USMLE WORLD QUESTIONS Quizlet

What are the two major microtubular motor proteins? Which

does anterograde axonal transport, which does retrograde
axonal transport?
Kinesin, Dynein
Kinesin: Anterograde
Dynein: Retrograde`

What do you think, immunologically speaking, when you see

someone with recurrent Neisseria infections?
Inability to form the membrane attack (MAC) complex
this is a common complement deficiency

What is the defect in Chronic Granulomatous disease? What

is the pathophysiology?
NADPH Oxidase deficiency leads to the inability to kill intracellular organisms

Characteristic triad of ataxia telangiectasia?

cerebellar ataxia, telangiectasias, increased risk of sinopulmonary infections

What is the major immune deficiency of ataxia

telangiectasia?
IgA deficiency, which predisposes to infections of the upper and lower
airways (and other mucous membranes)

There's a useful mnemonic for Ataxia Telangiectasia and the

gene that's mutated. What is it?
ATM
Ataxia
Telangiectasia
Mutated
ATM gene is responsible for DNA break repair

What is one reason that lead intoxication causes

hypochromic anemia?
Mitochondrial iron transport is important for Heme synthesis! It's inhibited by
lead. So you don't make heme in your mitochondria and you get
hypochromic anemia.

What is the biochemical problem in Lesch-Nyhan syndrome?

(And, only if you got that right, what are the really cool
symptoms of it?)
Defective purine catabolism, so buildup of purines. It's an X-linked recessive
disorder with mutated HGPRT gene (hypoxanthine-guanine
phosphoribosyltransferase, if you want to impress people).
Now, if you got HGPRT and purine catabolism right, you can say: selfmutilating behavior on top of mental retardation, choreoathetoid (think
Chorea) movements and spasticity.

What is the defect in Niemann-Pick disease?

What causes that?
What is the common macular finding?

Sphingolipid degradation is defective

Caused by an autosomal recessive defect in sphingomyelinase
Cherry Spot on the macula? Niemann Pick's or Tay Sach's.

If a baby gets exposed to an unclean knife (...) and

subsequently develops rigid paralysis, what is the diagnosis,
where do we think this might happen, and how do we
prevent it?
Neonatal Tetanus
Developing Countries
Maternal immunization with tetanus toxoid is the best way to prevent it
an adeuately immunized mom will transfer IgG's across the placenta to the
neonate

Which microtubule associated protein aids in anterograde

transport of intracellular vesicles and organelles? Which end
of the microtubule do they go towards?
Kinesin.
Towards the (+) rapidly growing end.

What is an early BRAIN finding of Ataxia-Telangiectasia and

how does it manifest itself?
Cerebellar atrophy
manifests as ataxia in the first years of life.

High yield path association for Alzheimer's disease?

Neurofibrillary tangles in the neocortex

High yield path association for Parkinson's disease?

Loss of neurons in the substantia nigra

High yield path association for Huntington disease?

Atrophy of caudate nucleus

What are the major manifestations of Ataxia-telangiectasia?

cerebellar ataxia, oculocutaneous tenlangiectasias, repeated sinopulmonary
infections, and an increased incidence of malignancy

If you heard: amenorrhea, bitemporal hemianopsia, and

enlargement of the pituitary gland on brain imaging, what
would you be thinking?
Prolactinoma, the most common pituitary adenoma.

What embryological layer is the anterior pituitary derived

from?
Surface ectoderm

What is the most common congenital abnormality associated

with the use of Sodium Valproate during pregnancy?
neural tube defects, e.g., meningocele
because valproate inhibits intestinal folic acid absorption resulting in
teratogenicity

What is the characteristic histology of a craniopharyngioma?

On light microscopy, cysts are lined by stratified squamous epithelium,
possibly with Keratin perals. Cysts are usually filled iwth a yellow, viscous
fluid that's rich in cholesterol crystals.

Where do craniopharyngyomas arise from?

Craniopharyngiomas are calcified cystic tumors that arise from remnants of
Rathke's pouch (embryonic precuros of the anterior pituitary)

Failure of what process leads due neural tube defects? What

can be seen in the amniotic fluid due to leakage of fetal
cebebrospinal fluid?
Failure of fusion of the neuropores.
Alpha-fetoprotein and Acetylcholinesterase may appear in the amniotic fluid

Can a competent patient refuse healthcare? Can a

competent patient refuse knowledge of their potential
health situation?
yes and yes

What is the consensus and professional standard regarding

the receiving of gifts from patients?
Don't do it. It's unethical to accept individual gifts from patients, especially of
signficant value.
AMA doesn't have clear cut answer, but they recommend careful
consideration be used. some general guidelines:
-cash gifts should never be accepted (this includes gift certificates)
-a gift should never influence treatment
-no specific dollar value is given; but as a rule of thumb, it shouldn't be
above patient's or physician's means
-psychiatrist must be super careful even with small gifts
-maintain consistency among all patients
-if physician would be embarrassed or uncomfortable if his colleagues found
out about the gift, don't accept it

Is displacement a mature or immature defense mechanism?

What is displacement?
Immature. A patient redirects emotions from the person or object that's
causing the emotions (e.g., wife), but who it woudl be completely
unacceptable to direct those emotions toward, to a more acceptable, but still
inappropriate, person or object (e.g., a wall or a vase).

Is sublimation a mature or immature defense mechanism?

How does it work?
Mature. Unacceptable drives are redirected toward completely acceptable
targets. (Workout hard if you're angry)

Is projection a mature or immature defense mechanism?

What is it?
Immature. Unacceptable or personally disagreeable impulses are attributed
to others; e.g., a student who wants to cheat on a test accuses his
classmates of cheating. Or the gayness thing

Is reaction formation immature or mature defense

mechanism? what is it?
immature, where unacceptable feeligns are IGNORED and the opposite
sentiment is adopted (forced). man who's mad at his wife instead
compliments her dress

Is splitting a mature or immature defense mechanism? what

is it?
immature. frequently employed by patients with borderline personality
disorder, everything is either "good or bad."

What do you do if you suspect child abuse? Ask the parents

or call child protective services?
Call Child Protective Services immediately!

Psychologically speaking, what phenomenon is "white coat

syndrome" associated with?
Classical Conditioning. In classical conditioning, a reflexive response normally
elicited by an unconditioned stimulus becomes evocable by a second,
formally neutral (conditioned) stimulus.

What three things can patients with bulimia develop (hint:

one isn't weight loss because bulimia doesn't work.)?
(1) bilateral partodi gland enlargement
(2) erosion of tooth enamel*
(3) irregular menses

What is the pulmonary capillary wedge pressure and what

does it indirectly measure?
Pressure in the pulmonary artey distal to the point of its occlusion by an
inflated intravascular balloon.
Since there's no significant blood flow towards the left atrium (LA) beyong
this point of occlusion, the pressure at the tip of the "wedged" pulmonary
artery catheter is an indirect measurement of LA Pressure.

What would we expect, in a normal patient, the relationship

to be between LA and LV pressure during diastole?
We would expect them to be nearly equale (both <12) since the open mitral
valve offers minimal resistance to flow between the 2 chambers

What is the characteristic finding via cardiac catheterization

in a patient with mitral valve stenosis? I.e., if we see what
value elevated while the other remains normal, when do we
think "Mitral Valve Stenosis."
Cardiac Catheterization will reveal a LA end diastolic pressure (via pulmonary
capillary wedge pressure) that is significantly greater than the LV end
diastolic pressure (LVEDP).
This abnormal pressure gradient implies increased resistance to flow
between the LA and LV, i.e., mitral valve stenosis.

Summarize the key points of pulmonary capillary wedge

pressures (PCWP) and how it helps us diagnose mitral valve
stenosis.
The Pulmonary capillary wedge pressure (PCWP) measures LAEDP. Under
normal conditions, the LAEDP is nearly equal to the LVEDP. Mitral stenosis
eleveates the LAEDP and PCWP relative to the LVEDP.

Generally speaking, regarding blood flow through our

vessels, the law of conservation of mass states that the total
flow of mass into a contained system must be equal to the
total outflow of mass from that system in a steady state.
What equation helps us prove the following condition: to
maintain a constant fluid flow througha tube with varying
diametes, how are cross-sectional area and flow velocities
related?
Volume in must equal volume out, right? Vol(in) = A1 V1 ; Vol(out) = A2V2
So any rearrangement of that equation holds true in a physiological system.
A2 = A1*V1 / V2 for example, works.
This applies for blood flow in the cardiovascular system.

What do you think when you hear a patient who has a heart
murmur presenting with the following physical exam
findings:
Bounding femoral pulses, carotid pulsations accompanied by
head-bobbing.
Aortic Regurgitation

How does the pathophysiology of aortic regurgitation

explain the characteristic findings of these patients? And
what are those findings again (2 major ones)?
(1) Bounding femoral pulses;
(2) Carotid Pulsations with head-bobbing (de Musset sign)
There is a large LVSV, a large regurgitant SV, and a large pulse pressure.
Bounding femoeral and carotid pulses marked by abrupt distention and quick
collapse ("water hammer" pulses) are the result of large pulse pressure
the head bobbing is due to the transfer of mementum from htel arge left
ventricular stroke volume to the head and neck

What is the order of cardiac tissue conduction velocity from

fastest to slowest?
Purkinje System
Atrial Muscle
Ventricular Muscle
AV node

What is the mnemonic to help you remember the order of

cardiac tissue conduction velocity?
P ark (purkinje's)
AT (atria)
VENT ura (ventricles)
AV enue (AV node)

Where does Atrial Natriuretic Peptide (ANP) come from? In

response to what?

Atrial Cardiomyocytes in response to atrial stretch, it is a signifier of volume

expansion

What is the ultimate action of ANP?

Lowers blood pressure through peripheral vasodilation, natriuresis, and
diuresis.

How does ANP affect the following organs:

(1) kidney?
(2) adrenal gland?
(3) blood vessels?
(1) Dilates the afferent arterioles, increasing GFR and urinary excretion of
sodium and water (diuresis); also limits sodium reabsorption (in proximal
tubule) and inhibits renin secretion
(2) restricts aldosterone secretion --> increase in sodium and water excretion
by the kidneys
(3) relaxes vascular smooth mucles, producing vasodilation; also increases
capillary permeability, leading to fluid extravasation to the interstitium and a
decrease in circulating blood volume

What major hormone comes from the renal juxtaglomerular

cells, and what is its net effect on the vasculature?
Renin, which catalyzes angiotensinogen --> ang I
angiotensin causes vasoconstriction, increased blood pressure, and
aldosterone release

What is the pathophysiology of CHF in general terms?

CHF occurs when the heart is unable to pump sufficient amounts of blood to
meet body's metabolic demands

How is the reduced cardiac output in CHF initially detected?

How does the body attempt to compensate?
A drop in blood pressure
Compensatory neurohormonal stimulation that is directed at maintaining
blood pressure and tissue perfusion
Chiefly mediated through:
(1)increased sympathetic nervous system activity,
(2)stimulation of the renin-angiotensin-aldosterone pathway,
(3) release of ADH

What are the adverse consequences of the body's

adaptations to CHF? There are 3 major ones to keep in mind.
(1) increased afterload from excessive vasoconstriction
(2) excess fluid retention
(3) deleterious cardiac remodeling, which perpetuates a downward spiral of
progressive cardiac deterioration

What is the most common cause of heart failure in

developed countries?
repeated bouts of myocardial ischemia

When do we most commonly (or typically for Step 1) hear an

S3 ventricular gallop?
in patients with left ventricular systolic failure or restrictive cardiomyopathy

When does S3 heart sound happen?

immediately following S2 during phase of rapid passive ventricular filling

How do we best auscultate an S3 gallop?

with the bell of the stethoscope at the ventricular apex

What 2 physical examination maneuvers can help bring out

an S3 more audibly?
(1) lying the patient in a left lateral decubitus position
(2) ask the patient to exhale completely while in that position by decreasing
the volume of the lungs and bringing heart closer to the chest wall

Summarize the key facts of the S3 sound or S3 gallop.

An S3 sound is a low frequency sound that can be physiologic in younger
individuals, but typically pathologic in older adults. In older adults, it results
from left ventricular systolic failure or restrictive cardiomyopathy. The S3
sound can be accentuated by having the patient lie in the left lateral
decubitus position and fully exhale.

What are the characteristic ECG findings of a patient in Afib?

(1) absent P waves replaced with chaotic f (fibrillatory) waves
(2) irregularly irregular R-R intervals
(3) narrow QRS complexes

What causes ventricular contraction rate in a patient in

atrial fibrillation?
Atrial fibrillation occurs due to irregular, chaotic electrical activity within the
atria
Some of the atrial impulses are transmitted to the ventricles, but most are
not.
this is due to the AV nodal refractory period.

What three pathologies do we associate a holosytolic

murmur with?
(1) tricuspid regurgitation
(2) mitral regurgitation
(3) ventricular septal defect

Does more or less blood return to the right heart during

inspiration? Why?
More blood returns because during inspiration intrathoracic pressure drops,
allowing more blood to return to the right heart

How do we differentiate a holosystolic murmur? I.e., how do

we know if it's tricuspid valve regurgitation vs. mitral
regurgitation vs. ventricular septal defect?
A tricuspid regurgitation murmur would be expected to increase in intensity
during inspiraiton, while the other two would not

Summarize the cardiac findings in a patient with a tricuspid

valve regurgitation.
A holosystolic murmur that increase in intensity on inspiration most likely
represents tricuspid regurgitaiton.

How do arterial baroreceptors monitor systemic blood

pressure?
Baroreceptors sense arterial wall stretch, which is an indicator of systemic
pressure in arterial circulation. When stimulated by:
(1) stretch: nerves innvervating those baroreceptors increase firing --> blood
pressure decrease through peripheral vasodilation and decreased cardiac
output
(2) hypotension: decreased baroreceptor signaling --> releases inhibition of
vasoconstrictor center and increases blood pressure

Which two nerves monitor the baroreceptors in the neck?

Glossopharyngeal nerve (IX) & Vagus nerve (X)

Which two anatomical landmarks are important loctaions of

barroreceptors that are especially important in blood
pressure control?
(1) the carotid sinus [located just above the bifurcation of the common
carotid artery]
(2) the aortic arch

Which nerve innervates the baroreceptors of the aortic arch?

the vagus nerve; fibers from the baroreceptors run within the vagus nerve
(X)

Which nerve is more associated with the carotid sinus? How

is it associated, and what is the name of the actual nerve /
who is that nerve a branch of?
(1) glossopharyngeal nerve
(2) AFferent fibers from the carotid sinus stretch receptors form a small
carotid sinus nerve called HERING'S NERVE, which is a branch of the
glossopharyngeal nerve

Where do all of our important baroreceptor nerves

terminate? I.e., fibers from the aortic arch baroreceptors
and the carotid sinus baroreceptors send their fibers to what
brain structure?
the solitary nucleus of the medulla

Describe the net impact on Mean Arterial Pressure (MAP) of

exercise on exercising muscle.
There is only a modest blood pressure increase! this is because of peripheral
vasodilation to skeletal muscle within the muscle significantly decreases the
total systemic vascular resistance.

In what condition do where hear a "snap" followed by a

rumbling diastolic murmur, best heard over the cardiac
apex?
Mitral Stenosis
Opening snap results from abrupt halting of motion of the stenotic mitral
valve leaflets during MITRAL VALVE OPENING (visualize where that is on a
pressure-volume curve) [the point between isoblumetric relaxation and

diastolic filling]
the diastolic murmur is the result of turbulent blood flow through the stenotic
mitral valve during LEFT ATRIAL CONTRACTION

What is the most common cause of mitral valve stenosis?

Prior rehumatic carditis

What is the classic physical exam finding in mitral valve

stenosis best heard over the apex of the heart?
MItral valve stenosis has a characteristic opening snap followed by a diastolic
rumbling murmur.

What are the two important formulae for cardiac output?

What principle underlies the second?
(1) CO = Stroke Volume * Heart Rate
(2) Oxygen Consumption / Arteriovenous O2 difference
*the second formula is explained by Fick's principle; it states that the cardiac
output is equal to the oxygen consupmtion by the tissues divided by
Arteriovenous Oxygen difference

What kinds of methods, invasive or noninvase, are used to

assess the necessary parameters (O2 consumption,
arteriovenous O2 difference) to determine cardiac output by
Fick's principle?
Invasive methods

When is the myocardium best perfused with blood? (this is a

unique property of myocardium)
DIASTOLE
The coronary circulation is unique in that only 10% of total perfusion through
the myocardial capillaries of the left ventricle occurs during systole
(contraction of the muscular left ventricle compresses the coronary arteries!)
The great majority of blood flow through the vascular beds supplied by the
coronary arteries to the LV occurs during diastole, when the blood vessels
are not compressed by myocardial contraction

What area of the heart is most prone to ischemia and

myocardial infarction and why?
The Left Ventricular subendocardial myocardium, because the systolic
reduction in coronary blood flow in this region is the greatest

What are the two most important factors that metabolically

autoregulate coronary blood flow?
Adenosine and Nitric Oxide (NO)

Which of the two major metabolites that regulates coronary

blood flow works more on small coronary arterioles?
Adenosine

Which of the two major metabolites that regulates coronary

blood flow works more on large arteries and pre-arteriolar
vessels of the heart?
Nitric Oxide

How does nitric oxide act within vascular smooth muscle to

affect vasodilation?
Nitric Oxide acts within smooth muscle with a soluble guanylate cyclase
enzyme to
INCREASE PRODUCTION OF CYCLIC GMP and CAUSE SMOOTH MUSCLE
RELAXATION

Does neuronal input typically have a strong impact on

coronary circulation?
no. nervous input generally has very little effect on coronary blood flow (so
NE, Ach, etc. doesn't have a lot to do with coronary flow... what does?
adenosine for small arterioles, NO for larger vessels)

What type of drug, generally speaking, is Verapamil? I.e.,

what is it's mechanism of action?
Verapamil is a calcium channel blocker

Why does verapamil only exhibit a minimal effect on skeletal

muscle?
Skeletal muscle does NOT require calcium to enter from the extracellular
space to cause calcium release from within the cell.

[review of skeletal muscle contraction: Calcium released from the

sarcoplasmic reticulum binds to Troponic C allowing actin and myosin to bind.
ATP bound to myosin is then hydrolyzed and contraction occurs]

What properties of cardiac muscle make it a better target

for calcium channel blockers such as verapamil?
In cardiac muscles, the L-type channel-RYR mechanical coupling mechanism
DOES NOT EXST.
In cardiac muscle, depolarization causes L-type calcium channels on the
plasma membrane to open and allow influx of EXTRACELLULAR CALCIUM.
This calcium then binds to and activates sarcoplasmic RyR-2 channels by a
mechanism known as calcium-induced-calcium-release, which then allows
calcium to move out of hte sarcoplasmic reticulum.
[contraction then proceeds in a similar manner to that seen in skeletal
muscle: Calcium binds to Troponin-C allowing actin and Myosin to bind, ATP
bound to myosin is then hydrolyzed and contraction occurs]

Medically speaking, how do we define palpitations? [I.e., not

just a black woman saying "You give me heart palpitations."]
subjective sensation and awareness of one's own heart beating

What is the most common cause of palpitations?

anxiety.
this was in there to remind you to THINK and not just "take the test"

Whenever you hear "irregularly irregular," you should think

of the most common chronic arrhythmia, which is what?
Atrial Fibrillation

What are some important precipitating factors for isolated

episodes of a-fib?
(1) binge alcohol consumption ("holiday heart syndrome")
(2) increased cardiac sympathetic tone
(3) pericarditis

What are the ECG hallmarks of A-Fib?

(1) absent p-waves
(2) irregularly spaced ventricular contractions
(3) variable r-r intervals (showing (2))

What is the most common paroxysmal tachycardia, and what

is its common pathophysiology?
Paroxysmal supraventricular tachycardia (PSVT)
PSVT typically results from a re-entrant impulse traveling through slowly and
rapidly conducting segments of the AV node

What are some simple maneuvers to treat PSVT?

carotid sinus massage and valsalva maneuver
both of these increase cardiac parasympathetic tone
the parasympathetic nervous system primarly functions to slow the heart
rate by slowing conduction through the AV node

How does the parasympathetic nervous system primarily

function to slow the heart rate?
Slowing conduction through the AV node

How does carotid sinus massage help a person in PSVT

recover?
The nerves innervating the carotid sinuses are constantly firing; when
pressure at the carotid bodies increases, the number of impulses sent to the
CNS also increases
Carotid sinus massage increases carotid sinus baroreceptor firing (involving
cranial nerve IX, not X like the aortic arch), thus increasing parasympathetic
influence on the heart and vessles
this ultimately prolongs the AV node refractory period which stops AV reentrant tachycardias

What is the clinical picture of congestive heart failure? What

is the super general pathophysiology?
Dyspnea, edema, and fatigue
poor cardiac output

What are early responses by our body makes to combat

CHF? How do these cause further problems?
Inadequate visceral perfusion causes activation of the sympathetic nervous
system and the renin-angiotensin-aldosterone system
Both the Sympathetic NS and the RAS system are meant to increase cardiac

output, but their effect on the diseased heart is to cause an inappropriately

high AFTERLOAD and CIRCULATING VOLUME
this leads to progressive heart disease

Where does our body synthesize ACE? What does ACE stand
for?
Lung endothelium
Angiotensin-converting-enzyme
(Ang I --> Ang II)

How, physiologically speaking, is cardiac relaxation

achieved, which is best detected by a rapid decrease in
cytoplasmic calcium levels?
Relaxation occurs subsequent to calcium efflux from the cytoplasm, which is
accomplished through the use of :
Calcium-ATPase and Na+/Ca2+ exchange mechanisms
the Ca2+ ATP-ase pump uses active transport to sequester calcium in the
sarcoplasmic reticulum and re-establish ion gradient
the sarcolemmal Na+/Ca2+ transmembrane protein does not require ATP
and acceps three Na+ ions in exchange for one intracellular Ca2+ ions

So, summarize the two important ways cardiac myocyte

relaxation is accomplished.
Calcium efflux, governed by the use of Ca2+-ATPase and Na+/Ca2+
exchange mechanisms

What does the Frank-Starling effect state?

As cardiac muscle is increasingly stretched (by venous return), the cardiac
output increases (up to a limit).
[This is essentially the same length-tension relationship that is seen in
skeletal muscle]

What would we expect in terms of cardiac output in a

patient with chronic anemia?
Cardiac output increases in an effort to meet the metabolic demands of the
tissues

What would we expect in anaphylaxis in terms of venous

return and cardiac output?
Anaphylaxis causes widespread venous and arteriolar dilation along with
increased capillary permeability and third-spacing of fluids
this results in a serious drop in venous return
cardiac contractility is also increased as the body attempts to maintain blood
pressure

How does acetylcholine and adenosine influence cardiac

pacemaker cells, particularly at Phase 4 (pacemaker
potential)?
Ach and adenosine reduce the rate of spontaneous depolarization in cardiac
pacemaker cells

What is unique to cardiac muscle actions potentials, and

what channel mediates it?
Plateua, characterized by the opening of L-type dihydropyridine-sensitive
Ca++ channels and the closure of some K+ channels
thus, the membrane becoems highly permeable to Ca++ ions and minimally
permeable to K+ ions

What are the 4 phases of a cardiac myocyte action

potential?
Phase
Phase
Phase
Phase
Phase

0:
1:
2:
3:
4:

rapid depolarization
intial rapid repolarization
plateua
late rapid repolarization
resting potential

the action potential is associated with increased membrane permeability to

Na+ and Ca++ and decreased permeability to K+

What is the major limiting factor for coronary blood flow?

the duration of diastole
most of the blood supply to the heart occurs during diastole and the duration
or length of diastole is a critical factor in determining coronary blood flow

What heart defect classically has a continueous murmur?

Patent Ductus Arteriosus

What heart defect is classically heard with a Patent Ductus

Arteriosus? Where do we best auscultate it?
PDA is associated with a continuous murmur best heard at the left
infraclavicular region with maximal intensity at S2

What patients are at greatest risks of PDA?

Kids born prematurely
Kids with cyanotic Heart Disease

What is the classic cardiac finding in Mitral Valve Prolapse?

Mitral Valve Prolapse classically results in a midsystolic click and mid-to-late
systolic murmur

From a cardiac pathophysiology standpoint, summarize

patent ductus arteriosus.
PDA is characterized by a continuous murmur heard best in the left
infraclavicular region with maximal intensity at S2.
A small PDA is often asymptomatic and detected incidentally during routine
cardiac auscultation.
It occurs most commonly in patients born prematurely and those with
cyanotic congenital heart disease.

How do natriuretic peptides (BNP and ANP) work?

they cause vasodilation, diuresis/natriuresis (as their name suggests...), and
a decrease in blood pressure

they counteract:
endothelin
sympathetic effects
angiotensin II

How can atrial fibrillation precipitate sudden heart failure?

the sudden loss of the contribution of normal atrial contraction to ventricular
filling (loss of the atrial systolic kick) decreases LV preload (end diastolic
volume)

What is the classic cardiac finding of mitral stenosis again?

Opening snap followed by rumbling murmur.

So what is the best auscultatory indicator of the severity of

mitral stenosis (MS)?
The length of the interval between S2 and the opening snap. The shorter the
interval, the more severe the stenosis

What condition do we associate an extra low-frequency

heart sound at the end of diastole just before S1 (known as
S4) with?
Left Ventricular hypertrophy... sounds like ba-dum BUM, ba-dum BUM, badum BUM, etc.
[may also occur in restrictive cardiomyopathy]

What is the phenomenon of hibernating myocardium, and

how does it explain why coronary artery bypass grafting is
an effective treatment of a failing left ventricle?
Repetitive ischemia of cardiac myocytes or persistent hypoperfusion of
myocytes can result in a chronic, but reversible, loss of contractile function
that's HIBERNATION

What is the characteristic cardiac finding on auscultation of

ventricular septal defect?
low-pitched holosytolic murmur heard best at the left sternal border with
accentuation during the hand-grip exercise
the hand-grip maneuver accentuates it because of increased afterload, which
results in an increase in the movement of blood from the left ventricle to the
right ventricle across the VSD

What are korotkoff sounds?

blood pressure sounds

What is pulsus paradoxus, and what disease do we

associated it with?
Pulsus Paradoxus is defined by a decrease in systolic blood pressure of
greater than 10 mmHg with inspiration, and is detected by inflating a blood
pressure cuff above systolic pressure and then SLOWLY releasing it [just
buzzword cap'd there]
as the kuff is deflated, korotkoff sounds first become audbile during
expiration and subsequently become audible during all phses of respiration
Inspiration causes increase in systemic venous return... so normally, this
results in expansion of right ventricle into the pericardial space with little
impact on the left side of the heart
in conditions that impair expansion into the pericardial space [PERICARDIAL
DISEASE], the increased right ventricular volume pushes the interventricular
septum to the left
therefore, the left heart diastolic volume and stroke volume are reduced,
resulting in decreased systemic blood pressure during inspiration and hence
pulsus paradoxus

Okay, short version. What is pulsus pardoxus? A disease of

what heart layer causes it?
Decreased systolic blood pressure during inspiration.
Pericardial Disease.

What are acute asthma exacerbations treated with?

Beta-adrenergic Agonists

How do beta-agonsists work? Why is this effective in acute

asthma exacerbations?
Beta-agonists produce relaxation of bronchial smooth muscle by stimulating
beta-2 receptors, which si a Gs protein-coupted receptor that activates
adenylyl cyclase and increases intracellular cAMP concentrations

Simply put, how do beta-agonists treat asthma attacks?

by causing bronchial smooth muscle relaxation by increasing intracellular
cAMP

What ist he classic auscultatory findings in mitral

regurigtation?
Blowing, holosystolic murmur heard best over the apex with radiation to the
axilla

What is a very common cause of mitral regurgitation in

developing countries? And what is the classic auscultatory
finding for mitral regurgitation?
Rheumatic Heart Disease
A blowing, holosystolic murmur heard best of the cardiac apex that radiates
to the axilla

What is the characteristic blood pressure of a patient with

aortic regurgitation?
Abnormally large (wide) pulse pressure is caused by aortic regurgitation, and
is responsible for many of the symptoms of Aortic Regurgitation

What is the syndromic name given to a condition in which an

accessory AV conduction pathway is used [i.e., the AV node
is bypassed and something else sets heart rhythm]?
Wolff-Parkinson-White syndrome

What is the characteristic triad of abnormalities

corresponding to ventricular pre-excitation [due to WolffParkinson-White syndrome]?
(1) shortened PR-interval
(2) delta wave at the start of the QRS complex
(3) widened QRS interval

What is the classic cardiac auscultation finding in aortic

stenosis?
A Harsh, crescendo-decrescendo systolic ejection murmur heard at the right
sternal border

Where do we hear the class cardiac auscultation finding in

aortic stenosis?
[and what does it sound like]
The right sternal border
harsh, crescendo-decrescendo systolic ejection murmur

What are the 3 main causes of valvular aortic stenosis?

(1) Congenitally abnormal valve with calcification
--e.g., a bicuspid aortic valve
(2) a calcified normal valve
(3) rheumatic heart disease
N.B. rheumatic heart disease is most common cause worldwide, calcific
aortic valve disease is more common in U.S.

A patient has deep venous thrombus and develops a stroke.

What type of embolus is this? Why?
A Paradoxical embolus, because it originated in the venous system but
crossed over into the arterial circulation (bypassing the lungs)

What does a paradoxical embolism usually indicate,

generally speaking?
That there is some abnormal connection between the right and left heart,
allowing the DVT to cross over from the venous system to arterial system
bypassing the lungs.

What classic heart defect would allow a DVT to become a

paradoxical embolus leading to a stroke in a patient?
Atrial Septal Defect

So a patient presents with a stroke after a DVT was

confirmed in his legs. You astutely recognize that since this
is a stroke it must be from a paradoxical embolus, and begin
to think "this gal must have an ASD, a common abnormal
connection between the right heart and left heart that would
let the embolus become paradoxical." Then, you confirm this
on physical exam by hearing what?
Wide splitting of S2 that does not vary with respiration.

What is the cardiac auscultatory finding in atrial septal

defect?
Wide splitting of S2 that does not vary with respiration.

What is the pathophysiology / pathology of tetralogy of

Fallot (ToF)?
PROVe it
(1)
(2)
(3)
(4)

Pulmonary artery stenosis

RVH
Overriding aorta (overrides the VSD)
VSD

How does squatting improve the symptoms in a patient with

Tetralogy of Fallot?

Compresses the femoral arterites, increases total peripheral resistance

thereby decreasing the R --> L shunt and direction more blood from the RV
to the lungs
compression-->resistance-->pressure

Again, how does squatting improve symptoms in Tetralogy

of Fallot patients?
Squatting increases Systemic Vascular Resistance (Total Peripheral
Resistance) and decreases R to L shunting, thereby increasing pulmonary
blood flow.
Squatting thus counteracts arterial desaturation during hypoxemic spells

How does the heart myocardium normally support its own

blood flow in coronary artery disease?
Coronary vessel occlusion can be bypassed by the natural existence and
compensatory recruitment of collateral vessels that help support blood flow
I.e., collateral circulation helps to alleviate ischemia and preserve myocardial
function

What types of drugs could potentially worsen myocardial

ischemia?
Coronary Arteriolar Dilators (e.g., Adenosine and Dipyridamole)

How could coronary arteriolar dilators worsen myocardial

ischemia? What is this phenomenon called?

Collateral microvessels form adjacent pathways for blood flow to areas distal
to an occluded vessel. Adenosine and dipyridamole are selective vasodilators
of coronary vessels that can cause the phenomenon of CORONARY STEAL in
which blood flow in ischemic areas is reduced due to arteriolar vasodilation in
nonischemic areas
I.e., coronary steal can lead to hypoperfusion and worsening of existing
ischemia

In a patient with an isolated diastolic heart failure (due to

smoking, perhaps), what would we expect to see regarding
these three parameters:
(1) LVEDP
(2) LVEDV
(3) LVEF
(1) Increased
(2) Normal
(3) Normal
[Diastolic heart fialure is characterized by a decrease in ventricular diastolic
compliance but normal ventricular contractile performance. As a result,
LVEDP must be increased in order to achieve a normal LVEDV and stroke
volume.]

So what do we think if we hear "heart failure with normal

ejection fraction?"
Some kind of a diastolic heart failure.

[This is a friendly but stern reminder to learn what a JVP

looks like on a graph... FirstAID.]

What is the first peak on a JVP tracing? When is it notably

absent?
The "a wave," which is generated by atrial contraction.
This is notably absent in patients with atrial fibrillation.

What is the classic murmur of aortic stenosis?

Systolic ejection-type, crescendo-decrescendo murmur that starts after the
first heart sound and typically ends before the A2 component of the second
heart sound.

What is the intensity of the Aortic Stenosis murmur

proprotional to?
The magnitude of the left ventricle-to-aorta pressure gradient during systole
[measured via catheter]

What aspect of Tetralogy of Fallot determines the degree of

right-to-left intracardiac shunting and thus hypoxemic
symptom severity?
The Degree of R.V. outflow tract obstruction, i.e., the degree of pulmonic
stenosis
PROVe
Pulmonary Stenosis
RVH
Overriding Aorta
VSD

What is the best, most reliable way to quantify the severity

of aortic regurgitation?
2D and Doppler Echocardiography

What is the classic auscultatory finding of mitral

regurgitation? What is the best physical exam finding
indicator of the severity of mitral regurgitation?
A holosystolic murmur that radiates to the axilla.
The presence of an audible S3;
i.e., the best indicator of a high regurgitant volume indicating severe Mitral
Regurgitation with left ventricular volume overload is the presence of a left
ventricular S3 gallop

What does not correlate well with the severity of Mitral

Regurgitation?
Intensity of a holosytolic murmur that radiates to the axilla; it does not
correlate well with regurgitatnt volume

What is the classic murmur of aortic regurgitation?

Early diastolic, high-pitched and blowing decresendo murmur heard best at
the left sternal border

What physical exam maneuvers help bring about an aortic

regurgitation murmur?

Have the patient lean forward (brings the valve close to the chest wall) and
at end expiration (listening during expiration often accentuates left-sided
heart murmur)

Summarize an Aortic Regurgitation Murmur.

The murmur of AR is a diastolic decrescendo murmur, heard loudest in early
diastole when the pressure gradient between the aorta and the left ventricle
is maximal. The murmur of AR is typically best heard at the left sternal
border with the patient leaning forward and at end expiration.

What is the clinical term for RVH (with or without congestive

right heart failure) caused by pulmonary hypertension?
Cor Pulmonale

In what heart condition do we hear the Ken-Tuck-y murmur?

It's a classic S3, which may be normal in young patients and in well-trained
athletes. In older adults, though, it's typically a sign of left ventricular failure
So will have patients of exertional dyspnea and difficulty sleeping

What do the auscultatory findings of a patient with Left

Ventricular Failure reflect?
The S3 sound of left heart failure is the result of increased left ventricular
end-systolic pressure; i.e., it's not pumping enough blood out of the LV

Given abrupt onset of total myocardial ischemia, how long

does it take to lose cardiomyocyte contractility?
60 seconds.

How long can we tolerate ischemia before it leads to

irreversible heart damage?
30 minutes [due to myocardial stunning]
after 30 minutes of total ischemia, the injury becomes irreversible

What is a major hemodynamic finding indicative of mitral

regurgitation?
Abnormally prominent (regurgitant) left atrial V-wave during catheterization
Left Atrial Pressure increases more than you would think towards the end /
after systole

In a patient with relatively acute aortic regurgitation, what

is the major hemodynamic adaptation that maintains cardiac
output?
An increase in the left ventricular end diastolic volume (LVEDV) in association
with ECCENTRIC left ventricular hypertrophy

In the heart, when do we see eccentric hypertrophy, and

when do we see concentric hypertrophy?

Eccentric: with volume overload (e.g., in chamber dilation de to increased

end diastolic volume
Concentric: pressure overload (e.g., in aortic stenosis or systemic
hypertension)

Generally speaking, what is cardiac tamponade?

Cardiac tamponade is pressure on the heart muscle which occurs when the
pericardial space fills up with fluid faster than the pericardial space can
stretch

What can cause cardiac tamponade?

hypothyroidism, physical trauma, pericarditis, iatrogenic trauma, myocardial
rupture

What is the classic triad (Beck's Triad) of cardiac

tamponade?
(1) hypotension
(2) distended neck veins
(3) distant or muffled heart sounds

Pathologic ventricular hypertrophy is accompanied not only

by morphologic changes, but by chanes in gene transcription
patterns as well. When there is prolonged hemodynamic
overload, there may be abnormal up-regulation or reexpression of fetal proteins fromboth atrial and ventricular
myoctyes. What type of mRNA might ventricular myocytes
express that is typically only expressed in atrial myocytes?

mRNA for natriuretic peptides. The main learning point is in the question
stem here.

How, in a physical sense, do we describe peripheral

resistance in the total body circuit? What about circulation
in an individual organ? What impact does that have on
resistance and calculating resistance?
Total body circulation is best described as a parallel circuit, whereas
circulation in an individual organ is often best described by a series
arrangement
Total body / parallel: 1 / TPR = 1/R1 + 1/R2 + 1/R3....
In an organ: TPR = R1+R2+R3.....

what is the treatment of choice for diabetic ketoacidosis?

Intravenous hydration with normal saline and insulin

How does I.V. hydration with normal saline and insulin help a
person in diabetic ketoacidosis?
decrease in:
serum glucose,
osmolality,
and potassium
Increase in:
serum bicarbonate
sodium

How do we relate blood flow and vessel radius?

Blood flow is directly related to the vessel radius raised to the fourth power.
Resistance to blood flow is inversely proportional to the vessel radius raised
to the fourth power.

What are 3 specific features that distinguish heart

circulation from the blood flow provided to skeletal muscle
and viscera? (this is a pretty vague question so if you don't
get it, just be sure to read the 3 points on the back)
(1) Heart muscle is perfused during diastole and consumes approximately
5% of cardiac output
(2) The myocardial oxygen requirement is very high [heart has a capillary
density far exceeding that of skeletal muscle, and oxygen extraction from
arterial blood is very effective within the heart: resting myocardium extracts
75% to 80% of oxygen from the blood, while myocardium at work extracts up
to 90% of oxygen from the blood]
(3) Coronary flow is regulated by local metabolic factors, including hypoxia
and adenosine accumulation

What organ is associated with max oxygen extraction from

the blood?
the heart

What is more related to the likelihood of a plaque causing

acute coronary syndrome: Plaque Size or Plaque Stability?
Plaque Stability

How to atherosclerotic plaques achieve max stability?

Plaque Stability depends significantly on mechanical strength o the fibrous
cap.

How can macrophages reduce plaque stability?

Inflammatory macrophages in the intima may reduce plaque stability by
secreting METALLOPROTEINASES, which degrade collagen.

Describe the pathogenesis of atherosclerosis.

Pathogenesis of atherosclerosis is thought to begin with endothelial cell
injury
in the response-to-injury model, chronic endothelial cell injury may result
from hypertension, hyperlipidemia, smoking, diabetes, homocysteine, toxins
(alcohol), viruses, and/or immune reactions
Such injury results in endothelial cell dysfunction and/or exposure of
subendothelial collagen
Endothelial cell dysfunction results in increased permeability as well as
monocyte and lymphocyte adhesion and migration into the intima
Endothelial cell denudation (fancy name for exposure of collagen) promotes
platelet adhesion
Growth factors produced by monocytes and platelets stimulate medial
smooth muscle cell migration into and proliferion in the intima
Increased endothelial cell permeability allows LDL cholesterol into the intima,
where it is phagocytosed by the accumulating macrophages and SMCs to
produce FOAM CELLS

Wow, simply put, describe atherosclerosis.

atherosclerosis is initiated by repetitive endothelial cell injury, which leads to

a chronic inflammatory state in the underlying intima of large elastic arteries
as well as large and medium-sized muscular arteries.

What compensatory mechanism can develop in the body to

avoid edema in the context of cor pulmonale (right sided
heart failure due to long standing pulmonary HTN)?
When the central venous pressure (CVP) is increased as in right heart failure,
the interstitial fluid pressure rises due to an increase in net plasma filtration.
As interstitial fluid pressure increases,
compensatory increase in LYMPHATIC DRAINAGE
allows for avoidance of edema.

What cell provides major proliferative stimuli for the cellular

components of atherosclerotic plaques? How / what are
these components?
Platelets release PDGR, which promotes migration of SMC from the media
into the intima and their subsequent proliferation in the intima.

A more concise look than above at the pathogenesis of

atherosclerotic plaques (atheromas) please?
Atherosclerotic plaques (atheromas) develop like this: endothelial cell injury
exposes subendothelial collagen. This promotes platelet adhesion,
aggregation, and release of factos that promte migration of smooth muscle
cells (SMCs) from the media into the intima, as well as SMC proliferation.
2 important factors are PDGF and TGF-beta, both released by platelets.

What causes isolated systolic hypertension in elderly

patients?
decrase in the compliance of the aorta and its proximal major branches

What cell types directly cause intimal changes and damage

in the formation of atherosclerotic plaques?
Smooth Muscle cells
The vascular reaction to endothelial and intimal injury is intimal hyperplasia
and fibrosis, predominantly mediated by reactive smooth muscle cells that
migrate from the media to the intima

What types of defects in hematology, platelet or clotting

factor, are more assocaited with hemarthroses? Which type
is associated with small petechial lesions on the skin?
Hemarthroses: clotting factor defect / coagulopathy
Small Petechial Lesions of the skin: platelet defects

What are teh 2 major effects of Carbon Monoxide (CO) on

oxygen delivery to tissues?
(1) it binds to hemoglobin with an affinity 250x that of Oxygen, reducing the
number of heme binding sites available to oxygen (CO-bound hemoglobin is
called CARBOXYHEMOGLOBIN). By decreasing the fraction of hemoglobin
available for oxygen binding, CO decreases the oxygen content of blood.
(2) CO poisoning causes a leftward shift of the hemoglobin dissociation
curve, reflecting a decreased tendency for oxygen to unload in the tissues

Does Carbon Monoxide affect the PaO2 and does it

precepitate methemoglobinemia?
No and no.
PaO2 remains normal (~95)
Methemoglobin is formed when the Fe2+ (ferrous) in heme is oxidzed to
Fe3+ (ferric iron). Methemoglobinemia results from drug exposures
(dapsone, nitrates) as well as enzyme deficiencies and hemoglobinopathies.

When treating an acute ST-elevation MI or ischemic stroke

with fibrinolytics such as TPA, what may develop? Is it
serious or benign?
Fibrinolytics may cause reperfusion arrhythmia on arterial re-opening, but
these arrhythmias are usually benign.
[Accerlerated idioventricular (AIVR) rhythm is a common reperfusion
arrhythmia]

What are 3 three plasmin-activating, clot-busting drugs?

Streptokinase
tPA
Urokinase

What are 3 fibrin-specific throbolytic/fibrinolytic drugs?

tPA, reteplase, tenecteplase
these act only on fibrin attached to recently formed clot without systemic
activation

What is a nonfibrin-specific fibrinolytic drug?

Streptokinase

How is blood that will be used for transfusion typically

stored? What electrolyte imbalance may develop in a patient
who receives a massive blood transfusion? What symptoms
will that electrolyte imbalance cause?
Prior to storage, whole blood is generally mied with solutions containing
citrate anticoagulant. Packed cells derived from these whole blood collections
also contain citrate
Infused citrate can chelate serum calcium in the receiving person, causing
hypocalcium
The patient may experience paresthesias due to hypocalcemia.

How does our body monitor total body iron?

Total body iron content is regulated through HEPCIDIN's effects on the
absorption of dietary iron
Hepcidin is an acute phase reactant synthesized mainly in the liver by
hepatocytes

Why is chloride much lower in arterial blood than in venous

blood?
Short answer: actions of carbonic anhydrase and chloride shift
Longer answer: Hb is responsible for carrying 15% of our CO2 as carbamate
and the rest of our CO2 is carried as bicarbonate ion within the RBCs.
[CO2 enters RBCs and is converted by carbonic anhydrase to form carbonic
acid and then HCO3- and H+]

Many of the bicarbonate ions diffuse out of the RBC into the plasma; to
maintain electrical neutrality chloride ions diffuse into RBCs to take their
place
This is called CHLORIDE SHIFT

What is the general pattern of airway resistance in the

lungs?
Medium and smalled sized bronchi greater than 2 mm in diameter (the first
10 generations of bronchi) account for the greatest summated frictional
resistance to airflow in normal airways.
The smallest bronchi and bronchioles have a larger total cross-sectional area,
so they don't contribute much to total airway frictional resistance.

What cells characterize the late phase of atopic asthma? (3

types)
eosinophils
basophils
neutrophils

What is the general histology of an eosinophil?

Bilobed nucleus packed with large granules of relatively uniform size and
inclusions seen on EM

What protein do eosinophils release that help them kill

parasites (helminths, e.g.)?

Eosinophils release major basic protein, a potent antihelminthic toxin that's

capable of causing damage to epithelial and endothelial cells (as it does it
atopic asthma)

What drugs are typically NOT used to treat asthma?

Antihistamines

What roles do leukotrienes (from mast cells, eosinophils,

basophils, and other cells that infiltrate bonchilal mucosa in
asthmatics) play in mediating asthma symptoms?
They cause bronchial constriction and hyperreactivity and also promote
mucosal edema and mucus hypersecretion

How do zafirlukast and montelukast offer long-term control

of atopic asthma?
They increase airway caliber and reduce mucosal inflammation by
antagonizing the leukotriene receptors

What is the major protease of extracellular elastin

degradation? What is the major serum inhibitor of this
extracellular elastase?
Neutrophil Elastase (comes from neutrophils and macrophages)
The major serum inhibitor of elastase is Alpha-1 Antitrypsin

What are the 3 most common causes of metabolic alkalosis?

(1) Loss of hydrogen ions from the body: e.g., vomiting and nasogastric
suction may cause loss of hydrochloric acid; this causes serum chloride to
decrease leadign to decrease in urinary cholirde (this would be SALINERESPONSIVE metabolic alkalosis)
(2) Thiazide and Loop Diuretics: cause increase renal losses of Na, followed
by excretion of Cl-; reabsorption of HCO3- increases to maintain electric
neutrality in cells; this is CONTRACTION ALKALOSIS
(3) Increased aldosterone secretion: seen in primary hyperaldosteronism
(Conn Syndrome) and associated with metabolic alkalosis; aldosterone
increases renal Na reabsorption and urinary lossess of K, Cl, and H with
relative increase in HCO3- resulting from H losses; urinary Cl concentration is
increased, but chloride doesn't correct it either (saline-resistant alkalosis)

What's the most important thing to do when doing a workup

of metabolic alkalosis?
Measure the urine chloride and ascertaining the patient's volume status.

How, immunologically speaking, are eosinophils recruited

and activated?
Eosinophils are recruited and activated by IL-5, which is secreted by Th2
helper T-cells

What is an important and easy equation to measure PaCO2?

Basal Metabolic Rate / alveolar ventilation

What is considered to be the main indicator of alveolar

ventilation?

Arterial PaCO2 (inversely related to alveolar hyperventilation)

So what does hypocapnia imply?

Ongoing alveolar hyperventilation

Again, what's a useful equation for PaCO2?

PaCO2 = Basal Metabolic Rate / alveolar hyperventilation

What is the general pathophysiology of centroacinar

emphysema?
Associated with chronic, heavy smoking predominantly involves intraalveolar
release of proteases, especially elastase, from infiltrating neutrophils and
from alveolar macrophages

More specifically, what is the pathophysiology of

centroacinar emphysema?
Oxidative injury to the respiratory bronchioles and activation of resident
macrophages --> neutrophil infiltrate
Neutrophils release NEUTROPHIL ELASTASE, proteinase 3, cathepsin G, and
matrix metalloproteinases, as well as generating OXYGEN-FREE RADICALS
The oxygen free radicals inhibit the antiprotease activity of alpha-1antitrypsin
the resultant net protease-antiprotease imbalance and oxidant-antioxidant
imbalance destroys acinar walls

What's the major factor in the development of centriacinar

emphysema?
excess neutrophil elastase activity

What is the clinical picture consistent with a COPD patient?

COPD encompasses chronic bronchitis and emphysema; heavy smoking is
the most common cause
hallmark of any obstructive PFT profile is DECREASED FEV1/FVC ratio due to
expiratory airflow obstruction
Emphysema also tends to increase TLC and RV

A mom brings in a 6 y.o. child who has had recurrent

sinusitis. You're worried about CF, so you order a "sweat
test" (chloride sweat test), but this comes back normal. You
next order a "nasal transepithelial potential difference" test.
Why would a patient with CF have a significantly more
negative nasoepithelial surface?
Increased luminal SODIUM ABSORPTION.
The CFTR normally SECRETES chloride ions into the lumen and has a tonic
inhibitory effect on the opening of apical sodium channel (which abosrbds
sodium into the cell)
Impaired CFTR functioning directly reduces ductal epithelial chloride
secretion and indirectly increases sodium absorption through lack of CFTR's
inhibitory effect on the apical sodium channel.
The result is dehydrated mucus and a widened, negative transepithelial
potential difference

What are the classic LFT findings in a patient with

emphysema (either a-1-antitrypisin deficiency or
centroacinar)?
FEV1/FVC: decreased (hallmark of obstructive lung disease)
Total Lung Volume: Increased (air can't get out)
Diffusing Capacity: decreased (due to destruction of alveoli and adjoining
capillary beds)

Why would we want to harvest the great saphenous vein?

For use in coronary bypass surgery

Where is the best place to harvest the great saphenous vein

from, surgically?
Just inferolateral to the pubic tubercle

Is the great saphenous vein located on the medial or lateral

side of the foot?
It originates on the medial side of the foot, courses anterior to the medial
malleolus, and then travels up the medial aspect of the leg and thigh. IT
drains into the femoral vein within the region of the femoral triangle, a few
centimeters inferolateral to the pubic tubercle

If you saw elastase in a healthy individual's bronchoalveolar

lavage, what cell did it come from?
Macrophages.

Macrophages and PMNs both make elastase, but this guy is healthy, so why
would he have neutrophils in his lungs? We always have some dust cells in
our lungs, so that's more likely.

Be sure to refer to FirstAid for the histological changes in

the cells lining our airway. Here's a verbal description of the
changes that we see from trachea to alveolus: (answer this
first: What's the last feature to disappear as the epithelium
changes along the respiratory tube?)
Cilia.
Bronchi have a pseudostratified columnar ciliated epithelium with goblet
cells and submucosal mucoserous glands and cartilage
Bronchioles, terminal bronchioles, and respiratory bronchioles lack:
goblet cells, glands, and cartilage
By the level of the terminal bronchioles, the airway epithelium is CILIATED
simple cuboidal.
Epithelial cilia persist up to the end of the respiratory bronchioles

What are lamellar bodies in Type II pneumocytes?

membrane-bound intracellular inclusions composed of stacked layeres of cell
membrane like material
they contain phospholipids (dipalmitoyl phosphatidylcholine..... surfactant.)

What is the major physiological function of surfactant?

to decrease the surface tension of fluid layer lining the alveolar surface

What is the result of insufficient surfactant (as seen in

neonatal respiratory distress syndrome, or maybe a guy who
doesn't have lamellar bodies in his type II pneumocytes)?
patchy atelectasis (collapse) of alveoli due to increased surface tension

Here's a high yield overview of the histology of the lungs:

Alveolar surface is 95% covered by flat Type I pneumocytes
Interspersed cuboidal type II pneumocytes are the source of pulmonary
surfactant (stored in lamellar bodies)
Type II pneumocytes are also the main cell type responsible for replacing the
alveolar epithelium after alveolar injury

What is unique about type II pneumocytes regarding

alveolar injury?
Type II pneumocytes are unique in their ability to proliferate in response to
injury

What are clara cells?

non-ciliated, secretory constituents of the terminal respiratory epithelium
they secrete clara cell secretory protein (CCSP), which INHIBITS NEUTROPHIL
RECRUITMENT and ACTIVATION as well as neutrophil-dependent mucin
production

Describe the pathogenesis and pathophysiology of Paget's

Disease of the Bone.

Disease process starts with marked osteoclastic activation, followed by an

increase in activity of bone forming cells osteoblasts. The net result is
increased bone resorption and also formation of abnormal bone. A new
collagen is laid down in a haphazard manner as compared to the normal,
linear manner. The end product is a
MOSAIC PATTERN
of lamellar bone with irregular sections linked by
CEMENT LINES
which represent previous areas of bone resorption

What are the 4 collagen subtypes, where is each found, and

what are associated diseases with each?
(1) Dermis, bone, tendons, ligaments, dentin, cornea, blood vessels, scar
tissue;
osteogenesis imperfecta
(2) cartilage, vitreous humor, nucleus pulposus
(3) skin, lungs, intestines, blood vessels, bone marrow, lymphatics,
granulation tissue
Ehlers-Danlos Syndrome (types 3 and 4)
(4) basement membranes
Alpart Syndrome

In the final stage of the healing process of myocardial

infarction, what type of collagen is deposited?
Type I

What intercellular connection connects osteocytes?

Gap Junctions
this is so they can send signals to modulate activity of surface osteoblasts,
thereby helping to regulate bony remodeling

What is the t(9;22) Translocation also called? What is its

associated disorder?
Philadelphia Chromosome
bcr-abl gene product
Associated with CML
"Philadelphia CreaML cheese"

What does the t(8;14) translocation cause? What disorder is

it associated with?
c-myc overexpression
Burkitt's Lymphoma

What does the t(14;18) translocation cause? What disorder

is it assocaited with?
bcl-2 activation
Follicular Lymphoma

What disorder does the t(15;17) cause? Why is this special?

M3 type of AML, which is responsive to all-trans retinoic acid.

What disorder is the t(11;33) translocation associated with?

Ewing's Sarcoma
11+22 = 33, Patrick EWING's number

What disorder is the t(11;14) translocation associated with?

Mantle Cell Lymphoma

What cause of mental retardation is associated with t(8,21)?

What disorder is further associated with this?
Down's Syndrome
ALL
"We ALL fall DOWN together."

Epigenetics: Acetylating histones vs. Methylating cytosine

and adenine?
A
cetylating
A
ctivates DNA
M
ethylation
M
utes DNA

What does genomic imprinting refer to?

The phenomenon in which an offspring's genes are expressed in a parentspecific manner
It occurs via an epigenetic process that alters phenotype of an organism
independent of genetic code
DNA methylation: mutes gene expression
is important in imprinting

What is the characteristic histological finding of many forms

of Acute Myelogenous Leukemia?
Auer Rods

Which type of AML is associated with many Auer Rods? What

chromosomal translocation? What's it's "specific"
differentiation / name? What do we treat it with?
M3
t(15;17)
Acute promyelocytic leukemia
all-trans retinoic acid

Which cyclooxygenase is an inducible enzyme that is

normally undetectable in most tissues except during
inflammation?

COX-2

What dermatological layers are apocrine glands found at?

Dermis and subcutaneous fat

What regions of the body have apocrine glands?

The dermis and subcutaneous fat of the:
breast areaolae,
axillae,
genital regions

If you're soaked with sweat, what types of glands are

responsible for the distinctive smell of you?
Apocrine glands
Initially odorless, but can become malodorous secondary to bacterial
decomposition on the skin surface

What are the classic signs of phenylketonuria (PKU)?

Mental retardation, eczema, and a mousy, musty body odor.

If a child pressents with mental retardation, eczema, and a

mousy, musty body odor, what disease are you thinking of?
PKU

How is PKU inherited?

Autosomal Recessive

People with Down Syndrome are at an increased risk to

develop what type of cancer?
ALL (we ALL fall DOWN together)
Also increased risk of AML

What's the term for the tendency of a study population to

affect an outcome due to the knowledge of being studied?
the Hawthorne Effect
i.e., if a doc knows someone is monitoring how often he takes a sexual
history, more likely to take lots of sexual histories

What is Berkson's bias?

Berkson's bias refers to selection bias created by selecting hospitalized
patients as control group

What is the pygmailion effect?

Describes researcher's beliefs in teh efficacy of treatment
this can potentially affect outcome

This is an important one: LEAD TIME BIAS. What is it?

Lead-time bias refers to apparent prolongation of survival after a SCREENING
TEST without any real effect on prognosis

So it's a biostats question and there's a lot of jargon about a

new screening test and patient's surviving longer? What do
you think about?
Lead-Time bias

In terms of vitamin D synthesis, where does sunlight

exposure fall?
It catalyzes the first reaction in the chain of active vitamin D synthesis:
7-dehydrocholesterol --> cholecalciferol (vitamin D3)

So, we should try to get lots of sunlight to catalyze the first

step in vitamin D synthesis, right?
No, excess sunlight exposure shunts previtamin D3 to a pathway that forms
inactive products
this is a mechanism to prevent against excessive Vitamin D

Once activated from 7-dehydrocholesterol to cholecalciferol

by sunlight, how many hydroxylations must Vitamin D3
undergo to become active? Where do each of these occur?

2
the first is in the liver by cytochrome P450 25-hydroxylase [this step is NOT
tightly regulated]
the second is in the kidney, performed by 1-alpha hydroxylase

What is a common clinical picture of Paget's disease of the

bone?
Older gentleman with pain and deformity in a bony area and hearing loss

What is the primary abnormality in Paget's disease of the

bone?
excessive OSTEOCLASTIC bone resorption; osteoclasts in Paget's disease are
typically very large and can have up to 100 nuclei
bone turnover is markedly increased in Paget's disease, culminating in
chaotic bone formation

What cell lineage do osteoclasts come from?

Mononuclear Phagocytic cell lineage (same as macrophages)

What are the 2 most important factors for osteoclastic

differentiation and where do these 2 factors come from?
M-CSF (macrophage colony-stimulating-factor) and RANK-L
these both come from osteoblasts

So what is paget's disease of the bone caused by?

excessive osteoclastic resorption
[childhood infection of osteoclasts by a paramyxovirus may be responsible]

Who has denser bones, black ladies or white ladies?

Statistically, black females have higher bone density than white females

There are 7 important risk factors for osteoporosis....

smoking
menopause
corticosteroid therapy
physical inactivity
caucasian race
low total body weight
alcohol use

What is the RANK receptor/RANK-L interaction essential for?

Formation and Differentiation of osteoclasts.
[2 most important factors for differentiation of osteoclasts: RANK-L and MCSF]

When you hear the term "humoral hypercalcemia of

malignancy" what does it sound like?

elevated serum calcium in the presence of cancer

[so, patient has risk factors for types of cancer, and an elevated calcium,
think this]

What is the cause of humoral hypercalcemia of malignancy?

The hypercalcemia is caused by release of parathyroid hormone-related
peptide (PTHrP)
PTHrP acts like PTH, although the degree of hypercalcemia is generally
higher with PTHrP than with primary hyperparathyroidism

What's the relationship between high/low calcium and

high/low phosphorous?
As a rule of thumb, if calcium levels are high, phosphorous levels are low,
and vice versa

What are the serum calcium and PTH findings in primary

osteoporosis (this is important, so know it)?
Serum calcium and PTH are typically within the normal range.

Again, what are the serum calcium and PTH findings in

primary osteoporosis?
In primary osteoporosis (osteoporosis not caused by a medical disorder),
serum calcium, phosphorous, and PTH levels are typically normal.

When considering disease epidemiology, what is the latent

period?
The time elapsed from initial exposure to clinically apparent disease

What 2 aspects of disease epidemiology can be related to

latent period and how?
(1) disease pathogenesis: exposure and how long it takes for symptoms
(2) exposure to risk modifiers (e.g., anti-oxidants)

What is a 95% confidence interval?

the range of values in which one can be 95% confident that the true mean o
the underlying population falls

How do we calculate "Standard Error of the Mean"

SEM = SD / (square root: n [sample size])

Statistically define incidence:

the number of new cases of a disease per year divided by the total
population at risk

Who is a tricky subset of a population who's NOT at risk to

get a disease, statistically speaking?

people who already have the disease!

population of 40 and 5 people have disease, population at risk is 35

What is a "positive predictive value" because you obviously

don't know...
The PPV reflects the number of true positives divided by the number of
subjects testing positive for a test

How is the positive predictive value related to disease

prevalence?
As the disease prevalence increases, the PPV also increases

Please allow access to your computers microphone to use

Voice Recording.

USMLE WORLD:
If a guy comes in with cervical lymphadenopathy, what do you look for in
terms of planning treatment?
Multiple, small rubbery nodes after a URI? Just watch.
Associated symptoms like fevers, chills, weight loss? Did the nodes grow? Are they
greater than 2cm? Consider biopsy.

Young person comes in with fevers, joint pain, and rash. The rash starts on
the face and spreads down her body. Also posterior lymphadenopathy.
What is it? And why isn't it EBV?
MEASLES.
EBV would involve CERVICAL LAD. Also accompanied by sore throat/pharyngitis.
Rash can occur but usually after administration of ampicillin.

If you intubate someone and there are now decreased breath sounds on
the left, what happened?
TUBE WENT DOWN RIGHT BRONCHUS. No air going to left lung. Wouldn't want to
increase tidal volume since that would worsen oxygenation imbalance.

Play audio for this term

If an old guy comes in with elevated alk phos but nothing else, what's
going on?
Paget's. Metastasis is possible but would see other symptoms like bone pain, lytic
lesions on imaging etc. PSA would be > 4 and you'd see elevated calcium

Hemorrhagic stroke vs. Ischemic stroke vs. Subarachnoid hemorrhage.

First test? How would hemorrhage appear vs ischemia?
Hemorrhagic stroke - symptoms manifest a little more gradually. HTN is the most
important risk factor.
Ischemic stroke - usually more sudden with a history of TIAs, carotid bruits, a-fib.
Subarachnoid hemorrhage - suden dramatic onset headache
First step is a non-contrast CT to distinguish between hemorrhagic or ischemic
stroke.
Hemorrhage = hyperdense (white)
Infarct = hypodense (black)

How do you treat restless leg syndrome?

Dopamine AGONISTS.

What are the signs of acromegaly?

HTN
Increase in finger size
Coarse features

Skin tags
Measure GH levels after glucose load. The PANCREATIC insulin that is released will
suppress GH release since that's converted to IGF-1 and you don't want TOO much
insulin.

HUS?
TTP?
ITP?
Vitamin k deficiency?
vWD?
Hemophilia A? B?
DIC?
HUS - thrombocytopenia, hemolytic anemia, PT/PTT normal
TTP - thrombocytopenia, mental status changes, normal PT/PTT
ITP = normal PT/PTT
Vitamin K deficiency = prolonged PT, normal PTT
vWD = isolated PTT due to carrying of factor 8
Hemophilia A = factor 8 = prolonged PTT
Hemophilia B = factor 9 = elevated PTT
DIC = elevated PT/INR

How would you differentiate aspiration PNA (pneumonia) from PE?

Infiltrates on CXR.

How do you calculate absolute risk reduction? NNT? (number needed to

treat)
Absolute risk reduction = 16-12
NNT = 1/ARR

How do you detect primary hyperparathyroidism? How does it present?

LAB! Isolated hypercalcemia is your only indication.

What's the best test to detect disseminated fungal infection?

Urine antigen.

How do you treat histoplasmosis?

ITRAconazole, not FLUconazole

What's a myasthenia gravis crisis?

Respiratory muscles are weakened so you can't clear infections, mucus, or sputum.
Increasing respiratory distress. Withdraw cholinergic drugs to decrease secretions
and INTUBATE

How do you treat hep C that's asymptomatic and with no LFT

abnormalities?
YOU DON'T! You only initiate antiviral therapy if LFTs are elevated.

How do you treat HOCM? (Hypertrophic Cardiomyopathy) What genetic

inheritance?
B-blockers. Slow rate, allow more time for filling, increased diastolic volume pushes
obstruction away.
Autosomal dominant

What is hereditary spherocytosis? What is a common presentation? How

do you definitively cure? What supplement do you need?
Decrease in spektrin, RBC membrane component. Greater fragility.
Cholecystitis!
Splenectomy.

Folate.

What's a marker for adrenal tumors?

DHEA-S

Intraparenchymal hemorrhagic stroke. How would these present?

-Putamen stroke
-Pontine hemorrhage
-Cerebellar hemorrhage
-Subarachnoid hemorrhage
Putamen = hemiparesis (internal capsule) + hemisensory deficit
Pontine = deep coma/paraplegia
Cerebellar = ataxia, occipital headaches, vomiting. NO HEMIPARESIS.

How do you treat MS ACUTELY? Or a RELAPSE? Progressive?

Acutely = steroids
Relapse = IFN-B
Progression = cyclosporine

What is primary sclerosing cholangitis? How does it appear? What

can it progress to?
Inflammation -> fibrosis -> stricturing/beading of intrahepatic/extrahepatic ducts.
-Onion skin pattern
-ESLD, cholangiocarcinoma

If you have hypovolemic shock, how does cardiac output change?

It decreases. HR jacks up, but SV is still reduced overall.

How do you diagnose ankylosing spondylitis?

All you need is an X-ray. MRI only if results are equivocal.

How do you diagnose polymyositis? How does it present?

Symmetric WEAKNESS. Difficulty getting up and mild pain.
-Elevation of CK
-Diagnose with muscle biopsy
-Treat with steroids, it's an -itis

How does fibromyalgia present? In which group? Do symptoms improve

with exercise? How do you treat?
General MSK pain in women 20-60 and NO SLEEP due to pain.
Excessive tenderness on palpation in 11/18 soft tissue sites.
Symptoms WORSEN with exercise.
Give AMITRIPTYLINE to treat. Also treats diabetic neuropathy.

Polymyalgia rheumatica?
Hip and shoulder pain. women > 50
ESR > 50, it's rheumatic.
Associated with temporal arteritis!

Seronegative spondyloarthropathy? ESR?

Psoriasis
Ankloysing spondylitits
IBD
Reiter's
ESR is NORMAL.
Pain IMPROVES with exercise

Woman with vague chest pain upon eating hot/cold food. Relieved with
nitro.

ESOPHAGEAL SPASM. Nitrates relax coronaries and esophageal myocytes.

How do you differentiate pulmonary edema caused by ARDS vs.

cardiogenic?
ARDS - PWCP < 18
Cardiogenic retrograde congestion - PWCP > 18

How do you test for or diagnose syphilis?

Test with RPR/DRL
Confirm with FTA-ABS
Rash begins in the trunk THEN spreads to palms/soles.
Rocky Mountain Spotted Fever = rash begins in hands/wrists, then spreads to trunk.

If a person has acute imbalance/vertigo and tinnitus, what do you look

for?
Aminoglycosides.
Furosemide can cause ototoxicity as well!

What is the finding triad for Meniere's?

Vertigo
Tinnitus
Hearing loss

What is BPPV? ( Benign Paroxysmal Positional Vertigo)

BPPV = recurrent vertigo brought on by HEAD MOVEMENT

If a person has signs of adrenal insufficiency, what do you want to rule

out? Then what do you do?

TB. Get a CXR + PPD.

Cosyntropin stimulation test.
> If no rise in cortisol, then Addison's.
> If rise in cortisol, r/o Addison's.
> If cortisol is low AND ACTH is low, then there's a problem at the secondary/tertiary
level.

How would you test for Cushing's disease?

Dexa suppression test.
-If you give low-dose dexa, it will suppress cortisol.
-If you give high-dose dexa and ACTH/cortisol drops, then you've suppressed a
pituitary adenoma.
-If you give HD dexa and ACTH/cortisol is still high, then you've got an ectopic ACTH
tumor, most likely small cell lung carcinoma, or an adrenal tumor

If a black guy comes in with painless hematuria, what do you think of?
Sickle cell trait
G6PD deficiency

How do you differentiate bronchiectasis from chronic bronchitis? What is

bronchiectasis? What is acute bronchitis?
Bronchiectasis = chronic PRODUCTIVE cough. Recurrent infections. Inherited form =
CF
Bronchitis = chronic UNPRODUCTIVE cough
Irreversible dilation of the airways due to inflammatory damage, resulting in loss of
elastic tissue. It's like emphysema of the bronchioles.
Acute bronchitis - no smoking history, throat pain + acute cough of yellow sputum
tinged with blood. Consider bronch only if massive hemoptysis. AFEBRILE!! If febrile,
then consider PNA.

What criteria do you use to place a chest tube?

pH < 7.2
Gluc < 60
+ Gram stain/culture

How do you differentiate HCC from colon mets?

AFP, only in HCC (HepatoCellular Carcinoma)

What does a KUB ( kidneys-ureters-bladder radiograph) miss in nephrolithiasis?

URIC ACID stones, small calcium stones (1-3 mm).
Get rid of uric acid stones with KCO3 or K-citrate to alkalize the urine and makethe
uric acid stones more soluble.

How do you diagnose chronic pancreatitis?

FECAL ELASTASE. Amylase and lipase aren't reliable because by this point parts of
the pancreas have become fibrotic.

What med would you avoid giving sildenafil with?

An alpha blocker. Unopposed vasodilation can cause dangerous hypotension.

What would you avoid giving in a cocaine-induced vasospasm?

BETA-BLOCKERS!

How do you treat Lyme disease? In pregnant women?

Doxycycline
Amoxicillin or azithromycin

What drugs can induce esophagitis?

KCl or bisphosphanates


If someone just got stuck with a Hep B needle and wasn't vaccinated,
what do you do?
HBIG and HBV vaccine

How would avascular necrosis present? What causes it?

Progressive hip pain. NORMAL range of motion. NORMAL X-ray results. Really need
an MRI to suspect.
SALT - steroids, alcohol, lupus, trauma

Vitamin C deficiency? Tea and toast diet?

Scurvy - perifollicular hemorrhages + gingival bleeding
Folate deficiency!

What is cauda equina syndrome? What should you think of?

Spinal cord compression that causes urinary/fecal incontinence, perianal anesthesia,
numbness in both extremities. It is ACUTE.
Prostate cancer metastases + epidural abscess
Diagnose with an MRI
Emergent surgery.

How do you treat prolactinomas? What are your cutoffs for surgery?
Prolactin inhibits GnRH which inhibits LH/FSH. Treat with dopamine since DA inhibits
prolactin.
Bromocriptine or CABERGOLINE.
If < 10 mm = medical. Only surgery if refractory to medication

When do you see acalculous cholecystitis?

Burns, trauma, TPN

If someone presents with massive water diarrhea and

hypokalemia/cramps, what should you think of?
VIPoma

How can you avoid calcium stones?

Avoid high-protein diets
Fluids + PO calcium

How do you treat ACD? (Anemia of chronic disease)

Underlying condition. So if RA for example, methotrexate.

In COPD, what are you afraid of with hypoventilation?

Hypoxemia, sure, but also hypercarbia-induced seizures/AMS

What cancer is notorious for going to the brain? What cancers do NOT?
Melanoma
1
2
3
4

prostate cancer
oropharyngeal cancer
skin cancer that is NOT melanoma
esophageal cancer

How should you adjust antibiotic treatment for aspiration PNA?

(pneumonia)
Clindamycin. Good gram - and anaerobe coverage

Where does glioblastoma multiforme manifest? Where do metastatic

tumors usually go?

GBM = frontal
Metastatic tumors = watershed zones or gray/white junctions

Pulsus paradoxus?
PTX, tamponade, asthma.

How often do you get colonoscopy if you have UC?

8 years after diagnosis, every year or two after that.

How do you treat essential tremor?

How do you treat early Parkinson's resting tremor?
Essential tremor = propranolol
Resting tremor Parkinson's = trihexyphenidyl

What skin lesions does blasto and coccidio present with?

Verrucous skin lesions that become crusted/warty/violet.
Coccidioides = erythema multiforme/nodosum

How do you treat mucormycosis?

Debride + IV amphotericin

What is pseudotomor cerebri?

-What makes it worse?
-In who?
-LP?
-Diagnosis of?
Idiopathic intracranial hypertension
-Headaches especially upon movement of the head
-Papilledema (risk of blindness)

-Usually young obese women

Causes of septic arthritis?

Staph then strep.
Gonococcus in a sexually active young'n.

CN III - ischemia vs. compression?

Ischemia = down and out
Compression = down and out + dilated fixed pupil, not reactive to light or
accommodation

How do you treat RA? (rheumatoid arthritis)

1. NSAID's at first
2. MTX once diagnosis is confirmed
3. Etanercept/infliximab (INF-inhibitors) only if refractory to MTX
Avoid steroids

First-line agents for HTN with no co-morbidities? With CKD or DM?

None - thiazide
CKD/DM - ACE-I's/ARB's

How do you differentiate chronic bronchitis from emphysema?

Chronic bronchitis - normal DLCo
Emphysema - low DLCo

What's a bad side effect of protease inhibitors in HIV treatment?

Crystalline nephropathy

If you have solid/liquid dysphagia, what is it?

If you have solid dysphagia THEN liquid dysphagia, what is it?
Solid/liquid = motility disorder (achalasia, esophageal spasm)
Solid then liquid = obstruction
Esophagram then endoscopy.

What affects HOCM and MVP murmurs?

Squatting = increased preload = reduction in murmur
Valsalva = decreased preload = increase in murmur

Respiratory distress a while AFTER sepsis/trauma?

PEEP
Tidal volume/RR
FiO2
ARDS
-Increase PEEP for suspected ARDS
-Tidal volume/RR for PCO2 control
-FiO2 increase at first but reduce after stabilization to avoid oxygen radical damage

How do you treat familial adenomatous polyposis?

Prophylactic proctocolectomy

Small cell vs. NSCLC? (not small cell lung cancer)

Small cell - all the acronyms = SIADH + ACTH + LE syndrome
NSCLC - PTHrP

-Spinal stenosis?
-What are two ways to differentiate neurogenic claudication vs. PVD
claudication?

Osteoarthritic degenerative changes of spinal canal -> narrowing -> neurogenic

claudication. Improved only on sittng or flexing spine.
Neurogenic claudication - pain on walking AND standing
PVD - pain only on walking + absent peripheral pulses

Herniated disc?
Hurts MORE with sitting
Radiculopathy
Straight leg test raise

Indications for dialysis?

Pericarditis
Uremia induced coagulopathy or encephalopathy
Hyperkalemia
Acidosis
Edema refractory to diuretics

How do you treat Reiter's?

NSAIDs

What histologic feature of A1AT? What's crazy about it?

A1AT can progress DIRECTLY to fulminant hepatic failure without any intervening
stage! PAS+ hepatocytes

Sarcoiditis is associated with uveitis.

What can you treat ALS with?

Riluzole - glutamate blocker

How do you differentiate v-tach/v-fib from a-fib?

A-fib DOES have QRS waves
V-fib - just squigglies everywhere
V-tach = QRS waves with no p-waves in between

How does hyperparathyroidism-hypercalcemia manifest if severe?

Moans, bones, stones, and psych overtones.
-Nephrolithiasis
-Bone pain
-Mood swings/depression

How would CHF cause low sodium urine?

Hypoperfusion to kidneys causes activation of RAAS which reclaims sodium from
urine.

Albumin and calcium?

If low albumin due to nephrotic syndrome, then overall calcium drops. But this is not
the TRUE degree of ACTIVE calcium in the body.
4-albumin * 0.8 = actual calcium

Stroke non-contrast CT to r/o hemorrhagic fibrinolytics if within 4.5

hours, ASA if longer

What can an aortic dissection cause?

Pericardium = tamponade
Carotids = ischemic stroke
Coronaries = MI


Person has recurrent oral/genital lesions similar to HSV but also erythema
nodosum over shins?
Behcet's vasculitis

What are indications for carotid endarterectomy?

If 70-99% occlusion = surgery
If 50-70% occlusion and with SX = surgery
If no sx and <50%, no surgery. Medication with ASA + statins

HIV patients
-Bright red, exophytic lesions?
-Brown/pink/violet plaques?
Bacillary angiomatosis 2/2 bartonella
Kaposi's

What electrolyte abnormality is associated with subarachnoid

hemorrhage?
Hyponatremia - inappropriate SIADH secretion after bleed

If a patient with uncomplicated pyelonephritis is on IV ceftriaxone and

improving, what do you do?
Switch to PO bactrim and d/c.

How do you treat v-tach medically?

Amiodarone or lidocaine.

Why don't you wait for cultures before starting ABx (antibiotics) in
neutropenic fevers?
Most of the infectious organisms are endogenous flora!


When do you use plavix?
Anyone with UA/NSTEMI (6 months, ASA indefinitely) or for 1 month after stent.

Bitemporal hemianopsia + hypopituitarism?

Pituitary adenoma, also a craniopharyngioma. Can see it in older people.

How do you treat Bartonella? How does it manifest?

Tender LAD. Give -mycins.

What's a side effect of acyclovir?

Renal tubular damage.

In a Marfanoid patient and a murmur, what's going on?

Aortic dissection --> aortic regurgitation

Why would a patient develop hypotension after pancreatitis?

Erosion into adjacent blood vessels causes massive retroperitoneal bleed - GreyTurner + Cullen's sign

If a male has evidence of a compression fracture, what happened?

Demineralization of vertebral body due to osteomalacia or osteoporosis.

How do you calculate ATTRIBUTABLE risk?

(aka how likely is it that this disease was caused by this risk factor) vs. relative risk
(if you have this risk factor, how likely is it you will develop this disease)
How do you calculate ABSOLUTE RATE REDUCTION? What can you derive
from that?

ARP = (1-RR)/RR
ARR = higher - lower
NNT = 1/ARR

* (ARP = attributable risk percent)

* ARR = attributable relative risk)
* NNT = number needed to treat)

What happens when you have a patient with GI complaints, periorbital

edema, and myositis?
Trichinellosis. Undercooked pork. Roundworm.

If a patient has evidence of nephrotic syndrome AND restrictive

cardiomyopathy, what should you think of?
Amyloid.

How do you treat hyperthyroidism?

Propranolol.
Radioactive iodine.
PTU/methimazole if pregnant or until you can do iodine treatment.
Surgery if refractory, definitive treatment.

Talk about Hep E

Fecal-oral. Endemic areas. NO VACCINE.
Vertical transmission.
No hepatitis, cirrhosis, or HCC, can progress directly to fulminant hepatitis.

What test should you order before giving sumatriptan?

Pregnancy test.

What's the most common cause of mitral regurgitation?

Mitral valve prolapse, NOT rheumatic disease, as that causes mitral stenosis. Both
predispose to a-fib though.

How do treat uremic coagulopathy?

NOT with platelets!!! Give DDAVP! If you give platelets, they won't work.

When do you use LASIX in an MI? What DON'T you use?

If flash pulmonary edema.
Beta-blockers!

What lab values should you check before giving metformin?

BUN/Cr. Can cause lactic acidosis and need to make sure kidneys can handle it.

What signs will you see in subacromial bursitis? What would you see in a
biceps tear? What would you see in axillary nerve compression?
Pain upon internal rotation/flexion.
Bulge in the arm, pain upon flexion.
Paralysis + atrophy of deltoid muscles.

How does HIV present acutely?

Lymphadenopathy + fever + malaise + GI sx + arthralgias

If you see a lymph node and biopsy shows SCC mets, what do you do?
Panendoscopy. Look for primary source, it's most likely upper body.

If someone drops with no pulse, what do you do?

DEFIBRILLATE. You don't know what rhythm caused it! V-fib/V-tach most likely.

What are anal warts called? What do you treat with? What causes them?
Condyloma acuminata. HPV. Dapsone.

If someone has temporal arteritis and then develops symptoms of

poylmyalgia rheumatica but WITHOUT AN ELEVATED ESR, what happened?
Steroid-induced myopathy.

Porcelain gall bladder picture.

Gallbladder carcinoma.

Nephrotic syndrome causes...

Proteinuria + hypocalcemia + hypercoagulable + ATHEROSCLEROSIS + infection

CNS lymphoma?
Periventricular.
Weakly enhancing.
EBV in CSF.

Post-MI complications?
Papillary muscle rupture --> mitral regurg
Free wall rupture --> tamponade
Septal rupture --> pansystolic murmur + thrill at LSB