MEDICINE REVIEW

Mark Jeremy P. Ramos, MD, FPCP, MHM (can.)

Internal Medicine
Assistant Professor- FEU-NRMF Institute of
Medicine
 CARDIOLOGY
• Blood pressure • taken in both arms
• supine and upright
• heart rate timed for
30s
• Examination of Retina
• Optic disc – edema
• Inspect arteries –
embolic plaques
• Abdomen • Abdominal aorta
• Liver- heart failure,
constrictive pericarditis
• Spleen – severe HF
• Edema

• Extremities • Palpate peripheral

arterial pulses
• Ankle brachial index
(ABI) – occlusive dse
BP Patterns Based on Office and Out-
of-Office Measurements
 Causes of secondary hypertension
Common Uncommon
Renal parenchymal disease 1-2% Pheochromocytoma 0.1-0.6%
Renovascular disease 5-34% Cushing’s syndrome <0.1%
Primary aldosteronism 8-20% Hypothyroidism <1%
Obstructive sleep apnea 25-50% Hyperthyroidism <1%
Drug or alcohol indued 5-10% Coarctation of aorta 0.1%
CVD risk factors common in patients
with hypertension
 Hypertension
• 2014 Evidence-Based Guideline for the Management of High
Blood Pressure in Adults Report From the Panel Members
Appointed to the Eighth Joint National Committee (JNC 8)

– 20-59 years old including DM and CKD patients- ----

initiate pharmacologic therapy with BP target <140/90
– 60 and above -- <150/90
• EBM showed reduction in risk for stroke, CHF, CHD
• No risk reduction for BP <140/90
2017 High Blood Pressure Clinical
Practice Guideline
 Basic and Optional Laboratory Tests
for Primary Hypertension
Basic Optional
Fasting blood glucose Echocardiogram
Complete blood count Uric acid
Lipid profile Urinary albumin to creatinine ratio
Serum creatinine with eGFR
Sodium, potassium, calcium
Thyroid function test
Urinalsysis
Electrocardiogram
Best Proven Nonpharmacological Interventions
for Prevention and Treatment of Hypertension
Intervention Approximate impact on SBP
Weight loss -5-8mmHg
Healthy diet -11mmHg
Reduced sodium intake -5-6mmHg
Enhanced potassium intake -4-5mmHg
Physical activity -5-8mmHg
Moderation in alcohol intake -4mmHg
 Hypertension
JNC 7 JNC 8/2017 ACC
Guidelines
5 drug classes 4 drug classes
recommended recommended
1. Beta blocker 1. Thiazide
2. Thiazide 2. ACE inhibitor
3. ACE inhibitor 3. ARB
4. ARB 4. CCB
5. CCB
Pulsus alternans Alternating weak and strong pulse
Severe cardiac tamponade
Pulsus bigeminus Caused by a premature ventricular
contraction
Pulsus paradoxus decrease in systolic arterial pressure that
normally accompanies the reduction in
arterial pulse amplitude during inspiration
Pericardial tamponade
Airway obstruction
Superior vena cava syndrome
Jugular Venous pulse Reflects phasic pressure changes in the
RA
a, c, v waves and x and y decents
Kussmaul’s sign Increase in JVP during inspiration
Severe right sided HF
Constrictive pericarditis
Point of maximal cardiac impulse Medial to the left midclavicular line 4th-
5th intercostal space
Thrills Palpable, low frequency vibrations
associated with heart murmurs
Heart sounds
S1 Closure of the mitral-tricuspid valve

S2 Closure of aortic-pulmonic valve

S3 Low pitched sound – frequent in normal

children, high cardiac output
S4 Low pitched, presystolic sound
MI
HEART MURMURS
Grades
I Faint; can be heard only with special
effort
II Mild to moderately loud murmur

III Moderate to loud murmur

IV Commonly accompanied by a thrill

V Murmur heard with edge of stethoscope

touching the chest
VI Audible murmur with stethoscope
removed from contact with chest
SYSTOLIC MURMURS

Holosystolic (Pansystolic)
rMR, TR
VSD
Midsystolic a.k.a. systolic ejection murmurs
AS
Hypertrophic cardiomyopathy
Young adult with thin chest
DIASTOLIC MURMURS

Early diastolic AR, PR

Mid diastolic MR
PDA, VSD
Acute, severe AR
Presystolic TS

Continuous PDA
Congenital or acquired AV fistula,
coronary AV fistula
 MIAS TIPS
(Systolic murmur)
 Case
• 52 year old male
• Hypertensive x 8 years– Losartan 50mg OD
• Non diabetic
• 20 pack year smoker
• BMI 30
• Chest heaviness after exercise lasting 10
minutes
 Considerations?
• GERD
• Angina pectoris
• Myocardial infarction
ISCHEMIC HEART DISEASE Inadequate supply of blood and oxygen
to a portion of the myocardium
Epidemiology US- 13million have IHD

Risk factors High fat and energy rich diet

Smoking
Sedentary lifestyle
Obesity
Diabetes mellitus
Coronary atherosclerosis Epicardial coronary arteries- major sites

Risk factors high plasma low-density lipoprotein (LDL)

low plasma high-density lipoprotein (HDL)
cigarette smoking,
Hypertension
diabetes mellitus
Segmental atherosclerotic narrowing of most commonly by the formation of a
epicardial coronary arteries plaque
-subject to rupture or erosion
Stable angina pectoris Due to transient myocardial ischemia

Incidence Male- 50s, Female- 60s

Chest pain heaviness, pressure, squeezing,

smothering, or choking
Levine’s sign- clenched fist over the
midsternum
Exercise induced
ECG May be normal
Stress test

Treatment (1) explanation of the problem and

reassurance
(2) identification and treatment of
aggravating conditions
(3) recommendations for adaptation of
activity as needed
(4) treatment of risk factors
(5) drug therapy
6) consideration of revascularization
Medications

NTG Vasodilators
ISDN/ISMN

BETA BLOCKERS Reduce cardiac workload, antiarrhythmic

CALCIUM CHANNEL BLOCKERS Amlodipine, Verapamil, Diltiazem
ANTIPLATELET DRUGS ASA, Clopidogrel
 Case
• 52 year old male
• Hypertensive x 8 years– Losartan 50mg OD
• Non diabetic
• 20 pack year smoker
• BMI 30
• Recurrent chest heaviness at rest throughout the
week lasting 20 minutes with increasing
intensity
• ECG: non-specific ST-T wave changes
 Considerations?
• Stable angina
• Unstable angina/MI
STABLE ANGINA UNSTABLE ANGINA/NSTEMI

chest or arm discomfort that may not be at least one of three features:
described as pain but is reproducibly (1) it occurs at rest (or with minimal
associated with physical exertion or stress exertion), usually lasting >10 min
(2) severe and of new onset (i.e., within
relieved within 5–10 min by rest and/or the prior 4–6 weeks);
sublingual nitroglycerin (3) it occurs with a crescendo pattern
 Unstable Angina/NSTEMI
Pathophysiology (1) plaque rupture or erosion with
superimposed nonocclusive
thrombus- most common cause
(2) dynamic obstruction [e.g., coronary
spasm, as in Prinzmetal's variant
angina]
(3) progressive mechanical obstruction
(4) increased myocardial oxygen
demand and/or decreased supply
s/sx Chest pain
Substernal, epigastric pain
Radiating to neck, left shoulder and arm
Cardiac biomarkers CK-MB, troponin
 Treatment (UA/NSTEMI)
ANTI ISCHEMIA

Nitrates IV when symptoms are not fully relieved

by sublingual nitrates
Beta blockers Metoprolol
Esmolol
Calcium channel blockers Verapamil
diltiazem
Morphine 2–5 mg IV dose
May be repeated every 5–30 min as
needed to relieve symptoms and maintain
patient comfort
ANTITHROMBOTIC THERAPY

ASA 162–325 mg followed by 75–162 mg/d

CLOPIDOGREL 300 mg followed by 75 mg/d

ABCIXIMAB

Eptifibatide

Tirofiban

Heparin
Fondaparinux
Bivalirudin
Enoxaparin 1 mg/kg SC every 12 h
 Recommendations for Use of an Early
Invasive Strategy
• Recurrent angina at rest/low-level activity despite Rx
• Elevated Troponin T or Troponin I
• New ST-segment depression
• Recurrent angina/ischemia with CHF symptoms, rales,
MR
• Positive stress test
• Ejection Fraction < 0.40
• Decreased BP
• Sustained VT
• PCI < 6 months, prior CABG
Fibrinolysis initiated within 30 min of presentation

principal goal - prompt restoration of full

coronary arterial patency
e.g. tPA, Streptokinase

Absolute contraindications 1. cerebrovascular hemorrhage

2. nonhemorrhagic stroke or other
cerebrovascular event within the past year
3. marked hypertension (a reliably
determined systolic arterial pressure >180
mmHg and/or a diastolic pressure >110
mmHg)
4. suspicion of aortic dissection
5. active internal bleeding (excluding
menses)
Relative contraindications 1. current use of anticoagulants
(FIBRINOLYSIS) 2. recent (<2 weeks) invasive or surgical
procedure or prolonged (>10 min)
cardiopulmonary resuscitation
3. known bleeding diathesis
4. Pregnancy
5. hemorrhagic ophthalmic condition
6. active peptic ulcer disease
7. severe hypertension (controlled)
Primary percutaneous coronary Angioplasty and/or stenting
intervention

applicable to patients who have

contraindications to fibrinolytic therapy

better short-term and long-term clinical

outcome

generally preferred when the diagnosis is in

doubt

cardiogenic shock is present

bleeding risk is increased

symptoms have been present for at least 2–3 h

when the clot is more mature and less easily
lysed by fibrinolytic drugs
ANTITHROMBOTIC THERAPY

ASA 162–325 mg followed by 75–162 mg/d

CLOPIDOGREL 300 mg followed by 75 mg/d

ABCIXIMAB

Eptifibatide

Tirofiban

Heparin
Fondaparinux
Bivalirudin
Enoxaparin 1 mg/kg SC every 12 h
 Complications (NSTEMI)
Ventricular dysfunction Ventricular Remodelling- series of changes in
shape, size, and thickness in both the infarcted
and noninfarcted segments
Hemodynamic assessment Pump failure – pulmonary rales and S3, S4 gallop

Killip classification I- no signs of pulmonary congestion (0-5%)

II- moderate heart failure (10-20%)
III- severe HF, pulmonary edema (35-45%)
IV- shock, cyanosis, confusion, oliguria (85-95%)
 Complications (NSTEMI)
Congestive heart failure

Cardiogenic shock Tx: diuretics, nitrates, ACE inhibitors

Right ventricular infarction 1/3 of inferior wall MI

Arrhythmias Ventricular premature beats

Ventricular tachycardia and fibrillation
Supraventricular arrhythmias
Sinus bradycardia
 Aortic diseases
Ascending aorta size 3cm in diameter

Thoracic aorta 2.5cm

Abdominal aorta 1.8-2cm

Aortic wall Thin intima

Thick tunica media
Adventitia
True aneurysm Involves all three layers of the vessel
Pseudoaneurysm intimal and medial layers are disrupted
and the dilatation is lined by adventitia
only
Fusiform aneurysm affects the entire circumference of a
segment of the vessel, resulting in a
diffusely dilated artery
Saccular aneurysm involves only a portion of the
circumference, resulting in an
outpouching of the vessel wall
 Aortic aneurysm
Etiology Atherosclerosis – most common
condition associated
Cystic medial necrosis - degeneration of Marfan syndrome
collagen and elastic fibers in the tunica Ehlers-Danlos syndrome type IV
media of the aorta and loss of medial cells Hypertension
that are replaced by multiple clefts of Congenital bicuspid aortic valves
mucoid material Familial thoracic aortic aneurysm
syndromes
 Thoracic aortic aneurysm
Cystic medial necrosis Ascending aortic aneurysms

Atherosclerosis Aortic arch and descending thoracic aorta

X- ray widening of the mediastinal shadow and

displacement or compression of the
trachea or left mainstem bronchus
Two-dimensional echocardiography-- assess the proximal ascending aorta and
transesophageal echocardiography (TEE) descending thoracic aorta
Contrast-enhanced computed assessment of aneurysms of the thoracic
tomography (CT) aorta and involvement of branch vessels
Magnetic resonance imaging (MRI)
Invasive aortography
Treatment Long term beta blockers
Control hypertension
Operative repair- symptomatic
 Abdominal Aortic Aneurysms
Males >Females

Related to atherosclerotic disease

No symptoms in most cases Pain usually a harbinger of rupture and

represents a medical emergency.
Acute rupture occurs without any prior
warning, and is always life-threatening
Treatment Operative repair and insertion of a
prosthetic graft - indicated for aneurysms
of any size that are expanding rapidly or
are associated with symptoms
 Acute aortic syndromes
• Aortic rupture
• Aortic dissection
• Intramural hematoma
• Penetrating atherosclerotic ulcer
 Aortic dissection
De Bakey Classification
Type I- intimal tear in the ascending
aorta but involves the descending aorta
also
II- dissection limited to ascending aorta
III- located in the descending aorta with
distal propagation of dissection Type I Type II

Stanford Classification
Type A – involves ascending aorta
Type B – limited to the descending aorta

Type III
 Aortic dissection
Clinical manifestations 6th and 7th decade

Sudden onset of pain, very severe and tearing

Pain localized to front or back of chest
Physical findings Hypertension or hypotension
Loss of pulses
Aortic regurgitation
Pulmonary edema
Neurologic (carotid obstruction)
Diagnosis Echocardiography
CT or MRI
 Aortic dissection
Treatment Medical therapy ASAP
Adrenergic blockers administered
parenterally
Calcium channel blockers
ACE inhibitors
Emergent surgery Type A dissections
Complicated Type B dissections
 Takayasu’s arteritis
Pulseless disease Frequent occlusion of large arteries
originating from the aorta

Pathology Panarteritis – mononuclear cells and occ.

giant cells

Prevalent in young females

Clinical manifestations Acute stage: fever, malaise, weight loss

Chronic: related to large artery occlusion
(claudication, cerebral ischemia, syncope)
Diagnosis MRA
CTA

Treatment Glucocorticoids (mainstay)

Angioplasty, bypass grafts (irreversible
arterial stenosis)
 Peripheral arterial disease
Definition stenosis or occlusion in the aorta or
arteries of the limbs
Atherosclerosis Leading cause of PAD in patients >40y/o

Other causes thrombosis, embolism, vasculitis,

fibromuscular dysplasia, entrapment,
cystic adventitial disease, and trauma
Pathology localized to large and medium-sized
vessels
Femoral and popliteal arteries (80–90%)
Tibial and peroneal arteries (40–50%)
Abdominal aorta and iliac arteries (30%)
 Peripheral arterial disease
Symptoms Intermittent claudication

Physical findings Decreased or absent pulses distal to the

obstruction
Bruits over the narrowed artery,
Muscle atrophy
Hair loss
Thickened nails
Smooth and shiny skin
Reduced skin temperature
Pallor or cyanosis
Ulcers or gangrene
 Peripheral arterial disease

Diagnosis Ankle brachial index (<0.90)

Segmental pressure measurements
Pulse volume recordings
Doppler flow velocity waveform analysis
Duplex ultrasonography
Transcutaneous oximetry
Stress testing
Treatment Antiplatelet therapy
Risk factor modification
Revascularization procedures
Thomboangiitis obliterans Most frequently in men <40 years
(Buerger’s Disease) Definite relationship to cigarette
smoking
Claudication of the affected extremity
Raynaud's phenomenon
Migratory superficial vein
Thrombophlebitis
Treatment Abstention from tobacco (only definitive
therapy)
Iloprost
Calcium channel blocker
Intermittent pneumatic compression
Raynaud’sPhenomenon

episodic digital ischemia, manifested clinically by the sequential development

of digital blanching, cyanosis, and rubor of the fingers or toes following cold
exposure and subsequent rewarming
Definition
Venous thrombosis
presence of thrombus within a superficial or deep
vein and the accompanying inflammatory response
in the vessel wall
 Venous thrombosis
Initial anticoagulation first few days (up to 10 days) following a
diagnosis of VTE
Most patients with acute venous
thromboembolism (VTE) require
anticoagulation for a minimum of three
months, with some patients requiring
longer finite periods of 6 to 12 months
Medical management Warfarin
Factor Xa and direct thrombin inhibitors
Aspirin
 Case
• 35F non hypertensive
• 5 months history of palpitation, easy
fatigability
• PMH: recurrent throat infection during
childhood
• PE: irregularly irregular rhythm, (+) diastolic
rumble
• ECG: Atrial fibrillation w/ MVR
 Answer
• Rheumatic heart disease
Valvular Heart Disease
Mitral stenosis Rheumatic heart disease is leading cause
Mitral valve orifice area 4-6cm2
<1cm2= severe MS
Risk factors Rheumatic fever
Congenital
Severe mitral annular calcification
SLE, RA
Symptoms Dyspnea, fatigue, palpitations,
hemoptysis, chest pain, AF
Physical findings Opening snap
Diastolic murmur-low pitched, rumbling
Malar flush- severe MS
Treatment Beta blockers
Nondihydropyridine calcium channel
blockers
Digoxin
Cardioversion for new-onset AF and HF;
Diuretics for HF
Warfarin
Penicillin for RF prophylaxis
Valve replacement
Mitral regurgitiation
Acute MR Endocarditis
Papillary muscle rupture (post-MI)
Trauma
Chordal rupture/Leaflet flail (MVP, IE)
Chronic MR Myxomatous (MVP)
Rheumatic fever
Endocarditis (healed)
Congenital (cleft, AV canal)
Mitral annular calcification
HOCM with SAM
Ischemic (LV remodeling)
Dilated cardiomyopathy
Symptoms Mild to mod MR- asymptomatic
Severe MR- Fatigue
exertional dyspnea
orthopnea
Auscultation Holosystolic murmur
Treatment Medical
Surgical
Mitral valve prolapse Systolic click murmur syndrome, Barlow’s
syndrome, floppy-valve syndrome,
billowing mitral leaflet syndrome
Excessive or redundant mitral leaflet
tissue
Cause Primary: degenerative disease in the
absence of identifiable connective tissue
disease, sporadic, or familial
Secondary: Marfan syndrome
Clinical features Female predisposition
Most are asymptomatic
Auscultation Mid or late systolic click
*Click and murmur occur earlier with
standing, during the strain of Valsalva,
and any maneuver decreasing LV volume
Treatment Reassurance
Beta blockers
Antiplatelet agents
Valve replacement
 Aortic stenosis
Congenital (bicuspid, unicuspid)
Degenerative calcific
Rheumatic fever
Symptoms Dyspnea (most common)
Angina pectoris
Exertional syncope
Physical findings Regular rhythm until late in the course
Pulsus parvus et tardus
Auscultation • A slow rate of rise in the carotid pulse
• Mid to late peak intensity of the
murmur
• Reduced intensity of the second heart
sound
(systolic murmur loudest in the second
right intercostal space was also
suggestive)

Management Valve replacement

Aortic regurgitation Valvular
Congenital (bicuspid)
Endocarditis
Rheumatic fever
Myxomatous (prolapse)
Traumatic
Syphilis
Ankylosing spondylitis
Root disease
Aortic dissection
Cystic medial degeneration
Marfan syndrome
Bicuspid aortic valve
Nonsyndromic familial aneurysm
Aortitis
Hypertension
Aortic regurgitation

Physical findings "water-hammer" pulse

Corrigan's pulse
Quincke's pulse
Traube's sign
Duroziez's sign
Widened arterial pulse
Systolic pressure elevation
Pulsation LV impulse is heaving and displaced
laterally and inferiorly
Auscultation high-pitched, blowing, decrescendo
diastolic murmur
Austin Flint murmur - a soft, low-pitched,
rumbling mid-diastolic murmur
Treatment Acute: IV diuretics and vasodilators
Chronic: surgery
control systolic BP
 Vegetation- mass of platelets, fibrin,
Infective endocarditis microcolonies of microorganisms, scant
inflammatory cells
Infection involves heart valves
Etiology Streptococci
Staphylococci
HACEK organisms
Primary portals Oral cavity, skin, upper respiratory tract

Pathogenesis Enter the bloodstream from mucosal

surfaces, skin, or sites of focal infection
Proliferate in the affected valve and
induce a procoagulant state
Diagnosis (Duke’s criteria) 2 major, 1 minor criteria
1 major, 3 minor criteria
5 minor criteria
JANEWAY LESIONS

SEPTIC EMBOLI
 Myocarditis
Causes Infectious process (Coxsackievirus B,
adenovirus, Hepatitis C, HIV)
Hypersensitivity
Irradiation, chemicals, physical agents
Clinical features preceding upper respiratory febrile illness
or a flulike syndrome,
viral nasopharyngitis or tonsillitis
NSSTTWC chest pain
Arrhythmias
CHF
Early death
Diagnosis Echocardiography
Cardiovascular magnetic resonance
EMB- cellular infiltrates, which are usually
histiocytic and mononuclear with or
without associated myocyte damage
Treatment Majority self limiting
Avoid strenuous activity
Correct CHF
 Dilated cardiomyopathy
Occur in 1/3 of CHF cases
Enlarged LV diameter with decreased
systolic function (low ejection fraction)
Genetic considerations a-cardiac actin,B- and a-myosin
heavy chain a-tropomyosin
Troponins T, I, and C
Other causes Ischemic cardiomyopathy
Stress-induced
Infectious
HIV
Toxic cardiomyopathy
Clinical features Left and right sided CHF develop gradually
Physical examination Variable degrees of cardiac enlargement
and CHF
Treatment Downhill course
Death due to progressive HF or ventircular
tachy- or bradyarrhythmia
Avoid Alcohol
Calcium channel blockers, NSAIDs
 Hypertrophic cardiomyopathy
LV hypertrophy of a nondilated chamber
Without obvious cause
Genetic considerations
Clinical features Most common cause of SCD in young
competitive athletes
Physical examination Double or triple apical precordial impulse
and a fourth heart sound
Echocardiogram LV hypertrophy
Septum >1.3x the thickness of LV free wall
Septum demonstrates “ground glass”
appearance (myocardial fibrosis)
Treatment Competitive sports and strenuous
activities should be avoided
Beta blockers, Verapamil
Surgical myotomy/myectomy of the
hypertrophied septum
 Restrictive cardiomyopathy
Hallmark Abnormal diastolic function
Ventricular walls are rigid and impede
ventricular filling
Causes Amyloidosis
Hemochromatosis
Radiation
Clinical features Exercise intolerance
Dyspnea
Edema
3rd and 4th heart sounds common
Echocardiography Symmetrically thickened LV walls
Normal or slightly reduced ventricular
volumes
Treatment No specific therapy
HF symptoms (loop diuretics, CCB, ACE,
beta blockers)
 Pericardial diseases
Pericardium Double layered sac (visceral and serous)

Acute pericarditis Most common pathologic process

involving the pericardium
Cardianal manifestations Chest Pain
(at least 2 of the following) Pericardial friction rub
ECG changes
Pericardial effusion
Pericardial friction rub High pitched, rasping, scratching, or
grating
Heard most frequently at end-expiration
with patient leaning forward and upright
Pericardial effusion “water bottle” configuration of cardiac
silhouette
Ewart’s sign Dullness and increased fremitus at left
lung base
 Acute pericarditis
Diagnosis Echocardiography-allows localization and
estimation of pericardial fluid
CT scan
MRI
Cardiac tamponade Accumulation of fluid in the pericardial
space sufficient to cause serious
obstruction to the inflow of blood
Causes Neoplastic
Idiopathic
Pericardial effusion sec to renal disease
Tuberculosis
Beck’s triad Hypotension
Soft or absent heart sounds
Jugular venous distention
Other symptom/findings Paradoxical pulse
Electrical alternans
Treatment Target underlying etiology
Idiopathic or viral: NSAIDs
Pericardiocentesis
ELECTRICAL ALTERNANS
 Chronic constrictive pericarditis
• Healing of acute fibrinous or serofibrinous
pericardits/Resorption of a chronic
pericardial effusion
•  obliteration of pericardial cavity
• Formation of granulation tissue
• Scar
 Chronic constrictive pericarditis
●Idiopathic or viral – 42 to 61 percent
●Post-cardiac surgery – 11 to 37 percent
●Post-radiation therapy – 2 to 31 percent,
primarily after Hodgkin disease or breast cancer
●Connective tissue disorder – 3 to 7 percent
●Postinfectious (tuberculous or purulent
pericarditis) – 3 to 15 percent
●Miscellaneous causes (malignancy, trauma, drug-
induced, asbestosis, sarcoidosis, uremic
pericarditis) – 1 to 10 percent
 Chronic constrictive pericarditis
Clinical and laboratory findings Weakness
Fatigue
Weight gain
Increased abdominal girth
Abdominal discomfort
Protuberant abdomen
Edema
Kussmaul’s sign
Broadbent’s sign
Treatment Pericardial resection (pericardiectomy)
 Case
• 35F non hypertensive
• 5 months history of palpitation, easy
fatigability
• PMH: recurrent throat infection during
childhood
• PE: irregularly irregular rhythm, (+) diastolic
rumble
• ECG: Atrial fibrillation w/ MVR
• Developed difficulty of breathing
• 2 pillow orthopnea
• Bipedal edema
• PE: Lung: crackles mid to base
 Heart failure
Epidemiology 2% in developed countries
6-10% over age 65
RHD major cause in Africa and Asia

Prognosis Symptomatic HF carries a poor prognosis

Cardinal manifestations Fatigue

Shortness of breath
Orthopnea
Paroxysmal nocturnal dyspnea
Cheyne stokes respiration
Acute pulmonary edema
Physical examination JVP elevation
Rales
Wheezing
Hepatomegaly
Ascites
Peripheral edema
 Heart Failure
Diagnosis
Routine labs Electrolytes, BUN, creatinine, hepatic
enzymes, urinalysis
DM screening
Lipid profile
12L ECG Assess cardiac rhythm
Determine LV hypertrophy or prior MI
Chest x ray Cardiac size and shape
2D ECHO with Doppler Assessment of LV size and function
Exercise testing Not routine
Useful in assessing need for cardiac
transplantation
 Heart failure
Treatment Preserved ejection
fraction
Control of congestion
Stabilization of heart rate
and BP
Improve exercise
intolerance
 Atrial Fibrillation
Mechanism Disturbance in impulse generation or
conduction
Tachyarrhythmia 1. Abnormal automaticity
2. Triggered activity
3. Reentry
Bradyarrhythmia 1. Failure of impulse generation within SA
node
2. Failure of the excitatory wavefront to
conduct from the atrium to the ventricle
through AV node

ECG Irregular RR intervals

No discernible or distinct P waves
Symptoms lethargy, palpitations, dyspnea, chest
tightness, sleeping difficulties,
and psychosocial distress
Atrial Fibrillation
 Atrial Fibrillation
Risk factors Heart failure
Hypertension
Valvular heart disease
Diabetes Mellitus
COPD
Obesity
Chronic kidney disease
Medications
Anticoagulants Warfarin
Heparin
Novel oral anticoagulants Dabigatran
(NOAC) Apixaban
Rivaroxaban
Rate control Digoxin
Beta blockers
Calcium channel blockers
 Atrial Fibrillation
Medications
Rhythm control Amiodarone
Sotalol
Flecainide
Propafenone
Ibutilide
Surgery AV node ablation
Pacemaker
Cardioversion
 MEDICINE REVIEW

Mark Jeremy P. Ramos, MD, FPCP

Internal Medicine
Assistant Professor- FEU-NRMF Institute
of Medicine
PULMONOLOGY
 COPD
Definition Airflow limitation that is not fully
reversible
emphysema anatomically defined condition
characterized by destruction and
enlargement of the lung alveoli
chronic bronchitis clinically defined condition with chronic
cough and phlegm
small airway disease small bronchioles are narrowed

Risk factors Smoking

Airway hyperresponsiveness
Respiratory infections
Occupational exposure
Ambient air pollution
Passive, or second hand, smoking
exposure
Genetic considerations (a-1 antitrypsin
deficiency)
 COPD
Pathophysiology
Airflow obstruction Determined by spirometry
Chronically reduced ratio of FEV1/FVC
Due to reduced elastic recoil of the lung
Hyperinflation Air trapping (increased residual volume)
Gas exchange Non-uniform ventilation
Ventilation-perfusion mismatching
Pathophysiology 1. Chronic exposure to cigarette smoke
may lead to inflammatory cell
recruitment within the terminal
spaces of the lung
2. Release elastolytic proteinases which
damage the extracellular matrix of the
lung
3. Loss of matrix –cell attachment leads
to apoptosis of structural cells
4. Ineffective repair of elastin
 COPD
• Clinical presentation
– Most common symptoms:
• Cough
• Sputum production
• Exertional dyspnea
• Physical findings
– Normal PE in early stages
– Advanced stages
• Cachexia
• Significant weight loss
• Diffuse loss of subcutaneous adipose tissue
 COPD
Laboratory findings
*airflow obstruction- hallmark of COPD
Chest x-ray- bullae, hyperaerated lung
Chest CT scan- definitive test for testing the presence or absence of
emphysema
A-1 Anti Trypsin
 COPD
Pharmacotherapy

*Smoking cessation Bupropion

Nicotine replacement therapy
Verenicline
Bronchodilators
Anticholinergic agents Ipratropium bromide
Tiotropium
Beta agonists LABA (Salmeterol, Formoterol)

Inhaled glucocorticoids
Oral glucocorticoids Not recommended for long term use
Theophylline

*Oxygen Only pharmacologic therapy to decrease

mortality in COPD
 COPD
Nonpharmacologic Therapies

General medical care Annual Influenza vaccine

Pneumococcal vaccine
Pulmonary rehabilitation Education and cardiovascular conditioning

Lung volume reduction surgery *can influence the natural history of

COPD patients (as with O2, smoking
cessation)

Lung transplantation Second leading indication

Acute exacerbations Bronchodilators

Antibiotics
Glucocorticoids
Oxygen
Mechanical ventilatory support
 Bronchial asthma
Definition Airflow obstruction
Reversible
Prevalence Affects 300 million people
Bronchial asthma
In the past 4 weeks, has the Well Partly Uncontrolled
patient had: controlled controlled
1. Daytime asthma symptom of
more than twice/week?
2. Any night waking due to asthma?
None of these 1-2 of these 3-4 of these
3. Reliever needed for symptoms
more than twice/week?
4. Any activity limitation due to
asthma?
 Treatment
Controllers Relievers

Inhaled glucocorticoids – most effective Rapid acting B2 agonists

Leukotriene modifiers Systemic glucocorticoids

Long acting B2 agonists Anticholinergics

Theophylline Theophylline

Cromones Short acting oral B2 agonists

Systemic glucocorticoids
Bronchial asthma
Inhaler technique
 Bronchiectasis
Bronchiectasis Abnormal and permanent dilatation of
the bronchi
May be focal or diffuse
Cylindrical bronchiectasis Bronchi appear uniformly dilated and end
(most common) abruptly at the point that smaller airways
are obstructed by secretions
Varicose bronchiectasis Irregular or beaded pattern of dilatation

Saccular bronchiectasis Ballooned appearance at the periphery,

ending in blind sacs
Etiology and pathogenesis Poor mucociliary clearance and
susceptibility to infection-microbial
colonization of bronchial tree
 Bronchiectasis
Infectious Adenovirus, influenza virus most
common
Staphylococcus aureus
Klebsiella
Anaerobes
Bordetella
TB
Noninfectious Exposure to toxic substance
Allergic bronchopulmonary aspergillosis
Yellow nail syndrome
Clinical manifestations Persistent cough and purulent sputum
production
Hemoptysis (50-70%)
Fatigue
Weight loss
Malaise
 Bronchiectasis
Treatement goals 1. Treatment of infection
2. Improved clearance of
tracheobronchial secretions
3. Reduction of inflammation
4. Treatment of an identifiable
underlying problem
Antibiotics – cornerstone of management
Mucolytics
For refractory cases Surgical resection/bronchial arterial
embolization- massive bleeding
 Interstitial lung disease
Categories (histopathologic patterns)

Alveolitis, interstitial Asbestos

inflammation, and fibrosis Fumes, gases
Granulomatous Inhalation of inorganic and organic dust
Sarcoidosis
Idiopathic pulmonary fibrosis (IPF)
Pulmonary fibrosis
 Interstitial lung disease
Signs and symptoms Dyspnea
Wheezing
Chest pain
Hemoptysis
Crackles
Diagnosis

Laboratory exams ANA, Rheumatoid factor

Anti basement membrane antibodies
Imaging studies Chest x ray
HRCT
Pulmonary function test Spirometry
ABG
Fiberobtic bronchoscopy
Bronchoalveolar lavage
Tissue and cellular exam Lung biopsy- most effective for
confirming the diagnosis and assessing
disease activity
 Interstitial lung disease
Treatment Goals: permanent removal of offending
agent
Early identification and aggressive
suppression of the inflammatory process
Glucocorticoids Mainstay of therapy
Low success rate
0.5-1mg/kg OD x 4-12 weeks
Cyclophosphamide 1-2mg/kg per day
Azathioprine
Lung transplantation
 Cystic Fibrosis
Genetic consideration Autosomal recessive
Mutations in the gene encoding CF
transmembrane conductance regulator
(CFTR)
Cause pancreatic insufficiency and high
sweat NaCl values
Lung pathophysiology Raised transepithelial electric potential
difference (PD)
Clinical features s/sx begin in childhood
Cough- first symptom
S. aureus, H. influenza, P. aeruginosa- first
organisms to appear in sputum
Chest x ray Hyperinflation- earliest finding
Luminous mucus impaction
Bronchial cuffing
Bronchiectasis
Right upper lobe – earliest and most
severe changes
 Cystic Fibrosis
Gastrointestinal tract Meconium ileus
Distal intestinal obstruction syndrome
Exocrine pancreatic insufficiency-
malabsorption
Genitourinary system Late onset puberty
Azoospermia
Infertility
Diagnosis

Sweat test Elevated sweat Cl values are

pathognomonic
CFTR mutation analysis

Nasal PD measurements
 Cystic Fibrosis
Treatment Promote clearance of secretions
Control infection
Provide adequate nutrition
Prevent intestinal obstruction
Lung disease Breathing exercise
Flutter valves
Chest physiotherapy
Inhaled hypertonic saline (7%)
Recombinant human DNAse
Antibiotics
Lung transplantation
GI disease Pancreatic enzyme replacement
Vitamin E and K
Megalodiatrizoate
Epidemiology
DVT and PE
DVT 3x more often than PE

Postphlebitic syndrome Major adverse outcome of DVT

Permanent damage to the venous valve
of the leg
Chronic calf swelling and aching
Skin ulceration in its severe form
Genetics Factor V Leiden
Prothrombin gene mutations
Acquired Long haul travel
Obesity
Cigarette smoking
Oral contraceptives
Pregnancy
Postmenopausal hormone replacement
Surgery
Trauma
APAS
Cancer
COPD
Non-imaging diagnostic modalities

D-dimer 80% sensitivity for DVT

95% sensitivity for PE
Not specific
MI, pneumonia, sepsis, cancer, pregnancy
Cardiac biomarkers Troponin – increased in RV
microinfarction
-predict complications and mortality in PE
ECG S1Q3T3 sign: s wave in lead I, Q wave in
lead III, inverted T wave in lead III
Insensitive
Non-invasive imaging modalities

Venous ultrasonography

Chest x-ray Westermark’s sign

Hampton’s hump
Palla’s sign
Chest CT w/contrast Principal imaging test for PE

Lung scanning Second line diagnostic test

Treatment Primary – thrombolysis, embolectomy
Secondary – IVC filter
Anticoagulants Heparin
Enoxaparin
Tinzaparin
Fondaparinux
Warfarin
Inferior vena cava filters 1. Active bleeding that precludes
anticoagulation
2. Recurrent thrombosis despite
intensive anticoagulation
Maintain adequate circulation Hydration
Inotropic agents
Fibrinolysis rtPA

Pulmonary embolectomy

Pulmonary thromboarterectomy
 Obstructive sleep apnea
Obstructive sleep apnea/hypopnea coexistence of unexplained excessive
syndrome (OSAHS) daytime sleepiness with at least five
obstructed breathing events per hour of
sleep
Apnea Breathing pauses lasting >10s
Hypopnea Ventilation reduced by at least 50% from
previous baseline during sleep lasting
>10s
Predisposing factors Obesity
Short mandible and/or maxilla
Hypothyroidism
Acromagaly
Male (40-65 years)
Myotonic dystrophy
Ehler Danlos syndrome
Smoking
 Obstructive sleep apnea
Clinical features Daytime sleepiness
Impaired vigilance, cognitive
performance, driving
Depression
Disturbed sleep
Hypertension
Choking
Decreased libido
Cardiovascular and Cerebrovascular Myocardial infarction (20% rise)
events Stroke (40%)
Diabetes mellitus Associated with insulin resistance

Liver Increased liver enzymes

Steatosis and fibrosis
 Obstructive sleep apnea
Diagnosis Overnight polysomnogram/ Sleep study
(Gold standard)
Treatment CPAP
Mandibular Repositioning Splint (MRS)
Surgery

Central Sleep Apnea Respiratory pauses caused by lack of

respiratory effort
Cardiac failure
Neurologic disease (stroke)
Investigation Esophageal pressure
Respiratory muscle electromyography
Treatment CPAP
Acetazolamide
Tuberculosis
Clinical Practice Guidelines
CLINICAL MANIFESTATION
EXTRAPULMONARY
TUBERCULOSIS
 Case Definitions
 Sub-categories of TB cases according to
the patient’s previous treatment:
tuberculosis
 Case Definitions
 Sub-categories of TB cases according to
the patient’s previous treatment:
tuberculosis
 Case Definitions
 Terminology of TB from the ATS (old) and WHO (new)
ATS Classification of Patients WHO Case Definitions
tuberculosis

0 - no TB exposure
Latent TB
1 – TB exposure, No evidence of infection

2 – TB infection, No evidence of disease

3 – TB clinically active

4 – TB not clinically active Active TB Case

Pulmonary or
5 – TB suspect (diagnosis pending) Extrapulmonary
Smear (+) or (-)

ATS classification not advocated by these guidelines.

 Diagnosis
 Initial recommended work-up
 sputum microscopy
tuberculosis

 most efficient way of identifying cases

 readily available, accessible, and affordable
 rapidly determined and correlate well with infectivity

 Sputum Collection

A. FRONTLOADING- spot-spot 1 hour apart

B. SPOT EARLY MORNING
1st: spot specimen collected at the time of first consult
2nd: early morning specimen

The two specimens should be collected at most within 3

days.
DIAGNSOSIS
 Available rapid diagnostic test (eg.
Xpert MTB/RIF)
 presumptive DRTB,
 persons living with HIV (PLHIV) with
signs and symptoms of TB
 smear negative adults with Chest Xray
findings suggestive of TB
 smear negative children
 Diagnosis
 Role of Chest Radiographs in Smear (+) TB
symptomatics:
tuberculosis

 not routinely necessary

 can be done if other concomitant diseases or life-
threatening conditions are being considered

 Value of PPD in Smear (+) TB symptomatics:

 not useful and is discouraged

 Value of various blood tests in Smear (+) TB

symptomatics:
 may be taken only when specific risks for possible
adverse events are present
 Diagnosis
 Sputum TB culture in Smear (+) patients
 allows early identification of Mycobacteria species and
tuberculosis

early susceptibility testing

 no compelling reasons to recommend a ROUTINE
TB culture
 TB culture recommended for the following
conditions:
 Smear (-) PTB patients, particularly those with HIV
 Patients suspected to have MDR whether smear (+) or
smear (-)
 All cases of relapse
 All cases of retreatment
 All cases of treatment failure
 Diagnosis
 Extra-pulmonary Tuberculosis
tuberculosis

 For all patients suspected of having extra-

pulmonary TB, appropriate specimens from the
suspected sites of involvement should be
obtained and processed for microbiologic
(sputum microscopy & culture) and
histopathologic examinations.

 Sputum specimens should also be sent for

microbiologic studies.
 Treatment
 Directly Observed Treatment, Short-Course
(DOTS) Strategy
tuberculosis

A Standardized
standardized short-course
recording and
Sustained
Uninterrupted
Access
reporting
to political
supply
quality-assured
system commitment
ofTB
enabling quality-
outcometo
sputum
chemotherapy
increase
assured human for allfinancial
anti-tuberculosis
and cases drugs
ofresources
TB under
with
microscopy
assessment
proper for
casedrug of
case
all
management detection
patients and
among
conditions,
and
reliable
make
assessment TB control
symptomatic
of the procurement
overalla nationwide
patients and
performance
including
priority directlytoobserved
integral
distribution thesystemstreatment
health system
of the TB control
(DOT) program
 Treatment
 Directly Observed Treatment, Short-Course
(DOTS) Strategy
tuberculosis

 Sustained political commitment

 Access to quality-assured TB sputum
microscopy
 Standardized short-course chemotherapy
 Uninterrupted supply of quality-assured anti-
tuberculosis drugs
 A standardized recording and reporting
system
 Treatment
 Dosages of Anti-TB Drugs
tuberculosis

Isoniazid Rifampicin Pyrazinamide Ethambutol Streptomycin

5 (4-6) 10 (8-12) 25 (20-30) 15 (15-20) 15 (12-18)

mg/kg mg/kg mg/kg mg/kg mg/kg

Not to Not to
Not to Not to Not to
exceed exceed
exceed 2g exceed exceed 1g
400mg 600mg
daily 1.2g daily daily
daily daily
 Adverse Drug Reactions
 Hepatotoxicity
tuberculosis

 restart on a regimen without pyrazinamide e.g.

HRES, with gradual reintroduction of isoniazid and
rifampicin.
 In the absence of symptoms, therapy should not
be altered because of modest asymptomatic
elevations of AST (< 5x normal), but the
frequency of clinical and laboratory monitoring
should be increased.

 For AST levels 5 or more times elevated with

or without symptoms or > 3x elevated with
symptoms, all hepatotoxic drugs should be
stopped immediately and patient should be
evaluated.
 Adverse Drug Reactions
 Restarting Medications
tuberculosis

 When the rash has improved, medications can be

restarted one by one at intervals of 2-3 days.

 Start with rifampicin followed by isoniazid and then

ethambutol or pyrazinamide.
 Pleural effusion
Definition Excess quantity of fluid in the pleural
space
Transudative Systemic factors alter pleural fluid
absorption and formation
• Nephrosis
• LV failure
• Cirrhosis
Exudative Local factors alter pleural fluid absorpton
and formation

•Bacterial pneumonia
•Malignancy, viral infection
•Pulmonary embolism
 Pleural effusion
• Diagnostic approach
– Chest ultrasound
• Quantify fluid and guide for thoracentesis

– Chest xray lateral decubitus

– LV failure- most common cause of pleural effusion

 Pleural effusion
• Factors indicating likely need for more invasive
measures than thoracentesis
1. Loculated pleural fluid
2. Pleural fluid pH <7.2
3. Pleural fluid glucose <3.3mmol/L (<60mg/dl)
4. Positive gram stain or culture of the pleural fluid
5. Presence of gross pus in the pleural space
 Pneumonia
Definition Infection of the pulmonary parenchyma

Pathophysiology Aspiration from oropharynx

Inhaled as contaminated droplets
Hematogenous
Pathology

Edema Presence of proteinaceous exudate in the

alveoli
Red hepatization Presence of erythrocytes in the cellular
intraalveolar exudate
Gray hepatization No new erythrocytes are extravasating,
instead are lysed and degraded
Resolution Macrophage is the dominant cell type
Pneumonia
Pneumonia
 Pneumonia
Clinical manifestations Fever
Tachycardia
Chills
Cough
DOB
Pleuritic chest pain
GI symptoms (nausea, vomiting)
Crackles
Diagnosis Chest x ray
Sputum GS/CS
Blood culture
Antigen test
PCR
Serology
 Clinical features of patients with CAP
according to risk categories
Low Risk CAP Moderate Risk CAP High Risk CAP
Stable vital signs Unstable vital signs Any of the clinical feature
-RR<30 breaths/min -RR  30 breaths/min of
-PR <125 beats/min -PR  125 beats/min moderate risk CAP plus
-Temp  40C or >35C any
Unstable comorbid on the following:
-SBP  90mmHg condition
-DBP  60 mmHg (i.e. uncontrolled diabetes 1. Shock or signs of
mellitus, active hypoperfusion
malignancies, progressing -hypotension
No or stable comorbid neurologic disease,
conditions -Altered mental state
congestive heart failure
(CHF) Class II-IV, unstable -Urine output < 30ml/hr
No evidence of coronary artery disease, 2. Hypoxia
extrapulmonary sepsis renal failure on dialysis (PaO2<60mmHg) or
uncompensated COPD, Acute Hypercapnea
decompensated liver (PaO2>50mmHg)
disease)
Phi Clinical Practice Guidelines, 2004
 Clinical features of patients with CAP
according to risk categories
Low Risk CAP Moderate Risk CAP High Risk CAP
No evidence of aspiration Evidence of
extrapulmonary sepsis
Ihepatic, hematologic, Chest X-ray:
gastrointestinal,
endocrine) -as in moderate risk CAP
Chest X-ray:
-Localized infiltrates
-No evidence of pleural Suspected aspiration
effusion nor abscess
-Not progressive within 24
hrs Chest X-ray:
-Multilobar infiltrates
-Pleural effusion or
abscess
-Progression of findings
to >50% in 24 hrs
Phi Clinical Practice Guidelines, 2004
 CAP Algorithm for the management –oriented risk stratification of
community –acquired pneumonia (CAP) in immunocompetent Adults

Any of the ff:

1. RR  30/min
2. PR  125/min
3. Temp  40C or <35C 1. Shock or signs of
4. SBP <90 mmHg; hypoperfusion
DBP ≤ 60 mmHg -hypotension
5. Altered mental status YES -altered mental state YES HIGH RISK
of acute onset -urine output
6.Suspected aspiration
2. PaO2<60mmHg or
7. Unstable comorbid
conditions Acute hypercaonea
8. CXR: multilobar, (PaCO2>50mmHg)
pleural effusion
abscess, progression
of lesion to >50% of
Initial within 24 hrs NO Intensive Care
NO
MODERATE RISK

LOW RISK

In-patient
Outpatient Phil Clinical Practice Guidelines, 2004
Pneumonia
Prevention Influenza vaccine
Pneumococcal vaccine
 MEDICINE REVIEW

Mark Jeremy P. Ramos, MD, FPCP

Internal Medicine
Assistant Professor- FEU-NRMF Institute
of Medicine
Nephrology
 Acute Kidney Injury
Rapid decline in GFR over hours to days

Causes 1. Diseases that cause renal

hypoperfusion (prerenal ARF)
2. Diseases that directly involve the renal
parenchyma (intrinsic ARF)
3. Diseases associated with urinary tract
obstruction (postrenal ARF)

Frequent clinical features Retention of nitrogenous waste products

Oliguria
Electrolyte and acid base abnormalities
 Acute kidney injury
Stages (KDIGO)
1 Increase in serum creatinine to 1.5 to 1.9 times baseline, or increase
in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L), or reduction
in urine output to <0.5 mL/kg/hour for 6 to 12 hours
2 Increase in serum creatinine to 2.0 to 2.9 times
baseline, or reduction in urine output to <0.5 mL/kg/hour for ≥12
hours
3 Increase in serum creatinine to 3.0 times baseline, or increase in
serum creatinine to ≥4.0 mg/dL (≥353.6 micromol/L), or reduction in
urine output to <0.3 mL/kg/hour for ≥24 hours, or anuria for ≥12
hours, or the initiation of renal replacement therapy
 Prerenal AKI
Prerenal azotemia Most common form
Reversible
Renal parenchymal tissue is not damaged
 Prerenal AKI
Clinical assessment Thirst
Orthostatic dizziness
Orthostatic hypotension
Tachycardia
Reduced JVP
Decreased skin turgor
Dry mucous membranes
Recent treatment with NSAIDs, diuretics,
ACE inhibitors, ARB
FENa < 1
Fluctuating creatinine levels parallel to
hemodynamic status
Treatment Fluid replacement

Dialysis Uremic syndrome

Refractory hypervolemia, hyperkalemia,
or acidosis
Intrinsic AKI (intrinsic renal vascular
disease)
 Intrinsic AKI
1. Ischemic or nephrotoxic tubular
injury
2. Tubulointerstitial diseases
3. Diseases of the microcirculation and
glomeruli
4. Diseases of the larger vessels
Ischemic ATN Initiation phase
Extension phase
Maintenance phase
Recovery phase
Nephrotoxic ATN Exposure to pharmacologic agents
Radiocontrast agents, Tacrolimus,
Cyclosporine
Pathology Patchy and focal necrosis of the tubular
epithelium
 Postrenal AKI
<5% of cases of hospital acquired ARF

Clinical assessment History of renal stones or prostatic

disease
Suprapubic flank pain
Colicky flank pain radiating to the groin
Radiologic findings Ultrasound
CT and MRI
Treatment Catheter (UB or bladder obstruction)
Stenting
 Chronic kidney disease
CRITERIA defined based on the presence of either
kidney damage or decreased kidney
function for three or more months,
irrespective of cause
1. Duration ≥3 months, based on
documentation or inference
2. Glomerular filtration rate (GFR) <60
mL/min/1.73 m2
3. Kidney damage, as defined by structural
abnormalities or functional abnormalities
other than decreased GFR
 Chronic kidney disease
Classification of Chronic Kidney Disease

Stage GFR

0 >90

1 90

2 60-89

3 30-59

4 15-29

5 <15

Applies to the process of continuing significant irreversible reduction in nephron

number, and typically corresponds to stage 3-5
 Chronic Kidney Disease
Recommended Equations for Estimation of Glomerular Filtration Rate (GFR) Using
Serum Creatinine Concentration (PCr), Age, Sex, Race, and Body Weight

1. Equation from the Modification of Diet in Renal Disease study

Estimated GFR (mL/min per 1.73 m2) = 1.86 x (PCr)–1.154 x (age)–0.203

Multiply by 0.742 for women

Multiply by 1.21 for African Americans

2. Cockcroft-Gault equation

(140-age)x wt in kg/72 x crea (mg/dl)

Multiply by 0.85 for women

 Chronic Kidney Disease

Etiology DM nephropathy- most common cause

Hypertensive nephropathy- elderly
Uremia Results from accumulation of toxins, fluid,
and electrolytes
Clinical and laboratory manifestations

Fluid and electrolyte disturbance Hyponatremia

Hyperkalemia
Endocrine-metabolic Sec. hypoparathyroidism
Vit. D deficiency
Neuromuscular Fatigue
Sleep disorders
 Chronic Kidney Disease
Cardiovascular Hypertension
CHF
Dermatologic Pruritus
hyperpigmentation
Gastrointestinal Anorexia
Nausea and vomiting
Hematologic and immunologic Anemia
Bleeding diathesis
 Chronic Kidney Disease
Evaluation Labs focused on underlying cause of the
disease
Renal ultrasound Bilateral small kidneys support CKD
diagnosis
Normal sized kidneys Diabetic nephropathy
Amyloidosis
HIV nephropathy
Doppler sonography, CT, MRI Renovascular disease

Renal biopsy Not advised

 Slowing the Progression of CKD

Protein restriction 0.60-0.75 g/kg per day protein

35 kcal/kg per day
Reduce intraglomerular hypertension and ACE and ARBs
proteinuria Calcium channel blockers
Slow down progression of diabetic renal 90-130mg/dl preprandial glucose
disease Hgba1c <7%
 Urinary Tract Infection
Anatomic categories Lower tract (urethritis and cystitis)
Upper tract (acute pyelonephritis,
intrarenal and perinephric abscess)

Microbiology Growth of 105 organisms per milliliter

from a properly collected midstream
"clean-catch"
Epidemiology Catheter-associated (nosocomial)
Non-catheter-associated (community-
acquired)
Etiology E. Coli – most common gram negative
bacilli
Alteration in normal vaginal flora
Genital infections
Contraceptives
Female more prone Proximity to the anus
Short urethra (4cm)
Termination beneath vagina
Sexual intercourse
 Urinary Tract Infection
Other conditions affecting pathogenesis Pregnancy
Obstruction
Neurogenic bladder dysfunction
Vesicoureteral reflux
Bacterial virulence factors
Genetics
Clinical presentation
Cystitis Dysuria
Frequency
Urgency
Suprapubic pain
Pyelonephritis Fever
Shaking chills
Nausea, vomiting
Abdominal pain
diarrhea
 Urinary Tract Infection
Catheter associated UTI Female
Prolonged catheterization
Severe underlying disease
Disconnection of the catheter and
drainage tube
Lack of systemic antimicrobial therapy
Diagnostic testing Urinalysis
Urine culture
Urologic evaluation For relapsing infections
History of childhood infections
Stones or painless hematuria
Recurrent pyelonephritis
 Antibiotic Treatment
(acute uncomplicated UTI)
• NITROFURANTOIN (100 mg QIDX5DAYS)

– Recommend first line of treatment due to

high efficacy, minimal resistance, minimal
side effects
– And low propensity for collateral damage
 Antibiotic Treatment
• TMZ-SMX (160/180mg BID x 3 days)

Used ONLY for culture proven susceptible

pathogen due to high prevalence of local
resistance and high failure rates
 Antibiotic Treatment
• Ampicillin and Amoxicillin should NOT be used for
empirical treatment

• Quinolones should NOT be used as first line drug

due to high propensity for collateral damage

• Beta lactam can be used if other recommended

agents cannot be used

• FOSFOMYCIN and PIVMECILLINAM can be used

 Antibiotic Treatment
• In healthy elderly women (>65yo), the
recommended duration of treatmnet is the
same as general population
ANTIBIOTICS DOSE (MG) DURATION
(DAYS)
TMP-SMX 800/160 BID 3
CIPROFLOXACIN 250 BID 3
OFLOXACIN 200 BID 3
NORFLOXACIIN 400 BID 3
LEVOFLOXACIN 250 OD 3
NITROFURANTOI 100QID 5
N
CEFIXIME 400 OD 3
CEFUROXIME 125-250 BID 3-7
COAMOXICLAV 625 BID 7
 Nephrolithiasis
Calcium salts Basic constituents of most kidney stones
Uric acid in the western hemisphere
Cystine
Struvite
Pathogenesis

Supersaturation

Crystallization Cell debris and other crystals present in

the urinary tract can serve as a template
to crystal formation + supersaturated
urine
Inhibitors of crystal formation

Treatment Combined medical and surgical approach

 Calcium stones (75-85%)
Idiopathic hypercalciuria Most common metabolic abnormality

Low sodium and low protein diets

Thiazide diuretics
Hyperuricosuria Due to excessive intake of purine from
meat, fish, and poultry
Low purine diet
Allopurinol
Primary hyperparathyroidism Hypercalcemia + elevated serum
concentrations of PTH
Hyperoxaluria Caused by excessive intake of high oxalate
foods (spinach, nuts, chocolate)
Enteric hyperoxaluria (jejunoileal bypass,
pancreatic insufficiency, Crohn’s)
Treatment Low oxalate diet
Avoid spinach, rhubarb, potato, vit. C
 Uric acid stones (5-10%)
Causes Gout
Metabolic syndrome
Myeloproliferative syndromes
Chemotherapy
Lesch-Nyhan syndrome
Treatment Supplemental alkali
Low purine diet
Allopurinol

Struvite stones (5-10%)

Result of infection with bacteria
(Proteus)

Treatment Complete removal of stone

Antibiotics- acute infection and
maintenance of sterile urine post-op
 Glomerular diseases
Nephritic syndrome 1–2 g/24 h of proteinuria
Hematuria with red blood cell casts
Pyuria
Hypertension
Fluid retention
Rise in serum creatinine associated with
a reduction in glomerular filtration
Nephrotic syndrome Heavy proteinuria (>3.0 g/24 h)
Hypertension
Hypercholesterolemia
Hypoalbuminemia
Edema/anasarca
Microscopic hematuria
Pulmonary-Renal syndrome Goodpasture's syndrome, Wegener's
granulomatosis, microscopic polyangiitis
Basement membrane syndrome Alport syndrome
Glomerular vascular syndrome Hypertensive nephrosclerosis
Infectious disease asssociated syndrome
 Acute nephritic syndromes
Post streptococcal glomerulonephritis Affects childrean ages 2-14 years
Skin and throat infections
Immune mediated
Renal biopsy Hypercellularity of mesangial and
endothelial cells
Glomerular infiltrates of
polymorphonuclear leukocytes
Granular subendothelial immune deposits
of IgG, IgM, C3, C4, and C5-9
Subepithelial deposits (which appear as
"humps")
Diagnosis Rheumatoid factor
Cryoglobulin and circulating immune
complexes
ANCA
ASO, anti DNAse
Treatment Antibiotics
Supportive
Endocarditis-associated Complication among untreated patients
glomerulonephritis Right sided endocarditis
Takes 10-14 days too develop immune
complex mediated injury
Pathology Subscapular hemorrhages with “flea-
bitten” appearance
Focal proliferation around foci of necrosis
Abundant mesangial, subendothelial, and
subepithelial immune deposits of IgG,
IgM, and C3
Gross or microscopic hematuria
Pyuria
Mild proteinuria
Normocytic anemia
Elevated ESR
Hypocomplementemia
High titers of rheumatoid factor, type III
cryoglobulins, and circulating immune
complexes
Treatment Eradication of infection with 4-6 weeks of
antibiotics
Lupus nephritis Common and serious complication of SLE
Results from the deposition of circulating
immune complexes, which activate the
complement cascade leading to
complement-mediated damage,
leukocyte infiltration, activation of
procoagulant factors, and release of
various cytokines
Proteinuria-most common sign
Hematuria
Hypertension
20% may require dialysis or
transplantation
 Lupus nephritis
Class I and II Minimal manifestation and normal renal
function
Excellent prognosis and no therapy
needed
Class III Most varied course
Mild proliferation involving small
percentage of glomeruli – respond well to
steroids alone
Class IV High anti-DNA antibody
Low serum complement
Worst prognosis
Mycophenolate, cyclophosphamide
High dose steroids
Class V Predisposed to renal vein thrombosis and
other thrombotic complications
Antiglomerular basement membrane
(anti-GBM) disease
Goodpasture’s syndrome Glomeruloneprhritis and lung
hemorrhage
Young men in their late 20s
Women in their 60s-70s
Renal biopsy Focal or segmental necrosis
Crescent formation in the Bowman’s
space
Anti-GBM and complement

Prognosis Worse if >50% crescents on biopsy

Advanced fibrosis
Creatinine 5mg/dl
Oliguria
Need for acute dialysis
Treatment Plasmapheresis
Steroids
IgA Nephropathy Episodic hematuria associated with the
deposition of IgA in the mesangium
One of the most common worldwide
Immune complex mediated
Diffuse mesangial IgA deposits often
associated with mesangial hypercellularity
Children Macroscopic hematuria during or
immediately following upper respiratory
infection (Henoch-Schonlein purpura)
Adults Asymptomatic microscopic hematuria

Treatment ACE inhibitors (proteinuria)

Tonsillectomy
Steroids
Fish oil
ANCA Small Vessel Vasculitis

Wegener’s Granulomatosis fever, purulent rhinorrhea, nasal ulcers,

sinus pain, polyarthralgias/arthritis,
cough, hemoptysis, shortness of breath,
microscopic hematuria, and 0.5–1 g/24 h
of proteinuria
Chest xray Nodules and persistent infiltrates,
sometimes with cavities
Biopsy Small vessel vasculitis and adjacent
noncaseating granulomas
Segmental necrotizing glomerulonephritis
without immune deposits
Microscopic polyangiitis

Churg-Strauss syndrome small-vessel vasculitis is associated with

peripheral eosinophilia, cutaneous
purpura, mononeuritis, asthma, and
allergic rhinitis
Biopsy Small-vessel vasculitis and focal
segmental necrotizing glomerulonephritis
Membranoproliferative Mesangiocapillary glomerulonephritis
Glomerulonephritis Lobar glomerulonephritis
Immune-mediated glomerulonephritis
characterized by thickening of the GBM
with mesangioproliferative changes
70% have hypocomplementemia
Type I Most proliferative
Tram-tracking
Type II Low serum C3
Dense thickening of the GBM containing
ribbons of dense deposits and C3
 Nephrotic syndrome
Classic presentation Heavy proteinuria
Minimal hematuria
Hypoalbuminemia
Hypercholesterolemia
Edema
Hypertension
Minimal change disease 10-15% of nephrotic syndrome in adults

Electron microscopy effacement of the foot process supporting

the epithelial podocytes with weakening
of slit-pore membranes
Abrupt onset of edema and nephrotic
syndrome
Treatement Prednisone
Immunosuppressive drugs
Focal segmental Glomerulosclerosis Proteinuria- most common clin. Finding
Primary (nephrotic syndrome)
Secondary (non-nephrotic)
Biopsy Prominent in glomeruli located at the
corticomedullary junction
Endocapillary hypercellularity
Collapsing glomerulopathy
Glomerular tip lesion
Poor outcome Nephrotic range proteinuria
African-American
Renal insufficiency
Treatment Primary Renin-angiotensin system inhibitors
Steroids
Cyclosporine
Secondary Treat underlying cause
Control proteinuria
Membranous glomerulonephritis 30% of cases of nephrotic syndrome in
adults
2:1 male to female ratio
Biopsy Uniform thickening of the basement
membrane along the peripheral capillary
loops
Worse prognosis Male
Older age
Hypertension
Persistent proteinuria
Complications Highest incidence of renal vein
thromboisis, pulmonary embolism, DVT
Treatment Control edema, dyslipidemia,
hypertension
Immunosuppressive drugs
Diabetic nephropathy Most common cause of CKD in the US

Mesangial sclerosis
Kimmelstiel-Wilson nodules
Normal to large kidneys
Microalbuminemia 30-300mg/24h
Appear 5-10 years after onset of DM
Treatment Intensive sugar control
BP control (<130/80)

Glomerular Deposition Diseases

Light chain deposition disease

Renal amyloidosis

Fibrillary immunotactoid
glomerulopathy
Fabry’s disease
 Tubulointerstitial disease
Primary Histologic and functional abnormalities
that involve the tubules and interstitium
Secondary Occur as consequence of progressive
glomerular or vascular injury
 Tubulointerstitial disease
Toxins

Exogenous Analgesic nephropathy

Lead nephropathy
Lithium
Miscellaneous
Metabolic Acute uric acid nephropathy
Gouty nephropathy
Hypercalcemic nephropathy
Extrarenal neoplasm Plasma cell dyscrasias
Amyloidosis
Immune disorders Allergic interstitial nephritis
Sjogren’s
miscellaneous Vesicoureteral reflux
Radiation nephritis
Analgesic nephropathy Papillary necrosis and tubulointerstitial
inflammation
Renal functions decline gradually
Anemia
“ring sign “ on pyelogram
“garland” pattern of calcified papilla (CT)
Transitional cell carcinoma
Lead nephropathy Pica from children
Occupational exposure
Lead accumulates in PCT
Elevated urinary excretion of lead, g-
aminolevulinic acid, coproporphyrin
Hyperuricemia
Treatment: removal from source of
exposure
Calcium disodium edetate
Lithium toxicity Insidious onset of chronic renal
insufficiency
Nephrogenic diabetes insipidus
Hypercalcemia, proteinuria
(hyperparathyroidism)
Biopsy: tubular atrophy and interstitial
fibrosis

Miscellaneous Cyclosporine - patchy interstitial fibrosis

and tubular atrophy
Hyalinosis, FSGS
Acute uric acid nephropathy Seen as part of tumor lysis syndrome in
patients given cytotoxic drugs for
lymphoproliferative or myelopreliferative
disorders
Deposition of uric acid crystals in the
kidney and collecting ducts
Treatment Allopurinol 200-800mg/d prior to
cytotoxic therapy
Diuretics (furosemide or mannitol)
Alkalinize urine to ph >7 (calcium
carbonate, acetazolamide)
Dialysis
Gouty nephropathy Crytalline deposits and monosodium
urate salts in the kidney parenchyma

u Incite obstruction and inflammatory

response
1. Lymphocytic infiltration
2. Foreign-giant cell reaction
3. Fibrosis (medullary and papillary
region of kidney)
Treatement Allopurinol
Hypercalcemic nephropathy Primary hyperparathyroidism
Sarcoidosis
Multiple myeloma
Vit. D intoxication
Metastatic bone disease
Early lesion Focal degenerative change in renal
epithelia (collecting ducts, DCT, loop of
Henle)
Inability to concentrate urine maximally
(polyuria and nocturia)

Treatment Reduce calcium concentration

Correct primary abnormality of calcium
metabolism
Allergic interstitial nephritis B-lactams
Sulfonamides
Fluoroquinolones
INH, RIF
Diuretics
NSAIDs
Proton pump inhibitors
Mesalazine
Enlarged kidneys
Interstitium of the kidney : pronounced
edema and infiltration with
polymorphonuclear leukocytes,
lymphocytes, plasma cells, and, in some
cases, large numbers of eosinophils
Treatement Discontinuation of drug
Steroids
Radiation nephritis Hyalinized glomeruli and arterioles
Atrophic tubules
Extensive interstitial fibroisis
Malignant hypertension
Anemia
Proteinuria
 Vascular injury to the kidney
Renal artery stenosis 5% of cases of hypertension
Increased sympathetic neural activity
-Flushing
-Loss of nocturnal BP decrease
-Autonomic instability
-Rapid BP swings
Doppler ultrasound (70% sensitivity)
Gadolinium enhanced 3D MRA -most
sensitive (90%) and specific (95%)
Treatment ACE inhibitors
Diuretics
Revascularization
Atheroembolic renovascular disease Cholesterol crystal embolization from
large arteries (aorta)
Male, elderly, hypertension, DM
Inciting events Vascular surgery
Arteriography
Angioplasty
Anticoagulation with heparin
Thrombolytic therapy
Clinical manifestations 1-14 days after inciting event
Fever, myalgia, headache, weight loss
Livedo reticularis, purple toes, gangrene
Laboratory findings Rising BUN and creatinine
Eosinophilia, eosinophiluria
Leukocytosis, elevated ESR, anemia
Hypocomplementemia
Treatment No effective therapy
Withdrawal of anticoagulation
Cholesterol lowering drugs
Hemolytic Uremic Syndrome Consumptive coagulopathies
Thrombotic Thrombocytopenic Purpura Microangiopathic hemolytic anemia
Thrombocytopenia
Renal involvement Microscopic hematuria (78%)
Subnephrotic proteinuria (75%)
Pathology Thrombotic microangiopathy
Microthrombi:
HUS- fibrin
TTP- platelet aggragates, fibrin, von
Willebrand factor
Etiology

HUS Shiga toxin-producing E. coli (0157;H7)

Non shiga toxin associated
TTP Deficient ADAMTS 13
Drug induced (mitomycin C, Ticlopidine,
Clopidogrel)
Treatment Antibiotics
Plasma exchange (plasmapheresis + FFP)
Dialysis
Renal transplant
Scleroderma (Progressive Systemic
Sclerosis)
Persistent urinary abnormalities – proteinuria, hypertension, mild
azotemia

Scleroderma renal crisis – rapid - malignant hypertension, oliguria,

deterioration of renal functions proteinuria, fluid retention,
microangiopathic hemolytic anemia, CNS
involvement
Treatment ACE inhibitors
Dialysis
Sickle cell nephropathy Sickling of RBCs in the microvasculature

Young individuals Renal hyperperfusion

Glomerular hypertrophy
Hyperfiltration
Renal complications Cortical infarcts – persistent hematuria,
perinephric hematomas
Papillary infarcts – increased risk of
bacterial infections
Functional tubule abnormalities –
nephrogenic diabetes insipidus
Management ACE inhibitors
 Gastroenterology
Esophagus Transport food bolus from mouth to
stomach
Prevent retrograde flow of GI contents
Heartburn Pyrosis
Burning retrosternal discomfort that may
move up and down the chest like a wave
Symptom of reflux esophagitis
Odynophagia Painful swallowing
Nonreflux esophagitis, herpes, pill
induced esophagitis
Barrett’s ulcer, carcinoma, caustic
damage, perforation
Regurgitation Effortless appearance of gastric or
esophageal contents in the mouth
 Esophageal diseases
Radiologic studies Barium swallow
Esophagogram
EUS
1. Carcinoma of esophagus 5. Long stricture (lye ingestion)

2. Leiomyoma 6. Peptic stricture

3. Barrett’s esophagus 7. Lower esophageal mucosal

(Schiatzki) ring
4. Monilial esophagitis
Esophagoscopy - Direct method of establishing the cause
of dysphagia
- Identify mucosal lesions not revealed by
barium swallow
- Biopsy
Esophageal motility Helpful for diagnosis of esophageal motor
disorders (achalasia, spasm, scleroderma)
Achalasia Esophageal body loses peristaltic
contractions and the LES does not relax
normally in response to swallowing
Pathophysiology Loss of intramural neurons

Clinical features Dysphagia

Chest pain
Regurgitation
Dysphagia to both liquids and solids and
aggravated by stress and hurried eating
Diagnosis Chest x ray – absence of gastric bubble
Barium swallow- normal peristalsis lost in
the lower 2/3 of esophagus
Beaklike appearance at terminal part of
esophagus
Treatment Nitrates, calcium channel blockers
Sildenafil
Botolinum toxin
Balloon dilatation
Heller’s extramucosal myotomy
Diffuse esophageal spasm Nonperistaltic contractions

Pathophysiology Dysfunction of inhibitory nerves

Patchy neural degeneration localized to
nerve processes
Clinical features Chest pain (retrosternal)
May mimic MI pain
Diagnosis Barium swallow – uncoordinated
simultaneous contractions (corkscrew
esophagus)
Manometry
Treatment Nitrates
Nifedipine
Reassurance and tranquilizers
Scleroderma esophagus Atrophy of smooth muscle
Weakness of lower 2/3 of esophagus
Incompetent LES
Clinical manifestation Dysphagia to solids
Dysphagia to liquids in recumbent
position
GERD
Diagnosis Barium swallow – dilatation and loss of
peristaltic contractions in the middle and
distal esophagus
Manometry – marked reduction in the
amplitude of smooth muscle contractions
Treatment Soft foods
Treat GERD and its complications
Gastroesophageal Reflux Disease Backflow of gastric acid and other gastric
contents into the esophagus due to
incompetent barriers at GEJ
Pathophysiology Reflux occurs when gradient of pressure
between LES and stomach is lost
Secondary causes of LES Scleroderma-like diseases
incompetence Myopathy
Pregnancy
Smoking
Anticholinergic drugs
Smooth muscle relaxants
Increased gastric volume
Gastric contents near gastroesophageal
junction
Increased gastric pressure
Clinical features Heartburn
Regurgitation of sour material into the
mouth
Chronic cough, laryngitis, pharyngitis
 GERD
Diagnosis History alone

Documentation of mucosal injury Barium swallow

Esophagoscopy
Mucosal biopsy
Bernstein test – 0.1N HCl
Documentation and quantitation Esophageal pH recording
of reflux
Treatment Weight reduction
Sleep with head elevated 4-6in
Lifestyle modification
H2 blockers
PPI – 8 weeks can heal erosive esophagitis
Antireflux surgery (fundoplication) –
gastric fundus wrapped around the
esophagus
Barrett’s esophagus Metaplasia of esophageal squamous
epithelium to columnar epithelium
Complication of reflux esophagitis
Low grade or high grade dysplasia
May progress to adenocarcinoma
HGD Close endoscopic follow up (every 3
months)
Esophagectomy
Endoscopic mucosal resection
Photodynamic therapy
LGD Endoscopy every 6-12 months initially
then yearly thereafter
Barrett’s esophagus without dysplasia Two examinations within the first year
and subsequently every 3 years
1. Carcinoma of esophagus 5. Long stricture (lye ingestion)

2. Leiomyoma 6. Peptic stricture

3. Barrett’s esophagus 7. Lower esophageal mucosal

(Schiatzki) ring
4. Monilial esophagitis
Diverticula Outpouchings of the esophageal wall

Zenker’s diverticulum Weakness in the post. Hypopharyngeal

wall (Killian’s triangle)
Halitosis and regurgitation of saliva and
food
Webs and rings Congenital or inflammatory

Plummer-Vinson syndrome Symptomatic hypopharyngeal webs and

iron deficiency anemia
Lower esophageal mucosal ring Schiatzki ring
Weblike constriction at the
squamocolumnar mucosal junction at or
near the border of LES
Lower esophageal muscular ring Contractile ring
Proximal to the site of mucosal rings
May represent an abnormal uppermost
segment of the LES
1. Carcinoma of esophagus 5. Long stricture (lye ingestion)

2. Leiomyoma 6. Peptic stricture

3. Barrett’s esophagus 7. Lower esophageal mucosal

(Schiatzki) ring
4. Monilial esophagitis
Hiatal hernia Herniation of part of stomach into the
thoracic cavity through the esophageal
hiatus
Sliding hiatal hernia GEJ and fundus of the stomach slide
upward
Mechanical trauma (esophageal rupture) 1. Damage from instrumentation or
external trauma
2. Increased intraesophageal pressure
associated with retching (spontaneous
rupture or Boerhaave’s syndrome)
3. Diseases of the esophagus (corrosive
esophagitis, esophageal ulcer,
neoplasm)
Diagnosis Xray
Chest CT scan (air in mediastinum)
Treatment Esophageal and gastric suction
Parenteral broad spectrum antibiotics
Surgical drainiage and repair ASAP
Mucosal tear (Mallory-Weiss Syndrome) Caused by vigorous vomiting, retching, or
vigorous coughing
Involves the gastric mucosa near the
squamocolumnar mucosal junction
s/sx Upper GI bleeding

Treatment Bleeding may resolve spontaneously

Vasopressin therapy
Angiographic embolization
 Peptic Ulcer Disease
Ulcer: break in the Duodenal ulcers Gastric ulcers
mucosal surface >5mm
Disruption of mucosal Disruption of mucosal
integrity of duodenum integrity of stomach
Relieved after food intake Aggravated by food intake
Pathology First portion of duodenum Can represent malignancy
(95%)
Malignant DU rare
Pathophysiology H. Pylori and NSAIDs H. Pylori and NSAIDs

H. Pyloi Gram negative microaerophilic rod

Always associated with chronic active gastritis
10-15% of infected individuals develop peptic ulcer
 Peptic Ulcer Disease
Pathogenetic factors in APD

Smoking Decrease healing rates

Impair response to therapy
Increase ulcer related complications
Genetics First degree relatives of DU patients are 3
times likely to develop an ulcer
Psychological stress neuroticism

Diet Alcohol
Caffeine
NSAID induced PUD
 Peptic Ulcer Disease
Clinical features Epigastric pain- gnawing, burning
Epigastric tenderness
Complications

GI bleeding Most common complication

More often in individuals >60 years old
Perforation Second most common complication
Penetration- ulcer bed tunnels to an
adjacent organ
Gastric outlet obstruction Least common
Secondary to ulcer related scar formation
and edema (peripyloric area)
Early satiety, nausea, vomiting, weight
loss, postprandial abdominal pain
 Peptic Ulcer Disease
Diagnostic evaluation

Barium study 80-90% sensitivity

Sensitivity decreased if ulcer <0.5cm,
previous scarring, postoperative patients
Endoscopy Most sensitive and specific
Tissue biopsy
Small lesions
Detects if ulcer is source of blood loss
Peptic Ulcer Disease
Peptic Ulcer Disease
 Peptic Ulcer Disease
Surgery Duodenal ulcer Gastric ulcer

1. Vagotomy and drainage 1. Antrectomy with Billroth I

2. Highly selective vagotomy 2. Csende’s procedure
3. Vagotomy with antrectomy 3. Kelling-Madlener
procedure
Surgery related 1. Afferent loop syndromes
complications 2. Dumping syndrome
3. Postvagotomy diarrhea
4. Bile reflux gastropathy
5. Maldigestion and malabsorption
6. Gastric adenocarcinoma
 Zollinger Ellison Syndrome
Zollinger Ellison syndrome Gastric acid hypersecretion due to
unregulated gastrin release from a non B
cell endocrine tumor (gastrinoma)
Epidemiology Males more commonly affected

Pathophysiology Hypergastrinemia originating from an

autonomous neoplasm
Tumor distribution Majority within the pancreas
80% at gastrinoma triangle
Duodenum - slow growing, less likely to
metastasize
Clinical manifestations Peptic ulcer- most common
Ulcers in unusual locations (2nd portion of
duodenum)
Ulcers refractory to medical therapy
Diarrhea (50%)
Gastrinoma in the presence of MEN 1
syndrome (25%)
 Zollinger Ellison Syndrome
Diagnosis Fasting gastrin (NV- <150 pg/ml)
Gastrinoma: 150-200pg/ml
 Zollinger Ellison Syndrome
Tumor localization Up to 50% have metastatic disease at
diagnosis
 Zollinger Ellison Syndrome
Treatment Ameliorate signs and symptoms
Curative resection of neoplasm
Control tumor growth in metastatic
disease
PPI Higher doses than for PU or GERD
Surgery Provide definitive cure
Chemotherapy May lead to toxicity without improvement
IFN –a in survival
Hepatic artery embolization
Gastrinoma 5 year survival rate 62-75%
10 year survival rate 47-53%
Entire tumor resected >90% (5 and 10 year survival rate)
Incompletely resected 5 years 43%
10 years 25%
 Peptic Ulcer Disease
Stress related mucosal injury Burns, trauma, head injury

Gastrointestinal bleeding Most common presentation

Cushing’s ulcer Stress ulceration after head trauma

Curling’s ulcer Stress ulceration after sever burns

Treatment Sucralfate
PPI- primary choice for stress prophylaxis
Gastritis Histologically documented inflammation
of the gastric mucosa
Acute Most common cause is infection (H.
pylori)
Chronic Inflammatory cell infiltrate consisting of
lymphocytes and plasma cells

Stages Superficial – limited to lamina propria

Atrophic – extends deeper into the
mucosa
Gastric atrophy – glandular structures lost
Type A gastritis Involve fundus and body (antral sparing)
Less common
Associated with pernicious anemia
Type B gastritis Antral predominant
More common
H. Pylori most common cause
Gastric cancer
Low grade B cell lymphoma
Gastric MALT lymphoma
 Disorders of Absorption
Diarrhea Symptom: decrease in stool consistency,
increase in stool volume, increase in
number of bowel movements
Sign: quantitative increase in stool water
or weight >220-225ml, or gram per 24h
Osmotic diarrhea Secondary to diminished absorption of
one or more dietary nutrients
Resolves on fasting
Secretory diarrhea Due to small and /or large intestinal fluid
and electrolyte secretion
Persistent even while fasting
Steatorrhea Caused by defects in the digestion and
absorption of dietary fat
 Celiac sprue
Celia sprue Nontropical sprue
Celiac disease
Gluten-sensitive enteropathy
Hallmark Presence of abnormal small-intestinal
biopsy and the response to elimination of
gluten from the diet
Etiology Unknown
1. Environmental – gliadin (wheat, rye)
2. Immunologic
3. Genetics
Diagnosis Small intestinal biopsy
1. Absence or reduced height of villi
2. Increased loss of villous cells with
increased crypt cell proliferation
3. Cuboidal appearance and nuclei that
are no longer oriented basally in
surface epithelial cells
4. Increased lymphocytes and plasma
cells in lamina propria
 Celiac sprue
Failure to respond to gluten restriction 1. Restriction of dietary protein
2. Glucocorticoids
3. Temporary response
4. Fail to respond to all measures and
have a fatal outcome
Mechanism of diarrhea 1. Steatorrhea
2. Secondary lactase deficiency
3. Bile acid malabsorption
4. Endogenous fluid secretion
Associated diseases Dermatitis herpetiformes
Type 1 DM
IgA deficiency
Complications CANCER
Refractory sprue
Collagenous sprue- do not respond to
gluten restriction and have poor
prognosis
Treatment Gluten restriction (90%)
 Tropical sprue
Affects 5-10% of population in some Chronic diarrhea
tropical areas Steatorrhea
Weight loss
Nutritional deficiencies (folate,
cobalamin)
Infectious agents G. Lamblia
Yersinia enterocolitica
C. Difficile
Cryptosporidium parvum
Diagnosis Intestinal biopsy: less villous architectural
alteration and more mononuclear cell
infiltrate in the lamina propria
Treatment Broad spectrum antibiotics
Folic acid
 Bacterial overgrowth syndrome
Diarrhea, steatorrhea, macrocytic anemia
Colonic type bacteria within the SI
Causes Functional stasis
Anatomic stasis
Direct communication between small and
large intestine
Pathogenesis E. coli, Bacteroides
Steatorrhea due to reduced concentration
of conjugated bile acids
Macrocytic anemia- cobalamin
Diagnosis Low serum cobalamin
Elevated serum folate
Normal Schilling test after 5 day
Tetracycline
Treatement Surgical correction
Tetracycline, metronidazole, co-amoxiclav,
cephalosporins can be given for 3 weeks
or until symtoms remit
 Irritable Bowel Syndrome
Functional bowel disorder characterized by abdominal pain or discomfort and
altered bowel habits in the absence of detectable structural abnormalities
 Irritable Bowel Syndrome
Clinical features 3x more often among females

Abdominal pain or discomfort Prerequisite clinical feature

Altered bowel habits Most consistent clinical feature

Constipation alternating with diarrhea

Gas and flatulence Impaired transit and tolerance of

intestinal gas loads

Upper gastrointestinal symptoms 25-50% complain of dyspepsia, heartburn,

nausea and vomiting

Pathophysiology Poorly understood

Abnormal gut motor and sensory activity
Central neural dysfunction
Psychological disturbance
Stress
Luminal factors
Treatment
duReassurance
Patient counseling and dietary alterations
Careful explanation of the functional
nature of the disorder
Avoid food precipitants
Stool bulking agents High fiber diet
Bran or hydrophilic colloid
Antispasmodics May provide temporary relief for
symptoms related to intestinal spasm
Antidiarrheal agents Most useful if taken before anticipated
stressful events that are known to cause
diarrhea
Antidepressant drugs Tricyclic antidepressants
Antiflatulence therapy
SSRI
Chloride channel activators Induces passive movement of sodium and
water into the bowel lumen and improves
bowel function
Diverticular Disease
 Diverticular Disease
Incidence and Epidemiology Affects nearly half of individuals over age
60
Only 20% develop symptomatic disease
True diverticula Saclike herniation of the entire bowel wall

False diverticula (pseudodiverticula) Involves only a protrusion of the mucosa

through the muscularis propria
Most common type affecting the colon
Pathophysiology Commonly affects sigmoid
Result of relative high-pressure zone
within the muscular sigmoid +
constipated, high fat content stool
Diverticulitis Inflammation of the diverticulum
Related to retention of particulate
material within the diverticular sac and
formation of fecalith
Diverticular bleeding Most common cause of hematochezia in
patients >60y
Localization done by colonoscopy
Massive bleeding- angiography
Vasopressin
Acute Uncomplicated Diverticulitis – 75% Abdominal pain
Fever
Leukocytosis
Anorexia/obstipation
CT scan Sigmoid diverticula
Thickened colonic wall >4mm
Inflammation within the pericolic fat
16% may present with abdominal abscess
Barium enema or colonoscopy should not
be performed (perforation risk)
Complicated diverticular disease – 25% Abscess 16%
Perforation 10%
Stricture 5%
Fistula 2%
 Diverticular Disease: Treatment

Medical management Asymptomatic: diet alterations

High fiber diet
Symptomatic: antibiotics and bowel rest
7-10 days treatment
TMP/SMZ
Ciprofloxacin
Metronidazole
Piperacillin
Surgical management 1. drainage, omental pedicle graft,
proximal diversion
2. Hartman’s procedure
3. Sigmoid resection with
coloproctostomy
4. Sigmoid resection with
coloproctostomy and proximal
diversion
 Inflammatory Bowel Disease
Immune mediated chronic intestinal condition
lc
 Ulcerative Colitis Crohn’s disease
Macroscopic findings Involves rectum and all part of Mouth to anus
the colon
Microscopic findings Diffuse mixed inflammation, Aphthoid ulcerations and
basal lymphoplasmacytosis, focal crypt abscesses with
crypt atrophy and irregularity loose aggregations of
macrophages, forming
noncaseating granulomas
Signs and symptoms Diarrhea, rectal bleeding, Ileocolitis
tenesmus, mucus passage, Jejunoileitis
crampy abdominal pain Colitis and perianal disease
Gastroduodenal disease
Diagnostics Sigmoidoscopy Elevated ESR and CRP
Barium enema: fine mucosal Endoscopy: rectal sparing,
granularity, “collar button” aphtous ulceration, fistula,
ulcers skip lesions
Cobblestoning
Complications Hemorrhage Perforation
Toxic megacolon Abscess
Strictures Obstruction
Hemorrhage
Malabsorption
 Treatment
5- ASA (Sulfasalazine) Antibacterial and anti-inflammatory
Effective inducing remission for mild to mod. UC and CD
Side effects: headache, nausea, anorexia, hypersensitivity
Glucocorticoids Prednisone 40-60mg/d for mod to severe UC and CD
No role in maintenance therapy
Side effects: fluid retention, abdominal striae, fat
redistribution, hyperglycemia, subcapsular cataracts,
osteonecrosis
Antibiotics No role in active or quiescent UC
Metronidazole, Ciprofloxacin – inflammatory, fistulous , and
perianal CD
Azathioprine and 6- Employed in management of glucocorticoid-dependent IBD
Mercaptopurine
Methotrexate Effective in inducing remission and reducing steroid dosage
Side effects: leukopenia, hepatic fibrosis
Cyclosporine
Tacrolimus
Anti-TNF antibody
 Pancreatitis
Acute pancreatitis

Signs and symptoms Abdominal pain: major symptom

Often severe, Steady and boring, located
at epigastrium and periumbilical region,
radiating to the back, chest flanks, lower
abdomen
Low grade fever
Tachycardia
hypotension
Shock 1. Hypovolemia
2. Increased formation and release of
kinin peptides
3. Systemic effects of proteolytic and
lipolytic enzymes
Pancreatitis
 Acute pancreatitis
Laboratory data 3x elevated serum amylase
Leukocytosis
Hyperglycemia
Hypocalcemia
Hyperbilirubinemia
Hypertrigliceridemia
Hypoxemia

CT scan
Treatment 85-90% self limited within 3-7 days
1. Analgesics for pain
2. IV fluids and colloids-most important
3. No oral alimentation
 Chronic pancreatitis
Clinical features

Abdominal pain Constant or intermittent

Eating may exacerbate pain
Maldigestion Chronic diarrhea
Steatorrhea
Weight loss
Fatigue
Chronic pancreatitis
 Treatment: chronic pancreatitis

Pain management Ductal decompression

octreotide
Endoscopic treatment Sphincterotomy, stenting, stone
extraction, drainage of pancreatic
pseudocyst
Pancreatectomy
Liver diseases
 Alcoholic Liver Disease
1. Fatty liver
2. Alcoholic hepatitis
3. Cirrhosis
Fatty liver Initial and most common histologic
response to hepatotoxic stimuli
Cessation of alcohol normalizes hepatic
architecture and fat within the liver
Alcoholic hepatitis Ballooning degeneration
Spotty necrosis
PMN infiltrate
Fibrosis in the perivenular and
perisinusoidal space of Disse
Precursor of cirrhosis
Reversible with cessation of alcohol
Alcoholic liver disease
 Alcoholic liver disease
Clinical features Hepatomegaly
RUQ discomfort
Nausea
Jaundice
Portal hypertension, ascites, varices
Laboratory features Ultrasound- detect fatty infiltration and
liver size
Prognosis Critically ill w/ alcoholic hepatitis have
mortality rate of >50%
Discriminant function 4.6 x [PT control] + serum bilirubin
(mg/dl)
>32: poor prognosis
Treatment Complete abstinence from alcohol
Glucocorticoids
Pentoxifylline
 Cirrhosis
Development of fibrosis with formation of regenerative nodules
Alteration in blood flow Decrease in hepatocellular mass and
function
 Alcoholic cirrhosis
Clinical features RUQ pain, nausea, fever, diarrhea,
anorexia, malaise
Ascites, edema, upper GI hemorrhage

Enlarged spleen and liver

Scleral iterus, spider angiomas, parotid
gland enlargement, digital clubbing,
muscle wasting
Laboratory Normal with early compensated cirrhosis

Diagnosis Liver biopsy is withheld until abstinence

has been maintained for at least 6 months
Treatment Cessation of alcohol use
 Cirrhosis due to Chronic Hepatitis
20-30% of chronic HCV develop cirrhosis
over 20-30 years
Pathology Small liver, shrunken with mixed micro-
and macronodular cirrhosis
Clinical features and diagnosis Fatigue, malaise, vague RUQ pain, lab
abnormalities
Treatment Specific therapy for complications
(varices, ascites, encephalopathy)
HBV: antiviral therapy
Lamivudine, adefovir, entecavir, tenofovir
 Primary Biliary Cirrhosis
Unknown cause
100-200/million
Female> Male
Elevated bilirubin and progressive liver
failure
Antimitochondrial antibodies (AMA)
present in 90% of patients
Pathology Chronic nonsuppurative destructive
cholangitis- earliest lesion
Mild fibrosis and bile stasis
Micro- and macronodular cirrhosis
Clinical features Most are asymptomatic
Fatigue out of proportion
Pruritus
Hyperpigmentation
Xanthelasma
Xanthoma
Laboratory Elevated GGT, ALP, aminotransferases
 Primary Biliary Cirrhosis
Diagnosis Liver biopsy most important in 10% of
AMA-negative patients
Treatment UDCA
Antihistamines, Naltrexone, rifampin ,
plasmapheresis for pruritus
 Primary Sclerosing Cholangitis
Unknown cause
Diffuse inflammation and fibrosis
involving the entire biliary tree
Clinical features Fatigue, pruritus, steatorrhea, deficiencies
in fat soluble vitamins
Laboratory findings Elevated aminotransferases
Decreased albumin
Prolonged PT
p-ANCA
Diagnosis MRCP- imaging technique of choice
- Multifocal stricturing and beading
involving intrahepatic and extrahepatic
biliary tree
Treatment No specific treatment
High dose UCDA
Endoscopic dilatation
Liver transplantation
Complications of Cirrhosis
 Cirrhosis
• Hepatic encephalopathy
●Grade I: Changes in behavior, mild
confusion, slurred speech, disordered sleep
●Grade II: Lethargy, moderate confusion
●Grade III: Marked confusion (stupor),
incoherent speech, sleeping but arousable
●Grade IV: Coma, unresponsive to pain
 Cirrhosis
Hepatic encephalopathy Management
Protein restriction and nutritional
support
Correction of precipitating causes
Lower blood ammonia (Lactulose,
Rifaximin)
INFECTIOUS
 Typhoid Fever
Typhoid fever Salmonella typhi
Gr negative bacilli
Enterobacteriaceae
Pathogenesis Begin with ingestion of contaminated
food or water
Infectious dose: 10 3- 10 6 CFU
Clinical course Fever – 75% (most prominent symptom)
Abdominal pain – 30-40%
Incubation period 10-14 days (5-21 days range)

Early findings Rose spots (30%)- first week

Hepatosplenomegaly (3-6%)
Epistaxis
Relative bradycardia (<50%)
Typhoid fever
 Typhoid fever
Diagnosis Culture
Blood culture 40-80% sensitive
Bone marrow culture 55-90% sensitive*
Stool culture 60-70% negative during first week
Positive during third week in untreated px
Serologic test Widal Test
Antigen and nucleic acid amplification
Treatment Fluoroquinolones- most effective
-resistance
Prevention
Ty21a Oral live attenuated S. typhi vaccine
Given on days 1, 3, 5 and 7, with booster
every 5 years
Minimum age: 6
Vi CPS Parenteral – purified Vi polysaccharide
from bacterial capsule
1 dose, booster every 2 years
Minimum age: 2
Malaria
 Malaria
Epidemiology P. Falciparum – predominates in Africa,
New Guinea, Haiti
P. Vivax – Central America
Clinical features Headache, fatigue, abdominal discomfort
Fever spikes, chills, rigors (P. vivax/ovale)
Anemia
Splenomegaly
 Malaria
Chronic Complications
Tropical splenomegaly Chronic repeated malarial infections
produce hypergammaglobulinemia
Normochromic normocytic anemia
Quartan Malarial Nephropathy Repeated infection with P. malariae
Cause soluble immune complex injury to
the renal glomeruli resulting to nephrotic
syndrome
Focal or segmental GN with splitting of
capillary basement membrane
Burkitt’s lymphoma and EBV Possibile malaria treated
immunosuppression provokes infection
 Chemoprophylaxis
Drug Usage Adult dose
Atovaquone/proguanil Prophylaxis in areas with 1 adult tablet PO
(Malarone) chloroquine- or
mefloquine-resistant
Plasmodium falciparum
Chloroquine phosphate Prophylaxis only in areas 300 mg of base (500 mg of
(Aralen and generic) with chloroquine-sensitive salt) PO once weekly
P. falciparum
Doxycycline (many brand Prophylaxis in areas with 100 mg PO qd
names and generic) chloroquine- or
mefloquine-resistant P.
falciparum
 Chemoprophylaxis
Drug Usage Adult dose
Mefloquine (Lariam and Prophylaxis in areas with 228 mg of base (250 mg of
generic) chloroquine-resistant P. salt) PO once weekly
falciparum
Primaquine An option for prophylaxis 30 mg of base (52.6 mg of
in special circumstances salt) PO qd
Hydroxychloroquine sulfate An alternative to 310 mg of base (400 mg of
(Plaquenil) chloroquine for primary salt) PO once weekly
prophylaxis only in areas
with chloroquine-sensitive
P. falciparum
 Tetanus
Definition Neurologic disorder characterized by
increased muscle tone and spasms
Etiologic agent Clostridium tetani- anaerobic, motile,
gram-positive rod
Epidemiology Always affects unimmunized persons
Partially immunized and fully immunized
individuals with low immunity
Follow an Acute injury (puncture,
laceration, abrasion)
Burns, frostbite, middle ear infection,
surgery, abortion, childbirth, drug abuse
Pathogenesis Toxin binds to peripheral motor neuron
terminals, enters the axon, then
transported to the nerve cell body in the
brainstem and spinal cord
Blocks inhibitory glycine and GABA
 Tetanus
Clinical manifestation

Generalized tetanus Most common form

Increased muscle tone and generalized
spasms
Median time of onset after injury: 7 days
Trismus noticed first by patient (lockjaw)
Risus sardonicus – grimace or sneer
Opisthotonos – arched back
Apnea
Laryngospasm
 Tetanus
Local tetanus Uncommon
Restricted to muscle near the wound
Excellent prognosis
Cephalic tatanus Rare
Follows head injury or ear infection
Involves one or more facial cranial nerves
High mortality
Diagnosis Based entirely on clinical findings
 Tetanus
Antibiotics Penicillin (10-12M units IV x 10 days)
(7-10 days duration) Metronidazole (500mg q6h)
Clindamycin
Erythromycin
Antitoxin Tetanus immune globulin (3000-6000U)
Tetanus antitoxin
Control of muscle spasm Diazepam
Lorazepam
Chlorpromazine
Neuromuscular blocking agents
Respiratory care Intubation or tracheostomy
 Tetanus
Prevention Given to all unimmunized and partially
immunized

Active immunization 1st and 2nd dose: given 4-8 weeks apart
3rd dose: 6-12 months after second dose
Booster: every 10 years
 Cholera
Definition Acute diarrhea that can result in rapidly
progressive dehydration and death

Microbiology and epidemiology Vibrio cholera

Coastal salt water and brackish estuaries
Type O blood are at greatest risk
Pathogenesis Cholera toxin – protein enterotoxin
colonizes the small intestine
cAMP inhibits the absorptive sodium
transport system -activates secretory
chloride transport system
Clinical manifestations 24-48h incubation
Painless watery diarrhea (voluminous)
Vomiting
“rice watery” stool- nonbilious, gray,
slightly cloudy fluid with flecks of mucus,
no blood, sweet inoffensive odor
 Cholera
Diagnosis V. Cholera in stool
TCBS agar – flat yellow colony
Treatment Rapid and adequate replacement of fluids
and electrolytes
Lactated Ringer’s IV
Doxycycline
Ciprofloxacin
Erythromycin
Azithromycin
Prevention Provision of safe water and facilities
Improve nutrition
Oral cholera vaccines (killed whole-cell)
Oral live cholera vaccine
 Leptospirosis
Etiologic agents Spirochetes
Leptospira interrrogans and L. biflexa
Coiled, thin, highly motile organisms
Epidemiology Rats- most important reservoir
Poor hygienic conditions favor pathogen’s
survival and distribution
Occur more in men
Transmission thru direct contact with
animal urine, blood, or tissue
Pathogenesis Leptospires enter through skin abrasions,
intact mucous membranes, drinking
contaminated water
Vasculitis- most important manifestation
 Leptospirosis
Clinical manifestations Mostly asymptomatic
Leptospiremic phase – fever 3-10 days
Immune phase – appearance of
antibodies

Anicteric leptospirosis Influenza like illness

Calf, back, abdominal pain
Intense headache (frontal, retroorbital)
Conjunctival suffusion- most common
finding (redness without exudate)

Severe leptospirosis Jaundice, renal dysfunction, hemorrhagic

(Weil’s syndrome) diathesis (4-9 days)
Mortality rate 5-15%
Renal failure – 2nd week of illness
Cough, dyspnea, chest pain, blood stained
sputum
Epistaxis, petechiae, purpura, ecchymoses
 Leptospirosis
Lab and radiologic findings Renal – urinary sediment changes
(hyaline or granular casts, leukocytes,
erythrocytes, proteinuria)
Elevated ESR
WBC count – 3,000-26,000
Thrombocytopenia
Elevated bilirubin , ALP, aminotransferases

Patchy alveolar pattern- scattered alveolar

hemorrhage in the lower lobes
Diagnosis Microscopic agglutinin test (MAT)
ELISA
CSF
Blood culture
Urine culture
Leptospirosis
Schistosomiasis
 Schistosomiasis
Etiology Cercariae – released from infected snails
in freshwater bodies
Pathogenesis and Immunity Cercaria once inside the
hostschistosomulalymphatic
vesselslungliver
Eggs lodge at pre sinusoidal sites and
form granulomashepatomegaly
Periportal pipestem fibrosis
Clinical features Occur in 3 stages
Cercarial invasion Swimmer’s itch- maculopapular rash on
the affected areas of the skin
Worm maturation Katayama fever – serum sickness like
(4-8 weeks after skin invasion) syndrome with fever, lymphadenopathy,
hepatosplenomegaly
Hepatosplenic phase RUQ “dragging” pain
(first year of infection) Bleeding esophageal varices
 Schistosomiasis
Clinical features
S. Japonicum, S. mekongi, Intestinal and hepatosplenic disease
S. interclatum
S. haematobium Dysuria, frequency, hematuria
Squamous cell carcinoma of the bladder
Diagnosis Travel history and exposure to freshwater
bodies
FAST-ELISA
EITB
Kato thick smear (stool)

Infection Drug of choice Adult dose and duration

S. mansoni, S. intercalatum, S. Praziquantel 20mg/kg, 2doses in 1 day
haematobium
S. japonicum, S. mekongi Praziquantel 20mg/kg, 3 doses in 1 day
 Meningococcal Infections
Neisseria meningitidis Gram negative aerobic diplococci
Have polysaccharide capsule
 Meningococcal Infections
Clinical manifestations

Upper respiratory tract infection

Meningococcemia Fever, chills, nausea, vomiting, myalgia

Rash – most distinctive feature
-erythematous macules become
petechial and purpuric (trunk and
lower extremities)
Waterhous-Friderichsen syndrome
Chronic meningococcemia
Meningitis Nausea, vomiting, neck stiffness, lethargy,
confusion
CSF: hypoglycorrhachia, elevated protein,
neutrophilic leukocytosis
Others Arthritis (10%)
Pneumonia
Conjunctivitis
Urethritis
 Meningococcal Infections
Diagnosis Blood, CSF, synovial fluid culture
Skin lesion biopsy
Gram stain
PCR
Throat or nasopharyngeal swab
Treatment
1. Ceftriaxone 2 g IV q12h (100 mg/kg per day) or cefotaxime 2 g IV q4h

2. For penicillin-sensitive N. meningitidis: Penicillin G 18–24 million units per day in

divided doses q4h (250,000 units/kg per day)

3. Chloramphenicol 75–100 mg/kg per day in divided doses q6h

4. Meropenem 1.0 g (children, 40 mg) IV q8h

5. In an outbreak setting in developing countries: Long-acting chloramphenicol in oil

suspension (Tifomycin), single dose Adults: 3.0 g (6 mL)
 Meningococcal Infections
Chemoprophylaxis
Rifampin (oral) 600 mg bid for 2 days
Ciprofloxacin (oral) 500mg, 1 dose
Ofloxacin (oral) 400mg, 1 dose
Ceftriaxone (IM) 250mg, 1 dose
Azithromycin (oral) 500mg, 1 dose
Vaccination
A, C, Y, W-135 vaccine (Memomune, Aventis Pasteur) or A, C vaccine

Single 0.5-mL subcutaneous injection

New C; A, C; and A, C, Y, W-135 meningococcal conjugate vaccines

 Rabies
Epidemiology Transmitted by bite of a rabid animal

Pathogenesis Incubation period 1-3 months

Once at the sensory motor neurons, virus
spreads centripetally at 100-400mm/day

Negri bodies- eosinophilic cytoplasmic

inclusions in brain neurons
Absence does not exclude the diagnosis
 Rabies
Laboratory investigations Nonspecific in early clinical stages

Diagnosis Not considered until late in the course

Serum, CSF, fresh saliva, brain tissue, neck
skin biopsy
Rabies virus specific antibodies- may be
detected within a few days after onset of
symptoms
RT-PCR- highly sensitive and specific –
fresh saliva, CSF, tissue
Direct Fluorescent Antibody testing –
brain tissue or skin biopsy
Treatment None

Prognosis Fatal
Only 6 documented survivors after
symptomatic rabies
Rabies
 Rabies
Prevention

Postexposure prophylaxis Local wound care

Active and passive immunization
Tetanus prophylaxis
Antibiotics (when indicated)
Passive immunization Previously unvaccinated – should be given
RIG no later than 7 days (20IU/kg)
Active immunization Day 0, 3, 7, 14, 28

Preexposure Rabies vaccination Occupational or recreational risk of rabies

exposure
Day 0, 7, 21, 28
Previously immunized: booster doses on
days 0 and 3
 Syphilis
Treponema pallidum
Sexually transmitted
Incubation period 2-6 weeks
Clinical manifestations
Primary syphilis Single painless papule that rapidly
becomes eroded (chancre)
Lesions usually located on the penis, anal
canal, mouth, cervix, labia
With regional lymphadenopathy
Chancre heals within 4-6 weeks
LN persists for months
 Syphilis
Secondary syphilis Localized or diffuse mucocutaneous
lesions
Generalized nontender
lymphadenopathy
Skin rash Macular, papular, papulosquamous,
occasionaly pustular
Condyloma lata Broad, moist, pink or gray-white, highly
infectious lesions (10%)
Mucous patches Oral or genital mucoa (10-15%)
Constitutional symptoms Sore throat, fever, weight loss, malaise,
anorexia, headache, meningismus
Acute meningitis (1-2%)
Syphilis
Latent syphilis Positive serologic test
History of primary or secondary lesions
Early latent syphilis Limited to the first year after infection
Late latent syphilis >1 year
Cardiovascular syphilis 10-40 years after infection
Aortitis, AR, saccular aneurysm, coronary
ostial stenosis
Gumma Solitary lesions
Granulomatous inflammation with central
area of necrosis
Indolent, painless, indurated nodular or
ulcerative lesions
Asymptomatic neurosyphilis Asymptomatic
CSF abnormalities: nononuclear
pleocytosis, increase protein, reactive
VDRL
Symptomatic neurosyphilis Meningeal, meningovesicular
parenchymatous syphilis- general paresis
and tabes dorsalis
 Syphilis
Clinical examinations
Serologic tests RPR, VDRL
FTA-ABS
TPHA

Evaluation for neurosyphilis CSF abnormalities

Pleocytosis (>5 WBC/mm3)
Increased protein (>45mg/dl)
VDRL reactivity
Syphilis
Syphilis
 Dengue fever
Carries 1 of 4 strains Aedes aegypti or Aedes albopictus
Dengue without warning signs Nausea/vomiting
-history of travel to endemic area + 2 of Rash
the following: Headache, eye pain, muscle ache, or joint
pain
Leukopenia
Positive tourniquet test
Dengue with warning signs Abdominal pain or tenderness
Persistent vomiting
Clinical fluid accumulation (ascites,
pleural effusion)
Mucosal bleeding
Lethargy or restlessness
Hepatomegaly >2 cm
Increase in hematocrit concurrent with
rapid decrease in platelet count
Severe dengue Severe plasma leakage leading to
shock and fluid accumulation with
respiratory distress
Severe bleeding (as evaluated by clinician)
Severe organ involvement
 MEDICINE REVIEW

Mark Jeremy P. Ramos, MD, FPCP

Internal Medicine
Assistant Professor- FEU-NRMF Institute
of Medicine
ENDOCRINOLOGY
 Diabetes Mellitus
Classification

Type 1 DM Result of complete or near-total insulin

deficiency
Type 2 DM Variable degrees of insulin resistance,
impaired insulin secretion, and increased
glucose production
 Diabetes Mellitus
Diagnosis 1. Symptoms of diabetes plus random
blood glucose conc. >11.1mmol/L
(200mg/dl) or
2. Fasting plasma glucose >7.0mmol/L
(126mg/dL) or
3. 2- hour plasma glucose >11.1 mmol/L
(200mg/dl) during an oral glucose
tolerance test
 Diabetes Mellitus
Pathogenesis (Type 1 DM) Result from autoimmune beta cell
destruction
 Type 2 DM
Genetic considerations Among identical twins (70-90%)
Both parents w/ DM (40%)
Pathophysiology Impaired insulin secretion
Insulin resistance
Excessive hepatic glucose production and
lipid production
Abnormal fat metabolism
Acute complications of DM
 Diabetic Ketoacidosis
Clinical features Nausea and vomiting often prominent
Severe abdominal pain
Kussmaul respiration, fruity breath odor –
classic signs
Pathophysiology Result from relative or absolute insulin
deficiency combined with
couterregulatory hormone excess
(glucagon, cortisol, growth hormone)
Laboratory abnormalities and diagnosis Hyperglycemia
Ketosis
Metabolic acidosis
Diabetic ketoacidosis
Diabetic ketoacidosis: Treatment
Hyperglycemic Hyperosmolar State
Clinical features Elderly individual
Several week history of polyuria
Weight loss
Diminished oral intake
Mental confusion
Lethargy, or coma
Profound dehydration and
hyperosmolality
Hypotension
tachycardia
Precipitated by a serious disease
(MI, stroke)
Pathophysiology Insulin deficiency
Inadequate fluid intake
Hyperglcyemia induces osmotic diuresis
Hyperglycemic Hyperosmolar State
Laboratory abnormalities and diagnosis Marked hyperglycemia
Hyperosmolality
Prerenal azotemia
Treatment Monitor fluid status
Correct underlying precipitating problems
Insulin IV bolus 0.1units/kg followed by
constant IV infusion rate of 0.1 units/kg
per hour
Chronic complications of DM
 Cardiovascular risk factors
Dyslipidemia Lower LDL
Raise HDL
Decrease triglycerides
LDL 100mg/dl for >40 y/o without
(Statins) cardiovascular disease
<70mg/dl if with cardiovascular disease
Triglycerides <150mg/dl
(Fibrates)
HDL 40mg/dl for males
50mg/dl for females
Hypertension <130/80
Lifestyle modification
ACE inhibitor or ARB – slow progression of
micro- , macroalbuminuria, renal
insufficiency
 Long term treatment

Patient education DM education

Nutrition
Exercise
Monitor level of glycemic control Self monitoring of blood glucose
Treatment: Type 1 DM
PARENTERAL EXAMPLES A1C AGENT DISADVANTAGE CONTRAINDICATIONS
MOA REDUCTION SPECIFIC
ADVANTAGE
Treatment: Type 2 DM
Treatment: Type 2 DM
Treatment: Type 2 DM
Thyroid diseases
HYPOTHYROIDISM
 Hypothyroidism
Symptoms:
 Tiredness, weakness
 Dry skin, feeling cold
 Hair loss
 Difficulty concentrating, poor memory
 Constipation
 Weight gain w/ poor appetite
 Dyspnea
 Hoarse voice
 Menorrhagia (oligomenorrhea, amenorrhea)
 Paresthesia
 Impaired hearing
 Hypothyroidism
Signs
 Dry coarse skin; cool peripheral extremities
 Puffy face, hands, feet (myxedema)
 Diffuse alopecia
 Bradycardia
 Peripheral edema
 Delayed tendon reflex relaxation
 Carpal tunnel syndrome
 Serous cavity effusions
 Hypothyroidism
ETIOLOGY
1. Primary hypothyroidism
2. Transient hypothyroidism
3. Secondary hypothyroidism
 HYPOTHYROIDISM
1. Primary hypothyroidism
ETIOLOGY :
 Autoimmune: Hashimoto’s, atrophic thyroiditis
 Iatrogenic: 131I- tx, thyroidectomy, ext. irradiation
 Drugs: I- (contrast, amiodarone), Li, ATD, ƿASA, IFN-α, other
cytokines, aminoglutethimide
 Congenital: absent, ectopic, dyshormonogenesis, TSH-R mutation
 I- deficiency
 Infiltrative: amyloidosis, sarcoidosis, cystinosis,
hemochromatosis, scleroderma, Riedel’s thyroiditis
 Overexpression type 3 deoI-ase infantile hemangioma
 HYPOTHYROIDISM
2. Transient Hypothyroidism
ETIOLOGY :
 Silent thyroiditis
 Postpartum thyroiditis
 Subacute thyroiditis
 Withdrawal of thyroxine treatment w/ intact thyroid
 After 131I tx or subtotal thyroidectomy for Graves’
disease
 Autoimmune Hypothyroidism
CLASSIFICATION
 Hashimoto’s or goitrous thyroiditis
 Atrophic thyroiditis

 Subclinical hypothyroidism
 Clinical or overt hypothyroidism
 Autoimmune Hypothyroidism
PREVALENCE
 Incidence: 4:1000 F, 1:1000 M
 Mean age: 60 yr
 Overt hypothyroidism ↑ w/ age
 Subclinical: 6-8% F, 3% M
 4% annual risk w/ (+) TPO Abs
 Autoimmune Hypothyroidism
PATHOGENESIS
 HLA-DR, CTLA-4 polymorphisms – account
for ½ genetic susceptibility
 Risk ↑ in ↑ I- (immunologic, direct toxicity)
 Tg & TPO Abs – clinically useful markers of
autoimmunity
 TSH-R blocking Abs (+) 20%
 TBII – confirm transient neonatal
hypothyroidism
 Autoimmune Hypothyroidism
LABORATORY INVESTIGATION
 TSH - ↑; for screening
 FT4 – ↓
 FT3 - ↓; normal in 25% → measurement not
indicated
 Autoimmune Hypothyroidism
TREATMENT:
Levothyroxine replacement
 Usually 1.6 μg/kg/day

Subclinical hypothyroidism
• No universally accepted recommendations
• Treatment not recommended when TSH values <10 mU/L
• Low dose levothyroxine (25-50ug/d)

Myxedema coma
• High mortality rate
• Reduced level of consciousness, seizure
• Hypothermia
• Levothyroxine 500ug IV bolus then 50-100ug/d
 Thyrotoxicosis
State of thyroid hormone excess
Hyperthyroidism –result of excessive thyroid function
 Thyrotoxicosis
Grave’s disease 60-80% of thyrotoxicosis
Occurs between ages 20-50
Pathogenesis HLA-DR, CTLR-4, PTPN22 polymorphisms
contribute to disease susceptibility
Stress
Smoking- minor risk factor for Graves but
major risk factor for ophthalmopathy
 Grave’s disease
Clinical manifestations Diffusely enlarged thyroid (2-3x)
 Grave’s disease
Clinical course Worsen without treatment
Remissions and relapses
Treatment Reduce thyroid hormone synthesis
Use antithyroid drugs
Reduce amount of thyroid tissue (RAIU)
thyroidectomy
Antithyroid drugs PTU – 100-200mg q6-8h
Carbimazole, methimazole- 10-20ug q8-
12h
Propranolol 20-40mg q6h
Radioiodine Can be used as initial treatmtent or for
relapses after trial of antithyroid drugs
Subtotal or near total thyroidectomy Relapse after antithyroid medication
 Grave’s disease
Thyrotoxic crisis/thyroid storm Life threatening exacerbation of
hyperthyroidism
Fever, delirium, seizure, coma, vomiting,
diarrhea, jaundice
Precipitated by acute illness, surgery, or
radioiodine treatment
Treatment PTU -500-1000mg loading dose and
250mg q4h (oral, NGT, per rectum)
Stable iodide one hour after PTU first
dose
Thyroiditis
 Thyroiditis
Acute thyroiditis Due to suppurative infection of the
thyroid
Elevated ESR and WBC ct
Normal thyroid function
Subacute thyroiditis De Quervain’s thyroiditis
Granulomatous thyroidits
Viral thyroiditis
1. Thyrotoxic phase
2. Hypothyroid phase
3. Recovery phase
Clinical manifestations Painful and enlarged thyroid
Treatment Large dose of ASA – to control symptoms
Steroids – prednisone 40-60mg
Goiter and nodular thyroid disease
Diffuse nontoxic (simple) Goiter Most commonly caused by iodine
deficiency
Exposure to environmental goitrogens:
cassava root, sprouts, cabbage,
cauliflower
Treatment Levothyroxine (50-100ug/d)
Nontoxic Multinodular Goiter Mostly asymptomatic, euthyroid
Conservative management
Toxic Multinodular Goiter May present with subclinical
hypothyroidism or mild thyrotoxicosis
Usually elderly
Treatment Antithyroid drugs w/ beta blockers can
normalize thyroid function
Stimulates growth of the goiter
radioiodine
Goiter and nodular thyroid disease
Hyperfunctioning solitary nodule Toxic adenoma
Have acquired somatic, activating
mutations in the TSH-R
Treatment Radioiodine ablation- treatment of choice
 Thyroid cancer
Most common malignancy of the
endocrine system
Unique features 1. Thyroid nodules readily palpable,
allowing early detection on biopsy
2. Iodine radioisotopes can be used to
diagnose and treat differentiated
thyroid cancer
3. Residual markers allow the detection
of residual or recurrent disease
Thyroid cancer
 Thryroid cancer
Pathogenesis
Radiation Predisposed to chromosomal breaks,
genetic rearrangement and loss of tumor
suppressor genes
Children are more prone to its effects
TSH and Growth factors Many differentiated cancers express TSH
receptors
Oncogenes and tumor suppressor genes Monoclonal in origin
Mutations of gene/proteins
 Thyroid cancer
Well differentiated thyroid cancer
Papillary cancer Most common (70-90%)
Biopsy: psammoma bodies, cleaved nuclei
with “orphan-Annie” appearance caused
by large nucleoli
Formation of papillary structures
Multifocal and tend to invade locally
within the thyroid gland and anterior neck
structures
Metastasis: bone and lung
Excellent prognosis
Follicular More common in iodine deficient regions
Difficult to diagnose
Hematogenous spread
Poor prognosis: distant metastasis, >50y,
primary tumor size >4cm, Hurthle cell
histology, vascular invasion
Thyroid cancer
 Thyroid cancer
Treatment
Surgery All should be surgically excised
Near total thyroidectomy
TSH suppressor therapy Levothyroxine - mainstay
Radioiodine

Anaplastic and other forms Poorly differentiated and aggressive

cancer
Most die within 6 months of diagnosis
Radioiodine, chemotherapy ineffective
Thyroid lymphoma Arises in the background of Hashimoto’s
thyroiditis
Rapidly expanding thyroid mass
Diffuse large-cell lymphoma – most
common
 Thyroid cancer
Medullary thyroid cancer 5-10% of thyroid cancers
3 familial forms: MEN 2A, MEN 2B, and
familial MTC without other features of
MEN
DISORDERS OF THE
ADRENAL GLAND
 OUTLINE
Disorders of the adrenal gland
• Glucocorticoid disorders
• Cushing’s syndrome
• Addison’s disease
CUSHING’S SYNDROME
CLINICAL MANIFESTATIONS
• Body fat – weight gain, central obesity,
rounded face, buffalo hump
• Skin – thin and brittle, facial plethora, easy
bruising, purple striae, acne, hirsutism
• Bone – osteopenia/porosis (vertebral
fractures)
• Muscle – weakness, myopathy (proximal),
atrophy (gluteal, upper leg)
 CLINICAL MANIFESTATIONS
• CVS – hypertension, hypokalemia, edema,
atherosclerosis
• Metabolism – glucose intolerance, DM,
dyslipidemia
• Reproductive system – decreased libido,
amenorrhea
• CNS – irritability, emotional lability, depression,
cognitive defects, psychosis
• Blood/immune system – increased susceptibility
to infection & WBC, eosinopenia,
hypercoagulation, increased DVT/PE risk
 ETIOLOGY
• ACTH-dependent
• Cushing’s disease (ACTH-producing pituitary
adenoma)
• Ectopic ACTH syndrome
• ACTH-independent
• adrenocortical adenoma
• carcinoma
• hyperplasia
 EVALUATION
• 24-hr urine free cortisol
• Dexamethasone overnight test
• Midnight plasma or salivary cortisol
• Plasma ACTH
• Adrenal CT
 TREATMENT
• Surgical removal of adrenal tumor
• Medical
• metyrapone
• ketoconazole
• mitotane
ADRENAL INSUFFICIENCY
 CLINICAL MANIFESTATION
• GC deficiency – fatigue, lack of energy, weight loss,
anorexia, myalgia, joint pain, fever, anemia,
lymphocytosis, eosinophilia, hypoglycemia, low BP,
hyponatremia
• MC deficiency – abdominal pain, nausea, vomiting,
dizziness, postural hypotension, salt craving, low BP,
inc. creatinine, hyponatremia, hyperkalemia
• Adrenal androgen deficiency – lack of energy, dry/itchy
skin, loss of libido and axillary/pubic hair in women
• POMC excess – hyperpigmentation
 ETIOLOGY
• Autoimmune – Isolated autoimmune
adrenalitis, APS 1 (APECED), APS 2, Cushing’s
disease, Ectopic ACTH syndrome
• Congenital – CAH, CLAH, AHC
• Destruction of the adrenal glands – infection,
hemorrhage, infiltration
 EVALUATION
• Screening/confirmation - Cosyntropin test or
Insulin tolerance test
• Plasma ACTH
• Adrenal antibodies
• Adrenal CT
 TREATMENT
• GC replacement – hydrocortisone
• MC replacement – fludrocortisone
• Adrenal androgen - DHEA