore, these patients typically require only continued monitoring.

109) causes of Elevated maternal serum alpha-fetoprotein (MSAFP) levels:

-identify fetuses with neural tube defects ;other benign causes (eg, multiple gestation,
incorrect dating).
—> Therefore, patients with elevated levels require fetal ultrasound.

110) Cell-free fetal DNA testing of maternal plasma

- a noninvasive and highly sensitive and specific screening test for fetal aneuploidy.
-It is performed at ≥10 weeks gestation
—> abnormal results are confirmed by chorionic villus sampling or amniocentesis
-

111) Chronic HT a RF for Abruptio placenta :

-Maternal chronic hypertension, regardless of well-controlled BP, is associated with
widespread endothelial dysfunction.
#Pathogenesis:
-This dysfunction impairs normal development of the spiral arteries that supply blood to the
fetus and placenta; the result is abnormally high-resistance spiral arteries that lead to
low placental perfusion, ischemia, and possible infarction, all of which increase the
risk of abruptio placentae.

-In addition, chronic endothelial dysfunction increases vessel frailty and the risk of
vessel rupture at the uteroplacental interface.

112) Pulm edema in Pre eclampsia:

-Pulmonary edema is a life-threatening complication of preeclampsia with severe features.
#Pathogenesis
-It is caused by increased systemic vascular resistance, capillary permeability, and
pulmonary capillary hydrostatic pressure + decreased serum albumin levels
 → -

117) Fetal heart rate accelerations require a mature sympathetic nervous system, which
develops at 26-28 weeks gestation; therefore, extremely premature fetuses (<28 weeks
gestation

**bradycardia only if HR< 110

119) Vacuum-assisted delivery

- indication: typically chosen when extraction is expected to be easy, although it is
relatively contraindicated in fetuses with a gestational age less than 34 weeks.

-S/E: scalp lacerations, cephalohematoma, brachia! plexus injury caused by shoulder

dystocia, retinal hemorrhage, and intracranial hemorrhage.
Vs
# Forceps are chosen when the extraction is expected to be more difficult and
require fetal head rotation.
# S/E: laceration, intracranial hemorrhage, facial nerve injury unilateral facial paralysis,
skull fracture, and ocular injury. Mothers can also suffer from lacerations, urinary tract
injury, and anal sphincter injury.

118) Quiet fetal sleep is the MCC of a nonreactive nonstress test (eg, no
accelerations). -Because a fetal sleep cycle can last as long as 40 minutes, a nonreactive
NSFis extended (eg, 40-120 min) to ensure that fetal activity outside of sleep is captured.

119) Perineal lacerations

- common after vaginal delivery and typically cause perineal edema and pain with
urination.
-Uncomplicated perineal lacerations (eg, no fever or purulence) are managed
conservatively (eg, nonsteroidal anti-inflammatory drugs, sitz baths).
 Strep agalactiae aka GBS, a common COLONIZER of maternal GIT & GUT. Asymptomatic in Pregnant Women but vertically transmitted to neonate
during Vaginal Delivery or ROM resulting in —> Neonatal GBS infection —> Sepsis, Pneumonia so SCREENING & USE OF INTRAPARTUM
PENICILLIN markedly reduces incidence of Neonatal GBS infection.

GROUP B STREPTOCOCCUS INFECTION (GBS)

Ante Natal

Don T 0
3638
ra
f of EIFFEL intomainmiryingemm

party

mzO
m.EE
Screening earlier at <36 wks
gestation can miss pts who
are not colonized with GBS
until layer in Pregnancy
Or
It can result in unnecessary
antibiotic prophylaxis so
increased risk of bacterial
resistance in pts who are no
longer colonized with GBS at
delivery.

infants delivered 37wks at

are risk for UBS
infection greater
dit immature immune
12

system
Page
120) Intrapartum antibiotic prophylaxis
- administered to prevent neonatal group B Streptococcus (GBS) infection in patients with
an unknown GBS status and the following risk factors for vertical transmission:

rupture of membranes for ≥18 hours, intrapartum fever, and fetal prematurity (<37
weeks gestation).

121) exercise C/I of pregnancy:

• Contact sports (eg, basketball, ice hockey, soccer)
• High fall risk (eg, downhill skiing, gymnastics, horseback riding)
• Scuba diving; Hot yoga

123) Mx of preterm labour at >34 wks: expectant

-At ≥34 weeks gestation, tocolytic agents, such as indomethacin and nifedipine, are not
recommended to temporarily halt preterm contractions and delay labor because the
risks of indomethacin (eg, oligohydramnios, closure of the ductus arteriosus)
and nifedipine (eg, maternal hypotension/tachycardia) outweigh the neonatal risks
of preterm delivery

-Therefore, patients in preterm labor at ≥34 weeks gestation who have no

contraindications to vaginal delivery (eg, placenta previa), receive expectant labor
management.

Uterine surgical history & vaginal birth

Trial of labor
Surgery
contraindicated?
Low transverse cesarean
No
delivery (horizontal incision)
Classical cesarean delivery
Yes
(vertical incision)
Abdominal myomectomy Yes-do urgent
with uterine cavity entry laparotomy and
Risk for rupture Cs
Abdominal myomectomy
No
without uterine cavity entry
126) fetal head compression
-Early decelerations are caused by fetal head compression; these occur when the fetal
head descends closer to the cervix, which contracts and causes narrowing of the fetal
anterior fontanelle.
*Pathogenesis:
-The narrowed anterior fontanelle causes a transient alteration in cerebral blood flow and
stimulates a vagal response, which slows the heart rate.

-Mx; Early decelerations are a benign, physiologic finding and do not indicate fetal hypoxia;
therefore, these decelerations do not require intervention.
127) Fetal dysmaturity syndrome
-occurs in post-term (≥42 weeks gestation) pregnancies due to age-related placental
changes and resultant uteroplacental insufficiency, meconium stained
#C/F:
-Neonates are small for gestational age, have a thin body with loose skin, and have
meconium-stained amniotic fluid.
128) Postpartum urinary retention Pathogenesis:
Delivery planning for a nonviable fetus
• Acardia
• Perineal trauma from a prolonged second stage

¥
• Anencephaly
• Bilateral renal of labor and/or perineal laceration: results in a
agenesis pudendal nerve injury—>decreased voiding
• Holoprosencephaly
Fetal diagnosis • Intrauterine fetal sensation—>thereby promoting urinary retention,
demise and cause external urethral sphincter dysfunction.
• Pulmonary
hypoplasia
• Thanatophoric • Reduced sensory and motor sacral spinal cord
dwarfism
impulses from regional neuraxial anesthesia (eg,
Obstetric • Vaginal delivery epidural anesthesia)—> suppress the
management • No fetal monitoring
micturition reflex and decrease detrusor tone—>
Neonatal • Palliative care if not
management stillborn bladder atony.

129) Immunity to rubella

- routinely evaluated at the initial prenatal visit.
-Patients without immunity are vaccinated in the immediate postpartum period with the
live-attenuated mumps-measles-rubella vaccine.
-Postpartum vaccination prevents future infection but avoids the theoretical risk of congenital
rubella.

130) vaccine safe in pregnancy: Tdap; inactivated influenza; Rho D Ig

 Physiologic changes of pregnancy
• ↑ Blood volume (plasma > RBC
Cardiovascula mass) .

r • ↓ Systemic vascular resistance

-
• ↑ Heart rate & cardiac output
Es
• ↑ Central respiratory drive
Pulmonary (hyperventilation)
• ↓ PaCO2 (respiratory alkalosis), ↑ PaO2
• ↑ Renal blood flow & urine output
• ↑ GFR, ↓ BUN & serum creatinine
• ↑ HCO3− excretion (metabolic
Renal
compensation)
v. • ↓ Serum Na+ concentration (↑ ADH
secretion)
• ↑ Prothrombotic coagulation factors
Hematologic • ↓ Hemoglobin concentration (dilutional
anemia)
Late- & post-term pregnancy
Thrombocytopenia in pregnancy
• Late-term: ≥41 weeks
• Isolated, mild (100,000-150,000/mm3) gestation
Definition
Gestational • Asymptomatic; resolves in 6 wk • Post-term: ≥42 weeks
• Diagnosis of exclusion gestation

Preeclampsia • Prior post-term pregnancy

• Nulliparity
with
• Moderate to severe (<100,000/mm3) Risk • Obesity
severe factors • Age ≥35
• Hypertension ± headache/scotomata
features/ • Fetal anomalies (eg,
• ± ↑ Creatinine, ↑ AST & ALT
HELLP anencephaly)
syndrome • Fetal/neonatal
Immune- • Isolated, moderate to severe (<100,000/ ◦ Macrosomia
mediated mm3) ◦ Dysmaturity syndrome
◦ Oligohydramnios
thrombocytop • Asymptomatic or mucosal bleeding/bruising Complicati ◦ Demise
enia (ITP) • Normal PT, aPTT ons • Maternal
Thrombotic
thrombocytop
-
• Severe (<30,000/mm3) ✓
• Neurologic symptoms (eg, confusion,
◦ Severe obstetric
laceration
◦ Cesarean delivery
enic seizure), fever, abdominal pain, petechiae ◦ Postpartum hemorrhage
purpura (TTP) • Normal PT, aPTT
• Frequent fetal monitoring (eg,
Disseminated • Moderate to severe (<100,000/mm3) Manageme nonstress test)
intravascular
coagulopathy
• Bleeding (eg, oozing intravenous sites)
± thrombosis
nt
gestation
•
• Delivery prior to 43 weeks

(DIC) • ↑ PT, ↑ aPTT, ↓ fibrinogen

#Patients with oligohydramnios, a marker for placental insufficiency, require immediate

→
delivery. No need for BPP
-
134) Cervical insufficiency criteria :
-Def: a structural weakness of the cervix that predisposes to second-trimester pregnancy
loss. It is diagnosed by any 1 of the following criteria:

• Painless cervical dilation in the current pregnancy (ie, examination-based) /

• A 2nd-TM cervical length of ≤2.5 cm + a prior preterm delivery (iultrasound-based) OR
• ≥2 prior consecutive, painless, 2nd-TM losses (ie, history-based), which typically
present with mild symptoms (eg, vaginal discharge, light spotting) followed by
precipitous delivery

#Prevention:
-Prophylactic cerclage is performed in the first trimester (ie, 12-14 weeks gestation) in
patients with a history of cervical insufficiency before it can recur in the 2nd TM

135)uterine inversion Mx:

-discontinuation of uterotonics (eg, oxytocin) and immediate manual replacement of
the uterus to prevent exsanguination.

2) 2nd line
-Uterine relaxants and laparotomy may be required if initial attempts at manual reduction
are unsuccessful.

*foll is not urgent:

-If the placenta is still attached to the uterine wall, it should not be removed until after
the uterus is replaced because of the risk of massive hemorrhage

136) Mx of polyhydramnois:
• severe / symptomatic polyhydramnios at preterm gestation
-Cx: are at increased risk for obstetric complications, including preterm labor and PPROM
-Mx. amnioreduction (ie, amniotic fluid removal by amniocentesis

• mild, asymptomatic polyhydramnios at term gestation:

- can undergo expectant management because obstetric outcomes are unchanged by
increased antenatal fetal surveillance or intervention.

137) maternal serum quadruple test

-Time: performed in the second trimester (15-20 weeks) and consists of maternal serum
α-fetal protein (MSAFP), β-hCG, estriol, and inhibin A.

#What if abnormal:
-Patients with abnormal quadruple screening results can be offered cell-free fetal DNA
testing, which measures circulating, free maternal and fetal DNA in maternal plasma and
has a sensitivity and specificity of up to 99%.
-An ultrasound should be performed to evaluate for fetal anomalies.
138) warning sign of shoulder dystocia:
-prolonged 1st / 2nd stage of labor and retraction of the fetal head into the perineum after it
delivers (eg, turtle sign).

139) D/D for No visible intrauterine pregnancy + Positive beta-HCG test :

1) an ectopic pregnancy (ie, pregnancy implanted outside the uterus) or
2) an abnormal, nonviable intrauterine pregnancy (eg, anembryonic gestation).

#Next Step for such cases :

When the diagnosis is uncertain, patients may undergo diagnostic dilation and
curettage, a procedure that samples tissue within the endometrial cavity.

• A negative or decreased β-hCG level after DNC: an abnormal intrauterine

pregnancy; these patients require reassurance and observation only because the
abnormal products of conception have been removed by the dilation and curettage.

• A persistent rise in β-hCG level after D & C : ectopic pregnancy (ie, the uterus has
been evacuated but an extrauterine pregnancy continues to produce β-hCG).
- needs MTX

140) FA in NTD:
-Because neural tube closure occurs at 5-6 weeks gestation, when most patients are
unaware of their pregnancy (particularly if menses are irregular), all women should begin
folic acid supplementation at least 1 month before conception to ensure adequate folate
levels.
#Mx:
-Average-risk patients require 0.4 mg daily;
-high-risk patients (eg, prior affected pregnancy, antiepileptic use) require 4 mg daily.

141) postpartum physiological changes:

-uterine contraction, lochia, breast milk excretion and milk letdown, and chills and shivering
causing hyperthermia or low-grade fever.

#Physiology: These changes are hormone-mediated (eg, increased oxytocin/prolactin

levels, decreased estrogen/progesterone levels).

#Mx; Patients with these normal findings are managed with routine postpartum care.

142) Postpartum fever

→
-T ≥38.0 C (100.4 F), exclusive of the first 24 hours after delivery.
-
Vs
-mild hyperthermia from normal postpartum shivering: 37.9 C (100.2 F) at 8 hours
postpartum
143) Amphetamine abuse during pregnancy :
preterm delivery, preeclampsia, abruptio placentae, FGR, and IUFD

144) Differentiating delayed PPH from normal lochia:

-features concerning for delayed PPH:

• Passage of large blood clots

• Increased pad counts (eg, saturation of ≥1 pad/hr for ≥2 consecutive hours)

• Signs and symptoms of anemia (eg, dizziness, chest pain) due to acute blood loss
Vs
#Normal lochia: In contrast, passage of small clots, normal vital signs, a benign
examination (eg, firm uterus, intact perineal repair), and an appropriate postpartum
hemoglobin level likely has normal lochia.

—> the best next step : observation and reassurance that this bleeding is normal and
may last for up to 6 to 8 weeks postpartum.

145) Neonatal hypoxic brain injury

-can occur with severe, acute decreases in placental perfusion or fetal oxygenation (eg,
severe placental abruption, shoulder dystocia) because the fetus has no time to adapt
to lower oxygen levels.
*Never tick that in Pre eclampsia
-Because preeclampsia causes chronically low uteroplacental perfusion, over time the
fetus adapts by preferentially shunting oxygenated blood from the body to the brain,
thereby sparing brain injury.
146) Postpartum endometritis
Maternal cardiopulmonary adaptations - Pathogenesis: the result of inoculation of the
to pregnancy
uterine cavity by vaginal flora during labor or
• Cardiac delivery and is a polymicrobial infection.
◦ ↑ CO
◦ ↑ Plasma volume
◦ ↓ SVR #microorganism:
Maternal • Respiratory
adaptations ◦ ↑ TV
-Normal vaginal flora includes a mix of gram + (eg,
◦ ↓ FRC, RVdec group B Streptococcus [GBS]), gram -ve bacilli (E coli),
◦ (elevation of and anaerobes (eg, Gardnerella vaginalis);
diaphragm)
-VC, FEV1 same
-therefore, treatment requires broad-spectrum Ab
• Peripheral edema
• ↓ Blood pressure therapy with coverage for all potential bacterial types.
Clinical
• ↑ Heart rate
manifestatio
• Systolic ejection
ns
murmur
-common regimen: clindamycin (gram-positives and
• Dyspnea anaerobes) + gentamicin (gram-negative bacilli)
Vs PID Rx: Ceftriaxone + doxycycline is a dual-therapy regimen that covers the MCC of
acute cervicitis, N gonorrhoeae and Chlamydia trachomatis
 Common problems related to lactation Tocolytics

Diagnosis Clinical features Drug Mechanism Side effects

e
Maternal
Engorge Bilateral, symmetric fullness, tenderness
-
• Gastritis
ment & warmth Indomethacin Cyclooxygenase
• Platelet dysfunction
Fetal
(<32 wk) inhibitor
Nipple Abrasion, bruising, cracking &/or blistering • Oligohydramnios
injury from poor latch • Closure of ductus
arteriosus
Plugged Focal tenderness & firmness &/or Maternal

I
duct erythema; no fever • Tachycardia/
Nifedipine Calcium channel palpitations
Galactoc Subareolar, mobile, well-circumscribed, (32-34 wk) blocker • Nausea
ele nontender mass; no fever • Flushing
• Headache
Mastitis Tenderness/erythema + fever Maternal
• Tachycardia/
Abscess Symptoms of mastitis + fluctuant mass Terbutaline β-Agonist palpitations
• Hypotension
• Pulmonary edema
147) Mx of galactocele:
-No intervention is required for an asymptomatic galactocele; symptomatic galactoceles
may be needle aspirated.
-Ultrasound is the first-line imaging modality for diagnosis; aspiration confirms the
diagnosis and is curative. Ice packs and a supportive, well-fitting bra provide symptomatic
relief.

148) Hyperemesis gravidarum (HG) next step

- Patients with a hydatidiform mole / multifetal gestation are at increased risk for HG.
-Therefore, a pelvic ultrasound should be performed on all patients with HG to evaluate for
these causes.

149) Fetal constitutional smallness

- associated with short maternal stature, low prepregnancy weight, and female sex.
-Constitutional smallness presents with an ultrasound-estimated fetal weight <10% for
gestational age, normal umbilical artery Doppler evaluation, and appropriate interval
growth. Constitutionally small infants have normal long-term outcomes.

150) next Best step in PPROM :

-initial evaluation includes a sterile speculum examination to assess for pooling of
fluid in the vagina, followed by a phenaphthazine test and microscopic examination of
the vaginal fluid to assess for ferning.

151) HCG produced by syncytiotrophoblast: maintains corpus luteum upto 10 wks

Vs
-after that, placental progesterone take up the responsibility to maintain endometrium
152) pathophysiology of HELLP
-microvascular damage with subsequent activation of intravascular platelets. These
platelets secrete substances that further enhance platelet agglutination and aggregation,
which in turn results in an overactivation of the coagulation cascade.
-In severe cases, this overactivation can lead to disseminated intravascular coagulation.

153) prophylaxis given in APLS:

-A regimen of low-dose aspirin and LMWH (enoxaparin), is the recommendation for
preventing thrombosis and pregnancy-related complications in pregnant APLS
Recurrent Pregnancy Loss (RPL)
D/D
SEPTIC ABORTION

uprompt Uterine
evacuation is
Necessary
so no need to
waitforMisoprostol

ELECTIVE ABORTION

INTRAUTERINE FETAL DEMISE (IUFD)

still birth IUFD

Risk factors:

Somost
Real time USG of the
times
Monitoring the coagulation profile
Unknown
40
Page
 Gynec

# ADR of TL
==> Patient with bilateral tubal ligation, which can increase risk of ectopic
pregnancy (because if patient does inadvertently become pregnant, very high risk
of ectopic pregnancy because tube is blocked) NBME 8
 Gyn case clue
1) Pelvic organ prolapse: ant/ post vaginal bulge outside the hymen with straining/
valsalva
-cervical conization increases risk for cervical insufficiency only not POP
2) Exernal anal sphincter dysfunction: decreased sphincter tone and anal
incontinence

3) Lactational mastitis: flulike Sx, focal U/L breast pain with surrounding erythema and
induration.
Vs
4) Breast abscess: mastitis Sx (fever, erythema; pain)+ fluctuant tender mass
#Rx:Ab: Dicloxacillin, cephalexin+ IND

5) Cervical CA: exophytic, friable, irregularly shaped lesion and with postcoital spotting,
-
-not heavy menses nor firm, round mass.

6) Endometrial cancer :thick endometrium is viewed on ultrasound.

-(thin endometrium rules it out)

7) Ovarian cancer: typically presents with an adnexal mass; advanced disease :ascites.

8) Endometrial hyperplasia:
-irregular menstrual or postmenopausal bleeding rather than heavy, regular menses

9) Endometriosis
-chronic pelvic cyclic pain and dysmenorrhea with small, nontender uterus that is
immobile (eg, fixed) vs boggy enlarged uterus in adenomyosis.
-cervical motion tenderness), dysmenorrhea, dyspareunia, and distorted pelvic anatomy
(eg, cervical displacement).
10) Adenomyosis:
-C/F: heavy mences wiht enlarged, symmetrical boggy uterine swelling; midline dull
pelvic pain

11) Sertoli leydig cell tumor:

-rapid onset (<1 year) of virilization; elevated testosterone and normal DHEAS level.
Vs
12) Adrenal tumor:
-rapid onset (<1 year) of virilization with elevated testosterone and elevated DHEAS level.

13)Menstruating F is not a C/I for IUD .

15)Endometrial polyps:
-Intermenstrual spotting without uterine enlargement is hallmark, no amenorrhea
Vs
Fibroid: heavy regular mences

16) vesicovaginal fistula:

-typically continuous, painless leakage of urine/ clear fluid into the vagina.

17) Retained tampon: located in the posterior vagina rather than inside the uterus at
the cervical os.
-O/E: tampon would be soft, foul-smelling, and <5 cm in size rather than a firm and
round mass

18) Pudendal nerve by perineal Lacerations:

-decreased perianal sensation and wink reflex

19) Vaginismus/ genitopelvic syndrome: Mx is pelvic floor exercise

-pain with both sexual and nonsexual vaginal penetration (eg, tampon insertion,
per speculum exam), likely due to involuntary pelvic floor contraction
Vs
20) Vestibular hypersensitivity (vulvodynia)
-persistent localized vulvar pain with light touch( pen, hand) with no detectable cause

21) Tubo-ovarian abscess (TOA),

-C/F: fever, abdominal pain, and a complex multiloculated adnexal mass with thick
walls and internal debris. (USG)

22) Ruptured ovarian cyst: sudden severe U/L lower abd pain immediately following
strenuous/ sexual activity

23) Granulosa cell tumor

- Adult subtype: Breast tenderness; AUB; PMB + complex ovarian mass.
-Juvenile: precocious puberty
-H/P: Call-Exner bodies (cells in rosette pattern)
-Endometrial biopsy (due to possibility of concomitant endometrial hyperplasia/CA
-Sx: uterus sparing in premenopausal/ puberty; else remove all

24) cyclic breast pain: every month; after 2 weeks of mences, no palpable mass;
benign..

25) cervical mucus prior to ovulation:

-mucus is clear, elastic, thin in consistency, and described similar in appearance to an
uncooked egg white at midcycle
26) Bacterial vaginosis : a thin white/ off white discharge with an odor
27) Candidiasis : thick white to yellow discharge + mucosal erythema (specific)

28) Chlamydia cervicitis : mucopurulent cervical discharge (NOT VAGINAL) + friable

cervix -

29) Vaginal squamous cell carcinoma

-typically vaginal bleeding, malodorous discharge, and an irregular vaginal lesion.

30) Vaginal cuff dehiscence:

Post hysterectomy, peritoneal leakage through the vagina may be seen and apex would
appear inflamed, indurated, or open.

31) Uterine sarcoma

-C/F and examination similar uterine fibroids but it occurs in postmenopausal F who have
taken tamoxifen / pelvic radiation.
-

32) U/L breast bloody discharge: normal skin: intraductal papilloma;

If eczematous skin: Pagets Ds.

33) corpus luteum cyst: normal menstrual cycle with mid cycle pain

34) müllerian agenesis

absent uterus and cervix with otherwise normal secondary sexual characteristics (eg,
breasts, external genitalia) and ovary
-normal estrogen, FSH

35)Pelvic congestion syndrome

-typically presents as a dull, ill-defined pelvic ache that worsens with intercourse or
during long periods of standing.
Vs
-In contrast 1o dysmenorrhea , those with pelvic congestion syndrome have pain
prior to menses that is then relieved by menses.

36) von Willebrand disease (vWD)

-patient with heavy, regular menses; anemia; and normal coagulation studies likely has von
Willebrand disease (vWD)
*Lab:
-prolonged BT; however, platelet count and PT are normal.
-may have a prolonged activated PTT,
but activated PTT can be normal in those with mild disease or in states of increased
vWF synthesis (eg, pregnancy, oral contraceptive use, acute stress, thyroid hormone
supplementation).
37) Pubertal gynecomastia
- a benign, physiologic condition
-MC age: boys 12-14 during midpuberty (Tanner stage 3-4) due to transiently
increased testicular production of estrogen compared with testosterone and
peripheral conversion of prohormones to estrogen.
-C/F: Patients typically have a small (<4 cm), firm, unilateral or bilateral, subareolar
mass that may be tender to the touch.

38) Because many adolescents become sexually active during or immediately after the
pubertal transition, the adolescent visit should include contraceptive counseling and
discussion of safe sex practices.

39) Annual Chlamydia trachomatis screening

- indicated for all sexually active women age <25 due to the increased incidence of
infection in this patient population.

-For this reason, dual contraception with condoms plus another contraceptive method is
recommended for adolescents

41) Thelarche:
-The first sign of breast development is breast buds, which are characterized by
enlargement of the areola, elevation of the papilla, and growth of a small mound of
breast tissue.
-O/E : a firm, retroareolar mass that may be slightly tender.
-Because breast growth is often asymmetric, it is normal for the breast bud to be
unilateral in early stages.

==> Pubertal changes in girls typically begin around age 10 and as early as age 8.

42) physiologic neonatal vaginal bleeding:

-bleeding typically occurs within the first 2 weeks of life and may last for several days.

-maternal hormones may lead to temporary breast bud and external genitalia
engorgement during the first month of life.
-Mx:
no required treatment, and parents should be reassured that this brief bleeding is
physiologic and normal
43) what condom should latex allergy Pt use????
-patient should avoid latex condoms given her
allergy, she could use non-latex (e.g.,
polyurethane) condoms.
43) primary dysmenorrhoea:
#C/F:
-midline lower abdominal pain 1 or 2 days prior to menses that resolves a few days after
onset of menses with /out Malaise, dizziness, Nausea, vomiting, diarrhea
• Normal pelvic examination

#Mx
• NSAIDS —> 1st line in Sexually non-active
• Combination OCP —> 1st line in Sexually Active

44) Mx of abnormal uterine bleeding:

A) Hemodynamically stable:
-1st-line treatment : IV estrogen (conjugated equine estrogen) or high-dose oral
estrogen/progestin contraceptive pills.
-High-dose progestins : patients with C/I to estrogen (eg, history of thromboembolism).

B) In hemodynamically unstable:
-anemic patients (eg, tachycardia, hypotension), a DNC and/or a packed RBC transfusion

45) Turner syndrome:

-Delayed and less Thelarche(as no Estrogen); low growth spurt cz absent X so less
estrogen
-cz TS does not affect the adrenal glands, normal adrenarche occurs and patients often
develop pubic and axillary hair.

46) primary amenorrhea

-Def: the absence of menarche in girls age ≥13 with no secondary sexual characteristics (or
girls age ≥15 with secondary sexual characteristics [eg, axillary/pubic hair]).
*Ix:
-Initial evaluation is with a pelvic ultrasound to determine the presence or absence of a
uterus.
-In those with a uterus the best next step is an FSH level, which helps distinguish
between central and peripheral causes of amenorrhea in the hypothalamic-pituitary-
ovarian (HPO) axis.

47) abnormal uterine bleeding (AUB),

defined during adolescence as menstrual bleeding <21 days or >45 days apart.

48) VWF dx: clinical, cystourethroscopy

RVF: fistulography, MRI, endosonography
 • I
** Fact : Absent breast development
during female puberty indicates a lack of
estrogen

Next best step: pelvic USG

2nd best step

13) Partial ovarian torsion:

-intermittent, self-resolving episodes of U/L pelvic
pain due to temporary ovarian vessel occlusion.
Vs
14) Partial torsion —> complete ovarian torsion.
-severe, constant, unilateral pelvic pain due to
ongoing ovarian ischemia; urgent lapro
 48) prognostic factors of breast cancer, in the order of decreasing significance:
1) TNM
2) ER+ and PR+ are good prognostic features.
3) Overexpression of the Her-2/neu oncogene is related to a worse prognosis.
4) histological grade : also tends to reflect the outcome. Poorly differentiated tumors have
the worst prognosis.

49) Mx of vaginal FB:

1) if easily visualized small foreign body (eg, toilet paper):
-an attempt at removal (after application of a topical anesthetic in the vaginal introitus) can
be made using vaginal irrigation with warm fluid or a swab.

2) when girl or the type of foreign body prohibits clinical evaluation??

-require the patient to undergo sedation or general anesthesia for examination (eg,
vaginoscopy) and foreign body removal.

50) fibrocystic changes of the breast:

-patient's diffusely nodular (eg, cordlike thickening) breasts and bilateral, nonfocal
premenstrual tenderness
-Rx: nsaids; OCP
52) intraductal papilloma
51) Benign breast disease -papillary tumor originating from the breast duct lining);
Diagnosis Clinical features -however, this benign growth is typically too small (≤1
• Solitary, well-circumscribed cm) to be palpable on clinical breast examination.
Breast cyst & mobile mass
#, it would not cause overlying skin retraction (ie,

I
• ± Tenderness constant
• Multiple, diffuse
invasion of suspensory ligaments) like DCIS
Fibrocystic nodulocystic masses
changes • Cyclic premenstrual 53) Phyllodes tumors
tenderness
• Solitary, firm, well-
-in the early stages of growth, shares similar
Fibroadenom
circumscribed & mobile characteristics with fibroadenomas (ie, unilateral,
mass isolated, firm, well circumscribed, mobile).
a
• Cyclic premenstrual
tenderness
• After trauma/surgery -However, phyllodes tumors typically grow much
Fat necrosis
• Firm, irregular mass
• ± Ecchymosis, skin/nipple
larger, resulting in changes to the shape, contour,
retraction and skin (eg, necrosis) of the affected breast.
53) ruptured ovarian cyst
-can cause hemoperitoneum, which presents with abdominal rigidity, rebound,
guarding, and referred shoulder pain. ; O/E: adnexal mass +/-
-Sudden-onset, severe, U/L lower abdominal pain immediately following strenuous or
sexual activity vs mild pain in mittelschmerz
-USG: pelvic free fluid
-Rx: stable widout infection/ hemoperitlneum: supportive; unstable: Sx

54) Fat necrosis

* similarity with breast CA:
- mimic breast cancer in its clinical and radiographic presentation
- it commonly presents as a fixed mass with skin or nipple retraction
- gives the appearance of calcifications on mammography.

* differentiating point:
-Ultrasonography : demonstrate a hyperechoic mass, which often correlates with a
benign etiology.
-Biopsy : diagnostic and typically shows fat globules and foamy histiocytes.
#Mx: remove it; no increase risk for breast CA

- • -

a .
 •

I NSAIDs;
=
supportive bra

56) • Physiologic nipple discharge : usually bilateral, multiductal, milky or nonbloody

and is expressed only with manipulation of the breast
—> typically caused by a benign process outside the breast (eg, hyperprolactinemia).

spontaneous
—> Etio: papilloma, carcinoma, abscess) is present within the breast.
i.
• Pathologic nipple discharge : usually unilateral, uniductal, bloody or serous, and

57) bloody nipple discharge:

1) with breast mass: invasive ductal carcinoma
2) Without rest mass: intraductal papilloma

58) Inflammatory breast carcinoma (IBC)

-an aggressive breast cancer that can present with unilateral breast rash, erythema, and
edema.
-Metastatic disease (eg axillary lymphadenopathy) is common on initial presentation.
-Dx: Patients require core needle breast biopsy and full-thickness skin punch
biopsy.
59) Mx of CIN 3:
-Dx gold std: Colposcopy:

-Rx of choice: cervical conization,

excision of the intact transformation
zone,

#Types of Cervical conization

a)(cold knife conization): with a
scalpel
b) loop electrosurgical excision
procedure (LEEP): via
electrocautery
60) Dx of choice in gynec:
#Pelvic ultrasound : the preferred initial imaging modality for suspected gynecological
tumors.;high sensitivity for diagnosing uterine fibroids and ovarian pathology.

#Diagnostic laparoscopy
- used to confirm clinical suspicion of endometriosis / pelvic adhesions, ademomyosis
both conditions are not reliably diagnosable by radiologic imaging.

61) evaluation prior to IUD insertion in AUB:

Contraindications to IUD placement
-IUD placement in patients with unexplained,
• Pregnancy
• Endometrial or cervical
abnormal vaginal bleeding can mask Sx
cancer
• Unexplained vaginal -Therefore, these patients require further
bleeding evaluation prior to IUD insertion, which typically
Copper IUD &
• Gestational
progestin IUD
trophoblastic disease includes: STI testing, endometrial biopsy, and
• Distorted endometrial pelvic USG.
cavity
• Acute pelvic infection
(eg, PID, cervicitis)
62)malignant adnexal mass:
-In the evaluation of an adnexal mass, ultrasound
• Active liver disease
Progestin IUD
• Active breast cancer findings concerning for ovarian malignancy :
Copper IUD • Wilson disease
complex appearance and abnormal internal
Emergency contraception
features (eg, irregular thickened septations,
Timing after
Method
intercourse
Efficacy Contraindications
papillary projections); ascites
• Acute pelvic
infection
-suspicious adnexal mass findings require further
Copper-containing
• Severe uterine
cavity
evaluation.
intrauterine
device
0-120 hr ≥99%
•
distortion
Wilson disease
-No role of BIOPSY as it could lead to rupture of
Best • Complicated
organ
the mass and result in spreading of the cancerous
transplant
failure cells throughout the abdomen
Ulipristal 0-120 hr 98%-99% • None
Levonorgestrel 0-72 hr 59%-94% • None 63) Protective for ovarian epithelial CA:
Oral
contraceptives*
0-72 hr 47%-89% • None -OC Pills; Multiparity; BF & Pregnancy
*Combined estrogen/progestin oral contraceptives containing
levonorgestrel or norgestrel.
#RF:HRT; Endometriosis; Infertility
64) Mx of fibroid: • Early menarche/late menopause
-Rx when Sx present; Asx: observe
-Rx:
a) Medical: OCP and progesterone IUD; GnrH agonist (short term); TXA
b) myomectomy sx
65) The genitourinary syndrome of menopause, / atrophic vaginitis
- vulvar and vaginal atrophy from loss of epithelial elasticity due to low estrogen levels.
- urogenital tissues thin, dry, and inelastic, making them more susceptible to injury (eg,
petechiae, vestibular fissures) and bleeding.
Vs
White plaques in LS

66) actinomycetes on pap:

-maybe normal flora/ cause PID
#Evaluation:
-patients with Actinomyces found incidentally on Pap testing require additional
evaluation for symptoms (eg, pelvic pain, abnormal vaginal discharge).

1) Asymptomatic patients: have minimal risk of infection.

-Therefore, they can maintain their IUD and require no further management.

2) symptomatic (eg, abnormal vaginal discharge, pelvic pain): -

- require IUD removal and empiric broad-spectrum antibiotics for PID

-The IUD is sent for culture;
-
-those with positive Actinomyces cultures require additional penicillin.

3) severe pelvic actinomycosis:

-C/F: systemic symptoms (eg, fever, weight loss) and a pelvic mass (ie, abscess).
- Rx:require IUD removal and culture, pelvic ultrasound, and prolonged penicillin
therapy (eg, 6-12 months).

67) puberty milestones:

1) Breast development (thelarche): 1st sign of puberty; age 8-12 in response to rising
estrogen levels.

2) Pubic hair development (pubarche) usually follows thelarche but can occur first.

3) (menarche) : expected around Tanner stage 4, approximately 2-2.5 years after

initial breast bud development i.e. 12.5;

4) In the 6 months preceding menarche, girls experience a growth spurt, a peak in

growth velocity.
 68) Ovarian hyperthecosis
- a cause of virilization but is typically diagnosed in postmenopausal women. Patients with

#
this condition also typically have signs of insulin resistance (eg, hyperglycemia, acanthosis
nigricans) and low/normal LH and FSH levels.
- Typical ultrasound findings : solid-appearing, enlarged ovaries rather than multiple cysts.

69) Aromatase deficiency:

-Normal internal genitalia + external virilization (eg, clitoromegaly) +
undetectable serum estrogen levels in a female patient
-transient masculinization of the mother that resolves after delivery.

#At birth: female infants have normal internal genitalia and ambiguous external
genitalia due to high levels of gestational androgens.

#In adolescence: delayed puberty, osteoporosis, undetectable estrogen levels (eg, no

breast development), and high concentrations of gonadotropins that result in polycystic
ovaries.
Vs
—> Similar above Fx + Hyponatremia >> Congenital Adrenal Hyperplasia

Diagnostic findings of amenorrhea

FSH LH Prolactin TSH
Ovarian failure ↑ ↑ Normal Normal
Functional hypothalamic
↓ ↓ Normal Normal
amenorrhea
Asherman syndrome Normal Normal Normal Normal
Prolactinoma ↓ ↓ ↑ Normal
Hypothyroidism ↓ ↓ ↑ ↑

70) -Breast cancer

- the 2nd MC cancer (after skin cancer) and the 2nd MCC of cancer death (after lung
cancer) in American women.

#BRCA testing:
--—>> Testing with F/H/O of cancer diagnosis at age <50, ovarian cancer at any age).
- Bilateral mastectomy can be offered to BRCA carriers.

71)All hormone-containing contraception is absolutely C/I in patients with breast cancer.

-A copper IUD is a safe, effective, hormone-free, long-term method of contraception.
 Absolute contraindications
72) #approach for suspected vulvar CA:
to combined hormonal contraceptives 1) 1st step: In suspected patients vulvar biopsy,
• Migraine with aura which distinguishes between benign (eg, lichen
• >15 cigarettes/day + age >35 sclerosus) and neoplastic disease.
• Hypertension >160/100 mm Hg
• Heart disease 2) 2nd step: In those with neoplastic changes,
• Diabetes mellitus with end-organ
damage -biopsy further determines the depth of invasion
• History of thromboembolic disease and differentiates between
• Antiphospholipid-antibody syndrome noninvasive (ie, vulvar intraepithelial neoplasia) /
• History of stroke invasive (ie, vulvar cancer) disease.
• Breast cancer
• Cirrhosis & liver cancer
• Major surgery with prolonged #Rx of benign biopsy:
immobilization - If this patient's lesion is benign on biopsy and is a
• Use <3 weeks postpartum recurrence of lichen sclerosus,
-she can be retreated with high-dose corticosteroids

#Rx of Malignant Ds:

1)noninvasive disease: either medical therapy (eg, imiquimod)
- / laser ablative therapy
2) invasive disease: require surgery (eg, wide local excision ± lymph node dissection)
.

and possible chemoradiation.

73) Primary infertility

1) <35 yrs: failure to conceive after a year of unprotected sexual intercourse
2) >35 yrs: After age 35, infertility investigation can begin after 6 months

#Evaluation:
1) HSG: best
-1st-line imaging to assess fallopian tube patency is a hysterosalpingogram,

2) A laparoscopy
-is useful for direct visualization and treatment of peritoneal adhesions and endometriosis.

3) A mid-cycle LH level is used to test for ovulation.

- The LH surge occurs 36 hours prior to ovulation and can be detected in urine and serum.
-if patient has regular menstrual cycles accompanied by mid-cycle pelvic pain
(mittelschmerz), which suggests ovulation. Therefore, an LH level would not be useful.

74) simple breast cyst:

-USG : posterior acoustic enhancement (indicative of fluid) and no echogenic debris or
-
=
solid components;
-aspiration, which should yield clear fluid and result in the disappearance of the mass

#F/U:As cystic fluid can reaccumulate, the patient should return in 2-4 months for a
follow-up clinical breast examination. 
-If the patient has no further s/o recurrence, annual screening can be resumed.
75) complex cyst:
-USG: echogenic debris, thick septa, solid components/ if the mass recurs or does not
disappear after aspiration.
-next step: core biopsy provides a tissue sample and is indicated.

Breast cancer warning signs

77) 5 alpha reductase deficiency
76) • axillary and pubic hair+
Clinical finding Pathophysiology
• Patients have no breast development (as
Nipple retraction Invasion of lactiferous ducts testosterone binds to the breast androgen
Nipple scaling or Epidermal infiltration by receptor and inhibits breast tissue
ulceration neoplastic cells proliferation)
Nipple discharge
Intraductal tumor growth ± Vs
necrosis
#Androgen insensitivity syndrome:
Invasion of suspensory -breast development, no secondary sexual
Skin retraction
(Cooper) ligaments
characteristics like pubic hairs
Obstruction of dermal
Peau d'orange
lymphatics
Invasion into adjacent breast
Fixed breast mass
tissue
Axillary Lymphatic spread to regional
lymphadenopathy lymph nodes

78) contraceptives in disabled adolescent: eg Down syndrome

-progestin-releasing subdermal implant, can be used for menstrual hygiene (eg, to decrease
menstrual bleeding)
Pap smear results requiring endometrial evaluation
Result Group requiring endometrial sampling
• Premenopausal women with:
Benign-appearing ◦ Abnormal uterine bleeding OR
endometrial cells Normal in
◦ Risk for endometrial hyperplasia
1st 10 days of mences
• Postmenopausal women
• Women age ≥35 OR at risk for
Atypical glandular cells
endometrial hyperplasia
Atypical glandular cells, favor
• All women
neoplastic

In women age ≥45, endometrial cells are reported because this finding is more
concerning for endometrial hyperplasia or cancer, particularly in patients who are
postmenopausal, symptomatic (ie, abnormal uterine bleeding), or at high risk (eg,
unopposed estrogen from obesity, chronic anovulation).
D/D of vaginal mass:
79) bartholin duct cyst
-soft, mobile, nontender, cystic mass is palpated behind /at base of posterior labium
majus

*Mx: Observation and expectant management are recommended for an asymptomatic

Bartholin cyst as spontaneous resolution may occur.
-Symptomatic cysts / abscesses : treated with IND followed by Word catheter placement.
-recurrent: marsupialisation

#Bartholin gland abscess:

localized erythema and induration and a tender, fluctuant mass

80) Gartner duct cyst

-appear along the lateral aspects of the upper anterior vagina —> do not involve the
vulva.
81) vulvar hematoma: tender, ecchymotic, firm mass from trauma

82) Skene glands :lateral to the urethral meatus (very anterior)

83) Mences just after menarche:

-Adolescents often have anovulatory cycles with irregular, heavy menstrual bleeding
due to an immature hypothalamic-pituitary axis.
-
#Rx: oral Progesterone normalizes menstruation by stabilizing unregulated endometrial
proliferation.

84) dermoid cysts

- surgically removed with either a laparoscopic ovarian cystectomy or oophorectomy
to reduce the risk of ovarian torsion and prevent complications (eg, infertility,
hemorrhage, sepsis) associated with ovarian necrosis.

85) Levonorgestrel IUD:

-efficacy : >99% and is approved for use in the United States for up to 5 years.
-S/E: amenorrhea, which can be used to improve anemia and abnormal uterine
bleeding.
-systemic side effects (eg, mood changes, breast tenderness, headaches).
Weight gain is not a side effect.

#MDPG: wt gain
90) ADR of tamoxifen:
-Hot flashes:MC; venous thromboembolism due to protein C resistance ; endometrial
hyperplasia

91) Mx of pelvic organ prolapse:

• Asymptomatic
◦ Observation
• Symptomatic
Pelvic floor muscle (Kegel) exercises; Vaginal pessary; Surgical repair

92) choriocarcinomas secrete markedly elevated hCG levels (>100,000 mIU/mL),

resulting in a positive pregnancy test

93)Endometriosis on bladder:
- Patients with bladder implants typically have cyclic hematuria, dysuria, suprapubic
tenderness, and negative urine culture.

94) perimenarche cycles:

-Anovulation typically resolves 1-4 years postmenarche, after which cycles normalize.

95) Mx of endometrial hyperplasia:

• Hyperplasia: progestin therapy or hysterectomy
• Cancer: hysterectomy with B/L salphingo oophorectomy with/out chemoradiation
—> Follow-up is with repeat endometrial biopsy (eg, every 3 months)
• On Biopsy, if stable or improved disease —> continue progestin therapy
• If progression to cancer —> hysterectomy

96) contraceptive in thromboembolism:

-Progestin-only contraceptives (eg, levonorgestrel-releasing intrauterine device) and the
copper-containing intrauterine device

98) physiological ovarian cyst : <3 cm

In premenopausal women, adnexal masses are typically benign, are related to ovulation
(CL cyst after mittleschmerz abd pain) , and resolve spontaneously.

—> Therefore, premenopausal patients with simple-appearing ovarian cysts are

managed with observation and repeat examination in 6 wks

99) Definitive diagnosis of adenomyosis is made histologically after hysterectomy, which is

also the treatment for patients who do not improve with conservative management (eg, oral
contraceptives/ progestin IUD ).
99) D/D of cervical motion tenderness
1) Dyspareunia + Dysmenorrhea + Cervical motion tenderness + Cervical displacement —
- -
>> most likely has endometriosis,ectopic endometrial implants within the intraabdominal
cavity.

2) PID —> Dyspareunia + cervical motion tenderness + fever or concomitant cervical

inflammation (ie, cervicitis),

100) contraception in BF:

-Nonhormonal (eg, copper-IUD and progestin-only contraception methods are preferred in
patients <1 month postpartum and BF as they do not increase thromboembolism risk
or affect breastfeeding unlike estrogen
101) Medications are a common
cause of galactorrhea :

Initial evaluation to - dopamine inhibition (eg,

identifying the cause : antipsychotics, antidepressants,
- serum prolactin, MRI
- TSH, Guaic test
opioids)
- pregnancy test. Serous/ bloody- stimulating pituitary lactotrophs (eg,
estrogen-containing contraceptives).
Grey, nonbloody
- cimetidine) can inhibit estradiol
metabolism and increase prolactin
levels

88) contraceptive during lactation:

-Lactation,is not considered a reliable form of birth control because ovulation can resume
while a mother is still BF. -so needs 2 contraception

89) Contraception in hypercoagulability inherited homozygous Ds:

-Patients with APLS/ hereditary thrombosis who desire pregnancy prevention should be
offered hormone-free options: copper IUD or permanent sterilization (eg, TL)
104) Management of hot flashes
depends on symptom severity and patient risk factors.

1) mild symptoms that do not interfere with daily activities :

- lifestyle modification (eg, wearing layers, weight loss)

2) Severe hot flashes :

- require pharmacologic therapy —>> hormone replacement therapy (HRT) is the first-line
treatment ;; SSRI if HRT C/I

# The only current indication for HRT?

- is vasomotor symptoms in women age <60 who have undergone menopause
within the past 10 years. (Cz increased risk for thromboembolism in old age)

105) Mx of endometriosis:
a) Indications for treatment of endometriosis include:
• Chronic pelvic pain
• Dysmenorrhea, / increasingly worse lower abdominal cramping throughout menses,
that is unrelieved by NSAIDS
• Dyspareunia
• Infertility (eg, due to pelvic adhesions)

b) asymptomatic endometriosis, including this patient who has minimal menstrual

cramping and no longer desires fertility (eg, tubal ligation)/ relieved with NSAIDS:
-require reassurance and observation only.
Endometrial biopsy indications
106) AGC on Pap testing
Age • Abnormal uterine bleeding
- investigated with colposcopy, >45 • Postmenopausal bleeding
endocervical curettage, and Abnormal uterine bleeding +:
endometrial biopsy to evaluate the • Unopposed estrogen (obesity, anovulation)
Age
ectocervix, endocervix, and endometrium. <45
• Failed medical management
• Lynch syndrome (hereditary nonpolyposis
colorectal cancer)
107) females with fragile X syndrome
Age
(FMR1 gene) premutation carriers (ie, >35
• Atypical glandular cells on Pap test
those with 50-200 CGG repeats):
#C/F :
- Primary Ovarian Insufficiency
- Neurobehavioral clinical features (eg, generalized anxiety disorder, autism)
- family history of fragile X syndrome

#Mechanism of POI :
Fragile X premutation causes an FMR1 mRNA overexpression, which is hypothesized
to have a cytotoxic effect on ovarian primordial follicles and result in accelerated
follicle depletion.
107) Premenstrual syndrome
-causes both physical and affective symptoms, which commonly include fatigue, bloating,
hot flashes, mood swings, and irritability.

-Diagnosis : supported with a symptom diary that reveals recurring symptoms in the
luteal phase (ie, 1-2 weeks prior to menses) that resolve with menses.
-
#-Mild PMS: exercise and stress reduction.
-moderate to severe PMS/PMDD: SSRIs (eg, fluoxetine) is the 1st line.

108) Breast conserving therapy

-typically consists of partial mastectomy and axillary sentinel lymph node biopsy,
followed by whole breast radiation therapy.
-Adequate surgical excision of the cancer requires negative margins.
Vs
#Modified radical mastectomy
- mastectomy (removal of the entire breast and nipple areolar complex) + axillary
lymph node dissection

109) # D/D of protruding vaginal mass:

1) urethral diverticulum:
- tender constant vaginal mass with purulent to discharge
- location: anterior vaginal wall,
- NO change with valsalva

2) Bartholin cyst abscess:

- tender constant vaginal mass with purulent to discharge
- location: posterior vaginal wall,
- NO change with valsalva

3) pelvic organ prolapse:

- nontender constant vaginal mass
- change with valsalva (CLUE)

110) lynch syndrome screening:

-Genetic testing should be performed in patients with a strong family history of colon
cancer (eg, >3 relatives involving multiple generations)- DNA mismatch repair gene.

—> Once the diagnosis of Lynch syndrome is established, patients should undergo
screening for colon cancer with colonoscopy +

—> Endometrial cancer screening with annual endometrial biopsy should begin at age
30-35.
—> Ovarian cancer risk is also increased and may present at a relatively younger age.
Therefore, prophylactic hysterectomy and bilateral oophorectomy is recommended
at age 40 or earlier if childbearing is complete.
 Ovarian Cancer Screening

- -

risk for ovarian cancer in the general population is low (~1.4%). 

In contrast, the risk for ovarian cancer significantly increases with familial cancer
syndromes such as BRCA1 (~40%), BRCA2 (~20%), and Lynch syndrome (~8%).
111)irreversible sign of virilisation:
-Voice deepening is a common (and possibly irreversible) sign of frank virilization as
excess androgens (eg, testosterone >150 ng/dL, dehydroepiandrosterone sulfate
[DHEAS] >700 µg/dL) lengthen and thicken the vocal cords, thereby changing their
acoustic frequency and changing the voice.

#Evaluation for Virilisation :

- ovarian and adrenal sources of androgen production with total testosterone, 17-
hydroxyprogesterone, and DHEAS levels.

112) Ovarian cyst rupture

-a common cause of acute, U/L lower abdominal pain in reproductive-aged women,
-ultrasound :thin-walled ovarian cyst with pelvic free fluid.

-Physiologic ovarian cysts are usually small (eg, <3 cm) and asymptomatic, but they can
become larger and rupture with vigorous activity (eg, intercourse)

#RF:
-patient's risk for ovarian cysts likely increased due to discontinuation of her combined
oral contraceptives that typically suppress cyst formation.

*Mx:
-Hemodynamically stable patients are managed with observation and reassurance.

113) MC RF For Endometrial adenocarcinoma: obesity and chronic anovulation.

115) Women age <45 with abnormal uterine bleeding who have failed medical
management (eg, oral contraceptives) require evaluation for endometrial hyperplasia/
cancer with an endometrial biopsy.

116) primary ovarian insufficiency: associated with hypothyroidism (autoimmune

Ds)and Turner syndrome. # Rx of infertility: IVF

118) Mx of LSIL on Pap test:

a) if the patient is 25 years of age or older: immediate colposcopy is performed

b) LSIL on a Pap smear who is 21–24 years of age:

—> Pap smear should be repeated twice at 12-month intervals
- The lesion usually spontaneously resolves over time and the risk of malignant
transformation into invasive cervical cancer is low.

-If repeat testing is negative twice, the patient may return to routine screening. If the
repeat Pap smear shows ASC-H , HSIL, or AGC, colposcopy should be performed.
117) Endometrial polyps
-premenopausal patient with regular monthly menses and intermenstrual bleeding
- Mx:Symptomatic endometrial polyps are Rx with hysteroscopic polypectomy.
-RF absent (normal BMI and regular menses)

Vs
#Endometrial hyperplasia
-typically presents as irregular, anovulatory menses in women with risk factors for
excess unopposed estrogen (eg, obesity, tamoxifen).

119) Inflammatory breast CA:

—> suspect even if normal mammography before a year as it may rapidly grow after
normal Mammography

#Prognosis:
-Due to early lymphatic involvement in IBC, there is typically rapid tumor growth and
metastasis (ie, within months), with the potential for interval development of IBC between
-
-
routine mammography screenings
-Patients commonly have metastatic disease at initial presentation.

#Mx:
-Patients with suspected IBC require breast biopsy (eg, core needle biopsy) and full-
thickness skin punch biopsy (evaluating for the classic finding of dermal lymphatic
invasion) for diagnosis.
#Rx;
-Due to high rates of metastasis, treatment for IBC is typically aggressive (eg,
chemotherapy, mastectomy, radiation).
 Flowchart in cervical cancer TCA Rx warts not
cervical ca
#Step 1: If Abnormal cervical CA screen/ Pap

#Step 2: Colposcopy
-provides an illuminated and magnified view of the vulva, vagina, and cervix, can
identify precancerous cervical lesions CIN

#Step 3: If unsatisfactory colposcopy

(ie, squamocolumnar junction not completely visualized) OR
high likelihood of cervical dysplasia OR
colposcopy with ectocervical biopsy showed CIN 1 (low risk of cancer progression)

#Step 4:endocervical curettage

!
sampling of the endocervical canal) to fully evaluate the cervix for lesions.

#Step 5: If CIN 3 diagnosed; it is a significant RF for concurrent invasive cervical

cancer. 

#Step 6: So Rx of CIN 3 (whether in the endo- or ectocervix) is with immediate

cervical conization. 
-Cervical conization :both a diagnostic and a therapeutic procedure, typically
removing the entire lesion and allowing for examination of the full depth of
invasion.

#Step 7: Post conization pathology results:

a) If there is no evidence of invasive cancer /-Ve margins (ie, all CIN removed):
Pap testing and HPV cotesting at 1 and 2 years as risk of recurrent CA persist

b) If invasive cancer /+ margins with residual CIN require additional surgical

excision with either repeat conization (if future fertility is desired) or hysterectomy
(if no future fertility is desired)
 123) How is Mx of HSIL different in
pregnancy???
1st step) :A Pap test is a screening
examination for precancerous lesions of
the uterine cervix.
2nd step) (HSILs) on Pap testing are concerning for underlying severe neoplasia (eg,
CIN2, CIN3) or invasive cervical cancer
—> all patients require evaluation with immediate colposcopy.
*Colposcopy:
-Colposcopy evaluates the cervix and vagina under magnification after application of acetic
acid to contrast and identify abnormal (eg, aceto-white changes) from normal cells;
→
abnormal vessels (a sign of high-grade lesions) also become more visible.

-Cervical neoplasia typically occurs at the transformation zone or squamocolumnar

junction.

3rd step) If these areas are not visualized during colposcopy (eg, an "inadequate"
colposcopy), an endocervical curettage is performed to evaluate the endocervical canal.

*Diff during pregnancy :

—> Endocervical curettage is an invasive procedure and is deferred during
pregnancy due to risk of miscarriage and preterm delivery.

—> Cervical biopsy is performed even in pregnancy if a lesion has high-grade

features (eg, abnormal vessels).
124) Approach to ovarian mass:
#Next step;
1) PELVIC USG —>> Showing Ovarian mass

2) CA-125 levels are measured in conjunction with pelvic ultrasonography findings to

categorize an ovarian mass as likely malignant or benign.

#why non-specific in premenopausal F?

- Elevations are also caused by common gynecologic conditions (eg, leiomyomata,
endometriosis) that are more likely present in premenopausal patients;

- therefore, the specificity of CA-125 levels is much greater in postmenopausal women.

# approach of Ovarian mass with CA 125:

1) In a postmenopausal patient, If there are suspicious features on ultrasound (eg, large
mass, solid components, septations) + CA-125 level is elevated,
-the patient should undergo further imaging (eg, MRI, CT scan) to assess the extent of
disease.

-Knowledge of the presence of metastatic implants from imaging is important to guide

surgical exploration ,which is recommended if malignancy is suspected based on clinical,
CA-125, and imaging findings.

2) If the adnexal mass has no malignant features on ultrasound (eg, small size, simple cyst)
and the CA-125 level is normal —> observed with periodic ultrasound.

125) Turner
-Dx: If karyotype is normal but suspicion for TS remains high, fluorescence in situ
hybridization is performed to detect mosaicism (eg, 45,XO/46,XX) that is beyond the
resolution of standard karyotyping.

-- Estrogen replacement therapy is given to girls with TS to promote normal sexual

maturation and reduce the risk of osteoporotic fractures.

126) sentinel LN biopsy:

-if positive, perform LN dissection of 3 more site
-if negative , stop

127) vwf deficiency with normal APTT:

-activated PTT can be normal in those with mild disease or in states of increased vWF
synthesis (eg, pregnancy, oral contraceptive use, acute stress, thyroid hormone
supplementation).
125) inflammatory breast carcinoma
-classically have symptoms of mastitis that do not improve with antibiotics.
-C/F: diffuse breast erythema, pain, and edema with skin thickening and dimpling (peau
d'orange appearance).

126) Ovarian hyperstimulation syndrome

- a complication of ovulation induction for infertility treatment.
#C/F:
-onset; 1-2 weeks
-abdominal pain; ascites; bilateral enlarged, cystic ovaries; and third spacing leading to
intravascular volume depletion (eg, hemoconcentration).
-Severe Cx : thromboembolism, multiorgan failure, and death

127) granulosa cell tumors

-Due to the association of granulosa cell tumors with endometrial cancer, patients with a
suspected granulosa cell tumor require an endometrial biopsy prior to surgical
staging to help guide management.

#monitoring Ds:
-After surgical management, inhibin levels can be monitored to evaluate for disease
progression or recurrence. -

128)B HCG <5 is considered negative—>rules out ectopic/ normal pregnancy

129) Fitz-Hugh–Curtis disease

-(PID) can be complicated by perihepatitis (eg, Fitz-Hugh–Curtis disease).

#C/F: typically have RUQ pain + classic PID symptoms (eg, fever, lower abdominal pain,
intermenstrual bleeds), in a young, sexually active not using barrier contraception F
Vs
Cholecystitis : no lower abd pain

130) Medroxyprogesterone S/E may be similar to pregnancy symptoms (eg, breast

tenderness, weight gain, fatigue).
—> Women of childbearing age with absence of menses for >1 month should be
evaluated for pregnancy. US Preventive Services Task Force
recommendations for breast cancer screening*
Definitely beneficial: • Mammogram every 2 years
recommended for women age 50-74
Possibly beneficial: • Mammogram in women age
individualize 40-49
• Mammogram in women age
Uncertain benefit
≥75
*For average-risk individuals.
131) Physiologic leukorrhea
- a white, odorless mucoid cervical discharge that typically occurs midcycle due to
increasing estrogen levels prior to ovulation.
-Microscopic examination of the discharge: no evidence of inflammation / infection (eg,
rare PMN leukocytes).
Intrauterine device
Cervical cancer screening
Type Levonorgestrel Copper
Demographics Screening guidelines
Duration of
3-5 years 10 years
• Onset of sexual intercourse efficacy
• At time of diagnosis
HIV • Cytotoxic
• Annually until ≥3 normal results, then
endometrial

Is
routine testing • Thickens
inflammation
cervical mucus
Immunosuppressed • Onset of sexual intercourse Mechanism • Impairs sperm
• Impairs
(SLE, organ transplant) • Annual Pap test with HPV cotesting function
implantation
• Impairs
Age <21 • No screening implantation
Age 21-29 • Cytology every 3 years • Nonhormonal
• Cytology every 3 years OR • Decreases • Can be used as
Benefits
menstrual flow emergency
• Cytology plus HPV testing every 5 years
Age 30-65 contraception
OR
• Primary HPV testing every 5 years • Active liver
disease • Wilson disease
• No screening if negative prior screens & • Breast cancer • Copper allergy
Age ≥65
low risk Contraindicati • Acute pelvic • Heavy menstrual
Hysterectomy • No screening if negative prior screens & ons infection bleeding
(with cervix removed) low risk -decreases • Acute pelvic
menstrual blood infection
HPV = human papillomavirus; SLE = systemic lupus erythematosus. flow

Contraception options 135) Ideal contraceptive of choice in adolescent

Type
Effectiveness with -Adolescents have more chance of (imperfect) use rates
typical use with many forms of contraception due to inconsistent
Intrauterine
>99%
compliance compared to other age groups.
device
Implant >99% -As a result, long-acting, reversible contraceptive
Injection 94% devices (LARCs) such as the levonorgestrel and
Pills, patch, ring 91% copper intrauterine devices
(IUDs) and subdermal progestin implant are first-line
Condom 80%
contraception options for adolescents.
Withdrawal 75%

-DMPA has a higher failure rate than LARCs.

-It is not recommended for long-term use (>2 years) in adolescents or young women
due to significant risk for loss of bone mineral density.

136) Mx of vaginismus:
-Pelvic floor physical therapy is the recommended initial treatment for patients with
vaginismus.
-Components of physical therapy such as internal manual techniques, patient education,
dilatation exercises, local tissue desensitization, and home exercises have been shown to
improve vaginal muscle mobility and help patients overcome vaginal penetration anxiety.
137) Test for abnormal uterine bleeding
1) Serum FSH levels
-differentiate between hypothalamic (eg, functional hypothalamic amenorrhea) and
ovarian (eg, perimenopause, primary ovarian insufficiency) causes of irregular bleeding.

2) progesterone withdrawal test

-is used in premenopausal women with secondary amenorrhea to determine estrogen
status (ie, no withdrawal bleed with low estrogen levels).

- It is not used in the evaluation of PMB because it cannot distinguish between benign
and malignant causes.

138) MC s/e of OCP: breakthrough bleeding

139) Role of HPV cotesting

1) LSILs :
-HPV) co-testing is performed to triage low-grade abnormalities on Pap testing,
including atypical squamous cells of undetermined significance and(LSILs), which may
or may not be due to HPV infection.

2) HSILs :
However, HPV infection is the cause of the high-grade lesions on Pap tests; therefore,
HPV co-testing is not performed.

-Further evaluation of HSIL results is required with colposcopy and biopsy - regardless
of presence or absence of HPV - due to the risk of malignancy.

140) Rx of fibrocystic breast Ds: NSAIDS, OCP

141) How to approach a patient with high risk for CA Breast ?

—> Ixs :
- MRI of the breast is used for the screening of high-risk patients (eg, BRCA carrier, first-
degree relative of known BRCA carrier) and the evaluation of disease extent and
chemotherapy response in breast cancer patients.

—> Mx :
- Prophylactic mastectomy can be considered in patients with a strong family history of
breast cancer, such as a patient with >1 first-degree relatives with breast cancer before age
50, or a hereditary oncogenic mutation.
141) 55) Mammary duct ectasia
#Pathogenesis:
Mammary duct ectasia, characterized by subareolar ductal dilation, inflammation, and
fibrosis, can cause a palpable breast mass (from scar tissue) with nipple discharge;
#C/F:
-the nipple discharge is classically green-brown and sticky (vs bloody in CA and none in
galactocele); the mass is classically subareolar
-common in perimenopause F vs galactocele post lactation
-USG: dilated ducts vs heterogenous echoec mass in galactocele
(vs peripheral), and involvement of the breast suspensory ligaments (ie, skin
retraction) in breast CA
 USG gynaecology appearance
1) Tubovarian abscess: complex multiloculated adnexal mass with thick walls and
internal debris- Rx with antibiotics

2) Endometriosis : homogenous cyst with internal echoes (eg, "ground glass":

#Endometriomas :
- USG: unilocular adnexal mass with homogeneous, low level echoes (ie, blood).

3) mature cystic teratoma:

-USG: ovarian cyst with solid components, hyperechoic nodules, and
calcifications: tooth and hyperechoeic bands: hair

4) Ovarian torsion
-USG :adnexal mass with absent Doppler flow to the ovary.

5) Ruptured ovarian cyst: pelvic free fluid

6) epithelial ovarian CA: solid mass and cystic mass with thick septation;
ascites

USG is superior to CT scan for evaluation of the pelvic organs, and CT scan is
reserved for detection of metastases from ovarian cancer.

7)hydrosalpinx
-Ultrasound : demonstrate a mass separate from the ovary rather than an
ovarian tumor.
#Divine podcast / amboss
● Pap f/u
○ Indeterminate/inadequate sample → repeat now
○ ASCUS → next do HPV testing as HPV is associated with cervical cancer/ repeat Pap
in 1 year
Do colposcopy after combo ASCUS+ HPV positive

■ If hrHPV present → colposcopy

○ Atypical glandular cells → colposcopy & endometrial bx
○ If CIN2+ /HSIL→ colposcopy
○ ASC-H (atypical squamous cells, cannot exclude high-grade) → colposcopy

117) Because submucosal fibroids distort the endometrial cavity and are the most
common fibroid type to cause abnormal bleeding,
-saline infusion ultrasonography (sonohysterography)is the Ix of test of choice.
 Male reproductive

#The risk of testicular cancer is increased in patients with cryptorchidism (ie, undescended
testis), but cancer is not a notable complication of varicocele.
 REPRODUC TIVE REPRODUCTIVE—PATHOLOGY
`  SEC TION III 653

Testicular tumors (continued)

Germ cell tumors
Seminoma Malignant Painless, homogenous testicular enlargement. Most common testicular
tumor. Analogous to ovarian dysgerminoma. Does not occur in infancy.

÷
Large cells in lobules with watery cytoplasm and “fried egg” appearance
on histology,  placental ALP (PALP). Highly radiosensitive. Late
metastasis, excellent prognosis.
Teratoma May be malignant Unlike in females, Mature teratoma in adult Males may be Malignant.
Benign in children.
Embryonal carcinoma Malignant Painful, hemorrhagic mass with necrosis. Often glandular/papillary
morphology. “Pure” embryonal carcinoma is rare; most commonly
mixed with other tumor types. May present with metastases. May be
associated with  hCG and normal AFP levels when pure ( AFP when
mixed). Worse prognosis than seminoma.
Yolk sac (endodermal Malignant, aggressive Yellow, mucinous. Analogous to ovarian yolk sac tumor. Schiller-Duval
sinus) tumor bodies resemble primitive glomeruli.  AFP is highly characteristic.
-
-
Most common testicular tumor in boys < 3 years old.
Choriocarcinoma Malignant Disordered syncytiotrophoblastic and cytotrophoblastic elements.
Hematogenous metastases to lungs and brain.  hCG, may produce

=
gynecomastia, symptoms of hyperthyroidism (α-subunit of hCG is
-

identical to LH, FSH, TSH).

Non-germ cell tumors
Sertoli cell tumor Mostly benign Androblastoma from sex cord stroma.
Leydig cell tumor Mostly benign Golden brown color; contains Reinke crystals (eosinophilic cytoplasmic
inclusions). Produces androgens or estrogens Ž gynecomastia in men,
precocious puberty in boys.
Testicular lymphoma Malignant, aggressive Most common testicular cancer in older men. Not a 1° cancer; arises
from metastatic lymphoma to testes.

Hormone levels in germ cell tumors

SEMINOMA YOLK SAC TUMOR CHORIOCARCINOMA TERATOMA EMBRYONAL CARCINOMA
PALP  – – – –
AFP –  – – –/ (when mixed)
β-hCG –/ –/  – 

#How to differentiate nonseminomatous from seminoma germ cell tumors??

-β-hCG is typically elevated in both seminomatous and nonseminomatous germ cell
tumors (SIMILARITY)
-but nonseminomatous germ cell tumors typically also produce AFP, which is not
produced by seminomas (DIFFERENCE)
-A large mediastinal mass with associated elevations of AFP and β-hCG is virtually
diagnostic of a nonseminomatous germ cell tumor.
1) Acute epididymitis Case clue
-posterior testicular pain/swelling, improvement of pain with testicular elevation, and
normal cremasteric reflex.
-Etiology: Chlamydia, Neisseria) in patients age <35; Rx: Ceftriaxone, doxycycline
- colonic pathogens (eg, Escherichia coli) in those age >35; Rx: levofloxacin

2) testicular torsion,
-severe, acute-onset scrotal pain episodes that does not resolve with elevation of
the testicle (negative Preen sign);
-abdominal pain; nausea vomiting
negative cremasteric reflex (ie, testes do not elevate with stroking of inner thigh).
-O/E: tender, high-riding testicle; a horizontal lie of the testis
-The scrotum is typically erythematous and markedly swollen; heterogenic echo texture
indicating necrosis ; small reactive hydrocele

-Most cases improve with detorsion and do not require orchiectomy.

3) Newborn hydroceles
-painless scrotal swelling that transilluminates on examination.
-Management : observation and reassurance, as most cases resolve spontaneously by
age 1 year.

5) Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS),

-chronic pelvic pain (including pain in the perineum and testes, which can radiate to the
back) for >3 months without an identifiable cause

-can present as voiding difficulties, irritative voiding symptoms (eg, frequency, urgency,
hesitancy), pain with ejaculation, or blood in the semen.
-generally afebrile and have little or no prostate tenderness with a normal urinalysis and
negative urine culture results.

#Rx: ab, alpha blockers, 5 alpha reductase inhibitor

-

6) Acute bacterial prostatitis: lower UTI Sx like UTI

-systemic illnes: fever chills; dysuria, leukocytosis, and tender, swollen prostate;
perineal pain specific
.
-Urine Gram stain and culture is then required to identify the pathogen:next best step
-Needs 6 wks of FQ/TMP-SMX
Vs

7) prostatic abscess
- prostatic fluctuance on digital rectal examination, failure to improve with antibiotics
Vs
8) Urethritis: urethral discharge present

9) chronic bacterial prostatitis:

-recurrent UTI, pain with ejaculation, and pyuria/bacteriuria
-transient improvement with antibiotics

10) obstructive azoospermia:

-absent sperm concentration with normal hormone levels (FSH, LH, testosterone).
Eg : CF

11) penile fracture (PF): next retrograde urethrography for urethral injury
-cause: blunt trauma (eg, sexual intercourse) to the erect penis.
-At the moment of rupture, patients often hear a snapping sound and experience sudden-
onset pain —> Afterward, as blood exits the engorged corpus cavernosum —> patients
experience rapid penile detumescence and formation of a penile shaft hematoma (eg,
swelling, ecchymosis)

12) Peyronie disease (PD):

- dorsal penile plaque and pain/curvature with erection

13) Leydig cell testicular tumors

-often cause feminization (eg, gynecomastia) due to the production of estrogen by tumor
cells.
-causes secondary inhibition of FSH and LH.
-Serum tumor markers (eg, β-hCG, AFP) are not usually elevated.

14) Fournier gangrene

-is a life-threatening necrotizing fascitis that typically affects perineal, scrotal, and lower
abdominal skin.
-C/F: rapid-onset swelling, tenderness, and crepitus of the affected region and significant
systemic symptoms (eg, hypotension, high fever).

-Rx: Rapid surgical intervention is required to prevent death and should not be delayed
for imaging.

15) Cryptorchidism
• Empty, hypoplastic, poorly rugated scrotum ± Inguinal fullness
• can impair testicular growth during puberty but does not delay the timing of pubertal
onset
#Mx: testes that have not descended by age 6 months —>> Orchiopexy (surgical pinning
of the testis) is performed, ideally before age 1, to reduce cx.

#Cx: Inguinal hernia; Testicular torsion; Subfertility; Testicular cancer

#Cx persisting after surgery: CA risk; but infertility and torsion reduces if performed early
16) evaluation of hypospadias:
-About 10% cases associated with cryptorchidism
-the condition may represent either virilization of a genotypic female (XX) /
undervirilization of a genotypic male (XY).

—>So 1st step :karyotype analysis.

—> Even if testes are present (indicating the presence of at least some functional Y
chromosome), a karyotype is still needed in severe hypospadias to evaluate for
mosaicism.
-Pelvic ultrasound may also be indicated to assess for internal genitalia (eg, uterus).

17) Approach to Prostate cancer:

1) 1st step: Rectal examination may help differentiate prostate cancer from BPH
2) 2nd step: PSA
3) 3rd step:: Prostate biopsy is indicated for patients with signs of prostate cancer
with USG guided needle

18) Patients with LUTS should have a urinalysis to evaluate for hematuria (eg, bladder
cancer, kidney stones) and infection.

20) Mx of varicocele:
-Gonadal vein ligation or embolization for those wanting fertility (boys & young
men with testicular atrophy)
-Scrotal support & NSAIDs (older men who do not desire additional children)

21) preventing gynecomastia in klinefelter:

-Selective estrogen receptor modulators (eg, tamoxifen)

22) Rx of ED: 23) Rx of premature ejaculation <1 min latency):

-1st line: PDE 5I even in MI SSRI (paroxetine,citalopram); topical anaesthetic
-2nd line: PGE analogue alprostadil
-testosterone in Hypogonadism cause
Vs Varicocele
Primary Secondary
• Compression of left renal • Extrinsic compression (renal
Pathophysiol vein between SMA and or retroperitoneal mass) of
ogy aorta IVC
• Incompetent venous valves • Venous thrombus
• "Bag of worms" mass
• "Bag of worms" mass
• Pubertal onset
Clinical • postpubertal onset
• Left-sided
features • Right-sided
• Decompresses when
• Persists when supine
supine
Initial • Reassurance and
• Abdominal ultrasound
management observation
 REPRODUC TIVE REPRODUCTIVE—EMBRYOLOGY
`  SEC TION III 647

Male/female genital homologs

Male Female
Glans penis Genital
Genital groove tubercle

Penile urethra Urogenital

fold Labioscrotal Clitoris
swelling
Urogenital Labia
Opening of
sinus minora
urethra
Scrotum Labia
Opening of majora
Anus vagina

Urachus Allantois Uterine

Vesical Urachus
Kidney tube
Urinary part Urinary
bladder Genital Kidney
Pelvic Urogenital bladder
tubercle part sinus
Testis Clitoris Ovary
Glans
penis Ureter Phallic
part Uterus
Ductus Rectum
Spongy
deferens Vagina
urethra
Dihydrotestosterone Estrogen
Glans penis Genital tubercle Glans clitoris
Corpus cavernosum
and spongiosum Genital tubercle Vestibular bulbs
Bulbourethral glands Greater vestibular glands
(of Cowper) Urogenital sinus (of Bartholin)
Prostate gland Urethral and paraurethral
Urogenital sinus glands (of Skene)
Ventral shaft of penis
(penile urethra) Urogenital folds Labia minora

Scrotum Labioscrotal swelling Labia majora

Congenital penile abnormalities

Hypospadias Abnormal opening of penile urethra on ventral Hypospadias is more common than
(under) surface due to failure of urethral folds epispadias. Associated with inguinal hernia,
to fuse. cryptorchidism, chordee (downward or upward
bending of penis).
Can be seen in 5α-reductase deficiency.

Epispadias Abnormal opening of penile urethra on dorsal Exstrophy of the bladder is associated with
(top) surface due to faulty positioning of epispadias.
genital tubercle.

#Physiologic changes in male sexual function due to aging

- delays in obtaining and maintaining an erection, longer refractory period between orgasms,
and decreased ejaculate force and volume
-These are normal changes that progress gradually with advancing age, and they are not
reflective of hormonal changes or decreased sexual desire.
24) Hypospadias and circumcission:
—> Urologic evaluation is required prior to circumcision because the foreskin may be
needed for hypospadias repair, and conventional circumcision techniques may be unsafe.

25) Initial management of priapism

-1st Line: aspiration of blood from the corpora cavernosa,
-2nd line: followed by intracavernous injection of phenylephrine to stimulate contraction
of cavernous smooth muscle and facilitate venous emptying.

Common causes of erectile dysfunction

Clinical features
• Cardiovascular risk factors (eg, hypertension, smoking,
diabetes)
Vascular
• Abnormal vascular examination (eg, bruits, decreased
pulses)
• Neurologic comorbidity (eg, diabetic neuropathy, multiple
Neurologic sclerosis, spinal injury/surgery)
• Gradual onset, loss of bulbocavernosus reflex
• Sudden onset
• Situational (eg, ED with partner, normal erection during
Psychogeni masturbation)
c • Normal nonsexual nocturnal erections( indicate intact vascular
and nerve function in the penis and are usually absent in
patients with organic causes)
• Additional symptoms due to underlying disorder
• Pituitary tumors can cause ED from low testosterone due to
Endocrine prolactin overproduction or compression of normal
gonadotrophs
• Abnormal hormone levels (eg, TSH, prolactin)
• Onset related to starting medication
Medications • Antihypertensives (beta blockers and thiazide diuretics), SSRIs,
anti-androgenic medications: Spironolactone, Cimetidine
• Gradual onset
Hypogonadi
• Decreased libido, gynecomastia, testicular atrophy
sm
• Low serum testosterone
26) Neonatal circumcision benefits
-reduced risk of UTI in the first year of life and penile phimosis, cancer, and
inflammatory disorders in adulthood.

-Although circumcision reduces the risk of acquiring HIV and certain STIs (eg, HPV)
through penile-vaginal sex, it does not protect against all STIs, including many of the
most common (eg, gonorrhea, chlamydia).
 Combined cause:
hypercortisolism;
cirrhosis

Common pathological causes of gynecomastia

29) Evalaution of B/L cryptorchidism
• Testicular, adrenal, or
Increased
hCG-secreting tumors
==> are concerning for a disorder of sex
estrogen development, such as congenital adrenal
• Obesity
production or
peripheral
• Cirrhosis hyperplasia (CAH)
• Thyrotoxicosis
conversion
• Androgen use
-Workup : karyotyping to distinguish a virilized
• Primary or secondary male genotypic female from an undervirilized
Androgen hypogonadism
deficiency • Hyperprolactinemia genotypic male.
• Renal failure
• Decreased androgen -In addition, electrolyte monitoring is
production (GnRH agonists, required to evaluate for salt-wasting CAH,
ketoconazole) which can result in a potentially fatal adrenal
• Decreased peripheral crisis.
conversion to
Medication effect
dihydrotestosterone (5-
alpha-reductase inhibitors)
• Inhibition of androgen
receptor (spironolactone,
bicalutamide)
 30) Mx of peyronie Ds:
- In many individuals, the pain and
deformity resolve spontaneously over 1-2
years.
- However, those with active or progressive
PD often require :
1) NSAIDs for pain;
2) pentoxifylline to reduce fibrosis; and/
3) intralesional injections of collagenase.
4) Surgery may be indicated in refractory
cases.

Malignant testicular neoplasms

Seminom • Retain features of spermatogenesis
Ger a • β-hCG, AFP usually negative
m
cell • ≥1 partially differentiated cells: yolk sac,
(95% Nonsemin embryonal carcinoma, teratoma, and/or
) oma choriocarcinoma
• β-hCG, AFP usually positive
• Often produces excessive estrogen
Leydig (gynecomastia) or testosterone (acne)
Stro • Can cause precocious puberty
mal
(5%) • Rare
Sertoli • Occasionally associated with excessive
estrogen secretion (eg, gynecomastia)
32) Testicular germ cell tumors
- common in young men and manifest primarily with a painless testicular mass.
#C/F of mets:
-a minority of patients may have symptoms of metastatic disease, including low back pain
(retroperitoneal lymphadenopathy) and dyspnea/cough (pulmonary nodules).

-Testicular examination : firm, ovoid testicular nodule

#Next step of Mx:
-should prompt a scrotal ultrasound and tumor markers to support the diagnosis.

33) Mx of penile fracture:

-Diagnosis of PF is usually clinical, and urgent surgical repair of the tunica albuginea is
the mainstay of treatment.
-However, because concomitant urethral injury occurs in approximately 20% of PF cases
(due to the close proximity of the corpus spongiosum), the following findings warrant
investigation with retrograde urethrography (or urethroscopy) prior to surgery:
 • Blood at the meatus
• Hematuria
• Dysuria
• Urinary retention
-If urethral injury is confirmed by urethrography, then the urethra should also undergo
repair at the time of surgery.

34) approach to testicular cancer:

•Elevated tumor markers (AFP, β-hCG, LDH) with NSGCTs).
•B/L Scrotal ultrasound: solid, hypoechoic lesion (seminoma) / a lesion with cystic
areas and calcifications (nonseminomatous germ cell tumor [NSGCT]).

#Rx: Radical inguinal orchiectomy and NOT scrotal orchiectomy , which is performed
to confirm the diagnosis histologically and provide definitive treatmen

36) Paraphimosis
-refers to the retraction and entrapment of the prepuce in an uncircumcised male patient.

-Management : urgent manual or surgical reduction of the prepuce to maintain vascular

flow of penis

37) Identifying urinary retention vs obstructive Sx of BPH:

-Bladder catheterization (either transurethral or suprapubic) is indicated in acute urinary
retention (AUR), a common complication of BPH.

-Although patient presents with features of bladder outflow obstruction due to prostatic
enlargement (e.g., poor stream, hesitancy), he does not complain of suprapubic or pelvic
pain, or a complete inability to pass urine or have a bladder that is palpable on physical
examination, all of which are features of AUR.

38) testicular torsion: pain starts in the groin and radiates to abdominal
Vs
#ureteral stone: pain starts in the abdomen and radiates to groin

39) testicular rupture)

-significant testicular pain/tenderness and/or testicular swelling
-abnormal contours and absence of B/L cremasteric reflex (retraction with stroking of
medial thighs)
 ENT

#when is imaging required in mastoiditis:

-Imaging is not required for diagnosis but is indicated if further complications (eg,
meningitis, neurologic deficits) are suspected, if the child appears toxic, if there is no
response to initial treatment, or if the diagnosis is unclear (eg, persistent otorrhea of
unclear etiology).

-CT scan of the temporal bones / MRI with contrast preferred over plain radiographs
 ENT case clues EAR
1) OE: tympanic membrane clear , no middle ear fluid

# Malignant/ necrotising OE: type of osteomyelitis ; MC : pseudo

-elderly DM; granulation tissue in ear canal; TM clear; severe pain At night;
#Rx: IV FQ x6-8wks +/- surgical debridement ;; NO surgical excision

2) Acute OM: bulging/ purulent middle ear effusion as air fluid level/ dec mobility of
TM ; red TM; so Rx with Ab.
C/F: classic fever, otalgia and irritability
Vs
O
# OME (OM with effusion): asymptomatic mostly; nonpurulent effusion; TM
noninflammed (No bulging/ erythematous); air fluid level e
-

-
-Mx:observe and evaluate; Tymapno tube only if hearing loss
-

#Purulent effusion: A pale yellow, opaque

T
TM with bulging

3) Cerumen impaction: inability to see TM; no redness

4) Otomycosis: fungal debris with fruiting bodies/ spores

5) Cholesteatoma: white mass/ granulation behind TM+ hearing loss

suspect when continuous ear drainage x several weeks despite Ab therapy; > with OM

6) Nasopharyngeal CA: endemic to China; recurrent epistaxis, OM; cervical

LNopathy; CN involvement (diff from polyp)

7) Meniere Ds: episodic vertigo, hearing loss and tinnitus x 20min- 24 hours; no
-
trigger
Vs
8) Perilymphatic fistula: head trauma causing episodic vertigo with nystagmus by
sudden pressure changes (Vatsalva)/ loud noises/sneezing/straining x a min
Vs
9) Benign paroxysmal positional vertigo
-typically have sudden, brief episodes of vertigo triggered by head movement.x (<1-min)
Vs
#Vestibular neuritis: vertigo following viral URTI

—> Head thrust test is usually abnormal —> In this test, the patient is asked to look at a
fixed target while the head is rapidly rotated.
1) Normal vestibular function : Patients maintain visual fixation;
2) Abnormal vestibular function such as in vestibular neuritis : the eyes move away and
then return to the target with a horizontal saccade.

10) Auricular hematoma: tender, fluctuant bloody swelling on anterior pinna

-Blunt trauma to the ear can cause an auricular hematoma, which is a collection of blood
between the perichondrium and cartilage of the outer ear.

-Mx: Prompt evacuation of the hematoma is required to avoid complications of

infection, avascular necrosis, and permanent cauliflower ear deformity.

11) Eustachian tube dysfunction: “Popping sensation”, retracted TM

12) Presbycusis: difficulty hearing in noisy/

loss vs better hearing in crowded in CHL
=
-
o
crowded environment; cochlear hair cell

13) Otosclerosis: conducting hearing loss in pregnancy

-a young pregnant patient with conductive hearing loss and a normal otoscopic
examination likely has otosclerosis. CLUE
Inheritance : AD pattern with incomplete penetrance.
-paradoxic improved speech discrimination in noisy environment; Otoscopy: red hue
behind TM; F/H +

11) Tympanosclerosis: Chalky, white patches on TM.

typically H/O otitis media (typically chronic) / previous tympanostomy tubes.

12) Relapsing polychondritis:

-inflammed pinna with sparing lobule ( as no cartilage in lobule)

14) conductive hearing loss: speech discrimination improves in noise as CHL dampens
the outer noise

SNHL : worse speech understanding with increasing background noise.

15) Drug induced ototoxicity :

-Aminoglycosides can be ototoxic to both the cochlea (resulting in sensorineural
hearing loss) and the vestibular system (resulting in imbalance).

16) Peripheral Vertigo :

- typically have shorter episodes,
- fatigable nystagmus inhibited by gaze fixation,
- preserved ambulation, and →
- no other CNS (eg, headache, diplopia, dysarthria).
 19) Chronic suppurative otitis media

±
- often preceded by an episode of acute
otitis media/ cholesteatoma
- defined as chronic (>6 weeks), purulent
otorrhea with tympanic membrane
perforation.

#Mx, ototopical fluoroquinolone to target

the most common pathogens,
Staphylococcus aureus and
Pseudomonas aeruginosa.

20) Mx of Meniere Ds:

-Initial management : restriction of sodium, caffeine, nicotine, and alcohol.
-Benzodiazepines, antihistamines, and antiemetics can relieve acute symptoms.
-Diuretics can be considered.
-interventional techniques (endolymphatic shunt placement):severe, intractable vertigo.

Interpretation of Rinne & Weber tests 17) Otalgia in the setting of a

Rinne result Weber result normal ear examination is likely
Normal AC > BC in both ears Midline referred pain (pain perceived at a
BC > AC in affected ear,
different site than its true origin).
Conductive Lateralizes to affected #Etio:
AC > BC in unaffected
hearing loss ear
ear -MCC of referred otalgia : dental
Sensorineural
Lateralizes to unaffected disease and temporomandibular
AC > BC in both ears ear, away from affected
hearing loss
ear
joint disorders.
-next: head and neck SCC
Mixed hearing BC > AC in affected ear, Lateralizes to unaffected
loss AC > BC in unaffected ear ear, away from affected ear

18) Repeated ear infections can result in conductive hearing loss, which may be
confused with certain pervasive and behavioral disorders of childhood.

-Hearing tests should be routinely conducted in all children presenting with social or
language deficits.

19) oral Ab in OM vs topical in otitis externa

20) Key idea: Elderly patients who have had chronic exposure to noise will first lose high-
frequency sounds (bilateral, symmetric sensorineural hearing loss), with young patients
with increased exposure to loud noises being able to lose the high-frequency sounds due
to destruction of hair cells at the cochlear base
19) #Difference between sporadic and inherited schwannoma?
-Sporadic vestibular schwannomas : typically unilateral and manifest around age 50.
Vs
- In contrast, the presence of bilateral, hereditary vestibular schwannomas in a young
patient: should raise suspicion for NF2.

#other condition having SNHL:

1) Jervell and Lange-Nielsen syndrome, a congenital long QT syndrome

-In contrast to NF2, congenital long QT syndrome typically presents in childhood with
profound bilateral deafness and episodes of arrythmia-induced syncope during
periods of stress.

20) smoking and AOM:

-Tobacco smoke exposure is linked to an increased need for tympanostomy tubes for
recurrent AOM, possibly related to smoke-induced dysfunction of the cilia in the URT
-A link between OE and smoking has not been established.

21) Tympanostomy tube placement

-ADR: otorrhea, persistent tympanic membrane perforations, and cholesteatoma.

22) next best step/ Ix of vestibular schwannoma:

• Audiogram
• MRI with contrast of internal auditory canal

23)Rx of recurrent OM
I) Treatment with oral antibiotics is recommended in specific situations:
• 1st-line therapy with amoxicillin if allergic - clindamycin/ TMP SMX
• #Indication: infants age <6 months and for children age ≥6 months with high fever
(>39 C [102.2 F]), severe pain, or bilateral disease.
•
• 2nd-line therapy with amoxicillin-clavulanate
• #Indication: refractory symptoms after 2-3 days of antibiotic therapy or recurrent
-
AOM (within 30 days) after antibiotic therapy. -

II) Tympanocentesis and culture during tympanostomy tube placement

should be considered for
-multiple episodes of AOM (eg, ≥3 episodes in 6 months)/
-persistent (>3 months) middle ear effusion with hearing loss.

24) Mx of vestibular neuritis: stays for 1-2 days

Because VN is usually self-limited, patients can be managed expectantly. Management
may also include vestibular suppressants (eg, meclizine), corticosteroids, and vestibular
rehabilitation.
 NOSE
1) polyps: constant sensation of dripping in the back of her throat ; persistent nasal
congestion and stuffiness.
-
Otoscopy: grey mass with inflammatory infiltrate
-

2) perforated nasal septum : typically a whistling noise on inspiration ( eg post

rhinoplasty)

3) Pyogenic granuloma: > pregnancy; vascular tumour on septum

4) Aspirin-exacerbated respiratory disease:

# triad: asthma +bronchospasm + nasal congestion/polyps/ chronic rhinosinusitis
following the ingestion of aspirin / NSAIDS by +
of LT (pro inflammatory) and inhibition of anti inflammatory PG
#Rx:
-Leukotriene pathway inhibitors (eg, zileuton, montelukast)
-If NSAIDs are absolutely required, desensitization is sometimes necessary.

5) Granulomatosis with polyangiitis

-commonly causes ear (otitis) + nasal (rhinorrhea, bloody discharge) sx

6) Nasal septal hematoma: soft, fluctuant swelling of septum B/L vs firm in deviated
septum; #Rx: urgent IND
-Cx If unRx: infection, septal perforation, and nasal deformities.

7)FB in the larynx or trachea : stridor but would present with life-threatening ARD. 
Vs
—>FB in the lower airways: would not present with stridor but with recurrent
pneumonias that do not resolve radiographically.

8) Bilateral choanal atresia

-shortly after birth with cyclic cyanosis that worsens during feeding and improves while
crying.
Vs
-Unilateral choanal atresia : presents during childhood as persistent, U/L nasal obstruction
and discharge.

9) CSF rhinorrhea: U/L watery rhinorrhea with salty/ metallic taste with bending/ increased
bowel movement
10) Allergic rhinitis :
• "Allergic shiners" (infraorbital edema & darkening)
• "Allergic salute" (transverse nasal crease)
• Pale, bluish, enlarged turbinates
• Pharyngeal cobblestoning
• "Allergic facies" (high-arched palate, open-mouth breathing)

#Rx: intranasa, steroids for weeks-months

11) Rhinitis medicamentosa:

-beefy red nasal mucosa as opposed to edematous pale mucosa in allergic rhinitis
-Rx: nasal glucocorticoids

12) Barotrauma to the ear

#C/F:
-significant shifts in barometric pressure (eg, during a plane's ascent and descent),
which can lead to stretching of the TM, causing ear pain and hearing loss.

-In severe cases, TM can rupture—> rapidly equalizes the pressure difference and
relieves the stretching and pain but may also result in minor bleeding (eg, drop of blood
on the finger).

#RF: Eustachian tube dysfunction by prior URTI

#Mx:
-Most barotraumatic TM injuries heal spontaneously within a few weeks.
-Tympanoplasty : used to repair persistent TM perforations.

13) serous otitis media.

-After appropriate treatment of an acute episode of otitis media, serous fluid may persist in

=
the middle ear for up to 3 months, referred to as serous otitis media.
#Prognosis:
-The effusion generally resolves spontaneously within 3 months; therefore, watchful
waiting is the recommended management, unless there are persistent symptoms of
infection, the effusion is bilateral, or >3 months have elapsed since the initial episode.

14) Adenoid hypertrophy

- the most common etiology of persistent nasal obstruction in the pediatric population.
-C/F: chronic congestion refractory to medical management; recurrent otitis and sinusitis.

-History may suggest chronic upper airway obstruction (eg, recurrent sinus and ear
infections, mouth breathing, sleep disturbances/snoring due to apnea).

-Adenoids are not easily accessible and not easily visualized during physical examination.
Mucopurulent nasal discharge, postnasal drip, and elongated/flattened facial features (due
to changes in the structure of the palate, jaw, and teeth) may suggest the diagnosis.
 Neck
1) Thyroglossal duct cyst: midline neck mass that moves superiorly with swallowing

2) SCC: MCC of tonsilar/ laryngeal ulcer in smoker

#SCC: usually presents as persistent nodular, erosive, or ulcerative lesions with
surrounding erythema or induration.
-Regional lymphadenopathy can be present as well.

Vs
#Leukoplakia:
-The white granular lesions; No induration; not scrappable vs scrappable in candidiasis

3) HPV: hoarseness due to finger like growth on vocal cords

4) Laryngomalacia :inspiratory stridor that worsens in the supine/feeding and

improves in the prone position.
#Mx: reassurance as it self resolves mostly till 18 yrs; Supraglottoplasty for severe
symptoms: feeding difficulties, tachypnea, cyanosis, or failure to thrive

5) Retropharyngeal abscess: enlarged prevertebral space on lateral Xray neck; CT is

diagnosis of choice
-C/F: neck pain, odynophagia, and fever, pain with neck extension

÷
-O/E: nuchal rigidity and bulging of the pharyngeal wall.
Vs
#Epiglottitis
-C/F: high fever, drooling, and stridor that can progress rapidly to life-threatening airway
obstruction and RS failure . #Lateral x-ray :swollen epiglottis ("thumb sign").
**1st step: intubation; if fails-surgical airway secure; 2nd step: Ab Ceftriaxone+ vanco
Vs

#Peritonsillar abscess : fever, muffled voice, and throat pain.

-Significant tonsillar swelling : uvular deviation to the contralateral tonsillar pillar.
Vs
#Tracheitis is caused by bacterial superinfection of the trachea following URTI and
presents with severe croup-like symptoms, including fever and stridor.
-Neck x-rays :tracheal narrowing.

6) Acute Tonsilitis: characterized by tonsillar erythema and exudates, often with tender
anterior cervical nodes and palatal petechiae.
Vs

7) Peritonsillar abscess:
-trismus, pooling of saliva, and uvular deviation
8) Acute necrotizing mediastinitis
-is a life-threatening complication characterized by fever, chest pain, dyspnea, and
odynophagia, and requires urgent surgical intervention.

9) Sialolithiasis:

→
Recurrent episode of sialadenitis i.e.: tender, swelling and jaw pain exacerbated by eating,
fever which resolved by Ab..

10) ludwigs angina: progressive cellulitis of the submandibular space and not LN
-After mandibular molar dental abscess, submandibular area is usually tender and
indurated, and the floor of the mouth is often elevated, displacing the tongue —> airway
obstruction; neck is brawny and woody..

#Mx:
-IV antibiotics (ampicillin-sulbactam, clindamycin) and removal of the inciting tooth.
-Drainage and surgery:
rarely required as the process is cellulitic and typically nonsuppurative, but they may
be required if there is no improvement with antibiotics.

-Impaired respiratory status requires prompt attention and early intervention with a
mechanical airway.

10) Torus palatinus (TP)

- benign bony growth (exostosis) located on the midline suture of the hard palate. It can
be congenital or develop later in life.

-TP is typically chronic and asymptomatic,

-Surgery is indicated: if the mass becomes symptomatic, interferes with speech or
eating, or causes problems with the fitting of dentures.

11) #Golden rule :

—> Constant or progressive hoarseness for >1 month minimum is often related to a
vocal cord lesion and should be evaluated by laryngoscopy.

12) Retropharyngeal abscess

-C/F: neck pain, odynophagia, and fever following
penetrating trauma to the posterior pharynx.

-Cx: Infection within the retropharyngeal space can

drain into the superior mediastinum.
I -Extension through the alar fascia into the
"danger space" can transmit infection into the
posterior mediastinum—> result in acute
BAP
necrotizing mediastinitis.
13) Mx of bisphosphonates induced Osteonecrosis :
-RF: It is often triggered by tooth extractions / other invasive dental procedures.
-Mx: The course can be intractable, and treatment is largely supportive with careful oral
→
hygiene and antibacterial rinse -
-

14) salivary gland ds

1) Sialadenosis: benign, noninflammatory enlargement of the salivary glands
-gradual nontender, B/L enlargement of the glands that does not fluctuate and is not associated
with eating.
-Recognition of this condition should prompt an investigation for underlying disease like alcoholism,
liver Ds, bulimia, malnutrition ,DM

2) Mumps Parotitis.
-C/F: typically painful parotid swelling and presents a few days after the onset of systemic symptoms
(eg, fever, headache, myalgias).

3)Pleomorphic adenoma
-a benign salivary neoplasm that can present with painless U/L enlargement of the parotid gland and a
distinct mass is typically palpated.

4)Salivary stones (sialolithiasis)

-swelling is usually fluctuating, painful, and associated with eating (which stimulates saliva secretion).

5)Sjögren syndrome
B/L swelling of the parotid glands due to lymphocytic infiltration.
-typically presents in women and is associated with dry mouth on examination.

6) parotid CA:
- firm, hard U/L swelling with CN 7 involvement: facial droop..

15) postoperative neck hematoma

-C/F: patient with an enlarging fluid collection (ballotable neck swelling) developing after
thyroidectomy likely has an expanding neck hematoma.

-Mx: should be recognized promptly and drained (reopen the incision) to avoid potentially
lethal upper airway obstruction.

16) Suppurative parotitis :exquisitely painful swelling of the parotid gland (Pre/post
Auricular swelling) exacerbated by chewing

#RF:
• Elderly, dehydrated, postsurgical
• Decreased oral intake (eg, NPO perioperatively)
• Medications (eg, anticholinergics)
• Obstruction (eg, calculi, neoplasm)
-Lab: Elevated serum amylase without pancreatitis
-Px: This postoperative complication can be prevented with adequate fluid hydration and
oral hygiene.

*Imaging:
-Although the diagnosis is typically evident after clinical evaluation,
-imaging (CT scan or ultrasound) should be obtained to assess for salivary stones
or neoplasms obstructing the duct, as well as to differentiate between suppurative
parotitis and an abscess.

#Rx:
-IV, broad-spectrum antibiotics (narrowed based on culture results), hydration,
sialagogues (increase salivary flow), and massage (expression of purulence from
the duct).

16) Refractory epistaxis:

- anterior: ligate greater palatine art
- post: sphenopalatine art
Mx of acute Epistaxis :
For the treatment of acute epistaxis,
1) nostril pinching is the first step in management.

2) Oxymetazoline (a topical vasoconstrictor) can be applied if direct compression alone is not

effective —> not useful for prevention and should not be used for more than 3 days due to the risk
of rebound congestion (ie, rhinitis medicamentosa).

3) A complete blood count is ordered in cases of severe epistaxis that may require transfusion

17) prevention of OE: amboss

-Application of acetic acid and/or alcohol-based ear drops helps to dry the ear and re-acidify the
ear canal.

-Other measures :carefully blow-drying the ear, wearing a bathing cap during water activities,
treatment of underlying dermatological disorders, and avoiding manipulation of the ear canal.
 ophthalmology

#Unusual case of 1st optic neuritis episode by MS UWSA1

-Visual acuity is reduced in the right eye but funduscopic examination is unremarkable
which developed after bathing in hot shower

-Classic: transient painful monocular vision loss that improves after several weeks.
 #Papilloema: only optic N
head involved
-Sx change with position
changes
Vs
#Optic neuritis:
= -entire nerves involved

#Ixs for Patients having Orbital Trauma :

All patients who sustain orbital trauma should undergo assessment of
1) visual acuity and extraocular movements.
2) CT scan is obtained if there is evidence of a fracture (eg, step-off on palpation),
changes in vision or extraocular movements, or the examination is limited due to soft-
tissue swelling or altered mental status.
 NEUROLOGY AND SPECIAL SENSES NEUROLOGY—OPHTHALMOLOGY
`  SEC TION III 539

Pupillary control
Miosis Constriction, parasympathetic:
ƒ 1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III
ƒ 2nd neuron: short ciliary nerves to sphincter pupillae muscles
Short ciliary nerves shorten the pupil diameter.
Pupillary light reflex Light in either retina sends a signal via CN II Visual field L eye Visual field R eye
to pretectal nuclei (dashed lines in image)
in midbrain that activates bilateral Edinger- Light Light Sphincter
Nasal pupillae
Westphal nuclei; pupils constrict bilaterally retina
muscles
(direct and consensual reflex). Temporal
retina Optic nerve
Result: illumination of 1 eye results in bilateral (CN II) Ciliary
pupillary constriction. Optic ganglion
chiasm

Edinger- Oculomotor
Westphal nerve (CN III)
nucleus

Lateral
geniculate
nucleus

Pretectal
nuclei

Mydriasis Dilation, sympathetic:

ƒ 1st neuron: hypothalamus to ciliospinal center of Budge (C8–T2)
ƒ 2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain
near lung apex, subclavian vessels)
ƒ 3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary
nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids
(minor retractors) and sweat glands of forehead and face.
Long ciliary nerves make the pupil diameter longer.

Marcus Gunn pupil Also called relative afferent pupillary defect (RAPD). When the light shines into a normal eye,
constriction of the ipsilateral (direct reflex) and contralateral eye (consensual reflex) is observed.
When the light is then swung to the affected eye, both pupils dilate instead of constrict due to
impaired conduction of light signal along the injured optic nerve. Associated with optic neuritis,
early multiple sclerosis.
540 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—OPHTHALMOLOGY
` 

Horner syndrome Sympathetic denervation of face Ž: PAM is horny (Horner).

ƒ Ptosis (slight drooping of eyelid: superior
Hypothalamus Ophthalmic division
tarsal muscle) of trigeminal nerve
ƒ Anhidrosis (absence of sweating) and Long ciliary nerve

flushing of affected side of face To sweat glands

ƒ Miosis (pupil constriction) of forehead

Associated with lesions along the sympathetic To smooth muscle of eyelid

To pupillary dilator
chain: Internal
carotid To sweat glands of face
ƒ 1st neuron: pontine hemorrhage, lateral artery
External carotid artery
medullary syndrome, spinal cord lesion C2
Third neuron
above T1 (eg, Brown-Séquard syndrome, First neuron
Superior cervical ganglion
late-stage syringomyelia)
Synapse in
ƒ 2nd neuron: stellate ganglion compression lateral horn T1
by Pancoast tumor Second neuron
ƒ 3rd neuron: carotid dissection (painful) Spinal cord

Ocular motility
Superior Superior Superior Superior CN VI innervates the Lateral Rectus.
rectus oblique rectus oblique
muscle muscle muscle muscle
CN IV innervates the Superior Oblique.
Medial CN III innervates the Rest.
Trochlea
rectus The “chemical formula” LR6SO4R3.
muscle
Lateral Medial
rectus rectus
muscle muscle

Lateral
Inferior Inferior rectus
oblique rectus muscle
muscle muscle
Inferior Inferior
rectus oblique
muscle muscle
Obliques go Opposite (left SO and IO tested
with patient looking right).
IOU: IO tested looking Up.
 NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PHARMACOLOGY
`  SEC TION III 573

Mixed agonist and antagonist opioid analgesics

DRUG MECHANISM CLINICAL USE NOTES
Pentazocine κ-opioid receptor agonist Analgesia for moderate to Can cause opioid withdrawal
and μ-opioid receptor weak severe pain. symptoms if patient is also
antagonist or partial agonist. taking full opioid agonist
(due to competition for opioid
receptors).
Butorphanol κ-opioid receptor agonist and Severe pain (eg, migraine, Causes less respiratory
μ-opioid receptor partial labor). depression than full opioid
agonist. agonists. Use with full opioid
agonist can precipitate
withdrawal. Not easily
reversed with naloxone.

Tramadol
MECHANISM Very weak opioid agonist; also inhibits the Tramadol is a slight opioid agonist, and a
reuptake of norepinephrine and serotonin. serotonin and norepinephrine reuptake
CLINICAL USE Chronic pain. inhibitor. It is used for stubborn pain, but
can lower seizure threshold, and may cause
ADVERSE EFFECTS Similar to opioids; decreases seizure threshold;
serotonin syndrome.
serotonin syndrome.

Glaucoma therapy  IOP via  amount of aqueous humor (inhibit synthesis/secretion or  drainage).
BAD humor may not be politically correct.
DRUG CLASS EXAMPLES MECHANISM ADVERSE EFFECTS
β-blockers Timolol, betaxolol, carteolol  aqueous humor synthesis No pupillary or vision changes
α-agonists Epinephrine (α1),  aqueous humor synthesis via Mydriasis (α1); do not use in
-
apraclonidine, vasoconstriction (epinephrine) closed-angle glaucoma
brimonidine (α2)  aqueous humor synthesis Blurry vision, ocular
(apraclonidine, brimonidine) hyperemia, foreign body
sensation, ocular allergic
reactions, ocular pruritus
Diuretics Acetazolamide  aqueous humor synthesis No pupillary or vision changes
via inhibition of carbonic
anhydrase
Prostaglandins Bimatoprost, latanoprost  outflow of aqueous humor via Darkens color of iris
(PGF2α)  resistance of flow through (browning), eyelash growth
uveoscleral pathway
Cholinomimetics (M3) Direct: pilocarpine, carbachol  outflow of aqueous humor via Miosis (contraction of pupillary
Indirect: physostigmine, contraction of ciliary muscle sphincter muscles) and

=
echothiophate and opening of trabecular cyclospasm (contraction of
meshwork ciliary muscle)
Use pilocarpine in acute angle
closure glaucoma—very
effective at opening meshwork
into canal of Schlemm
 Case clue ophthal
1) Anterior uveitis
-presents with a painful, red eye associated with photophobia, tearing, and diminished
visual acuity, constricted
. pupils
-O/E: ciliary flush, hypopyon, Keratic precipitates ("mutton fat") and iris nodules

2) Acute angle-closure glaucoma

-red, painful eye with diminished visual acuity and is MC in older patients and most patients
have headache, nausea, and vomiting

3) Bacterial conjunctivitis :conjunctival edema and hyperemia and a purulent

discharge,

-viral conjunctivitis :conjunctival redness with a watery or mucoid discharge

4) Episcleritis: disappears by phenylephrine

-o
-acute redness and tearing with injection of conjunctival and episcleral vessels.
-mild irritation, but overt pain and diminished visual acuity are absent
-
5) Allergic conjunctivitis: episodic vs once in viral conjunctivitis
- intense itching, hyperemia, tearing, and edema of the conjunctiva and eyelids B/L eyes

6) Atopic keratoconjunctivitis
-severe form of ocular allergy.
-itching, tearing, thick mucus discharge, photophobia, and blurred vision.

-diff from AC by more severe sx with a prolonged course, potential visual

impairment due to corneal involvement, and thickening of the eyelids and
surrounding skin.

7) Viral keratitis
-typically have corneal vesicles, opacification, and/or dendritic ulcers.

#Bacterial keratitis
-usually occurs in contact lens wearers, following corneal trauma / entry of a foreign body.
-C/F: central ulcer and adjacent stromal abscess; Hypopyon may be present.

#Fungal keratitis
-after corneal injury in agricultural workers or immunocompromised patients.
-The cornea shows multiple stromal abscesses.

8) lens dislocation (ectopia lentis):

-Poor vision is typically the first sign of dislocation, and a tremulous iris (vibration of the
iris during left and right movement)
10) Postoperative endophthalmitis: basically infection of vitreous
-onset: usually occurs within 6 weeks of surgery.
-pain and decreased visual acuity; swollen eyelids and conjunctiva, hypopyon, corneal
edema and infection.

#Dx:
-The vitreous can be sent for Gram stain and culture.
#Rx: Based on the severity, intravitreal antibiotic injection or vitrectomy is done.

11) Cavernous sinus thrombosis : B/L eyes involved, CN involved 3,4,5,6

-proptosis, ophthalmoplegia, chemosis, and visual loss due to hematogenous spread from
an infected, inflamed sinus, papilloedma
#Dx: MRI; Rx: IV Ab

12) Orbital cellulitis: U/L; Dx: CT scan of orbit and sinus

-Painful eye movements, Ophthalmoplegia; Proptosis; Visual changes
#Etio:
• 1) Local infection
• sinusitis ethmoid or maxillary sinuses- MC
• dental infection in maxillary teeth (which are close to the sinuses and orbits)
• skin infection: Streptococcus species, Staphylococcus aureus
• 2) Orbital trauma

13) Graves ophthalmopathy

-characterized by ocular irritation, impaired extraocular motion, and proptosis

14) Cataract:
-usually report painless blurring of vision, bothersome glare, and often halos around lights
at night due to scattering of light in the lens.

15) DM retinopathy:
-floaters, decreased visual acuity, focal visual field defects, and acute monocular
vision loss.
-vs Gradually progressive blurring with glare and halos is more consistent with
cataracts.

16) HT retinopathy: acutely with monocular vision loss in long standing HT

17) surgery is the primary option for paediatric glucoma +/- anti glaucoma drops

18) Retinoblastoma
#Diagnosis is confirmed with MRI of the brain and orbits (red circle).
-Biopsy is not performed due to risk of tumor seeding.
536 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—OPHTHALMOLOGY
` 

Glaucoma Optic disc atrophy with characteristic cupping (normal A versus thinning of outer rim of optic
nerve head B ), usually with elevated intraocular pressure (IOP) and progressive peripheral visual
field loss if untreated. Treatment is through pharmacologic or surgical lowering of IOP.
Open-angle glaucoma Associated with  age, African-American race, family history. Painless, more common in US.
Primary—cause unclear.
Secondary—blocked trabecular meshwork from WBCs (eg, uveitis), RBCs (eg, vitreous
hemorrhage), retinal elements (eg, retinal detachment).
Closed- or narrow- Primary—enlargement or anterior movement of lens against central iris (pupil margin)
angle glaucoma Ž obstruction of normal aqueous flow through pupil Ž fluid builds up behind iris, pushing
peripheral iris against cornea C and impeding flow through trabecular meshwork.
Secondary—hypoxia from retinal disease (eg, diabetes mellitus, vein occlusion) induces
vasoproliferation in iris that contracts angle.
Chronic closure—often asymptomatic with damage to optic nerve and peripheral vision.
Acute closure—true ophthalmic emergency.  IOP pushes iris forward Ž angle closes abruptly.
Very painful, red eye D , sudden vision loss, halos around lights, frontal headache, fixed and
mid-dilated pupil, nausea and vomiting. Mydriatic agents contraindicated.
A B C D

Normal

Normal Cupping Angle closure Acute angle closure

Uveitis Inflammation of uvea; specific name based on location within affected eye. Anterior uveitis: iritis;
A
posterior uveitis: choroiditis and/or retinitis. May have hypopyon (accumulation of pus in anterior
chamber A ) or conjunctival redness. Associated with systemic inflammatory disorders (eg,
sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27–associated conditions).

Age-related macular Degeneration of macula (central area of retina). Causes distortion (metamorphopsia) and eventual
degeneration loss of central vision (scotomas).
A
ƒ Dry (nonexudative, > 80%)—Deposition of yellowish extracellular material (“Drusen”) in
between Bruch membrane and retinal pigment epithelium A with gradual  in vision. Prevent
progression with multivitamin and antioxidant supplements.
ƒ Wet (exudative, 10–15%)—rapid loss of vision due to bleeding 2° to choroidal
neovascularization. Treat with anti-VEGF (vascular endothelial growth factor) injections
(eg, bevacizumab, ranibizumab).
19) optic nerve injury.:
-relative afferent pupillary defect (RAPD) following head trauma

20) Dacrocystitis:
-sudden onset of pain and redness in the medial canthal region with purulent discharge
from the punctum.

22) Chalazion
-chronic, granulomatous inflammation of the meibomian gland which appears as a hard,
painless lid nodul

23) photokeratitis:
-B/L eye pain and photophobia 6-12 hrs after playing in the snow with B/L punctate
defects on staining

24) Optic Glioma:

-NF1 pt develops decreased visual acuity, alterations in color vision, optic nerve
atrophy, and proptosis.

25) Presbyopia:_ altered lens elasticity

-middle-aged individual who has to hold books at an arms length to read is classic.

26) Orbital compartment syndrome

-eye pain and vision loss due to rapidly increased intraorbital pressure from trauma.
-O/E: tight orbit (eg, periorbital swelling, hard eyelid, proptosis) and ARPD
-Mx: immediate surgical decompression (medial canthotomy with cantholysis) to
prevent permanent vision loss.

27) Sympathetic ophthalmia

-patient with a traumatic injury to the left eye has developed inflammation (eg, conjunctival
erythema, uveitis ) and decreased vision in the uninjured right eye.
-This is most consistent with, an autoimmune condition that can occur when T cells
become sensitized to previously sequestered eye antigens.
-Mx: remove injured eye if poor prognosis, else steroids

28) RP:
-onset- 10 yrs and blind till 40
-nyctalopia, mid peripheral visual field loss as Rodes are max here
-fundus:waxy pallor yellow disc, bony black spicules in mid periphery,retinal vessel
attenuation
30) Mx of acute angle closure: epinephrine is C/I
• Topical therapy: multidrug topical therapy (eg, timolol, pilocarpine, apraclonidine)
• Systemic therapy: acetazolamide (consider mannitol) rapid action
• Laser iridotomy definitive Rx
#Mx of CRAO:
31) -CRAO is an ophthalmologic emergency, and
attempts at recovering vision (eg, anterior
chamber paracentesis, ocular massage,
revascularization) should be considered.
-Workup also includes noninvasive imaging of the
carotids to evaluate for stenosis.
Rx:
-Atherosclerotic treatment (eg, aspirin, statin),
-in cases of cardioembolic phenomenon, long-term
anticoagulation (eg, warfarin) are often initiated.

34)–pupil-involving CN III palsies

- frequently caused by mass effect
and should be considered due to an
intracranial aneurysm until proved
otherwise.

-Next step: immediate MR or CT

angiography of the head for
evaluation.
 Preseptal vs orbital cellulitis 33) Blepharospasm
Diagnosi Preseptal
Orbital cellulitis
- a form of focal dystonia characterized by
s cellulitis
recurrent forceful contraction of the eyelid
• Symptoms of preseptal
• Eyelid cellulitis
muscles.
Clinical erythema + -B/L, symmetric vs U/L, red in uveitis
features & swelling • Pain with EOM, proptosis &/
• Chemosis or ophthalmoplegia with
diplopia -Bright lights may trigger symptoms, whereas
Treatment
• Oral • Intravenous antibiotics touching or brushing the skin around the eye may
antibiotics • ± Surgery
terminate the spasm. /
EOM = extraocular movements.

#Mx: Mild cases : trigger avoidance,

-but botulinum toxin injection : needed for more significant symptoms.

Conjunctivitis treatment 35) ectopic lentils after mild

trauma
• Erythromycin ointment
• Polymyxin-trimethoprim drops -Lens dislocation typically occurs
Bacterial after blunt trauma to the eye.
• Azithromycin drops
conjunctivitis
• Preferred agent in contact lens wearers:
fluoroquinolone drops -However, ectopia lentis following
Viral • Warm or cold compresses minimal or no trauma should
conjunctivitis • ± Antihistamine/decongestant drops prompt
• Over-the-counter antihistamine/ ==> evaluation for Marfan
decongestant drops for intermittent syndrome, including
Allergic
symptoms
conjunctivitis
• Mast cell stabilizer/antihistamine drops for echocardiography to detect
frequent episodes (olopatadine, azelastine) associated aortic root disease.

36) High-dose systemic glucocorticoids —>> IV MP (methylprednisolone) x 3 days

then oral steroids for the treatment of :
1) anterior ischemic optic neuropathy in giant cell (temporal) arteritis.
2) optic neuritis (eg, due to multiple sclerosis).

37) #Work up for Anterior Uveitis :

Anterior uveitis can be idiopathic but often occurs in association with systemic
inflammatory disorders.
- Further evaluation depends on the presence of associated features that could suggest a
systemic disease:

• No evidence of systemic disease: CXR and serum RPR should be obtained

because both sarcoidosis and syphilis can be silent.

• Evidence of systemic symptoms: For back pain or enthesitis, x-ray of the

sacroiliac joints should be obtained to rule out spondylarthritis (eg, ankylosing
spondylitis).
9) CMV retinitis
-CD4 counts <100/mm3 with blurred vision, floaters, and photopsia (sensation of flashing
lights).
-Funduscopy: yellow-white, fluffy, hemorrhagic lesions adjacent to the fovea and
retinal vessels

#Mx:
-CMV retinitis are usually treated with oral antivirals (eg, valganciclovir).
- Lesions near the fovea or optic nerve typically require concomitant intravitreal
injections to reduce the risk of blindness and retinal detachment due to retinal
scarring.

-ART should also be initiated (usually 2 weeks after beginning CMV treatment) to
prevent CMV recurrence and progression.

19) Diabetic retinopathy

-it is the leading cause of blindness in the USA. It occurs in both insulin dependent and
non-insulin dependent diabetes mellitus.

#There are 3 main categories:

1 background or simple retinopathy - consists of microaneurysms, hemorrhages,
exudates, and retinal edema
2 Nonproliferative—damaged capillaries leak blood lipids and fluid seep into retina —
> hemorrhages and macular edema. Rx: blood sugar control.

3) Proliferative—chronic hypoxia results in new blood vessel formation with resultant

traction on retinaretinal detachment.
-Rx: anti-VEGF injections, peripheral retinal photocoagulation, surgery.

20) Mx of CRVO:
#Etiology :
- caused by thrombosis of the central retinal vein
#RF:
- most common in patients with coagulopathy, hyperviscosity, chronic glaucoma, and
atherosclerotic risk factors (eg, age, diabetes, hypertension).

#Ix :
- Confirmed with Fundus fluorescein angiography (FFA).
#Mx:
1) No significant macular edema or neovascularization:conservatively with close
observation.

2) Significant macular edema : Intravitreal injection of anti- VEGFs.

—> No treatment is particularly effective, but some patients may have partial recovery
of vision within the first 3 months.
—> Strict control of underlying Etiology is required otherwise recurrences are possible.
Neonatal conjunctivitis 21) choroid rupture:
Ons -Features similar to RD but
Type et Findings Treatment **
age
crescent-shaped streak
• Mild conjunctival irritation & concentric to the optic nerve.
<24
Chemical tearing after silver nitrate Eye lubricant
hr
ophthalmic prophylaxis
• Marked eyelid swelling -C/F: The usual complaint is blurred
Single IM dose of
Gonococc 2-5 • Profuse purulent
3rd- generation
vision following blunt trauma.
al days discharge
cephalosporin
• Corneal edema/ulceration
• Mild eyelid swelling
Chlamydi 5-14 • Watery, serosanguineous, Oral
al days or mucopurulent eye erythromycin
discharge
27) D/D of central scotoma:
a) Optic neuritis : young age
- acute onset of monocular vision loss with central scotoma, afferent pupillary defect
(paradoxical pupillary dilation (x miosis) of the affected eye with the swinging-
flashlight test); changes in color perception, and pain with eye movement.

-There is a strong association between optic neuritis and multiple sclerosis.

#Dx:
• MRI of the orbits & brain, CT
• Funduscopy is usually normal as inflammation occurs behind the optic nerve
head (dont get misguided)
Vs

b) Macular degeneration: old age

- painless, progressive loss of central vision
-RF:occurs in older patients, especially those with vascular risk factors.
*Diff:
-Both eyes are often affected, and funduscopic abnormalities (eg, drusen [yellow
deposits]) are prominent.
27) HSV vs CMV in HIV pt:
a) HSV and VZV
-rapidly progressing bilateral necrotizing retinitis/ "acute retinal necrosis syndrome"
-initial sx : keratitis and conjunctivitis
- severe, acute retinal necrosis associated with pain, keratitis, uveitis,
- fundus: peripheral pale lesions and central retinal necrosis.
Vs

b) CMV retinitis
-painless, not usually associated with keratitis or conjunctivitis
-Fundus: hemorrhages and fluffy / granular lesions around the retinal vessels.

28) Open globe laceration (OGL)

#Types of injury:
a) small, high-velocity particles
-sent airborne by power tools, explosions, lawn mowers, or motor vehicle accidents.

b) Large OGL
- present with globe deformity, extrusion of vitreous or iris/ visible entry wound.

-Other manifestations : a peaked or teardrop pupil, asymmetric anterior chamber

depth, loss of visual acuity/ afferent pupillary response, and reduced IOP
#Dx: fluorescien drops

29) Strabismus (ocular misalignment)

-eye deviation, asymmetric corneal light and red reflexes, and an abnormal cover test.

-Next step: Dilated funduscopic to detect retinoblastoma

30) vitreous hemorrhage

-Once a diabetic patient presents with a sudden onset of visual loss with numerous
floaters, a vitreous hemorrhage is most likely to have occurred.
#Fundoscopy: loss of fundus details, floating debris and a dark red glow.

#Conservative Mx:
-For patients with underlying medical conditions, conservative treatment (i.e., upright
position during sleep, which enhances settling of the hemorrhage) is recommended.

31) Amblyopia : a functional reduction in the visual acuity of one or both eyes and is
caused by disturbances in binocular vision during early childhood.

• Unilateral (MC): ≥2-line difference in vision between eyes (eg, 20/30 & 20/50)
• Bilateral: vision worse than 20/40 at age ≥4
• Because of compensation by the normal eye, the presentation of refractive amblyopia
is often delayed until the normal eye is occluded (eg, pirate patch)
#Management
- strengthening the amblyopic eye by applying a patch / cycloplegic vision-blurring drops
(eg, atropine) to the eye with better vision.
-typically require prescription lenses to correct the refractive error.

32) external hordeolum

- an acute inflammatory disorder of the eyelash follicle or tear (moll/Zeis) and presents as
an erythematous, tender nodule at the lid margin.
Vs
#internal hordeolum:
-A similar process arising in the meibomian gland (internal hordeolum) presents as a
tender nodule visible at the palpebral conjunctiva but is less common.

# Natural course of stye:

-Within a few days, a minute pustule may appear at the lid margin (pointing), which will
then rupture with discharge of pus and relief of pain.

**So next best step:

-Warm compresses are advised to accelerate the process and NOT ab
-For patients with a persistent hordeolum (eg, >1-2 weeks) or a large chalazion: additional
IND

Conjunctivitis
Symptoms Viral Bacterial Allergic
Distribution U/L; B/L U/L; B/L B/L
<30 minutes to
Duration 1-2 weeks 1-2 weeks
perennial
Watery/
Discharge Purulent Watery
mucoid
Associated Viral Unremitting ocular
Ocular pruritus
findings prodrome discharge

a
-

34) #Mx of Chemical burns :

—>> In either case, the most important and urgent step in management is to restore a
neutral pH by flushing the eye copiously with water or saline.

#Duration of ocular irrigation :

- Normalization of pH typically takes 30-60 minutes but may take greater than >2 hours for
alkali burns
-after cessation of irrigation, the eye's pH should be remeasured with litmus paper to
confirm that it remains neutral.
35) Presence of RAPD is either due to
1) Extensive Retina damage in Advanced Glaucoma /Advanced Diabetics
Retinopathy or
2) Optic nerve damage.

36) 29) Amaurosis fugax

-The MC etiology: retinal ischemia due to atherosclerotic emboli originating from the
ipsilateral carotid artery;
-So patients with vascular risk factors should receive a duplex ultrasound of the neck.
Vs
If a amaurosis fugax+ FND/AMS/seizures: suspect structural Brain Ds so CT/MRI

17) Macular degeneration

-causes decreased acuity of central vision; It occurs in 2 primary forms:
a) atrophic (dry): slowly progressive, vision loss that involves one or both eyes and is
usually associated with scotoma (ie, blind spot);

b) exudative/neovascular (wet), :U/L, aggressive vision loss, often starting with

straight line distortion by grid test (dx)

37) congenital dacrostenosis:

-may spontaneously resolved in 95% cases by age 1 to 2 years
-NLD probing only if persist >6 mon

38) Retinopathy of prematurity

#Pathogenesis:
-premature( <30 wks) infants retinal vessels have not grown upto the periphery yet..
-so peripheral part remains ischaemic and starts secreting VEGF—>
neovascularisation —> if severe can cause RD

18) Open-angle glaucoma

-insidious, gradual loss of peripheral vision.
-This may lead to near-miss motor vehicle collisions, but night driving is not
preferentially affected like cataract

#Rx:
1st line: topical PG analogues- latanoprost, bimatoprost
2nd line: topical B blockers- Timolol
3rd line :Sx laser trabeculoplasty

39) Rx of anterior uveitis:

-cyclopentolate dilator drops: relieves ciliary muscle spasm
-topical steroids to relieve inflammation
 Musculoskeletal

==> Key idea: Two main causes of back pain with a positive straight leg test are disc
herniation and osteophyte (same pathophysiology with spinal root compression)

==> Key idea: The two main diseases that affect the DIP joints of the hand (at least on
NBME exams) are osteoarthritis and psoriatic arthritis
 446 SEC TION III MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE ANATOMY AND PHYSIOLOGY
` 

MUSCULOSKELETAL, SKIN, AND CONNECTIVE TISSUE—ANATOMY AND PHYSIOLOGY

` 

Rotator cuff muscles Shoulder muscles that form the rotator cuff: SItS (small t is for teres minor).
A
ƒ Supraspinatus (suprascapular nerve)—
abducts arm initially (before the action Acromion
Supraspinatus

of the deltoid); most common rotator

Humerus
Glenoid cuff injury (trauma or degeneration and Coracoid

impingement Ž tendinopathy or tear [arrow

Greater tubercle
in A ]), assessed by “empty/full can” test Infraspinatus

ƒ Infraspinatus (suprascapular nerve)—

externally rotates arm; pitching injury Teres minor
ƒ teres minor (axillary nerve)—adducts and
externally rotates arm Lesser tubercle Subscapularis
Humerus
ƒ Subscapularis (upper and lower subscapular
nerves)—internally rotates and adducts arm
Innervated primarily by C5-C6.

Arm abduction
DEGREE MUSCLE NERVE
0°–15° Supraspinatus Suprascapular
15°–100° Deltoid Axillary
> 90° Trapezius Accessory
> 100° Serratus Anterior Long Thoracic (SALT)

#Suprascapular nerve entrapment

-C/F: presents with shoulder pain and
weakness of shoulder abduction
" (supraspinatus)and external
rotation(infraspinatus) .

#Etio: caused by external compression

of the nerve at the suprascapular notch
= (eg, use of a heavy backpack), a direct
#Claw toe and hammer toe deformities reflect blow, or repetitive motion at the
an imbalance in strength and flexibility shoulder.
between the flexor and extensor muscle
groups.
-In a patient with longstanding diabetes, these
deformities may suggest underlying diabetic
peripheral neuropathy.
-Other complications of diabetic neuropathy :
callusing, ulceration, joint subluxation, and
Charcot arthropathy.
 MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE ANATOMY AND PHYSIOLOGY
`  SEC TION III 447

Upper extremity nerves

NERVE CAUSES OF INJURY PRESENTATION
Axillary (C5-C6) Fractured surgical neck of humerus Flattened deltoid
Anterior dislocation of humerus Loss of arm abduction at shoulder (> 15°)
Loss of sensation over deltoid and lateral arm
Musculocutaneous Upper trunk compression  biceps (C5-6) reflex
(C5-C7) Weakness of forearm flexion and supination
Loss of sensation over lateral forearm
Radial (C5-T1) Compression of axilla, eg, due to crutches or Wrist drop: loss of elbow, wrist, and finger
sleeping with arm over chair (“Saturday night extension
palsy”)  grip strength (wrist extension necessary for
Midshaft fracture of humerus maximal action of flexors)
Repetitive pronation/supination of forearm, eg, Loss of sensation over posterior arm/forearm and
due to screwdriver use (“finger drop”) dorsal hand
Median (C5-T1) Supracondylar fracture of humerus Ž proximal “Ape hand” and “Pope’s blessing”
lesion of the nerve Loss of wrist flexion, flexion of lateral fingers,
Carpal tunnel syndrome and wrist laceration thumb opposition, lumbricals of index and
Ž distal lesion of the nerve middle fingers
Loss of sensation over thenar eminence and
dorsal and palmar aspects of lateral 31⁄2 fingers
with proximal lesion
Ulnar (C8-T1) Fracture of medial epicondyle of humerus “Ulnar claw” on digit extension
“funny bone” (proximal lesion) Radial deviation of wrist upon flexion (proximal
Fractured hook of hamate (distal lesion) from lesion)
fall on outstretched hand Loss of wrist flexion, flexion of medial fingers,
abduction and adduction of fingers (interossei),
actions of medial 2 lumbrical muscles
Loss of sensation over medial 11/2 fingers
including hypothenar eminence
Recurrent branch of Superficial laceration of palm “Ape hand”
median nerve (C5-T1) Loss of thenar muscle group: opposition,
abduction, and flexion of thumb
No loss of sensation
Humerus fractures, proximally to distally, follow the ARM (Axillary Ž Radial Ž Median)
C5
C6
C7
Axillary nerve C8
T1
Median nerve
Axillary nerve
Musculocutaneous nerve Ulnar nerve
Intercostobrachial
Radial nerve nerve
Radial nerve Radial nerve
Medial brachial
Radial nerve in
cutaneous nerve Palm of hand
spiral groove

Median nerve Musculocutaneous

Ulnar nerve Medial antebrachial
nerve
cutaneous nerve Median nerve
Radial nerve
Ulnar nerve
Radial nerve
Recurrent branch
of median nerve Radial nerve

Dorsum of hand
448 SEC TION III MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE ANATOMY AND PHYSIOLOGY
` 

Brachial plexus lesions

Erb palsy (“waiter’s tip”) C5 Upper Lateral Randy
Klumpke palsy (claw hand) Musculocutaneous Travis
Wrist drop C6 Drinks
Axillary
Winged scapula
Middle Posterior Cold
Deltoid paralysis C7 (Extensors) Median (flexors) Beer
“Saturday night palsy” (wrist drop)
Difficulty flexing elbow, variable Radial
C8 Lower Medial
sensory loss
Decreased thumb function, Ulnar
“Pope’s blessing” T1
Trunks Divisions Cords Branches
Intrinsic muscles of hand,
claw hand
Long thoracic

Roots
Erb-Duchenne palsy
CONDITION INJURY CAUSES MUSCLE DEFICIT FUNCTIONAL DEFICIT PRESENTATION
(”waiter’s tip”)
Erb palsy (“waiter’s Traction or tear Infants—lateral Deltoid, Abduction (arm
tip”) of upper trunk: traction on neck supraspinatus hangs by side)
C5-C6 roots during delivery Infraspinatus Lateral rotation (arm
Adults—trauma medially rotated)
Biceps brachii Flexion, supination
Herb gets DIBs (arm extended and
on tips pronated)

Klumpke palsy Traction or tear Infants—upward Intrinsic hand Total claw hand:
of lower trunk: force on arm muscles: lumbricals normally
C8-T1 roots during delivery lumbricals, flex MCP joints and
Adults—trauma interossei, extend DIP and PIP
(eg, grabbing a thenar, joints
tree branch to hypothenar
break a fall)
Thoracic outlet Compression Cervical rib Same as Klumpke Atrophy of intrinsic A
syndrome of lower trunk (arrows in A , palsy hand muscles; C5

and subclavian Pancoast tumor ischemia, pain, C6

C7
vessels, most =
and edema T1
commonly due to vascular
within the compression
scalene triangle
Winged scapula Lesion of long Axillary node Serratus anterior Inability to anchor B
thoracic nerve, dissection after scapula to thoracic
roots C5-C7 mastectomy, cage Ž cannot
(“wings of stab wounds abduct arm
heaven”) above horizontal
position B
462 SEC TION III MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE ANATOMY AND PHYSIOLOGY
` 

Lower extremity nerves

NERVE INNERVATION CAUSE OF INJURY PRESENTATION/COMMENTS
Iliohypogastric
(T12-L1)
→
Sensory—suprapubic region
Motor—transversus abdominis
Abdominal surgery Burning or tingling pain in
surgical incision site radiating
and internal oblique to inguinal and suprapubic
region
Genitofemoral nerve Sensory—scrotum/labia Laparoscopic surgery  upper medial thigh and
(L1-L2) majora, medial thigh anterior thigh sensation
Motor—cremaster beneath the inguinal
ligament (lateral part of the
femoral triangle); absent
cremasteric reflex
Lateral femoral Sensory—anterior and lateral Tight clothing, obesity,  thigh sensation (anterior and
cutaneous (L2-L3) thigh pregnancy, pelvic procedures lateral)
Obturator (L2-L4) Sensory—medial thigh Pelvic surgery  thigh sensation (medial) and
Motor—obturator externus, adduction
adductor longus, adductor
brevis, gracilis, pectineus,
adductor magnus

Femoral (L2-L4) Sensory—anterior thigh, Pelvic fracture  leg extension ( patellar

medial leg reflex)
Motor—quadriceps, iliacus,
pectineus, sartorius

Sciatic (L4-S3) Motor—semitendinosus, Herniated disc, posterior hip Splits into common peroneal
semimembranosus, biceps dislocation and tibial nerves
femoris, adductor magnus

Common (fibular) Superficial peroneal nerve: Trauma or compression of PED = Peroneal Everts and
peroneal (L4-S2) ƒ Sensory—dorsum of foot lateral aspect of leg, fibular Dorsiflexes; if injured, foot
(except webspace between neck fracture dropPED
hallux and 2nd digit) Loss of sensation on dorsum
ƒ Motor—peroneus longus of foot
and brevis Foot drop—inverted and
Deep peroneal nerve: plantarflexed at rest, loss of
ƒ Sensory—webspace eversion and dorsiflexion;
between hallux and 2nd “steppage gait”
digit
ƒ Motor—tibialis anterior
 MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE ANATOMY AND PHYSIOLOGY
`  SEC TION III 463

Lower extremity nerves (continued)

NERVE INNERVATION CAUSE OF INJURY PRESENTATION/COMMENTS
Tibial (L4-S3) Sensory—sole of foot Knee trauma, Baker cyst TIP = Tibial Inverts and
Motor—biceps femoris (long (proximal lesion); tarsal Plantarflexes; if injured, can’t

F-
head), triceps surae, plantaris, tunnel syndrome (distal stand on TIPtoes
popliteus, flexor muscles of lesion) Inability to curl toes and loss of
foot sensation on sole; in proximal
lesions, foot everted at rest
with weakened inversion and
plantar flexion

Superior gluteal Motor—gluteus medius, gluteus Iatrogenic injury during Trendelenburg sign/gait—
(L4-S1) minimus, tensor fascia latae intramuscular injection pelvis tilts because weight-
to superomedial gluteal bearing leg cannot maintain
region (prevent by choosing alignment of pelvis through
superolateral quadrant, hip abduction
preferably anterolateral Lesion is contralateral to the
region) side of the hip that drops,
ipsilateral to extremity on
which the patient stands

Trendelenburg
Normal sign

Inferior gluteal (L5-S2) Motor—gluteus maximus Posterior hip dislocation Difficulty climbing stairs, rising
from seated position; loss of
hip extension
Pudendal (S2-S4) Sensory—perineum Stretch injury during  sensation in perineum and
Motor—external urethral and childbirth, prolonged cycling, genital area; can cause fecal
anal sphincters horseback riding and/or urinary incontinence
Features of lumbosacral radiculopathy Can be blocked with local
anesthetic during childbirth
Nerve using ischial spine as a
Reflex affected Sensory loss* Weakness
Root
landmark for injection
•
Anterome • Hip flexion (iliopsoas)
L2-L4** • Patellar dial thigh • Hip adduction
• Medial • Knee extension (quadriceps)
shin
• Foot dorsiflexion &
• Lateral
inversion (tibialis anterior)
shin
L5 • None • Foot eversion (peroneus)
• Dorsum
• Toe extension (extensor
of the foot
hallucis and digitorum)
• Posterior
• Hip extension (gluteus
calf
maximus)
S1 • Achilles • Sole &
• Foot plantarflexion
lateral
(gastrocnemius)
foot
•
• Urinary or fecal incontinence
S2-S4** Anocutan • Perineum
• Sexual dysfunction
eous
*Radicular pain typically has a similar distribution to sensory loss.
** Difficult to distinguish between individual nerve roots clinically.
 MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE ANATOMY AND PHYSIOLOGY
`  SEC TION III 465

Ankle sprains Anterior talofibular ligament—most common

Anterior inferior
ankle sprain overall, classified as a low ankle Fibula
tibiofibular ligament
sprain. Due to overinversion/supination of foot. Posterior inferior
Tibia
Anterior talofibular
tibiofibular ligament ligament
Always tears first.
Navicular
Anterior inferior tibiofibular ligament—most Posterior talofibular Cuneiform bones
ligament
common high ankle sprain. Talus

Calcaneus Cuboid

Calcaneofibular
ligament
Tarsals Metatarsals Phalanges

Signs of lumbosacral Paresthesia and weakness related to specific lumbosacral spinal nerves. Intervertebral disc (nucleus
radiculopathy pulposus) herniates posterolaterally through annulus fibrosus (outer ring) into central canal due to
thin posterior longitudinal ligament and thicker anterior longitudinal ligament along midline of
vertebral bodies. Nerve affected is usually below the level of herniation.

Disc level
herniation L3-L4 L4-L5 L5-S1
Nerve root L4 pedicle (cut)

÷
L4 L5 S1
L4 body
L4 nerve root
L4-L5 disc
protrusion

L5 body
Dermatome L5 nerve root
L5-S1 disc
protrusion

S1 nerve root

S2 nerve
Weakness of knee extension Weakness of dorsiflexion Weakness of plantar flexion
Clinical root
↓ patellar reflex Difficulty in heel walking Difficulty in toe walking
findings .
↓ Achilles reflex

Neurovascular pairing Nerves and arteries are frequently named together by the bones/regions with which they are
associated. The following are exceptions to this naming convention.

← LOCATION
Axilla/lateral thorax
NERVE
Long thoracic
ARTERY
Lateral thoracic
Surgical neck of humerus Axillary Posterior circumflex
Midshaft of humerus Radial Deep brachial
Distal humerus/cubital fossa Median Brachial
Popliteal fossa Tibial Popliteal
Posterior to medial malleolus Tibial Posterior tibial
464 SEC TION III MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE ANATOMY AND PHYSIOLOGY
` 

Knee exam Lateral femoral condyle to anterior tibia: ACL. Femur

Medial femoral condyle to posterior tibia: PCL.
LAMP.
Lateral Medial
condyle condyle

ACL PCL

LCL MCL

Lateral Medial
meniscus meniscus

Fibula Tibia

TEST PROCEDURE

Anterior drawer sign Bending knee at 90° angle,  anterior gliding of

t
tibia (relative to femur) due to ACL injury ACL tear
Lachman test also tests ACL, but is more
sensitive ( anterior gliding of tibia [relative to
femur] with knee bent at 30° angle)
Posterior drawer sign Bending knee at 90° angle,  posterior gliding of
tibia due to PCL injury
PCL tear

Abnormal passive Also called valgus stress test.

abduction Knee either extended or at ~ 30° angle, lateral Abduction
(valgus) MCL tear
(valgus) force Ž medial space widening of force
tibia Ž MCL injury

Abnormal passive Also called varus stress test.

adduction Knee either extended or at ~ 30° angle, medial Adduction
(varus) LCL tear
(varus) force Ž lateral space widening of tibia force
Ž LCL injury

McMurray test During flexion and extension of knee with

Internal
rotation of tibia/foot (LIME): rotation
Lateral
meniscal
ƒ Pain, “popping” on internal rotation and
tear
varus force
and varus force Ž Lateral meniscal tear
(Internal rotation stresses lateral meniscus)
ƒ Pain, “popping” on external rotation and External Medial
valgus force Ž Medial meniscal tear rotation meniscal
and tear
(External rotation stresses medial meniscus) valgus force
 Ortho rheumatology medicine clues
1) Septic arthritis:
systemic findings (eg, fever, chills) and restricted movement in the joint with pain, swelling,
or warmth; acute monoarthritis

2) Osteonecrosis/ a vascular/ atruamatuc or ischaemic necrosis:

-it can present with groin pain and reduced hip range of motion.
-have nocturnal or rest pain,
-reduced ROM (particularly internal rotation and abduction) and joint instability.
-RF: all have a history of GC use, SCD or heavy alcohol use

3) Deep venous thrombosis (DVT)

-typically presents with U/L calf or thigh pain and leg swelling with warmth, tenderness, or
erythema.

4) Achilles tendinopathy:
-ankle pain, Swelling, tenderness 2-6 cm proximal to tendon insertion following
strenuous exercise/ FQ/GC; negative Thompton test:absence of plantar flexion of
ankle on calf squeezing
#Mx: Acute: activity modification, ice, NSAIDs; Chronic: eccentric resistance exercises

5) Polymyalgia rheumatica (PMR)

->50 yrs; B/L pain and stiffness in the neck, shoulders and pelvic girdle x >1 month;
elevated ESR; no focal tenderness/ inflammation

6) Fibromyalgia (FM)
#Rx:
-initial try: aerobic exercise; if fails Med
-1st line: TCA- amitryptilline; 2nd line: SNRI duolexitin, milnacioram; pregabalin
-3rd line: combo of CBT, pain meds

7) Herniated disk:
-radicular pain radiating along the thigh to below the knee

8) Spinal epidural abscess

-triad of fever, severe localized back pain, and CNS deficits (eg, motor weakness,
paresthesias, bowel/bladder dysfunction)

9) Inflammatory back Ds: eg AS, seronegative arthritis

-typically worse in the morning and improves throughout the day.
10) vertebral compression fracture (VCF)
-acute(1 day) back pain and midline local lumbar tenderness after sudden bending,
coughing, or lifting/minimum trauma ; decreased spinal mobility, CNS exam normal
-RF must be + osteoporosis in elder after minimum trauma else think something else

11) Aortoiliac atherosclerosis

-pain is typically in the entire leg (buttock, thigh, and calf) with activity. Impotence
-distal pulses :diminished.

12) Meralgia paresthetica

-causes burning pain and paresthesias at the lateral thigh; Sx unaffected by motion.

14) Morton neuroma

-pain betwen the 3rd & 4th toes on the plantar surface and with a clicking sensation
(Mulder sign) that occurs when palpating this space and squeezing the metatarsal
joints.

16) stress fracture

-usually causes sharp and localized pain over a bony surface (MC the 2nd, 3rd, or 4th
metatarsals) and not joints that worsens with athletic activity
#Mx:
-# of the 2nd, 3rd, and 4th metatarsals are managed conservatively as the surrounding
metatarsals act as splints and nonunion is uncommon.
-#of the 5th metatarsal shaft :at increased risk for nonunion and are usually managed
with casting or internal fixation

17) Meniscal tear: medial joint line tenderness and palpable locking or catching
when the joint is rotated or extended while under load

18) Pes anserinus pain syndrome: includes bursar and non bursar causes
-localized pain and tenderness over the medial tibial condyle below the joint line..
-Mx: quadriceps strengthening exercises

19) Hand OA
worsening hand Pain( DIP, PIP; nodes) with extensive use of hand tools or other
strenuous motor tasks (eg, opening jars).

20) Lumbosacral strain:

-lumbar paravertebral muscles that does not radiate below the level of the knee. (Diff
that from disc prolapse which is below knee)
-Straight-leg raising testing : negative
22) Osteoarthritis of the hip joint:
-upper lateral thigh pain, but deep anterior groin pain is more typical, and loss of
sensation is not seen vs meralgia paresthetica
-X-ray: loss of the normal joint space, periarticular osteophytes, sclerosis of the acetabular
surface.

23) Anterior cruciate ligament tear /ACL

-presents with pain, swelling, and a popping sensation in the knee upon pulling the tibia
forward / positive anterior drawer test.
-Significant swelling (effusion/hemarthrosis) unlike menisci tear and MCL injury ;
Joint instability

24) Osteoid osteoma

-a benign bone tumor that typically occurs at the proximal femur and causes nighttime leg
pain in adolescents which resolved with NSAIDs

25) Ganglion cyst:

-Rubbery, round, well-circumscribed cystic nodule with + transillumination
-Rx: Observation for asymptomatic cysts; Surgical excision: Even if recurrences
after Aspiration

26) Inflamed epidermal cyst :

- a painful, nontransilluminating nodule with an overlying punctum.

27) subcutaneous rheumatoid nodules :

- hard, fixed nodules at pressure points (not rubbery, mobile nodules at the dorsal wrist).
- Transillumination would be negative.

28) Langerhans cell histiocytosis

• Lytic bone lesions (eg, skull, jaw, femur, vertebrae): asymptomatic / associated with
local pain and an overlying tender mass
• Skin rash: (purplish papules, eczematous rash)
• Lymphadenopathy, hepatosplenomegaly
• Pulmonary cysts/nodules —> cough
• Central DI (polyuria, hypernatremia)

#Rx::Chemotherapy (prednisone ± vinblastine)

• Desmopressin for diabetes insipidus

29) Stress # vs shin splints

-Medial tibial stress syndrome (shin splints) : diffuse area of tenderness;> in
obese
Vs
-stress # of tibia: point tenderness; > in undernourished; neg Xray
30)

31) Mx of clavicular #:
A) Uncomplicated fractures of the middle 1/3 of the clavicle :
-MC #
- treated nonoperatively with rest, ice, and either a sling or figure of eight bandage.
-If a patient has signs of vascular injury (brachial art) —> additional assessment must be
performed first.

B) Fractures of the distal 1/3 of the clavicle :

- require open reduction and internal fixation to prevent nonunion.

32) Charcot joint (neurogenic arthropathy)

#RF: DM, B12 def, spinal cord injury
#C/F:
• Foot & ankle deformity (swelling, collapsed arch, decreased range of motion)
• O/E : skeletal deformity, skin calluses, neuropathic ulcers
• Mild pain d/t loss of underlying sensations
• X-ray: bone & joint destruction (deformity, fragmentation), subluxation/
dislocation, decreased bone mass, osteophyte formation, and loss of joint spaces
.
#Mx: Mechanical offloading & correction of joint mechanics (eg, casting, orthotics) to
decrease further Trauma

33) Septic arthritis: infection of joint

Vs
Osteomyelitis: chronic, indolent bone infection associated with a neuropathic ulcer
with sinus tracts or exposure of the underlying bone;

x-ray: bone necrosis with surrounding sclerosis and periosteal thickening, rather than
collapse of the joint.
34) Mx of stress # in Anorexia N: start with diet history

35) Stress Fracture sites :

1) Tibia,
2) metatarsals,
3) tarsal bones (eg, navicular, calcaneus),
4) less commonly, the femur and pelvis.

35) Osteoarthritis knee Mx:

- strengthen the quadriceps muscles
- Intraarticular injection of hyaluronic acid derivatives (ie, viscosupplementation) is
occasionally used for OA of the knee when noninvasive measures fail.

36) Myositis ossificans

-painful, firm, mobile Intramuscular mass with local swelling /induration
-Onset: Days to weeks following injury; MC site: Quadriceps & brachialis

37) Gout nodules : painful

Vs
#Calcinosis cutis: painless
vs
#Rheumatoid nodules: firm, flesh-colored, and nontender. They typically occur over
pressure points such as the elbow and extensor surface of the proximal ulna.

38) Rx of GCA
• PMR only: low-dose oral glucocorticoids (eg, prednisone 10-20 mg daily)

• GCA: intermediate- to high-dose oral glucocorticoids (eg, prednisone 40-60 mg daily)

• GCA with vision loss: pulse high-dose IV glucocorticoids (eg, methylprednisolone

1,000 mg daily) for 3 days followed by intermediate- to high-dose oral glucocorticoids
 39) vertebral fracture in AS:
-Pathogenesis: long-standing ankylosing spondylitis can develop bone loss due to
increased osteoclast activity in the setting of chronic inflammation(TNF a, IL 6) +
spinal rigidity contributes
-C/F: vertebral fracture(local bone tenderness), from minimal trauma.
40) DMARDs include,
40)
#nonbiologic agents (eg, MTX, HCQ, sulfasalazine,
leflunomide, AZN )
#biologic agents (eg, etanercept, infliximab,
adalimumab, tocilizumab, rituximab).

#NSAIDS and GC won’t modify the disease severity

41) RA atlantoaxial subluxation:
-an important and potentially life-
threatening complication
-C/F: spinal cord compression and
difficulties with intubation (eg, during
anesthesia).

-Features of cervical myelopathy in RA :

neck pain, progressive spastic
quadriparesis, and sensory deficits in
the hands and feet.
41) hereditary hemochromatosis (HH) vs OA
• Onset at age <40 versus >40 with OA
• Predilection for the 2nd and 3rd (MCP) joints and wrists vs DIP joints and thumb
bases with OA
• Presence of chondrocalcinosis (ie, cartilage calcification)
#Mx:
-symptomatic (eg, acetaminophen, NSAIDS ),
-but therapeutic phlebotomy is necessary to minimize other systemic complications of HH
(eg, liver disease).

42) Upper extremity DVT:

-Etiology:Central catheter or PICC line within 7-14 days; Young, athletic males
(spontaneous); Repetitive arm motions (eg, baseball pitching); Weight lifting;
Malignancy

-Types: spontaneous and catheter related

-Rx: 3 months anticoagulation; Thrombolysis (non–catheter-related); PICC line can

often remain in place.
 Mnemo Pb KTL: prostate, breast,
43) mets bone: vertebral mc as BF here is slow nic: kidney, thyroid, lung cancers
-Prostate CA: osteoblastic "lead
-MM: osteolytic Pb = symbol for lead
kettle"

44) SLE induced pancytopenia:

-indicates concurrent peripheral, immune-mediated destruction of all 3 cell lines.
-platelet: TTP, ITP as well

21) Malingering
-pain in a nonanatomic distribution, tenderness to light palpation over a broad region, and
a change in neurologic examination while distracted.

22) fat embolism syndrome: after 72 hrs of trauma

-RS distress; CNS dysfunction; Petechial rash
-Mx: supportive care; ventilation only if respiratory failure/ failure to respond to O2.

23) Initial Mx of septic arthritis :

-IV antibiotics + adequate drainage of purulent material.
1) For easily accessed joints (like the knee Joint): needle aspiration may be performed

2) For deep joints (eg, hip) / when needle aspiration does not facilitate adequate
drainage: arthroscopic irrigation / open surgical drainage may be needed.

—>Regardless of drainage technique, serial procedures (eg, daily needle aspirations)

are often required to completely clear the infection
Risk factors for osteoarthritis Osteoporosis risk factors
in absence of trauma or other secondary Nonmodifiable Modifiable
causes of OA,
• Advanced age • Smoking
risk of primary OA is low before age 40 • Postmenopausal • Excessive alcohol
Modifiable Nonmodifiable • Low body weight intake
• White or Asian • Sedentary lifestyle
• Advanced age ethnicity • Medications (eg,
• Sedentary lifestyle
• Female sex • Malabsorption glucocorticoids,
• Obesity

I
• Family history disorders anticonvulsants)
• Occupational joint
• Abnormal joint • Hypercortisolism, • Vitamin D

=
loading hyperthyroidism, deficiency,
alignment
• Diabetes mellitus hyperparathyroidism inadequate calcium
• Prior joint trauma
• Inflammatory intake
disorders (eg, • Estrogen deficiency
#Osteoporosis in a young or middle-aged rheumatoid arthritis) (eg, premature
• Chronic liver or renal menopause,
man suggests a secondary cause. disease hysterectomy/
• oophorectomy)
-celiac disease ;hyper Th not hypo;RTA; #In patients with osteoporosis, the risk for
drugs ;hyper PTH fragility fracture is highest in those with
a prior history of fragility fracture.
25) when to suspect secondary causes of osteoporosis??
-in the absence of fracture (eg, vertebral compression fracture, which could cause
localized spine tenderness), nonlocalized bone pain and tenderness, are uncommon
in postmenopausal osteoporosis and also suggest secondary causes of bone loss (eg,
osteomalacia, malignancy).

26) D/D of takayasu

1) Aortic coarctation
-pulse deficits
-BP discrepancies (U/E and L/E) vs BP discrepancy between both U/E in takayasu
and dissection
- MC age group for coarctation: neonates and young children

2) Aortic dissection
-C/F: acute chest pain radiating to the back.
- It is most common in patients with underlying hypertension.
-> 20 mmHg BP discrepancy between 2 arms

3) Takayasu arteritis
- BP discrepancy between 2 arms; decreased pulse..

27) Drugs causing SLE:

-Most common: procainamide, hydralazine, penicillamine
-Others: minocycline, TNF-alpha inhibitors (eg, etanercept, infliximab), isoniazid

28) Bone scan: tracer uptake by dense bone

-not useful in the diagnosis of MM as they detect only osteoblastic activity
-In MM, the lesions are osteoclastic (lytic), so a skeletal survey (series of Xray) ,
rather than a bone scan, is needed

29) psychosis in SLE:

-patient's history of arthralgia and psychosis, together with thrombocytopenia,
hematuria, and proteinuria, is concerning for systemic lupus erythematosus (SLE).
- classic malar rash seen in SLE is often absent and should not be relied on for
diagnosis.

30) myasthenia gravis

:#Triggers:
Medications: antibiotics (eg, FOs, aminoglycosides), neuromuscular blocking agents, cardiac
medications (eg, BBs), MgSO4, penicillamine
• Physiologic stress: pregnancy/childbirth, surgery (especially thymectomy), infection

• Surgery, exposed to a neuromuscular blocking agent (eg, rocuronium) during intubation —>
Unmasking of symptoms.
#C/F:
-fluctuating, fatigable weakness that is most prominent in the ocular (eg, ptosis,
diplopia), bulbar (eg, dysphagia, dysarthria), facial (eg, myasthenic sneer), and
proximal (eg, difficulty holding up the head or lifting the arms) muscles.

#Mx:
1)1st line: AChEI DOC- pyridostigmine
2) 2nd line: immunotherapy- steroids; AZN
3) 3rd line: thymectomy

#+Celecoxib:
used as NSAIDs

=
only if GIT Ds
-S/E: > cvs
problem and less
effective than
Brufen

Indications for imaging in low back pain,

:infection, malignancy, or bony abnormalities (eg,
compression fracture)
• Acute onset midline spine
tenderness —> Osteoporosis/
X-ray
compression fracture
• Suspected malignancy —>
MRI used to
constant dull Nocturnal pain
confirm Xray
• Ankylosing spondylitis (AS) (eg,
findings
insidious onset, nocturnal pain,
better with movement)
• Sensory/motor deficits
• Cauda equina syndrome (eg,
MRI
urine retention, saddle anesthesia)
(without
• Suspected epidural abscess/
LMN preceding X-
infection (eg, fever, intravenous
ray indications)
drug abuse, concurrent infection,
hemodialysis)
Radionuclide
• Indications for, but patient not able
bone scan or CT
to have, MRI
33) Vascular injury by clavicle # scan
- middle 1/3 of the clavicle overlies the brachial plexus and the subclavian artery and vein in the
thoracic outlet —>> so clavicular fractures require a careful neurovascular assessment.

—>> Clinical examination is usually adequate to rule out significant brachial plexus injury in the
acute phase —>> If a chronic thoracic outlet syndrome develops, nerve conduction studies could
be considered later.
 #Because displaced
clavicular fractures
can injure the
pleura/lung (eg,
Proximal to joint line pneumothorax),
subclavian vessels,
and/or brachial
plexus, they are
best evaluated with
Distal to joint line CT scan of the chest
(typically with
intravenous
contrast).

34) acute gouty arthritis: exquisitely painful vs tophi : generally painles

#Diagnosing septic monoarthritis in gout pt:

-gout flares: typically an abrupt onset with maximal symptoms within 12-24 hours
Vs
-whereas septic arthritis develops gradually like 3 days so take joint aspiration

35) Pagets Ds bone:

-ALP > 10 times normal; Ca PO3- normal;
-radionuclide bone scan is useful to fully stage the disease.

36) Pseudogout in hyperPTH:

-symptomatic hypercalcemia (fatigue, constipation, nephrolithiasis [likely calcium
stones]), suggesting primary hyperparathyroidism who now has acute inflammatory
arthritis s/o - Psuedogout.
37) a) Primary RP typically affects young
Joint fluid characteristics
Monoarthritis —> Gout, Septic arthritis patients (ages 15-30, often female),
Noninflammatory
Inflammatory -have symmetric episodic attacks without
Normal (eg, crystals, Septic joint
(eg, OA)
RA)
tissue injury.
Translucent or
-Rx: preventive: CCB; abortive: nitrates
Appearance Clear Clear Opaque
opaque
50,000-150,
WBCs (mm3) <200 200-2,000 2,000-100,000
000
PMNs <25% 25% Often >50% >80%-90%

b) secondary RP : generally older (age >40, often male) and have asymmetric attacks
with clinical features of tissue ischemia (eg, numbness, ulcers) and systemic
disease (autoimmune or vascular).
-Rx: CCB for persisitent Sx despite Rx underlying Ds
-aspirin for digital ulcer
38) vertebral osteomyelitis
fever, leucocytosis not required to diagnose vertebral osteomyelitis
-clue: tenderness to gentle percussion
-but ESR grossly elevated
-Dx: MRI is the most sensitive diagnostic study.

-There should be a very high index of suspicion for vertebral osteomyelitis in patients with a
history of injection drug use or recent distant site infection (eg, urinary tract infection).

39) Pes anserine bursitis

-C/F: presents as a swelling over the upper medial tibial region.
-Etiology: typically caused by overuse and poor knee mechanics.

-Rx: quadriceps and hamstring strengthening exercises to optimize strength, flexibility,

and stability of the knees.

41) Lateral epicondylitis tennis

- a tendinopathy of the wrist extensors at the lateral epicondyle origin.
-pain most severe 1 cm distal to the lateral epicondyle; elicited by resisted wrist extension.

#Rx:
• Initial treatment: activity modification, counterforce bracing/strap
• Refractory symptoms: short-term NSAIDs, corticosteroid injection, surgery

42) Baker cyst

-Mechanism: due to extrusion of synovial fluid from the knee joint into the gastrocnemius or
semimembranosus bursa,
-RF:common in patients with underlying arthritis/ injury
-C/F: Posterior bulge behind the knee that enlarges with extension and disappears with
flexion

-Diff ruptured cyst leg edema from DVT: An arc of ecchymosis is often visible distal to the
medial malleolus ("crescent sign").
# next step: Ultrasound can rule out DVT and confirm the popliteal cyst.

43) NCS and EMG are indicated for patients with chronic or refractory CTS who are being
considered for surgery.
-They are not usually needed in the initial diagnosis (which is typically based on clinical
features) but can be considered if the diagnosis is uncertain.
-Dx of choice: clinical/ Nerve conduction study; NEVER MRI
 43) Mixed cryoglobulinemia is
- small-vessel vasculitis that commonly presents with palpable purpura (leukocytoclastic
vasculitis), arthralgias, fatigue, peripheral neuropathy, liver involvement, and renal
disease.
-It is strongly associated with hepatitis C infection,
- characteristic laboratory : hypocomplementemia, polyclonal IgG, and RF
Vs
HSP: IgA nephropathy+ systemic vasculitis; follows Abd pain

44) xray of osteoarthritis: narrow joint space; osteophytes

Vs
RA: periarticular erosions

#prosthetic joint infection (PJI): WBC usually elevated to >1000/mm3 but is often < than
in septic native joints (usually >50,000/mm3).

45) Mx of olecranon bursitis:

-Rx: activity modification, nonsteroidal anti-inflammatory drugs, and elbow padding.

#Indication of bursal fluid aspiration:

-redness, warmth, or significant pain suggests an infectious or inflammatory etiology and
warrants bursal fluid aspiration.
 48) Giant cell arteritis
-suspected by new headache and
elevated inflammatory markers in
patients age ≥50;
-cx : permanent vision loss.

No role of smoking

49) Dupuytren contracture : painless

-results from progressive palmar fascia fibrosis, leading to puckering of the skin and
fibrotic nodule and cord formation along the flexor tendons 3rd, 4th & 5th digits.

-Patients develop contractures that limit extension at the metacarpophalangeal and

proximal interphalangeal joints.
-Dx: made clinically; no imaging is needed.
#Rx:
-modify hand tools, needle aponeurotomy, intralesional steroid, Surg

Vs
#Tenosynovitis and calcific peritendinitis : red, pain
Vs
50) Diabetic cheiroarthropathy ("diabetic stiff hand syndrome") :
- Decreased collagen degradation leads to thickened scleroderma-like skin, sclerosis of
the tendon sheaths, and stiffness in the joints.
- Pt can’t tightly oppose the palms in prayer posture: PRAYER SIGN

51) Role of Ice Pack Test in myasthenia gravis Dx :

- to support the Dx

an ice pack is applied over the eyelids for several minutes, leading to an improvement in
ptosis.
-MOA: The cold temperature improves muscle strength by inhibiting the breakdown of
acetylcholine at the neuromuscular junction, thereby increasing acetylcholine
availability to the nicotinic receptor.
52) Venous insufficiency (valvular incompetence) pitting
- the MCC of LE edema.
-classically worsens throughout the day and resolves overnight when the patient is
recumbent.
Vs
#lymphedema: classically affects the dorsa of the feet and causes marked thickening and
rigidity of the skin. Non pitting

Extraarticular manifestations of rheumatoid arthritis Medications to avoid in

myasthenia gravis
• Fever
Systemic • Magnesium sulfate
• Weight loss

3¥
• Fluoroquinolones,
• Pulmonary fibrosis
Pulmonary aminoglycosides
• Pulmonary hypertension
• Neuromuscular blocking
Cardiovasc • Atherosclerosis agents
ular • Vasculitis • CNS depressants
Musculoskel • Muscle relaxants
• Osteopenia/osteoporosis • Calcium channel blockers
etal
• Beta blockers
Dermatologi • Opioids
• Rheumatoid nodules
c • Statins
Hematologic • Anemia Acute vertebral compression fracture
• Low back pain & decreased spinal mobility
• Compressive neuropathy (eg, • Pain increasing with standing, walking, lying on back —>> Pain
Neurologic carpal tunnel syndrome) in each positions
• Cervical myelopathy • Midline Tenderness at affected level —> not paraspinal

• Sjögren syndrome Chronic/gradual

Other • Raynaud phenomenon • Painless
• Progressive kyphosis
• Scleritis, episcleritis • Loss of stature

56) DOC for stabilizing bony metastatic lesions to prevent hypercalcemia of

malignancy and pathologic fractures: Bisphosphonates (zoledronic acid, pamidronate)

57) Hypercalcemia of malignancy

- generally due to either osteolytic bone metastases or the release of PTHrP. Differentiation
can be made with whole-body bone scan and PTHrP testing.

-normal whole-body bone scan (no metastatic bone lesions) indicates that the source of his
hypercalcemia is PTHrP.

58) Rx of back pain benign:

-1st line:(NSAIDs) are first-line drug therapy for acute, uncomplicated low back pain.
-2nd line: If NSAIDs are ineffective, a short course of a nonbenzodiazepine muscle
relaxant (eg, cyclobenzaprine, tizanidine) can provide additional pain relief.
59) osteomalacia
• X-rays may show thinning of cortex with reduced bone density
• Bilateral & symmetric pseudofractures (Looser zones) are characteristic radiologic
findings

60) Examination findings suggesting OA in the knee include:

• Periarticular bony hypertrophy and tenderness
• Limited range of motion with crepitus and pain
• Small joint effusion without erythema or warmth
• Varus or valgus angulation
• Popliteal (Baker) cyst behind the joint

Inj. GC

61) Radial tunnel syndrome

#Pathogenesis:
-caused by compression of the radial nerve where it passes under the supinator.

#C/F:
-Although it may cause lateral elbow pain resembling lateral epicondylitis, the
tenderness is typically greatest at the margin of the supinator several centimeters
distal to the elbow,
Vs
-rather than at the lateral epicondyle (eg, lateral distal humerus 1 cm Distal to
elbow)
 Differential diagnosis of neck pain
63) Polyarteritis nodosa
Condition Clinical clues - marked by segmental, transmural
Strain
• Antecedent history of neck injury inflammation of medium-sized arteries,
• Pain/stiffness with neck movement
which leads to luminal narrowing,
• Older individuals
Facet osteoarthritis • Pain/stiffness worse with movement thrombosis, and organ ischemia.
• Relieved with rest
• Pain radiates to shoulder/arm -MC site: kidneys (eg, renal infarction) and
• Dermatomal sensory/motor/reflex GIT (eg, mesenteric ischemia, bowel
Radiculopathy
findings
• Positive Spurling test perforation) are often affected.
• LE weakness, gait/bowel/bladder
Spondylitic
myelopathy
dysfunction -Dx: Mesenteric angiography- multiple
• Lhermitte sign
arteries with microaneurysms, irregular
• Young men
Spondyloarthropat • HLA-B27
luminal narrowing, and distal occlusions.
hy • Relieved with exercise
• Prolonged morning stiffness
• Constant pain
Spinal metastasis • Worse at night
• Not responsive to position changes
• Focal tenderness
Vertebral • Fevers & night sweats
osteomyelitis • IVDU, immune compromise, or
recent infection

65) De Quervain tendinopathy

-presents with lateral wrist pain over the tendons of the abductor pollicis longus and
extensor pollicis brevis.
-RF: > in women age 30-50, with an increased frequency during the postpartum
period. -O/E: tenderness at the radial side of the wrist (1st external component)

+ Finkelstein test (reproduction of pain on adduction of the wrist with the fingers closed
over the thumb) due to stretching of tendons

66) Postthrombotic syndrome

-occurs in >50% of patients with a H/O acute DVT and is marked by the development of
chronic venous insufficiency distal to the site of thrombus.
#C/F;
-usually presents with leg pain, edema, fatigue, superficial venous dilation, and/or ulcer
but negative ultrasound for active DVT

#Treatment : exercise and compression.

67) Osteoarthritis of the hands is primarily a clinical diagnosis;

-imaging (eg, x-ray) is less sensitive than examination findings and is usually
unnecessary for diagnosis or management.

68) acute Rx of gout:

-NSAIDs avoided in HT; colchicine avoided in renal and hepatic failure
 Pedia rheumat
1) Transient synovitis vs septic arthritis:
• Transient synovitis well appearing children- afebrile / low-grade fever.
-acute hip pain and limited mobility of the affected joint but can usually bear weight.
-lab Normal, holds hips flexed to relieve pain
Vs
•septic arthritis :Ill appearing, febrile, (severe pain), non wt bearing and abnormal
laboratory lab (mod elevated WBC, ESR, CRP)

#what if overlap?.
A) 1st step: When the diagnosis is unclear, bilateral hip ultrasound is performed.
-Joint effusion in septic arthritis is unilateral, whereas 25% of patients with transient
synovitis have bilateral hip effusions (even with unilateral symptoms).

B) what If hip ultrasound shows a unilateral effusion??

- arthrocentesis is required to evaluate for septic arthritis.

2) suspecting child abuse:

• Bruises/fractures at various stages of healing 3) Osgood-Schlatter disease : pain
• Femur fracture in nonambulatory infant occurs over the tibial tuberosity
• Posterior rib fractures
• Metaphyseal corner fractures -Pain worsens with activities involving
• Retinal & subdural hemorrhages repetitive running, jumping, or kneeling
(eg, soccer, basketball, gymnastics).

—> Pain improves with rest

- > unilateral than bilateral.
Vs
#patellar tendinitis:
-point tenderness is present at the
inferior pole of the patella.

Vs
# Patellofemoral pain
- Pain is usually localized to the patella
and associated with a sensation of
5) Juvenile idiopathic arthritis (JIA) instability or "buckling" at the knee.
-polyarticular: involves ≥5 joints within 6 months of disease onset .in toddler and
adolescent girls
Vs
#Oligoarticular JIA: the MC form, is characterized by involvement of ≤4 joints (ie, <5
joints) within the first 6 months of disease onset.
Vs
#systemic juvenile idiopathic arthritis (JIA):
≥2 weeks of daily fever (quotidian fever), fixed arthritis (>1 joints) lasting ≥6 weeks,
and a pink macular rash that worsens during fever.

- As with other rheumatologic disorders, the joint pain and stiffness are classically worse
in the morning and improve throughout the day.

-Lab: - leukocytosis; thrombocytosis; markedly elevated inflammatory markers (eg,

erythrocyte sedimentation rate, C-reactive protein)
-Rx: 1st line: NSAIDs; 2nd line: MTX
6) Adolescent Scoliosis :
#C/Fs :
- Rib hump,
- asymmetric scapulae,
- unilateral thoracic/lumbar prominence on forward bend test. Club foot

#why greatest progression occurs in early adolescence ?

-at the time of the pubertal growth spurt, after which progression slows and
subsequently stops once bone ossification is complete.

7) Developmental dysplasia of the hip:

-Barlow and Ortolani maneuvers assess joint stability: and a palpable "clunk"
-Dislocated hip: Limited hip abduction .
-Limb length discrepancy: Galeazzi test
-Asymmetric ◦gluteal/inguinal/thigh creases

#Mx:
◦ Age <4 months: Hip ultrasound; Infants with abnormal examination should undergo
bilateral hip ultrasonography
◦ Age >4 months: Hip radiograph; After age 4 months, when the femoral head and
acetabulum are ossified, x-rays are preferred

◦ Confirmed DDH is treated with a Pavlik harness, a splint that holds the hip in flexion
and abduction while preventing
 MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE PATHOLOGY
`  SEC TION III 473

Childhood musculoskeletal conditions

Radial head Also called nursemaid’s elbow. Common elbow injury in children < 5 years. Caused by a sudden
subluxation pull on the arm Ž immature annular ligament slips over head of radius. Injured arm held in
Humerus slightly flexed and pronated position.
Ulna
Radiu
s

Osgood-Schlatter Also called traction apophysitis. Overuse injury caused by repetitive strain and chronic avulsion of
disease the secondary ossification center of proximal tibial tubercle. Occurs in adolescents after growth
spurt. Common in running and jumping athletes. Presents with progressive anterior knee pain.

Patellar
tendon
Tibial
tuberosity

Patellofemoral Overuse injury that commonly presents in young, female athletes as anterior knee pain.
syndrome Exacerbated by prolonged sitting or weight-bearing on a flexed knee.

Patella

Femur

Developmental Abnormal acetabulum development in newborns. Risk factor is breech presentation. Results in hip
dysplasia of the hip instability/dislocation. Commonly tested with Ortolani and Barlow maneuvers (manipulation of
newborn hip reveals a “clunk”). Confirmed via ultrasound (x-ray not used until ~4–6 months
because cartilage is not ossified).
Legg-Calvé-Perthes Idiopathic avascular necrosis of femoral head. Commonly presents between 5–7 years with
disease insidious onset of hip pain that may cause child to limp. More common in males (4:1 ratio). Initial
x-ray often normal.
Slipped capital Classically presents in an obese young adolescent with hip/knee pain and altered gait. Increased
femoral epiphysis axial force on femoral head Ž epiphysis displaces relative to femoral neck (like a scoop of ice
cream slipping off a cone). Diagnosed via x-ray.
8) Distal spiral tibial #/ Toddler fracture
-age: seen in ambulatory children age ≤3 (accidental trauma)
# Mechanism of injury: twisting injury during a low-impact fall in the early walking yrs
#Rx:involves immobilization and pain control with no additional workup

9) Radial head subluxation/ Nursemaids elbow:

#Mechanism of injury:
- (child lifted/ innocent swinging of a young child by the arms or pulling a child's arm while
in a hurry)
#C/F:
•The child is usually not in distress at presentation but may cry at any attempt to move the
elbow or forearm.
• Arm held extended & pronated
• No swelling, deformity, or focal tendernes; Xray normal

#Mx: Hyperpronation of forearm: closed reduction by applying pressure on the radial head
-Sign of success: A pop may also be heard on successful reduction.

10) Mx of club foot:

-1st line: gentle manipulation and stretching with serial molding cast in neonatal period.
-2nd line: Once an optimal position is achieved by casting, long-term bracing is typically
required;
-3rd line: surgical correction is reserved for refractory cases / recurrence of clubfoot
after nonsurgical treatment

#If untreated: abnormal gait with weight bearing on the lateral aspects of the feet.

11) Growing pain:

-pattern: Occurs primarily at night & resolves by morning
-MC site: B/L LE (eg, thighs, calves); Normal physical examination & activity
-Rx: Parental education & reassurance; Massage, stretching exercises, heat & analgesics

12) Septic arthritis flare in JIA:

-septic arthritis synovial fluid:>50 k; atypical single acute join flare: pain, swelling
Vs
-JIA flare synovial fluid: < 50 k; morning stiff

13) #physiologic genu varum include: #Blount disease/ pathologic bowlegs:

• Symmetric bowing -due to abnormal cartilage growth.
• Normal stature -C/F: leg length discrepancy, asymmetrical
• No leg length discrepancy bowing, and lateral thrust with ambulation.
• No lateral thrust when walking
 14) septic arthritis in SCD
Vs
Sickle cell pain crisis: never occurs <6
month as HbF still present.

15) serum sickness-like reaction

fever, urticaria, and joint pain, which began
after 1-2 weeks of administration of β-
lactams (eg, penicillin, amoxicillin, cefaclor)
or trimethoprim-sulfamethoxazole
16) Osteomyelitis in children,
fever, leg pain,
refusal to bear weight

17) Adolescent idiopathic scoliosis (AIS): lateral curvature (ie,

Cobb angle >10 degrees) of the spine without a specified
etiology.
1) Monitoring:
-mild (ie, Cobb angle 10-30 degrees) and can be monitored
clinically every 6 months
2) A thoracolumbosacral spinal brace
- indicated in a child with growth potential remaining and Cobb
angle ≥30 degrees to help reduce curve progression
3) Surgical fixation
-severe curvature (ie, Cobb angle ≥40-50 degrees)
# when is MRI indicated in scoliosis??
-Scoliosis due to pathologic causes (eg, mass, dysraphism) may present with neurologic
symptoms, severe back pain, rapid progression (>10o/yr) /vertebral abnormalities on
x-ray.

18) drop arm test: rotator cuff tear

-A complete supraspinatus tear causes weakness in the middle of above head
abduction: rotator cuff injury
-*The arm is held in 90-degree abduction & released; inability to hold the arm steady
suggests a tear.

19) Slipped capital femoral epiphysis

- Feet are pointed laterally due to limited internal rotation of the affected hip, and external
rotation of the thigh during passive hip flexion is a characteristic examination finding.
- x-ray : posterior displacement of the femoral head, unlike damaged femur head in
legg calve. Vs
21) Approach for monoarthritis
Common etiologies include:
• Traumatic injury – patients almost always recall recent joint trauma.

• Bacterial joint infection – significant systemic symptoms (eg, fever, malaise,

tachycardia) and severe joint pain, erythema, and warmth.

• Inherited blood disorders – Both sickle cell anemia (vasoocclusive crisis) and
hemophilia (hemarthrosis) typically cause severe (not mild) knee pain, and
hemophilia typically occurs in male patients (X-linked) and presents in childhood

-Thoroughly reviewing the patient's history can often elicit less common causes of
monoarticular knee effusion.

# How to elicit H/O of rare causes of monoarthritis ?

-Inquiring about the presence of a recent rash is important for diagnosis because a rash
frequently precedes or accompanies several causes of monoarticular arthritis, including

1) late Lyme disease (spreading, annular rash)with mild, monoarticular knee joint arthritis
2) juvenile arthritis (evanescent, macular, salmon-colored rash), and
3) serum sickness (pruritic urticarial rash) and JIA: high fever and polyarthritis.
23) RF for curve progression in scoliosis:
22) Treatment of ankylosing spondylitis • Female sex
• Exercise (postural exercises,
Nonpharmac
ROM/stretching exercises) • Age <12
measures
• Physical therapy • Early pubertal status (eg, premenarchal)
Initial treatment
• NSAIDs (eg, ibuprofen, naproxen) • Skeletal immaturity
• COX-2 inhibitors (eg, celecoxib) • Severe curvature (ie, Cobb angle ≥25
• TNF-α inhibitors (eg, degrees)
Treatment etanercept, infliximab)
failure/ • Anti–IL-17 antibodies (eg, -premenarchal status of scoliosis indicates
disease secukinumab) that patient still has significant remaining
progression • Both Have significant toxicity and
are not used as 1st-line treatment growth potential.

24) HSP: criteria

-Palpable petechiae/purpura is required for diagnosis + ≥2 of the following:

• Arthritis/arthralgia:MC in LE and may cause refusal to walk in young children

• Colicky abdominal pain due to intestinal edema, which can also lead to nausea,
vomiting, gastrointestinal bleeding, and intussusception
• Renal disease (hematuria ± proteinuria) Ig A Nephropathy
#Mx:
-oral hydration,rest, NSAIDs ; if not improved/ inability to maintain hydration use steroids
-BP measurements and S creat for IgA nephropathy
25) SCFE:
-U/L: antalgic gait; B/L: waddling

26) Mx of carpal tunnel

syndrome in pregnancy:

-nocturnal Wrist splinting is safe

and effective during pregnancy,
and unlikely to cause fetal harm;

-Rx need not be delayed until

after delivery.

--Surgical intervention can be

considered during pregnancy for
severe symptoms (eg, motor
weakness, thenar atrophy);
27) supracondylar # complications: look for distal humerus part displacement
-If posterior displaced—> median N + brachial art compressed by proximal humerus
-if anterior displaced—>ulnar N compressed
-compartment syndrome
#Rx:
-if displaced- Sx; non displaced: splint

28)y SCFE MC in pt with underlying thyroid disorder??

-Because thyroid hormone promotes ossification of the growth plate, patients with
hypothyroidism are also at increased risk.

-Children with endocrinopathies often have SCFE at an earlier age (<10) and are more
likely to develop bilateral disease.

29) intussusception of HSP:

-most pediatric cases of idiopathic intussusception: typically ileocolic.
-intussusception in HSP : small bowel (ileoileal).
#Mx
*Rx: Although ileocolic intussusceptions are treated with air or contrast enema
Vs
ileoileal intussusceptions that do not reduce spontaneously often require surgical
management.

30) Limb length discrepancy

-Growth arrest caused by a fracture involving the growth plate (physis)metaphysis can
lead to limb length discrepancy.
Not diaphyseal #
31) Greenstick fractures of the forearm
- common in children due to relatively strong periosteum, which limits the fracture line
from extending through the width of the bone.
-Rx: immobilization to prevent refracture, and no long-term cx are expected.

33) Mx of fibular #?.

-If x-ray reveals a distal fibular fracture, most cases can be managed with a hard (eg,
plaster, fiberglass) or soft (eg, air cushion) splint.

-Surgical intervention is considered for some proximal fibular fractures as well as

for complicated (eg, comminuted, spiral) distal fibular fractures.

34) Drug of choice in gout:

-NSAIDS avoid in high risk bleeding like on anticoagulant
- avoid colchicine in elderly and Renal dysfunction

35) Dermatomyositis: perimysial/ perifascicular infiltrates

Polymyositis: endomysial/ intrafascicular infiltrates

36) 20) Legg calve perthes Ds:

-Insidious hip pain, limp; Restricted hip abduction, internal rotation
• Positive Trendelenburg sign
-Xray: Femoral head flattening,; fragmentation, sclerosis
#Rx: Patients are made non–weight bearing and managed conservatively with bracing /
splinting.
-Surgery indicated in cases in which the femoral head is not well contained within the
acetabulum.
Lambert-Eaton myasthenic syndrome
Lambert-Eaton syndrome Myasthenia gravis
• Antibodies to
• Antibodies to presynaptic
postsynaptic
Pathogenesis voltage-gated calcium
acetylcholine
channels at NMJ
receptors at NMJ
• Muscle weakness:
◦ Ocular (ptosis,
• Proximal limb weakness
diplopia)
(legs > arms)
◦ Bulbar
• ↓ or absent reflexes
(dysphagia,
Clinical • Improvement in strength
dysarthria)
features & reflexes following
◦ Proximal limbs
isometric contraction
(arms > legs)
• Autonomic dysfunction
• Normal reflexes
(eg, dry mouth)
• Weakness that
worsens with activity
Electrophysiologi • ↑ Action potential • ↓ Action potential
c amplitude with repetitive amplitude with
studies nerve stimulation repetitive stimulation
Associated
• Small cell lung cancer • Thymoma
neoplasm
1) shoulder dislocation: Ortho surgery
-hand externally rotated +/- humeral neck # with/ with out blood flow disruption

2) osteosarcoma:
A child with P/H/O retinoblastoma has X-ray of the knee shows a lytic lesion that has ill-
defined margins on the femoral condyle surrounded by concentric layers of reactive
bone.

3) Meniscal tear:
-locked/ catching sensation in knee; With the knee held in internal and external
rotation, flexion and extension at the knee elicits moderate pain and crepitus.
-twisting injury while the foot is in a fixed position.
-Thessaly test; McMurray test

4) Iatrogenic septic bursitis:

-presenting with acute pain several days after an initial positive response to
corticosteroid injection.
Vs
-steroid-induced chemical synovitis): typically occurs rapidly and resolves within 48
hours.

5)

7) Stenosing tenosynovitis ("trigger thumb")

-pain over the palmar aspect of the first MCP joint;
-associated with a catching sensation during movement or locking of the thumb in
flexion

8) Scaphoid fractures
-typically occur during forceful FOOSH.
--typically present with pain at the radial wrist proximal to the base of the thumb And
tenderness at a anatomical snuff box

9) Acromioclavicular (AC) joint sprain:

-maximal tenderness over the AC joint and pain with adduction of the arm across
the torso vs weakness with suprascapular N entrapment
. Vs abduction problem in rotator cuff tendinopathy and tear

25) Greater trochanteric pain syndrome:

-presents with lateral hip pain and tenderness over the greater trochanter (bursa
between gluteus medius and minimus) during flexion

#Mx: supportive; if resistant: corticosteroid injection

10) Pectoralis major strain
-results from activities involving repetitive pushing movements, such as bench presses.
-present with chest wall soreness rather than shoulder pain.

11) Brachial plexus injury (eg, thoracic outlet syndrome)

-acute pain in the supraclavicular area that radiates down the arm. 
-Neurologic symptoms (eg, weakness or numbness) +edema, claudication

12)Calcaneal apophysitis
#Pathogenesis: an overuse injury caused by repetitive microtrauma to the calcaneal
apophysis (heel growth plate)

#C/F: Chronic Heel pain (50% bilateral) that is worse with activity, particularly when
wearing shoes without heel support; MC in 8-12 yrs

-Pain with calcaneal palpation (squeezing heel) / compression/on palpation at the

base of the heel over the apophysis.
-limited ankle dorsiflexion may be present due to an associated tight Achilles’ tendon
-unlike TTS, the pain does not radiate to the toes and is typically dull (DIFF POINT)
Vs
#Achilles tendinopathy :
-tenderness is over the Achilles tendon (posterior ankle), not the heel.
Vs

13) Plantar fasciitis :MC U/L rather than B/L.

-Pain is worst on first stepping out of bed and improves throughout the day.
-When the toes are dorsiflexed, there is tenderness between the heel and forefoot
(anteromedial heel)
-X-ray may show calcifications in the proximal fascia (heel spurs)

14) calcaneal stress fracture: > in obese

-the pain typically is localized in the posterior calcaneus and elicited by lateral squeezing
the medial and lateral calcaneus (calcaneal squeeze test).

#Dx/ next best step : don’t jump to rx

-confirmed on imaging; x-ray typically shows a zone of lucency or sclerosis in the posterior
calcaneus. If x-ray is nondiagnostic, MRI has a higher sensitivity.

#Rx:
-analgesics and reduction of weight-bearing activities.
-Heel pads or walking boots that dissipate impact during ambulation recommended.
#Prognosis: Calcaneal stress fracture usually heals well with conservative mx.
18) D/D of Diff abduction post injury
rotator cuff injury: impaired arm abduction but intact sensation (as MC muscle:
supraspinatus); Etiology: post shoulder dislocation
Vs
Axillary N damage in anterior shoulder dislocation: above + impaired sensation
Vs
AVN head of humerus: impaired arm abduction but delayed onset after injury vs
immediate in RCI

19) Rotator cuff tendinopathy: pain with abduction without weaknesses

Rotator cuff tear: weakness with abduction
Dx: MRI shoulder

20) Quadriceps tendon rupture

-an audible pop, rapid swelling, inability to actively extend the knee against gravity.

a) tears (proximal to the patella in the rectus femoris tendon): the patella rides low —
> indicating an intact connection to the tibia, with a palpable defect above the patella

b) Patellar tendon tears (distal to the patella): the patella rides high, often with a
palpable defect below the patella (the nomenclature can be confusing as the
patellar tendon is actually a ligament)
#Rx: surgical repair

21) Patellofemoral pain syndrome

-young, physically active women, anterior pain reproduced by squatting (isometric
quadriceps contraction.
#patellofemoral compression test (reproduction of pain when the patella is compressed
into the trochlear groove)
-Rx: Strengthening the quadriceps and hip abductors

22) Achilles tendon rupture:

-best .evaluated on physical examination with the calf squeeze test, which simulates
gastrocnemius contraction. —>Absent foot plantar flexion in response to calf squeeze is
diagnostic
-also results in an impaired ability to walk on the tips of the toes.

23) Compartment syndrome: supra chondylar #; tibia #

-suspected in a patient with increasing swelling and pain that is unresponsive to escalating
analgesics.
-red flags: "4 Ps": stretch pain (early) pallor, paresthesia, pulselessness, and paralysis
(last)
Vs no neurological deficit in DVT
 26) Spondylolysis : pars interarticularis
defects (eg, fractures) that are often due
to overuse injury and can be unilateral
or bilateral.
Vs
Spondylolisthesis:
-characterized by forward slip of a vertebral
body (usually L5) and develops in patients in
spondylolysis who have bilateral defects.

- It is MC during adolescent (age 10-19) growth spurts due to increased physiologic

lumbar lordosis (exposing L5 vertebra) and decreased bone mineralization.

28) Mx of open book pelvic # with H’age:

- To prevent exsanguination during ongoing resuscitation efforts and evaluation, rapid, external
stabilization with a pelvic binder asap in hemodynamically unstable
-MOA: decreases pelvic volume and promotes tamponade of venous bleeding.

#Evaluation after Mx with Pelvic Binders :

1) CT scan of the abdomen and pelvis —> for intraabdominal injury and provide 3D
visualization of the pelvic fractures.

2) Retrograde cystourethrogram —> to assess for urethral injury, especially given the finding of blood at th
urethral meatus.

29) Septic bursitis: acute redness, warmth vs

absent in noninflammatory bursitis

#Etiology of bursitis : rule out by bursal fluid aspiration- send for Gm stain, culture, cell
count
-due to infection (ie, septic bursitis),
-crystalline arthropathy (eg, gout), or
-autoimmune conditions (eg, rheumatoid arthritis).
#Mx:
-systemic antibiotics;
-Drainage : if bursitis fails to improve after 36-48 hours of antibiotic therapy or compressive
symptoms (eg, neurovascular compromise) are present.
- A knee compression wrap and ice application —> for noninflammatory bursitis due to
overuse.
30) colles #: MC nerve involved- median N and brachial art

31) Hip neck fractures: MC hip # in elderly

-external rotation, abduction and shortening is more typical of femoral neck fracture cz due to
contraction of the psoas and iliacus without the normal acetabular counterforce).

A) Intracapsular fractures: femoral head and neck

- NO significant ecchymoses
-higher risk of avascular necrosis.

B) Extracapsular fractures : intertrochanteric or subtrochanteric)

-higher risk for displacement
-visible ecchymosis.

#Mx: Both types generally require surgical correction (eg, open reduction with internal fixation)
within 48 hrs
Vs
32) Femoral shaft fracture
-shortening of the leg, often with angulation.
Vs
33) Posterior hip dislocation (> MC than ant )
-typically presents with adduction and internal rotation at the hip vs abducted nd externally
rotated in ant dislocation

#Cx: sciatic N injury, femur head injury, labrum tear, AVN

#Mx: #Treatment of hip dislocation

-requires expedited reduction, typically within 6 hours of injury to prevent AVN
• Dislocation without associated fracture :closed (ie, nonoperative) reduction (eg, in the emergency
room).
• Dislocation with fracture : open (ie, operative) reduction.

34) # associated with AVN:

-MC in areas of bone with limited blood supply such as the scaphoid, femoral head, or
metadiaphyseal junction of the fifth metatarsal

35) Salter-Harris type III

-fracture of the distal tibial epiphysis and lateral physis (ie, growth plate)
- MC age: adolescents when the physis is partially fused.
- growth arrest and lead to persistent limb-length discrepancy.
 Salter Harris Fracture & its Complications

T Growth plate
M

All 3
E

Salter Harris Fracture:

—> A child has an ankle injury with diffuse swelling and an inability to bear weight;
- initial imaging with x-ray is appropriate,
- CT scan may be needed to fully visualize a fracture —>>
CT scan reveals a combination of: a distal tibial epiphysis fracture + a growth plate (ie, physeal) fracture,
as suggested by growth plate widening —>>
combination of fractures is known as a Salter-Harris type III (juvenile Tillaux fracture).

Complications in Salter Harris Fracture :

- The distal tibial growth plate typically closes around age 14 in boys (age 12 in girls),
- fractures involving the maturing, partially fused, physis (eg, Salter-Harris type III and IV
fractures) carry an increased risk for long-term complications.
1) In particular, injury to the growth plate can cause growth arrest and lead to persistent limb-length
discrepancy.
2) formation of physeal bars (bony bridges across the growth plate),
3) premature osteoarthritis,
4) decreased range of motion.
 36) Further Mx after immediate reduction of post dislocated knee:
- Given the risk of vascular (eg, popliteal artery) injury, reduction should be followed by a
meticulous vascular examination that includes:
• Palpation of the popliteal and distal pulses
• Measurement of the ankle-brachial index (ABI)
• Duplex ultrasonography (if available)

# Role of ABI
- Because pulse examination alone is of limited accuracy in diagnosing vascular injury,
obtaining and documenting the ABI are critical.

1) normal pulses +ABI >0.9 : virtually excludes clinically significant vascular injury.
2) Any signs (eg, diminished pulse, ABI ≤0.9) of vascular injury:
-warrant emergency imaging (eg, CT angiography) and vascular consultation.
Modified Wells criteria for pretest probability
of deep venous thrombosis DVT
-Noninvasive evaluation with compression

4¥
• Previously documented DVT
• Active cancer USG is recommended as an initial test in
• Recent immobilization of the legs patients with moderate or high probability of
• Recently bedridden >3 days
• Localized tenderness along vein
DVT Vs D dimer If low probability
.
Score 1 point
distribution
for each feature
present • Swollen leg -Patients with clinical evidence of(PE)
• Calf swelling >3 cm than other leg
• Pitting edema should be started on anticoagulation if
• Collateral superficial nonvaricose veins there are no C/I (eg, active bleeding) while
• Alternate diagnosis more likely (−2 undergoing diagnostic evaluation.
points)
Total score for • 0 points = Low probability
clinical • 1 or 2 points = Moderate probability
—> Those with features of DVT only,
probability • ≥3 points = High probability should have the diagnosis confirmed
prior to starting anticoagulation as
37) Shoulder dislocation: anticoagulation itself has risks
1) Anterior dislocation: arm held in abduction/external rotation, anterior prominence of
humeral head
2) Posterior dislocation: arm held in adduction/internal rotation, loss of anterior contour,
prominence of coracoid & acromion
#Cx:Fracture (glenoid, proximal humerus, clavicle); Rotator cuff injury; Recurrent dislocation

#recurrent dislocation due to

-Hill-Sachs defect (ie, avulsion fracture of the posterolateral humeral head)
-labral tears (ie, Bankart lesion),
-ligamentous laxity due to overuse, and
-underlying multidirectional joint instability
#Mx: For patients with no associated fracture and no other evidence of neurovascular (eg, radial artery, axillary
nerve) injury, closed reduction under sedation can generally be attempted (eg, in the emergency department).
—> Postreduction care : immobilization of the shoulder x 2-3 weeks, followed by a progressive physical
therapy program
38)Indication for external fixation:
-External fixation (eg, with external pins) is used in cases of polytrauma; severe,
comminuted open fractures with defects in skin, bone, or soft tissue; and some burn-
related injuries.

39) radial nerve neurapraxia due to midshaft humeral fracture

-resolves in up to 90% of cases, including with nonsurgical management.
-EMG can be considered if radial nerve function does not recover following surgery.

40) open reduction and surgical exploration of any # are indicated if:
-open fractures,
- significant displacement (eg, arm shortening),
-neurovascular compromise (eg, asymmetric radial pulses
-polytrauma, and pathologic fractures.

Features of cervical radiculopathy

Nerve root Reflex
Sensory loss* Weakness
(Disc space) affected
C5 • Lateral • Shoulder abduction (deltoid)
• Biceps
(C4-5) upper arm • Elbow flexion (biceps)
• Biceps • Elbow flexion (biceps)
• Thumb
C6 • • Forearm pronation/
• Index
(C5-6) Brachiora supination (brachioradialis)
finger
dialis • Wrist extension

(C6-7)
C7

—> M/C involved

• Triceps
• Dorsal
forearm
• Middle
• Wrist flexion
• Finger extension
is
• Elbow extension (triceps)

Nerve Root finger

• Ring &
C8 • Finger • Finger flexion & extension
little
(C7-T1) flexors** • Thumb flexion & abduction
fingers

T1 • Finger
• Medial • Finger abduction &
(T1-2) flexors**
forearm adduction
*In addition to neck/shoulder pain, radicular pain typically has a similar distribution to
sensory loss.
**Not typically evaluated clinically.

41) cervical radiculopathy:

-Shoulder abduction reduces tension on the impinged nerve root, and improvement of
radicular symptoms when the hand is placed on the top of the head (ie, shoulder
abduction relief test) and exacerbated by lateral neck flexion
Vs
It worsens pain in thoracic outlet syndrome due to more compression
 Post-amputation pain
43) scaphoid avascular necrosis and
Acute stump • Tissue & nerve injury nonunion:
pain • Severe pain lasting 1-3 weeks
-Nondisplaced fractures may not be
• Swelling, skin discoloration immediately visible on x-ray.
• Wound breakdown
Ischemic pain
• ↓ Transcutaneous oxygen
tension -If initial x-rays are negative, CT scan
←
• Weeks to months after
amputation
or MRI is recommended, or the wrist
should be immobilized and x-rays
• Focal tenderness, altered local repeated after 7-10 days
Post-traumatic
sensation
neuroma
• ↓ Pain with anesthetic
injection-diagnostic
-Rx: neuroma excision
• Onset usually within 1 week
• Increased risk in patients with
Phantom limb
severe acute pain
pain
• Intermittent cramping, burning
felt in distal limb

24) Supracondylar #: -child 2-7 yrs;

-# line with wide anterior fat pad (normally
narrow or absent) and a posterior fat pad = .

(normally absent).
#Mx: -Nondisplaced: long arm splint & sling
-Displaced: surgical reduction & pinning

25) Mx of plantar fasciitis with/out spur:

-Initial management : activity modification (eg, avoiding walking barefoot, reducing high-
impact exercise),
physical therapy (eg, fascial stretching, muscle strengthening exercises), and
padded heel inserts, which reduce strain on the fascia.
-About 80% of patients recover within 1 year.

-Calcaneal spurs are incidental and do not require treatment.

26) Common fibular neuropathy

-Etiology: leg immobilization, leg crossing, or protracted squatting.
#C/F: usually transient (lasting hours) , foot drop and sensory changes over the dorsal
foot and lateral shin.

27) Tibial stress fractures Mx:

-managed in most cases with pneumatic splinting, reduced weightbearing, and a
graduated exercise program.
-Most patients may resume full-intensity exercise within 12 weeks, but the program may
need to be delayed if the patient develops recurrent pain.
 I =

• Injury to the ulnar nerve at the wrist (eg, hamate fracture, compression from a
bicycle handlebar) :
numbness and paresthesia at the medial side of the hand + intrinsic hand weakness that
patients may describe as "clumsiness." (Dont mix this with below)

• Injury at the elbow : similar symptoms +decreased grip strength due to

denervation of the flexor muscles in the forearm.

27) Mx of phantom limb pain:

Treatment of PLP is typically multimodal and may include:
• pharmacotherapy: antidepressants (eg, tricyclics), antiepileptics (eg, gabapentin), N-
methyl-d-aspartate (NMDA) receptor antagonists (eg, ketamine), and analgesics (eg,
acetaminophen, opioids). NO ROLE OF NSAIDS IN NEUROPATHIC PAIN

• adjuvant therapies: biofeedback, CBT, and mirror therapy (ie, using a mirror to watch
the reflection of the residual limb moving at the location of the absent limb).

28) Cervical facet dislocation

-Injury: typically occurs with forced flexion of the cervical spine (eg, falling onto a flexed
neck);
-a single facet is usually dislocated results in radiculopathy of the corresponding N. root.

#MC site: The MC affected vertebral bodies are C5/C6, which lead to C6 radiculopathy,
and C6/C7, which lead to C7 radiculopathy.
-Imaging : anterior subluxation of the vertebral bodies.

29) uncomplicated Lumbosacral radiculopathy (sciatica)

-Etiology: due to nerve root compression by a herniated disc / lumbar spondylosis;
less commonly by epidural abscess and CA
-Mx: Most patients experience spontaneous resolution.
-Initial management : focused on short-term relief with NSAIDS / acetaminophen.

-NO NEED of MRI; MRI only if complicated Sx like saddle anaesthesia; FND
27) Patellar dislocation
-Mode of injury: Quick, lateral twisting motion around a flexed knee
• Feeling of knee giving way, severe pain, popping noise

#O/E: lateral dislocation of patella (Large, Immobile mass on lateral side),

-decreased extension, hemarthrosis and
-tenderness along the medial patella (reflecting tear of the medial patellofemoral ligament)

#Mx: often reduces spontaneously

—> closed reduction is required for patients without spontaneous resolution
#-Surgeons often choose to confirm the diagnosis by measuring compartment pressures
(eg, needle manometry); a delta pressure (diastolic blood pressure − compartment
pressure) ≤30 mm Hg is suggestive of CS.

--Time to fasciotomy is the most critical prognostic indicator and should be performed
without delay.
30) Complex regional pain syndrome
-typically follows local trauma or surgery and is characterized by severe burning
(allodynia) / tingling pain in a regional (not dermatomal) distribution.
-It is often associated with edema, erythema, and trophic skin, hair, or nail changes.
-X-ray may show patchy demineralization.

-NO fever, lab abnormality (leukocytosis, raised inflammatory markers) unlike

cellulitis
#Mx:
• Physical & occupational therapy, exercise
• Medications: NSAIDs, antineuropathic medications (eg, pregabalin, TCAs), BP

32) Adhesive capsulitis

-results from contracture of the glenohumeral joint capsule and presents with gradual onset
shoulder pain and reduced active and passive range of motion.
#Rx:
-Treatment includes gentle range of motion exercises; adjunctive measures include
NSAIDS and corticosteroid injections.

33) Mx of DVT:
-Major surgery is a significant risk factor for deep venous thrombosis (DVT). At least 3
months of anticoagulation is recommended for provoked DVT. Stable patients can be
treated with anticoagulation as early as 48-72 hours after surgery.
*Rx:
-Patients started on warfarin must be started on an additional anticoagulant (eg, heparin) at
the same time because warfarin temporarily causes a prothrombotic state.

LMWH is not recommended in end-stage renal disease.

—> diverticular bleeding is not C/I

35) Bisphosphonates (eg, alendronate, risedronate)
- the 1st-line treatment for most women with postmenopausal osteoporosis.
*Monitoring:
-After initiation, bone density is typically remeasured after 2 years to assess
response to therapy.
#Rx: usually discontinued after 5 years due to a risk of atypical fracture with prolonged
use.
—> WHEN TO START DRUGS FOR OSTEOPOROSIS :
- women with osteoporosis confirmed by DXA (ie, T-score ≤−2.5) or with an osteoporotic
fragility fracture warrant pharmacologic antiresorptive therapy.
/osteopenia (T-score between −1 and −2.5) who are at high risk for fragility fracture.

17) septic bursitis: active ROM not affected; passive

Vs
Septic arthritis: passive and active ROM affected

15) The tibialis anterior muscle tendinopathy:

presents with anterior ankle (not heel or toe) pain, worsened by ankle dorsiflexion

16) Tarsal tunnel syndrome:

-posterior tibial nerve compression beneath the flexor retinaculum in the medial
ankle.
- burning pain or numbness(neuropathic pain) in the posteromedial ankle, heel, sole, and
toes, which is elicited by tapping on the nerve (ie, Tinel sign).

36) When elderly patient has co-morbidities along with hip fracture:
—>> In general, surgical repair should be done as soon as feasible to relieve pain,
minimize complications, and reduce length of hospital stay.

- However, surgery may be delayed up to 72 hours if needed to address unstable

medical comorbidity. (Pre op )

#If there is a history of sudden fall on ground without standing above ground level :
Evaluation:
- chest x-ray, EKG , cardiac markers to determine the etiology of fall and assess
preoperative risk prior to surgical correction of his fracture.

- If evidence of pulmonary edema and pleural effusion: echocardiogram is needed.

- Once it is determined that patient is otherwise medically stable, patient may be cleared
for surgical intervention.
37) Ix of choice: NBME 8
• Key idea: Indications for x-ray in setting of low back pain is (1) Osteoporosis or
compression fracture (2) Suspected malignancy (3) Ankylosing spondylitis

• Key idea: Indications for MRI in setting of low back pain is (1) Sensory/motor deficits
(2) Cauda equina syndrome (3) Suspected epidural abscess or infection

38) when is arthrocentesis indicated for osteoarthritis???

-Initial management of knee osteoarthritis : exercise, weight loss, NSAIDs

-Joint aspiration with synovial fluid analysis should be considered when treatment
fails conservative measures, especially when significant warmth, joint tenderness,
or effusion is present: suspect other causes like CPP
Osteosarcoma versus Ewing sarcoma 39) Rx of patellar tendon rupture
Diagnosis Osteosarcoma Ewing sarcoma -Surgical repair is the treatment of
• Most common pediatric choice and should be performed as
bony malignancy • Second most common
Epidemiolog • All races pediatric bony malignancy soon as possible to optimize
y • Bimodal incidence: • White recovery of knee function and
Adolescent boys & age • Adolescent boys
>65 decrease the likelihood of long-term
• Chronic, localized pain & disability.
• Chronic, localized pain
swelling
& swelling
• Long-bone diaphyses & axial
Clinical • Long-bone
skeleton (eg, pelvis) -Delayed treatment can lead to
features metaphyses
• Rare systemic
• More common systemic limited range of motion of the knee,
symptoms (eg, fever,
symptoms
leukocytosis) quadriceps muscle atrophy, and
• "Onion skinning" (lamellated contracture formation.
• "Sunburst" periosteal periosteal reaction)
X-ray reaction • "Moth-eaten"/mottled
findings • Periosteal elevation appearance
(Codman triangle) • Periosteal elevation (Codman
triangle)

40) Mx of PAD:
-1st line exercise therapy
-2nd line: cilostazol
-3rd line: percutaneous transluminal angioplasty / bypass Sx

41) Mx of humerus shaft #:

-1) nonsurgically (eg, closed reduction followed by arm immobilization with a coaptation or
sugar-tong splint) most cases of isolated diaphyseal (midshaft) humeral fracture can be treated
non Sx.

2) open reduction and surgical exploration are indicated :

-open fractures,
- significant displacement (eg, arm shortening)
-neurovascular compromise (eg, asymmetric radial pulses, as in this patient),
-polytrauma, and pathologic fractures.
 42) Why to avoid closed
reduction in dislocations
associated with humeral neck
fractures??
-closed reduction may lead to
further displacement of the
fracture.
-Therefore,such fractures should
not be reduced in the
emergency department but
require open surgical repair.

43) #Mx of acromioclavicular

sprain:
-mild cases of AC sprain:
immobilization with a sling
- more severe cases: operative
management.

44) Mx of colles #:
—>> Neurovascular compromise (eg, absent radial pulse, diminished median nerve
sensation) is an indication for immediate fracture reduction.
1) first step in management :
- Closed reduction often resolves most neurovascular deficits and exacerbation of any
neurovascular injuries during the procedure is unlikely.

2) If evidence of neurovascular compromise persists after closed reduction

—> CT angiography and/or emergency orthopedic surgery consultation for possible open
reduction and exploration is warranted.

45) Pseudogout Mx:

-intra articular steroids, NSAIDs, colchicine
476 SEC TION III MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE PATHOLOGY
` 

Lab values in bone disorders

DISORDER SERUM Ca2+ PO 43− ALP PTH COMMENTS
Osteoporosis — — — —  bone mass
Osteopetrosis —/ — — — Dense, brittle bones. Ca2+  in severe, malignant
disease
Paget disease of bone — —  — Abnormal “mosaic” bone architecture
Osteitis fibrosa cystica
Primary     “Brown tumors” due to fibrous replacement of
hyperparathyroidism bone, subperiosteal thinning
Idiopathic or parathyroid hyperplasia, adenoma,
carcinoma
Secondary     Often as compensation for CKD ( PO43−
hyperparathyroidism excretion and production of activated
vitamin D)
Osteomalacia/rickets     Soft bones; vitamin D deficiency also causes 2°
hyperparathyroidism
Hypervitaminosis D   —  Caused by oversupplementation or
granulomatous disease (eg, sarcoidosis)
  = 1° change.

Primary bone tumors Metastatic disease is more common than 1° bone tumors. Benign bone tumors that start with o are
more common in boys.
TUMOR TYPE EPIDEMIOLOGY LOCATION CHARACTERISTICS
Benign tumors
Osteochondroma Most common benign Metaphysis of long bones Lateral bony projection of growth
bone tumor plate (continuous with marrow space)
Males < 25 years old covered by cartilaginous cap A
Rarely transforms to chondrosarcoma
Osteoma Middle age Surface of facial bones Associated with Gardner syndrome
Osteoid osteoma Adults < 25 years old
Males > females
=
Cortex of long bones Presents as bone pain (worse at night)
that is relieved by NSAIDs

⇐
Bony mass (< 2 cm) with radiolucent
osteoid core B
Osteoblastoma Males > females Vertebrae Similar histology to osteoid osteoma
Larger size (> 2 cm), pain unresponsive
to NSAIDs
Chondroma Medulla of small bones of Benign tumor of cartilage
hand and feet
Giant cell tumor 20–40 years old Epiphysis of long bones Locally aggressive benign tumor
(often in knee region) Neoplastic mononuclear cells that
express RANKL and reactive
multinucleated giant (osteoclast-like)
cells. “Osteoclastoma”
“Soap bubble” appearance on x-ray C
 MUSCULOSKELETAL, SKIN, AND CONNEC TIVE TISSUE PATHOLOGY
`  SEC TION III 477

Primary bone tumors (continued)

TUMOR TYPE EPIDEMIOLOGY LOCATION CHARACTERISTICS
Malignant tumors
Osteosarcoma Accounts for 20% of 1° Metaphysis of long bones Pleomorphic osteoid-producing cells
(osteogenic sarcoma) bone cancers. (often in knee region). (malignant osteoblasts).
Peak incidence of 1° Presents as painful enlarging mass or
tumor in males < 20 pathologic fractures.
years. Codman triangle D (from elevation of
Less common in periosteum) or sunburst pattern on
elderly; usually 2° to x-ray E (think of an osteocod [bone
predisposing factors, fish] swimming in the sun).
such as Paget disease Aggressive. 1° usually responsive to
of bone, bone infarcts, treatment (surgery, chemotherapy),
radiation, familial poor prognosis for 2°.
retinoblastoma,
Li-Fraumeni syndrome.
Chondrosarcoma Medulla of pelvis, proximal Tumor of malignant chondrocytes.
femur and humerus.
Ewing sarcoma Most common in White Diaphysis of long bones Anaplastic small blue cells of
patients. (especially femur), pelvic neuroectodermal origin (resemble
Generally males < 15 years flat bones. lymphocytes) F .
old. Differentiate from conditions with
similar morphology (eg, lymphoma,
chronic osteomyelitis) by testing for
t(11;22) (fusion protein EWS-FLI1).
“Onion skin” periosteal reaction in
bone.
Aggressive with early metastases, but
responsive to chemotherapy.
11 + 22 = 33 (Patrick Ewing’s jersey
number).
A B C

Round cell lesions

Ewing sarcoma
Diaphysis

Myeloma Fibrous dysplasia

Osteoid osteoma D E F
Simple bone cyst
Epiphysis Metaphysis

Osteosarcoma
Osteochondroma

Physis
Giant cell tumor
Renal

#Mx of renal biopsy RPGN:

-needs to be immediately treated with
corticosteroids (such as IV methylprednisolone)
 Switching Antibiotics in pyelonephritis during pregnancy

#Normal duration of Rx in pyelonephritis:

-The treatment course for pyelonephritis (regardless of pregnancy status) typically requires 5-14 days to
completely eliminate bacteria from both the upper (eg, kidney, renal collecting ducts) and lower urinary
tract.

#Ideal candidates for antibiotic transition :

-Following initial treatment with broad-spectrum antibiotics, patients who show clinical improvement (ie,
no fever for 48 hours) are typically at low risk for disease progression and/or complications (eg, renal
abscess); therefore, these patients can transition to oral antibiotics to complete the treatment course.

#Antibiotic of choice during pregnancy:

-The choice of oral antibiotic during pregnancy is guided by fetal safety profile and urine culture
sensitivity testing.
o
I
-

**SAFE:, penicillins, cephalosporins, and fosfomycin are safe during all trimesters.

#Follow up Rx in pregnancy:
-Following completion of treatment, pregnant patients also require a repeat urine culture (due to a high
risk for persistent bacteriuria) and daily antibiotic prophylaxis (eg, cephalexin, nitrofurantoin) for the
remainder of the pregnancy to prevent recurrence.

#Avoid following in pregnancy:

1) Ciprofloxacin, a fluoroquinolone, can be used to treat acute complicated urinary tract infections in
nonpregnant patients; however, it is generally avoided during pregnancy because its fetal effects are not
well studied.

-
pregnancy; - o
2) Nitrofurantoin and trimethoprim-sulfamethoxazole are commonly used to treat acute cystitis during

*why not in pyelonephritis but only cystitis?

—> however, both achieve poor concentration in the kidneys and are therefore inadequate for the
treatment of pyelonephritis.
- In addition, trimethoprim-sulfamethoxazole is generally avoided near term gestation because of the risk
for neonatal kernicterus.
 592 SEC TION III RENAL RENAL—PHYSIOLOGY
` 

Acid-base physiology
pH PCO2 [HCO3–] COMPENSATORY RESPONSE
Metabolic acidosis    Hyperventilation (immediate)
Metabolic alkalosis    Hypoventilation (immediate)
Respiratory acidosis     renal [HCO3–] reabsorption (delayed)
Respiratory alkalosis     renal [HCO3–] reabsorption (delayed)
Key:   = compensatory response.

[HCO3−]
Henderson-Hasselbalch equation: pH = 6.1 + log
0.03 Pco2
Predicted respiratory compensation for a simple metabolic acidosis can be calculated using the

⇐ Winters formula. If measured Pco2 > predicted Pco2 Ž concomitant respiratory acidosis; if
measured Pco2 < predicted Pco2 Ž concomitant respiratory alkalosis:
Pco2 = 1.5 [HCO3–] + 8 ± 2
-
-

#diarrhea from laxative abuse : severe hypokalemia (K loss In stool)

Acidosis and alkalosis and metabolic alkalosis (increased aldosterone from volume depletion)
Vs -
Check arterial pH Simple diarrhoea: met acidosis

opH < 7.35 pH > 7.45

Acidemia Alkalemia

Pco2 > 44 mm Hg HCO3– < 20 mEq/L Pco2 < 36 mm Hg HCO3– > 28 mEq/L
=
=
Respiratory Respiratory
Metabolic acidosis Metabolic alkalosis
acidosis alkalosis

Hypoventilation Check anion gap Hyperventilation H+ loss/HCO3– excess

_
= Na + – (CI– + HCO3 )
Airway obstruction Anxiety/panic attack Loop diuretics
=
Acute lung disease Hypoxemia (eg, high altitude) Vomiting
-
Chronic lung disease Salicylates (early) Antacid use
Opioids, sedatives Tumor Hyperaldosteronism
Weakening of respiratory Pulmonary embolism
muscles

> 12 mEq/L 8–12 mEq/L Pco2 =

45 Metabolic
40 mm Hg
Nagma 40 Respiratory
alkalosis

! Anion gap Normal anion gap acidosis

Plasma [HCO3– ] (mmol/L)

35 Mixed
MUDPILES: HARDASS: 30 alkalosis
Methanol (formic acid) Hyperchloremia/hyperalimentation
Uremia Addison disease 25
Buffer line
Diabetic ketoacidosis Renal tubular acidosis 20 Mixed
Propylene glycol Diarrhea acidosis
15
Iron tablets or INH Acetazolamide
Lactic acidosis Spironolactone 10 Respiratory
Ethylene glycol (oxalic acid) Saline infusion Metabolic alkalosis
5 acidosis
Salicylates (late)
6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9
pH
# urine anion gap (urine Na + urine K − urine Cl)
-indication: calculated when there is a normal anion gap metabolic acidosis.
#Inference: UAG helps determine if such acidosis is due to the renal or intestinal bicarbonate losses.
a) Renal losses of bicarbonate: occur in - distal RTA (+ urine anion gap) / CAI use. .

b)GIT loss of bicarbonate:occurs classically in diarrhea (-ve urine anion gap).

1) NAGMA
- large-volume fluid losses from the pancreas (eg, pancreatic duct leak) or small
intestine (eg, high ileostomy output, enterocutaneous fistula).

2) D/D of hypokalemia, alkalosis and normotension:

1 Surreptitious vomiting
2 Diuretic abuse
3 Bartter syndrome
⇐
4 Gitelman's syndrome

-distinguish vomiting from other entities (e.g., diuretic abuse, Bartter's syndrome)
using the urine chloride concentration.

3) D/D of hypovolemia with U. na >:

•Normally, dehydrated patients with hyponatremia are expected to have low urine
sodium (<20 mEq/L);
however, if elevated urine sodium suggests salt wasting (eg, diuretic use, cerebral
salt wasting [CSW], adrenal insufficiency).

I
• Normally, patients with hypokalemia respond by reducing urine potassium
excretion, except in cases of renal potassium wasting (eg, diuretic use,
hyperaldosteronism, renal tubular acidosis).

• Hypochloremia is likely a result of diuresis and contraction alkalosis; urine chloride

levels can vary.

D/D
1) cerebral salt wasting:
0
CSW presents with hypovolemia and hyponatremia with high urine sodium (>20 mEq/L).
However, CSW always occurs due to a neurologic insult (injury or surgery).
Vs
2) Diuretic abuse leads to increased excretion of water and electrolytes by the kidneys,
resulting in dehydration, weight loss, orthostatic hypotension, hyponatremia, and
hypokalemia.
-Urinary sodium and potassium will be elevated.
Vsr u n
?
#Laxative abuse : hypotension and hypovolemia.
-However, elevated urine sodium indicates that sodium loss is through the urinary tract
(eg, diuretic use) rather than the gastrointestinal tract (eg, laxative use).
 Hypovolemia stimulating RAAS

Hyper Na state by increased RAAS

I
Common medications that cause hyperkalemia
Medication Mechanism
#Inhaled beta-2 agonists (eg,
albuterol) and insulin move
ACE inhibitor, Decreases aldosterone secretion (inhibition
ARB of AT II/AT II receptor) + inhibits ENaC
potassium intracellularly by
activating the Na+/K+-ATPase in
Cyclosporine Blocks aldosterone activity
skeletal muscle.
Digitalis Inhibits Na+/K+-ATPase They are often used to rapidly
Heparin Blocks aldosterone production reduce serum potassium in
Nonselective hyperkalemic emergency; they
Interferes with β2-mediated intracellular
β-adrenergic
potassium uptake do not increase serum
blocker potassium.
Decreases renal perfusion → decreased
NSAID
potassium delivery to the collecting ducts
Potassium-
sparing Inhibits ENaC or aldosterone receptor
diuretic
Succinylcholin Causes extracellular leakage of potassium
e through acetylcholine receptors
Trimethoprim Inhibits ENaC
 RENAL
Lumen - urine `R̀ENAL—PHYSIOLOGY
α-intercalated cell
Interstitium - blood

HCO₃-
SEC TION III 617
CO2 + H2O α-intercalated cell
K+ CA II
ATP ATP
H2CO3
H+ H+

Renal tubular acidosis H+ H+ HCO₃– K+ HCO₃–

HCO₃-
RTA 1 CI– ATP CI–
HCO₃-
ATP
H+
Distal renal tubular acidosis Proximal renal tubular Hyperkalemic tubular
(RTA type 1) acidosis (RTA type 2) acidosis (RTA type 4)
Lumen - urine Interstitium - blood Lumen - urine Interstitium - blood
α-intercalated cell Proximal convoluted tubule Aldosterone
Lumen - urine Interstitium - blood
CO2 + H2O RTA 2 Proximal convoluted tubule
Na+
K+ CA II
ATP HCO₃- H+ H+ + HCO₃– HCO₃- + +
H2CO3 NH₃ NH3 production K+
H+ H₂ CO₃
H₂ CO₃
CA
H+ H+ HCO₃–
HCO₃- CO₂ + H₂O CO₂ + H₂O
ATP RTA 1 CI–

7 ATP
α-intercalated cell
RTA 4
R Aldosterone
+ H+
HCO₃- NH₄
α-intercalated cell
Lumen - urine
Proximal convoluted tubule
Interstitium - blood K+ HCO₃–
ATP ATP CI–
RTA 2 H+ H+
Na+
K+ HCO₃–
HCO₃- H+ H+ + HCO₃– HCO₃-
HCO₃-
ATP CI–
H+
H₂ CO₃

CO₂ + H₂O
DEFECT Inability of α-intercalated Defect in PCT HCO3– Hypoaldosteronism or
Aldosterone
cells to secrete H+ Ž no reabsorption
Lumen - urine Interstitium - bloodof
Ž  excretion
Proximal convoluted tubule
aldosterone resistance;
new HCO3– is generated HCO3– in +urine Ž metabolic hyperkalemia Ž  NH3
+
HCO₃- NH3 production +

Ž metabolic acidosis
α-intercalated cell
acidosis
NH₃ K
synthesis in PCT Ž  NH4+
ATP Urine can be acidified by excretion
H+
α-intercalated cells in
K+ HCO₃– α-intercalated cell

HCO₃-
ATP CI– collecting ATP
duct, Rbut RTA 4 not
Aldosterone
H+
enough to overcome  HCO3–
+ H+
NH₄
K+ HCO₃–
excretion ATP CI–
H+

URINE pH > 5.5 Aldosterone < 5.5 when plasma HCO3– < 5.5 (or variable)
below reduced resorption
Lumen - urine Interstitium - blood
Proximal convoluted tubule

+ +
NH3 production K+
threshold
NH₃
> 5.5 when filtered HCO3–
exceeds resorptive threshold
SERUM K+  α-intercalated cell  
RTA 4
CAUSES Amphotericin
NH₄
+ H+
B toxicity,
ATP R Aldosterone Fanconi syndrome, multiple  aldosterone production (eg,

=
analgesic nephropathy,
HCO₃– myeloma, carbonic anhydrase diabetic hyporeninism, ACE
3As K +

I
congenital
ATP
H+ anomalies CI– inhibitors inhibitors, ARB, NSAIDs,
(obstruction) of urinary tract, heparin, cyclosporine, adrenal
autoimmune diseases (eg, insufficiency) or aldosterone
SLE) resistance (eg, K+-sparing
diuretics, nephropathy due to
obstruction, TMP-SMX)
ASSOCIATIONS  risk for calcium phosphate  risk for hypophosphatemic
kidney stones (due to  urine rickets (in Fanconi syndrome)
pH and  bone turnover
related to buffering)

#Renal tubular acidosis

- caused by a defect in either hydrogen excretion or bicarbonate resorption in the kidney.
In infancy, it most commonly presents with failure to thrive due to a chronic, normal anion
gap metabolic acidosis.
-Treatment : oral bicarbonate replacement.
 Saline responsive met alkalosis:
-Vomiting causes a significant loss of gastric H+ from the body. It also causes loss of
water and salt (NaCl), with relatively more loss of Cl- than Na+ due to the high gastric
quantity of hydrochloric acid (HCl).
-These losses trigger characteristic electrolyte abnormalities resulting in hypokalemic,
hypochloremic metabolic alkalosis.

• The loss of H+ reduces the amount of carbonic acid (H2CO3) buffer in the body,
resulting in an increase in the relative quantity of bicarbonate (HCO3-). Metabolic
alkalosis is initiated with increased serum HCO3-.

• Volume loss decreases renal perfusion and activates the renin-angiotensin-

aldosterone system. The secondary hyperaldosteronism stimulates Na+ reabsorption
in the distal tubules at the expense of increased K+ and H+ excretion. This leads to
hypokalemia and worsens the metabolic alkalosis.

• The loss of Cl- from the stomach and kidneys (which is relatively greater than the
passive Cl- reabsorption that aldosterone stimulates along with Na+ reabsorption)
leads to profound total body Cl- depletion and hypochloremia.

-Because adequate Cl- delivery to the distal renal tubules is required for appropriate
excretion of HCO3- (via the pendrin exchanger), the Cl- depletion causes impaired
HCO3- excretion and perpetuates the metabolic alkalosis.

-Urine sodium and urine chloride are low due to total body depletion and aldosterone-
mediated renal tubular reabsorption. Clinically, low urine chloride is an important indicator
of the etiology and appropriate treatment of metabolic alkalosis.

-It is the expected finding in etiologies of metabolic alkalosis that are primarily driven by
Cl- depletion (eg, severe vomiting, diuretic overuse), and indicates that repletion of
volume and Cl- with normal saline will shut off the mechanisms perpetuating the alkalosis
and allow serum electrolytes to normalize (saline responsive).

#1st step for post op urinary retention Amboss:

-Acute urinary retention is a common problem in the postoperative setting. After
confirming urinary retention by ultrasound,
—> the first step is to check the Foley catheter, which is easily kinked or bent during
postoperative patient transfer (e.g., when the patient is moved from the operative table to
the stretcher).
 Mx of hyperkalemia
a) serve hyperK (>6.5/ rapid escalation in serum potassium during tissue breakdown,
or symptomatic hyperkalemia (eg, ECG changes, cardiac arrhythmia) :

-Urgent treatment (IV calcium gluconate, insulin + glucose)

-

b)mild-moderate hyperK: moderate, chronic elevation of potassium and a creatinine level

that is at baseline, do not require urgent treatment (unless they have concomitant
oliguria or endstage renal disease).

*Mx:
-a low-potassium diet (eg, <40-70 mEq/day)
- avoidance of other medications (NSAIDS) that raise serum potassium.
-oral cation exchange agent (eg, patiromer, zirconium cyclosilicate) not oral Ca
carbonate
a
→
#MOA:
-These insoluble compounds bind potassium in the colon in exchange for calcium or
sodium and are then excreted in the stool, thereby eliminating potassium from the body.

-Patients with CKD who are hypervolemic also sometimes receive a thiazide (eg,
hydrochlorothiazide) or loop diuretic (eg, furosemide), which increase potassium
excretion in the urine.
Contrast-induced nephropathy
• Age >75
• Chronic kidney disease (especially
Risk diabetic nephropathy)
factors • Reduced renal perfusion (eg,
hypotension)
• High-contrast load
• Periprocedural saline hydration
Preventi • Use lowest volume of contrast
on agent possible
• Hold NSAIDS
 596 SEC TION III RENAL RENAL—PATHOLOGY
` 

Nephritic syndrome NephrItic syndrome = Inflammatory process.

Acute Most frequently seen in children. ~ 2–4 weeks after group A streptococcal infection of pharynx or
poststreptococcal skin. Resolves spontaneously in most children; may progress to renal insufficiency in adults. Type
glomerulonephritis III hypersensitivity reaction. Presents with peripheral and periorbital edema, tea or cola-colored
urine, HTN. ⊕ strep titers/serologies,  complement levels (C3) due to consumption.
ƒ LM—glomeruli enlarged and hypercellular A
ƒ IF—(“starry sky”) granular appearance (“lumpy-bumpy”) B due to IgG, IgM, and C3
deposition along GBM and mesangium
ƒ EM—subepithelial IC humps
Rapidly progressive Poor prognosis, rapidly deteriorating renal function (days to weeks).
(crescentic) ƒ LM—crescent moon shape C . Crescents consist of fibrin and plasma proteins (eg, C3b) with
glomerulonephritis glomerular parietal cells, monocytes, macrophages ,
Several disease processes may result in this pattern which may be delineated via IF pattern. steroid
ƒ Linear IF due to antibodies to GBM and alveolar basement membrane: Goodpasture
syndrome—hematuria/hemoptysis; type II hypersensitivity reaction. Treatment: plasmapheresis CYP
ƒ Negative IF/Pauci-immune (no Ig/C3 deposition): granulomatosis with polyangiitis
(Wegener)—PR3-ANCA/c-ANCA, eosinophilic granulomatosis with polyangiitis (Churg-
Strauss) or Microscopic polyangiitis—MPO-ANCA/p-ANCA
ƒ Granular IF—PSGN or DPGN
Diffuse proliferative Often due to SLE (think “wire lupus”). DPGN and MPGN often present as nephrotic syndrome
glomerulonephritis and nephritic syndrome concurrently.
ƒ LM—“wire looping” of capillaries D
ƒ IF—granular; EM—subendothelial, sometimes subepithelial or intramembranous IgG-based
ICs often with C3 deposition
IgA nephropathy Episodic hematuria that usually occurs concurrently with respiratory or GI tract infections (IgA is
(Berger disease) secreted by mucosal linings). Renal pathology of IgA vasculitis (HSP).
ƒ LM—mesangial proliferation
ƒ IF—IgA-based IC deposits in mesangium; EM—mesangial IC deposition
Alport syndrome Mutation in type IV collagen Ž thinning and splitting of glomerular basement membrane.
Most commonly X-linked dominant. Eye problems (eg, retinopathy, anterior lenticonus),
glomerulonephritis, sensorineural deafness; “can’t see, can’t pee, can’t hear a bee.”
ƒ EM—“basket-weave” appearance due to irregular thickening of GBM
Membrano- MPGN is a nephritic syndrome that often co-presents with nephrotic syndrome.
proliferative Type I may be 2° to hepatitis B or C infection. May also be idiopathic.
glomerulonephritis ƒ Subendothelial IC deposits with granular IF
Type II is associated with C3 nephritic factor (IgG autoantibody that stabilizes C3 convertase Ž
persistent complement activation Ž  C3 levels).
ƒ Intramembranous deposits, also called dense deposit disease
Both types: mesangial ingrowth Ž GBM splitting Ž “tram-track” on H&E and PAS E stains.
A B C D E

-HIV : FSGN
-Hep B: membranous (MC); MPGN
 RENAL RENAL—PATHOLOGY
`  SEC TION III 597

Nephrotic syndrome NephrOtic syndrome—massive prOteinuria (> 3.5 g/day)

Minimal change Also known as lipoid nephrosis. Most common cause of nephrotic syndrome in children.
disease Often 1° (Idiopathic) and may be triggered by recent Infection, Immunization, Immune stimulus
(4 I’s of MCD). Rarely, may be 2° to lymphoma (eg, cytokine-mediated damage).
1° disease has excellent response to corticosteroids.
ƒ LM—Normal glomeruli (lipid may be seen in PCT cells)
ƒ IF—⊝
ƒ EM—effacement of podocyte foot processes A
Focal segmental Most common cause of nephrotic syndrome in African-Americans and Hispanics.
glomerulosclerosis Can be 1° (idiopathic) or 2° to other conditions (eg, HIV infection, sickle cell disease, heroin abuse,
massive obesity, interferon treatment, or congenital malformations).
1° disease has inconsistent response to steroids. May progress to CKD.
ƒ LM—segmental sclerosis and hyalinosis B
ƒ IF—often ⊝ but may be ⊕ for nonspecific focal deposits of IgM, C3, C1
ƒ EM—effacement of foot processes similar to minimal change disease

=-
Membranous Also known as membranous glomerulonephritis.
nephropathy Can be 1° (eg, antibodies to phospholipase A2 receptor) or 2° to drugs (eg, NSAIDs, penicillamine,
gold), infections (eg, HBV, HCV, syphilis), SLE, or solid tumors.
1° disease has poor response to steroids. May progress to CKD. w
ƒ LM—diffuse capillary and GBM thickening C
ƒ IF—granular due to immune complex (IC) deposition
ƒ EM—“Spike and dome” appearance of subepithelial deposits
Amyloidosis Kidney is the most commonly involved organ (systemic amyloidosis). Associated with chronic
conditions that predispose to amyloid deposition (eg, AL amyloid, AA amyloid).
ƒ LM—Congo red stain shows apple-green birefringence under polarized light due to amyloid
deposition in the mesangium
Diabetic glomerulo- Most common cause of ESRD in the United States.
nephropathy Hyperglycemia Ž nonenzymatic glycation of tissue proteins Ž mesangial expansion; GBM

=
thickening and  permeability. Hyperfiltration (glomerular HTN and  GFR) Ž glomerular
-
hypertrophy and glomerular scarring (glomerulosclerosis) Ž further progression of nephropathy.
ƒ LM—Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis
(Kimmelstiel-Wilson lesions D )
A B C D

#Pathogenesis for nephrotic syndrome:

1) Circulating immune complexes /immune complex-mediated glomerulopathies : SLE,
post-streptococcal glomerulonephritis, etc.
2) Cell-mediated injury: idiopathic crescentic glomerulonephritis.
3) Non-immunologic kidney damage: diabetic nephropathy, hypertensive nephropathy, etc.
4) Membranoproliferative glomerulonephritis, type 2/ dense deposit ds: persistent
activation of the alternative complement pathway.
 RENAL RENAL—PATHOLOGY
`  SEC TION III 601

Acute kidney injury

Prerenal azotemia Intrinsic renal failure Postrenal azotemia
ETIOLOGY Hypovolemia Tubules and interstitium: Stones
 cardiac output ƒ Acute tubular necrosis BPH
 effective circulating volume (ischemia, sepsis, infection, Neoplasm
(eg, HF, liver failure) nephrotoxins) Congenital anomalies
ƒ Acute interstitial nephritis
Glomerulus:
ƒ Acute glomerulonephritis
Vascular:
ƒ Vasculitis
ƒ Malignant hypertension
ƒ TTP-HUS
PATHOPHYSIOLOGY  RBF Ž  GFR In ATN, patchy necrosis Outflow obstruction (bilateral)
Ž  reabsorption of Na+/H2O Ž debris obstructing tubules
and urea and fluid backflow Ž  GFR
In ATN, epithelial/granular
casts

É E
URINE OSMOLALITY (mOsm/kg) >500 <350 <350
URINE Na+ (mEq/L) <20 >40 Varies
FENa <1% >2% Varies
SERUM BUN/Cr >20 <15 Varies

SpecificI gravity >1.02 < 1.02

Acute interstitial Also called tubulointerstitial nephritis. Acute Associated with fever, rash, hematuria, pyuria,
nephritis interstitial renal inflammation. Pyuria
(classically eosinophils) and azotemia
=
and costovertebral angle tenderness, but can be
asymptomatic.
occurring after administration of drugs that Remember these 5 P’S:
act as haptens, inducing hypersensitivity ƒ Pee (diuretics)
(eg, diuretics, NSAIDs, penicillin derivatives, ƒ Pain-free (NSAIDs)
proton pump inhibitors, rifampin, quinolones, ƒ Penicillins and cephalosporins
sulfonamides). Less commonly may be 2° to ƒ Proton pump inhibitors
other processes such as systemic infections ƒ RifamPin
(eg, Mycoplasma) or autoimmune diseases ƒ Sulfa drugs

→
(eg, Sjögren syndrome, SLE, sarcoidosis).

# Pathogenesis of HT in PSGN Cms

—Hypertension associated with poststreptococcal glomerulonephritis is caused by salt and
fluid retention resulting in volume overload.
-Fluid retention can lead to generalized edema including periorbital, pretibial, and pedal
edema. It can also lead to complications involving heart failure, pulmonary edema, and
respiratory distress.
 Case clue renal Pedia
1) CKD in children
-H/O frequent(UTIs), fatigue, hypertension( 130/80), and proteinuria in addition to daytime
and nighttime enuresis.

2) Nocturnal enuresis secondary to obstructive sleep apnea

-child with
. bedwetting +inattention, behavioral concerns, HT, and/ tonsillar
hypertrophy.
-Evaluation :nocturnal polysomnography

3) Secondary enuresis:
- new-onset nighttime wetting after a ≥6-month period of urinary continence, may be
caused by an underlying medical condition (eg, urinary tract infection) or a psychological
stressor.
—>>The 1st step in evaluation is urinalysis

4) Pyuria: > 5 WBC; hematuria: > 3 RBC

:
=3
←

- -

-
.

5) False + Hematuria:
- red/brown urine that is heme positive but negative for red blood cells.
2 causes: Hburia, Myoglobinuria

6) The MCC of gross hematuria in children: nonglomerular (eg, UTI, perineal/meatal

irritation, trauma
-1st step- renal and bladder USG; 2nd step- CT for small calculi

#Color of hematuria:
1) brown: glomerulonephritis
2) bright red: non glomerular cause
7) Evaluation of GN:
1) 1st step) Low C3 is suggestive of(PSGN), the MC glomerulonephritis in children, /
lupus nephritis.
2) 2nd step)Antistreptolysin O (seen in PSGN) and ANA (seen in SLE) testing can help
differentiate these conditions.
3) 3rd step) If laboratory evaluation is unrevealing and symptoms persist, renal biopsy may
be indicated for diagnosis (eg, IgA nephropathy, membranoproliferative glomerulonephritis).

8) #approach to elevated creatinine in child :

1) 1st step:
-assessment of oliguria (normal urine output is at least one void per day of life),
edema, and hypertension, which would suggest renal disease.
→
⇐
A) if any of the above signs +;
-require possible renal ultrasound and additional laboratory evaluation (eg, trending
serum creatinine), -

particularly if there are risk factors for renal injury (eg, nephrotoxic medications, perinatal
hypoxia).

B) if above signs -;
—> If a neonate has a normal urine output and unremarkable physical examination (eg,
normotensive, expected weight loss) — suggest normal kidneys but has elevated serum
creatinine level — reflective of the mother's creatinine level from renal failure.

9) Normal elevated creatinine in neonate:

-Serum creatinine at birth is equivalent to the serum creatinine of the mother
-as creatinine
- passes across the placenta.
it
0
-Course: In healthy term infants, creatinine normalizes over the first 2 weeks of life to a
nadir that reflects neonatal muscle mass.

10) bilateral renal agenesis:

-serum creatinine rises abnormally after birth;
—> no or minimal urine output is expected

11)Nephrotoxocity in infants:
-nephrotoxicity is not observed until at least 48-72 hours after the initial dose due to the
intracellular accumulation of gentamicin within the proximal tubule;

12)Mx of PSGN
-Supportive care
• Volume overload: loop diuretics (Furosemide) 1st line
• Indications of adjuvant antihypertensives (CCB nifedipine DOC) :hypertensive
encephalopathy, hypertension refractory to diuresis.
• Refractory cases: hemodialysis
13) #Evaluation of neonatal AKI:
—> All neonates with oliguria require further evaluation with the following:
• History and physical examination to evaluate for possible risk factors (eg,
nephrotoxins, family history, renal anomaly) and volume status
• Renal and bladder ultrasound (RBUS), which documents vascular abnormalities /
congenital anomalies

*Y renal USG should be done before fluid resuscitation???

-establishing normal renal anatomy is required first because in obstructive uropathy / renal
dysplasia, fluid bolus could lead to volume overload, since the kidneys are unable to
remove the excess fluid.

14) Mx of posterior urethral Valve:

--The first step in evaluation is a renal and bladder ultrasound.

÷
Findings: dilated bladder with bilateral hydroureters and hydronephrosis vs non
dilated in renal agenesis

-Voiding cystourethrogram is performed if ultrasound is abnormal; evidence of posterior

urethral dilation confirms the diagnosis.

15) physiologic hydronephrosis of pregnancy.

-because there is an increase in maternal blood volume that requires increased renal
filtration, resulting in greater renal vasculature and interstitial tissue.
#timing:
-begins during the 1st trimester as high progesterone levels cause ureteral dilation and
decreased peristalsis.
-Hydronephrosis becomes more pronounced in the 2nd and 3rd trimesters as uterine
enlargement compresses the ureters at the pelvic brim, which results in dilation of the
proximal ureters and bilateral hydronephrosis.

#Side: Right hydronephrosis is often more pronounced due to dextrorotation of the uterus

#Mx: requires no additional management.

16) Primary nocturnal enuresis:

• Nighttime urinary incontinence age ≥5 who has never achieved a prolonged period
(≥6 months) of dryness overnight
• typically have no other urinary tract symptoms (eg, daytime incontinence, urgency,
dribbling).

#Mx: 1st line: behavioural; 2nd line: vasopressin; 3rd line: imipramine
 17) safe antibiotics for pyelonephritis in pregnancy:
**SAFE:, penicillins, cephalosporins, and fosfomycin 18)Mx of postpartum SUI:
-< 6 weeks: observation; kegel
exercise
-> 6week persist: pessary;
midurethral sling Sx

19) Minimal change disease

- the MCC of nephrotic syndrome in
young children.

—> Renal biopsy is not required for

initial diagnosis as the condition is
highly responsive to
- steroids(85%) <— best next step

-indications of Renal biopsy :

children age >10 with nephrotic syndrome, / in any child with nephritic syndrome or minimal
change disease that is unresponsive to steroids.

20) Children age <2 years with a 1st febrile (UTI)

-should receive 1-2 weeks of antibiotics +a renal and bladder ultrasound to evaluate for
abnormalities that may lead to
-
recurrent UTIs.

21) Normal pregnancy Renal changes:

- trace proteinuria —> 1+ is common; creatinine is expected to decline.
- blood pressure typically declines in early pregnancy; the presence of hypertension indicates
underlying pathology.

25) Diabetic nephropathy in pregnancy:

-Pregnancy can cause worsening of diabetic nephropathy (already existing DM) leading to
hypertension, elevated creatinine, and frank proteinuria.
Vs
-Preeclampsia also causes hypertension and proteinuria but occurs later in pregnancy;
findings prior to 20 weeks gestation are usually due to preexisting nephropathy.

==> The development of significant proteinuria (>300 mg/day; 1+ protein) prior to 20

weeks gestation suggests underlying renal disease that was likely present
preconception.
Vs
-Gestational hypertension : new-onset hypertension but does not cause proteinuria and
occurs exclusively at ≥20 weeks gestation.
Medical conditions causing enuresis
Etiology Symptoms Findings
• Infrequent & hard stools
• Encopresis: fecal incontinence,a sign of
Constipatio • ± Palpable
constipation characterized by leakage around
n* stool mass
impacted stool.
• Firm left abdomen (clue)
• ± Recurrent
Bladder • Daytime incontinence
urinary tract
dysfunction* • Weak stream, urgency, straining
infections
Urinary tract • Dysuria, urgency, frequency • Positive urine
infection • Abdominal pain culture
• Hypertension
Chronicj • Daytime incontinence • (130/80 is HT
kidney • Weight loss, fatigue in child)
disease =
Evaluate by S creat and renal imaging • Proteinuria,

Diabetes • Polyuria, polydipsia, polyphagia

• hematuria

• Glucosuria
mellitus • Weight loss, fatigue
Diabetes • Low urine
• Polyuria, polydipsia
insipidus specific gravity
Obstructive • Snoring • Adenotonsillar
sleep apnea • Hyperactivity, inattention hypertrophy
*Often a clinical diagnosis.

27) voiding cystourethrogram indications in children:

-to assess for predisposing urologic abnormalities (eg, vesicoureteral reflux) in a
child with ≥2 febrile urinary tract infections, abnormal renal ultrasound, high fever
with an unusual pathogen, or signs of chronic kidney disease (poor growth; HT)

#y USG is not enough?

-A renal ultrasound should be obtained following an initial UTI in any child and can be
repeated in case of recurrent febrile UTI; it may detect hydronephrosis suggestive of
VUR but is not sensitive for the diagnosis.

-Therefore, a voiding cystourethrogram (VCUG) is often obtained in children with UTI in

whom VUR should be excluded

#Mx of high grade VUR (grade 4/5): daily prophylactic antibiotics

-Mild to moderate VUR : continuous antibiotic prophylaxis, behavioral modification (e.g.,
timed voiding), and regular surveillance.
-severe VUR: surgical or cystoscopic repair of the vesicoureteric junction.
28) #Dx plan for VUR:
-1st line: definitive is voiding cysturethrogram
-renal USG to screen Hydronephrosis
-Renal scintigraphy with dimercaptosuccinic acid: preferred modality for long-term
evaluation for renal scarring.
-Renal function should be followed by serial creatinine.

29) A significant risk factor for recurrent cystitis (ie, ≥2 episodes in 6 months or ≥3
episodes in a year) in women is sexual intercourse.

r
.
-Mx: Postcoital antibiotic prophylaxis (eg, nitrofurantoin, trimethoprim-
-
sulfamethoxazole) can reduce the rate of recurrence.
-

30) Cx of unRx pyelonephritis in Pregnancy:

• Preterm labor • Low birth weight. • ARDS
#Mx:
-Due to the high risk of severe Cx, Mx in pregnancy :hospitalization and empiric IV Ab
(eg, ceftriaxone).

31) The increased incidence of UTI > women : due to the shorter length of the female
urethra compared to males.
Vs
#A shorter distance between the anus and urethra in women :associated with a higher
incidence of recurrent UTIs within the female population,
but is not the main reason for the difference in UTI frequency between men and women.

32) Rx of UTI in infants: 3o cephalosporin

33) Key idea: Treating strep throat will reduce risk of rheumatic fever, but does not
reduce risk of post-strep glomerulonephritis NBME 8

34) Orthostatic proteinuria : the MCC of proteinuria in adolescents.

-The degree of proteinuria is mild and other significant renal abnormalities (eg,
hematuria, acute kidney injury, hypertension) are absent.
#Dx:
-Orthostatic proteinuria can be diagnosed by split (day and night) 24-hour urine
collection showing elevated daytime but normal nighttime protein excretion
rates.
#Pathogenesis:
-Possible mechanisms of proteinuria include an exaggerated normal response to upright
posture, increased glomerular capillary pressure due to an exaggerated angiotensin II
response with standing, subtle glomerular abnormality (eg, focal mesangial
hypercellularity and/or basement membrane thickening), or left renal vein entrapment.
 RENAL RENAL—PATHOLOGY
`  SEC TION III 599

Hydronephrosis Distention/dilation of renal pelvis and calyces A . Usually caused by urinary tract obstruction (eg,
A
renal stones, severe BPH, congenital obstructions, cervical cancer, injury to ureter); other causes
include retroperitoneal fibrosis, vesicoureteral reflux. Dilation occurs proximal to site of pathology.
Serum creatinine becomes elevated if obstruction is bilateral or if patient has an obstructed
solitary kidney. Leads to compression and possible atrophy of renal cortex and medulla.

Urinary incontinence Mixed incontinence has features of both stress and urgency incontinence.
Stress incontinence Urgency incontinence Overflow incontinence
MECHANISM Outlet incompetence (urethral Detrusor overactivity Ž leak Incomplete emptying
-
hypermobility or intrinsic with urge to void immediately (detrusor underactivity or
sphincter deficiency) Ž leak outlet obstruction) Ž leak
with  intra-abdominal .
with overfilling,  postvoid
pressure (eg, sneezing, lifting) residual on catheterization or
=
⊕ bladder stress test (directly
observed leakage from urethra
ultrasound

upon coughing or Valsalva

maneuver)
ASSOCIATIONS Obesity, vaginal delivery, UTI Polyuria (eg, diabetes), bladder
prostate surgery outlet obstruction (eg, BPH),
neurogenic bladder (eg, MS)
TREATMENT Pelvic floor muscle Kegel exercises, bladder Catheterization, relieve
strengthening (Kegel) training (timed voiding, obstruction (eg, α-blockers
exercises, weight loss, distraction or relaxation for BPH)
pessaries techniques), antimuscarinics
(eg, oxybutynin for overactive
bladder), mirabegron

-All patients with urinary incontinence (eg, stress, urgency, mixed) require initial
evaluation for urinary retention (eg, postvoid residual) and infection (eg, urinalysis); both
tests.

#Rare case:
-mid urethral sling Sx done for stress incontinence can be a RF for urge incontinence.
So Rx now differs
 Renal medicine

1) Mx of mixed urine incontinence: usually stress+ urge

1) voiding diary
-tracks fluid intake, urine output, and leaking episodes in order to classify the
predominant type of urinary incontinence and determine optimal treatment.

2) Non pharmac:
-All patients generally require bladder training with
*lifestyle changes (eg, weight loss, smoking cessation, decreased alcohol and caffeine
-
intake) and
*pelvic floor muscle exercises (eg, Kegels).

3) Pharmacotherapy
-depending on predominant type:

-Urodynamic testing
typically reserved for patients with complicated urinary incontinence (ie, those who do
not respond to treatment) / who are considering surgical intervention.

4) Rx of systemic sclerosis renal crisis: ACEI

2) Bladder CA:
-Adults age >40 who have painless hematuria require prompt investigation for bladder
cancer when no evidence of infection (eg, dysuria, pyuria, bacteriuria), GN (eg, red
blood cell casts, dysmorphic red blood cells)/ nephrolith are present.

-The gold-standard initial test: urinary cystoscopy, which allows direct visualization of
the bladder wall and biopsy of suspicious masses.
-Abdominal CT is then generally necessary for staging.
3) Evaluation of hyperK :
-Initial evaluation of hyperkalemia : ECG to evaluate for conduction abnormalities.

- The next step is to exclude acute treatable secondary causes (eg, uncontrolled
hyperglycemia, tumor lysis syndrome).

-Patients should then have a review of recent/current medications as they frequently

can cause hyperkalemia.
—> Patients with persistent, unexplained hyperkalemia: should be evaluated further for
hypoaldosteronism with serum renin and aldosterone levels.

4) RCC:
-varicocele that fails to disappear in recumbent; polycythemia; hematuria; flank pain
-Lab: anaemia/polycythaemia, thrombocytosis, hypercalcaemia (PNS)
-best next step: CT scan

5) post op urinary retention:

-if POUR is present (eg, >600 mL on bedside ultrasound, with different sources listing
different cutoffs), urinary catheterization (>300 ml) is typically performed

-Dont rush directly to cath if not distended bladder. Confirm with bladder USG first

-Anti-hypertensive medication is not recommended when hypertension is due to

urinary retention. Upon draining the bladder (removing the sympathetic stimulus), the
hypertension will spontaneously resolve.

6) RAS: 1st non invasive Renal duplex USG / CT or MR angiography

 }

Oral not IV
NSAIDs
-

8) Role of kidney buffer in met acidosis compensation:

a) increased HCO3− reabsorption
-this leads to leads to increased urinary chloride (Cl−) excretion to maintain electro
negativity in body
b) H+ excretion.
-in the form of ammonium (NH4+) / titratable acid, dihydrogen phosphate (H2PO4−).

—> Carbonic anhydrase is necessary for HCO3− reabsorption in the renal proximal tubule;
therefore, activity is increased in response to acidosis

9) crystal-induced acute kidney injury

#RF: Acyclovir; Sulfonamides; MTX; Ethylene glycol; PI; Uric acid (tumor lysis)
mm
-

#C/F: onset: AKI 24-48 hrs to <7 days of starting drug

• UA: Hematuria, pyuria & crystals
-

• Increased risk with volume depletion, CKD

#Rx:
-Discontinuation of drug; Volume repletion; Loop diuretic
 Clinical features of hyperkalemia
• Tall, peaked T waves with
shortened QT interval
• PR interval prolongation
Sequence of
• QRS complex widening
ECG changes
• Disappearance of P wave
• Conduction blocks, ectopy, or sine
-
wave pattern
Cardiac membrane
• Calcium infusion
E -

E
stabilization
• Insulin with glucose
Rapidly acting
• β2-adrenergic agonists
treatment options

Removal of
-
• Sodium bicarbonate

• Diuretics
v.
potassium
=,
• Gastrointestinal cation exchangers
from body (slow
• Hemodialysis
acting)

9) Mx of lower Urinary Sx:

1st step: URM for infection and hematuria ; 2nd step: PSA;

I
3rd step: S creat in suspected CKD; raised by B/L obstruction;
4th step: renal USG if elevated creat
-Hydronephrosis if found is relieved by catherisation
-

10) cardiorenal syndrome (HF) in acute Pre renal AKI:

-Although prerenal AKI usually results from total body volume depletion, it can also occur
in volume overloaded states that involve reduced effective arterial blood volume
(EABV).

*Case: if patient has volume overload due to an acute heart failure exacerbation, and his
AKI is most likely due to cardiorenal syndrome.

#Mechanism:
-Elevated central venous pressure (CVP) is the major driver of AKI in cardiorenal
syndrome.
-The elevated CVP leads to elevated renal venous pressure and congestion, which may
reduce the perfusion pressure across the glomerular capillaries and cause a consequent
reduction in glomerular filtration rate (GFR).

F
-Rx: diuretics are usually the most effective therapy for AKI due to cardiorenal syndrome;
the resulting reduction in CVP improves renal perfusion and increases GFR.
11) mixed acid base disorder:
-sepsis due to LE cellulitis: primary metabolic acidosis due to lactic acidosis.
-sepsis due to pneumonia:
-vomiting with opiod overdose:Mixed metabolic alkalosis and respiratory acidosis
12) Ideal candidates for oral antibiotic
transition in pyelonephritis ??
clots are unusual in glomerular disease
-patients who show clinical improvement
(ie, no fever for 48 hours) are typically at
low risk for disease progression and/or
complications (eg, renal abscess);

—> not necessarily same group of oral

Ab as IV ab (TMP after IV ceftr is ok )

13) Calcium oxalate stones

get
if the cancer originates from the
bladder neck or trigone. - the MC type of kidney stone;

-Risk factors : dehydration, excess

sodium or oxalate in the diet, obesity,
hyperparathyroidism, and malabsorptive
disorders; RTA

15) Hepatorenal syndrome:

-severe liver cirrhosis have increased nitric oxide generation in the splanchnic circulation
secondary to portal hypertension —> cause systemic vasodilation—> reduces peripheral
vascular resistance and BP, causing renal hypoperfusion—> Pre renal failure

#clue: patients do not respond to intravenous fluids and withdrawal of diuretics, and
renal function continues to decline.

#Rx:Splanchnic vasoconstrictors (midodrine, octreotide, norepinephrine); Liver.

transplantation
-avoid precipitating factor
16) MCC of death in ESRD:
-Cardiovascular disease accounts for approximately 50% of all deaths in this population
Cardiovascular risk factors in ESRD patients
• HT, DM & dyslipidemia
Traditional risk • LVH
factors • Advanced age & low physical
activity
• Anemia of chronic kidney
disease
ESRD-specific risk • Vascular calcifications (↑
factors phosphorus, ↑ calcium)
• Oxidative stress related to uremia
and dialysis

Osmolal gap = measured serum osmolality

− calculated serum osmolality
= 350 – 297 = 53 mOsm/kg H2O (normal
<10),
where calculated serum osmolality =
(2*sodium) + (glucose/18) + (blood urea
nitrogen/2.8)

18) Most patients with ADPKD are asymptomatic until age 30-40, when renal cysts
become large and numerous.

#C/F: B/L upper abdominal masses are typically palpable on physical examination, and
HT is an early disease manifestation that typically precedes a progressive decline in renal

D
function.
#Cx: Cerebral aneurysms; Hepatic & pancreatic cysts; MVP, AR; Colonic diverticulosis;
- -
Ventral & inguinal-hernias -

#Rx: ACEI for HT; Dx: USG

—> vasopressin-2 receptor antagonists (eg, tolvaptan) may slow disease

progression

19) y chronic diarrhoea/ ileal resection is causes uric acid stone??

-Chronic diarrhea can cause urine to be hyper-concentrated and abnormally acidic
due to ongoing gastrointestinal bicarbonate and water losses. Such urine predisposes to
uric acid kidney stone formation.
-Urine alkalinization helps prevent precipitation of uric acid stones.
 Hyponatremia
Serum
ECV Urine findings Cause
osmolality
• Nonrenal salt loss (eg, vomiting,
UNa <40 mEq/L
Hypovolemi diarrhea, dehydration)
c • Renal salt loss (eg, diuretics,
UNa >40 mEq/L
primary adrenal insufficiency)
Low
• Psychogenic polydipsia
(<275 UOsm <100 mOsm/kg
- • Beer potomania
mOsm/kg) Euvolemic
UOsm >100 mOsm/kg • SIADH (rule out hypothyroidism,
& UNa >40 mEq/L
Ig
secondary adrenal insufficiency)
Hypervole • CHF, hepatic failure, nephrotic
Variable
mic syndrome
• Pseudohyponatremia (eg,
Normal
paraproteinemia, hyperlipidemia)
High Variable
• Hyperglycemia
(>295
-
• Exogenous solutes (eg, mannitol)
mOsm/kg)
CHF = congestive heart failure; ECV = extracellular volume; SIADH = syndrome of
inappropriate antidiuretic hormone; UNa = urine sodium; UOsm = urine osmolality.

# Resistant HypoK in alcoholic

* Pathogenesis:
-Intracellular magnesium is thought to inhibit potassium secretion by renal outer
medullary potassium (ROMK) channels in the collecting tubules of the kidney.
-Therefore, low intracellular magnesium concentrations result in excessive renal potassium
loss and refractory hypokalemia.

—> Normalization of magnesium levels restores ROMK channel potassium transport

regulation, decreases renal potassium losses, and allows for successful correction of
hypokalemia with oral (preferred) or intravenous potassium replacement.

-Hypomagnesemia should be suspected in patients with hypokalemia that is difficult

to correct with potassium replacement.

20) Renal and perinephric abscesses

-C/F: manifest with insidious onset of flank pain and systemic symptoms (eg, fever, weight
loss), typically in patients with a history of urinary tract infection or extrarenal infection (eg,
bacteremia) in the prior 1-2 months.

-In most cases, the urinalysis demonstrates pyuria, bacteriuria, and proteinuria, but it may
remain normal if the abscess is not in contact with the collecting ducts.

-Mx: Management includes antibiotic therapy

and percutaneous drainage.
20) contrast induced Nephropathy:
-clue: acute rise in creatinine within 24-48 hours of contrast administration followed
by a gradual return to baseline in 1 week vs persist >2 weeks in ch embolism
-Mechanism: Direct toxicity causing ATN and renal VC causing pre-renal injury

21) Nephrotic syndrome is a clinical complex characterized by:

1 Proteinuria (> 3-3.5 g/day - most important manifestation)
2 Hypoalbuminemia
3 Oedema
4 Hyperlipidemia and lipiduria

22) Hyponatremia:
-Adaptations to normalize brain volume (eg, extrusion of osmolytes from brain cells)
typically take ~48 hours.
#C/F:
-mild/moderate symptoms : nausea, malaise, headache, and confusion, whereas
severe symptoms : seizure, coma, and respiratory arrest
#Types:
a) Acute hyponatremia (present for <48 hr)
-is poorly tolerated, ;Cx: patients are at high risk of brain herniation.

a-
#Indication of hypertonic saline: serum sodium of <130 mEq/L with any symptoms of
elevated intracranial pressure
-Because neural adaptations have not occurred, patients are at relatively low risk of
osmotic demyelination syndrome (ODS).

b) Chronic hyponatremia (present for ≥48 hr)

- typically better tolerated;

#Indication of hypertonic saline : often reserved for those with severe hyponatremia
(<120 mEq/ L), severe symptoms (eg, seizure), or concurrent intracranial
pathology (eg, masses, hemorrhagic stroke).

#Rx:
-The goal of hypertonic saline infusion : to raise serum sodium levels by 4-6 mEq/L over
a period of hours, which markedly reduces the risk of herniation.
-The maximum rate of correction : 8 mEq/L in 24 hours to prevent ODS.
23) Sx like BPH in young male- urethral stricture
-Postvoid residual volume is increased.
-diagnosis is confirmed on urethrography or cystourethroscopy;
-
-
-Rx: urethral dilation or surgical urethroplasty.

24) Mx of BPH:
-1st line: alpha 2 blocker
-2nd line: 5 alpha reductase inhibitor

25) When to treat met acidosis???

-S/E: Administration of sodium bicarbonate may cause myocardial depression and
increased lactic acid production;

-therefore, in patients with pH >7.1, the relatively small benefits of sodium bicarbonate do
not typically outweigh the risks.
-Indication: pH <7.1

26) dietary recommendations for patients with renal calculi are:

1 Increased fluid intake
2 Decreased sodium intake; increased K intake
3 Normal dietary calcium intake;

28) inadequate pain control acid base:

-develop respiratory alkalosis with a high RR and normal O2 saturation due to inadequate
pain control.

Appropriate compensatory PaCO2 or bicarbonate

Recurrent urinary tract infection changes in acid-base disorders
Definitio • ≥2 infections in 6 months Metabolic
n • ≥3 infections in 1 year acidosis Expected PaCO2 = (1.5 × bicarbonate)
(acute or + 8 ± 2 (Winters formula)
• History of cystitis at ≤15 years chronic)
Risk • Spermicide use
Metabolic
factors • New sexual partner alkalosis ~7 mm Hg ↑ in PaCO2 per 10 mEq/L
• Postmenopausal status (acute or ↑ in bicarbonate
Evaluati • Urinalysis chronic)
on • Urine culture Respiratory ~4 mEq/L ↑ in bicarbonate per 10 mm
acidosis
• Behavior modification (chronic only*) Hg ↑ in PaCO2
• Postcoital or daily antibiotic
Preventi Respiratory
prophylaxis
on alkalosis ~4 mEq/L ↓ in bicarbonate per
• Topical vaginal estrogen for
(chronic only*)
postmenopausal patients
31) Calcineurin inhibitors (eg, tacrolimus, cyclosporine)
-have vasoconstrictive properties on afferent
- -
and efferent ar- responsible for toxicity.
-RF: often triggered by impaired hepatic clearance of the drug eg CYP inhibitors
-C/F: presents with hypertension and prerenal acute kidney injury.
32) Acute interstitial nephritis when becomes
chronic is chronic tunulointerstitial nephritis

-Patients are typically asymptomatic with an

elevated creatinine found incidentally.
-Patients can also develop painless and
=WBC cast prominent hematuria due to papillary
ischemia from analgesic-induced
vasoconstriction of medullary blood vessels
(vasa recta).
In] -Significant papillary necrosis and sloughing
may cause renal colic.
33) RAS:
-O/E: asymmetric renal size>1.5 cm; abd bruit
-Lab: 2o hyperaldosteronism by RAAS +; rise in S creat >30% after ACEI;
-imaging: unexplained atrophic kidney
-dx of choice: renal ultrasound with Doppler
34) Pathophysiology of edema:
a) nephritic syndrome:
Primary glomerular damage leads
to decreased glomerular filtration
rate with eventual development of
significant volume overload

b) nephrotic syndrome:

I
- excessive albumin loss

*How is hypoalbuminemia

E-
different from other causes
peripheral edema??

-It can cause significant

peripheral edema but usually
does not cause pulmonary
edema.
35) Pathogenesis of oxalate stone:
-Under normal circumstances, calcium binds oxalate in the gut and prevents its
absorption. In patients with fat malabsorption, calcium is preferentially bound by fat
leaving oxalate unbound and free to be absorbed into the bloodstream—> urine

-Failure to adequately absorb bile salts in states of fat malabsorption also cause
decreased bile salt reabsorption in the small intestine.
-Excess bile salts may damage the colonic mucosa and contribute to increased oxalate
absorption.

36) Rhabdomyolysis lab abnormalities:

• Hyperkalemia and hyperphosphatemia, :release of these electrolytes from lysed
muscle cells into the bloodstream.
-• Hypocalcemia, : deposition of calcium in damaged muscle tissue.
• Moderate transaminase elevations, : greater elevation in aspartate aminotransferase
(AST) than(ALT) due to relatively higher levels of AST in skeletal muscle.

#AKI:
-from decreased renal perfusion (due to intravascular volume depletion from shifting of
fluid into damaged muscle tissue)
- direct renal tubular toxicity of heme pigments, which are contained in myoglobin
proteins released from lysed muscle cells.

37) D/D of renal colic but absent stone on Xray:

1 Radiolucent stones (uric acid stones, xanthine stones)

2 Small calcium stones (<1-3 mm in diameter)
3 Nonstone ureteral obstruction (eg, blood clot, tumor)
38) Rx of uric acid stone:
-1st step: alkalinisation of urine by potassium citrate; hydration; low purine diet
-MOA Of citrate : a stone inhibitor and reduces crystallization; solubilises urate

-2nd step:Allopurinol can be added if symptoms recur despite initial measures,

especially if hyperuricosuria or hyperuricemia occurs.
-NOT thiazides

39) after treatment and resolution of urinary symptoms, she continues to have
persistent proteinuria.
-In the context of her long-standing diabetes and poorly controlled hypertension,
persistent proteinuria suggests diabetic nephropathy (DN).
Indications for urgent dialysis (AEIOU) 40) Common causes of asterixis:
• Metabolic acidosis -hepatic encephalopathy, uremic
Acidosis ◦ pH <7.1 refractory to medical therapy encephalopathy, and hypercapnia.
• Symptomatic hyperkalemia
◦ ECG changes or ventricular arrhythmias -Treating the underlying cause (eg
Electrolyte
abnormalities
• Severe hyperkalemia dialysis in RF) will improve
◦ Potassium >6.5 mEq/L refractory to
neurological status and resolve
medical therapy
asterixis.
• Toxic alcohols (methanol, ethylene glycol)
• Salicylate
Ingestion 41) Acute pyelonephritis
• Lithium
• Sodium valproate, carbamazepine -can result in Gram-negative
Overload • Volume overload refractory to diuretics sepsis.
• Symptomatic: -Urine (and blood) cultures should
◦ Encephalopathy be obtained routinely before
Uremia ◦ Pericarditis administration of empiric
◦ Bleeding antibiotics.

#Indication of Urological imaging in pyelonephritis:

-typically reserved for patients with persistent clinical symptoms despite 48-72 hours of
therapy, history of nephrolithiasis, complicated pyelonephritis, or unusual urinary
findings (eg, gross hematuria, suspicion for urinary obstruction).

42) Simple Renal cyst:

-Simple renal cysts are almost always benign and do not require further evaluation.
-Features concerning for malignant renal mass : a multilocular mass, irregular walls,
thickened septa, and contrast enhancement.
↳
43) # How will you differentiate stress incontinence from UTI??
*Similarity: both causes leakage of urine with valsalva

*Difference:
-Stress incontinence: bladder descent due to intrinsic sphincter deficiency/ urethral
-

hypermobility
- UTI: no bladder descent ;
Here, urine leakage with valsalva is due to bladder irritation.

46) Acute salicylate intoxication

-mixed primary respiratory alkalosis and primary metabolic acidosis
with arterial pH often within the normal range.
-Don’t tick any 1 side of pH

47) Analgesic nephropathy

- the MC form of drug-induced chronic renal failure.

*Incidence:
-It accounts for 3-5% of end stage renal disease in the USA,
-MC seen in females (peak at age 50-55 years)

*Dose:
- It is generally seen after cumulative ingestion of 2-3 kg (4.4-6.6 lbs) of the index
drug.
#Pathology:
-Papillary necrosis and chronic tubulointerstitial nephritis are the MC pathologies seen.
-Hypertension, mild proteinuria, and impaired urinary concentration commonly occur as the
disease advances.
-In severe cases: nephrotic range proteinuria can be seen.

* other Ds:
-Patients with chronic analgesic abuse are also more likely to develop premature aging,
atherosclerotic vascular disease, and urinary tract cancer.

48) In any patient, the pH and PaCO2 are the two lab values that provide the best
picture of acid-base status;
-the HCO3- can be calculated from these values using the Henderson-Hasselbalch
equation.

49) Hypertensive nephrosclerosis

-develops in patients with chronically uncontrolled hypertension and is characterized by
hyaline arteriolosclerosis and ischemic glomerulosclerosis.

# Pathogenesis
• Elevated creatinine (decreased glomerular filtration rate)
•
•
-
Ultrasonographically small, atrophic kidneys
o
Bland (ie, no white/red blood cells) urinalysis with mild proteinuria (<1 g/day).

-Over time, azotemia, anemia (decreased renal erythropoeitin production), and other
chronic kidney disease (CKD) manifestations (eg, fatigue) develop.

-Azotemia is typically slowly progressive (over years) and irreversible.

Vs
# This contrasts with bilateral renal artery stenosis
which may present similarly to HN (though typically with more rapid renal deterioration) but
-
often improves with treatment (eg, angioplasty, stenting).
-
50) interstitial cystitis (ie, painful bladder syndrome)
-a chronic pain disorder classically characterized by suprapubic pain that worsens with
bladder filling and is relieved with voiding, resulting in increased urinary frequency.

O
#Rx:
-Interstitial cystitis is often treated with amitriptyline, and those with worsening symptoms
may require an increased dose
 #New onset dysuria in interstitial
cystitis:
However,if patient's develops new-onset
pain with urination (ie, dysuria) is atypical
for interstitial cystitis and requires
evaluation for other disorders

-The MCC of dysuria in young sexually

active women : cystitis and urethritis,
—> initial evaluation: urinalysis and urine
culture.

52) Scleroderma renal crisis

-typically presents with acute renal failure
(without previous kidney disease) +
malignant hypertension (eg, headache,
blurry vision, nausea).

-Urinalysis :mild proteinuria.

-PS: MAHA with fragmented red blood
cells (eg, schistocytes) +
thrombocytopenia.
-Onset SRC usually occurs within the first 5 years of SSc diagnosis.
#Pathogenesis
-The likely mechanism involves increased vascular permeability, activation of the
coagulation cascade, and increased renin secretion.

#Rx: ACEI, hemodialysis

# Rhabdomyolysis: UWSA1
-initially pigmented cast but false hematuria by acute kidney injury
- later muddy brown cast when it converts to ATN

53) Mx of bladder CA:

-
No muscle invasion: TURBT &
intravesical immunotherapy
• Muscle invasion: radical
cystectomy & systemic
chemotherapy
• Metastatic: systemic chemotherapy
& immunotherapy
54) Obstructive nephropathy :
*Case: patient with LUTS (eg, urinary frequency, nocturia, impaired flow) with (BPH) has a
slowly rising creatinine level; urinalysis does not show evidence of albuminuria,
hematuria, or pyuria, making intrinsic kidney disease less likely.

-This presentation raises suspicion for BPH-induced obstructive uropathy (eg, enlarged
prostate, palpable bladder), which may result in permanent kidney damage due to
blockage of free flow of urine.

#Mx:
-With obstructive uropathy, a renal ultrasound examination (which should be performed
in all patients being evaluated for creatinine elevation or chronic kidney disease) typically
reveals hydronephrosis; it can also help assess the extent of kidney injury.

-If irreversible kidney damage (eg, cortical atrophy on sonogram due to increased
pressure) has not yet occurred, management of BPH may improve creatinine levels.
Vs

#ACE inhibitors (eg, lisinopril)

- cause an elevation in creatinine level, but this elevation would be rapid and would
occur within 3-5 days of starting the medication, not over 12-24 months
Treatment of acute cystitis & pyelonephritis in nonpregnant women #RF for progressive/ ESRD in IgA
• Nitrofurantoin for 5 days (avoid in suspected Nephropathy:
pyelonephritis or creatinine clearance <60 mL/min)
• Trimethoprim-sulfamethoxazole for 3 days (avoid if • Often self-resolves
Uncomplicat local resistance rate >20%)
ed cystitis • Fosfomycin single dose
• Fluoroquinolones only if above options cannot be
• End-stage renal disease in
used some patients
• Urine culture needed only if initial treatment fails ◦ RF: ↑ creatinine, ↑ BP,
• Fluoroquinolones** (5-14 days), extended-spectrum persistent proteinuria(>1 g)
antibiotic (eg, ampicillin/gentamicin) for more
Complicated

=
severe cases
cystitis*
• Obtain sample for urine culture prior to initiating ◦ Slowly progressive (>10 yr)
therapy & adjust antibiotic as needed
• Outpatient: Fluoroquinolones (eg, ciprofloxacin,
levofloxacin)
Pyelonephriti • Inpatient: Intravenous antibiotics (eg, fluoroquinolone,
s aminoglycoside ± ampicillin)
• Obtain sample for urine culture prior to initiating
therapy & adjust antibiotic as needed
*Associated with diabetes, pregnancy, renal failure, urinary tract
obstruction, indwelling catheter, urinary procedure (eg, cystoscopy),
immunosuppression & hospital-acquired.
**Do not use fluoroquinolones in pregnancy. Consider cefpodoxime,
cephalexin, amoxicillin-clavulanate & fosfomycin. CAFE
 Causes of urinary incontinence in the elderly 56)Evaluation:
• ↓ Detrusor contractility, detrusor overactivity -Acute infections, especially (UTIs),
• Bladder or urethral obstruction (eg, tumor, are leading causes of UI in elderly
Genitourinary BPH)
• Urethral sphincter or pelvic floor weakness patients.
• Urogenital fistula
• Multiple sclerosis -Reversible causes of UI DIAPPERS
• Dementia (eg, Parkinson, Alzheimer, normal should be identified and managed
Neurologic
pressure hydrocephalus) before evaluating for chronic causes.
• Spinal cord injury, disc herniation
• Delirium —> As older adults often lack typical
• Infection (eg, UTI) signs or symptoms of UTI, urinalysis
• Atrophic urethritis/vaginitis
• Pharmaceuticals (eg, alpha blockers, with culture should be obtained
Potentially diuretics) routinely.
reversible • Psychological (eg, depression) -Once infection is excluded, additional
• Excessive urine output (eg, diabetes testing is based on clinical findings
mellitus, CHF)
• Restricted mobility (eg, postsurgery)
that suggest other etiologies (CNS).
• Stool impaction

58) Thrombosis of the renal

vein
-can be acute
-C/F; present with abdominal
pain, fever, and hematuria,

- RVT is more commonly

progressive, causing gradual

-
worsening of renal function
and proteinuria in an
asymptomatic patient.
*MC NS:
-RVT can occur in any etiology
of nephrotic syndrome,
but > membranous
glomerulopathy.

E
-a

-FMD decreases perfusion to the kidneys, which increases

both renin and aldosterone levels (secondary
hyperaldosteronism).
-aldosterone : renin activity ratio is ~10 (<20).
 Prevention of recurrent nephrolithiasis 61) Calcium stones:
• Increased fluids (produce >2 L urine/day) -Most patients have hypercalciuria
• Reduced sodium (<100 mEq/day)
• Reduced protein
→
(24-hour U ca excretion >4 mg/kg).
Dietary
• Normal calcium intake (1200 mg/day) #Rx:
measures
• Increased citrate (fruits & vegetables) -The mild volume depletion caused
• Reduced-oxalate diet for oxalate stones
(dark roughage, vitamin C) by thiazide diuretics leads to a
compensatory rise in reabsorption
• Thiazide diuretic
Drug • Urine alkalinization (potassium citrate/
of sodium and water with resulting
therapy bicarbonate salt) increased passive reabsorption of
• Allopurinol (for hyperuricuria-related stones) calcium.

-Thiazides are also thought to modulate calcium channels on the tubular membrane.

Acute pyelonephritis 63) indicator of kidney perfusion

-Urine output is a good indicator of
• Otherwise healthy, nonpregnant
• Primarily Escherichia coli
kidney perfusion, which is an
Uncomplicate • Oral fluoroquinolone, trimethoprim- indicator of overall organ perfusion.
d sulfamethoxazole -Maintaining organ perfusion is the
• Intravenous antibiotics if vomiting, primary goal of IV fluid therapy in
elderly, septic burn patients.
• Diabetes, urinary obstruction/ -Initially, the approximate volume of
instrumentation, renal failure, fluid required may be estimated
immunosuppression, hospital-acquired (e.g., via the Parkland formula),
• ↑ Risk of antibiotic resistance/treatment
Complicated
failure
however this is merely a starting
• Intravenous fluoroquinolone, point,
aminoglycoside, extended spectrum
beta-lactam/cephalosporin

and IV fluid volume should be titrated to maintain a urine output of 0.5 mL/kg/h in adults (1
mL/kg/h in children). Although heart rate and blood pressure should be monitored in
patients with burns, these parameters are not good indicators of overall organ perfusion.
Asymptomatic bacteriuria in pregnancy
Asymptomatic bacteriuria (ASB) refers to the growth of
≥100,000 (105) colony-forming units/mL of a single type
of bacteria from a clean catch urine specimen in the
absence of urinary tract infection symptoms. Risk factors
for ASB include pre-gestational diabetes mellitus and
multiparity. The increased progesterone levels in
pregnancy cause smooth muscle relaxation and ureteral
dilation, thereby increasing the risk for pyelonephritis
and other obstetrical complications (eg, preterm
delivery, low birth weight, increased perinatal
mortality) from ASB.
Therefore, all patients at the initial prenatal visit (12-1
weeks gestation) are screened for ASB. Patients whose
screening urine cultures are positive are treated with
antibiotics. The most common pathogen is scherichia
coli. First-line antibiotics include cephalexin, amoxicillin-
clavulanate, and nitrofurantoin. A repeat urine culture is
performed after antibiotic completion (after a week) to
determine clearance of infection.
Monthly urine cultures are recommended for the duration of the pregnancy to monitor for recurrent infection.
Patients with persistent bacteriuria after ≥2 courses of therapy require daily suppressive therapy (eg,
nitrofurantoin) for the duration of the pregnancy.

=
 3. Pyelonephritis
PYELONEPHRITIS
- Patients with uncomplicated pyelonephritis should have urine culture prior to empiric oral antibiotics
against Gram-negative organisms (eg, fluoroquinolone).
- Hypotensive patients:
1. Require hospitalization and blood cultures to determine the causative organism, evaluate for
bacteremia, and check for drug-resistant organisms.
2. Aggressive resuscitation with IV fluids and empiric IV antibiotics.
1 - Uncomplicated pyelonephritis does not require routine urological imaging (eg, CT of abdomen/pelvis),
especially if the patient is improving clinically. Imaging is typically reserved for patients with persistent
clinical symptoms despite 48-72 hours of therapy, history of nephrolithiasis, or unusual urinary findings
(eg, gross hematuria, suspicion for urinary obstruction).
, - Complicated pyelonephritis: involves progression of the initial pyelonephritis to renal corticomedullary
abscess, perinephric abscess, emphysematous pyelonephritis, or papillary necrosis. Patients can
develop sepsis with multiorgan failure, shock, and renal failure. Complicated pyelonephritis occurs
more commonly in patients with conditions such as diabetes, kidney stones, immunosuppression, or
other anatomic abnormalities of the urinary tract. These patients usually require imaging to evaluate
for these complications, urological evaluation, and prompt therapy (medical/surgical).

- Diabetic pts are usually managed initially with IV antibiotics

- Unless there is a concurrent disorder affecting urinary tract that would impair clear the infection, most
patients can be shifted to oral therapy within 48-72 hours
- Oral therapy options: fluoroquinolones and TMP-SMX, but treatment is based individually on the basis
of culture and antibiotic sensitivity
- ral antibiotics should be continued for treatment 10-1 days.

I
36
Page

urinary alkalization (pH >8) raises suspicion for a urease-producing bacterium such as Proteus
mirabilis (most commonly) or Klebsiella pneumoniae.
Most hospitalized patients can be transitioned to culture-guided oral antibiotics if symptoms
are improved after 48 hours.
 Renal Surg
1) bladder injury
bladder dome rupture: intraperitoneal rupture
Vs anterior bladder rupture: extra peritoneal rupture; FAST -
Vs

2) urethral injury: can’t pass the catheter

-Patients with suspected urethral injury (eg, blood at the urethral meatus, high-riding
prostate) should undergo retrograde urethrography.

#Mx:
-After imaging, anterior urethral injuries: typically repaired urgently (eg, within 24 hours),
Vs
-most PUIs are treated with temporary urinary diversion via suprapubic catheter,
followed by delayed repair. This allows time for healing the injury

2) #Common complications of TURP :

- urethral stricture formation,
-urinary incontinence, and
-bladder neck stenosis, but not iatrogenic pudendal nerve injury.
-recurrence of BPH cz it can’t prevent regrowth

3) renal injury:
-Blunt trauma can cause renal injury. 
-C/F: flank pain and ecchymosis, costovertebral area tenderness, and hematuria. 

-Next: These findings, or a concerning mechanism of injury, should prompt CT scan of the
abdomen and pelvis.

4) Blunt trauma to a full bladder

-MC site: can cause it to rupture at the weakest point, the dome.
-Diversion of urine from the urinary tract (eg, inability to void) into the peritoneal cavity can
cause urinary ascites
-
-Lab: increased BUN and creatinine from peritoneal reabsorption.

-Onset of urinary ascites: short within a day

Vs
Liver ascites: within weeks- months

#Retrograde cystography (or retrograde CT cystography)

- the preferred test used to diagnose bladder rupture, once urethral injury has been
excluded (by retrograde urethrography or successful Foley catheter insertion).
5) • Young woman with recent total abdominal hysterectomy who is anuric with drain
creatinine = serum creatinine, AKI and mild bilateral hydronephrosis consistent with
ureteral ligation/damage due to surgery

•Key idea: Drain fluid creatinine: Serum creatinine > 1 consistent with urine leak
• Key idea: Hysterectomy and other female GU operations are highly associated with
ureteral damage (especially in NBME exams)

6)Mx of kidney stones

a) Alpha blockers such as tamsulosin :facilitate stone passage in stable patients with
relatively small (<10 mm) ureteral stones.
Xx: not recommended for patients with larger stones / those with clinical instability such
as infection or acute kidney injury.

b)Shock-wave lithotripsy :
-used in the management of uncomplicated proximal ureteral stones.
-Disadvantage: However, it may not lead to immediate relief of ureteral obstruction.
-As a result, unstable patients with infection or acute kidney injury first require
decompression with percutaneous nephrostomy or ureteral stenting.

c) percutaneous nephrostomy or ureteral stent placement.

-Patients with obstructing ureterolithiasis associated with infection, acute kidney injury, or
severe pain that has failed initial measures require decompression of the upper urinary
tract with percutaneous nephrostomy or ureteral stent placement.

7) #How to differentiate distal RTA from renal failure??

#Normally,
When there is a gradual loss of nephrons, the remaining nephrons maintain the kidney's ability to excrete a daily
acid load by producing more NH3 buffer that removes H+ as NH4+ in the urine.
#CKD:
-As a result, metabolic acidosis in chronic kidney disease is rarely seen until there is advanced renal dysfunction
(glomerular filtration rate <20 mL/min; elevated creat)

#Distal RTA:
Non-anion gap metabolic acidosis and hyperkalemia that occur out of proportion to the renal
dysfunction( presence of preserved kidney function ; near normal creat) indicate a renal tubular disorder.

#Acquired RTA in DM:

Hyperkalemic RTA is commonly seen in elderly patients who have poorly controlled diabetes with damage to
the juxtaglomerular apparatus, which causes a state of hyporeninemic hypoaldosteronism.
 Poisoning

#opioid toxicity: hypothermia not hyperthermia

594 SEC TION III PSYCHIATRY PSYCHIATRY—PATHOLOGY
` 

Psychoactive drug intoxication and withdrawal

DRUG INTOXICATION WITHDRAWAL
Depressants
Nonspecific: mood elevation,  anxiety, sedation, Nonspecific: anxiety, tremor, seizures,
behavioral disinhibition, respiratory depression. insomnia.
Alcohol Emotional lability, slurred speech, ataxia, Alcoholic hallucinosis
(usually visual)
coma, blackouts. Serum γ-glutamyltransferase
(GGT)—sensitive indicator of alcohol use. AST Withdrawal seizures

value is 2× ALT value (“ToAST 2 ALcohol”). Tremors, insomnia, diaphoresis,

Delirium tremens
agitation, GI upset
Treatment: supportive (eg, fluids, antiemetics).
0 3 6 12 24 36 48 96

Time from last drink (hours)

Treatment: longer-acting benzodiazepines.

Barbiturates Low safety margin, marked respiratory Delirium, life-threatening cardiovascular
depression. Treatment: symptom management collapse.
(eg, assist respiration,  BP).
Benzodiazepines Greater safety margin. Ataxia, minor Seizures, sleep disturbance, depression.
respiratory depression. Treatment: flumazenil
(benzodiazepine receptor antagonist, but
rarely used as it can precipitate seizures).
Opioids Euphoria, respiratory and CNS depression, Sweating, dilated pupils, piloerection (“cold
 gag reflex, pupillary constriction (pinpoint turkey”), rhinorrhea, lacrimation, yawning,
pupils), seizures,  GI motility. Most common nausea, stomach cramps, diarrhea (“flu-like”
cause of drug overdose death. Treatment: symptoms). Treatment: symptom management,
naloxone. methadone, buprenorphine.
Inhalants Disinhibition, euphoria, slurred speech, Irritability, dysphoria, sleep disturbance,
disturbed gait, disorientation, drowsiness. headache.
Effects often have rapid onset and resolution.
Perinasal/perioral rash with repeated use.
Stimulants
Nonspecific: mood elevation,  appetite, Nonspecific: post-use “crash,” including
psychomotor agitation, insomnia, cardiac depression, lethargy,  appetite, sleep
arrhythmias, tachycardia, anxiety. disturbance, vivid nightmares.
Amphetamines Euphoria, grandiosity, pupillary dilation,
prolonged wakefulness, hyperalertness,
hypertension, paranoia, fever, fractured teeth.
-

Skin excoriations with methamphetamine use.

-
Severe: cardiac arrest, seizures. Treatment:
benzodiazepines for agitation and seizures.
Caffeine Palpitation, agitation, tremor, insomnia. Headache, difficulty concentrating, flu-like
symptoms.
 PSYCHIATRY PSYCHIATRY—PATHOLOGY
`  SEC TION III 571

Psychoactive drug intoxication and withdrawal (continued)

DRUG INTOXICATION WITHDRAWAL
Cocaine Impaired judgment, pupillary dilation,
hallucinations (including tactile), paranoia,
angina, sudden cardiac death. Chronic use
may lead to perforated nasal septum due
to vasoconstriction and resulting ischemic
necrosis. Treatment: benzodiazepines;
consider mixed α-/β-blocker (eg, labetalol) for

I
hypertension and tachycardia. Pure β-blocker
usage is controversial as a first-line therapy.
Nicotine Restlessness. Irritability, anxiety, restlessness,  concentration,
 appetite/weight. Treatment: nicotine patch,

Hallucinogens
→
gum, or lozenges; bupropion/varenicline.

Lysergic acid Perceptual distortion (visual, auditory), Visual hallucination

diethylamide depersonalization, anxiety, paranoia,
psychosis, flashbacks (usually nondisturbing).
Marijuana Euphoria, anxiety, paranoid delusions, Irritability, anxiety, depression, insomnia,

•
E-
E-
(cannabinoid) perception of slowed time, impaired judgment, restlessness,  appetite.
social withdrawal,  appetite, dry mouth,
a
conjunctival injection, hallucinations.
Pharmaceutical form is dronabinol: used
as antiemetic (chemotherapy) and appetite
stimulant (in AIDS).
MDMA (ecstasy) Hallucinogenic stimulant: euphoria, Depression, fatigue, change in appetite,
hallucinations, disinhibition, hyperactivity, difficulty concentrating, anxiety.
-
 thirst, bruxism, distorted sensory and time
perception. Life-threatening effects include
hypertension, tachycardia, hyperthermia,
←hyponatremia, serotonin syndrome.
.

Phencyclidine Violence, impulsivity, psychomotor agitation, Onset of action: <8 hrs

nystagmus, tachycardia, hypertension,
Rx of agitation: IV BZD
analgesia, psychosis, delirium, seizures.
Trauma is most common complication.

Alcohol use disorder Physiologic tolerance and dependence on alcohol with symptoms of withdrawal when intake is
interrupted.
Complications: vitamin B1 (thiamine) deficiency, alcoholic cirrhosis, hepatitis, pancreatitis,
peripheral neuropathy, testicular atrophy.
Treatment: naltrexone (reduces cravings), acamprosate, disulfiram (to condition the patient to
abstain from alcohol use). Support groups such as Alcoholics Anonymous are helpful in sustaining
abstinence and supporting patient and family.
Wernicke-Korsakoff Results from vitamin B1 deficiency. Symptoms can be precipitated by administering dextrose
syndrome before vitamin B1. Triad of confusion, ophthalmoplegia, ataxia (Wernicke encephalopathy). May
progress to irreversible memory loss, confabulation, personality change (Korsakoff syndrome).
Treatment: IV vitamin B1 (before dextrose).
 Poisoning clues
1) organophosphate poisoning:
-diaphoresis, nausea and vomiting, fecal incontinence, bronchospasm and diffuse
weakness with muscle fasciculation after working in an agricultural field has signs of
cholinergic toxicity

2) frostbite:
Severity can range from superficial pallor to mummification
• Superficial pallor & anesthesia; Blistering, eschar formation
• Deep tissue necrosis & mummification stiff or waxy texture.
#Mx: rapid rewarming in 37-39 C water bath followed by other measures like wound care;
angiography to assess for thrombosis and thrombolysis in severe limb ischaemia

3)

4) Methemoglobinemia
-presents with cyanosis after exposure to an oxidizing agent (eg, dapsone, nitrites,
anesthetics).
-Pulse oximetry saturation is typically low and does not improve with the administration
of oxygen;, PaO2 is normal.

Vs CO poisoning improves by 100% O2

5) Caustic alkali ingestion

-causes immediate esophageal injury with liquefactive necrosis.
—> In stable patients with no evidence of perforation, endoscopy should be performed
within the first 24 hours to assess the severity of the injury and guide further
management.
#acidic substances : cause coagulation necrosis (eg, protein denaturation) that
results in an eschar, thereby preventing further acid penetration and injury.

#alkaline substances (eg, many cleaning supplies) : cause liquefactive necrosis (eg, cell
membrane dissolution) that often leads to deeper penetration of tissues and therefore
more severe injuries.

6) 1) NPPV:
*Indication because it does not protect against aspiration, it should not be used in
somnolent patients who cannot protect their airway.

2) Endotracheal intubation with mechanical ventilation:

*Indication: This is performed if airway protection is required (eg somnolent to
prevent aspiration) or if adequate oxygenation cannot be achieved with less
invasive strategies.
7) SSRI toxicity:
-Isolated overdose of (SSRIs) is usually well tolerated and asymptotic

—> When a patient with SSRI overdose has altered mental status and abnormal
physical examination findings, levels of common coingestants (eg, salicylates, ethanol)
should be obtained. -

Vs
Autonomic dysfunction, altered vitals and clonus in serotonin syndrome caused by
taking 5HT potentiating drugs

8) Tricyclic antidepressant overdose

- present with CNS, cardiac, and anticholinergic findings.
QRS duration >100 msec is associated with increased risk for ventricular arrhythmia
and seizures and is used as an indication for sodium bicarbonate therapy.
Best predictor of Cx
9) BZD toxicity
- In the absence of coingestion, benzodiazepine intoxication typically presents with
normal vital signs and pupillary size (2-4 mm in bright light).

- Respiratory depression may develop when coingestion (eg, opioids, alcohol) has
occurred or when benzodiazepines are administered intravenously.

10) Loxosceles reclusa (brown recluse) spider bite

-initially have a small, red papule that can progress to form a larger necrotic wound
(loxoscelism).
-Mx: Most cases will resolve with the application of cold packs and local wound care.

11) Isopropyl alcohol ingestion vs

Ocular & CNS Fxs

✓
• High osmolar gap
• CNS depression
• No increased anion gap
• Disconjugate gaze
or metabolic acidosis
___
• Absent ciliary reflex

#All alcohol has high osmolar

Methanol poisoning gap and anion gap MA but
isopropyl alcohol has No MA
Ocular & CNS Fxs
• Visual blurring, • High osmolar gap
central scotomata • Increased anion # severe lactic acidosis in CN
• Afferent pupillary gap metabolic
-

poisoning: > 10 lactate

defect acidosis
• Altered mentation
12) Salicylate Toxicity : confusion, hyperthermia, tachypnea, elevated lactate, Epigastric
tenderness, Nausea/vomiting, anion gap metabolic acidosis, tinnitus
Vs
13) CO Poisoning : Carboxyhemoglobin level is elevated —> confusion, lactic acidosis,
anion gap metabolic acidosis.

14) 2 types of antivenom for North American snake bites:

1) Crotalidae polyvalent immune Fab (ovine), brand name CroFab (FabAV),
-which can be used for all North American snake bites,

2) Crotalidae Immune F(ab')2 (equine), brand name Anavip (Fab2AV),

-which can be used only for confirmed rattlesnake bites.

15) antivenom snake indication:

• no need:
Given the risk of anaphylaxis, patients with mild envenomation (eg, mild, localized
swelling; normal laboratory studies) should be observed for 12-24 hours because
delayed toxicity can occur.

• venom
-progressing or pronounced Sx (eg, pronounced swelling and ecchymosis), abnormal
-

coagulation (eg, oozing), or CVS compromise (eg, hypotension) should receive

antivenom and be admitted to the ICU

16) lead screening

-Capillary (fingerstick) blood specimens are widely used in screening for lead
poisoning, but FP results due to environmental contamination and improper collection.
—> Confirmatory venous lead measurement is required: if a screening capillary Pb
level ≥5 µg/dL.

#Mx of lead toxicity: notify public health Dept

-Dimercaptosuccinic acid (succimer) :Pb levels 45-69 µg/dL.
-Dimercaprol (British anti-Lewisite) + calcium disodium edetate (EDTA)emergently:
if Pb ≥70 µg/dL / acute encephalopathy. 2c

17) CO poisoning Rx:

1) 1st line: administration of 100% oxygen via nonrebreather facemask

2) 2nd line: Hyperbaric oxygen is sometimes used in severe cases that are
unresponsive to facemask-administered oxygen.
 E-
19) acute iron poisoning
-C/F:abdominal pain, diarrhea, and hematemesis;
-hypovolemic shock within a few hours due to gastrointestinal losses.
-Lab: an anion gap metabolic acidosis, ; x-ray : radiopaque tablets in stomach

20) #acute lead toxicity,

• GIT: abdominal pain, constipation
• Neuropsychiatric : (eg, forgetfulness), motor and sensory neuropathies (eg, extensor
weakness, stocking-glove distribution)
• Hematologic :microcytic anemia
--o-
.

-Nonspecific symptoms (eg, fatigue, irritability, insomnia) are common.

#Chronic lead exposure : hypertension and nephropathy.

#H/O clue: occupation (eg, battery manufacturing, plumbing, home restoration) ,distillation
of alcohol through parts with lead soldering), old homes

21) Opioid intoxication:

-patient with altered mental status, hypothermia (dont mistake it as cold exposure),
bradypnea, and hypoxia most likely has opioid intoxication (OI).
-The most reliable and predictive sign :decreased RR

* Target of Naloxone :titrated to achieve a RR >12/min but not to achieve normal

mental status.
Vs

#Rx of opioid withdrawal: methadone

 Acute Vs Chronic Salicylate Toxicity :
#Chronic toxicity :
- more common in young children and the elderly; eg after chronic use of topical
methyl salicylate
- It’s often not associated with a history of recent, heavy ingestion

- It can present with milder symptoms, with only minimally elevated (or even normal)
salicylate levels, making the diagnosis very challenging.

#Acetazolamide is C/I for Salicylate Poisoning :

—>> Although acetazolamide, a carbonic anhydrase inhibitor with diuretic effects,
alkalinizes urine, it is contraindicated in patients with salicylate toxicity.

- It acts by increasing urinary bicarbonate loss, thereby lowering arterial pH, which
encourages salicylate diffusion into the CNS, increasing its neurotoxicity.
23) Synthetic cathinones ("bath salts"):
-have amphetamine-like properties that can cause severe agitation, combativeness,
psychosis, delirium, myoclonus, and, rarely, seizures.

÷
-Tachycardia and increased BP are often present.
-prolonged action: may take up to a week to subside.
-undetected in tox screen urine

24) Bedbug bites

-C/F: small, pruritic, erythematous papules, often arranged in a linear pattern on
exposed areas and each with a central hemorrhagic punctum.
-Management : supportive, but definitive treatment requires eradication of the bugs.

25) Cocaine
-C/F: a stimulant that produces increased energy, decreased appetite, and reduced
need for sleep; mood changes (eg, euphoria, irritability) and weight loss secondary
to decreased appetite.

—> The diagnostic hallmark :erythema of the nasal mucosa, which is a common
finding in individuals who snort cocaine.

#psychiatric complications of cocaine use: anxiety, panic attacks, grandiosity, and

psychosis (ie, delusions and hallucinations)

—> Physical signs of sympathetic nervous system activation can help differentiate
cocaine-induced symptoms from primary mood and psychotic disorders.

26) BZD withdrawal:

-patient's tremulousness, hallucinations, and elevated vital signs (eg, hypertension,
tachycardia) in the context of a psychiatric history consistent with a prescription of
benzodiazepines (eg, anxiety, insomnia) are suggestive of delirium due to benzodiazepine
withdrawal.
-In severe cases, benzodiazepine withdrawal can result in seizures.
27) Caffeine is a stimulant that, when used in excessive amounts, can cause sympathetic
hyperactivity, leading to anxiety, jitteriness, insomnia, palpitations, and tremors.
Vs
Alcohol withdrawal: needs H/O heavy drinking not just 1-2 drinks a day
 Standard urine drug screen
28) Smoking cessation
Duration of positive Duration of positive
Drug
test (short-term use) test (long-term use)
False positives
#the 3 available FDA-approved,
• Atenolol, 1st-line pharmacological
propranolol
Amphetamine ≤2 days ≤4 days • Bupropion treatments for smoking cessation.
• Nasal
decongestants
Cocaine ≤2 days ≤7 days • High specificity 1) Nicotine replacement therapy
Cannabis ≤3 days 1-2 months
• Hemp- (NRT),
containing foods
2) varenicline: nicotine Ach
Opioids*
Morphine ≤3 days ≤3 days • Poppy seeds receptor partial agonist
Heroin
3) bupropion:NE DA reuptake I
•Dextromethor
phan

•Diphenhydra
Phencyclidine ≤7 days ≤7 days
mine,
doxylamine
• Ketamine
• Tramadol
• Venlafaxine
*Standard urine drug screens do not detect semisynthetic (eg, hydrocodone,
hydromorphone, oxycodone) or synthetic (eg, fentanyl, meperidine, methadone, tramadol)
opioids.

29) Theophylline toxicity

- manifest as CNS stimulation (eg, headache, insomnia, seizures),
-GIT disturbances (eg, nausea, vomiting), and cardiac toxicity (arrhythmia).

-RF: Inhibition of the cytochrome oxidase system by other medications, diet, or

underlying disease can alter its narrow therapeutic window.

30) Methamphetamine use is associated with cardiomyopathy, which likely occurs due
to both ischemic and nonischemic mechanisms —> HF

31) Bites from imported fire ants cause sterile pustules that should be left intact to prevent
secondary infections.
-Pustules and small local reactions require no treatment.
-Large local reactions : treated successfully with antihistamines and topical steroids.

32) Acute erosive gastropathy

- hemorrhagic lesions after ischemia or the exposure of gastric mucosa to various
injurious agents (eg, alcohol, aspirin, cocaine).

33) Alcohol abuse :

#Mx:
-1st line: Acambrosate (x In renal impairment) Naltrexone (C/I in opioid abuse and liver Ds)
( x Naloxone)
-2nd line: Disulfiram ( after self motivation and abstinence)
34) Awake seizure
1)scorpion stings
#Mechanism:
-neuronal membrane hyperexcitability —>uncontrolled, repetitive firing of axons.
#C/F:
- However, this commonly results in fasciculations and jerking of the extremities rather
than fixed, extensor posturing; furthermore, patients typically remain awake and complain of
intense pain at the site of the bite.

2) Strychnine
#Mechanism:
-an ingredient in rodenticide and some illicit drugs, blocks inhibitory (glycine)
neurotransmission within the spinal cord and can result in powerful, uncontrollable
muscle contractions.
#C/F:
-However, it classically causes episodic contractions appearing like tonic-clonic activity in a
fully awake patient (sometimes termed an "awake seizure").
Clinical features of caustic ingestion 35) inhalant abuse.
• Chemical burn or liquefaction necrosis injury -Commonly abused inhalants : glue,
Clinical • Affects lips, tongue, oral mucosa & esophagus toluene, nitrous oxide ("whip-its"),
presentati • Patients can develop chest & abdominal pain,
on vomiting with occasional hematemesis & dysphagia/ amyl nitrite ("poppers"), and
odynophagia spray paints.
Prehospital #C/F:
• Decontamination (eg, remove contaminated clothing, -acute intoxication : brief transient
brush off visible chemical, irrigate exposed skin)
• Do not induce vomiting or give charcoal
euphoria and loss of
Emergency department consciousness and vary depending
• Confirm decontamination; chest & abdominal x-rays on the specific chemicals inhaled.
Managem • Endotracheal intubation for significant oropharyngeal
#MOA:
=
ent injury
• Consider gastric lavage if nasogastric tube is placed -Inhalants are highly lipid soluble
Inpatient —>produce immediate effects that
• Endoscopy within 12-24 hr if hemodynamically stable
& without respiratory distress or perforation typically last 15-45 minutes.
• Serial x-rays to rule out perforation -They act as CNS depressants and
• Tube feedings & surgical intervention for severe injury may cause death.

#Other changes:
-LFT may be elevated with repeated use.
-Chronic abuse of nitrous oxide :vitamin B12 deficiency and resultant polyneuropathy,
.

-H/O clue: in young boys which may go unnoticed as common household products are
used and no drug paraphernalia is found.
36) Mx of alcohol abuse dependence
• Acamprosate: 1st line
-MOA: a glutamate modulator at metabotropic glutamate receptor 5,
- C/I and Ix: It is excreted mostly unchanged by the kidneys, and can be used safely in
patients with liver disease but requires dosage adjustment in patients with RF

• Naltrexone: 1st line

-MOA: a mu-opioid receptor antagonist,
-C/I: associated with hepatotoxicity and is contraindicated in patients with liver disease
and those taking prescribed opioid medication.

—> xx Naloxone is a short-acting opioid antagonist used to treat acute opioid intoxication

#Candidates for disulfiram

-must be highly motivated or supervised because they may skip a dose to avoid the averse
reaction when alcohol is desired.
-2nd-line agent for use when naltrexone and acamprosate are either ineffective or C/I
Vs

#Benzodiazepines (eg, chlordiazepoxide)

- indicated for the treatment of moderate to severe alcohol withdrawal.
-They do not treat AUD and have a high risk of abuse.

38) Key idea: Ingestion of household bleach is often considered a benign ingestion,
=
whereas ingestion of industrial-grade bleach is very severe/morbid NBME 8

39) The presence of persistent chest pain and neurologic symptoms in a patient with recent
cocaine use after IV BZD should raise suspicion for acute dissection of the ascending
aorta.
-Rapid diagnosis is essential and can be made by CT angiography of the chest.

40) Acute cocaine intoxication Rx:

-treated supportively and withdrawal is self-limited.
-Long-term treatment of cocaine use disorder :psychosocial interventions, including
individual psychotherapy and 12-step groups (eg, Cocaine Anonymous, Narcotics
Anonymous).
-Although this is an active area of research, no medication has shown consistent efficacy
for cocaine use disorder.
41) cannabinoid hyperemesis syndrome (CHS) amboss
-a condition characterized by cyclic episodes of colicky abdominal discomfort, nausea,
and vomiting in a patient with a history of chronic cannabis use.
-The symptoms of nausea and vomiting associated with CHS are classically relieved with
hot showers
#Mx:
- The only known effective long-term treatment for CHS is cannabis cessation
-Other therapies that may have limited benefit : topical capsaicin, benzodiazepines, and
antiemetics (e.g., ondansetron).

42) Polyneuropathy:
-tingling and symmetric distal sensory loss
-sensory ataxia, as indicated by the positive Romberg test, lower motor neuron weakness,
and hyporeflexia further support this diagnosis.

-Causes: axonal disorders (e.g., diabetes, alcohol use disorder, HIV, Charcot-Marie-Tooth
disease) or demyelinating diseases (e.g., Guillain-Barré syndrome).
 A
its absence does not exclude the diagnosis

-results from environmental exposure and impaired

thermogenesis, and can occur even at room temperature in
severely intoxicated patients.

dog
 Skin

⇐
Pyoderma gangrenosum f
- a neutrophilic dermatosis that is usually associated with inflammatory bowel disease or
an arthritides.
-Lesions typically begin as inflammatory nodules, pustules, or vesicles and quickly
evolve to ulcers; however, they are usually quite painful.
Vs

#Ecthyma gangrenosum
- MC seen in immunocompromised patients with Pseudomonas aeruginosa bacteremia.
-Manifestations :rapid evolution of >1 skin lesion from an erythematous/ H’agic macule
to a pustule or bullae and then into a nonpainful gangrenous ulcer.
-Fever and systemic signs of illness are common.
 Case clue
1) allergic contact dermatitis:
A) Mild, acute cases :erythematous, indurated plaques;
• severe acute cases: vesiculation and bullae may appear,

B) Chronic: scaling, lichenification, fissuring by low-level exposure to an allergen (eg, nickel

clothing fasteners)
• Itching is a dominant feature in all cases

2)SJS: skin/ lesion pain instead of pruritus; preceded by flu

3) TSS
-C/F: high fever, hypotension, and multisystem involvement (eg, diarrhea), + macular rash
resembling a sunburn

4) keratosis Pilaris:
-small, painless papules, a roughened skin texture, and mottled perifollicular erythema.
-MC site: KP can occur anywhere on the body but is most common on the posterior surface
of the upper arm.
-association: atopy, ichthyosis
-Rx: emollients and topical keratolytics (eg, salicylic acid, urea).
5) RF for Hideradenitis suppuretiva:
-smoking, metabolic syndrome (obesity, diabetes)

6)SCC
-Scaly plaques/nodules
• ± Hyperkeratosis or ulceration
• Neurologic signs (if perineural invasion)
Vs
#SCC in situ: slow-growing, red, scaly patches/plaques

#Mx:
1) Small or low-risk lesions : usually managed with surgical
excision or local destruction (eg, cryotherapy, electrodessication);
2) high risk lesions/ located in cosmetically sensitive areas:
should be referred for Mohs micrographic surgery

7) Pyoderma gangrenosum
- characterized by rapidly progressive, painful ulcers with a purulent base and violaceous
border, often following local trauma (pathergy).

-Many patients have underlying systemic inflammatory disorders (eg, rheumatoid arthritis,
inflammatory bowel disease).
 Perianal dermatoses 8) congenital melanocytic nevus
Diagnosis
Contact Candida Perianal -presents within the first few months of life
dermatitis dermatitis Streptococcus - isolated hyperpigmented patches with an
Most common Second most School-aged increased density of hair follicles.
Epidemiolog cause in common children
y infants cause in
Vs
infants
Spares Beefy-red rash Bright, sharply 9) Congenital dermal melanocytosis
creases/ involving demarcated (Mongolian spots)
Examination skinfolds skinfolds with erythema over
satellite perianal/
-flat, gray-blue patches that are poorly
lesions perineal area circumscribed and will fade with time.
Topical barrier Topical Oral antibiotics -MC site: classically located on the lower
Treatment ointment or antifungal back and sacrum,
paste therapy

10) Nevus simplex lesions

- typically located on the eyelids, glabella, and nape of the neck and fade with time;
Vs
11) nevus flammeus lesions (port-wine stains)
do not regress with time and are usually unilaterally located on the face.

12)epidermal Inclusion cyst

-dome-shaped, firm, and freely movable cyst or nodule with a central punctum (small,
dilated, pore-like opening

13) Chemotherapy-induced hair loss

-anagen effluvium
-Culprit: antimicrotubule drugs (paclitaxel), alkylators (cyclophosphamide), and antibiotic
chemotherapy agents (doxorubicin).

14) SCC in situ: limited to epidermis; plaque like lesions; not elevated.
Vs
SCC CA: nodule indurated/ ulcerated

15) Behcets syndrome

-recurrent aphthous ulcers on oral cavity, genitals; uveitis; EN; pathergy

16) 2o syphilis rash: very similar to P rosea i.e. follows skin cleavage line But unlike P.
Rosea it occurs on palm and sole

17)
17) statis dermatitis:
-warm, erythema, malleolar ulcers, varicosity, woody indurated feet, decreased pulse
-Mx: next step is Doppler USG to confirm venous HT and reflux
Vs
#Arterial insufficiency:
-absent pulse, cool and atrophied limb; Next step: ABI

18) melasma
-RF: estrogen and progesterone also stimulate melanocyte proliferation in Pregnancy; darker
skin color, thyroid dysfunction, medications (eg, antiepileptics), and cosmetic use.
Vs
#SLE malar rash:
-similarity: both spare nasolabial fold;
-Difference: SLE rash typically is erythematous and scaly appearing. Additional clinical
features may include hypertension, anemia, thrombocytopenia, and proteinuria.

19) D/D of EN :
- streptococcal infection,
- sarcoidosis,
- tuberculosis (TB),
- endemic fungal disease (eg, histoplasmosis),
- inflammatory bowel disease (IBD),
- Behçet disease.

20) EN and IBD:

—> association between EN and IBD is well recognized and more commonly occurs in
Crohn disease than ulcerative colitis.

Erythema Nodosum & IBD Severity :

- EN mirrors IBD disease activity, meaning that it worsens during severe IBD flares and
resolves as those flares improve.

21) Use of protective clothing

• Key idea: Sunscreen not commonly used in infants under 6 months of age with best
strategy to keep infants in the shade especially during the middle of the day and to use
protective clothing

22) Mx of rosacea:
-only erythema and telangiectasias: topical brimonidine and avoidance of trigger

-papular / pustular lesions: topical metronidazole / azelaic acid.

-Oral antibiotics :more severe or refractory cases.
 23) Nail melanomas :
-present as longitudinal, pigmented
bands in the nail plate+ extends into
nailbed (longitudinal melanonychia).
Vs

# Longitudinal melanonychia:
that involves multiple nails, is
stable over years, or is <3 mm
wide is usually benign.

-However, lesions that are larger, have indistinct borders, change appearance over time, or
extend into the nail folds are suggestive of melanoma.

Sun-protective measures
• Sun avoidance, especially age
Exposur <6 months
e • Reduce exposure 10:00 AM–
4:00 PM
• SPF ≥30
• Apply 15-30 minutes prior to
Sunscre
sun exposure
en
• Reapply every 2 hours & after
swimming
• Long sleeves, broad-brim hats
Clothing
• Tight weave, dark color
 Hidradenitis suppurativa 27) Keloids
• Disordered folliculopilosebaceous units: -benign fibrous growths that develop
Pathogenes
◦ Ductal keratinocyte proliferation → follicular in scar tissue 2o to an
occlusion → follicular rupture → inflammation
is
• Risk factors: smoking, metabolic syndrome (obesity,
overproduction of extracellular
diabetes) matrix and dermal fibroblasts.
• Chronic & recurrent lesions in intertriginous areas
Clinical
• Mild: painful nodules, draining abscesses #Rx: Intralesional glucocorticoids
• Moderate: sinus tracts & scarring
presentation
• Severe: extensive sinus tracts, widespread
are the preferred means of treating
disease most keloids
• Mild: topical clindamycin
• Moderate: oral tetracycline
Treatment
• Severe: tumor necrosis factor-α inhibitors (eg,
adalimumab), surgical excision
Complicati • Depression & suicide
ons • Squamous cell carcinoma of skin

29) Biopsy in melanoma:

-Data suggest that 1–2 cm surgical margins confer the best possible survival
advantage for surgically excised superficial spreading melanoma that is 1.01–2 mm
thick in Breslow depth.
-Results from a sentinel lymph node study help with prognosis and regional disease
control. These results also determine the necessity of adjuvant treatment and the eligibility
of patients for clinical trials.
-A sentinel lymph node study is recommended if tumor thickness is > 1 mm.
30) acral lentiginous melanoma
-A painless, irregularly shaped, brown-black pigmented lesion
involving the toe and nail bed
-This subtype mainly affects dark-skinned and Asian
populations.
-C/F: night sweats, which may be a symptom of malignant
disease.

31) P versicolor: dont tick woods lamp as it’s just 30%

confirmatory
- KOH mount will help
32) Ix of choice in Stasis dermatitis
-C/F: scaling, weeping, superficial erosions, and pitting edema. Chronic findings include
red/brown discoloration, woody induration, fibrosis, and chronic ulcers.
#Dx:
-diagnosis is primarily based on clinical findings, although duplex ultrasonography can
confirm venous hypertension and reflux.
33) Angiosarcomas
- rare malignant tumors derived from the internal lining of blood vessels / lymphatic vessels.

#Types of angiosarcoma :
1) Primary angiosarcoma can occur anywhere in the body (eg, liver, breast),
2) angiosarcoma secondary to breast cancer therapy is typically confined to the skin.

*RF: localized radiation therapy is the strongest risk factor.

-patients with chronic axillary lymphedema, often precipitated by surgical lymph node
resection, are at increased risk.

#C/F:
multiple ecchymoses or purpuric masses on the skin of the breast, axilla, or upper arm
-Onset of 2o CA: 4-8 years following completion of breast cancer therapy.
#Hematogenous spread
#Rx:surgical resection, poor prognosis for 2o

34) BCC: biopsy with 3-5 mm margin

Melanoma: 1-3 mm margin
 Ethics

#Clinical decision support systems (CDSS) assist providers in achieving reliability

(minimizing harmful variations of care) and adhering to evidence-based guidelines in
diagnostic and therapeutic processes.
-CDSS can potentially reduce medication errors (eg, mathematical errors resulting from
incorrect conversion of opioid equivalents).
 #overworked
- (working for > 80 hours
per week, > 24 hours of
consecutive hours on
duty, and/or on call more
often than every third
night).

#Analysing driving in elderly

-Factors that can contribute to impaired driving in older patients include medical conditions
(eg, cerebrovascular disease, movement disorders, arthritis, epilepsy), medication effects
(eg, benzodiazepines, anticholinergics), delayed reaction time, hearing and vision loss,
and cognitive impairment (eg, impaired spatial processing, executive dysfunction, impaired
judgment).

-Evaluating older drivers requires a careful evaluation of the patient's functional capacity to
drive and balancing patient autonomy and confidentiality with public safety.
 278 SEC TION II PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—HEALTHCARE DELIVERY
` 

PUBLIC HEALTH SCIENCES—HEALTHCARE DELIVERY

` 

Disease prevention
Primary disease Prevent disease before it occurs (eg, HPV vaccination)
prevention
Secondary disease Screen early for and manage existing but asymptomatic disease (eg, Pap smear for cervical cancer)
prevention
Tertiary disease Treatment to reduce complications from disease that is ongoing or has long-term effects
prevention (eg, chemotherapy)
Quaternary disease Quit (avoid) unnecessary medical interventions to minimize incidental harm (eg, imaging studies,
prevention optimizing medications to reduce polypharmacy)

Major medical insurance plans

PLAN PROVIDERS PAYMENTS SPECIALIST CARE
Exclusive provider Restricted to limited panel No referral required
organization (except emergencies)
Health maintenance Restricted to limited panel Most affordable Requires referral from
organization (except emergencies) primary care provider
Point of service Patient can see providers Higher copays and Requires referral from
outside network deductibles for out-of- primary care provider
network services
Preferred provider Patient can see providers Higher copays and No referral required
organization outside network deductibles for all services
Accountable care Providers voluntarily enroll Medicare Specialists voluntarily enroll
organization

Healthcare payment models

Bundled payment Healthcare organization receives a set amount per service, regardless of ultimate cost, to be divided
among all providers and facilities involved.
Capitation Physicians receive a set amount per patient assigned to them per period of time, regardless of how
much the patient uses the healthcare system. Used by some HMOs.
Discounted fee-for- Insurer and/or patient pays for each individual service at a discounted rate predetermined by
service providers and payers (eg, PPOs).
Fee-for-service Insurer and/or patient pays for each individual service.
Global payment Insurer and/or patient pays for all expenses associated with a single incident of care with a single
payment. Most commonly used during elective surgeries, as it covers the cost of surgery as well as
the necessary pre- and postoperative visits.
#Pay-for-performance programs
-link financial incentives to provider actions (eg, completing cancer screening). They can
promote clinicians' delivery of evidence-based care and high-value health care (ie, care
that optimizes patient outcomes and quality while avoiding unnecessary treatment).
- so they improve cancer screening follow up referrals and chronic condition monitoring

-However, P4P programs do not address factors outside provider control (eg, patient
socioeconomic status, health care access) and have not yet improved health outcomes
(eg, mortality).
 PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—HEALTHCARE DELIVERY
`  SEC TION II 279

Medicare and Medicare and Medicaid—federal social MedicarE is for Elderly.

Medicaid healthcare programs that originated from MedicaiD is for Disadvantaged.
amendments to the Social Security Act.
Medicare is available to patients ≥ 65 years old, The 4 parts of Medicare:

}
< 65 with certain disabilities, and those with ƒ Part A: hospital Admissions, including
end-stage renal disease. hospice, skilled nursing
Medicaid is joint federal and state health ƒ Part B: Basic medical bills (eg, physician
assistance for people with limited income and/ fees, diagnostic testing)
or resources. ƒ Part C: (parts A + B = Combo) delivered by
approved private companies
ƒ Part D: prescription Drugs

Hospice care Medical care focused on providing comfort and palliation instead of definitive cure. Available to
patients on Medicare or Medicaid and in most private insurance plans whose life expectancy is
Patients are free to leave hospice at < 6 months.
any time to pursue curative
treatments and can return later. During end-of-life care, priority is given to improving the patient’s comfort and relieving pain
(often includes opioid, sedative, or anxiolytic medications). Facilitating comfort is prioritized
over potential side effects (eg, respiratory depression). This prioritization of positive effects over
negative effects is called the principle
- of double effect.

Common causes of death (US) by age

< 1 YR 1–14 YR 15–34 YR 35–44 YR 45–64 YR 65+ YR
#1 Congenital Unintentional Unintentional Unintentional Cancer Heart disease
malformations injury injury injury
#2 Preterm birth Cancer Suicide Cancer Heart disease Cancer
#3 Pregnancy Congenital Homicide Heart disease Unintentional Chronic
complications malformations injury respiratory
disease
#visiting nurse with adequate skills can supervise the medication and health status, but
cannot stay with the patient permanently.

#home hospice Not round the clock

—> Home hospice personnel can reduce caregiver burden but are usually present on-site
for only a few hours a day; assistance from family caregivers in the home is recommended
for optimal 24-hour care.
Vs
#home health aide : HHA responsibilities do not include medication and periodical health
evaluation.
-can relieve caregiver burden but would not be as effective as trained hospice personnel in
facilitating high-quality palliative care for a patient with terminal illness and would not replace
hospice services.

#Inpatient hospice
- most commonly used for patients with symptoms that are inadequately controlled by
home hospice (eg, intractable pain or nausea).
 ● Kiddo with multiple bouts of pneumococcal sepsis, giardia, family members with multiple severe infections:
Bruton's agammaglobulinemia
o Et: X-linked mutation @ Bruton's tyrosine kinase (B-cell maturation)
● "humoral immunity defect/antibody defect"
● Vs. T cell @ PCP, viral, fungal infections
o Sx: show up after 6mos because mom's Ab protects until then
o Dx: low levels of every Ig
o Tx: monthly IVIG
● Kiddo with recurrent infections, petechiae on skin, bleeds when mom tries to brush teeth, eczema: Wiskott
Aldrich syndrome
o Et: X-linked immunodeficiency
o Sx: thrombocytopenia, eczema, recurrent infections
● Kiddo with recurrent abscesses with bacteria: CGD
o Et: mutation in NADPH oxidase (oxidative burst)
o Sx: infection with catalase positive organisms (i.e. Staph, Serratia)
● Kiddo with immunodeficiency, seizures, recurrent parainfluenza, prolonged QT interval: diGeorge syndrome
o Et: failed development of 3rd/4th pouches (where T-cells reach puberty)
● T-cell deficiency --> infections
● Hypocalcemia --> prolonged QT, seizures
● DDx: infants of diabetic moms
● Sx: hypoglycemia 2/2 hyperinsulinemia developed in utero, VSD, HOCM
● Pediatric seizure, on desmopressin for nocturnal enuresis: hyponatremic seizure 2/2 ADH-analog over-secretion
o DDx volume depleted kiddo: replenish with isotonic saline

Cross checked? YES

----------------------------------------------------------------------------------------------------------------------------

Episode 123: Ethics I

● 32 yo M s/p drug overdose in the ICU on a ventilator. No brainstem reflexes can be elicited. He is
homeless and estranged from family. Girlfriend says that the pt wouldn’t want this. Family wants
everything done. NBS?
○ Withdraw care
○ Principle: If you have an accurate, recent representation of a pt’s wishes, you should strongly
consider following these wishes.

● Pt is septic with hallucinations and waxing-and-waning levels of consciousness. They don’t want you to
place IV to administer fluids and antibiotics. They say “I don’t want any of those medications. Don’t give
me any of those poisons.”
○ NBS? Administer abx and fluids against pt’s wishes
○ Principle: If the patient isn’t “with it” mentally, then their wishes don’t count. Instead, do what the
“rational person” would decide to do.
J
● 4 week old infant was brought to ED with 2-3 days of bilious vomiting. He has a hypokalemic
hypochloremic metabolic acidosis. Upper GI series shows malrotation with volvulus. You recommend
immediate surgical intervention. Parents do not want surgery. NBS?
○ Proceed with surgery against the parents’ wishes

233
 ○ Principle: If something is life-threatening to a kid, perform the medically indicated intervention
regardless of parents’ wishes
○ Another example: child of Jehovah’s witnesses that needs blood transfusion

● Adult with clear mentation has a life-threatening condition. You explain that they will die without
treatment. They reiterate that they don’t want the intervention. NBS?
○ Do NOT give treatment
○ Principle: adults with clear mentation have autonomy

● Man with hx Alzheimer’s dementia is hospitalized. He has no written directives. Over the past several
weeks, he’s been jaundiced and has lost 15 lbs. Imaging shows metastatic pancreatic cancer. A study
states that similar pts there is no survival with xyz intervention. Family member wants xyz intervention
to be done. NBS?
○ Comfort care measures
○ Do NOT do something that is not medically indicated even if the family wants it
○ Principle: if it’s not medically indicated, don’t do it

● 14 yo kid with a medical condition requiring surgery. The child is developmentally normal and clearly
mentating. The child does not want the surgery. Parents want the surgery. NBS?
○ Proceed with the surgery
○ Principle: If pt is < 18 yo, their don’t matter (see exceptions below).
■ Exception: mental health
■ Exception: reproductive health (e.g. decisions regarding continuing pregnancy &
abortion)
■ Exception: child married before age 18
■ Exception: emancipated minor

● Pt comes in with diffuse lymphadenopathy & chronic diarrhea. He reports inconsistent condom use with
multiple partners. He tests positive for HIV. He doesn’t want to tell his partner. NBS?
○ Inform the health department. The health department will perform partner notification.
○ Do NOT promise the patient that you won’t inform authorities or that partners won’t be told.
○ Similar to Tarasoff case (duty to warn when the pt expresses intention to harm another person)

● Pt says that he’s going to kill his wife. You call the wife. Option 1 = tell the wife to get away and go
somewhere safe. Option 2 = tell the wife all the details of how he is going to attempt to kill her.
○ Option 1 is best. Only give enough information so the other person can get out of the unsafe
situation.

● Pt that is depressed. Pt says “I don’t think I can take this anymore” and “I can’t continue like this much
longer.” NBS?
○ Further screening for suicide OR hospitalization
○ Trick answer will be “give antidepressants.” They will take too long to go into effect and the
person may already be dead.

● Pt expresses suicidal ideation. NBS? Option 1 = ask the pt how they feel about hospitalization. Option 2
= more forceful approach, where you tell the pt that they will be involuntarily admitted.
Option 1 is best. Try to convince the pt to voluntarily be admitted before pursuing
involuntary admission. 234
● “Mental status exam is negative for evidence of suicidality” → you do NOT need to bring
this pt into the hospital
 ● Newborn should receive which vaccine before they leave the hospital? Hep B
● When do you give mom Rhogam?
○ 24-28 weeks
○ After any invasive procedure (e.g. amnio)
○ After delivery (use Kleihauer-Betke test) to determine dose
● HIV-positive mom delivery baby. Baby has IgG to p24 antigen. Do they have HIV? Not necessarily!
○ IgG can cross the placenta
○ If they have IgM, that’s concerning because IgM does not cross the placenta. NBS? HIV RNA
testing

● CO is a surrogate for SBP. SVR is a surrogate for DBP.

○ Causes of widened pulse pressure?
■ Aortic regurg
■ PDA
■ Milrinone (PDE inhibitor)
● Increases cAMP →
○ Increases contraction of cardiac muscle
○ Relaxation of vascular SM muscle → decrease SVR
■ Septic shock
● Inflammatory mediators → vasodilation → decrease SVR
● CO increases (easier for blood to flow out of heart)

-------------------------------------------------------------------------------------------------------------------------------

Episode 228: CLEAN-SP 1 Palliative

● #1 COD in the US? Heart disease

○ But incidence is decreasing
● #2 COD in the US? Cancer
○ Trend is increasing
● Most healthcare spending goes to chronic disease
○ Most goes toward the last few years of a person’s life
○ Increasing trend of hospitalizations & ICU admissions near end of life (e.g. last 30-60 days)
● Terminal illness = reasonable medical expectation that person won’t survive beyond the next 6 months

● Palliative care is part of comprehensive care for chronic disease

● Principles of palliative care
○ Manage sxs
○ Avoid invasive diagnostic testing & exams
○ Goals of care discussions on a regular basis

● Why don’t physicians initiate goals of care discussions?

○ Fear of bringing up death
○ Time constraints
● Communication skills for goals of care discussion

451
 ○ Normalize: this is a discussion I have with all my pts, I have these discussions so pts can
maintain their autonomy in their care even if they become incapacitated
○ Start open-ended

● How to break bad news to pt

○ P = prepare for discussion
○ S = setting
○ P = patient’s perception (assessing pt’s understanding)
○ I = information (how much would you like to know?)
○ K = knowledge
○ E = empathy & acknowledge emotions
○ S = sharing next steps & summarize

● Advanced directives
○ Living will → patient complete while coherent, details specific wishes for various scenarios
○ Healthcare proxy / durable POA → person that the pt designates to make healthcare decisions
if they cannot

Patient safety culture

-------------------------------------------------------------------------------------------------------------------------------

Episode 230: CLEAN-SP 2 Quality/Safety

● Quality control
○ Example: resident checks EVERY med student note to make sure if has all the required

=
components
● Quality assurance
○ Periodic audit
○ Example: resident does weekly checks of med student notes to make sure they’re up to par
● Quality improvement
○ You’ve identified a problem & designed an intervention to improve things

● Hawthorne effect = people act differently when they know they’re being observed

● Weber effect = if you are tracking adverse events, the incidence of that adverse event will go down (for
-
the first year)

=
-

● Safety champion = person in charge of quality & safety

● High value care

○ Value = service x quality / cost
○ Example: residents are a high value resource because they provide a lot of services that are
pretty high quality at a low cost

● PDSA cycle ....basically the scientific method

○ P = plan
○ D = do
○ S = study
452
 ○ A = act

● Lean model = find inefficiencies in a process, and eliminate them

○ Goal = reduce waste

● DMAIC
○ D = define
○ M = measure
○ A = analyze
○ I = improve
○ C = control
○ Data-driven improvement model

● Six sigma model = no more than 3 defects per million products (this is 6 standard devs)
○ High-fidelity process
○ Goal = eliminate defects

● FMEA = failure mode & effects analysis

○ “What are the different ways in which something might fail?”
○ “What are the consequences of these failures?”
○ PROSPECTIVE TOOL
○ Find the different ways this thing can fail and rank them, then focus on the biggest error

● Root cause analysis

○ Like FMEA but RETROSPECTIVE TOOL

● Swiss cheese model

○ Multiple steps in a process need to fail (holes in the cheese align) in order to cause the error
○ When you design a process, you want to create multiple safeguards to error
○ Example: ordering the wrong dose (off by a zero)
■ the EMR flags the order
■ the pharmacist sees that the dose is not reasonable

--------------------------------------------------------------------------------------------------

Episode 231: Military Part 2

1. Vaccines/protection for military personnel:
I. MMRV, Tdap, typhoid, influenza, polio, hep A + depending on location may give (yellow fever,
anthrax, smallpox).
II. DEET on skin and permethrin on clothes
III. If medic→ Hep B
IV. Sexually active→ Hep B
V. Outbreak of meningitis→ N. meningitidis, use ceftriaxone or ciprofloxacin for treatment and
rifampin ppx for all close contacts.

453
 Episode 234 pt care new
● Pathophys: cardiac tamponade, CHF, post-MI --> CO decreased (heart cannot pump fluid forward), SVR increased -->
fluid backs up in the heart --> CVP/PCWP increased
o CO is low --> tissues get very efficient at extracting oxygen --> O2 sat of blood returning to RA is very low (MVO2
decreased)
● Tx
o Positive inotropic = digoxin, dobutamine (b1 agonist), milrinone
● Milrinone = PDE inhibitor --> increased cAMP --> increased cardiac contractility, decreased vascular
resistance
▪ Pulse pressure increases due to increased SBP + decreased DBP
Hypovolemic shock
● Pathophys: bleeding out --> body volume goes down --> preload goes down --> CO decreased, SVR increased -->
PCWP/CVP decreased, MVO2 decreased
● Tx: fluids

● *QSOFA criteria (1+): AMS, RR >=22, SBP<=100* used clinically

-------------------------------------------------------------------------------------------------------------------------------

Episode 234: CLEAN-SP 2 Medication/Transition of Care

● Medication error = any error that occurs between the clinician prescribing the medication and the
medication arriving to the pt

● Adverse drug event = any type of harm that is experienced by a pt as a result of taking a drug

● RF for adverse drug event

○ #1 = polypharmacy
○ Elderly pt
○ Pediatric pt (weight-based dosing can be confusing)
○ Low health literacy STOPP (Screening Tool of Older Persons' Prescriptions) and START (Screening
○ Drugs that look alike Tool to Alert to Right Treatment) are criteria used as a tool for clinicians to review
■ Similar tablets potentially inappropriate medications in older adults and have been endorsed as
a best practice by some organizations.
■ Similar names

● Screening tools for inappropriate rx in the elderly

○ BEERS criteria
○ STOPP criteria

● 4 drugs responsible for 50% adverse drug events

○ Insulin
○ Warfarin
○ Antiplatelets
○ Opioids

● Drugs NOT to prescribe

○ Benzos in the elderly
○ Opioids for dental procedures or small surgical procedures

● Pathway from clinician to pt & ways to prevent error

460
 ○ Clinician orders
■ Prescribe conservatively (reduce # of rxs)
■ Computerized order entry systems w/ clinical decision support system (e.g. “This pt has
valvular Afib dx in EHR. NOAC may not be appropriate”)
■ Medication reconciliation
○ Pharmacist transcribes Electronic health record
■ EHR has helped eliminate transcribing errors due to poor handwriting
○ Pharmacist dispenses
■ Pharmacist must oversee the process
■ Tall man lettering (helps distinguish drugs with similar names)
■ Automated dispensing cabinets
○ Nurse/caregiver administers
■ 5 Rights Rule
● Right med
● Right dose
● Right time
● Right route
● Right pt
■ Barcode scanners help ensure you’re giving right med to right pt
■ Minimize interruptions in the process of med administration
■ Use a smart infusion pump for IV meds
■ Use a multicompartment medication device when pt is discharged on lots of meds
● IV meds are more prone to error than oral meds due to more calculations required for dosing
●
O
MC type of medication error? Administering med at the wrong time
-
● Opioid safety

o
○ Biggest issue is overprescribing
○ Appropriate for:
■ Acute traumatic pain
■ Cancer-related pain
■ SOB in c/o cancer (morphine)
○ Use prescription monitoring program
-
○ Use short course of opioids
○ Use only when it’s clinically warranted

● Transition of care = moving of pt from one healthcare setting to another

○ E.g. ward → ICU
○ E.g. hospital → LTAC
● Two mostly likely complications of poor transition of care

et
○ Readmission
○ Adverse drug events
● Measures to improve transition of care
○ Clearly written discharge instructions
○ Explain instructions to pt & use teach back
○ Give detailed records to rehab facility/nursing home M
○ Medication reconciliation
○ Arrange definitive f/u (get them an appt!)
461
 ○ Discharge checklist

● Reduce error in pt handoffs

○ Well-written instructions for the other team
○ Done in an environment free of interruptions
○ Use I-PASS method
■ I = illness severity
■ P = pt summary
■ A = action list (to-dos for the night team)
■ S = situation awareness (if-then statements)
■ S = synthesis by receiver (teach back from new team)

● SBARR method for nurse-physician or physician-physician communication

○ S = situation (e.g. this pt’s BP is going down)
○ B = background (e.g. hx of MIs, recurrent V-tach episodes)
○ A = assessment (e.g. I see ST elevations. I think he’s having another MI)
○ R = recommendation (e.g. please put the pt on O2. I’m coming down)
○ R = response
----------------------------------------------------------------------------------------------------------------------------
Episode 237: (HIV)
1) Envelop has gp41 and gp120 glycoprotein (bind to CD4 and ccr5 or cxcr4), and matrix p17
protein and capsid has p24 protein. 2 ssRNA copies.
2) Transmitted with any body fluids. Semen, blood, from mother to baby.
3) Homozygous for E32 mutation, which affects CCR5 mutation→ resistant to HIV, heterozygous is
slower course.
4) Acute retroviral syndrome→ pharyngitis, fever, lymphadenopathy, loss of weight. Happens 2-6
weeks after exposure. Higher risk of transmission. Loss of 100 CD4 per year, latent for 10
years, then starts to have AIDS.
5) AIDS defining illness→ PCP, esophageal candida, CMV, toxoplasma, cervical cancer, or Kaposi.
6) Key disease at CD4 marks:
a) <500 → esophageal candida, lymphoma
b) <200→PCP, but he also mentions crypto, coccidio and histo
c) <100→ PML (JC virus, can also happen from natalizumab), toxoplasma
d) <50→ CMV retinitis, Bacillary angiomatosis, primary CNS lymphoma
7) Diagnose: ELISA checks for IgM and IgG only, known as 3rd generation (99% sensitivity), or
ELISA (IgM and IgG antibodies) + p24 antigen this is known as 4th generation immunoassay
(Sen and Spec 100%), confirm with western blot (antibodies against 2 different HIV proteins,
specificity is 100%)
8) After diagnosis: Check viral load, HLA B57 check (abacavir hypersensitivity), CCR5 check if
they have E32 mutation. Do PPD (5 mm is positive), check lipid profile and glucose when they
start antiretroviral therapy.
9) More common cause of death now is cardiovascular disease because of metabolic syndrome
from antiretroviral therapy

462
 Clues
1) Failure mode and effects analysis (FMEA)
- prospective, systematic, team-based approach that consists of identifying steps in a
process and finding solutions to any problems that may arise, with the goal of ensuring
safe outcomes.
-FMEA can be performed before any problems are identified.
Vs
-As with control chart analysis and RCA, near-miss analysis : performed
retrospectively

2) drug-seeking behavior
- "lost" or "stolen" medication, premature refill requests, and pain inconsistent with
examination findings or known pathology.

3) Help-rejecting patients who are hopeless about treatment can lead the physician to
become frustrated and confrontational and to desire to refer the patient to another
provider.
—> Clear expression of empathy and a collaborative approach with limited goals are
the most effective approaches.

3) Contraceptive counseling
-The adolescent well-child visit should include contraceptive counseling and discussion of
safe sex practices.
-Contraceptive counseling is an opportunity to develop a trusting health care provider–
patient relationship and to decrease the rates of unintended pregnancies and sexually
transmitted infections

4) Malingering
- suspected when a patient is reluctant to be examined or treated and there is a
discrepancy between symptoms and objective findings.
Eg: sensory loss in glove like distribution in entire right hand and denied exam

5) Gender variance: When gender identity or gender expression differ from social norms
and/or expectations, it is referred to as gender variance or gender nonconformity.

Eg: he dressed like opposite gender but not sad with his own gender
Vs
#Gender dysphoria : characterized by persistent distress due to a discrepancy
between assigned gender and innately felt gender.
6) Under the Health Insurance Portability and Accountability Act, patients have the legal
right to obtain copies of their medical records within a timeframe(30 days of request)

7) Team approach for spitting:

*Case: patient's polarized views of the admitting senior resident as "good" (eg, "You're a
great doctor") and the first-year resident as "bad" (eg, "You're not good at your job") has
led to an impasse in treatment and potential division within the treatment team.

—> The optimal approach to manage splitting in the inpatient setting is for all providers to

→
see the patient jointly as a team.
-This allows the team to present a united front, providing clear and consistent information,
preventing miscommunication, and minimizing the potential for splitting to divide the team
or interfere with treatment.

8) Incapacitated patients (intoxicated) may regain capacity as their condition

improves.
-These patients should be reassessed for capacity before health care decisions are made
in non emergency conditions

9) decision making capacity in psychotic pt

-Patients with psychotic illness do not necessarily lack decision-making capacity.

—> If a patient's psychotic symptoms do not interfere with understanding or ability

to communicate a choice regarding medical treatment, the patient has the right to
refuse treatment, even if it would be lifesaving.

#Dont get misguided by this:

-flat affect, general suspiciousness, and hearing nonthreatening voices on mental status
examination are consistent with mild severity of schizophrenic illness and are not impairing
his ability to weigh this specific decision.

#when can a psychiatric patient not consent??

- patient who has severe delusions related to the medical condition,
disorganization, or cognitive impairment may lack capacity and require a surrogate
decision maker)

10) blunt end flaw: latent error

O

11) AMA against medical advice

-When a patient chooses to prematurely discontinue treatment (eg, leaving a hospital
against medical advice), the provider should clearly inform the patient of the risks of
doing so. (Autonomy)
-If the patient insists on discontinuing treatment, the provider should continue to act in
the patient's best interest, including offering appropriate (even if less effective)
alternate treatment options. ( beneficiary) -

12) Directive counseling

#when only 1 medically reasonable treatment option??
-when there is only 1 medically reasonable treatment option that has clearly superior
evidence-based support, it is ethically appropriate for the physician to provide directive
counseling, in which a single treatment option is recommended to the patient.

-Patients with complete placenta previa should be counseled that cesarean delivery is
medically necessary.

13) Mx agitated non violent pt:

-Verbal deescalation techniques should be used to calm agitated but nonviolent
patients and may include the offer of something to eat and drink.

==> IM antipsychotic medication and physical restraints are indicated when verbal
deescalation has failed and violence by a patient is imminent.
Vs
Violent pt: antipsychotic
14) Criteria for eligibility for hospice
-To qualify for hospice, patients must elect to discontinue curative or life-prolonging
treatments; however, they may continue palliative treatments (eg, surgery, palliative
radiotherapy) that are primarily provided for control of symptoms.

#Case: patient has a terminal diagnosis (eg, advanced RCC) but would not qualify for
hospice if she continues immunotherapy, which is considered a curative treatment.

-However, she could enroll in hospice and still continue radiotherapy (which is palliative
therapy for spinal metastasis pain) and other measures that promote comfort

15) taking nonurgent consent from psych pt:

-Valid informed consent for nonurgent treatment requires intact capacity.
-When the patient's decision-making capacity is impaired by reversible factors (eg,
acute psychosis), it should be restored by treating the underlying cause.

-eg giving antipsychotic first in psychiatric patient before treating his lipoma which was
talking with the pt

16) Reducing Hospital readmissions:

-Hospital readmissions are used as a quality metric because they are often preventable
through improved patient communication and follow-up.

-Telephone-based outreach shortly after discharge reduces readmissions rates by

*preventing loss to follow-up,

*increasing patient engagement (proactively identifying and addressing potentially serious
concerns) and
*care coordination (effective transition between inpatient and outpatient care).

17) According to ethical guidelines, permission must be obtained from the family (or
from the patient prior to death) before procedures can be performed on a newly
deceased patient for training purposes

18) Adverse drug events :

-Prescriptions should also communicate plain-language instructions (eg, "morning and
before bed," rather than "twice a day"), intervals (eg, "wait 1 hour before second dose"),
and limits (eg, "maximum 2 pills per day")

-Preventable adverse drug events (ADEs) are a major patient safety concern; risk
increases with vague prescription instructions (eg, "as directed"). Plain-language
medication teaching improves patient health literacy and reduces ADE risk.
20) Intimate partner violence has a high prevalence and significant morbidity and
mortality and is underreported.
-Therefore, screening is required in all women of child-bearing age at routine medical
visits.
Vs
#Mammography screening : begins between ages 40 and 50 in average-risk women,
depending on the guidelines used.

# In patients age ≥30, a Pap test with human papillomavirus cotesting should be
-
performed every 3-5 years for cervical cancer screening.
21) PDSA
-Once a QI issue is identified (eg, elevated rate of failed extubations among preterm
infants), a 4-step process is put in place to address it, as follows:

• Plan: put a plan in place to carry out a cycle (eg, new protocol and checklist

I
development, training in preparation for implementation).

• Do: Implement the plan (ie, new protocol) while making sure to collect data and
document problems and unexpected observations.

• Study (or Check): Using the data gathered, complete a data analysis that compares the
results obtained to the objectives set (eg, evaluate variations in failed extubation rates).

• Act: Based on these data, identify changes that need to be made and lessons learned,
and then begin work on the next cycle if needed to achieve the objective.

22) ecchymoses due to suspected partner violence:

—> next best statement: Tell me more about the bruises on your body

NOT the below statement immediately:

—> Do you have a safety plan to leave the situation?

-At some point in the conversation, the physician should discuss a safety plan with the
patient. However, before making specific recommendations, it is necessary to
understand the nature of the possible abuse and explore what options she may have
already considered.

-The physician should ask open-ended questions to allow patients to describe their
situation on their own terms. The first priorities are to obtain an accurate and thorough
understanding of the abuse and take any necessary action to ensure patient safety.

23) Jehovah's Witnesses

-The Health Care Consent Act has been applied to Jehovah's Witnesses to allow
transfusion to preserve a patient's life in an emergency when no blood refusal card is
present.
—> The patient's fiancé is not a legal next of kin and cannot serve as a substituted
decision-maker
24) Run charts
-A run chart is a quality improvement tool that graphs a process performance outcome
(eg, no-show rate) over time (eg, before and after a quality improvement intervention).

#Inference:
-Presence of a desired trend (ie, consistent directional change for 5 or more data points
in a row) post-intervention suggests
potential effectiveness; persistent underperformance or excessive variation suggests
the intervention only partially addresses factors influencing performance.

25) Interprofessional rounds (ie, involving a

team of professionals from different disciplines)

improve teamwork, communication, and

oversight, reducing the risk of sentinel events
such as wrong-patient error.

26) Pts inappropriate demand

==> "Although I understand your concern, we should address it tomorrow because
it is not an emergency."

-Physicians should respond politely but firmly to inappropriate patient requests.

Maintaining professional boundaries is an important component of the physician-patient
relationship.

27) Transgender name issues:

-Transgender patients experience significant health disparities, including communication
errors (eg, addressed as incorrect name/pronoun), that increase emotional distress and
reluctance to seek care.

#Prevention:
-prevented by redesigning physical systems, including improving visibility of key patient
information eg: placing preferred name and gender in bold text as a chart header/
creating an electronic alert with the preferred name when the chart is accessed

28) Physical environmental reengineering (eg, improving number and placement of

hand hygiene stations) is a systems approach that increases provider likelihood of hand
hygiene compliance.
29) medication reconciliation
-Errors in medication reconciliation (ie, the process of reviewing and updating the
current medication regimen) occur frequently during the transfer of care.
#Prevention
-includes independent review by multiple care team members, interprofessional review
(eg, physicians, nurses, pharmacists), and updated review prior to medication orders.

30) Patient-centered care

-incorporates patient preferences and values, with emphasis on measuring and monitoring
outcomes prioritized by patients (eg, pain level, functional status).

-Shared decision-making optimizes care in chronic conditions featuring multiple reasonable

management strategies (eg, pain management, cancer treatment), promoting selection of
treatments aligned with patient priorities.

31) Conflict of interest

-occurs when the process of informed consent is influenced or biased by a provider's
self-interest.
—>Providers are obligated to inform patients of all medically reasonable alternatives and
provide care that is most likely to yield the greatest benefit to the patient.

32) Patients with serious Ds like HIV (who may anytym devastate) who wish not to inform
family members of their medical information should designate an alternate surrogate
decision-maker (eg close frnd if they don’t trust their family)

33) Psychological safety strengthens safety culture by enabling team members to

express questions and concerns without fear and regardless of status.

—> Team-based safety briefings, used by high-reliability organizations (eg, aviation),

improve communication skills and psychological safety by encouraging
collaborative discussion and monitoring.

#Never choose this

-Observing roles and communication driven by hierarchy, rather than mutual
collaboration and merit, is likely to worsen fear linked to perceived lower status and reduce
the student's psychological safety.

34) DNR orders are most commonly intended to avoid ventilator dependency and
prolongation of terminal illness. However, many patients who have signed DNR orders
are willing to receive care for temporary or correctable conditions (eg, acute
infection).

-In addition, although DNR orders typically apply to implementation of advanced cardiac
life support (ACLS) algorithms for terminal arrhythmias, they generally are not intended as
a refusal of supportive care (including vasopressors)
35) Voluntarily Stopping of Eating and Drinking
-is a decision by patients with terminal illness to cease all food and fluid intake, often as a
symbolic acceptance of death.

-When a patient requests VSED, the physician should proceed as follows:

• Confirm that the patient is cognitively intact and that the request for VSED is
voluntary and not influenced by mental illness
• Counsel the patient (and family members) regarding possible consequences,
including severe thirst and associated discomfort

• Discuss alternatives to VSED (eg, continuing fluids only, decreasing rather than
eliminating oral intake)
• Discuss and clearly record the patient's preferences for managing discomfort
(eg, small sips of fluids, oral swabbing, ice chips) because delirium and
cognitive impairment may occur

36) Time-out and site verification procedures are critical safety practices that
emphasize team communication and redundancy. These procedures involve the
following:

• Preoperative verification of operative site and patient identity (using 2 identifiers)

by at least 2 providers: This process should involve the patient (or surrogate).

• Site marking, in which the surgeon clearly marks each operative site with permanent
marker: Nonoperative sites should not be marked because doing so may cause
ambiguity’
• Final time-out immediately prior to incision involving the entire team: This verifies
surgical site, surgery side, and patient identity.

37) incase of impaired physician due to alcohol, do not confront him as he l deny/ change
-instead inform the local health care programme

38) Never events

- adverse events that are unambiguous, serious, and usually preventable.
#Eg: Unintentionally leaving a foreign object (e.g., surgical instrument) in a patient's body
following surgical intervention, wrong-site surgery, patient death/serious injury due to
contaminated drugs/devices/biologics supplied by a health care facility, patient suicide
during hospitalization, and patient death/serious injury due to administration of the
wrong medication.
39) alert fatigue
-Def: the phenomenon of clinician desensitization to alarms. Although computerized
alerts were created to improve patient safety, the high number of alarms encountered has
led healthcare personnel to become desensitized to such warnings.

-This desensitization is worsened by the high proportion of alarms that are clinically
inconsequential. As a result, physicians often ignore these warnings or do not react
appropriately.

40) research trial rules:

a) According to regulations established by the Office for Human Research Protections
(OHRP) of the U.S. Department of Health and Human Services, all subjects enrolled in a
study have the right to discontinue their participation at any given time, for any or no
reason, without incurring a penalty or loss of benefit to which the subject was entitled to
for participating in the study.
-The investigator cannot obtain any further information without the subject's consent.

B) If the study is not subject to FDA review and the subject requests that the already
collected data be destroyed, the investigator may honor the subject's requests depending
on the protocol set up by the institutional review board.

—> For studies subject to FDA review, the investigator cannot destroy this information or
exclude it from analysis.

C) For interventional studies, data regarding adverse events might be important to protect
the safety of other research subjects, and the OHRP, therefore, recommends that the
investigator clarifies with the subject whether they wish to withdraw completely from the
trial or only from the primary interventional component.

-If the subject wishes to withdraw only from the primary interventional component, follow-
up data collection can continue after reobtaining the subject's consent.

41) Irrespective of state laws, if a physician believes that a patient cannot drive safely, the
physician must share their concerns with the patient and ask them to stop driving until
they have been evaluated and treated by a driver rehabilitation specialist.

-Alternatively, the patient can be recleared for driving by the state licensing authority (e.g.,
Department of Motor Vehicles). However, the laws for reporting impaired drivers differ
between states.
42) Conference funding
-Moreover, a pharmaceutical company cannot invite a physician to present at a medical
conference. Instead, the institution organizing the conference or meeting may accept
commercial support (i.e., from the pharmaceutical company) and independently decide the
appropriate use of its funds (e.g., content, presenters, fees, reimbursement).

43) Phase 3 trial

-While phase III drug trials are often industry-sponsored, the lead researcher should have
complete responsibility for the conduct of the trial, data analysis, and research publication;
even unfavorable results from the trial should be reported.

-The company's interference for trial funding jeopardizes the integrity of research.
Therefore, the attending physician should not accept the trial funding.

-Industry-sponsored research is only permissible if there are no conflicts of interest, the

institutional review board gives permission, and all sources of funding are duly disclosed.

44) according to AMA, 1-2 years of physician patient relationship termination is

required before starting romantic relationships

45) Whom to inform??

-In the case of billing fraud, the appropriate investigatory authority of the insurance
provider (e.g., CMS office in cases of Medicaid or Medicare fraud) should also be
informed.
-If the alleged misconduct potentially violates any criminal statutes, law enforcement
authorities should also be informed.

-When a violation of a medical licensing provision is suspected to be due to physician

impairment, it is appropriate to first inform the local Physician Health Program (PHP),
which is supervised by the SMLB and can make recommendations to the SMLB if
required.
But if the head of institute is guilty, there is no one above him..so directly inform state
board
PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY AND BIOSTATISTICS
`  SEC TION II 261

Clinical trial Experimental study involving humans. Compares therapeutic benefits of ≥2 treatments, or of
treatment and placebo. Study quality improves when study is randomized, controlled, and double-
blinded (ie, neither patient nor researcher knows whether the patient is in the treatment or control
group). Triple-blind refers to the additional blinding of the researchers analyzing the data. Five
phases (“Can I SWIM?”).
Crossover study Compares the effect of a series of ≥2 treatments on a participant. Order in which participants
receive treatments is randomized. Washout period occurs between treatments.
Allows participants to serve as own controls.
Intention-to-treat analysis: All patients are analyzed according to their original, randomly assigned
treatment. No patients are excluded. Attempts to avoid misleading bias from patients dropping out.
Per protocol analysis: Only patients who complete the study “per protocol” are included in analysis.
Patients who fail to complete treatment as originally, randomly assigned are excluded. Risk of bias
from non-random noncompliance.
DRUG TRIALS TYPICAL STUDY SAMPLE PURPOSE
Phase 0 Very small number of either healthy volunteers Initial pharmocokinetic and pharmacodynamic
or patients with disease of interest. assessment. Uses <1% of therapeutic dose. No
safety or toxicity assessment.
Phase I Small number of either healthy volunteers or “Is it Safe?” Assesses safety, toxicity, dosage,
patients with disease of interest; more than pharmacokinetics, and pharmacodynamics.
Phase 0.
Phase II Moderate number of patients with disease of “Does it Work?” Assesses treatment efficacy, and
interest. adverse effects.
Phase III Large number of patients with disease of interest “Is it as good or better?” Compares the new
randomly assigned either to the treatment treatment to the current standard of care (any
under investigation or to the standard of care Improvement?).
(or placebo).
Phase IV Postmarketing surveillance of patients after “Can it stay on the Market?” Detects rare or
treatment is approved. long-term adverse effects and evaluates cost-
effectiveness.

Bradford Hill criteria A group of principles that provide limited support for establishing evidence of a causal relationship
between presumed cause and effect.
Strength Association does not imply causation, but the stronger the association, the more evidence for
causation.
Consistency Repeated observations of the findings in multiple distinct samples.
Specificity The more specific the presumed cause is to the effect, the stronger the evidence for causation.
Temporality The presumed cause precedes the effect by an expected amount of time.
Biological gradient Greater effect observed with greater exposure to the presumed cause (dose-response relationship).
Plausibility A conceivable mechanism exists by which the cause may lead to the effect.
Coherence The presumed cause and effect do not conflict with existing scientific consensus.
Experiment Empirical evidence supporting the presumed cause and effect (eg, animal studies, in vitro studies).
Analogy The presumed cause and effect are comparable to a similar, established cause and effect.
 Step 3 concepts
1) refusal to know genetic test result:
According to the ethical guidelines of the World Health Organization, "the wish of
individuals and family not to know genetic information, including test results, should be
respected, except in testing of newborn babies or children for treatable conditions."

2) release information to employer

-The HIPAA Privacy Rule limits disclosure to the "minimum necessary" information
required to complete a request for information. Eg: fit to join work
-after release of information consent from pt to employer.

3) wait before effect of antidepressants

-An inadequate trial (<6 weeks) is a common cause of a patient's poor response to
antidepressant medication.

4) incase of disagreement between multiple 1o surrogates:.

-In such cases of conflict, the hospital's ethics committee should be involved to act as a
mediator between the different family members

5) Rx family member:
-Treating family members is generally considered to be ethically problematic.
-Acute and limited care may be appropriate when no other physician is available.

6) Overdisturbing on non urgent issues:

-Excessively needy patients who demand attention for nonurgent concerns are best
managed by setting limits in a firm but empathic manner.

-Educating patients about specific guidelines for contacting the physician outside
of office hours and providing alternate resources for routine questions are helpful
strategies.

7) Email communication
-Patient-physician email communication regarding simple, nonurgent health care issues is
useful in clarifying instructions, improving rapport, and increasing patient satisfaction.
-Physicians should set clear parameters early on with patients regarding appropriate
use of email.

8) urgent Rx of jehovahs pt denying BT:

-Intravenous fluids and vasopressors are important supportive measures that should be
administered to Jehovah's Witnesses who have suffered significant blood loss.
References
9) vaccine hesitancy:
-The best approach to vaccine hesitancy or refusal is an open, honest conversation that
includes listening to parental concerns, correcting misinformation, and discussing risks
and benefits of immunization.
—> Continued vaccine refusal can be managed with ongoing dialogue at each visit.

10) Regarding disagreement between doc and patient relatives about end of life care

11) Undesired medical outcomes (eg, errors, inefficiencies, delays) often result from
inadequate patient handoffs between medical providers. Use of sign-out procedures that
incorporate systematic checklists and templates can reduce the incidence of poor
outcomes.

12) According to the American Society of Human Genetics, if attempts to encourage

disclosure by the patient have failed, then disclosure of genetic information to
relatives is permissible only if such a disclosure would serve to ameliorate or
prevent a highly likely and forseeable harm to the identified individual.

-Eg: informing his family members about Huntington disease would not be expected
to prevent or ameliorate harm, as his disease status does not change the disease's
incurable nature or modify its course in his relatives
13) homebound
Patients must also meet the criteria for being "homebound," which includes >1 of the
following:
• Use of a supportive device (eg, crutch, cane, wheelchair, walker) for mobility
• Ability to leave home only with the assistance of another individual
• Medical contraindication to leaving home

#skilled care :physical and occupational therapy and medication adherence assistance.
#nonskilled care: bathing, grooming, dressing).
—> Having a terminal disease with <6 months of life expectancy would qualify a
patient for hospice services; terminal illness is not a requirement for home health
services.

14) non emergency consent for a child:

-consent from nanny or caretaker won’t do.. take consent from parents/ legal guardian;
verbal consent if not available will also help.

15) Skilled nursing facilities

- appropriate when patients cannot live at home or require continuous monitoring (eg,
post-stroke rehabilitation, severe cognitive impairment).
Vs
16) Home health care
-a form of care coordination (eg, safe transition of care), provides home-based,
interdisciplinary health services (eg, physical therapy, home safety assessment,
management of complex medication regimen) by skilled professionals (eg,
nurses, social workers).
-It improves safety (eg, reducing fall risk in the elderly) and health care quality while
maintaining patient independence, autonomy, and engagement.

17) Physicians have the right to terminate their relationships with patients only
after giving them reasonable notice or providing a referral to another health care
provider who is willing to accept the patient.
-Ensuring continuity of care is fundamental to patient safety.
-Failure to adhere to these guidelines may lead to lawsuits for patient abandonment.
 Alcohol use (abuse) screening
• Have you felt you should cut down on
your drinking?
• Have others annoyed you by criticizing
your drinking?
CAGE • Have you ever felt bad or guilty about
your drinking?
• Have you ever taken a drink first thing in
the morning (eye-opener) to steady your
nerves?
Single- • How many times in the past year have
item you had 5 (4 for women) or more drinks
screening in a day?
• How often do you drink alcohol?
• How many drinks do you have on a
AUDIT-C typical day when you are drinking?
• How often do you have 6 (4 for women)
or more drinks on 1 occasion?
• 10-item screen assessing frequency,
AUDIT number of drinks & psychosocial
consequences
 Pediatrics

#spinal muscular atrophy

-the bilateral lower brainstem motor nuclei and anterior horns degenerate, leading to
progressive, symmetric muscular weakness and a lower motor neuron-pattern of
dysfunction (eg, decreased tone, hyporeflexia, fasciculations, early-onset atrophy).

-Deficits typically progress during the course of months, which differentiates spinal
muscular atrophy from the acute descending motor weakness of botulism.
#C/F:
-The first sign of CP is often delayed gross motor milestones during infancy.
-Diagnosis is typically established by age 2 based on movement and tone subtypes
*tone subtypes:
1) spastic (ie, resistance to passive muscle stretch): MC ←

2) dyskinetic (ie, involuntary movement), or

3) ataxic (ie, incoordination).

 -

= .

Maternal serum alpha-fetoprotein screening 1) AFP

↑ MSAFP ↓ MSAFP -source: produced by the fetal yolk sac, liver, and
• Open neural tube • Aneuploidies (eg, gastrointestinal tract.
defects (eg, trisomy 18 & 21) -Maternal serum AFP (MSAFP) is measured at 15-20
anencephaly,
open spina bifida) weeks gestation (optimally at 16-18 weeks) to
• Ventral wall screen for fetal anomalie
defects (eg,
omphalocele,
gastroschisis) —> next step: An ultrasound should be performed
• Multiple gestation to evaluate the fetal anatomy.

Routine newborn care 2) CHD monitoring:

• Intramuscular vitamin K
-1/3rd of patients with critical CHD are asymptomatic
Preventi for the first few days of life (due to patent ductus
• Erythromycin eye ointment
ve
• Hepatitis B vaccine arteriosus) and may remain undetected during
• Newborn screen (metabolic/ hospitalization.
genetic disorders)
• Hyperbilirubinemia
• Hearing screen -Universal screen with pre-ductal (right arm) and
Screeni
ng
• Pre- & post-ductal pulse post-ductal (either leg) oxygen saturations allows
t
oximetry (congenital heart
disease)
early detection of critical CHD and decreases
• Hypoglycemia (select morbidity and mortality associated with delayed
populations) diagnosis.

#Acrocyanosis: refers to a blue-to-purple color of the acral extremities (hands, feet) and
around the mouth, which is commonly seen in healthy neonates.
-It typically resolves within the first few days of life.
1. Normal Development in Children

←
f- feeding a doll)

-
:

→ .

*
*
.

e-
 €
-

#Tracking midline:
-Around 3 months, babies can cross the midline with their eyes as they visually track an object
moved in an arc in front of them.

- By 6 months they begin reaching across the body with one hand, and around 8 months they cross
the midline with both hands by transferring objects from one hand to the other.

#Raking grasp:
-Raking grasp, wherein the fingers, but not including the thumb, do all the holding. Palmar grasp,
wherein the fingers squeeze against the palm, instead of against themselves as in the raking grasp.

-Routine well-child visits are an opportunity to assess growth and development, as delays
can signify a serious medical condition.
 Case clue
1) Normal growth velocity in infants:
-Infants grow rapidly during the first 6 months of life, gaining approximately 1 oz (30 g)
a day for the first 3 months and doubling their birth weight by age 4 months.
-By age 12 months, an infant's weight triples and height increases by 50%

2) Disorders of speech (eg, delayed articulation) and language (eg, receptive language
delay) are often associated with hearing loss.
—> The first step in management is a hearing test.

3) speech becomes 100% intelligible at 4 years of age.

4) physiologic weight loss in healthy newborn:

-healthy neonates normally lose up to 7% of their birth weight in the first 5 days of life
due to excretion of excess fluid acquired in utero and during labor.
-Birth weight should be regained by age 10-14 days.

-Mx: Frequent BF should be encouraged, and education about dehydration should be

provided.

5) average diaper rule:

-As a general rule,the number of wet diapers should = age in days for 1st week of life.
-For example, a 4-day-old neonate should have >4 wet diapers per day.
-After the first week, infants should have >6 wet diapers per day.

6) age Limit for rear-facing car seat:

-Children should remain in a rear-facing car seat as long as possible and transition to a
forward-facing car seat only once they surpass the height or weight limit of their
specific car seat, as determined by the manufacturer.

-There is no absolute height, weight, or age that determines the transition. At least upto
2
7) normal sexual behaviour in children:
-It is normal for curious young children to touch their own or other young children's
genitals, undress themselves or others, and make masturbatory movements.
-These behaviors are typically brief, intermittent, and distractible.
*abnormal:
—> Age-inappropriate knowledge or simulation of sexual acts, however, should raise
concern for possible abuse.

8) HIV neurocognitive disorder:

MRI :usually reveals diffuse brain atrophy, ventricular enlargement, and diffuse increased
white matter intensity
vs
-PML: well-delineated, asymmetric (rather than diffuse)/ focal white matter lesions

9) Wilson disease:
-New-onset psychosis in an adolescent with neurologic dysfunction (eg, tremor,
parkinsonism) raises concern for Wilson disease.
-Pathogenesis : defective hepatocellular copper transport, leading to copper accumulation
in the liver and basal ganglia.

10) physiologic GER reflux:

-onset: first 6 months of life (peak symptoms at age 4 months) with spit-up or vomiting of
partially digested breast milk or formula after feeding.
-physiologic GER does not cause discomfort while spitting up, infants continue to feed
eagerly, with normal weight gain—> "happy spitters."
Vs

#Signs of pathologic GER : irritability, poor feeding, and/or weight loss.

11) deliberate scald injuries

- burns with sharp lines of demarcation,
uniform depth, lack of splash marks,
- spared flexural creases.
11) anterior fontanel :closes typically occurs at age Down syndrome comorbidities
12-15 • Intellectual disability
Neurology
• Early-onset Alzheimer disease
12) Atlantoaxial instability in Down • Complete atrioventricular
-It is seen in >10% of patients with Down syndrome Cardiology
septal defect
• Ventricular septal defect
• Atrial septal defect
-weakness, gait changes, urinary/fecal
Gastroenterolog • Duodenal atresia
incontinence, and vertebrobasilar symptoms such y • Hirschsprung disease
as dizziness, vertigo, imbalance, and diplopia. • Hypothyroidism
Endocrinology • Type 1 diabetes mellitus
-UMN findings :spasticity, hyperreflexia, and a • Obesity

Babinski sign (ie, upgoing big toe) are often present. Hematology • Acute leukemia
Vs Rheumatology • Atlantoaxial instability
-
Normally hypotonia in Down syndrome
Neonatal sepsis 14) Neonatal sepsis:
-Because physical examination does not
• Group B Streptococcus
reliably distinguish among different types
• Escherichia coli
Etiology
• Listeria monocytogenes (age of serious neonatal bacterial infections
(eg, meningitis, bacteremia, urinary tract
I
<7 days)
infection), neonates with suspected
• Temperature instability (fever or
hypothermia)
infection urgently require a full evaluation.
• CNS signs (eg, lethargy,
irritability, apnea) -This includes a CBC with DC, URM, (CSF)
Clinical • Poor feeding analysis, and cultures of all 3 fluids (blood,
features • Respiratory distress (eg, urine, CSF).
tachypnea, grunting)
• Jaundice 15) Normal crying:
• Abnormal leukocyte count (high -Intermittent, <3 hr/day; consolable
or low); bandemia Vs
• Blood, urine & cerebrospinal
Diagnosis
fluid cultures #Colic: - crying for no apparent reaso
• Parenteral antibiotics • Inconsolable
Treatment • ≥3 hr/day (usually evening), ≥3 days/
(ampicillin & gentamicin)
week
• Healthy infant age <3 months
• cause of colic is may be related to gut immaturity or suboptimal feeding techniques
(eg, excessive swallowing of air)
#Mx:
-Soothing techniques should be reviewed and include using a pacifier; holding, rocking,
or swaddling the baby; and minimizing environmental stimuli (eg, dark room).
-Use of swings, carriers, and strollers can also be calming and allows parents to rest from
active soothing.

-adjusting feeding techniques (eg, upright feeding position in bottle-fed babies) may help
reduce air swallowing and relieve colic.
16) iron and Vit D supplements for preterm:
-Full-term infants are born with adequate iron stores to prevent anemia for the first 4-6
months of life regardless of dietary intake.
-Preterm infants are at significantly increased risk for iron deficiency anemia.

—> Iron supplementation should be started at birth in exclusively breastfed preterm

infants and continued until age 1 year.
—> All exclusively breastfed infants should also be started on daily 400 U vitamin D
supplementation until 1 yr

17) D/D of Hydrops fetalis:

-parvovirus: maternal infection; neg indirect Coombs
-Rh incompatibility: + indirect Coombs; mom must be alloimmunized
-Hb barts; Fetal aneuploidy, CVS abnormalities
#Mx:
-Fetal hydrops has a high risk of fetal demise, and affected patients require serial
ultrasounds and possible intrauterine transfusion.

18) Dehydration in infants:

1 Mild dehydration (3-5% volume loss) :
-H/O decreased intake or increased fluid loss with minimal or no clinical symptoms.

2 Moderate dehydration (6-9% volume loss)

-C/F: decreased skin turgor, dry mucus membranes, tachycardia, irritability, a delayed
capillary refill (2-3 seconds), and decreased urine output.

3 Severe dehydration (10-15% volume loss)

-C/F: cool, clammy skin, a delayed capillary refill (>3 seconds), cracked lips, dry mucous
membranes, sunken eyes, sunken fontanelle (if still present), tachycardia, lethargy, and
minimal or no urine output.

-Patients can present with hypotension and signs of shock when severely dehydrated.

#Mx:
1) mild to moderate dehydration: Oral rehydration therapy
2) moderate to severe dehydration: immediately resuscitated with intravenous fluids to
restore perfusion and prevent end organ damage.
—> Isotonic crystalloid is the only crystalloid solution recommended for intravenous fluid
resuscitation in children.

Resumption of postpartum menstruation

Formula feeding 8-14 weeks postpartum
Exclusively >6 months postpartum
breastfeeding (variable)
19) Small for gestational age infants
- a weight < 10th percentile for gestational age at birth
-complications : hypoxia, polycythemia, hypoglycemia, hypothermia, and hypocalcemia.
-
Vs
FGR: same but in Utero vs above was after birth

20) Microcephaly
- head circumference >2 SD below the mean (ie, <2nd percentile).

==> In a child with normal development and an otherwise normal examination,

the next step :measure parental HC to assess for benign familial microcephaly.

#Findings that are suggestive of benign microcephaly include:

• Absence of syndromic features

v
-

• Normal development .

-
• Mildly restricted HC with open fontanelle as closed 1 suggest genetic Ds

#Etiology :
- Microcephaly may signify :
1) an underlying genetic syndrome : microcephaly+ dysmorphic face
2) perinatal brain insult (eg, infection) : CMV
3) benign in many cases.

21) Fetal USG S/o Fetal Hydrops:

-fetus has ascites (eg, echolucent
-
abdominal fluid), skin edema, polyhydramnios
-
(single deepest pocket ≥8 cm), and placental thickening (reflecting intravillous edema)
consistent with hydrops fetalis (fetal hydrops); pleural and pericardial effusion.

23) universal screening newborns in USA

- hypothyroidism, phenylketonuria and galactosemia, CF

24) Macrocephaly
-HC >97th percentile.
-The condition is most likely benign (eg, familial) in a patient with normal development
and normal examination (eg, no syndromic features, no signs of increased ICP)

-Mx: reassurance and observation.

25) Older siblings rivalry

-Older siblings often react to the birth of a baby with regressive behavior (loss of toilet
training, separation anxiety) and sometimes aggression toward the infant.

-Parents should be counseled to spend one-on-one time with their older children to
reinforce their importance and sense of security.
 Pediatric neck masses
26) No front facing rear seat till
• Tract between foramen cecum & base of
anterior neck 2 minimum
Thyroglossal Midlin • Cystic, moves with swallowing or tongue No chocking round food like
duct cyst e protrusion
• Often presents after upper respiratory
tract infection
O
grapes, peanuts until 4

• Cystic mass with trapped epithelial 27) Intraosseous lines

Dermoid cyst Midline
debris -can be placed rapidly when
• Occurs along embryologic fusion planes
• No displacement with tongue protrusion
emergency access is necessary
• Tract may extend to the tonsillar fossa
and peripheral access cannot be
obtained.

E
(2nd branchial arch) or pyriform recess
Branchial cleft cyst Lateral (3rd branchial arch)
• Anterior to the sternocleidomastoid
muscle -Intraosseous access can be
Reactive • Firm, often tender performed with less required skill
Lateral
adenopathy • Multiple nodules and practice than central venous
Mycobacterium • Necrotic lymph node access.
avium Lateral • Violaceous
#
discoloration of skin .

lymphadenitis • Frequent fistula formation

27) atypical BHS:
Posteri
Cystic hygroma
or
• Dilated lymphatic vessels -Patients with atypical BHS (eg,
multiple daily episodes, duration
Breath-holding spell (BHS) vs seizure of apnea >1 min) / F/H/O cardiac
Cyanotic BHS Pallid BHS Seizure disease / sudden death
• Any age
Epidemiol
• Age 6 months to 2 years
• ↑ Risk with iron deficiency
• ↑ Risk with history
of febrile seizure or
O
should undergo an ECG to
ogy
anemia developmental
evaluate for arrhythmias (eg,
delay prolonged QT syndrome).
• Minor
Triggers
• Crying/ trauma • Often unprovoked -classic pallid BHS does not
frustration • Pain or • Sleep deprivation require cardiac evaluation.
fear
•Bradycardia,
apnea &
• Apnea & • LOC → tonic-
pallor →
cyanosis clonic
LOC
Clinical → LOC movements
• ± Brief (<5
features • Rapid • Prolonged (>5
min)
return to min) postictal
confusion
baseline -
confu
or
sleepiness

28)How many infections rates/year considered normal in healthy child??

-Healthy young children who attend day care or have older siblings may experience up to 12
respiratory infections per year.
-The majority of these infections are viral in origin and do not require antibiotics
-
29) Uric acid stains Normal in neonate :
- appearance of "pink stains" or "brick dust" in neonatal diapers represent uric acid
crystals.
-Uric acid excretion is especially high at birth and decreases until adolescence, when
adult levels are observed.
-Uric acid crystals are commonly seen during the first week as the mother’s milk is coming
Is
in, or in later months with the morning void after the infant begins to sleep through the
night.

30) bilirubin induced neurological dysfunction:

#Pathogenesis
-BIND occurs when bilirubin concentration dramatically rises (total bilirubin ≥30 mg/dL) and
-
exceeds the binding capacity of albumin.
-Unbound bilirubin crosses the blood-brain barrier and deposits in the basal ganglia and
brainstem nuclei (eg, oculomotor, auditory), causing neuronal damage.

÷
#C/F:
• Acute BIND typically presents with lethargy; tone abnormalities; and high-pitched,
inconsolable
-
crying. However, symptoms may be subtle or overlooked.

• Prolonged, unrecognized or untreated hyperbilirubinemia can lead to chronic BIND

(ie, kernicterus), typically presenting after early infancy with irreversible neurologic
damage.

-Common manifestations : hyperkinetic movements (eg, choreoathetosis, dystonia),

sensorineural
-
hearing loss, and abnormal eye movements (eg, upward gaze
palsy). Developmental delay (eg, inability to push up when prone at age 4
-

months) is also typical.

#Prevention of chronic :
-Serial examinations and/or bilirubin monitoring in the early neonatal period,
particularly in patients with risk factors, as well as early treatment of hyperbilirubinemia
(eg, phototherapy) can help prevent BIND.

#D/D:
1) Physiologic chorea of infancy refers to benign, chorea-like movements in normal
newborns. It resolves by age 8 months.
-Neither hearing loss nor gaze abnormalities are seen.

2) Autoimmune injury to the basal ganglia describes Sydenham chorea, a manifestation

of acute rheumatic fever (ARF)
31) Screening in children:
#Vision is evaluated at every well-child visit, as early detection of eye abnormalities can
prevent long-term vision loss.
-Formal visual acuity testing : starting at age 4 as well as in cooperative 3-year-olds

*referral:
-Visual acuity worse than 20/40 at age 4 or worse than 20/30 at age ≥5 should prompt
ophthalmologic evaluation for refractive errors.
-Additional indications for referral : pupillary asymmetry of ≥1 mm, nystagmus, and
ptosis or other conditions obstructing the visual field.

#Autism screening is routinely performed at ages 18 months and 2 years,

# depression screening starts at age 12.

34) Diff simple hand biting (normal behaviour)

from lesch Nyhan causing permanent disfigurement

35) central cyanosis: typically indicates low arterial oxygen saturation

-peripheral cyanosis have normal arterial oxygen saturation and increased oxygen
extraction due to sluggish blood flow through the capillaries.
 33) #infant dyschezia
*Classic clue: This otherwise healthy infant with straining and crying prior to passing
normal soft stool most likely has infant dyschezia, a common, benign functional stooling
disorder.

#C/F:
-crying, turning red in the face, and straining for greater than 10 minutes, followed by
passage of a soft, nonbloody stool.
-Infants are otherwise well-appearing with no abnormalities on examination.

#Mx:
*Prognosis:As the infant's gut nervous system matures, defecation becomes more
coordinated, and infant dyschezia resolves spontaneously, typically by age 9
months.
Benign neonatal rashes
-Mx: education and reassurance alone. Diagnosis Onset Clinical features Management/resolution
Genetic disorders associated with autism • Pustules with
Birth to
Erythema erythematous • Observation
Syndro toxicum
age
base on trunk • Resolves within a
Etiology Key features* 3
me neonatorum & proximal week
days
extremities
Fragile • More severe in boys
• Trinucleotide • Firm, white • Observation
X • Dysmorphic facies (eg, long
repeat in FMR1 Milia • Birth papules on • Resolves within a
syndro face, large ears)
gene face month
me • Macroorchidism
Any
• Almost exclusively in girls age, • Avoid overheating
Rett Erythematous,
• MECP2 • Developmental regression but (eg, cool
syndro papular rash
mutation • Loss of purposeful hand Miliaria not
on occluded &
environment, thin/
me rubra pres cotton clothing)
movements intertriginous
ent • If severe, topical
areas
Tuberou at corticosteroid
• Dermatologic findings (eg, ash- birth
s • TSC1/2
leaf spots)
sclerosi mutation •
• Seizures
s Nonerythemato
us pustules →
• Dysmorphic facies (eg, evolve into • Observation
Down
upslanting palpebral fissures, Neonatal hyperpigmente • Pustules resolve
syndro • Trisomy 21 pustular Birth d macules with within days
epicanthal folds)
me melanosis collarette of • Hyperpigmentation
• Congenital heart disease
scale may last months
Prader- • Diffuse, may
• Loss of paternal involve palms
Willi • Obesity/hyperphagia
allele on Cr & soles
syndro • Hypogonadism
15q11-q13
me Around • Erythematous • Observation
Neonatal age papules & • Resolves in weeks
Angelm • Loss of • Microcephaly cephalic 3 pustules on to months
an maternal allele • Ataxic gait/tremors pustulosis wee face & scalp • If severe, topical
syndro on Cr 15q11- • Happy demeanor, inappropriate ks only corticosteroid
me q13 laughter

36) Obesity in children:

-In children, overweight : BMI at or above the 85th percentile and below the 95th
percentile for age and gender,
-while obesity : BMI at or above the 95th percentile.
-Common causes of childhood obesity : consuming an excessive amount of total calories,
a diet rich in unhealthy, calorie-rich foods, and a lack of sufficient exercise.
37) assistance with the initiation of breathing
-The initiation of breathing following delivery is crucial for the newborn. A substantial portion
of neonates require assistance with the initiation of breathing.
*
-Initial, universal steps after delivery include an assessment of the newborn's heart and
respiratory rates, muscle tone, reflexes, and color, and immediate warming, drying, and
tactile stimulation, all of which are helpful for stimulating spontaneous respirations.

#Mx:
-Neonates who fail to respond to gentle tactile stimulation should be immediately supported
with more invasive support techniques, such as bag and mask ventilation or endotracheal
intubation.
—> Tactile stimulation and oxygen therapy are noninvasive and are therefore an appropriate
initial step.

38) spinal dysraphism:

• Male newborn who has lower limb paralysis and numbness with a full bladder, most
consistent with a spinal cord injury affecting the lower extremities
• Spinal dysraphism = Type of neural tube defect
Vs
• Cerebral palsy: Delayed motor milestones, comorbid seizures/intellectual disability,
abnormal muscle tone
• Muscular dystrophy: Waddling gait, hip weakness, Gower sign in a toddler

39) Walking is a gross motor milestone that normally occurs at age 9-16 months. Evaluation
and treatment should be considered if a child is not walking by age 16 months or delays
are present in multiple developmental categories.

40) goats milk: folate deficiency megaloblastic anemia

** cows milk and honey C/I at <1 yr

41) ideal formula feed for infant with NEC: amino acid containing cz of loss of functional gut
 Surgery

# airway Mx in neck Hematoma

-Cricothyroidotomy and tracheostomy may be indicated in cases of airway compromise in
which endotracheal intubation is unsuccessful.

-However, in cases of an expanding, arterial neck hematoma, these maneuvers may be

difficult or impossible depending on the location of the hematoma. So do ET
-Additionally, inadvertent decompression of an arterial hematoma in the neck may result in
exsanguination along with additional airway compromise via hemorrhage into the newly
created ostomy.
 Case clue
1) Care of an amputated part eg finger
-begin with gentle removal (eg, saline irrigation) of gross contamination debris).
-Following this, the part should be wrapped in sterile saline-moistened gauze and
sealed in a plastic bag.
-The bag should be then placed in a container of ice water to be transported

2) Ideal most fluid for hypovolemia:

-Lactated Ringer solution, a balanced fluid, is preferred because it contains near-
physiologic levels of electrolytes and includes a buffer that helps correct acidosis and
-7
maintain normal blood pH. -

#Y NS not ideal??
-Normal saline is associated with the development of hyperchloremic metabolic
acidosis as it has supra physiological level of Chloride

#Indication of Hypotonic fluid??

-MOA: Dextrose 5% in water is initially a slightly hypotonic crystalloid solution that
quickly becomes markedly hypotonic with the metabolism of dextrose;
—> Indication: free-water deficit (ie, hypernatremia).

3) Hemorrhagic shock:
-the MC type of shock in trauma patients.
—> Areas where large amounts of blood can be lost (or hidden) are "the
floor" (external bleeding) "and 4 more": chest, abdomen, pelvis/retroperitoneum,
and thigh.

*How to reach the cause of bleeding:

-if patient has no evidence of external bleeding or major hemorrhage into the chest
(bilateral breath sounds), abdomen (nondistended, soft, no intraperitoneal free fluid), or
thighs (normal muscle tone).
—> Therefore, pelvic/retroperitoneal bleeding should be suspected.
6) Superficial wound dehiscence
-separation of the epidermis and/or subcutaneous tissue with an intact fascia,
- Mx: conservatively with regular dressing changes.
Vs
-deep (fascial) dehiscence: involves the fascia and is a surgical emergency
Risk of strangulation and Bowel evisceration

7) Platelets are typically transfused for a platelet count <10,000/mm3 (risk of

spontaneous hemorrhage)/ platelet count <50,000/mm3 with active bleeding.

—>Cryoprecipitate is considered with low fibrinogen (eg, <100 mg/dL).

8) Massive transfusion protocols, developed to standardize resuscitation, are likely

required in patients with ≥2 of the following (>3 units in 30 min)

• Penetrating mechanism of injury

• Positive focused assessment with sonography in trauma examination (ie,
evidence of hemorrhage)
• SBP ≤90 mm Hg
• P ≥120/min

9) Blood products should be administered early in patients with signs of hemorrhagic

shock.
—> They should be administered in a ratio of 1:1:1 (fresh frozen plasma/packed red
blood cells/platelets) to reduce coagulopathy, a leading contributor to mortality in
trauma patients.

10) BT should be initiated early in patients with hemorrhagic shock.

-Group O, Rh D-negative blood (universal donor) should be transfused while waiting for
type-specific blood to be available.

11) In acutely injured trauma patients, excess crystalloid use exacerbates the lethal,
trauma-induced triad of hypothermia, acidosis, and coagulopathy, increasing
mortality.
-Research supports limited crystalloid administration (eg, 1 L) in patients with
hemorrhagic shock when blood is not immediately available.

12)Central venous catheter:

-ideal placement of a tip: in the lower superior vena cava.
-To avoid myocardial perforation, tip should be proximal to either cardiac silhouette /
the angle between the trachea and the right mainstem bronchus
 13) Catheter (central line)-associated infection
-Coagulase-negative staphylococci (eg, Staphylococcus epidermidis) are a constituent
of normal skin flora, and are also the most frequent cause of bloodstream infection in
patients with intravascular devices.

#Factors that favor infection over contamination include:

• Systemic signs, such as fever, hypotension, or leukocytosis
• Erythema and tenderness at the catheter entry site (the absence of local signs does not
rule out an infection)
• Culture growth within 48 hours and in both aerobic and anaerobic bottles
• Two or more blood culture samples with the same organism and drug susceptibility
Vs

# surgical site infection SSI: occurs in same time line as catheter related infection but the
wound is red, dirty

14) Abdominal aortic injuries due to BAT are rare (<1%).

-Many patients with traumatic aortic injury die from exsanguination before reaching the
hospital.
—> Those who survive (because bleeding has been contained within the
retroperitoneum) typically would not have a large amount of intraperitoneal free fluid
on FAST.
15) Indications for lower extremity
amputation include:
Rib fracture location & associated injuries • Critical limb ischemia without the
Location Associated injuries
ability, either anatomically or due to
comorbidity contraindications, to
Subclavian vessels, brachial plexus,
Ribs 1-3
mediastinal vessels (eg, aorta)
perform revascularization
• Unsalvageable lower extremity soft
Ribs 3-6 Cardiovascular
tissue (eg, trauma, gangrene,
Intraabdominal: liver (right), spleen (left), kidney frostbite)
Ribs 9-12
(posterior ribs 11 & 12)
• Life-threatening infection (eg,
Any level Pulmonary infected gangrene, necrotizing soft-
tissue infection)
16) An avulsed permanent tooth
-should be reimplanted asap within 15 minutes to 1 hour to increase the likelihood of tooth
survival
-The tooth can be briefly stored in cold milk / saliva and manually reimplanted by
splinting adjacent tooth after gentle rinsing of the tooth and socket with normal
saline.

17) Chronic critical limb ischemia :pain at rest, nonhealing wounds and gangrene. Ischemic
rest pain is typically described as a burning pain in the arch or distal foot that occurs while
the patient is recumbent but is relieved when the patient returns to a position in which the
feet are dependent.
-ABI 0.4 or less, an ankle systolic pressure of 50 mm Hg or less, or a toe systolic pressure
of 30 mm Hg or less. Intervention may include conservative therapy, revascularization or
17) #diaphragmatic paralysis post cervical trauma:
1) Immediate diaphragmatic paralysis:
-After a high cervical spine injury, patients are at risk for immediate diaphragmatic paralysis
because the diaphragm is innervated by cervical nerve roots from C3-C5.
Vs
2) delayed diaphragmatic paralysis:
-However, if the spinal cord is injured lower than C5, a delayed diaphragmatic paralysis
may occur due to ascending edema.

#Mx of trauma:
-As in all trauma patients, primary survey includes assessment of the airway (in addition
to breathing and circulation).

*intubation of choice in cervical trauma:

-In patients with impending respiratory failure, the best next step in management is
orotracheal intubation, even with evidence of an unstable cervical spine injury, because
this procedure can be rapidly performed and is relatively noncomplex.

- Typically, this is done with manual stabilization of the cervical spine to minimize neck
movement during intubation.

18) Cx of laparoscopy:
-Laparoscopic intraabdominal surgery (eg, cholecystectomy) requires insufflation of CO2
into the abdomen to create space for surgical maneuvering and visibility.

-The increased intraabdominal pressure stimulates stretch receptors on the

peritoneum —>that respond by triggering an increase in vagal tone—> severe
bradycardia, atrioventricular block, and sometimes asystole.

- The increased intraabdominal pressure can also cause a mechanical increase in systemic vascular
resistance leading to elevations in blood pressure.
- Increased intraabdominal pressure —> caval compression would lead to decreased venous return with
a reduction in cardiac output and a reflexive increase in heart rate.

#Other Possible Complications :

1) CO2 gas embolization :
- a rare complication of CO2 insufflation, usually resulting from inadvertent insertion of
the insufflation needle directly into an artery, vein, or organ (eg, liver).

- Affected patients typically develop end-organ infarction (arterial embolism) or

hypotension and obstructive shock (venous embolism).

2) CO2 systemic absorption :

- Systemic absorption of intraabdominal CO2 can occur during laparoscopic procedures,
leading to an increase in blood PaCO2 —>> causes peripheral vasodilation with a
reflexive increase in heart rate.
19) burn Mx:
-After initial stabilization, burn patients who require aggressive fluid resuscitation (eg,
due to burns covering a large total body surface area) should undergo urethral
catheterization as soon as possible.

*further steps.
-Following urethral catherization, treatment of this patient's burns involves copious
irrigation and gentle gauze debridement of affected areas.
-This is followed by application of topical antimicrobial agents (eg, topical antibiotic) and
nonstick dressings

20) Postoperative incisional pain in the absence of signs of infection, fluid

collection, and wound dehiscence is managed with observation and reassurance.

—> mild induration and diffuse tenderness to deep palpation over her incision are
consistent with normal healing.
21) Use of CVC (venous) :
Antibiotics for SSI prevention
-administration of critical care
Wound medications (eg, pressors, hypertonic
Procedure Typical Antibiotic
classificatio saline) and
examples contaminants prophylaxis
n
-in the setting of difficult vascular access/
Skin flora: 1st-line: -need for long-term medication (eg,
Cardiac, Streptococcus, cefazolin
chemotherapy).
neurological, Staphylococcus
Clean* - for Hemodynamic monitoring.
orthopedic, aureus & Alternative:
vascular coagulase-negative vancomycin
staphylococci clindamycin #Access sites for CVC :
Based on - The preferred points of central venous
surgical site, access are
Gastrointestinal, Skin flora, gram-
broader 1) internal jugular vein (typically by
Clean- genitourinary, negative bacilli,
coverage ultrasound guidance) or
contaminate gynecologic/ enterococci &
often
d** obstetric, head & endogenous flora of
indicated: i
2) subclavian vein (typically by
neck, thoracic the viscus anatomic landmark guidance).
pro/metro/
Piptaz
*Uninfected, uninflamed, the viscus is not entered.
**Viscus (eg, alimentary, genitourinary, respiratory systems) is
entered under controlled conditions.
SSI = surgical site infection.
 General

#Transillumination +Ve:
• Hydrocephalus in newborns or infants
• Hydrocele in males
• Breast lesions or cysts in females General test-taking strategy: When asked to
- pneumothorax in newborn mostly provide best initial diagnostic test, often a
-ganglion cyst non-invasive answer is the correct answer
58 SEC TION II BIOCHEMISTRY `B̀IOCHEMISTRY—GENETICS

Disorders of imprinting Imprinting—one gene copy is silenced by methylation, and only the other copy is expressed
Ž parent-of-origin effects.
Prader-Willi syndrome Angelman syndrome
WHICH GENE IS SILENT? Maternally derived genes are silenced Paternally derived UBE3A is silenced
Disease occurs when the paternal allele is deleted Disease occurs when the maternal allele is
or mutated deleted or mutated
SIGNS AND SYMPTOMS Hyperphagia, obesity, intellectual disability, Seizures, Ataxia, severe Intellectual disability,
hypogonadism, hypotonia inappropriate Laughter
Set SAIL for Angel Island
CHROMOSOMES INVOLVED Chromosome 15 of paternal origin UBE3A on maternal copy of chromosome 15
NOTES 25% of cases are due to maternal uniparental 5% of cases are due to paternal uniparental
disomy disomy
POP: Prader-Willi, Obesity/overeating, Paternal MAMAS: Maternal allele deleted, Angelman
allele deleted syndrome, Mood, Ataxia, Seizures
P = Paternal
M = Maternal
Normal Mutation
Active gene
P M P M
Silenced gene (imprinting)
Gene deletion/mutation

Prader-Willi syndrome

Angelman syndrome

¥-0
'

e-
-
1) black widow spider bite:
Case clue
-more pronounced local and systemic manifestations due to effects of the toxin
compared to brown recluse bite

#C/F:
-muscle pain (a prominent finding); abdominal rigidity (like a surgical abdomen);
muscle cramps (>60%).
Vs
2) Loxosceles reclusa (brown recluse) spider bite
-initially have a small, red papule that can progress to form a larger necrotic wound
(loxoscelism).
-Mx: Most cases will resolve with the application of cold packs and local wound care.
-
-
3) Heat exhaustion:
-hyperthermia (typically ≤40 C [104 F])
-weakness, dizziness, profuse sweating, headache, and/or nausea.
==> Mentation remains normal, unlike in exertional heat stroke.
-Mx: cooling (eg, cool water shower) and oral hydration with salt-containing fluids.
Vs
# Rx differs in exertional and non exertional heat stroke:
-in exertional heat stroke [eg, following strenuous exercise in a hot, humid
4) Heat stroke:
environment]:ice water immersion
-T > 104 F/ 40C
-altered mentation -Non exertional stroke: evaporative techniques.
5) types of heat stroke:
1) nonexertional heat stroke
-which typically affects individuals at the extremes of age who are incapable of obtaining
adequate fluids and removing themselves from a hot environment,

2) Exertional heatstroke :
-occurs most commonly in those exposed to hot/humid environments while performing
extreme physical activity (eg, landscaping,).

6) a) Type 1 decompression sickness is relatively mild

• "the bends": painful joints that are nontender to palpation and have normal range of
motion. 
• Cutaneous :pruritus and erythema.
• Lymphatic involvement lymphadenopathy and localized edema.
Vs
B) Type 2 decompression sickness is severe
- CNS "the staggers": ataxia, dizziness, visual disturbance, and spinal cord involvement
(eg, weakness, paresthesia, loss of bladder control). 
-RS ("the chokes") : rare ; obstructive shock due to venous gas embolism occluding the
pulmonary vasculature.
#Mx of decompression sickness:
-Intravenous fluids & 100% oxygen
-Hyperbaric oxygen therapy as soon as possible
•

7) high altitude sickness

A) AMS acute mountain sickness:
-Onset: within the first 24 hours of arrival

I
-C/F: mild symptoms of fatigue, headache, and disturbed sleep.
-common and generally resolves within a few days with / out Rx (eg, oxygen,
acetazolamide).

b) HACE high altitude cerebral edema: end-stage AMS

- onset: 12 hours - 3 days after AMS onset.
-C/F: encephalopathic symptoms (eg, drowsiness, confusion, ataxia)
-If left untreated, coma and death due to brain herniation
-Rx: Dexamethasone

C) HAPE high-altitude pulmonary edema

◦ Uneven hypoxic vasoconstriction
◦ Dyspnea, cough ± hemoptysis, respiratory distress

8) large local reactions: exaggerated local allergic responses called large local reactions,
Reactions to Hymenoptera envenomation range from
1) mild (1-5 cm or erythema and swelling at the sting site) to
2) severe (anaphylaxis, toxic reactions), with approximately 10% of individuals
developing LLR.

9) Exercise-associated postural hypotension

-characterized by collapse (with no loss of consciousness)/ inability to walk
immediately after completion of exercise with a sensation of lightheadedness or
dizziness due to abrupt dec in CO as the skeletal muscle suddenly stops to
contract
-Rx: trendelenburg position, hydration
-vs other causes of exercise-associated collapse (eg, exertional heat stroke (>104F) ,
sweat-induced hyponatremia): unalert with abnormal mental status.

10) pitting vs non-pitting oedema:

1) protein rich: non pitting
-Congenital lymphedema typically presents at birth with edema that is generally
nonpitting due to the high protein content in the interstitial fluid.

2) protein poor: pitting

-In contrast, the pitting edema seen with liver failure (hypoalbuminemia), nephrotic
syndrome (proteinuria), and congestive heart failure (ventricular hypocontractility) is
caused by low protein concentration in the interstitial fluid
11) CHARGE syndrome
-Coloboma, Heart defects, Atresia choanae, Retardation of growth, and
Genitourinary and Ear abnormalities.

12) chronic lymphedema:

-Early: soft skin, pitting edema
-Late: firm, dry & thickened skin; nonpitting edema
-Inability to lift the skin on the dorsum of the second toe (positive Stemmer sign) is highly
specific for lymphedema.

13) Acute lymphangitis

- a common complication of injection drug use due to inoculation of skin flora into
subcutaneous tissue.
-C/F: generally marked by tender red streaks up the lymphatic channels with painful,
swollen, erythematous regional lymphadenitis

14) Necrotizing myositis

-severe systemic toxicity (eg, high fever, hypotension, toxic appearance) and rapidly
progressive skin changes (eg, discoloration, gangrene).

15) iliofemoral deep venous thrombosis:

-U/L leg edema, warmth, and erythema with evidence of dilated superficial veins and
increased calf/thigh diameter on examination.

16) benefits of enteral nutrition <48 hrs: EN

-Route: NG/OG tube
-reduction in infections (eg, pneumonia) and mortality.
-EN may also help maintain gut integrity, preventing atrophy of gut- and mucosa-
associated lymphoid tissue

17) Total parenteral nutrition (TPN)

-Route: central venous catheter because the high osmotic load is damaging to peripheral
veins.
-Indications: used only for patients with contraindications to EN (eg, intestinal
discontinuity, prolonged ileus)
-Disadvantage: early initiation may increase the risk of infection (eg, central line–
associated bloodstream infection) and lead to prolonged ICU and hospital stays.
18) Amyloidosis
-Etiology: complication of a chronic inflammatory condition (eg, chronic infections,
inflammatory bowel disease, rheumatoid arthritis)
-C/F: NS; asymptomatic proteinuria; Hepato-megaly; neuropathy; macroglossia; bleeding
diathessi; waxy skin thickening

- Treatment :Rx of the underlying inflammatory disease; colchicine for prevention and Rx

19) #Number of alcohol drinks per day that have adverse effects :
—> National Institute on Alcohol Abuse and Alcoholism has found evidence of negative
health effects for
a) women of all ages and men age ≥65 who consume >7 drinks in a week or >3 in a
day b)men age <65, the cutoffs are >14 drinks in a week or >4 drinks in a day).

20) #How alcohol affects sleep..?

—> Individuals with alcohol use disorder frequently seek primary care due to sleep
disturbance and/or anxiety symptoms from mild withdrawal.

—> These individuals may use alcohol to fall asleep, but as the blood alcohol level
drops, CNS hyperarousal occurs and results in multiple awakenings.

21) cancer Rx:

a) Adjuvant therapy :Rx given in addition to standard therapy.

b) Consolidation therapy :given after induction therapy with multidrug regimens to

further reduce tumor burden.

c) Induction therapy: an initial dose of treatment to rapidly kill tumor cells and send the
patient into remission (<5% tumor burden).

d) Maintenance therapy :usually given after induction and consolidation therapies (or
→
initial standard therapy) to kill any residual tumor cells and keep the patient in remission.

e) Neoadjuvant therapy :Rx given before the standard therapy for a particular disease.
Preparation for bariatric surgery 22) indications of weight loss meds:
• BMI ≥40 kg/m2 - BMI ≥30 kg/m2 (obese) and BMI of 25-29.9 kg/
• BMI ≥35 kg/m2 with serious m2 (overweight) with weight-related
Indication comorbidity (eg, T2DM, complications.
s hypertension, OSA)
• BMI ≥30 kg/m2 with resistant
T2DM or metabolic syndrome #Primary options: orlistat, lorcaserin,
• Review previous attempts at naltrexone/bupropion, phentermine/topiramate,
weight loss, diet, exercise habits
Intake
• Review psychiatric history, coping
and liraglutide;
assessme
skills, readiness to change
nt
• Review risk for cardiac (eg, CAD)
and pulmonary (eg, OSA) disease
 23) Burn sepsis:
-Evidence of organ hypoperfusion and/or
dysfunction, such as oliguria or new-onset
enteral feeding intolerance (eg, high gastric
residual volumes) after a period of tolerance,

-which may reflect splanchnic hypoperfusion

leading to gastrointestinal hypomotility and
ileus (distended, tympanitic abdomen;
decreased bowel sounds)

24) When to suspect Burns Wound Infection (BWI) :

-when there is a change in wound appearance, loss of a viable skin graft, or
development of infectious features (eg, erythema) in noninjured surrounding tissue.

#Types of BWI:
a) Invasive wound infections : systemic manifestations (eg, confusion, tachycardia) of
infection + on biopsy, show microbial invasion into unburned tissue.

#Rx : Ab covering Pseudomonas aeruginosa and Staphylococcus aureus.

piperacillin-tazobactam /carbapenem (eg, meropenem): Pseudomonas
+vancomycin, :MRSA.

b) Noninvasive wound infections : minimal / no systemic symptoms and no microbial

invasion into surrounding healthy tissue.
-Rx : Narrower-spectrum Ab eg, cefazolin, clindamycin that target gram+skin
bacteria.

25) Vitamin C deficiency

- ecchymosis, petechiae, poor wound healing, perifollicular hemorrhage, coiled hairs,
and gingivitis;
-platelet count, prothrombin time, and partial thromboplastin time :normal.

26) Nutrient deficiency in CF:

-Patients with cystic fibrosis are at risk for fat-soluble vitamin (ie, A, D, E, and K)
deficiency due to fat malabsorption from pancreatic insufficiency.
-Vitamin K deficiency causes easy bruising and mucosal bleeding.
 Drugs/supplements that affect warfarin 27) Drug interaction with warfarin :
metabolism (selected) 1) Foods containing high levels of
CYP450 • Antibiotics (eg, vitamin K, such as leafy green
Inhibitors metronidazole, macrolides) vegetables (eg, spinach, Brussels
↑ Warfarin • Azole antifungals sprouts),
effect • Amiodarone —> decreases the therapeutic effect of
(↑ bleeding • Cimetidine warfarin and leads to reduction in
risk) • Grapefruit juice therapeutic efficacy (eg, subtherapeutic
INR)
CYP450
• Carbamazepine
Inducers 2) Acetaminophen use (>2-3 grams/
• Phenytoin
↓ Warfarin day) can prolong INR in those on
• Phenobarbital
effect
• Rifampin warfarin due to interruption of vitamin
(↓ in
• St. John's wort K recycling in the liver.
efficacy)

3) antibiotics reduce bacterial vitamin K production in the gut, which can raise INR (lower
vitamin K availability)

27) Although cervical lymphadenopathy is common with infectious processes, a large

supraclavicular node, is highly suspicious for malignancy.

28) hereditary hemorrhagic telangiectasia

-site:AVMs tend to occur in the mucous membranes, skin, and gastrointestinal tract, but
may also be present in the liver, brain, and lung.
#Pulm AVM:
-AVMs in the lungs can shunt blood from the right to the left side of the heart, causing
chronic hypoxemia, digital clubbing, and a reactive polycythemia.
-can also present as massive, sometimes fatal, hemoptysis.

29) all patients with HIV should receive vaccinations for

-hepatitis A, hepatitis B, and zoster (unless they have documented immunity);
immunization for Meningococcus and Streptococcus pneumoniae should also be given.

31) United States Preventive Services Task Force, recommend one-time DEXA screening
for osteoporosis in
—>all women age >65+ women age <65 who have an equivalent risk of osteoporotic
fracture.
32) Pap tests for cervical cancer screening :
- recommended every 3 years in women age 21-65 /
-every 5 years in women age 30-65 if combined with testing for human papillomavirus

#Not required:
-for women age >65 / for those who have had their cervix removed for a reason other than
cancer.

33) Annual low-dose chest CT

- patients age 50-80 with a >20 pack-year smoking history (who are currently smoking
or quit within the last 15 years) has been shown to reduce lung cancer mortality
35) Beckwith-Wiedemann syndrome (BWS)
WAGR syndrome/11p deletion syndrome -macrosomia, macroglossia, hemihyperplasia,
Pathogene • Gene deletion on chromosome umbilical hernia/omphalocele, and neonatal
sis 11p13 hypoglycemia.
• Wilms tumor
• Aniridia #CA risk and screening:
Clinical
features
• -Wilms tumor and hepatoblastoma,
Genitourinary abnormalities
• Intellectual disability -Abdominal USG and AFP: every 3 months from
(previously MR)
birth to age 4
- renal USG: every 3 months from age 4-8.
36) effect of alcohol on CNS development:
-MOA: negatively impacts the fetal brain via inhibition of NMDA and hyperactivation of
GABA receptors.
-Deficits in development of the corpus callosum, cerebellum, and basal ganglia result in
abnormal reflexes, tone—> difficulty with writing and clumsiness.
-A decrease in the volume of the frontal lobe and dysfunction of the amygdala result in
deficits in executive functioning, impulse control, and emotion regulation.

-Other Sx:(ADHD) cognitive impairment, seizures, learning disabilities, and social skill
deficits.

37) Hypoxic-ischemic brain injury (eg, drowning)

-can lead to widespread neuronal cell death, cerebral edema, and increased intracranial
pressure (ICP). Severely increased ICP can cause Cushing triad,

38) Neimann pick Ds:

-hepatosplenomegaly; areflexia, cherry red macula
Vs
#tay Sach Ds:
-no hepatosplenomegaly; hypereflexia; cherry red macula
38) catheterisation in prolonged ICU admission:
#Y radial artery preferred??
- Adv: due to its accessibility (ie, superficial location) and the typical presence of
collateral circulation (ie, ulnar artery) to the hand.

# benefits of brachial artery catheterisation:

-increased reliability (ie, lower occlusion rates) and accuracy (ie, closer correlation with
central aortic pressure)
- if there are technical difficulties with radial artery cannulation.

#disadvantages of brachial artery catheterisation :

-Median nerve injury -resolves on its own
-thrombosis—> acute limb ischaemia leading to cool hands

39) balanced resuscitation :

1) Limiting use of crystalloids (eg, ≤1 L), which dilute existing coagulation (eg, clotting)
factors and platelets, thereby increasing coagulopathy; non anion met acidosis; hypothermia
by low room temperature than body temp

2) Replacing lost intravascular volume with blood products (rather than crystalloids),
transfused in a ratio similar to that of whole blood (eg, 1:1:1 ratio of packed red blood cells/
plasma/platelets)

3) Permitting hypotension (ie, permissive hypotension) to limit ongoing hemorrhage and/

or prevent clot disruption and rebleeding

-With balanced resuscitation, blood products are administered only as needed to maintain a
blood pressure (eg, mean arterial pressure ~65 mm Hg) sufficient for tissue perfusion, until
definitive hemorrhage control (eg, surgical intervention) can be achieved.

41) Mx of osteoblastic vertebral mets :

-Osteoblastic metastasis in the axial skeleton is the most common type of metastasis in patients with
advanced prostate cancer and often causes pain and functional impairment.
-External beam radiotherapy is the treatment of choice for patients with symptomatic, localized
skeletal metastasis that is limited to one or a few sites, such as this patient. It provides rapid pain
relief and improves mobility.
-In addition, denosumab or zoledronic acid can be administered as an adjunct to reduce the risk of
complications (e.g., pathologic fracture, spinal cord compression).
41) Delayed emergence from anesthesia
- defined as the failure to return to consciousness within the expected window of the last
administration of an anesthetic or adjuvant agent (typically 30-60 minutes).
#Etio: →
• Drug effect: Preoperative drug ingestion (eg, opiates, benzodiazepines, illicit drugs,
anticholinergic drugs, antihistamines) may potentiate anesthetic effects.
• Metabolic disorder: hyper- or hypoglycemia, hyper- or hypothermia, hyponatremia,
and liver disease.
• Neurologic disorder: Intraoperative stroke, seizure (or postictal state), or elevation of
intracranial pressure can cause prolonged alterations in mental status.
#Mx: includes ventilatory support (eg, bag and mask, reintubation); reversal agents (eg,
naloxone) may also be indicated.

42) common mistakes in screening cancer:

-Although smoking and family history of bladder cancer can indicate increased risk,
bladder cancer screening does not provide conclusive benefit.

* lung cancer screening only for–80 years with >20 pack yr history.... not young age
with >20 pack year history
-18 yrs of 1/2 pack yr smoking= 9 years of pack smoking

43) Clinical indicators of thermal and smoke inhalation/ upper airway injury include:
• Burns on the face
• Singeing of the eyebrows
• Oropharyngeal inflammation
• Blistering or carbon deposits
• Carbonaceous sputum
• Stridor
• Carboxyhemoglobin level >10%
• History of confinement in a burning building.

==> The presence of ≥1 of these indicators warrants early intubation to prevent upper
airway obstruction by edema.

44) Wilms tumor: flank mass; hematuria, HT ; 2-5 yrs

Vs
Neuroblastoma: arises anywhere in SANS; common as abd mass in adrenal gland; <2
yrs; no hematuria

45) 1st step in drowning Mx: RS support

-Drowned patients often require respiratory support to correct hypoxia.

* indications of invasive ventilation in drowning:

-In patients who are unable to protect their airway (somnolent) or who are hypoxic
despite supplemental oxygen, intubation with mechanical ventilation should be
performed.
46) VHL:
• Cerebellar & retinal hemangioblastomas
• Pheochromocytoma; RCC(clear cell subtype)

47) Refeeding syndrome

-Pathogenesis: reintroduction of carbohydrates (ie, tube feeding) leads to increased
insulin secretion —> This stimulates the cellular uptake of electrolytes (ie, phosphate,
potassium, magnesium) and increases phosphate utilization during glycolysis (eg,
formation of ATP, 2-3 diphosphoglycerate)

-C/F: muscle weakness (which can include the muscles of respiration), arrhythmias,
congestive heart failure, rhabdomyolysis, and neurologic dysfunction (eg, paresthesia,
seizure).

48) Poor prognostic factors for drowning: #Cx:

• Submersion time >5 min • ARDS
• Delay in initiation of cardiopulmonary resuscitation • Cerebral edema
• Prolonged resuscitative efforts • Arrhythmia
• Age >14; Arterial blood pH <7.1
50) High-voltage electrical
Intravenous fluids injuries
Tonicity Fluid type Clinical use
-frequently cause more severe
damage to internal structures (eg,
0.9% (normal) saline Volume resuscitation
(eg, hypovolemia,
muscle) than external structures
Isotoni
Lactated Ringer solution shock) (eg, skin).
c Volume replacement,
Albumin (5% or 25%)* treatment of -Cx:
SBP or HRS Skeletal muscle necrosis is a
Dextrose 5% in water** frequent complication that can result
Free water deficit in
Hypoto 0.45% (half-normal) saline
nic acute compartment syndrome,
Dextrose 5% in 0.45% (half- Maintenance
normal) saline** hydration rhabdomyolysis, and
heme pigment–induced AKI
Hyperto Severe, symptomatic
3% (hypertonic) saline
nic hyponatremia
# Pathogenesis:
HRS = hepatorenal syndrome; SBP = spontaneous bacterial
peritonitis. -Because bone (with its high
*Colloid solution; all other listed fluid types are crystalloid resistance to electrical current)
solutions. generates the most heat as
**Dextrose 5% in water (initially slightly hypotonic) & current passes through the body,
dextrose 5% in 0.45% saline (initially hypertonic) become
markedly hypotonic due to metabolism of glucose.
thermal injury to internal tissues
surrounding the bone (eg, skeletal
muscle)
 Clinical manifestations of trace mineral
deficiencies 52) Copper deficiency
Chromiu • Impaired glucose control in -Etio: typically occurs in patients with a history of
m diabetes
gastric surgery (eg, bariatric), chronic malabsorption
• Brittle hair (eg, inflammatory bowel disease), or excessive zinc
• Skin depigmentation
• Neurologic dysfunction (eg, ingestion.
Copper ataxia, peripheral -Sx: slowly progressive myeloneuropathy similar to that
neuropathy)
• Anemia: microcytic hypo of vitamin B12 deficiency (eg, distal extremity
• Osteoporosis paresthesia, numbness, sensory ataxia), anemia, hair
Iron • Microcytic anemia fragility, skin depigmentation, hepatosplenomegaly,
• Thyroid dysfunction edema, and osteoporosis.
Selenium • Cardiomyopathy
• Immune dysfunction Vegan diet
• Alopecia
• Pustular skin rash (perioral • Complete abstinence from
region & extremities) animal-derived foods
Zinc • Hypogonadism Composition
• Emphasis on fruits, vegetables,
• Impaired wound healing
• Impaired taste legumes
• Immune dysfunction
• Lower blood glucose &

E-
cholesterol
Potential benefits • Reduced risk of cardiovascular
disease (eg, heart disease,
stroke)
Potential • Common: vitamin B12, vitamin
nutritional D, calcium
deficiencies • Possible: iodine, iron, zinc

• Baby born with excessive skin

on back of neck, swelling of
hands/feet and heart murmur
which are classically seen in
patients with Turner syndrome

• Key idea: Noonan syndrome is

basically the male version of
Turner syndrome (although
Noonan can also be seen in a
female patient
 BIOCHEMISTRY `B̀IOCHEMISTRY—GENETICS SEC TION II 63

Autosomal trisomies
Down syndrome Findings: intellectual disability, flat facies, Incidence 1:700.
(trisomy 21) prominent epicanthal folds, single palmar Drinking age (21).
crease, incurved 5th finger, gap between 1st 2 Most common viable chromosomal disorder
toes, duodenal atresia, Hirschsprung disease, and most common cause of genetic
congenital heart disease (eg, ASD), Brushfield intellectual disability.
spots. Associated with early-onset Alzheimer First-trimester ultrasound commonly shows
disease (chromosome 21 codes for amyloid  nuchal translucency and hypoplastic nasal
-
precursor protein),  risk of AML/ALL. bone. Markers for Down syndrome are HI up:
-

95% of cases due to meiotic nondisjunction  hCG,  inhibin.

( with advanced maternal age; from 1:1500 in The 5 A’s of Down syndrome:
women < 20 to 1:25 in women > 45 years old). ƒ Advanced maternal age
Single palmar crease 4% of cases due to unbalanced Robertsonian ƒ Atresia (duodenal)
translocation, most typically between ƒ Atrioventricular septal defect
chromosomes 14 and 21. Only 1% of cases are ƒ Alzheimer disease (early onset)
due to postfertilization mitotic error. ƒ AML/ALL
Edwards syndrome Findings: PRINCE Edward—Prominent Incidence 1:8000.
(trisomy 18) occiput, Rocker-bottom feet, Intellectual Election age (18).
disability, Nondisjunction, Clenched fists with 2nd most common autosomal trisomy resulting
overlapping fingers, low-set Ears, micrognathia in live birth (most common is Down syndrome).
(small jaw), congenital heart disease, VSD
omphalocele, myelomeningocele. Death
usually occurs by age 1 year.
Overlapping fingers

Patau syndrome Findings: severe intellectual disability, rocker- Incidence 1:15,000.

(trisomy 13) bottom feet, microphthalmia, microcephaly, Puberty (13).
cleft liP/Palate, holoProsencephaly, Defect in fusion of prechordal mesoderm
Polydactyly, cutis aPlasia, congenital heart Ž midline defects.
=
(Pump) disease, Polycystic kidney disease,
-
omphalocele. Death usually occurs by age 1. ☒
Cutis aplasia

Nondisjunction in meiosis I Nondisjunction in meiosis II 1st trimester screening

Trisomy β-hCG PAPP-A
Meiosis I 21  
18  
Nondisjunction 13  

Meiosis II 2nd trimester screening

Trisomy β-hCG Inhibin A Estriol AFP
Nondisjunction
21    
18  — or   
Gametes 13 — — — —

n+1 n+1 n–1 n–1 n n n–1 n+1

Trisomy Monosomy Normal Monosomy Trisomy
56) Ehlers-Danlos syndrome is a collection of genetic connective tissue disorders.
-joint hypermobility/laxity, multiple joint dislocations, tissue fragility, poor wound
healing, and cigarette, paper-like scarring.
# recurrent joint dislocation
Clinical features of Ehlers-Danlos & Marfan syndromes in EDS versus recurrent joint
Classic Ehlers-Danlos Marfan fractures in marfan
• Transparent &
hyperextensible
Skin • Easy bruising, poor healing • No features other than striae 58) Hypotonia in Down:
•
=
Velvety with atrophy &
scarring
-Hypotonia is a common
finding in neonates with Down
• Joint hypermobility • Joint hypermobility
• Pectus excavatum • Pectus excavatum or syndrome.
Musculoskeletal • Scoliosis carinatum -Poor muscle tone and a
• Scoliosis
• High, arched palate • Tall with long extremities weak suck are key findings.
• Progressive aortic root
Cardiac • Mitral valve prolapse dilation -Additional features of
• Mitral valve prolapse
Down :upslanting palpebral
• Abdominal & inguinal
Other hernias
• Lens & retinal detachment fissures, a protruding tongue,
• Spontaneous pneumothorax
• Uterine prolapse and a single palmar crease.
• COL5A1 & COL5A2
• FBN1 mutation
Genetics mutation
• Autosomal dominant
• Autosomal dominant
 #Percutaneous transluminal
angioplasty with stenting
-can be used to revascularize
peripheral vessels.
-Percutaneous transluminal
angioplasty with stenting is only
considered once conservative and
pharmacological treatment have failed
to provide symptomatic relief, or if
there is evidence of critical limb
ischemia on physical exam.

-otherwise use exercise graded

programme

#Critical limb ischaemia: non healing

ulcer with necrosis, claudication,
stenosis on MR angio

iz
CNG
59) dialysis related amyloidosis
-Along with sustained elevation of B2-microglobulin, several connective tissue
components (eg, glycosaminoglycans, type I collagen) participate in amyloid fibril
stabilization.

-This may explain DRA's affinity for osteoarticular structures, resulting in the following
classic Triad
• Scapulohumeral periarthritis: shoulder pain/hypertrophy with increased rotator
cuff thickness and hyperechogenic deposits on imaging

• Carpal tunnel syndrome:

• Bone cysts: possible pathologic fracture vs tertiary hyperparathyroidism which

shows hypercalcemia
 Amyloidosis
• Extracellular deposition of insoluble
protein fibrils
◦ AL: produced by clonal plasma cells
Etiology ◦ AA: secondary to chronic
inflammation
◦ ATTR: age-related or hereditary
◦ AB2-m: dialysis-related
• Nephrotic syndrome (AL & AA)
• Hepatomegaly with/without
splenomegaly (AL & AA)
• Restrictive cardiomyopathy (AL &
Clinical
ATTR)
presentatio
• CTS, scapulohumeral periarthritis
n*
(AB2-m)
• Peripheral/autonomic neuropathy
• Periorbital purpura, waxy skin,
macroglossia

61) C/F of fragile X in children:

-In addition to autism, patients with FXS often have:
• Developmental delay (eg, first step at age 2) and intellectual disability
• Neuropsychiatric comorbidities, with features of attention deficit hyperactivity disorder
(eg, difficulty remaining seated, trouble transitioning)

• Aggression, anxiety, and self-injurious behavior (eg, hand biting) vs deformity in leach
nyhan
—> risk of MVP and MR amboss
Vs
#FXR in adults:
Typical physical features of FXS (eg, elongated face, large ears, enlarged testes) may not
present until adolescence.

62) dont mix deep vein valvular insufficiency with DVT

•Deep venous valvular insufficiency –> dilated veins with edema of the extremity due to
poor filling
• Superficial thrombophlebitis –> Tender nodular thickening of the vein, often
associated with pancreatic cancer

• Superior vena cava syndrome –> similar to deep venous valvular insufficiency with
swelling of the face as well
• Thoracic outlet syndrome –> SVC syndrome with atrophy of intrinsic hand muscles
due to compression of the lower trunk of the brachial plexus,
÷

É
 Immunology

# annual influenza vaccine in USA is killed IM: oct- april above 6 yrs

#Stem cell transplantation is a treatment option for congenital mixed immunodeficiencies,

such as severe combined immunodeficiency, Wiskott-Aldrich syndrome, and hyper-
IgM syndrome
116 SEC TION II IMMUNOLOGY IMMUNOLOGY—IMMUNE RESPONSES
` 

WAC, cvid, AT: Cancer

Immunodeficiencies
DISEASE DEFECT PRESENTATION FINDINGS
B-cell disorders
X-linked (Bruton) Defect in BTK, a tyrosine Recurrent bacterial and Absent B cells in peripheral
agammaglobulinemia kinase gene Ž no B-cell enteroviral infections after 6 blood,  Ig of all classes.

I
maturation; X-linked recessive months ( maternal IgG) Absent/scanty lymph nodes
Rx: IV IG not ( in Boys) and tonsils (1° follicles
stem cell and germinal centers
absent) Ž live vaccines
transplant
contraindicated
Selective IgA Cause unknown Majority Asymptomatic  IgA with normal IgG, IgM
deficiency Most common 1° Can see Airway and GI levels
immunodeficiency infections, Autoimmune  susceptibility to giardiasis
disease, Atopy, Anaphylaxis to -
Can cause false-positive β-hCG
IgA-containing products test
Common variable Defect in B-cell differentiation. May present in childhood  plasma cells,
immunodeficiency Cause unknown in most cases but usually diagnosed after  immunoglobulins
puberty
 risk of autoimmune disease, ITP, RA, AIHA, vitiligo,
bronchiectasis, lymphoma,
sinopulmonary infections
autoimmune thyroiditis
T-cell disorders
Thymic aplasia 22q11 microdeletion; failure CATCH-22: Cardiac defects  T cells,  PTH,  Ca2+
to develop 3rd and 4th (conotruncal abnormalities Thymic shadow absent on
pharyngeal pouches Ž absent [eg, tetralogy of Fallot, truncus CXR
thymus and parathyroids arteriosus]), Abnormal facies,
DiGeorge syndrome—thymic, Thymic hypoplasia Ž T-cell
parathyroid, cardiac defects deficiency (recurrent viral/
Velocardiofacial syndrome— fungal infections), Cleft
palate, facial, cardiac defects palate, Hypocalcemia 2° to

e-
parathyroid aplasia Ž tetany
IL-12 receptor  Th1 response; autosomal Disseminated mycobacterial  IFN-γ
deficiency recessive and fungal infections; may Most common cause of
present after administration of Mendelian susceptibility
BCG vaccine to mycobacterial diseases
(MSMD)
Autosomal dominant Deficiency of Th17 cells due to Cold (noninflamed)  IgE
hyper-IgE syndrome STAT3 mutation Ž impaired staphylococcal Abscesses,  eosinophils
(Job syndrome) recruitment of neutrophils to retained Baby teeth, Coarse
Learn the ABCDEF’s to get a
sites of infection facies, Dermatologic problems
Job!
(eczema),  IgE, bone
Fractures from minor trauma
Chronic T-cell dysfunction Persistent noninvasive Candida Absent in vitro T-cell
mucocutaneous Impaired cell-mediated albicans infections of skin and proliferation in response to
candidiasis immunity against Candida sp mucous membranes Candida antigens
Classic form caused by defects Absent cutaneous reaction to
in AIRE Candida antigens
 IMMUNOLOGY IMMUNOLOGY—IMMUNE RESPONSES
`  SEC TION II 117

Immunodeficiencies (continued)
DISEASE DEFECT PRESENTATION FINDINGS
B- and T-cell disorders
Severe combined Several types including Failure to thrive, chronic  T-cell receptor excision
immunodeficiency defective IL-2R gamma diarrhea, thrush circles (TRECs)
chain (most common, Recurrent viral, bacterial, Absence of thymic shadow

n =
X-linked recessive); adenosine fungal, and protozoal (CXR), germinal centers

✗ deaminase deficiency
(autosomal recessive);
RAG mutation Ž VDJ
recombination defect
infections (lymph node biopsy), and
T cells (flow cytometry)

AKE

_
Ataxia-telangiectasia Defects in ATM gene Ž failure Triad: cerebellar defects  AFP .

A to detect DNA damage (Ataxia), spider Angiomas  IgA, IgG, and IgE
Ž failure to halt progression (telangiectasia A ), IgA Lymphopenia, cerebellar
of cell cycle Ž mutations deficiency atrophy

Hyper-IgM syndrome
accumulate; autosomal
recessive
Most commonly due to
⇐
 sensitivity to radiation (limit
x-ray exposure)
Severe pyogenic infections
 risk of lymphoma and
leukemia
Normal or  IgM

R
defective CD40L on Th cells early in life; opportunistic  IgG, IgA, IgE
✗ Ž class switching defect; infection with Pneumocystis, Failure to make germinal
X-linked recessive
→
Cryptosporidium, CMV centers
Wiskott-Aldrich Mutation in WAS gene; WATER: Wiskott-Aldrich:  to normal IgG, IgM
syndrome leukocytes and platelets Thrombocytopenia, Eczema, - IgE, IgA

xn
unable to reorganize actin Recurrent (pyogenic) Fewer and smaller platelets
cytoskeleton Ž defective infections
antigen presentation; X-linked  risk of autoimmune diseaseMx: stem cell transplant
recessive and malignancy
Phagocyte dysfunction
Leukocyte adhesion Defect in LFA-1 integrin Late separation (>30 days) of  neutrophils in blood
deficiency (type 1) (CD18) protein on umbilical cord, absent pus, Absence of neutrophils at
-reduced CD18 antigen on the
surfaces of neutrophils. CD18 is a key
phagocytes; impaired dysfunctional neutrophils infection sites Ž impaired
component of integrins migration and chemotaxis; Ž recurrent skin and wound healing
autosomal recessive mucosal bacterial infections .
-

Chédiak-Higashi Defect in lysosomal trafficking PLAIN: Progressive Giant granules ( B , arrows) in

syndrome regulator gene (LYST) neurodegeneration, granulocytes and platelets.
Microtubule dysfunction in Lymphohistiocytosis, Pancytopenia
.

B
→
phagosome-lysosome fusion;
autosomal recessive
Albinism (partial), recurrent
pyogenic Infections,
Mild coagulation defects

peripheral Neuropathy

Chronic Defect of NADPH oxidase  susceptibility to catalase ⊕ Abnormal dihydrorhodamine

granulomatous Ž  reactive oxygen organisms (flow cytometry) test ( green
disease species (eg, superoxide) fluorescence)

N and  respiratory burst in Nitroblue tetrazolium dye

✗
neutrophils; X-linked form reduction test (obsolete) fails
-

-
most common to turn blue
 IMMUNOLOGY IMMUNOLOGY—IMMUNE RESPONSES
`  SEC TION II 111

Vaccination Induces an active immune response (humoral and/or cellular) to specific pathogens.
VACCINE TYPE DESCRIPTION PROS/CONS EXAMPLES
Live attenuated Microorganism rendered Pros: induces strong, often Adenovirus (nonattenuated,
vaccine nonpathogenic but retains lifelong immunity. given to military recruits),
capacity for transient Cons: may revert to virulent typhoid (Ty21a, oral),
growth within inoculated form. Contraindicated polio (Sabin), varicella
host. Induces cellular and in pregnant and (chickenpox), smallpox,
humoral responses. MMR immunodeficient patients. BCG, yellow fever, influenza
and varicella vaccines can be (intranasal), MMR, rotavirus.
given to people living with “Attention teachers! Please
HIV without evidence of vaccinate small, Beautiful
immunity if CD4 cell count young infants with MMR
≥ 200 cells/mm3. regularly!”
Killed or inactivated Pathogen is inactivated by heat Pros: safer than live vaccines. Hepatitis A, Typhoid
vaccine or chemicals. Maintaining Cons: weaker immune (Vi polysaccharide,
epitope structure on surface response; booster shots intramuscular), Rabies,
antigens is important for usually required. Influenza, Polio (SalK).
immune response. Mainly A TRIP could Kill you.
induces a humoral response.
Subunit Includes only the antigens that Pros: lower chance of adverse HBV (antigen = HBsAg),
best stimulate the immune reactions. HPV (types 6, 11, 16, and
system. Cons: expensive, weaker 18), acellular pertussis
immune response. (aP), Neisseria meningitidis
(various strains), Streptococcus
pneumoniae, Haemophilus
influenzae type b.
Toxoid Denatured bacterial toxin with Pros: protects against the Clostridium tetani,
an intact receptor binding bacterial toxins. Corynebacterium diphtheriae.
site. Stimulates the immune Cons: antitoxin levels decrease
system to make antibodies with time, may require a
without potential for causing booster.
disease.
 Divine 250 vaccine
1)Hep B vaccine given to newborn before it leave hospital. But if mom has +HBsAg, then
given Hep B IVig as well in another buttock as Hep B may inactive the IV ig

2) all live virus C/I in child < 1 yrs, except rotavirus which is given at 6;10;14 wks/
2;4; 6 months

3) PPCV13: conjugated so both humoral and cell mediated response

-C so conjugated
-13 comes 1st, so it’s given 1st before 23
-13 is given to all

vs 23 only for > 65 yrs/ high risk groups like organ failure, Ig def,chronic Ds , CSF leak
and cochlear implant < 65 yrs

4) general rule for childhood vaccines:

-mostly 3 doses minimum
-most doses: 2, 4, 6 months 246 rule (except live virus )

#exeception to above rule:

-Hep B 0; 2 months; 6-18 month
-Tdap:5 doses: 2,4,6 mon; 6-18 mon; 4-6 yrs ;; after adolescence; Td booster 10 yrly
-H flu: 2,4 month; 12-15 month 3

-polio: 2,4,6 mon; 4-6 yrs

-influenza: yrly
- - -7
-Both live MMR & varicella: 12-15 mon; 4-6 yrs .

-Hep A: 2nd yr Of life—> 2nd dose after 6 months

5) adolescent vaccine:
-Td boosters
-Meningococcal vaccine: 11-12 yrs—> 16 yrs
-HPV vaccine: 9-26 yrs

6) old age vaccine:

-Zoster vaccine (different from varicella) at age of 50 yr—> then 6 months apart
-PPSV 23 >65

7) every pregnancy needs Tdap vaccine; between 27-36 wks

 Routine Pediatric & Adults vaccination Schedule
Pediatric Vaccination Schedule

@ Birth : HBV (Not given if weight <2 kg)

@ 2 Months of Chronological Age :

- HBV 2nd Dose DR PC
- Rotavirus : Live
.

2B
- DPT : Toxoid + Subunit
( To be)
- Pneumo / Hib : Capsulated
- Polio : Inactivated

@ 1 Year of Chronological Age :

==> All Live except Rotavirus
- MMRVr
- MMR , Varicella

— Preterm more susceptible for vaccine

preventable diseases
— Preterms are given vaccine as per their
chronological age not Calculated gestational
age

Adults Vaccination Schedule

Influenza, Meningococcal, HPV vaccine schedule is as follows :
— As it’s not mentioned in above schedule

1) Meningococcal Vaccine : As it’s a Teenager Prone disease so Given before Teenage

—> Has serotypes A,C,Y, W135
Meningococcal
Serotype B
vaccine : Age 16-18

Also for Asplenia

—>> vaccination is also recommended before travel to highly endemic environments,

such as most of sub-Saharan Africa and the Muslim hajj pilgrimage to Mecca, Saudi
Arabia.
—>> Primary vaccination can also be given to adults age >18 who are at increased risk
for invasive meningococcal disease (eg, complement deficiency, functional or anatomic
asplenia).

2) Influenza : IM Inactive annually

3) HPV Vaccine :
-Individuals age ≥15 require 3 doses of the(HPV) vaccine to achieve immunity.
-In contrast, individuals age <15 require only 2 doses administered 6 months apart to
achieve equivalent immunity.
4) Vaccines for international travel
 Case clues immunology

2) Posttransplantation lymphoproliferative disorder

- a plasmocytic/ lymphoid proliferation that occurs in those on high-dose
immunosuppressive following transplantation.
-Etiology: Epstein-Barr virus (EBV) MC

-C/F: reticuloendothelial manifestations (eg, lymphadenopathy, hepatosplenomegaly,

cytopenias) and elevated EBV titers.

4) leukocyte adhesion deficiency:

SO MARKED LEUKOCYTOSIS IN BLOOD BUT NO WBC AT INFECTION SITES.
—> Lack of Purulence at infection site

5) SCID:
-Lymphopenia (defective T cell development) + hypogammaglobulinemia (defective B
cell)
-Routine screening; absent TREC (T cell receptor excision circle)
8) Medical exemption from vaccination:
-Currently, all states allow medical exemption from vaccination (eg, allergy to vaccine
components).
-Some states also allow for exemption based on a parent's religious and/or personal
beliefs.

9) C/I for DPT vaccine

1) anaphylaxis develops following DTaP administration
2) Unstable neurologic disorders (eg, infantile spasms, uncontrolled epilepsy) and
encephalopathy (ie, coma, decreased level of consciousness, prolonged seizures >5
min) within a week - mayb by pertussis component
—> as a result, diphtheria and tetanus toxoids should be administered without
pertussis.

10) Transient hypogammaglobulinemia of infancy (THI)

• physiologic nadir in infant IgG levels occurs around age 3-6 months, at which
time infants typically start to produce their own IgG, and levels begin to rise
again.
• in THI, IgG synthesis is delayed, and the physiologic nadir is prolonged beyond
age 6 months.
#Lab:
• Leukocyte count is normal
• ↓ IgG (± ↓ IgA and/or IgM mostly normal)
• Normal antibody response to vaccines (eg: elevated Tetanus and Diphtheria
specific IgG) DIFF CLUE
• Normal B and T lymphocytes

11) S/E of calcineurin inhibitors:

-Nephrotoxicity, hypertension, neurotoxicity: tremors, glucose intolerance , gingival
hypertrophy, cancers like SCC skin and lymphoma

12) X-linked agammaglobulinemia

-Flow cytometry: ↓ CD19+ B cells& normal T cells
#Rx:
• 1st line:Ig replacement therapy x monthly for lifelong
• 2nd line: Prophylactic antibiotics if severe and if IV Ig therapy is unsuccessful.

13) vaccination in preterm:

-Vaccinations for preterm infants should not be delayed;
-they are safe and proven to induce an adequate antibody response to confer immunity.
14) Vaccines prerequisites at birth:
—> The 1st hepatitis B vaccine is administered when the patient weighs ≥2 kg (4 lb
6 oz), typically at birth.
-All other vaccines are administered based on chronologic age.
15) X linked agammaglobulinemia:
-absent/dec B cells; dec all Ig
Vs
#CVID: normal B cells; dec all Ig

16) when to suspect humoral deficiency???

-Normal resp. infections are common in childhood
and can occur up to 10 times a year

—> However severe and recurrent sinopulmonary

infections (intubation, early tympanostomy tube
placement, poor growth) raise concern for
humoral deficiency

—> Also in fully immunised child, infection with

capsulated organism raises suspicion.

17)Annual influenza vaccine is recommended > 6

month

18) GVHD:
-onset: within 100 days
• rash involving palms, soles, and face that may generalize is typical),
• Profuse, watery diarrhea that has a secretory pattern with crampy abdominal pain,
nausea, and vomiting - can be blood-positive diarrhea
• Liver inflammation : damage to the biliary tract epithelium, elevated bilirubin, ALP, and
-
-
transaminases

#Dx: biopsy (eg, colonoscopy with biopsy) after common infections such as
Clostridioides difficile and cytomegalovirus are ruled out.
#Rx: Glucocorticoids

Vs
—> chemotherapy induced nausea and vomiting: generally resolve within a week;
-symptoms 3 weeks later would be very atypical.

19) Conditioning chemotherapy

- administered prior to transplantation to destroy active immune cells (immunoablative) or
to destroy hematopoietic stem cells in the bone marrow to create room for transplanted
stem cells (myeloablative).
20) transfusion reaction : 22) Vaccine in splenectomy
a) Anaphylaxis: Stop BT; Rx and dont resume -pneumococcus, H influenza,
Vs meningococcus, influenza, HAV, HBV,
b) urticarial: stop BT; Rx and can resume tdap
-Timing: either >14 days before/after OT

Vaccines for adults with HIV

Vaccine Indications Recommended vaccines for patients with
• Chronic liver disease (including HBV & HCV) chronic liver disease
• Men who have sex with men
HAV • IV drug users Tetanus Every 10 years
• administered to those with no serologic evidence
of immunity. Influenza Annually
• All patients without documented immunity to HBV Pneumococcal At diagnosis & at age 65
HBV • Immune: +hepatitis B surface antibody & - core/
surface antigen) Hepatitis A Initiate series if not immune
HPV • All patients age 11-26 Hepatitis B Initiate series if not immune
• Annually in fall for all patients (inactivated
Influenza
formulation) 24) Pertusis vaccine schedule
• vaccination should be given to all patients with -primary series at 2, 4, 6, and 15-18
HIV
Meningococcu • booster :every 5 years. months and at 4-6 years,
s • All patients age 11-18 with booster doses in adolescence and
(serogroups A, • Large groups living in close proximity (eg,
C, W, Y) college students, military recruits, incarcerated adulthood.
individuals); sub Saharan Africans
• Asplenia or complement deficiency
25) Varicella vaccination :
• PCV13 once ( conjugate)
Pneumococcu
• PPSV23 ( polysaccharide)8 weeks later, 5 years given to children in 2 doses (age 12-15
s
later & at age 65 months and 4-6 years).
• Tdap once (considered to address waning
Tetanus, pertussis immunity, particularly in those who have
diphtheria & not previously received Tdap.; repeat with each 26) ==>Any lung transplant recipient with
pertussis pregnancy in women) new infiltrates and fever should undergo
• Td every 10 years
Live vaccines (eg, MMR, varicella-zoster) are
a comprehensive workup for both ACR
contraindicated if CD4+ cell count <200/mm3 (acute cell rejection) and infection,
• Zoster – vaccination should generally be administered to those often with bronchoscopy and lung
born after 1979 who have no evidence of immunity (negative anti-
varicella IgG). biopsy.
-The recombinant (inactivated) vaccine can be given to patients
with CD4 counts <200/mm3 but the immunogenic response is often
muted; therefore, it is frequently delayed until CD4 counts are
improved following antiretroviral therapy initiation.

-CMV: acute onset

-PCP: over weeks; less
likely if pt on TMP SMX

-
=.
25) TACO Transfusion-associated circulatory overload
-RF: occur when a large volume of blood product is rapidly transfused, particularly in
children age <3 with chronic anemia/>60 yrs

-C/F: RS distress, HT by overload, tachycardia, and pulmonary edema-B/L rales, S3,

raised JVP within 6 hours of transfusion initiation.

-Management : diuresis (eg, furosemide).

26) In the USA, the hepatitis A vaccine became part of routine childhood vaccinations
in 2006;

27) Patients with CGD should receive antimicrobial prophylaxis with TMP SMX and
itraconazole.
-Patients with severe phenotypes benefit from interferon-gamma injections.

28) asplenia are at risk for fulminant infection with encapsulated bacteria

-due to deficits in antibody response and antibody-mediated phagocytosis/

complement activation

>1 yr who has Neonate;

been exposed pregnancy
← within 5 days
 Humoral immunodeficiency syndromes 29) CD19+= B cell
B cell T cell= CD 4 and 8
Condition IgG IgA IgM IgE
count
CD40 ligand deficiency Norma
↓ ↓ ↑ ↓
(hyper-IgM syndrome) l
Common variable Norma
↓ ↓ ↓ ↓

:
immunodeficiency l
Job syndrome (hyper- Norma Nor Nor Nor
↑
IgE syndrome) l mal mal mal
Selective IgA Norma Nor Nor Nor
↓
deficiency l mal mal mal
X-linked
↓ ↓ ↓ ↓ ↓
agammaglobulinemia

30) #Risk factors for anaphylaxis

-immune disorders such as asthma and mast cell disorders.

-Patients with underlying pulmonary or cardiovascular comorbidities are at

increased risk for poor outcomes.

-Medications such as NSAIDS or beta-adrenergic blockers can exacerbate

anaphylaxis by resulting in nonimmunologic mast cell activation / unopposed alpha-
adrenergic effects, respectively.

31) chronic enteroviral illness in childhood is highly specific for X linked

agammayinemia

32) Meningococcal vaccination

-Schedule: to all adolescents at age 11-12, with a booster recommended at age 16.
-Candidates: complement deficiency or asplenia, military recruits, college students living
in dormitories, and travelers to sub-Saharan Africa.

33) Yellow fever vaccine:

-Vaccination for yellow fever is recommended prior to travel to some countries in central
Africa, many of which require evidence of vaccination for entry.

-C/I: for live-attenuated vaccine include:

• Allergy to vaccine components (eg, eggs)
• AIDS (CD4 <200/mm3), certain immunodeficiencies (including those associated with
thymus disorder), recent stem cell transplantation
• Immunosuppressive therapy (eg, TNF antagonists, high-dose systemic corticosteroids),

bradykinin-mediated angioedema, unlike mast cell–mediated angioedema, does not

cause rash (eg, wheals).
34) Acute renal allograft rejection
- predominantly T-cell mediated and usually occurs within the first 6 months following
transplant.
-Affected patients typically experience an asymptomatic rise in serum creatinine.
-diagnosis : renal biopsy showing lymphocytic infiltration of the intima,
- Rx: high-dose intravenous glucocorticoids.

34) Sickle cell disease patients are at high risk of delayed hemolytic transfusion
reactions due to alloimmunization from frequent transfusions.
-Onset: >24 hours after transfusion and can cause hemolytic anemia.
-Diagnosis :newly positive Coombs test.

35) Hemodynamics in anaphylaxis

-Arteriolar vasodilation—> decreases SVR to cause hypotension,
- venular vasodilation —> decreases CVP and PCWP

36) MMR vaccine:

-2 doses (at age 1 and 4) generates immunity in >95%

-For planned international travel, an additional dose between age 6 and 11 months is also
recommended.

39) Mx of TRALI: RS supportive care including ventilation

Vs
TACO: needs diuretics and they have HT and not hypotension like TRALI

38) No need to give varicella Ig to mom after exposure if she already has positive
VZV IgG (already previously performed immunity )

Acute respiratory failure due to transfusion

Feature TRALI TACO
Pulmonary symptoms Acute dyspnea Acute dyspnea
Diffuse bilateral Diffuse bilateral
Chest x-ray
infiltrate infiltrate
Jugular venous
Absent Present
distension
Crackles/rales ±
Auscultation Crackles/rales
S3
Ejection fraction Normal Decreased
BNP Normal High
39) inactivated influenza vaccine in pregnancy: Nov
- safe during every trimester of pregnancy and while breastfeeding.
-This vaccine prevents maternal influenza-related illness and provides passive
neonatal immunity, thereby decreasing the risk of influenza-related illness in
newborns.

40) post exposure prophylaxis for hepatitis B:

- This unvaccinated HCW (health care worker) should receive both the HB vaccine +
immune globulin —> with follow-up serological testing for viral hepatitis.

*Schedule:
-1st dose of the vaccine: preferred within 12 hours, with the next 2 doses according to
the standard schedule.
-HB immune globulin as soon as possible, preferably within 24 hours.

Nonallergic rhinitis Allergic rhinitis 41) nonallergic rhinitis (NAR), /

• Nasal congestion,
• Watery rhinorrhea, vasomotor rhinitis.
sneezing, eye
rhinorrhea, sneezing,
symptoms -In contrast to patients with allergic
postnasal drainage
• Later onset (age >20)
• Earlier age of onset rhinitis, patients with NAR usually
• Identifiable allergen or
Clinical
common
seasonal pattern cannot identify specific allergic triggers

f-
• No obvious allergic
feature
s
trigger
• Pale/bluish nasal
mucosa
(eg, pollen counts), and they typically
• Perennial symptoms
(may worsen with
• Associated with other have negative testing for aeroallergens.
allergic disorders (eg,
season changes)
eczema, asthma,
• Erythematous nasal
mucosa
eustachian tube -However, many have very specific
dysfunction)
behavioral triggers (eg, walking into cold
=
• Mild: intranasal
antihistamine or • Intranasal air, eating).
Treatm
glucocorticoids glucocorticoids
ent
• Moderate to severe: • Antihistamines
combination therapy

-patients with NAR typically lack the sneezing and allergic conjunctivitis (eg, itchy eyes,
injected conjunctivae) that classically accompany allergic rhinitis.

#Mx
-First-line treatment for both allergic rhinitis and NAR is intranasal glucocorticoids.
Intranasal antihistamines (eg, azelastine, olopatadine) or intranasal ipratropium bromide
can also be used.
-Combination therapy is often required for patients with moderate to severe symptoms.

42) Recurrent bacterial infections in an adult (20-40 yrs)

-should raise suspicion for CVID- do Quantitative S. Ig levels for Dx
Vs
CF: diagnosed before adulthood
43) The rotavirus vaccine
-schedule: recommended at age 2-8 months as the greatest risk for dehydration from
severe gastroenteritis is during early infancy.
—> The vaccine is not administered past this age range.
44) Allograft rejection:
- • Patient with recent liver transplant presents weeks later with fever, eosinophilia (in a
patient taking prednisone where we would otherwise expect low eosinophils), elevated
LFTs and a biopsy showing a mononuclear infiltrate with eosinophils in the hepatic triads,
consistent with allograft rejection
• Key idea: Graft eosinophilia is a sensitive and specific marker of acute rejection
in liver allografts

45) Mx of acute haemolytic transfusion reaction

#Cx: Patients may feel anxious or short of breath, but oxygen saturation and lung sounds
are typically normal. Severe cases may progress to acute renal failure (eg, oliguria,
anuria) or disseminated intravascular coagulation (eg, oozing from the IV insertion site).
#Mx:
-AHTR is a medical emergency. 1st step :immediate cessation of the transfusion.
-Aggressive hydration with IV normal saline is indicated for hemodynamic stabilization and
prevention of renal injury.

-In addition to hydration, supportive care measures (eg, supplemental oxygen,

vasopressors) may be required

46) egg allergy in vaccine:

-Most live influenza vaccines (LAIVs) and inactivated influenza vaccines (IIVs) contain a
limited amount of egg protein, but they are no longer contraindicated in patients with an
allergy according to the Centers for Disease Control (CDC).

-Patients with a severe allergy (i.e., anaphylaxis) should be closely monitored for adverse
effects under supervision of a health care provider after receiving the vaccine.
-More importantly, the LAIV is not Recommended vaccines for asplenic adult patients
approved until 2 years of age and • Sequential PCV13 & PPSV23
the IIV is only recommended for Pneumococcus • Revaccination with PPSV23 5 years later
& at age 65
children age 6 months and older; an
influenza vaccination is therefore not Haemophilus
• 1 dose Hib vaccine
influenzae
indicated at this time.
• Meningococcal quadrivalent vaccine
Meningococcus
• Revaccinate every 5 years
-The MMR vaccine contains virtually
Influenza • Inactivated influenza vaccine annually
no egg protein and is generally
• HAV
considered safe in individuals with • HBV
egg allergies. Other vaccines
• Tdap once as substitute for Td, then Td
every 10 years
47) <7 yrs: DTaP
> 7 yrs: Tdap
#Lower-case letters mean it contains a lower dose of the vaccine. DTaP contains full doses
of diphtheria, tetanus, and whooping cough vaccines. Tdap contains a full dose of the
tetanus vaccine and a lower dose of diphtheria and whooping cough vaccines

48) 7) Cyclic neutropenia

-recurrent episodes of reduced peripheral neutrophils, fever, sore throat, and
lymphadenopathy, commonly occurring every 3 weeks.

49) The WHO recommends typhoid fever vaccination, which contains the Vi capsular
polysaccharide antigen, to those traveling to high-risk areas (East and Southeast
Asia, Latin America, Africa).

50) delayed anemnetic Hemolytic anemia : prevented by extended Ab cross matching as

it’s formed against Minor antigens

51) Neither mild acute illness (e.g., upper respiratory tract infection, otitis media, low-grade
fever, mild diarrhea) nor current antibiotic therapy are contraindications for vaccination
(except for oral live typhoid vaccine, because antibiotics might compromise the
immune response to this vaccine)

52) HCV screening

-The United States Preventive Services Task Force recommends screening for hepatitis C
virus (HCV) infection in all adults 18–79 years of age. Most individuals only need to be
screened for this condition once,
-but more frequent screening is recommended for individuals with risk factors for HCV
infection, such as a history of injection drug use, solid-organ transplantation, long-term
hemodialysis, or HIV infection
 Post Transplantation Lymphoproliferative Disorder
Case :
—> In a 6 yrs old after 8 months of organ transplant,
a febrile illness with lymphadenopathy and leukopenia while taking immunosuppressive medications with
presence of an elevated Epstein-Barr virus (EBV),

Dx..?

Oncogenic Potential of EBV :

- EBV is an oncogenic virus because it produces proteins (eg, latent membrane protein) that lead to B-cell
proliferation and generates prosurvival nuclear transcription factors (EBNA) that lead to B-cell
immortalization.
- Subsequent cell spread through the reticuloendothelial system results in lymphadenopathy,
hepatosplenomegaly, bone marrow infiltration (eg, leukopenia, anemia), and/or B-symptoms.
- Diagnosis is often suspected due to a markedly elevated EBV titer, but biopsy may be required for
confirmation.
 Serum sickness & serum sickness–like reaction
SS SSLR
Foreign proteins in
Medications,
Common antivenom, antitoxin,
particularly cefaclor,
triggers or monoclonal
penicillin & TMP-SMX
antibody
Immune
High titer Mild or none
complexes
Compleme
nt Extensive Minimal or none
activation
5-14 days after 5-14 days after
Onset
exposure exposure
Fever High Low-grade
Arthralgia Yes Yes
Urticaria Yes Yes
Spontaneous
Resolution Spontaneous (discontinue drug if still
receiving)

-thought to be due to genetic deficiencies in eliminating the metabolic by-products of

these medications, which leads to hapten-mediated cytotoxic T-cell injury or direct
cytotoxicity.

SSLR is most common in children and usually presents 5-14 days after medication
initiation.

-Most patients have a mildly pruritic urticarial rash that persists >24 hours. Significant
multiarticular joint pain is usually present.

-Examination usually reveals pain with joint movement, but signs of arthritis (eg, joint
warmth, swelling, erythema) are usually absent. Low grade fever and generalized
lymphadenopathy often occur.

-Symptoms of SS and SSLR resolve completely over several days as the medication
is eliminated by the mononuclear phagocyte system (SS) or by metabolic pathways
(SSLR).
INDICATIONS FOR SPECIALIZED RBC TREATMENTS

LEUKOREDUCED

CALCIUM GLUCONATE INFUSION

WARMING

25
Page
 Biphasic Anaphylaxis
#Indications for hospitalisation in anaphylaxis:

1) protracted anaphylaxis (ie, symptoms lasting hours to days despite treatment) should be admitted.

2) patients who experience complete resolution of symptoms with treatment should be admitted under
the following circumstances:
• Severe symptoms (eg, hypotension, upper airway edema, respiratory distress) occurred at
presentation
• Multiple doses of epinephrine were required to achieve symptom resolution.

#biphasic anaphylaxis
-Above patients are believed to have a higher risk of biphasic anaphylaxis (ie, recurrence of symptoms after
an initial period of resolution), which can be fatal.
-Because both the timing and severity of symptom recurrence are unpredictable, admission for extended
observation is recommended.

#RF for fatal anaphylaxis:

-asthma: Greatest RF
-older age,
-cardiovascular comorbidities, and
-delayed administration of epinephrine.

#Types of anaphylaxis
-symptoms may recur or persist despite treatment, according to the following patterns:

• Biphasic anaphylaxis: characterized by an initial anaphylactic reaction followed by an

asymptomatic period (typically 1-30 hr) and then a recurrence of symptoms.

• Protracted anaphylaxis (less common) : anaphylactic symptoms that last hours or

days despite treatment.

#Mx:
-Patients with biphasic or protracted anaphylaxis (or those unresponsive to the initial dose)
should receive additional IM epinephrine.
-If symptoms persist after 3 IM doses, intravenous epinephrine infusion may be required.
 114 SEC TION II IMMUNOLOGY IMMUNOLOGY—IMMUNE RESPONSES
` 

Blood transfusion reactions

TYPE PATHOGENESIS TIMING CLINICAL PRESENTATION DONOR BLOOD HOST BLOOD
Allergic/ Type I hypersensitivity Within minutes Allergies: urticaria, IgE
(anti-IgA)
anaphylactic reaction against plasma to 2-3 hr (due to pruritus

=⇐
reaction proteins in transfused release of preformed Anaphylaxis:
blood inflammatory wheezing,
IgA-deficient individuals mediators in hypotension,
should receive blood degranulating mast respiratory arrest,
Donor plasma proteins, Host mast cell
products without IgA cells) shock including IgA

Acute Type II hypersensitivity During transfusion Fever, hypotension,

hemolytic reaction or within 24 hr tachypnea,
transfusion Typically causes (due to preformed tachycardia,
reaction intravascular hemolysis antibodies) flank pain,
(ABO blood group hemoglobinuria Donor RBC with A and/ Host anti-A, anti-B IgG,
or B group antigens IgM
incompatibility) (intravascular),
jaundice
(extravascular)
Febrile Cytokines created by Within 1-6 hr (due Fever, headaches,
nonhemolytic donor WBCs accumulate to preformed chills, flushing
transfusion during storage of blood cytokines) More common in
reaction products children Donor WBC releases Host anti-HLA, anti-
Leukoreduction also reduces the risk of human preformed cytokines leukocyte IgG
Reactions prevented by
leukocyte antigen alloimmunization and
leukoreduction of blood transmission of cytomegalovirus (which
products typically resides in leukocytes).
Transfusion- Two-hit mechanism: Within minutes to Respiratory distress,
related acute ƒ Neutrophils are 6 hr noncardiogenic
lung injury sequestered and pulmonary edema Host
neutrophils
primed in pulmonary
vasculature due to
recipient risk factors Donor antileukocyte
IgG
ƒ Neutrophils are activated
by a product (eg,
antileukocyte antibodies)
in the transfused blood
and release inflammatory
mediators Ž  capillary
permeability
Ž pulmonary edema
Delayed Anamnestic response to Onset over 24 hr Generally self limited
hemolytic a foreign antigen on Usually presents and clinically silent
transfusion donor RBCs (Rh [D] or within 1-2 wk Mild fever,
reaction other minor blood group (due to slow hyperbilirubinemia
Donor RBC with Host IgG
antigens) previously destruction by foreign antigens

=
encountered by recipient reticuloendothelial
Typically causes system)
extravascular hemolysis
→
_­
 Biostat concepts

#A confidence interval (CI) is constructed by taking a sample value (eg, difference in

sample percentages) and adding and subtracting a margin of error.
-Consequently, the interval always contains the sample value, and the sample value is
typically at the center of the interval.

• A CI that includes 0 indicates that there is no difference in group means.

• A CI that excludes 0 indicates that there is a difference in group means.
260 SEC TION II PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY AND BIOSTATISTICS
` 

Highest accuracy
Receiving operating ROC curve demonstrates how well a diagnostic Ideal test (AUC = 1)
1
characteristic curve test can distinguish between 2 groups (eg, 1)
<
disease vs healthy). Plots the true-positive rate UC
<A
(sensitivity) against the false-positive rate .5
t (0

TP rate (sensitivity)
)
(1 – specificity). 0.5

s
l te
C=

ua
The better performing test will have a higher (AU

Act
e
alu
area under the curve (AUC), with the curve ev
ic tiv
closer to the upper left corner. pred
No

FP rate (1 – specificity) 1

Bias and study errors

TYPE DEFINITION EXAMPLES STRATEGIES TO REDUCE BIAS
Recruiting participants
Selection bias Nonrandom sampling Berkson bias—cases and/ Randomization
or treatment allocation or controls selected from Ensure the choice of the right
of subjects such that hospitals are less healthy and comparison/reference group
study population is not have different exposures than
representative of target general population
population. Attrition bias—participants lost
Most commonly a sampling to follow up have a different
bias. prognosis than those who
complete the study
Performing study
Recall bias Awareness of disorder alters Patients with disease recall Decrease time from exposure
recall by subjects; common in exposure after learning of to follow-up
retrospective studies similar cases
Measurement bias Information is gathered in a Using a faulty automatic Use objective, standardized,
systemically distorted manner sphygmomanometer to and previously tested methods
measure BP of data collection that are
Hawthorne effect—participants planned ahead of time
change behavior upon Use placebo group
awareness of being observed
Procedure bias Subjects in different groups are Patients in treatment group Blinding (masking) and
not treated the same spend more time in highly use of placebo reduce
specialized hospital units influence of participants and
Observer-expectancy Researcher’s belief in the An observer expecting researchers on procedures and
bias efficacy of a treatment changes treatment group to show signs interpretation of outcomes
the outcome of that treatment of recovery is more likely to as neither are aware of group
(aka, Pygmalion effect) document positive outcomes assignments

#Response bias
-occurs when participants in cross-sectional studies (eg, surveys, polls,
questionnaires) purposely give desirable responses to questions about topics
perceived to be sensitive (eg, health behaviors).
 PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY AND BIOSTATISTICS
`  SEC TION II 261

Bias and study errors (continued)

TYPE DEFINITION EXAMPLES STRATEGY TO REDUCE BIAS
Interpreting results
Confounding bias Factor related to both exposure An uncontrolled study shows Multiple/repeated studies
and outcome (but not on an association between Crossover studies (subjects act
causal path) distorts effect drinking coffee and lung as their own controls)
of exposure on outcome (vs cancer. However, coffee Matching (patients with
effect modification, in which drinkers also smoke more, similar characteristics in both
the exposure leads to different which can account for the treatment and control groups)
outcomes in subgroups association
stratified by the factor)
Lead-time bias Early detection is confused Early detection makes it seem Measure “back-end” survival

E-
with  survival like survival has increased, (adjust survival according to
but the disease’s natural the severity of disease at the
history has not changed time of diagnosis)
Length-time bias Screening test detects diseases A slowly progressive cancer A randomized controlled trial

=
with long latency period, is more likely detected by a assigning subjects to the
while those with shorter screening test than a rapidly screening program or to no
latency period become progressive cancer screening
symptomatic earlier

#Lead-time bias
- should always be considered while evaluating any screening test.
-This bias occurs when there is an incorrect assumption or conclusion of prolonged
apparent survival and better prognosis due to a screening test.

-What actually happens is that detection of the disease was made at an earlier point in time,
but the disease course itself or the prognosis did not change, so the screened patients
appeared to live longer from the time of diagnosis to the time of death.

#(USMLE tip: think of lead-time bias when you see "a new screening test" for poor
prognosis diseases like lung or pancreatic cancer.)

-False positive ratio = 1- specificity.

-False negative ratio = 1 - sensitivity.

#If a test result is negative, the probability of having the disease is 1 - NPV
 Biostat review

Likelihood ratio
 PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY AND BIOSTATISTICS
`  SEC TION II 257

Evaluation of Sensitivity and specificity are fixed properties Disease

–
diagnostic tests of a test. PPV and NPV vary depending on

it
disease prevalence in population being tested. PPV
TP FP = TP/(TP + FP)

Test
#overall proportion of negative – FN TN
NPV
= TN/(TN + FN)

tests: (FN + TN) / (TP + FP + TN + Sensitivity Specificity Prevalence

TP + FN
= TP/(TP + FN) = TN/(TN + FP) (TP + FN + FP + TN)
FN).
Sensitivity (true- Proportion of all people with disease who test = TP / (TP + FN)
positive rate) positive, or the probability that when the = 1 – FN rate
disease is present, the test is positive. SN-N-OUT = highly SeNsitive test, when
Value approaching 100% is desirable for ruling Negative, rules OUT disease
out disease and indicates a low false-negative High sensitivity test used for screening
rate.
Specificity (true- Proportion of all people without disease who = TN / (TN + FP)
negative rate) test negative, or the probability that when the = 1 – FP rate
disease is absent, the test is negative. SP-P-IN = highly SPecific test, when Positive,
Value approaching 100% is desirable for ruling rules IN disease
in disease and indicates a low false-positive High specificity test used for confirmation after a
rate. positive screening test
Positive predictive Probability that a person who has a positive test PPV = TP / (TP + FP)
-.
value result actually has the disease. PPV varies directly with pretest probability
(baseline risk, such as prevalence of disease):
high pretest probability Ž high PPV
Negative predictive Probability that a person with a negative test NPV = TN / (TN + FN)
-
value result actually does not have the disease. NPV varies inversely with prevalence or pretest
probability

*
Blue I
0
Possible cutoff values for (+) vs (-) test result

o
Disease Disease A = 100% sensitivity cutoff value
,
Number of people

absent present B = practical compromise between specificity and sensitivity

C = 100% specificity cutoff value

TN TP Lowering the cutoff value: ↑ Sensitivity ↑ NPV

↑ ↑ ↑
100% 100 B A (↑ FP FN) Specificity PPV
↑

Sn FN FP %Sp
Raising the cutoff value: ↑ Specificity ↑ PPV
A
- B + C B C (↑ FN FP)
↑ ↑ - ↑
Sensitivity NPV
-
↑

Test results
=

Likelihood ratio Likelihood that a given test result would be sensitivity TP rate
LR+ = =
expected in a patient with the target disorder 1 – specificity FP rate
compared to the likelihood that the same result
would be expected in a patient without the 1 – sensitivity FN rate
LR– = =
target disorder. specificity TN rate
LR+ > 10 indicates a highly specific test, while
LR– < 0.1 indicates a highly sensitive test.
LRs can be multiplied with pretest odds of
disease to estimate posttest odds.

-overall accuracy of the test : (TP + TN) / (TP + FP + TN + FN)

-it represents the probability that an individual will be correctly classified by a test.
-defined as the proportion of true results (true positive and true negative) out of all the
results of a given diagnostic test.
#Biostat review:
-the lesser the overlap between 2 curves, higher the sn and sp

#Effect modification
-If stratification doesn’t erase effects → effect modification
Example: When you stratify by BMI, the difference in BP reduction is still present. Implies
that there’s something about obesity that makes the drug more effective in that population
-Example: The increased risk of cancer in smokers is even higher among those who also
drink heavily.
 PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY AND BIOSTATISTICS
`  SEC TION II 259

Incidence vs # of new cases Incidence looks at new cases (incidents).

Incidence = (per unit of time)
prevalence # of people at risk
# of existing cases (at a point in Prevalence looks at all current cases.
Recurrence Prevalence =
Total # of people time)
Incidence
in a population
Prevalence Prevalence = average duration
Incidence rate ×
1 – prevalence of disease
Mortality Cure
Prevalence ≈ incidence for short duration disease -
Prevalence ∼ pretest probability.
(eg, common cold).  prevalence Ž  PPV and  NPV.
Prevalence > incidence for chronic diseases, due to
large # of existing cases (eg, diabetes).
SITUATION INCIDENCE PREVALENCE

 survival time — 
 mortality — 
Faster recovery time — 
Extensive vaccine administration  
 risk factors  

Precision vs accuracy
Precision (reliability) The consistency and reproducibility of a test. Random error  precision in a test.
The absence of random variation in a test.  precision Ž  standard deviation.,narrow CI

=
 precision Ž  statistical power (1 − β).
Accuracy (validity) The closeness of test results to the true values.
The absence of systematic error or bias in a test. -✓ Systematic error  accuracy in a test.

Ar High
Accuracy
Low High
Accuracy
Low
** Here systemic error
includes measurement,
confounding and
measurement bias

High High Low Low

Precision Precision

#A perfectly valid diagnostic test should have sensitivity and specificity equal to 1,
but this is seldom possible.
-The more sensitive the test, the less specific it is (and vice versa).
 b/d bc
a/(a + b)
258
Relative risk =
SEC TION II PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY
`  c/(c + d)AND BIOSTATISTICS
a c
Attributable risk =
a+b c+d

Disease or outcome
Quantifying risk Definitions and formulas are based on the classic
2 × 2 or contingency table.

or intervention
Exposure
a b

c d

TERM DEFINITION EXAMPLE FORMULA

Odds ratio Typically used in case-control If in a case-control study, 20/30 lung a/c ad
OR = =
studies. Represents the odds of
-
cancer patients and 5/25 healthy b/d bc
exposure among cases (a/c) vs individuals report smoking, the OR a b
odds of exposure among controls is 8; so the lung cancer patients are 8 20 5
(b/d). times more likely to have a history of c d
10 20
smoking.
Relative risk Typically used in cohort studies. If 5/10 people exposed to radiation are a/(a + b)
RR =
#Ratio of Risk of developing disease in the diagnosed with cancer, and 1/10 people c/(c + d)
-
probability exposed group divided by risk in not exposed to radiation are diagnosed a b
the unexposed group. with cancer, the RR is 5; so people 5 5 →
of event in RR = 1 Ž no association between exposed to radiation have a 5 times c d
exposed vs exposure and disease. greater risk of developing cancer.
-
1 9

non RR > 1 Ž exposure associated with For rare diseases (low prevalence), OR
 disease occurrence. approximates RR. RR = (Ratetreatment / Ratecontrol)
exposed RR < 1 Ž exposure associated with

-
 disease occurrence.
Relative risk The proportion of risk reduction If 2% of patients who receive a flu RRR = 1 − RR
e- -
reduction % attributable to the intervention as shot develop the flu, while 8% of -RRR = (Ratecontrol − Ratetreatment) /
compared to a control. unvaccinated patients develop the flu, Ratecontrol
/ relative reduction then RR = 2/8 = 0.25, and RRR = 0.75.
-

g
-
-RRR = ARR/control rate
Attributable The difference in risk between If risk of lung cancer in smokers is 21% a c
AR = −

z
-
risk exposed and unexposed groups. and risk in nonsmokers is 1%, then the a+b c+d
attributable risk is 20%. RR − 1
Just substraction AR% =
RR
× 100
=
Absolute The difference in risk (not the If 8% of people who receive a placebo c a
- ARR = −
risk proportion) attributable to the vaccine develop the flu vs 2% of people c+d a+b
reduction intervention as compared to a who receive a flu vaccine, then ARR =
ARR = (Ratecontrol − Ratetreatment)
control. 8%–2% = 6% = 0.06.
Number Number of patients who need to NNT = 1/ARR
needed to be treated for 1 patient to benefit.
treat Lower number = better treatment.
Number
needed to
Number of patients who need to
be exposed to a risk factor for 1
→
NNH = 1/AR

harm patient to be harmed. Higher

= number = safer exposure.
Case fatality Percentage of deaths occurring If 4 patients die among 10 cases of deaths
CFR% = × 100
rate among those with disease. meningitis, case fatality rate is 40%. cases

# types of Odds ratio:

1) exposure odds ratio,
in which the exposure of RF in cases is compared to the exposure (controls).
-used in case control study

2) Prevalence odds ratio: calculated in cross-sectional studies to compare the prevalence of a disease between
different populations.
268 SEC TION II PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY AND BIOSTATISTICS
` 

Statistical hypothesis testing

Null hypothesis (H0) Hypothesis of no difference or relationship (eg, there is no association between the disease and the
risk factor in the population).
Alternative hypothesis Hypothesis of some difference or relationship (eg, there is some association between the disease
(H1) and the risk factor in the population).
p-value The probability of obtaining test results at least as extreme as those observed during the test,
assuming that H0 is correct.

Outcomes of statistical hypothesis testing

Correct result Stating that there is an effect or difference when Reality

PI
one exists (H0 rejected in favor of H1). H1 H0 .

Stating that there is no effect or difference when

TP p
none exists (H0 not rejected). Power α
Study rejects H0
( 1 – β) Type I error

Ft
Study does not reject H0
-
β ft .

¥
Type II error

Blue shading = correct result.

Testing errors
Type I error (α) Stating that there is an effect or difference when Also called false-positive error.
none exists (H0 incorrectly rejected in favor of 1st time boy cries wolf, the town believes there
H1). is a wolf, but there is not (false positive).
α is the probability of making a type I error You can never “prove” H1, but you can reject the
(usually 0.05 is chosen). If p < α, then H0 as being very unlikely.
assuming H0 is true, the probability of
obtaining the test results would be less than
the probability of making a type I error. H0 is
therefore rejected as false.
Statistical significance ≠ clinical significance.
Type II error (β) Stating that there is not an effect or difference Also called false-negative error.
when one exists (H0 is not rejected when it is 2nd time boy cries wolf, the town believes there is
in fact false). no wolf, but there is one.
β is the probability of making a type II error. β is If you  sample size, you  power. There is power
related to statistical power (1 – β), which is the in numbers.
probability of rejecting H0 when it is false.
 power and  β by:
ƒ  sample size
ƒ  expected effect size
ƒ  precision of measurement
 Biostat concepts
1) relative chance (ie, risk, probability) of
an outcome of interest in cohort studies is
the relative risk (RR).

;
2) Attributable risk percentage (ARP)
describes the % of disease in an exposed
group that can be attributed to the
exposure.
-the difference in risk of disease between
the exposed and nonexposed groups
divided by the risk of disease in the
exposed group:
ARP = [(RR − 1) / RR] × 100

ARP = [(Riskexposed − Risknonexposed) /

Riskexposed] × 100

4) Hazard ratios
- the ratio of an event rate occurring in the treatment group versus the non-treatment group.
==> Ratios <1 indicate that the treatment group had a lower event rate and ratios >1
indicate that the treatment group had a higher event rate.

** Hazard ratio and median survival are commonly used in cohort studies and
experimental designs to compare total and median survival times, respectively, in ≥2
groups of patients

5) what if group A (placebo) pt deteriorates and has to be given group B Rx??

-Grouping them with patients from both the groups may lead to erroneous analysis and
weaken the conclusions that can be drawn from the study.
-To avoid selection bias in studies, patients are randomly assigned to treatments to minimize
potential confounding variables.

#Types of analysis in such case:

a) intention-to-treat (ITT) analysis:
-An ITT analysis compares the initial randomized treatment groups (the original
intention) regardless of the eventual treatment to avoid counting crossover patients.

b) Conversely, as-treated analysis/ per protocol

-compares the groups based on the actual treatment received.
-it is performed to gauge the effectiveness of the treatment itself, with less regard for
potential confounders.
6) Power
-Def: Power describes a study's ability to detect an effect (eg, difference between groups)
when one truly exists.

}
• ↑ sample size ↑ power
• ↓ outcome variability ↑ power
• ↑ effect size (difference in 2 results) ↑ power
• ↑ significance level (alpha) ↑ power

#Unsual study where power increased after the results:

the power of the study increased from 80% (before the study started) to 92% (at the end
of the study). Such an increase in statistical power can occur only if above reason.

==> Therefore, the most likely explanation is that the difference in mean serum
triglycerides (ie, effect size) was greater than expected.
7) confidence level C
-refers to how often a CI includes the true
population value if the calculation process is
repeated multiple times.

-CI : estimate a population value (eg,

population mean) is constructed by + and
subtracting a margin of error based on a
desired confidence level from the sample
value (eg, sample mean).

==> A 95% CI has a 95% confidence level

and a 100% − 95% = 5% significance
level; it captures the central 95% of the
distribution.

*
dependent (eg, outcome) and independent
(eg, exposure, risk factor)
Eg: t test
• The quantitative dependent variable : duration of work rounds in minutes.
• The categorical independent variable : type of attending physician supervision (with
categories "increased direct supervision" and "standard supervision").
 8) Per-protocol analysis
includes only nondropouts)

-This approach tends to

provide an estimate of the true
effect of an intervention for a
perfect scenario, but it can
overestimate the effect of the
intervention in a practical
clinical setting.

9) Types of RCT
1) factorial design : involves 2/> experimental →
interventions, each with 2 />variables that are
studied independently.
Vs
2)Parallel design: just 1 variable, rest same

10) approximate proportion (%) of decreased risk in exposed vs non exposed?/ /

relative reduction
==> Dont get confuse by this; they r asking for RRR

11) A confounder is an extraneous factor that has properties linking it with both the
exposure and the outcome of interest.

12) type I and II errors go inversely.

-reduction in sample size results in a greater probability of a type II error and a lower
probability of a type I error (known as alpha [α]).

13) NPV is the probability of being free of a disease if the test result is negative.
Remember: the NPV will vary with the pretest probability (RF) of a disease.

-A patient with a high probability of having a disease will have a low NPV, and a
patient with a low probability of having a disease will have a high NPV.

14) Ecological study:

-Results about associations at the population level may not translate to the individual level:
Ecological fallacy
15) The pre-test probability
-sets your expectations before performing the diagnostic test. It describes the existing
probability of a patient to have the disease in question even before using a particular
diagnostic test.

°
-Statistically, the prevalence is directly related to the pre-test probability.
Vs

=
#post-test probability:
-(PPV) describes the probability of having the disease if the test result is positive.

==>The post-test probability of having the disease is directly related to the PPV.
-

16) Examples of long and short latency:

-Most infectious diseases have relatively short latency periods (ie, the time elapsed
from initial exposure to clinically apparent disease).
-In contrast, some disease processes (eg, cancer, heart disease) have a long latency
period before clinical manifestations develop.

#Latency from risk modifier:

-Sometimes, a significant amount of time must pass before exposure to a risk modifier
has a clinically evident effect on the disease process.

- Eg: at least 1 year of high-dose statin therapy was required to show a significant
protective advantage over moderate-dose therapy.

17) ideal study type for comparing incidence between 2 groups:

-Cohort NOT case control

18) Dont mix the inference:

-Increase the probability that a person with HCV truly has a positive test result :
sensitivity—> Ds comes 1st

-probability that a person with a positive test result will truly have HCV: PPV —> test
comes 1st
Vs

#Likelihood ratio (LR) is the probability of a given test result occurring in a patient with a
disease compared to the probability of the same result occurring in a patient without the
disease. (Likely test result interpreted before taking the test )

LRs are calculated from sensitivity and specificity, so they are not affected by disease
prevalence.
20) natural history of a disease
-It is very important to consider the natural history of a disease when evaluating any drug
trial.
#Case:
-The common cold is a self-limiting disease, which generally resolves within a week. For
this reason, conclusions are difficult to draw regarding the effectiveness of the drug.

-The resolution of symptoms in the 90% of the study population may be due to natural
resolution rather than the drug.

*Prevention:
-For such drug trials, a control group is useful since it helps exclude the bias due to natural
resolution of the disease.

21) #Disadvantage of Cross sectional study:

-it is biased in favor of longer-lasting and milder conditions.

—> More severe chronic conditions tend to be rapidly fatal and are therefore less
likely to be found in a snapshot of the population.

-This means that a cross-sectional study may not be able to estimate the prevalence of
severe chronic conditions. This phenomenon is known as late-look (or Neyman) bias.
22) odds of an event pretest probability of disease
—> the ratio of the probability P that the event happens to the probability that the event
does not happen:
Odds = P / (1 − P)

-def: The pretest probability of disease is the probability of having the disease before
testing.
*Case:
-A useful measure of pretest probability is disease prevalence in the population of interest
(ie, proportion of patients with the disease in a particular population). In this question, 80
individuals have genital human papillomavirus (HPV) and 120 do not, for a sample size of
80 + 120 = 200.
-The pretest probability (ie, prevalence in
this case) of HPV in this population is
80/200 = 0.40. This means that P = 0.40
and (1 − P) = 1 − 0.40 = 0.60

23) Strength of association and dose dependent relation:

1) strong association:
-the RR for bronchogenic cancer in smokers is >2, thereby indicating a strong
association between smoking (risk factor/exposure) and bronchogenic cancer
(outcome).

2) dose-response effect:
-When exposure is measured on a continuous scale (eg, number of packs per day
[PPD]), the classification in 2 or more ordinal categories enables the risk to be
assessed as a function of exposure, and the dose-response effect can be calculated
for the exposure and outcome.

24) Post-hoc analysis

-refers to performing unplanned statistical tests on patterns that were identified
after the fact in data from a completed study.
-This can lead to incorrect conclusions, particularly if the appropriate statistical
measures have not been taken to account for these additional tests.
25) 3) correlation:
-r>0/<0 indicates direction
-r>0.5/ < 0.5 indicates strength of relation:

# r is positive(r>0) if both variable goes in same direction and negative (r<0) if vice
versa
==> values closer to −1 or 1 indicate stronger relationships)
Vs
relationship is very weak if r is closer to 0 than to 1

26) Prevalence ratio

- a ratio of 2 prevalence estimates commonly used in cross-sectional studies to compare
the prevalence of disease among exposed and nonexposed groups of people.

* y not from case control study ??

-In case-control studies, cases and controls are selected from a pool of potential cases and
controls that do not represent the real frequency (ie, prevalence) of disease in the
population.
-Therefore, estimating the prevalence of disease in case-control studies is incorrect and
would lead to bias.

27) for the same data, a CI with a greater confidence level (eg, 95 CI %) is always wider
(eg, capturing 95% of the distribution) than a CI with a lower confidence level (eg,
90% CI).

-the narrower 90% CI, the lower and upper boundaries may both be positive values; but for
the wider 95% CI, the lower boundary may be a negative value whereas the upper
boundary may be a positive value.

-Therefore, the statistical significance of the 95% CI cannot be determined

 28)
a) Effective modification:
- not necessarily change from
non significant to significant after
stratification
—> but RR becomes >
significant (I.e increases in
number from 1 to 3 )
—> only associated with Ds

Vs
# Confounding:
-stratification causes
significant to non significant

—> associated with both Ds

and RF
29) Dontget confused by
word “risk” (it’s same
as RR)
30) when does a study have
insufficient power??
-Failure to show a statistically
significant association
between a risk factor and an
outcome is often due to
insufficient power (eg, due to a
small sample size) to detect an
association.
31) Framing null hypothesis in different type of study design:
a) Cross sectional: Use the word “association”
- a statement of no association between variables of interest.

b) case control: use the word “risk factor”

-In cross-sectional study, the temporal relationship between the 2 variables cannot be
determined. So this can’t be used there

c) cohort study: “risk” word

-“ The risk of colon cancer is the same for subjects with and without elevated CRP levels”
-cz here, individuals with and without elevated CRP levels are followed over time to
determine the risk of colon cancer.
32) dont mix the following inferences:
-accuracy : the probability that an individual is correctly classified by the test
Vs
-PPV: probability that a positive test result correctly identifies an infected individual
-NPV: the probability that a negative test result correctly identifies an uninfected
individual.
Vs
-negative likelihood ratio: (ie, probability of a negative test result occurring in an infected
patient compared to an uninfected patient)

33) inference from below case:

-The odds ratio for tampon use among patients with TSS compared to healthy subjects
(controls) was reported as 5.0 (95% confidence interval [4.7-5.2], p <0.01).
-The authors concluded that the risk of TSS was approximately 5 times higher in tampon
users

Above both sentence represents OR=RR. So TSS is a rare Ds

34) volunteers bias /subtype of selection bias.

-A sample of volunteers (eg, nonrandom) is likely to misrepresent its target population
because individuals who volunteer for a study may differ from those who do not.

35) rare case RF ideal study:

*Case: the patient was diagnosed with a rare type of cancer (adenoid cystic
carcinoma, ACC) and asks about risk factors for ACC.

-This means that the study must be analytical (ie, able to test hypotheses about
associations between risk factors and ACC)
==> The case-control study is the most appropriate analytical design to study
uncommon (rare) diseases and diseases with a long latent period.

36) ANOVA
#what does statistically significant in ANOVA mean??
-Analysis of variance (ANOVA) compares the means of ≥3 independent groups.
—> However, a statistically significant ANOVA indicates only that at least 1 group mean
is different from the rest.

#How to overcome this shortcomings of ANOVA??

- Therefore, further evaluation is required to determine which group means differ.
-It is possible to use confidence intervals (CIs) to determine whether means of >2
groups are different.
• If CIs do not overlap: significant difference between the groups' means.
• If CIs overlap: may / may not be a significant difference between the groups' means.
PUBLIC HEALTH SCIENCES PUBLIC HEALTH SCIENCES—EPIDEMIOLOGY AND BIOSTATISTICS
`  SEC TION II 269

Confidence interval Range of values within which the true mean H0 is rejected (and results are significant) when:
of the population is expected to fall, with a ƒ 95% CI for mean difference excludes 0
specified probability. ƒ 95% CI OR or RR excludes 1
CI = 1 – α. The 95% CI (corresponding to ƒ CIs between two groups do not overlap
α = 0.05) is often used. As sample size H0 is accepted (and results are significant)
increases, CI narrows. when:.
CI for sample mean = x ± Z(SE) ƒ 95% CI for mean difference includes 0
For the 95% CI, Z = 1.96. ƒ 95% CI OR or RR includes 1
For the 99% CI, Z = 2.58. ƒ CIs between two groups do overlap

Meta-analysis A method of statistical analysis that pools summary data (eg, means, RRs) from multiple studies
for a more precise estimate of the size of an effect. Also estimates heterogeneity of effect sizes
between studies.
Improves power, strength of evidence, and generalizability (external validity) of study findings.
Limited by quality of individual studies and bias in study selection.

Common statistical tests

t-test Checks differences between means of 2 groups. Tea is meant for 2.
Example: comparing the mean blood pressure
between men and women.
ANOVA Checks differences between means of 3 or more 3 words: ANalysis Of VAriance.
groups. Example: comparing the mean blood pressure
between members of 3 different ethnic groups.
Fisher’s exact test Checks differences between 2 percentages or Example: comparing the percentage of 20 men
proportions of categorical, nominal outcomes. and 20 women with hypertension.
Use instead of chi-square test with small
populations.
Chi-square (χ²) Checks differences between 2 or more Pronounce chi-tegorical.
percentages or proportions of categorical Example: comparing the proportion of
outcomes (not mean values). members of 3 age groups who have essential
hypertension.

Variables to be compared

Numerical (means) Categorical (proportions)

2 groups ≥ 3 groups Small sample size Large sample size

t-test ANOVA Fisher’s exact text Chi-square test

If n <10/20
37) The Kaplan-Meier survival curve
- a commonly used graphic representation of the probabilities that subjects survive
in a study without an event of interest.
-The event-free survival rates of ≥2 study groups can be compared;

-The statistical test that compares KM survival curves is the log-rank test.
38) A study with a smaller sample size can control
for potential confounders as much as a study with a
larger sample size.

oii
-this implies even if control size increases
>cases
39) Limitations of cohort

: -A cohort study begins by identifying individuals

as exposed or nonexposed to 1 risk factor and
ends by comparing the incidence of ≥1
=
outcomes (ie, disease) between the 2 groups.

Vs
#Limitation of Case-control studies :
- consider only 1 outcome (ie, disease) per study but can evaluate exposure to ≥1 risk
factors.

40) #case control study clue

-whenever individuals were initially selected based on their status for a particular disease
(ie, case: ARTI; control: no ARTI) and then categorized based on past exposure to a risk
factor (ie, attendance at a social gathering), the study is a case-control design.

- questionnaire can also be used in case control study like cross sectional study
. So don’t mix css as they mostly give prevalence

41) Meta analysis: biostat review

-employed to increase the power of the study
-if the outcome is rare and Diff between 2 groups is small, meta analysis is conducted
*disadv:
- it also adds up all the bias and limitations of all the study

-
42) coefficient of
determination= squaring the
correlation coefficient
-this expresses % of variability
in the outcome factor that is
explained by the predictor
factor
-if for eg: r=0.8, them co of
deter = 0.64
 ÷
-

43) odds of increase of any variable= OR variable - 1 (null OR) = in %

44) Attributable risk %= attributable risk/ incidence of Ds in exposed

Or
1- RR/ RR

# Inference: 50% of the yearly RS Ds in smokers is attributed to smoking

45) Population attributable risk % describes the impact of exposure on the entire study
population
= attributable risk ( incidence of Ds in whole population- incidence in placebo)/
incidence of the Ds in population

#Inference: x% of the yearly RS Ds in the study population is attributable to smoking

47) don’t mix ecological study with cross sectional area:

-if entire data is used as a whole—> ecological
Vs
-if only +Ve syphilis cases were retrieved from the healthcare survey to determine the
prevalence of syphilis and genitourinary chlamydia at a single point in time is consistent
with a cross-sectional study.
 ##Step 3
40) The attributable risk percent (ARP) is a measure of excess risk. It estimates the
proportion of the disease in exposed subjects that is attributed to exposure status.

-ARP = (Risk in exposed - Risk in unexposed) / Risk in exposed.

-The second uses relative risk (RR): ARP = (RR - 1) / RR

41) The percentage of ischemic strokes in the observed population that is attributable to
smoking is given by the population attributable risk percent (PARP).
-Unlike attributable risk percent, PARP is the measure of excess risk in the total population,
not only in exposed subjects. PARP compares 2 risks (or incidences):

PARP = (Risk in total population - Risk in unexposed) / Risk in total population

-Given the risk of stroke among the exposed (0.1%) and the unexposed (0.05%), as well as
the proportion of exposure in the population (0.5), the risk in the total population can be
calculated as a weighted average:

Risk in total population = (Risk in smokers)(Proportion of smokers) + (Risk in

nonsmokers)(Proportion of nonsmokers) = (0.1%)(0.5) + (0.05%)(0.5) = 0.075%.

42) LRs can be used to calculate post-test odds (post-test odds = pre-test odds * LR),
providing clinically relevant information for individual patients based on their pre-test odds of
disease.

-Other advantages of LRs are that they can be used with tests that have >2 possible test
results and they can be used to combine the results of multiple diagnostic tests.

43) verification bias/ workup bias:

-a type of measurement bias that occurs when a study uses gold standard testing
selectively in order to confirm a positive (or negative) result of preliminary testing; this can
result in overestimates (or underestimates) of sensitivity (or specificity).

—> A possible method to reduce verification bias is to perform gold standard testing in a
random sample of participants with negative results

44) Contamination bias

-occurs when the control group unintentionally receives the treatment or the intervention,
thereby reducing the difference in outcomes between the control and treatment group.

45) Publication bias

- occurs when studies with significant, positive results are published or considered for
inclusion in systematic reviews and meta-analyses, but studies with negative or
nonsignificant results are not.
Pharmacology
550 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PHARMACOLOGY
` 

Inhaled anesthetics Desflurane, halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, N2O.

MECHANISM Mechanism unknown.
EFFECTS
 cerebral metabolic demand.
O
Myocardial depression, respiratory depression, postoperative nausea/vomiting,  cerebral blood flow,
-

ADVERSE EFFECTS Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane,

epileptogenic), expansion of trapped gas in a body cavity (N2O).
Malignant hyperthermia—rare, life-threatening condition in which inhaled anesthetics or
succinylcholine induce severe muscle contractions and hyperthermia. Susceptibility is often
inherited as autosomal dominant with variable penetrance. Mutations in voltage-sensitive
ryanodine receptor (RYR1 gene) cause  Ca2+ release from sarcoplasmic reticulum.
Treatment: dantrolene (a ryanodine receptor antagonist).

Intravenous anesthetics
AGENT MECHANISM ANESTHESIA USE NOTES
Thiopental Facilitates GABA A (barbiturate) Anesthesia induction, short  cerebral blood flow. High lipid
surgical procedures solubility
Effect terminated by rapid
redistribution into tissue, fat
Midazolam Facilitates GABA A Procedural sedation (eg, May cause severe postoperative
(benzodiazepine) endoscopy), anesthesia respiratory depression,  BP,
induction anterograde amnesia
Propofol Potentiates GABA A Rapid anesthesia induction,
short procedures, ICU
May cause respiratory
depression, hypotension VE
sedation -

Ketamine NMDA receptor antagonist Dissociative anesthesia  cerebral blood flow

- preserve respiration Sympathomimetic Emergence reaction possible
with disorientation,
hallucination, vivid dreams
Etomidate: suppress cortisol

Local anesthetics Esters—procaine, tetracaine, benzocaine, chloroprocaine.

Amides—lIdocaIne, mepIvacaIne, bupIvacaIne, ropIvacaIne (amIdes have 2 I’s in name).
MECHANISM Block Na+ channels by binding to specific receptors on inner portion of channel. Most effective in
rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then
bind to ion channels as charged form.
Can be given with vasoconstrictors (usually epinephrine) to enhance local action— bleeding,
 anesthesia by  systemic concentration.
In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane
effectively Ž need more anesthetic.
Order of nerve blockade: small-diameter fibers > large diameter. Myelinated fibers > unmyelinated
fibers. Overall, size factor predominates over myelination such that small myelinated fibers
> small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.
Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.
CLINICAL USE Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.
ADVERSE EFFECTS CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension,
arrhythmias (cocaine), methemoglobinemia (benzocaine).
 NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PHARMACOLOGY
`  SEC TION III 551

Neuromuscular Muscle paralysis in surgery or mechanical ventilation. Selective for Nm nicotinic receptors at
blocking drugs neuromuscular junction but not autonomic Nn receptors.
Depolarizing Succinylcholine—strong ACh receptor agonist; produces sustained depolarization and prevents
neuromuscular muscle contraction.
blocking drugs Reversal of blockade:
ƒ Phase I (prolonged depolarization)—no antidote. Block potentiated by cholinesterase inhibitors.
ƒ Phase II (repolarized but blocked; ACh receptors are available, but desensitized)—may be
reversed with cholinesterase inhibitors.
Complications include hypercalcemia, hyperkalemia, malignant hyperthermia.
Nondepolarizing Atracurium, cisatracurium, pancuronium, rocuronium, tubocurarine, vecuronium—competitive
neuromuscular ACh antagonist.
blocking drugs Reversal of blockade—cholinesterase inhibitors (eg, neostigmine, edrophonium) are given with
anticholinergics (eg, atrophine, glycopyrrolate) to prevent muscarinic effects, such as bradycardia.

Spasmolytics, antispasmodics
DRUG MECHANISM CLINICAL USE NOTES
Baclofen GABA B receptor agonist in Muscle spasticity, dystonia, Acts on the back (spinal cord).
spinal cord. multiple sclerosis.
Cyclobenzaprine Acts within CNS, mainly at the Muscle spasticity. Centrally acting. Structurally
brain stem. related to TCAs. May cause
anticholinergic side effects,
sedation.
Dantrolene Prevents release of Ca2+ from Malignant hyperthermia Acts Directly on muscle.
sarcoplasmic reticulum of (toxicity of inhaled anesthetics
skeletal muscle by inhibiting and succinylcholine) and
the ryanodine receptor. neuroleptic malignant
syndrome (toxicity of
antipsychotic drugs).
Tizanidine α2 agonist, acts centrally. Muscle spasticity, multiple
sclerosis, ALS, cerebral palsy.

Opioid analgesics
MECHANISM Act as agonists at opioid receptors (μ = β-endorphin, δ = enkephalin, κ = dynorphin) to modulate
synaptic transmission—close presynaptic Ca2+ channels, open postsynaptic K+ channels
Ž  synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.
EFFICACY Full agonist: morphine, heroin, meperidine, methadone, codeine, fentanyl.
Partial agonist: buprenorphine.
Mixed agonist/antagonist: nalbuphine, pentazocine, butorphanol.
Antagonist: naloxone, naltrexone, methylnaltrexone.
CLINICAL USE Moderate to severe or refractory pain, diarrhea (loperamide, diphenoxylate), acute pulmonary
edema, maintenance programs for heroin addicts (methadone, buprenorphine + naloxone).
ADVERSE EFFECTS Nausea, vomiting, pruritus, addiction, respiratory depression, constipation, sphincter of Oddi
spasm, miosis (except meperidine Ž mydriasis), additive CNS depression with other drugs.
Tolerance does not develop to miosis and constipation. Treat toxicity with naloxone (competitive
opioid receptor antagonist) and prevent relapse with naltrexone once detoxified.
 566 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PHARMACOLOGY
` 

Barbiturates Phenobarbital, pentobarbital, thiopental, secobarbital.

MECHANISM Facilitate GABA A action by  duration of Cl− channel opening, thus  neuron firing (barbidurates
 duration).
CLINICAL USE Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).
ADVERSE EFFECTS Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by
alcohol use); dependence; drug interactions (induces cytochrome P-450).
Overdose treatment is supportive (assist respiration and maintain BP).
Contraindicated in porphyria.

Benzodiazepines Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide,

alprazolam.
MECHANISM Facilitate GABA A action by  frequency of Cl– channel opening (“frenzodiazepines”  frequency).
 REM sleep. Most have long half-lives and active metabolites (exceptions [ATOM]: Alprazolam,
Triazolam, Oxazepam, and Midazolam are short acting Ž higher addictive potential).

=
CLINICAL USE Anxiety, panic disorder, spasticity, status epilepticus (lorazepam, diazepam, midazolam), eclampsia,
detoxification (eg, alcohol withdrawal/DTs; long-acting chlordiazepoxide and diazepam are
preferred), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic
(insomnia). Lorazepam, Oxazepam, and Temazepam can be used for those with liver disease who
drink a LOT due to minimal first-pass metabolism.
ADVERSE EFFECTS Dependence, additive CNS depression effects with alcohol and barbiturates (all bind the GABA A
receptor). Less risk of respiratory depression and coma than with barbiturates. Treat overdose with
flumazenil (competitive antagonist at GABA benzodiazepine receptor). Can precipitate seizures
by causing acute benzodiazepine withdrawal.

#Non BZD:
a) Zaleplon :very short half-life (∼ 1 hour).
-Use: Therefore, it is effective for the treatment of sleep-onset insomnia

b) Zolpidem : a longer half-life than Zaleplon (up to 4.5 hours).

-It is used for patients that have difficulty with sleep onset and/or sleep maintenance.

*Adv over BZD:

-Non-benzodiazepines have marked sedative effects and are not associated with drug
dependence. Because of their more favorable side effect profile, they are preferred
over benzodiazepines for the treatment of sleep disorders, particularly among elderly
persons (except zolpidem increases the risk for falls in elderly).
-However, like benzodiazepines, they are not approved for long-term use.
568 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PHARMACOLOGY
` 

Parkinson disease The most effective treatments are non-ergot dopamine agonists which are usually started in
therapy younger patients, and Levodopa (with carbidopa) which is usually started in older patients. Deep
brain stimulation of the STN or GPi may be helpful in advanced disease.
STRATEGY AGENTS
Dopamine agonists Non-ergot (preferred)—pramipexole, ropinirole; toxicity includes nausea, impulse control disorder
(eg, gambling), postural hypotension, hallucinations, confusion.

I
Ergot—bromocriptine rarely used due to toxicity.
 dopamine availability Amantadine ( dopamine release and  dopamine reuptake); toxicity = peripheral edema, livedo
reticularis, ataxia.
 L-DOPA availability Agents prevent peripheral (pre-BBB) l-DOPA degradation Ž  l-DOPA entering CNS Ž  central
l-DOPA available for conversion to dopamine.
ƒ Levodopa (l-DOPA)/carbidopa—carbidopa blocks peripheral conversion of l-DOPA to
dopamine by inhibiting DOPA decarboxylase. Also reduces side effects of peripheral l-DOPA
conversion into dopamine (eg, nausea, vomiting).
ƒ Entacapone and tolcapone prevent peripheral l-DOPA degradation to 3-O-methyldopa
(3-OMD) by inhibiting COMT. Used in conjunction with levodopa.
Prevent dopamine Agents act centrally (post-BBB) to inhibit breakdown of dopamine.
breakdown ƒ Selegiline, rasagiline—block conversion of dopamine into DOPAC by selectively inhibiting MAO-B.
ƒ Tolcapone—crosses BBB and blocks conversion of dopamine to 3-methoxytyramine (3-MT) in
the brain by inhibiting central COMT.
Curb excess Benztropine, trihexyphenidyl (Antimuscarinic; improves tremor and rigidity but has little effect on
cholinergic activity bradykinesia in Parkinson disease). Tri Parking my Mercedes-Benz.
DOPA
DECARBOXYLASE CIRCULATION
Dopamine 3-OMD
INHIBITOR
– L-DOPA
COMT INHIBITORS
Carbidopa DDC COMT – (peripheral)

BLOOD-
BRAIN Entacapone
BARRIER Tolcapone

L-DOPA

DDC COMT INHIBITOR

(central)
PRESYNAPTIC
Dopamine –
TERMINAL FROM THE Tolcapone
SUBSTANTIA NIGRA COMT
3-MT
DOPAC

–
Autoregulatory MAO TYPE B
receptor INHIBITORS
Reuptake
Selegiline
Rasagiline

DOPAMINE +
AVAILABILITY

Amantadine

Dopamine receptors + DOPAMINE AGONISTS

POSTSYNAPTIC
TERMINAL IN
THE STRIATUM Pramipexole (non-ergot)
Ropinirole (non-ergot)
Bromocriptine (ergot)
448 SEC TION III HEMATOLOGY AND ONCOLOGY HEMATOLOGY AND ONCOLOGY—PHARMACOLOGY
` 

Cancer therapy—cell cycle

Bleomycin Microtubule inhibitors
Taxanes
– Vinca alkaloids
– –

G2 Mit M
os
Double check is
repair
–
is
nes
oki
Cy t
Topoisomerase inhibitors
Etoposide

INT
Teniposide RP

E
Irinotecan HASE Duplicate
–
Topotecan DNA cellular content
synthesis Cell cycle–independent drugs
Antimetabolites – G1 Platinum compounds
Cladribine* GO Alkylating agents:
Cytarabine S Resting Anthracyclines
5-fluorouracil Busulfan
Hydroxyurea Dactinomycin
Methotrexate Rb, p53 modulate Nitrogen mustards
*Cell cycle Pentostatin G1 restriction point Nitrosoureas
nonspecific Thiopurines Procarbazine

Cancer therapy—targets
Nucleotide synthesis DNA RNA Protein Cellular division

MTX, 5-FU: Vinca alkaloids:

Alkylating agents, platinum compounds:
↓ thymidine synthesis inhibit microtubule formation
cross-link DNA

Thiopurines: Taxanes:
Bleomycin:
↓ de novo purine synthesis inhibit microtubule disassembly
DNA strand breakage

Hydroxyurea: Anthracyclines, dactinomycin:

inhibits ribonucleotide DNA intercalators
reductase
Etoposide/teniposide:
inhibits topoisomerase II

Irinotecan/topotecan:
inhibits topoisomerase I
 PHARMACOLOGY PHARMACOLOGY—AUTONOMIC DRUGS
`  SEC TION II 249

Phosphodiesterase Phosphodiesterase (PDE) inhibitors inhibit PDE, which catalyzes the hydrolysis of cAMP and/or
inhibitors cGMP, and thereby increase cAMP and/or cGMP. These inhibitors have varying specificity for
PDE isoforms and thus have different clinical uses.
TYPE OF INHIBITOR MECHANISM OF ACTION CLINICAL USES ADVERSE EFFECTS
Nonspecific PDE  cAMP hydrolysis Ž  cAMP COPD/asthma (rarely used) Cardiotoxicity (eg, tachycardia,
inhibitor Ž bronchial smooth muscle arrhythmia), neurotoxicity
Theophylline relaxation Ž bronchodilation (eg, seizures, headache),
abdominal pain
PDE-5 inhibitors  hydrolysis of cGMP Erectile dysfunction Facial flushing, headache,
Sildenafil, vardenafil, Ž  cGMP Ž  smooth Pulmonary hypertension dyspepsia, hypotension in
tadalafil, avanafil muscle relaxation by Benign prostatic hyperplasia patients taking nitrates; “hot
enhancing NO activity (tadalafil only) and sweaty,” then headache,
Ž pulmonary vasodilation heartburn, hypotension
and  blood flow in corpus Sildenafil only: cyanopia (blue-
cavernosum fills the penis tinted vision) via inhibition of
PDE-6 (six) in retina
PDE-4 inhibitor  cAMP in neutrophils, Severe COPD Abdominal pain, weight loss,
Roflumilast granulocytes, and bronchial depression, anxiety, insomnia
epithelium
PDE-3 inhibitor In cardiomyocytes: Acute decompensated HF with Tachycardia, ventricular
Milrinone  cAMP Ž  Ca2+ influx cardiogenic shock (inotrope) arrhythmias, hypotension
Ž  ionotropy and
chronotropy
In vascular smooth muscle:
 cAMP Ž MLCK inhibition
Ž vasodilation Ž  preload
and afterload
“Platelet inhibitors” In platelets:  cAMP Intermittent claudication Nausea, headache, facial
Cilostazola Ž inhibition of platelet Stroke or TIA prevention (with flushing, hypotension,
Dipyridamoleb aggregation aspirin) abdominal pain
Cardiac stress testing
(dipyridamole only, due to
coronary vasodilation)
Prevention of coronary stent
restenosis
a
Cilostazol is a PDE-3 inhibitor, but due to its indications is categorized as a platelet inhibitor together with dipyridamole.
b
Dipyridamole is a nonspecific PDE inhibitor, leading to inhibition of platelet aggregation. It also prevents adenosine reuptake
by platelets Ž  extracellular adenosine Ž  vasodilation.
1) Phenytoin ADR:
-commonly causes megaloblastic anemia and gingival hyperplasia due to impaired folic
acid absorption in the jejunum. Supplementation with FA prevents this.

-Calcium and vitamin D supplementation are also usually given to counter alterations in
bone mineral metabolism that impair bone density

2) Mx steps of NMS:
-onset: anytime anytime but usually within 2 weeks of antipsychotic/ antiemetic Rx
• Stop antipsychotics or restart dopamine agents
• Supportive care (hydration, cooling), intensive care unit
• Benzodiazepines: improve agitation and relaxes muscles
• Bromocriptine / dantrolene/ amantadine if refractory
Disease-modifying antirheumatic drugs
Agent Mechanism Adverse effects
• Hepatotoxicity-Avoid Alcohol
• Stomatitis, Painful oral ulcers, Rash
Methotrexate • Folate antimetabolite—
• ILD
> Megaloblastic anemia
• Cytopenias
1st line DMARDs for RA (MCV>100)
Mx :
• folinic acid, even for Hepatotoxicity
• Pyrimidine synthesis • Hepatotoxicity
Leflunomide
inhibitor • Cytopenias
• Retinopathy
Hydroxychloroquine • TNF & IL-1 suppressor
—>> Bull’s eye maculopathy
• Hepatotoxicity
Sulfasalazine • TNF & IL-1 suppressor • Stomatitis
• Hemolytic anemia
• Neutropenia —> Infection —>
TNF inhibitors Reactivation of Latent TB (so start
(eg, adalimumab, after negative PPD)
certolizumab, etanercept, • Demyelination
golimumab, infliximab) • Congestive heart failure
• Malignancy

4) TCA cardiotoxicity
-MOA: TCA inhibition of fast sodium channels in the His-Purkinje system and myocardium.
This decreases conduction velocity, increases the duration of repolarization, and prolongs
absolute refractory periods.
-QRS prolongation and ventricular arrhythmias (eg, ventricular tachycardia, ventricular
fibrillation) may result.

#Sod bicarbonate
A QRS interval >100 msec / ventricular arrhythmia in the setting of TCA overdose is an
indication for sodium bicarbonate therapy.

-Sodium bicarbonate likely improves cardiac toxicity through the following mechanisms:
• Increasing serum pH makes the TCA less pharmacologically active, decreasing its
avidity for sodium channels.
 • Increasing extracellular sodium concentration raises the electrochemical gradient
across cardiac cell membranes, decreasing the impact of the TCA-induced sodium
channel blockade.

Sodium bicarbonate infusion also improves TCA-induced hypotension, which is caused by

alpha-1 adrenergic receptor antagonism

5) Duration of action of common benzodiazepines

Short
hepatic metabolism via phase II glucuronidation
Triazolam, midazolam, MTs instead of phase I cytochrome P450 oxidation
(half-life <6 hr)
Intermediate are preferred in patients with evidence of liver
Oxazepam, alprazolam, lorazepam,
(half-life 6-50
clonazepam COLA dysfunction. Oxazepam, temazepam, and
hr)
lorazepam fulfill these criteria
Long
(half-life >50 Diazepam, chlordiazepoxide, flurazepam
hr)

6) Calcineurin inhibitors
-nephrotoxicity, hypertension, neurotoxicity (eg, tremor), and impaired glucose control

7) Glucocorticoid myopathy:
-the only cause of painless myopathy

8) Isoniazid, idiosyncratic liver injury with a histological picture similar to viral hepatitis
must be considered
. with -Ve Viral serology

9) MOA of drugs
1)Statins : inhibit HMG-CoA reductase, a rate-limiting enzyme in the intracellular
biosynthesis of cholesterol that converts HMG-CoA to mevalonate.

2)Immune-mediated reactions
-drug-induced conditions such as membranous glomerulonephritis induced by captopril.

3)Cell surface receptor blockage

- primary action of many cardiovascular drugs (eg, beta blockers, alpha blockers, calcium
channel blockers).
-This action is also responsible for some of the noncardiac adverse effects seen with
nonselective beta blockers (eg, bronchospasm).

4)ACE inhibitors (eg, lisinopril) : extracellular enzyme blockers

10) EPO:
#Indication: All patients with significant renal failure and a hemoglobin <10 g/dL are
candidates for ESAs after iron deficiency has been ruled out.
#ADR:
-Onset: Up to 30% of patients on erythropoietin therapy develop new or worsening
hypertension, which typically occurs 2-8 weeks after treatment initiation.

-Hypertension is generally mild but can be severe, leading to end-organ damage (eg,
encephalopathy, seizures).
-RF: Large doses of erythropoietin or rapidly rising hemoglobin soon after administration
increase the risk of hypertension.

-Monitoring: patients started on erythropoietin require close BP monitoring.

11) even inhaled GC can cause:

-neutrophilia, eosinopenia and lymphopenia

12) Beta blocker overdose vs no AMS and hypoglycaemia in CCB overdose

-C/F: bradycardia, hypotension, wheezing (specific), hypoglycemia, delirium,
seizures, and cardiogenic shock.

-Mx: priority: Rx consists of airway management, followed by correction of

hypotension and hypoglycemia.
• 1st Line: IV fluids, Secure airway GI decontamination; IV fluid boluses
• IV atropine
• IV glucagon if refractory

13) anticoagulation of choice in RF:

-unfractionated heparin is preferred over LMWH, fondaparinux, and rivaroxaban in patients
with severe renal insufficiency (estimated GFR <30 mL/min/1.73 m2) as reduced renal
clearance increases anti-Xa activity levels and bleeding risk.

14) hyperkalemia with trimethoprim:

-MOA: due to blockade of the epithelial sodium channel in the collecting tubule. Enac
-also competitively inhibits renal tubular creatinine secretion and may cause an artificial
increase in serum creatinine without affecting the glomerular filtration rate.

15) ACEI induced cough:

-At risk population: Women and individuals of Chinese descent
a tickling or scratching sensation in the throat (as reported by this patient) is a common
feature.
—> If the cough is significantly bothersome, discontinuing the drug typically results in
resolution of the cough within days.
 Drugs for neuropathic pain 16) Rx of neuropathic pain in
cardiac pt:
Drug Mechanism of action -Although amitriptyline is effective for
Tricyclic reducing neuropathic pain, it should
antidepressants be used with caution in patients
• ↓ Reuptake of serotonin &
(eg, amitriptyline, age >65 due to its anticholinergic
norepinephrine
nortriptyline)
SNRIs (eg,
• Inhibition of pain signals effects, and
duloxetine)
-it is not recommended in patients
Anticonvulsants
• Decreased depolarization of with pre-existing cardiac disease
(eg, gabapentin,
neurons in CNS due to the risk of precipitating
pregabalin)
conduction abnormalities.
• Activation of central opioid
Opioids
receptors
• Loss of membrane potential in
Capsaicin (topical)
nociceptive fibers
• Decreased depolarization of
Lidocaine (topical)
neurons in peripheral nerves

#Pregabalin MOA:
-a structural analogue of GABA and decreases pain by inhibiting the release of excitatory
NT by binding to voltage-gated ca modulators on nerve terminals. -Common S/E:
drowsiness, weight gain, and fluid retention.

17) y conventional B blockers unsafe in diabetes??

a) glucose intolerance
#Pathogenesis :
-Normally, alpha-1 receptor stimulation causes vasoconstriction, which reduces
glucose uptake into skeletal muscles (due to reduced skeletal muscle blood flow);
beta-2 receptor stimulation opposes this effect.

-In the presence of beta blockade, alpha-1‒mediated effects are unopposed, leading to
further reduction in glucose uptake, higher levels of circulating glucose, and resultant
increased insulin secretion from the pancreas.

b) wt gain
-Insulin resistance is effectively increased (ie, insulin sensitivity is reduced). As a result,
patients experience weight gain.
A reduction in lipolysis in adipocytes (which is largely beta-1 receptor–mediated)
likely also contributes to weight gain.

#then which drugs are safer ??

-In contrast, beta blockers with combined vasodilatory alpha-1 receptor‒blocking properties
(eg, carvedilol, labetalol)
18) y BZD avoided in dementia ??
-Benzodiazepines (eg, lorazepam) generally do not have a role in the treatment of
dementia-related neuropsychiatric symptoms due to their significant

-potential for adverse effects (eg, worsening gait/falls, physical dependence,

paradoxical disinhibited agitation).

*Indication in akathisia:
-Although benzodiazepines are sometimes used to symptomatically treat symptoms of
akathisia, this approach is reserved for cases in which dose reduction or
discontinuation has failed.

19) opioids
-Management options for acute
pain (including opioids) will be
similar for all patients regardless
of substance use history,
although those with a history of
opioid addiction who are given
opioid analgesics may need close
follow-up care to avoid relapse.

-Transdermal fentanyl : indicated

for long-term management of
pain in patients who require daily,
continuous pain relief.

-Methadone is used in maintenance therapy for patients with opioid addiction and is
occasionally used for its analgesic effects in patients with chronic pain.

20) Succinylcholine
- a depolarizing neuromuscular blocker that can cause life-threatening hyperkalemia in
patients with a condition leading to upregulation of postsynaptic acetylcholine
receptors (eg, skeletal muscle trauma, burn injury, stroke).

#Mx:
-Nondepolarizing neuromuscular blocking agents (eg, vecuronium, rocuronium) should be
used with these patients.
21) anaesthesia ADRs :
1) Halothane :halothane-associated liver toxicity.

2) Etomidate :
- inhibits 11β-hydroxylase and can lead to adrenal insufficiency.
- RF: elderly and patients with critical illness (eg, sepsis)

3) Nitrous oxide :
- inactivates vitamin B12, leading to inhibition of methionine synthase activity;

4) Propofol :
- Severe hypotension due to myocardial depression is a common ADR of propofol.
- avoided/ used with extreme caution in patients with ventricular systolic dysfunction.

22) OTC Medicines for Cold causing Acute onset Psychosis in children :
1) Over-the-counter antihistamines (eg, diphenhydramine, doxylamine) decrease nasal
discharge also have anticholinergic properties —> cause confusion & hallucinations.

2) Alpha-adrenergic agents (eg, phenylephrine, pseudoephedrine) —> agitation &

psychosis via sympathomimetic properties.

3) cough suppressant dextromethorphan, which is an NMDA antagonist, can result in —

> dissociative symptoms and hallucinations.

Side effects of over-the-counter medications may be cumulative when used in combination

or in excess of recommended doses.

Vs
-Children often use imaginary friends to comfort themselves in times of stress.

—>the acute onset of hallucinations following initiation of new medications is more

likely a medication side effect, especially considering that the parents have reported
this as unusual behavior for the child.

23) A mild rash may develop in up to 10% of those treated with lamotrigine, whereas life-
threatening SJS/TEN may occur in 0.1%.
*Mx:
-Any occurrence of rash during the treatment of lamotrigine requires immediate
discontinuation of the drug.
 24) Aspirin and beta blockers exacerbating asthma
Short-term use of cardioselective beta blockers is usually safe in patients with mild-to-
moderate asthma, but all beta blockers should be used with caution.

25) Medication-induced psychotic disorder

- characterized by the acute onset of delusions and/or hallucinations that are temporally
associated with the use of a new medication.
-Glucocorticoids, particularly at high doses, are often implicated in new-onset psychotic

Methotrexate-induced lung injury

26) Secondary hypogonadism
Pathoge • Idiosyncratic (ie, not dose dependent) - a common adverse effect of
nesis hypersensitivity pneumonitis opioids, which suppress GnRH and
& risk • Risk factors: rheumatoid arthritis, LH secretion, leading to reduced
factors parenchymal lung disease Leydig cell testosterone
• Onset 1-12 months: pneumonitis → synthesis.
fibrosis (restrictive PFTs)
27) Key idea: Many antiepileptics
• CT scan with variable mix of patterns: (including phenobarbital and
inflammation (eg, GGO, consolidation) carbamazepine) lead to induction
Clinical
& fibrosis (eg, reticulation)
features of the cytochrome P-450 system,
• BAL: lymphocytosis; peripheral blood:
which leads to increased
eosinophilia metabolism of vitamin D and can
• Trial of MTX cessation is diagnostic & lead to vitamin D deficiency (seen in
therapeutic up to 50% of patients taking long-
term anti-epileptic therapy)
GGO = ground-glass opacities

-Key idea: Carbamazepine also associated with folate deficiency, but that would not
affect bone health and would instead lead to a megaloblastic anemia

28) MOA of orthostatic hypotension by different drugs:

a) Vasodilators
-increase (rather than decrease) venous capacitance (eg, pooling of blood)—>
impairs mobilization of blood back to the heart and contribute to orthostatic hypotension
and syncope.

b) alpha 1 blocker:
-With smooth muscle alpha-1 receptors blocked (on both capacitance veins and
peripheral arterioles), vasoconstrictive sympathetic output is disrupted; therefore,
on standing, blood cannot be mobilized from capacitance veins to increase venous return
and systemic vascular resistance cannot be increased to help maintain BP.

-Consequently, cardiac output and cerebral perfusion drop, and syncope can occur.
-a decrease in alpha 1 mediated arteriolar smooth M contractility
 MICROBIOLOGY MICROBIOLOGY—ANTIMICROBIALS
`  SEC TION II 189

Cephalosporins
MECHANISM β-lactam drugs that inhibit cell wall synthesis Organisms typically not covered by 1st–4th
but are less susceptible to penicillinases. generation cephalosporins are LAME:
Bactericidal. Listeria, Atypicals (Chlamydia, Mycoplasma),
MRSA, and Enterococci.
CLINICAL USE 1st generation (cefazolin, cephalexin)—gram ⊕ 1st generation—⊕ PEcK.
cocci, Proteus mirabilis, E coli, Klebsiella
pneumoniae. Cefazolin used prior to surgery to
prevent S aureus wound infections.
2nd generation (cefaclor, cefoxitin, cefuroxime, 2nd graders wear fake fox fur to tea parties.
cefotetan)—gram ⊕ cocci, H influenzae, 2nd generation—⊕ HENS PEcK.
Enterobacter aerogenes, Neisseria spp., Serratia
marcescens, Proteus mirabilis, E coli, Klebsiella
pneumoniae.
3rd generation (ceftriaxone, cefotaxime, Can cross blood-brain barrier.
cefpodoxime, ceftazidime, cefixime)—serious Ceftriaxone—meningitis, gonorrhea,
gram ⊝ infections resistant to other β-lactams. disseminated Lyme disease.
Ceftazidime—Pseudomonas.

E
4th generation (cefepime)—gram ⊝ organisms,
-
with  activity against Pseudomonas and gram
⊕ organisms. -

O
5th generation (ceftaroline)—broad gram ⊕ and
gram ⊝ organism coverage; unlike 1st–4th
generation cephalosporins, ceftaroline covers
MRSA, and Enterococcus faecalis—does not
cover Pseudomonas.
ADVERSE EFFECTS Hypersensitivity reactions, autoimmune
hemolytic anemia, disulfiram-like reaction,
vitamin K deficiency. Low rate of cross-
reactivity even in penicillin-allergic patients.
 nephrotoxicity of aminoglycosides.
MECHANISM OF RESISTANCE Inactivated by cephalosporinases (a type of
β-lactamase). Structural change in penicillin-
binding proteins (transpeptidases).

β-lactamase inhibitors Include Clavulanic acid, Avibactam, CAST (eg, amoxicillin-clavulanate,

Sulbactam, Tazobactam. Often added to ceftazidime-avibactam, ampicillin-sulbactam,
penicillin antibiotics to protect the antibiotic piperacillin-tazobactam).
from destruction by β-lactamase.
 Medication-induced orthostasis Common drugs affecting lithium levels
Mechanism Examples • Thiazide diuretics
• NSAIDs
• Terazosin, prazosin, doxazosin Increase
• ACE inhibitors & ARBs
α-1 blockade–mediated lithium
• Antipsychotics (eg, risperidone) • Antibiotics (eg,
vasodilation levels
• Antihistamines, TCAs tetracycline,
• ACE inhibitors & ARBs metronidazole)
• Dihydropyridine CCBs Minimal
Other vasodilation • Calcium channel blockers
• Hydralazine, nitrates effect on
(eg, amlodipine)
• Phosphodiesterase inhibitors lithium
• Loop diuretics
levels
• Diuretics
Volume depletion Decrease • Osmotic diuretics (eg,
• SGLT-2 inhibitors
lithium mannitol)
• Beta blockers levels • Theophylline
Sympathetic blockade
• Clonidine

31) mc anti epileptic drug causing SJS : lamotrigine; valproate is rare

32) NE induced necrosis of digits:

-symmetric digits, toes.

33) Trastuzumab induced cardiotoxicity

-Therapy should be discontinued in patients who develop symptomatic heart failure or a significant decline
in ejection fraction (eg, >16 percentage points from baseline).

The cardiotoxicity associated with trastuzumab is typically reversible, with patients experiencing complete
recovery of cardiac function following treatment discontinuation.

34) Bupivacaine is a long-acting, amide-type local anesthetic with an onset of ∼ 10 minutes and duration of
action of 4–8 hours. Bupivacaine is commonly used for local infiltration if prolonged anesthesia or extended
pain relief is required.

35) rare but important side effect of trimethoprim-sulfamethoxazole (TMP-SMX) is agranulocytosis (dec
WBC) , which is thought to be mediated by direct toxicity of TMP (or its metabolites) to granulocytes,
particularly neutrophils, meaning patients are at an increased risk of infection.
Step 1 FA
94 SEC TION II BIOCHEMISTRY `B̀IOCHEMISTRY—METABOLISM

Lipoprotein functions Lipoproteins are composed of varying proportions of cholesterol, TGs, and phospholipids. LDL and
HDL carry the most cholesterol.
Cholesterol is needed to maintain cell membrane integrity and synthesize bile acids, steroids, and
vitamin D.
Chylomicron Delivers dietary TGs to peripheral tissues. Delivers cholesterol to liver in the form of chylomicron
remnants, which are mostly depleted of their TGs. Secreted by intestinal epithelial cells.
VLDL Delivers hepatic TGs to peripheral tissue. Secreted by liver.
IDL Delivers TGs and cholesterol to liver. Formed from degradation of VLDL.
LDL Delivers hepatic cholesterol to peripheral tissues. Formed by hepatic lipase modification of IDL in
the liver and peripheral tissue. Taken up by target cells via receptor-mediated endocytosis. LDL is
Lethal.
HDL Mediates reverse cholesterol transport from peripheral tissues to liver. Acts as a repository for
apolipoproteins C and E (which are needed for chylomicron and VLDL metabolism). Secreted
from both liver and intestine. Alcohol  synthesis. HDL is Healthy.

Abetalipoproteinemia Autosomal recessive. Mutation in gene that encodes microsomal transfer protein (MTP).
A Chylomicrons, VLDL, LDL absent. Deficiency in ApoB-48, ApoB-100. Affected infants present
with severe fat malabsorption, steatorrhea, failure to thrive. Later manifestations include retinitis
pigmentosa, spinocerebellar degeneration due to vitamin E deficiency, progressive ataxia,
acanthocytosis. Intestinal biopsy shows lipid-laden enterocytes A .
Treatment: restriction of long-chain fatty acids, large doses of oral vitamin E.

Familial dyslipidemias
TYPE INHERITANCE PATHOGENESIS  BLOOD LEVEL CLINICAL
I—Hyper- AR Lipoprotein lipase or Chylomicrons, TG, Pancreatitis,
chylomicronemia ApoC-2 deficiency cholesterol hepatosplenomegaly, and
eruptive/pruritic xanthomas
(no  risk for atherosclerosis).
Creamy layer in supernatant.
II—Hyper- AD Absent or defective IIa: LDL, cholesterol Heterozygotes (1:500) have
cholesterolemia LDL receptors, or IIb: LDL, cholesterol, cholesterol ≈ 300 mg/dL;
defective ApoB-100 VLDL homozygotes (very rare) have
= cholesterol ≥ 700 mg/dL.
Accelerated atherosclerosis (may
have MI before age 20), tendon
(Achilles) xanthomas, and
corneal arcus.
III—Dysbeta- AR ApoE (defective in Chylomicrons, VLDL Premature atherosclerosis,
lipoproteinemia type thrEE) tuberoeruptive and palmar
xanthomas. ApE’s palms.
IV—Hyper- AD Hepatic VLDL, TG Hypertriglyceridemia (> 1000
triglyceridemia overproduction of mg/dL) can cause acute
VLDL pancreatitis. Related to insulin
resistance.
670 SEC TION III REPRODUC TIVE REPRODUCTIVE—PATHOLOGY
` 

Primary dysmenorrhea Painful menses, caused by uterine contractions to  blood loss Ž ischemic pain. Mediated by
prostaglandins. Treatment: NSAIDs.

Ovarian cysts
Follicular cyst Distention of unruptured Graafian follicle. May be associated with hyperestrogenism, endometrial
hyperplasia. Most common ovarian mass in young females.
Theca lutein cyst Also called hyperreactio luteinalis. Often bilateral/multiple. Due to hCG overstimulation.
Associated with choriocarcinoma and hydatidiform moles.

Ovarian tumors Most common adnexal mass in females > 55 years old. Present with abdominal distention, bowel
obstruction, pleural effusion.
Risk  with advanced age, infertility, endometriosis, PCOS, genetic predisposition (eg, BRCA1 or
BRCA2 mutations, Lynch syndrome, strong family history).
Risk  with previous pregnancy, history of breastfeeding, OCPs, tubal ligation.
Epithelial tumors are typically serous (lined by serous epithelium natively found in fallopian tubes,
and often bilateral) or mucinous (lined by mucinous epithelium natively found in cervix). Monitor
response to therapy/relapse by measuring CA 125 levels (not good for screening).
Germ cell tumors can differentiate into somatic structures (eg, teratomas), or extra-embryonic
structures (eg, yolk sac tumors), or can remain undifferentiated (eg, dysgerminoma).
Sex cord stromal tumors develop from embryonic sex cord (develops into theca and granulosa cells of
follicle, Sertoli and Leydig cells of seminiferous tubules) and stromal (ovarian cortex) derivatives.

Surface
Epithelial tumors epithelium

Egg
Germ cell tumors
Follicle
Sex cord stromal tumors Cortex
(stroma)

TYPE CHARACTERISTICS
Epithelial tumors
Serous cystadenoma Benign. Most common ovarian neoplasm.
Mucinous Benign. Multiloculated, large. Lined by mucus-secreting epithelium A . Can result in
cystadenoma pseudomyxoma peritonei intraperitoneal accumulation of mucinous material.
Brenner tumor Usually benign. Solid, pale yellow-tan tumor that appears encapsulated. “Coffee bean” nuclei on
H&E stain.
Serous carcinoma Most common malignant ovarian neoplasm. Psammoma bodies.
-
Mucinous carcinoma Malignant. Rare. May be metastatic from appendiceal or other GI tumors.
 REPRODUC TIVE REPRODUCTIVE—PATHOLOGY
`  SEC TION III 671

Ovarian tumors (continued)

TYPE CHARACTERISTICS
Germ cell tumors
Mature cystic Also called dermoid cyst. Benign. Most common ovarian tumor in young females. Cystic mass
teratoma with elements from all 3 germ layers (eg, teeth, hair, sebum) B . May be painful 2˚ to ovarian
enlargement or torsion. Monodermal form with thyroid tissue (struma ovarii C ) may present with

I
hyperthyroidism. Malignant transformation rare (usually to squamous cell carcinoma).
Immature teratoma Malignant, aggressive. Contains fetal tissue, neuroectoderm. Commonly diagnosed before age 20.
Typically represented by immature/embryonic-like neural tissue.
Dysgerminoma Malignant. Most common in adolescents. Equivalent to male seminoma but rarer. Sheets of
uniform “fried egg” cells D . Tumor markers:  hCG,  LDH.
Yolk sac tumor Also called endodermal sinus tumor. Malignant, aggressive. Yellow, friable (hemorrhagic) mass.
50% have Schiller-Duval bodies (resemble glomeruli, arrow in E ). Tumor marker:  AFP. Occurs
in children and young adult females.
Sex cord stromal tumors
Fibroma Benign. Bundle of spindle-shaped fibroblasts.
Meigs syndrome—triad of ovarian fibroma, ascites, pleural effusion. “Pulling” sensation in groin.
Thecoma Benign. May produce estrogen. Usually presents as abnormal uterine bleeding in a postmenopausal
female.
Sertoli-Leydig cell Benign. Small, grey to yellow-brown mass. Resembles testicular histology with tubules/cords lined
tumor by pink Sertoli cells. May produce androgens Ž virilization (eg, hirsutism, male pattern baldness,
clitoral enlargement).
Granulosa cell tumor Most common malignant sex cord stromal tumor. Predominantly occurs in females in their
50s. Often produces estrogen and/or progesterone. Presents with postmenopausal bleeding,
endometrial hyperplasia, sexual precocity (in preadolescents), breast tenderness. Histology shows
Call-Exner bodies (granulosa cells arranged haphazardly around collections of eosinophilic fluid,
resembling primordial follicles; arrow in F ). Tumor marker:  inhibin. “Give Granny a Call.”
A B C

D E F
690 SEC TION III RESPIRATORY RESPIRATORY—PHYSIOLOGY
` 

Oxygen content of O2 content = (1.34 × Hb × Sao2) + (0.003 × Pao2).

blood Hb = hemoglobin concentration; Sao2 = arterial O2 saturation.
Pao2 = partial pressure of O2 in arterial blood.
Normally 1 g Hb can bind 1.34 mL O2; normal Hb amount in blood is 15 g/dL.
O2 binding capacity ≈ 20 mL O2/dL of blood.
With  Hb there is  O2 content of arterial blood, but no change in O2 saturation and Pao2.
O2 delivery to tissues = cardiac output × O2 content of blood. ABG
Hb CONCENTRATION % O2 SAT OF Hb DISSOLVED O2 (PaO2) TOTAL O2 CONTENT
CO poisoning Normal  (CO competes with O2) Normal 

¥
Anemia  Normal Normal 
Polycythemia  Normal Normal 
Methemoglobinemia Normal  (Fe poor at binding O2)
3+
Normal 
Cyanide toxicity Normal Normal Normal Normal

Methemoglobin Iron in Hb is normally in a reduced state (ferrous Dapsone, local anesthetics (eg, benzocaine), and
Fe2+; “just the 2 of us”). Oxidized form of Hb nitrites (eg, from dietary intake or polluted/
(ferric, Fe3+) does not bind O2 as readily as Fe2+, high-altitude water sources) cause poisoning by
but has  affinity for cyanide Ž tissue hypoxia oxidizing Fe2+ to Fe3+.
from  O2 saturation and  O2 content. Methemoglobinemia can be treated with
Methemoglobinemia may present with cyanosis methylene blue and vitamin C.
(does not improve with supplemental O2) or
with chocolate-colored blood.

Oxygen-hemoglobin ODC has sigmoidal shape due to positive

100
dissociation curve cooperativity (ie, tetrameric Hb molecule can Hemoglobin
in
bind 4 O2 molecules and has higher affinity 90
og
lob
My

for each subsequent O2 molecule bound). 80

Myoglobin is monomeric and thus does 70
Left Right
Hb saturation (%)

not show positive cooperativity; curve lacks 60 (↓ P50) (↑ P50)

sigmoidal appearance. P50

50
Shifting ODC to the right Ž  Hb affinity
40
for O2 (facilitates unloading of O2 to tissue)
30
Ž  P50 (higher Po2 required to maintain
50% saturation). In peripheral tissue,  H+ 20

from tissue metabolism shifts curve to right, 10 Venous blood Arterial blood
unloading O2 (Bohr effect). 0
(deoxygenated) (oxygenated)

Shifting ODC to the left Ž  O2 unloading 0 10 20 30 40 50 60 70 80 90 100

PO2 (mm Hg)
Ž renal hypoxia Ž  EPO synthesis
Left shift Right shift
Ž compensatory erythrocytosis. ( O₂ unloading to tissue) ( O₂ unloading to tissues)
Fetal Hb (2 α and 2 γ subunits) has higher Left = lower ACE BATs right handed
affinity for O2 than adult Hb (due to  affinity H+ ( pH, base) H+ ( pH, Acid)
for 2,3-BPG) Ž dissociation curve is shifted PCO₂ PCO₂
2,3–BPG Exercise
left, driving diffusion of O2 across the placenta Temperature 2,3–BPG
from pregnant patient to fetus. CO High Altitude
MetHb Temperature
HbF
622 SEC TION III RENAL `R̀ENAL—PATHOLOGY

Kidney Can lead to severe complications such as hydronephrosis, pyelonephritis, and acute kidney injury. Obstructed
stones stone presents with unilateral flank tenderness, colicky pain radiating to groin, hematuria. Treat and prevent
by encouraging fluid intake.
CONTENT PRECIPITATES WITH X-RAY FINDINGS CT FINDINGS URINE CRYSTAL NOTES
Calcium Calcium Radiopaque Radiopaque Shaped like Calcium stones most common (80%); calcium
oxalate: envelope A oxalate more common than calcium
hypocitraturia or dumbbell phosphate stones.
/dipyramidal Can result from ethylene glycol (antifreeze)
ingestion, vitamin C overuse, hypocitraturia
(associated with  urine pH), malabsorption
(eg, Crohn disease).
Treatment: thiazides, citrate, low-sodium diet.
Calcium Radiopaque Radiopaque Wedge- Treatment: low-sodium diet, thiazides.
phosphate: shaped
 pH prism
Ammonium  pH Radiopaque Radiopaque Coffin lid B Account for 15% of stones. Caused by infection
magnesium with urease ⊕ bugs (eg, Proteus mirabilis,
phosphate Staphylococcus saprophyticus, Klebsiella)
(struvite) that hydrolyze urea to ammonia Ž urine
alkalinization. Commonly form staghorn
calculi C .
Treatment: eradication of underlying infection,
surgical removal of stone.
Uric acid  pH Radiolucent Visible Rhomboid D About 5% of all stones. Risk factors:  urine
or rosettes volume, arid climates, acidic pH.
Strong association with hyperuricemia
(eg, gout). Often seen in diseases with  cell
turnover (eg, leukemia).
Treatment: alkalinization of urine, allopurinol.
Cystine  pH Faintly radi- Moderately Hexagonal E Hereditary (autosomal recessive) condition in
opaque radiopaque which Cystine-reabsorbing PCT transporter
loses function, causing cystinuria. Transporter
defect also results in poor reabsorption
of Ornithine, Lysine, Arginine (COLA).
Cystine is poorly soluble, thus stones form
in urine. Usually begins in childhood. Can
form staghorn calculi. Sodium cyanide
nitroprusside test ⊕.
“Sixtine” stones have six sides.
Treatment: low sodium diet, alkalinization
of urine, chelating agents (eg, tiopronin,
-
penicillamine) if refractory.
-
A B C D E
50 SEC TION II BIOCHEMISTRY `B̀IOCHEMISTRY—CELLULAR

Collagen Most abundant protein in the human body. Type I - Skeleton

Extensively modified by posttranslational Type II - Cartilage
modification. Type III - Arteries
Organizes and strengthens extracellular matrix. Type IV - Basement membrane
SCAB
Type I Most common (90%)—Bone (made by Type I: bone, tendone.
osteoblasts), Skin, Tendon, dentin, fascia,  production in osteogenesis imperfecta type I.
cornea, late wound repair.
Type II Cartilage (including hyaline), vitreous body, Type II: cartwolage.
nucleus pulposus.
Type III Reticulin—skin, blood vessels, uterus, fetal Type III: deficient in vascular type of Ehlers-
tissue, early wound repair. Danlos syndrome (threE D).
Type IV Basement membrane (basal lamina), lens. Type IV: under the floor (basement membrane).
Defective in Alport syndrome; targeted by
autoantibodies in Goodpasture syndrome.

Collagen synthesis and structure

Synthesis—translation of collagen α chains
Fibroblast Preprocollagen
Pro α-chain backbone (Gly-X-Y)
(preprocollagen)—usually Gly-X-Y (X and
Y are proline or lysine). Collagen is 1⁄3
Nucleus
OH
Hydroxylation of proline and glycine; glycine content of collagen is less
OH lysine (requires vitamin C)
Collagen mRNA variable than that of lysine and proline.
Sugar
Glycosylation
Hydroxyproline is used for lab quantification
Cytoplasm OH
OH of collagen.
RER
Hydroxylation—hydroxylation
Triple helix formation (“hydroxCylation”) of specific proline
Procollagen
and lysine residues. Requires vitamin C;
Golgi
deficiency Ž scurvy.
Exocytosis
Glycosylation—glycosylation of pro-α-chain
Extracellular
hydroxylysine residues and formation of
space procollagen via hydrogen and disulfide
Cleavage of procollagen bonds (triple helix of 3 collagen α chains).
C- and N-terminals
Problems forming triple helix Ž osteogenesis
Tropocollagen
imperfecta.
Formation of cross-links Exocytosis—exocytosis of procollagen into
(stabilized by lysyl oxidase) extracellular space.
Proteolytic processing—cleavage of
Collagen fiber
disulfide-rich terminal regions of procollagen
Ž insoluble tropocollagen.
Cross-linking—reinforcement of many
staggered tropocollagen molecules by
covalent lysine-hydroxylysine cross-linkage
(by copper-containing lysyl oxidase) to make
collagen fibrils. Cross-linking of collagen
increases with age. Problems with cross-
linking Ž Menkes disease.
 BIOCHEMISTRY `B̀IOCHEMISTRY—CELLULAR SEC TION II 51

Osteogenesis Genetic bone disorder (brittle bone May be confused with child abuse.
imperfecta disease) caused by a variety of gene defects Treat with bisphosphonates
= to  fracture risk.
A
(most commonly COL1A1 and COL1A2). Patients can’t BITE:
Most common form is autosomal dominant Bones = multiple fractures
with  production of otherwise normal type I I (eye) = blue sclerae
collagen (altered triple helix formation). Teeth = dental imperfections
Upper Manifestations include: Ear = hearing loss
extremity ƒ Multiple fractures and bone deformities
B
(arrows in A ) after minimal trauma (eg,
during birth)
ƒ Blue sclerae B due to the translucent
connective tissue over choroidal veins
ƒ Some forms have tooth abnormalities,
including opalescent teeth that wear easily
due to lack of dentin (dentinogenesis
imperfecta)
ƒ Conductive hearing loss (abnormal ossicles)

Ehlers-Danlos Faulty collagen synthesis causing A B

syndrome hyperextensible skin A , hypermobile joints B ,
and tendency to bleed (easy bruising).
-
Multiple types. Inheritance and severity vary.
Can be autosomal dominant or recessive. May
be associated with joint dislocation, berry and
aortic aneurysms, organ rupture. -

-
I Hypermobility type (joint
-
instability): most
common type.
Classical type (joint and skin symptoms):
Z caused by a mutation in type V collagen (eg,
COL5A1, COL5A2).
Vascular type (fragile tissues including vessels
z [eg, aorta], muscles, and organs that are prone
to rupture [eg, gravid uterus]): mutations in
type III procollagen (eg, COL3A1).

Menkes disease X-linked recessive connective tissue disease caused by impaired copper absorption and transport
due to defective Menkes protein ATP7A (Absent copper), vs ATP7B in Wilson disease (copper
Buildup). Leads to  activity of lysyl oxidase (copper is a necessary cofactor) Ž defective collagen.
Results in brittle, “kinky” hair, growth and developmental delay, hypotonia,  risk of cerebral
aneurysms.
544 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PATHOLOGY
` 

Adult primary brain tumors

TUMOR DESCRIPTION HISTOLOGY
Glioblastoma Grade IV astrocytoma. Common, highly Astrocyte origin, GFAP ⊕. “Pseudopalisading”
malignant 1° brain tumor with ~ 1-year pleomorphic tumor cells B border central areas
median survival. Found in cerebral of necrosis, hemorrhage, and/or microvascular
hemispheres. Can cross corpus callosum proliferation.
(“butterfly glioma” A ). Associated with EGFR
amplification.
Oligodendroglioma Relatively rare, slow growing. Most often in Oligodendrocyte origin. “Fried egg” cells—round
frontal lobes C . nuclei with clear
= cytoplasm D .
Often
= calcified. “Chicken-wire” capillary pattern.
Meningioma Common, typically benign. Females > males. Arachnoid cell origin. Spindle cells
Most often occurs near surfaces of brain and concentrically arranged in a whorled pattern F ;
in parasagittal region. Extra-axial (external psammoma bodies (laminated calcifications).
to brain parenchyma) and may have a dural
attachment (“tail” E ). Often asymptomatic;
may present with seizures or focal neurologic
signs. Resection and/or radiosurgery.
Hemangioblastoma Most often cerebellar G . Associated with von Blood vessel origin. Closely arranged, thin-

=
-
Hippel-Lindau syndrome when found with walled capillaries with minimal intervening
retinal angiomas. Can produce erythropoietin parenchyma H .
-
Ž 2° polycythemia.
A B C D

E F G H
546 SEC TION III NEUROLOGY AND SPECIAL SENSES NEUROLOGY—PATHOLOGY
` 

Childhood primary brain tumors

TUMOR DESCRIPTION HISTOLOGY
Pilocytic astrocytoma Low-grade astrocytoma. Most common 1° Astrocyte origin, GFAP ⊕. Bipolar neoplastic

EEE
brain tumor in childhood. Usually well cells with hair-like projections. Associated with
circumscribed. In children, most often found microcysts and Rosenthal fibers (eosinophilic,
in posterior fossa A (eg, cerebellum). May be corkscrew fibers B ). Cystic + solid (gross).
supratentorial. Benign; good prognosis.
Medulloblastoma Most common malignant brain tumor in Form of primitive neuroectodermal tumor
childhood. Commonly involves cerebellum (PNET). Homer-Wright rosettes, small blue
C . Can compress 4th ventricle, causing cells D .
noncommunicating hydrocephalus →
Synaptophysin ⊕.
Ž headaches, papilledema. Can involve the
cerebellar vermis Ž truncal ataxia. Can send
“drop metastases” to spinal cord.
Ependymoma Most commonly found in 4th ventricle E . Can Ependymal cell origin. Characteristic
cause hydrocephalus. Poor prognosis. perivascular pseudorosettes F . Rod-shaped

=
blepharoplasts (basal ciliary bodies) found near
-

the nucleus.
Craniopharyngioma Most common childhood supratentorial tumor. Derived from remnants of Rathke pouch
-
May be confused with pituitary adenoma (ectoderm). Calcification is common G H .
(both cause bitemporal hemianopia). Cholesterol crystals found in “motor oil”-like
Associated with a high recurrence rate. fluid within tumor.
Pinealoma Tumor of pineal gland. Can cause Parinaud Similar to germ cell tumors (eg, testicular
syndrome (compression of tectum → vertical seminoma).
gaze palsy); obstructive hydrocephalus
(compression of cerebral aqueduct); precocious
puberty in males (hCG production).
A B C D

E F G H
238 SEC TION II PHARMACOLOGY PHARMACOLOGY—AUTONOMIC DRUGS
` 

G-protein–linked second messengers

RECEPTOR G-PROTEIN CLASS MAJOR FUNCTIONS
Adrenergic
α1 q  vascular smooth muscle contraction,  pupillary dilator muscle contraction
(mydriasis),  intestinal and bladder sphincter muscle contraction
α2 i  sympathetic (adrenergic) outflow,  insulin release,  lipolysis,  platelet
aggregation,  aqueous humor production
β1 s  heart rate,  contractility (one heart),  renin release,  lipolysis
β2 s Vasodilation, bronchodilation (two lungs),  lipolysis,  insulin release,
 glycogenolysis,  uterine tone (tocolysis),  aqueous humor production,
 cellular K+ uptake
β3 s  lipolysis,  thermogenesis in skeletal muscle,  bladder relaxation
Cholinergic
M1 q Mediates higher cognitive functions, stimulates enteric nervous system
M2 i  heart rate and contractility of atria
M3 q  exocrine gland secretions (eg, lacrimal, sweat, salivary, gastric acid),
 gut peristalsis,  bladder contraction, bronchoconstriction,  pupillary
sphincter muscle contraction (miosis), ciliary muscle contraction
(accommodation),  insulin release, endothelium-mediated vasodilation
Dopamine
D1 s Relaxes renal vascular smooth muscle, activates direct pathway of striatum
D2 i Modulates transmitter release, especially in brain, inhibits indirect
pathway of striatum
Histamine
H1 q  nasal and bronchial mucus production,  vascular permeability,
bronchoconstriction, pruritus, pain
H2 s  gastric acid secretion
Vasopressin
V1 q  vascular smooth muscle contraction

V2 s  H2O permeability and reabsorption via upregulating aquaporin-2 in

collecting twobules (tubules) of kidney,  release of vWF

“After qisses (kisses), you get a qiq (kick) out of siq (sick) sqs (super qinky sex).”
H1, α1, V1, Gq DAG Protein HAVe 1 M&M.
Receptor Phospholipase C
M1, M3 kinase C
Lipids PIP2 +
IP3 [Ca2+]in Smooth muscle contraction

β1, β2, β3, D1, Gs ATP

Receptor
H2, V2
Adenylate cyclase [Ca2+]in (heart) People who are
Gi too (2) MAD
– cAMP Protein kinase A
M2, α2, D2 Receptor – inhibit themselves.
Myosin light-chain
kinase (smooth
muscle)
 242 SEC TION II PHARMACOLOGY PHARMACOLOGY—AUTONOMIC DRUGS
` 

Sympathomimetics
DRUG ACTION HEMODYNAMIC CHANGES APPLICATIONS

Direct sympathomimetics
Albuterol, salmeterol, β2 > β1  HR (little effect) Albuterol for Acute asthma/COPD. Salmeterol
terbutaline for Serial (long-term) asthma/COPD.
Terbutaline for acute bronchospasm in asthma
and tocolysis.
Dobutamine β1 > β2, α / BP,  HR,  CO Heart failure (HF), cardiogenic shock (inotropic
> chronotropic), cardiac stress testing.
Dopamine D1 = D2 > β > α  BP (high dose),  HR, Unstable bradycardia, HF, shock; inotropic and
 CO chronotropic effects at lower doses due to β
effects; vasoconstriction at high doses due to α
effects.
Epinephrine β>α  BP (high dose),  HR, Anaphylaxis, asthma, open-angle glaucoma;
 CO α effects predominate at high doses.
Significantly stronger effect at β2-receptor than
norepinephrine.
Fenoldopam D1  BP (vasodilation),  HR, Postoperative hypertension, hypertensive crisis.
 CO Vasodilator (coronary, peripheral, renal, and
splanchnic). Promotes natriuresis. Can cause
hypotension and tachycardia.
Isoproterenol β1 = β2  BP (vasodilation),  HR, Electrophysiologic evaluation of
 CO tachyarrhythmias. Can worsen ischemia.
Has negligible α effect.
Midodrine α1  BP (vasoconstriction), Autonomic insufficiency and postural
 HR, / CO hypotension. May exacerbate supine
hypertension.
Mirabegron β3 Urinary urgency or incontinence or overactive
bladder. Think “mirab3gron.”
Norepinephrine α1 > α2 > β1  BP,  HR, / CO Hypotension, septic shock.
Phenylephrine α1 > α2  BP (vasoconstriction), Hypotension (vasoconstrictor), ocular procedures
 HR, / CO (mydriatic), rhinitis (decongestant), ischemic
priapism.
Indirect sympathomimetics
Amphetamine Indirect general agonist, reuptake inhibitor, also Narcolepsy, obesity, ADHD.
releases stored catecholamines
Cocaine Indirect general agonist, reuptake inhibitor Causes vasoconstriction and local anesthesia.
Caution when giving β-blockers if cocaine
intoxication is suspected (can lead to
unopposed α1 activation Ž extreme
hypertension, coronary vasospasm).
Ephedrine Indirect general agonist, releases stored Nasal decongestion (pseudoephedrine), urinary
catecholamines incontinence, hypotension.
#Dobutamine is a potent inotropic agent
-MOA:strong affinity for beta-1 receptors and a weak affinity for beta-2 and alpha-1
receptors.
-Dobutamine stimulates increased myocardial contractility leading to improved EF,
reduced LV ESV, and symptomatic improvement of decompensated heart failure.
250 SEC TION II PHARMACOLOGY PHARMACOLOGY—TOXICITIES AND SIDE EFFECTS
` 

PHARMACOLOGY—TOXICITIES AND SIDE EFFECTS

` 

Ingested seafood Toxin actions include histamine release, total block of Na+ channels, or opening of Na+ channels to
toxins cause depolarization.
TOXIN SOURCE ACTION SYMPTOMS TREATMENT

E?
Histamine Spoiled dark-meat Bacterial histidine Mimics anaphylaxis: oral Antihistamines
(scombroid fish such as tuna, decarboxylase converts burning sensation, facial Albuterol +/–
poisoning) mahi-mahi, histidine to histamine flushing, erythema, epinephrine
mackerel, and Frequently urticaria, itching; may
bonito misdiagnosed as fish progress to bronchospasm,
allergy angioedema, hypotension
Tetrodotoxin Pufferfish Binds fast voltage-gated Nausea, diarrhea, Supportive
Na+ channels in nerve paresthesias, weakness,

= ⇐
tissue, preventing dizziness, loss of reflexes
depolarization
Ciguatoxin Reef fish such as Opens Na+ channels, Nausea, vomiting, diarrhea; Supportive
barracuda, snapper, causing depolarization perioral numbness;
and moray eel reversal of hot and cold
sensations; bradycardia,
heart block, hypotension

Age-related changes It’s how aging bodies are MADE.

in pharmacokinetics
Metabolism  hepatic mass,  hepatic blood flow and  drug metabolism.
Phase I metabolism lost first with aging. Drugs metabolized during phase II (eg, lorazepam,
acetaminophen) are safer than drugs metabolized during phase I (eg, diazepam). Thus
 therapeutic doses may suffice in elderly.
Absorption  gastric pH,  gastric emptying.
Drug absorption influenced via drug-drug/food interactions.
Distribution  body fat content ( Vd for lipophilic drugs, eg, propofol).
 albumin ( binding of acidic drugs).
 total body water ( Vd for hydrophilic drugs, eg, digoxin).
Elimination  GFR and  tubular secretion.
 plasma concentration of renally excreted drugs; thus  therapeutic doses may suffice in elderly.

Beers criteria Widely used criteria developed to reduce potentially inappropriate prescribing and harmful
polypharmacy in the geriatric population. Includes > 50 medications that should be avoided in
elderly patients due to  efficacy and/or  risk of adverse events. Examples:
ƒ α-blockers ( risk of hypotension)
ƒ Anticholinergics, antidepressants, antihistamines, opioids ( risk of delirium, sedation, falls,
constipation, urinary retention)
ƒ Benzodiazepines ( risk of delirium, sedation, falls) So fracture
ƒ NSAIDs ( risk of GI bleeding, especially with concomitant anticoagulation)
ƒ PPIs ( risk of C difficile infection)
 PHARMACOLOGY PHARMACOLOGY—TOXICITIES AND SIDE EFFECTS
`  SEC TION II 255

Drugs affecting pupil  pupil size (mydriasis)  pupil size (miosis)

size Anticholinergics (eg, atropine, TCAs, Sympatholytics (eg, α2-agonists)
tropicamide, scopolamine, antihistamines)
Indirect sympathomimetics (eg, amphetamines, Opioids (except meperidine)
cocaine, LSD), meperidine
Direct sympathomimetics Parasympathomimetics (eg, pilocarpine),
organophosphates

Cytochrome P-450 Inducers (+) Substrates Inhibitors (–)

interactions (selected) St. John’s wort Theophylline Sodium valproate

E
Griseofulvin OCPs Isoniazid
Carbamazepine Anti-epileptics Cimetidine
Chronic alcohol overuse Warfarin Ketoconazole
Rifampin Fluconazole
Modafinil Acute alcohol overuse
Nevirapine Chloramphenicol
Phenytoin Erythromycin/clarithromycin
Phenobarbital Sulfonamides
Ciprofloxacin
Omeprazole
Metronidazole
Amiodarone
Ritonavir
Grapefruit juice

St. John grimaced at the carbs The OCPs are anti-war SICKFACES.COM (when I
in chronic alcohol overuse, am really drinking grapefruit
refused more, and never juice)
again forgot his phen-phen

Sulfa drugs Sulfonamide antibiotics, Sulfasalazine, Scary Sulfa Pharm FACTS

Probenecid, Furosemide, Acetazolamide,
Celecoxib, Thiazides, Sulfonylureas.
Patients with sulfa allergies may develop
fever, urinary tract infection, Stevens-
Johnson syndrome, hemolytic anemia,
thrombocytopenia, agranulocytosis, acute
interstitial nephritis, and urticaria (hives).
 BIOCHEMISTRY `B̀IOCHEMISTRY—METABOLISM SEC TION II 93

Key enzymes in lipid transport

Cholesteryl ester Mediates transfer of cholesteryl esters to other lipoprotein particles.
transfer protein
Hepatic lipase Degrades TGs remaining in IDL and chylomicron remnants.
Hormone-sensitive Degrades TGs stored in adipocytes. Promotes gluconeogenesis by releasing glycerol.
lipase
Lecithin-cholesterol Catalyzes esterification of 2⁄3 of plasma cholesterol (ie, required for HDL maturation).
acyltransferase
Lipoprotein lipase Degrades TGs in circulating chylomicrons.
Pancreatic lipase Degrades dietary TGs in small intestine.
PCSK9 Degrades LDL receptor   serum LDL. Inhibition   LDL receptor recycling    serum LDL.

Liver

Transfer of
LCAT Mature CETP cholesteryl
Nascent
HDL esters to
HDL
VLDL, IDL,
LDL

Small intestine

Major apolipoproteins
Chylomicron
Apolipoprotein Function Chylomicron remnant VLDL IDL LDL HDL
E Mediates remnant uptake ✓ ✓ ✓ ✓ ✓
(everything except LDL)
A-I Found only on alpha- ✓
lipoproteins (HDL), activates
LCAT
C-II Lipoprotein lipase cofactor that ✓ ✓ ✓ ✓
catalyzes cleavage.
B-48 Mediates chylomicron ✓ ✓
secretion into lymphatics
Only on particles originating
from the intestines
B-100 Binds LDL receptor ✓ ✓ ✓
Only on particles originating
from the liver
228 SEC TION II PATHOLOGY PATHOLOGY—NEOPLASIA
` 

Important Determine primary site of origin for metastatic tumors and characterize tumors that are difficult to
immunohistochemical classify. Can have prognostic and predictive value.
stains
STAIN TARGET TUMORS IDENTIFIED
Chromogranin and Neuroendocrine cells Small cell carcinoma of the lung, carcinoid
synaptophysin tumor, neuroblastoma
Cytokeratin Epithelial cells Epithelial tumors (eg, squamous cell carcinoma)
Desmin Muscle Muscle tumors (eg, rhabdomyosarcoma)
GFAP NeuroGlia (eg, astrocytes, Schwann cells, Astrocytoma, Glioblastoma
oligodendrocytes)
Neurofilament Neurons Neuronal tumors (eg, neuroblastoma)
PSA Prostatic epithelium Prostate cancer
S-100 Neural crest cells Melanoma, schwannoma, Langerhans cell
histiocytosis
TRAP Tartrate-resistant acid phosphatase Hairy cell leukemia
Vimentin Mesenchymal tissue (eg, fibroblasts, endothelial Mesenchymal tumors (eg, sarcoma), but also
cells, macrophages) many other tumors (eg, endometrial carcinoma,
renal cell carcinoma, meningioma)

P-glycoprotein ATP-dependent efflux pump also known as multidrug resistance protein 1 (MDR1). Classically
seen in adrenocortical carcinoma but also expressed by other cancer cells (eg, colon, liver). Used
to pump out toxins, including chemotherapeutic agents (one mechanism of  responsiveness or
resistance to chemotherapy over time).

Psammoma bodies Laminated, concentric spherules with dystrophic calcification A , PSAMMOMaS bodies are seen
A
in:
ƒ Papillary carcinoma of thyroid
ƒ Somatostatinoma
ƒ Adrenals (calcifying fibrous pseudotumor)
ƒ Meningioma
ƒ Malignant Mesothelioma
ƒ Ovarian serous carcinoma
ƒ Prolactinoma (Milk)
ƒ Serous endometrial carcinoma

Cachexia Weight loss, muscle atrophy, and fatigue that occur in chronic disease (eg, cancer, AIDS, heart
failure, COPD). Mediated by TNF-α, IFN-γ, IL-1, and IL-6.
1) To remember the sections of small intestine and pertinent nutrient absorbed in each, use
mnemonic Iron Fist Bro for Iron (duodenum), Folate (jejunum) and B12 (ileum)