A 45-year-old man presents to the emergency department complaining of chest

pain, which began twenty minutes before while he was filling

up his car with gasoline. He describes the pain as substernaI, intense, dulI, and
squeezing. It does not change with respiration. He also
complains that he is nauseated. He has never experienced anything like this
before. His temperature is 37.5 C (99.5 F), blood pressure is
124/76 mm Hg, pulse is 80/min, respiratory rate is 22/min, and oxygen saturation
is 95% on room air. On physical examination, he is
diaphoretic. His lungs are clear, his heart rate is regular, and he has a normaI S1
and S2 without murmur, rub, or gallop. The examiner
estimates that his jugular venous pressure is elevated to the angle of the jaw. His
abdomen is nontender, with normal bowel sounds. An
electrocardiogram is performed, which reveals sinus rhythm, normal axis, normal
intervals, and ST elevation in leads lI, III, and aVF. A chest x-
ray film reveals no apparent cardiac or pulmonary abnormalities.
Question 1 of 7

Which of the following is the most likely diagnosis?

/A. Acute myocardial infarction
/B. Aortic dissection
/C. Gastroesophageal reflux
/D. Pericarditis
/E. Pulmonary embolus

Explanation - Q: 1.1 Close

The correct answer is A. The differential diagnosis of chest pain is broad

and includes all the answers on this list, all of which can present, as in this
patient, with a relatively normal examination of the heart and lungs. Acute
myocardial infarction is the only one of these findings that is associated with
ST segment elevation in an anatomical distribution (in this case, the "inferior"
leads). His elevated jugular venous pressure is also a clue to abnormal
cardiac function; however, this might be present in severe constrictive
pericarditis or pulmonary embolism as well.

Aortic dissection (choice B) often presents with chest pain or pain radiating
to the back. It is not, however, typically associated with ST segment changes
on the EKG, unless the dissection extends proximally into the ostia of the
coronary arteries, obstructing flow, and resulting in secondary acute
myocardial infarction, in which case a patient could present like this.
However, this presentation would be an uncommon presentation of a
relatively uncommon disease. The risk for aortic dissection is increased with
long-standing essential hypertension, other peripheral vascular disease,
hyperlipidemia, and advanced age, as well as connective tissue disorders
such as Marfan syndrome or Ehlers-Danlos syndrome.
 Patients with gastroesophageal reflux (choice C) may complain of intense
substernal chest pain that is difficult to distinguish from the pain of myocardial
infarction. However, the ST elevations on the EKG suggest transmural
ischemia of the myocardium and do not occur with isolated gastroesophageal
reflux. Do not let relatively normal vital signs and gastrointestinal symptoms
such as nausea fool you!

Pericarditis (choice D), an inflammatory disease of the pericardium, presents

with chest pain and is often associated with ST elevation on the EKG, as well
as PR interval depression. However, the ST elevation usually involves
multiple leads of the EKG, and is not in a strictly anatomic distribution.
Pericarditis is often associated with a friction rub.

Pulmonary thromboembolism (choice E) can also present with chest pain. A

patient who has had a large PE, however, typically will not have normal vital
signs, and is likely to have tachycardia, tachypnea, and possibly hypoxemia.
Hemodynamically significant pulmonary embolism can present with elevated
JVP due to right heart strain. The patient might have ST depression in the
inferior leads, but will not have ST elevation. The pain associated with
pulmonary embolus is generally pleuritic in nature, that is, lateralizing, and
changing with inspiration. Risk factors for pulmonary embolism include
hypercoagulable states, immobilization, and vascular injury (Virchow's triad).
Question 2 of 7
What is the pathophysiologic process most likely to be responsible for this
patient's presentation?
/A. Atherosclerotic plaque rupture resulting in thrombus formation
/B. Buildup of atherosclerotic stenosis to produce high-grade obstruction of the
artery
/C. Dissection of the vessel
/D. Embolization of blood clot, air, or foreign material
/E. Myocardial hypertrophy resulting in vessel narrowing
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Explanation - Q: 1.2 Close

The correct answer is A. Acute coronary syndromes are thought to be the

result of rupture of a pre-existing atherosclerotic plaque, often one that is not
producing high-grade stenosis. When the endothelial surface covering the
lipid core of an unstable plaque ruptures, a platelet plug forms and the clotting
cascade is activated, rapidly propagating thrombus formation and suddenly
occluding the vessel. This results in transmural ischemia, which becomes
infarction, should the clot fail to recanalize quickly.

Atherosclerotic stenosis (choice B) is an important pathologic component of

coronary artery disease. However, high-grade coronary stenoses most
frequently cause stable angina, that is, chest pain and myocardial ischemia
 induced when an increase in myocardial oxygen demand exceeds the fixed
supply that can be obtained through a severely stenotic vessel. As vessels
progressively narrow over time, they produce ischemia, but not sudden
infarction. Often distal to a narrowed vessel, collaterals will form from less
diseased vessels, compensating for the reduced flow.

Coronary artery dissection (choice C) is a rare phenomenon that can

produce transmural ischemia and infarction, but most commonly occurs in the
setting of instrumentation of the vessel.

Embolization (choice D) is a relatively rare phenomenon in the coronary

circulation under normal circumstances. Foreign material can only enter the
left side of the heart via right-to-left intracardiac shunt, pulmonary vein
interruption, or surgical opening of the left heart. Thrombus that forms in the
left atrium (usually the result of low-flow states such as mitral stenosis or
atrial fibrillation) can also embolize; patients with atrial fibrillation are
anticoagulated to reduce the risk of cerebral embolization of left atrial clot.

Myocardial hypertrophy (choice E) can restrict subendocardial oxygen supply

by creating high capillary pressure relative to arteriolar pressure. This does
not occur in large coronary vessels, but can produce subendocardial
ischemia in disease states that are associated with hypertrophic myocardium,
such as aortic stenosis, long-standing essential hypertension, and idiopathic
hypertrophic subaortic stenosis (IHSS).
Question 3 of 7
Which of the following vessels is most likely to be diseased in this patient?
/A. Coronary sinus
/B. Left anterior descending coronary artery
/C. Left circumflex coronary artery
/D. Left main coronary artery
/E. Right coronary artery
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Explanation - Q: 1.3 Close

The correct answer is E. Acute myocardial infarction is usually due to

obstruction of one coronary vessel. The right coronary artery exits the right
sinus of Valsalva of the aorta and gives off branches to the right ventricle, the
SA nodal artery (in 70% of patients), the AV nodal artery, and, in the 85% of
patients whose circulations are said to be "right-dominant," the posterior
descending artery, which supplies the inferior wall of the RV and the LV as
well as the posterior 1/3 of the interventricular septum. This patient has EKG
signs of an inferior myocardial infarction, with ST elevation in the inferior
leads, II, III, and aVF. He also has a physical sign of right ventricular
dysfunction (elevated jugular venous pressure).
 The coronary sinus (choice A) is the principal vein draining the left ventricle
and runs alongside the circumflex artery in the posterior AV groove. It is not a
common site for atherosclerotic disease or for obstruction.

The left anterior descending artery (choice B) supplies the anterior and
anteroseptal portions of the left ventricle. Obstruction would produce ST
elevation in the anterior (V2-V6) and occasionally the lateral (I, aVF) leads of
the EKG, with possible "reciprocal" ST depression in the inferior leads.

The left circumflex artery (choice C) supplies the lateral wall of the left
ventricle. 85% of patients have a "right-dominant" coronary anatomy. That is,
the right coronary artery gives off the posterior descending artery (PDA). In
the "left-dominant" remaining 15%, the PDA comes off the circumflex. Isolated
inferior EKG lead changes are, therefore, most likely to be due to RCA
obstruction; circumflex obstruction typically produces EKG lead changes in
the lateral (I, aVL, V5, V6) leads.

The left main coronary artery (choice D) exits the aorta at the left sinus of
Valsalva and divides into the left anterior descending and left circumflex
arteries. Obstruction of the left main makes the entire left ventricle ischemic,
often resulting in cardiogenic shock. This would produce ST segment
elevation in leads I, aVL, and V2-V6.

Question 4 of 7

This patient is given aspirin in the emergency department. Decreased production

of which of the following mediators is responsible for the
beneficial effects of aspirin in this disorder?
/A. cAMP
/B. PIatelet glycoprotein lIB/IIIA
/C. Prostacyclin
/D. Thromboxane A2
/E. Ubiquinone (coenzyme Q)

Explanation - Q: 1.4 Close

The correct answer is D. Aspirin irreversibly inhibits the enzyme

cyclooxygenase, which produces all the prostaglandin mediators from
arachidonic acid. Cyclooxygenase in platelets produces thromboxane A2,
which is a potent promoter of platelet aggregation and vasoconstriction. By
blocking this, aspirin irreversibly inhibits platelet function, preventing
aggregation at the site of plaque rupture. Platelets, having no nuclei, are
unable to synthesize more cyclooxygenase, and therefore thromboxane
production is inhibited for the life of the platelet, approximately 10 days.
 Cyclic AMP (choice A) is an intracellular small molecule responsible for
multiple signal transduction pathways. In cardiac myocytes, it activates
protein kinases responsible for the phosphorylation of calcium channels,
promoting entry of calcium into the cell. cAMP is broken down by
phosphodiesterase, the inhibition of which is responsible for the beneficial
effects of inotropic phosphodiesterase inhibitors such as milrinone.

Platelet surface glycoprotein IIb/IIIA (choice B) binds fibrinogen and von

Willebrand factor, promoting aggregation and clot formation. It is inhibited by
drugs like eptifibatide and tirofiban, which are used in acute coronary
syndromes to further inhibit platelet aggregation and thrombus formation.

Prostacyclin (choice C) is produced by cyclooxygenase in endothelial cells,

where it promotes vasodilation and inhibits platelet aggregation. Prostacyclin
should therefore be a beneficial mediator. Aspirin inhibits prostacyclin
formation, however, endothelial cells can produce more cyclooxygenase and
are able to continue to synthesize adequate amounts of prostacyclin.

Ubiquinone (choice E), or coenzyme Q, is a naturally occurring coenzyme

that plays a vital role in the mitochondrial electron transport chain. Studies
have shown an association between decreased levels of coenzyme Q and
heart disease, so inhibition of ubiquinone production would not likely be
beneficial.

Question 5 of 7
EIevation of which of the following serum proteins is the most specific
biochemical marker for this patient's condition?
/A. AIanine aminotransferase
/B. Creatine phosphokinase
/C. Lactate dehydrogenase
/D. Transferrin
/E. Troponin
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Explanation - Q: 1.5 Close

The correct answer is E. Troponins (in isoforms troponin C, troponin I, and

troponin T) are required for actin-myosin cross linking in cardiac muscle.
Small elevations in serum troponin levels are currently the most sensitive
clinical serum markers for myocardial injury, elevating within 3-12 hours of
infarction. Levels remain elevated for 5-14 days.

Alanine aminotransferase (choice A) occurs in both cardiac muscle and in

the liver, and has been used in the past as a marker of cardiac injury.
However, currently, its more common clinical use is as a marker of
hepatocyte injury. Its time course of elevation in MI is intermediate between
 CPK and LDH (see below).

Creatine phosphokinase (choice B) has been the mainstay of diagnosis of

myocardial injury for many years. CPK has several isoforms, of which the MB
isoform is specific for cardiac muscle. The fraction of the total CPK that is the
MB isoform has been used to differentiate myocardial injury from other injury
processes elevating CPK. CPK is also elevated with skeletal muscle and with
brain injury, but neither of these tissues contains significant amounts of MB
isoform. In MI, CPK levels usually rise within 8 to 24 hours and return to
normal after 48 to 72 hours.

Lactate dehydrogenase (choice C) is, like alanine aminotransferase, an

enzyme that is released both with cardiac injury and with hepatocellular injury.
It can also be elevated in hemolysis and with some neoplasms. In MI, it
generally rises within 12 hours and peaks after 24-48 hours, remaining
elevated for 10-14 days. These properties made LDH, prior to the introduction
of troponin assays, the test used to detect MI occurring more than a day
previously.

Transferrin (choice D) is a plasma protein responsible for the uptake of iron

after absorption in the small intestine, and is responsible for iron-binding
capacity in the blood. It is measured (usually as "total iron-binding capacity")
in the differential diagnosis of the anemias.
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Question 6 of 7
Three days after hospital admission, the patient suddenly develops shortness of
breath and becomes hypotensive. His heart rate is 100/min,
with a normaI PR and QRS intervaI. His blood pressure is 75/50 mm Hg. His
respiratory rate is 38/min and his oxygen saturation on 2 Iiters
via nasal cannula drops to 60%. A chest x-ray reveals bilateral fluffy infiltrates in
the lung fields. Which of the following complications of his
condition has most likely occurred?
/A. Dilation of the left ventricle
/B. Dressler syndrome
/C. Rupture of the left ventricular free wall
/D. Rupture of the posteromedial papillary muscle
/E. Ventricular tachycardia

Explanation - Q: 1.6 Close

The correct answer is D. This patient is suddenly in cardiogenic shock with

severe pulmonary edema. This could be the result of arrhythmia, cardiac
tamponade, or left ventricular valvular dysfunction. He had an inferior MI,
which is most likely due to thrombosis of the right coronary artery. The
posteromedial papillary muscle is supplied by the RCA alone in most patients
 and is prone to rupture in inferoposterior MI. Rupture leads to acute and
severe mitral valve dysfunction, resulting in pulmonary edema and poor
forward ejection.

Dilation of the left ventricle (choice A) typically occurs after extensive

damage occurs, which would have appeared on this patient's acute EKG as
ST elevation in the anterior leads. Dilation can result in mitral regurgitation,
but typically of an insidious onset.

Dressler syndrome (choice B) is a late complication of MI that may occur

weeks to months later, characterized by symptoms of pericarditis including
pleuritic chest pain, fever, friction rub, and elevated white blood cell count.
Patients can also develop early postinfarction pericarditis in the days to
weeks following MI with friction rub and pericardial effusion. This is seldom
associated with cardiac tamponade.

Rupture of the LV free wall (choice C) is a complication more likely to occur

with more extensive damage to the LV than is produced in an inferior MI such
as this patient had. However, LV free wall rupture would produce cardiac
tamponade, which could produce this clinical picture.

Ventricular tachycardia (VT) (choice E) is a complication of MI (though risk is

highest early in the course of infarction) and could also produce this clinical
picture. However, it is excluded by the EKG, which reveals an atrial-
ventricular conducted rhythm (VT displays no P waves) and a narrow-
complex QRS (VT typically has a QRS much greater than 0.12 s).
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Question 7 of 7
The patient is taken emergently to the operating room. During surgery, a sample
of affected myocardial tissue is sent to the pathology
Iaboratory for examination. Which of the following would be the likely pathologic
finding(s)?
/A. Acellular fibrosis
/B. Monocyte infiltration, absent nuclei and striations
/C. Myocyte disarray
/D. Myocyte edema, hemorrhage, and dense neutrophil infiltration
/E. Wavy myofibers with eosinophilic contraction bands

Explanation - Q: 1.7 Close

The correct answer is B. Three days after infarction, coagulation necrosis is

complete, with complete loss of cellular structure (hence the high risk of
mechanical complications such as rupture) and infiltration of monocytes to
phagocytize debris.

Acellular fibrosis (choice A) replaces necrosis after many weeks when debris
 is removed and fibroblasts have invaded the dead tissue and replaced it with
collagen.

Myocyte disarray (choice C) is associated with hypertrophic subaortic

stenosis (IHSS), rather than myocardial infarction.

Myocyte edema, with hemorrhage and neutrophil infiltration (choice D)

occurs within 4-12 hours after infarction.

Wavy myofibers and contraction bands (choice E) are the first light
microscopic pathologic changes to occur after MI, and appear within 1-3
hours after infarction.

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A 52-year-old man presents to the emergency department because of severe
chest pain. The excruciating pain began abruptly, 30 minutes
previously, and feels to the patient as if something were "ripping." When asked to
point to where the pain is worst, the patient points to the
precordium. The man additionally reports that the pain seems to be changing in
position slowly.
Question 1 of 6
Which of the following is most likely causing the patient's severe pain?
/A. Aortic dissection
/B. Atherosclerotic aortic aneurysm
/C. Esophageal reflux
/D. Myocardial infarction
/E. Peptic ulcer

Explanation - Q: 2.1 Close

The correct answer is A. This patient has a classic presentation of aortic

dissection. Any time a patient in excruciating chest pain describes the pain as
"tearing" or "ripping," you should strongly consider the diagnosis of aortic
dissection. The pain may move with time as the dissection progresses. Aortic
dissection is a highly lethal condition that may lead to aortic rupture, most
often into the pericardial cavity or left pleural space. The two most common
sites of origin of the dissection are in the proximal aorta within 5 cm of the
aortic valve and in the descending thoracic aorta just distal to the origin of the
left subclavian artery. CT scan with contrast is often used to confirm the
diagnosis suspected clinically. Therapy is promptly initiated with medications
that lower the blood pressure to try to prevent extension of the dissection.
Surgery is usually then performed in patients in which the dissection begins in
the proximal aorta near the aortic root; medical therapy alone can sometimes
be used for those with distal aortic dissection that has not compromised blood
 flow to limbs or organs.

Atherosclerotic aortic aneurysm (choice B) more commonly involves the

abdominal aorta, and, when rupturing, may produce excruciating pain that is
usually referred to the lower abdomen and back.

The pain of esophageal reflux (choice C) is rarely excruciating, and usually

does not produce a ripping or tearing sensation.

Myocardial infarction (choice D) can produce severe precordial chest pain,

but the pain usually does not move with time and does not have a tearing or
ripping character.

Peptic ulcer pain (choice E) may be severe and referred to the chest, but
patients are more likely to use terms like "burning" than ripping or tearing, and
the pain does not slowly change position.
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Question 2 of 6
Extension of this patient's disease process would be most likely to produce which
of the following?
/A. Aortic insufficiency
/B. Aortic stenosis
/C. Mitral insufficiency
/D. Mitral stenosis
/E. Tricuspid stenosis

Explanation - Q: 2.2 Close

The correct answer is A. Dissecting aneurysms tend to start near the root of
the aorta, and aortic insufficiency is a common complication. This can be very
helpful in the initial evaluation of the patient, since up to 2/3 of the patients
with proximal aortic dissection demonstrate, on auscultation, the
characteristic murmur of aortic insufficiency, which is a pandiastolic
decrescendo murmur that is loudest over the sternum and left lower sternal
border. Aortic stenosis (choice B) usually does not occur.

Involvement of the mitral (choices C and D) and tricuspid valves (choice E)

would be very rare, and probably only seen if the aortic dissection interrupted
the orifices of the coronary arteries and induced a secondary myocardial
infarction.

Question 3 of 6
If enzyme chemistries were sent, which would be the most likely results?
/A. Decreased AST, elevated CK, decreased LDH
/B. EIevated AST, elevated CK, normal to decreased LDH
/C. EIevated AST, normaI CK, normaI LDH
/D. NormaI AST, elevated CK, elevated LDH
/E. NormaI AST, normaI CK, normal to elevated LDH
Explanation - Q: 2.3 Close

The correct answer is E. Unless aortic dissection secondarily causes a

myocardial infarction secondary to occlusion of the coronary arteries,
aspartate aminotransferase (AST) and creatine kinase (CK) levels should be
normal. Lactic dehydrogenase (LDH) levels may be normal, or elevated if
some hemolysis is occurring within the area of dissection.

In general, AST can be elevated (choices B and C) in a variety of cardiac

diseases (e.g., myocardial infarction, heart failure, myocarditis, pericarditis),
muscle damage (e.g., myositis, muscular dystrophy, trauma), and damage to
liver, pancreas, kidney, or brain. AST is decreased (choice A) in pyridoxine
(vitamin B6) deficiency and in the terminal stages of liver disease. In general,
CK can be elevated (choices A, B, and D) in disease or damage involving
heart, muscle, or brain. Decreased CK has no medical significance. Lactic
dehydrogenase (LDH) can be elevated (choice D) in myocardial infarction,
pulmonary infarct, hemolytic and pernicious anemia, hematologic
malignancies, and disease of liver, kidney, or brain. Decreases in LDH
(choices A and B) are not medically significant.

Question 4 of 6
If surgery is necessary to repair this problem, the surgeon will be required to
understand the anatomic relationship of the aorta to the
surrounding structures. Which of the following most accurately describes the
descending portion of the thoracic aorta?
/A. It descends on the right side of the thoracic vertebrae
/B. It flattens the posterior aspect of the trachea
/C. It is to the left of the esophagus at the hiatus
/D. It is to the left of the thoracic duct at the T10 Ievel
/E. It is to the right of the inferior vena cava

Explanation - Q: 2.4 Close

The correct answer is D. The thoracic duct is the main lymphatic duct and it
lies on the bodies of the inferior seven thoracic vertebrae. It conveys most of
the lymph of the body to the venous system. It passes superiorly from the
cisterna chyli (the expanded inferior end of the thoracic duct) through the
aortic hiatus in the diaphragm. The thoracic duct ascends in the posterior
mediastinum, on the right of the thoracic aorta and to the left of the azygos
vein. At the level of T4, T5, or T6, the thoracic duct crosses to the left,
 posterior to the esophagus and ascends to the superior mediastinum. The
thoracic duct empties into the venous system near the union of the left
internal jugular and subclavian veins.

As a continuation of the aortic arch, the descending aorta begins on the left
side of the inferior border of the body of the T4 vertebra and descends in the
posterior mediastinum on the left sides of T5 to T12 (choice A).

The trachea travels in the superior mediastinum and does not have direct
contact with the descending thoracic aorta. The trachea is kept patent by a
series of C-shaped tracheal cartilages. The posterior aspect is flat where it is
applied to the esophagus, not the aorta (choice B).

At the level of the esophageal hiatus (choice C), the esophagus lies anterior
to the descending thoracic aorta.

The inferior vena cava (choice E) is located to the right of the abdominal
aorta, not the thoracic aorta. The IVC returns blood from the lower limbs,
most of the abdominal wall, and the abdominopelvic viscera. This vessel
begins anterior to L5 vertebra by union of the common iliac veins. It then
ascends on the right psoas major muscle to the right of the median plane and
aorta. It passes through the vena caval foramen in the diaphragm at the level
of T8 to enter the right atrium.

Question 5 of 6
Which of the following would be most likely to be seen on pathological
examination of a specimen removed from this patient at surgery?
/A. Bacterial vegetations
/B. Cystic medial degeneration
/C. Multiple small granulomas
/D. Parasitic organisms
/E. Polyarteritis nodosa

Explanation - Q: 2.5 Close

The correct answer is B. Cystic medial degeneration is a disruption and

fragmentation of the elastic tissue in aortic media, with formation of areas
devoid of elastin. These changes weaken the aortic wall, predispose for
dissection, and are seen in the majority of cases of aortic dissection.

Bacterial vegetations (choice A) are a feature of endocarditis.

Multiple small granulomas (choice C) can be seen in temporal arteritis and

Takayasu arteritis.

Parasitic organisms (choice D) do not usually affect the aorta; the organisms
 of trichinosis and Chagas disease can affect the heart.

Polyarteritis nodosa (choice E) is a focal inflammation that usually involves

smaller blood vessels than the aorta.
Question 6 of 6
Which of the following conditions has been associated with this patient's
disease?
/A. Cushing syndrome
/B. Dandy-Walker syndrome
/C. Kawasaki syndrome
/D. Marfan syndrome
/E. Tourette syndrome

Explanation - Q: 2.6 Close

The correct answer is D. Marfan syndrome is an autosomal dominant

connective tissue disease characterized by skeletal changes (e.g., tall
stature, long limbs, long fingers, lax joints), a tendency to develop
dislocations of the lens of the eye, and a tendency to develop aortic
dissection secondary to prominent cystic medial degeneration in the aortic
media. A similar condition, Ehlers-Danlos syndrome, also predisposes for
dissecting aneurysm. Other predisposing factors include congenital
cardiovascular abnormalities (e.g., coarctation of the aorta, patent ductus
arteriosus, bicuspid aortic valve) that increase the turbulence of blood flow in
the aorta, atherosclerosis, and trauma (including iatrogenic trauma during
arterial catheterization and cardiovascular surgical procedures). The other
conditions listed in the choices are unrelated to aortic dissection.

Cushing syndrome (choice A) is a characteristic pattern of physical changes

(truncal obesity, moon face, buffalo hump), biochemical/hormonal changes
(hypertension, altered carbohydrate and protein metabolism, amenorrhea),
and sometimes psychiatric disturbances that are seen in patients with
increased levels of adrenocortical hormones.

Dandy-Walker syndrome (choice B) is a congenital abnormality of the

cerebellum and fourth ventricle.

Kawasaki syndrome (choice C) is a febrile childhood disease that

predisposes for the formation of tiny aneurysms of the coronary arteries.

Tourette syndrome (choice E) is a motor and vocal tic disorder.

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A 35-year-old man with no significant past medical history presents to clinic with
a six week history of worsening chest discomfort and pain.
He describes the pain as a substernal burning sensation that occasionally wakes
him up at night and is often worse after he eats. He
sometimes notices a sour taste in his mouth when he wakes up in the morning.
He has no dysphagia or odynophagia. The pain is unrelated
to exertion, and he jogs 3 miles every other day without difficulty or chest pain.
His vital signs and physical examination are normaI.
Question 1 of 6
Which of the following is the most likely diagnosis?
/A. Acute viral pericarditis
/B. Aortic dissection
/C. Candida esophagitis
/D. Gastroesophageal reflux disease (GERD)
/E. Stable angina

Explanation - Q: 3.1 Close

The correct answer is D. A patient who presents with chest discomfort that
is burning in nature, and worsened after eating without symptoms of
dysphagia or odynophagia, most likely has gastroesophageal reflux disease
(GERD). GERD occurs when there is reflux of gastric contents into the
esophagus. This may occur with or without inflammation. It is often caused by
inappropriate relaxation of the lower esophageal sphincter. Certain foods
such as peppermint, caffeine, and high-fat and spicy foods are often
associated with GERD.

Acute viral pericarditis (choice A) would present with more severe and
sudden onset of chest pain that is relieved with leaning forward or sitting up.
Acute viral pericarditis is often associated with a prodrome and usually
presents with a fever. Occasionally, a pericardial friction rub can be heard on
exam.

Aortic dissection (choice B) would also present as sudden onset of severe

chest pain, which often radiates to the back. Patients can have hypotension,
depending on the severity of the dissection. Patients can also have unequal
pulses in their extremities if the dissection affects one of the major arteries
branching off the aortic arch.

Candida esophagitis (choice C) would present with dysphagia and

odynophagia. Patients also have oral thrush, and generally are
immunocompromised. These patients usually have a fever.

Stable angina (choice E) should present with typical chest pain that is
worsened after exertion. The fact that this patient can jog 3 miles without
 difficulty goes against stable angina. Furthermore, he is young and does not
have any risk factors for cardiac disease such as hypertension, diabetes, or
hypercholesterolemia.
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Question 2 of 6
Which of the following tests would be most likely to confirm the probable
diagnosis?
/A. 24-hour ambulatory esophageal luminal pH monitoring
/B. Cardiac angiogram
/C. Chest radiograph
/D. Exercise treadmill test
/E. Serologic blood tests for H. Pylori infection

Explanation - Q: 3.2 Close

The correct answer is A. Twenty-four hour ambulatory esophageal luminal

pH monitoring is one of the most sensitive tests for GERD. In most cases, the
disease is diagnosed clinically by history, but pH monitoring would help
confirm the diagnosis.

Cardiac angiograms (choice B) are used to evaluate the coronary arteries for
signs of blockage, to evaluate heart function, or to evaluate cardiac valve
function.

A chest radiograph (choice C) can be used to evaluate the structures in the

thorax, but will not help confirm the diagnosis because GERD patients
generally have normal chest radiographs.

An exercise treadmill test (choice D) is used to evaluate patients who are

believed to have underlying coronary heart disease or to rule out heart
disease.

Serologic blood testing for H. pylori infection (choice E) only documents the
presence of a current infection or the history of an H. pylori infection. A past or
present infection does not confirm a diagnosis, because GERD can occur in
the setting with or without H. pylori. Furthermore, the role of H. pylori in
GERD is still unclear.
Question 3 of 6
The patient is treated with cimetidine, which completely relieves his symptoms.
Which of the following is the mechanism of action of this
medication?
/A. Beta-1 adrenergic blockade
/B. Histamine H2 receptor blockade
/C. Inhibition of cell wall synthesis
/D. Inhibition of cyclooxygenase
/ E. Smooth muscle relaxation
Explanation - Q: 3.3 Close

The correct answer is B. Cimetidine and other histamine H2 receptor

blockers such as ranitidine block the action of histamine on H2 receptors,
resulting in a decrease in gastric acid production, thus decreasing the
symptoms of GERD.

Beta-1 adrenergic blockade (choice A) (e.g., atenolol, metoprolol) is used to

lower blood pressure, which is not related to GERD.

Inhibition of cell wall synthesis (choice C) (e.g., amoxicillin) is a mechanism

that is used by many antibiotics. GERD can be associated with the presence
of H. pylori, but the treatment of H. pylori with antibiotics in GERD patients
remains controversial, and its benefit remains questionable.

Inhibition of cyclooxygenase (choice D) (e.g., ibuprofen, naproxen) does not

play a role in the treatment of GERD. GERD may or may not be associated
with inflammation of the esophagus, but anti-inflammatory agents may
actually worsen symptoms.

Smooth muscle relaxation (choice E) (e.g., nitroglycerin) does play a role in

the relief of esophageal spasm, but this patient does not complain of
dysphagia or odynophagia.

Question 4 of 6

The physician cautions the patient about cimetidine because of which of the
following potential side effects?
/A. CNS depression
/B. Hypertensive crisis
/C. Inhibition of hepatic metabolism
/D. Masking symptoms of hypoglycemia
/E. Ototoxicity

Explanation - Q: 3.4 Close

The correct answer is C. Many drugs can lead to clinically significant drug
interactions via inhibition of the hepatic drug-metabolizing enzymes,
particularly the cytochrome P450 isozymes. This can lead to unwanted
elevations of plasma drug levels. Cimetidine is a classic example of one of
these drugs. Other examples include erythromycin, ketoconazole,
sulfonamides, quinidine, and disulfiram.

Benzodiazepines and barbiturates are examples of drugs that can cause

 CNS depression (choice A).

MAO inhibitors prior to the ingestion of tyramine-containing foods can cause a

hypertensive crisis (choice B).

Beta blockers can mask the symptoms of hypoglycemia (choice D).

Aminoglycosides can produce ototoxicity (choice E). The risk of ototoxicity

may be further increased if the patient is also taking loop diuretics.

Question 5 of 6

The patient's symptoms are initially controlled on cimetidine. After 10 years, he

develops refractory symptoms, and the physician places him
on a proton pump inhibitor. Which of the following medications was most likely
prescribed?
/A. Lansoprazole
/B. Loperamide
/C. Metoclopramide
/D. Ondansetron
/E. Ranitidine

Explanation - Q: 3.5 Close

The correct answer is A. Lansoprazole is a proton pump inhibitor and acts

directly to inhibit the gastric parietal cell hydrogen-potassium ATPase. It can
be used as the initial treatment for GERD, or for refractory cases.

Loperamide (choice B) is an anti-diarrheal agent, which inhibits peristalsis.

Using it in this setting may worsen the symptoms of GERD.

Metoclopramide (choice C) stimulates upper gastrointestinal motility. It can

be used in refractory cases of GERD, but it is not a proton pump inhibitor.

Ondansetron (choice D) is an antiemetic and acts by selectively antagonizing

serotonin 5-HT3 receptors. It is primarily used is severe cases of nausea,
such as in patients receiving chemotherapy for cancer treatment.

Ranitidine (choice E) is also an histamine H2 receptor blocker, like

cimetidine. Some patients who do not respond to one histamine H2 receptor
blocker, may respond to another, but ranitidine blocks the action of histamine
on H2 receptors, resulting in a decrease in gastric acid production. It is not a
proton pump inhibitor.

Question 6 of 6
Histologic examination of the affected tissue shows Barrett's esophagus. This is
most correctly described as which of the following?
/A. Adenocarcinoma
/B. Esophageal stricture
/C. H.Pylori infection
/D. Localized outpouching of the esophageal wall
/E. Metaplasia of the squamous epithelium

Explanation - Q: 3.6 Close

The correct answer is E. Patients who have long-standing GERD are at risk
for development of Barrett's esophagus, which is the replacement of the
normal esophageal squamous epithelium with columnar epithelium
(metaplasia). This is a premalignant lesion that needs to be monitored
regularly for the development of adenocarcinoma.

Adenocarcinoma (choice A) is a malignant lesion that can result from cellular

metaplasia, but Barrett's esophagus is the premalignant lesion that occurs
before the development of adenocarcinoma of the esophagus.

Esophageal strictures (choice B) can occur in patients with long-standing

GERD, but the presence of a stricture does not mean that there is cellular
dysplasia, or Barrett's esophagus.

H. pylori infection (choice C) can occur in the setting of GERD, but it is not
synonymous with Barrett's esophagus.

An esophageal diverticulum is a localized outpouching of the esophageal wall

(choice D). This is unrelated to Barrett's esophagus.

A 45-year-old man presents with a 3-day history of persistent, severe chest pain.
Prior to this, he had flu-Iike symptoms for 2 weeks, including
fever, cough, myalgias, and arthralgias. His pain is worse when he takes a deep
breath and is improved when he sits up. On physical
examination, he is febrile, and his pulse is 110/min. His oxygen saturation is
normaI, and his breath sounds are equal and clear to
auscultation over all lung fields. There is a scratching and scraping, high-pitched
sound on auscultation of the heart over the left third
intercostal space, which is increased when the patient is sitting forward.
Question 1 of 4

Which of the following is the most likely diagnosis?

/A. Acute pericarditis
/B. Aortic dissection
/C. Pneumonia
/D. Pulmonary embolus
/E. Tension pneumothorax

Explanation - Q: 4.1 Close

The correct answer is A. This patient has symptoms that are typical of
inflammation of the pericardial sac. In addition, the sound that is heard over
his heart is a pericardial friction rub. Acute pericarditis is often associated with
viral syndromes, connective tissue diseases, renal failure, myocardial
infarction, and tumor invasion of the pericardium.

Aortic dissection (choice B) will also present with severe chest pain, but it is
tearing in quality, and is not positional, nor pleuritic in nature.

Pneumonia (choice C) may present similarly, but auscultation of the lung

fields should reveal abnormal breath sounds, and a pericardial friction rub
should not be heard.

Pulmonary embolus (choice D) can present with chest pain that is worse with
deep breaths. However, it is not positional in nature, and it is not associated
with a pericardial friction rub. Depending on the size of the embolus, the
oxygen saturation may be abnormal.

Tension pneumothorax (choice E) is not associated with flu-like symptoms

nor a pericardial friction rub. Furthermore, there should be an absence of
breath sounds over the affected part of the lung.
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Question 2 of 4
Which of the following would help confirm the diagnosis?
/A. Angiogram showing a clot in one of the coronary arteries
/B. Chest radiograph showing multiple emphysematous bullae
/C. CT scan of the chest showing a widened mediastinum
/D. EIectrocardiogram showing diffuse ST elevation
/E. Endoscopy revealing esophageal varices

Explanation - Q: 4.2 Close

The correct answer is D. Acute pericarditis often presents with diffuse ST

 elevation on an electrocardiogram.

An angiogram showing a clot in one of the coronary arteries (choice A) would

be seen in a patient having an acute myocardial infarction.

A chest radiograph showing multiple emphysematous bullae (choice B)

would be seen in a chronic smoker, and would be a possible cause of
spontaneous pneumothorax.

CT scan of the chest showing a widened mediastinum (choice C) would be

seen in a patient with an acute aortic dissection.

Endoscopy revealing esophageal varices (choice E) is seen in patients with

chronic liver disease or portal hypertension.

Question 3 of 4
Other than an antecedent viral syndrome, which of the following conditions can
predispose a patient to this problem?
/A. AIcohol abuse
/B. Liver failure
/C. Peptic ulcer disease
/D. Recent total hip replacement
/E. Renal failure

Explanation - Q: 4.3 Close

The correct answer is E. Patients with renal failure or uremia can often
present with a fibrinous or serofibrinous pericarditis.

Alcohol abuse (choice A) and liver failure (choice B) do not necessarily

predispose a patient to pericarditis, nor are they associated with pericarditis.

Peptic ulcer disease (choice C) may cause epigastric pain that can be
confused with chest pain, and patients may have recurrent bleeding, but this
disorder is not associated with pericarditis.

A recent total hip replacement (choice D) predisposes patients to the

development of a deep venous thrombosis, which can embolize and cause a
pulmonary embolus. This is not associated with pericarditis.

Question 4 of 4
The patient is treated with a nonsteroidal anti-inflammatory agent. Which of the
following was prescribed?
/A. AIIopurinol
/B. Gemfibrozil
/C. Indomethacin
/D. Labetalol
/E. Methocarbamol

Explanation - Q: 4.4 Close

The correct answer is C. Indomethacin or any of the other nonsteroidal anti-

inflammatory agents can be used in the treatment of acute pericarditis.

Allopurinol (choice A) is used for the treatment of gout. It inhibits xanthine

oxidase, which decreases the production of uric acid.

Gemfibrozil (choice B) is a lipid lowering agent used in patients with

hypercholesterolemia.

Labetalol (choice D) is a beta blocker and is used in hypertensive

emergencies.

Methocarbamol (choice E) is a muscle relaxant, which helps to relieve pain

associated with muscle spasms.

A 62-year-old white man is brought to the emergency department after

experiencing twenty minutes of sudden onset, crushing, substernal
chest pain radiating to his neck and left shoulder. The pain started when the
patient was lifting a heavy trolley. He denies shortness of breath,
back pain, or loss of consciousness. In the emergency department, he is given
sublingual nitroglycerin tablets, which relieve the pain almost
immediately. The patient has a history of hypertension, drinks beer several times
a week, smokes one pack of cigarettes per day, and does
not exercise. He is not on any medications. On physical examination, he is a
diaphoretic patient with a temperature of 36.6 C (98 F), blood
pressure of 150/80 mm Hg, pulse of 84/minute, and respirations of 16/minute.
His heart and breath sounds are normaI, his abdomen is soft
and non-tender, and no bruits were heard. A chest radiograph is normaI. An
electrocardiogram confirms T-wave inversion in leads V2 and
V3, with an otherwise normal sinus rhythm. The patient is started on atenoloI, a
nitroglycerin paste patch, and aspirin. He is admitted into the
hospitaI, where he remains pain free. Troponin levels taken every eight hours for
the next 24 hours are all within normal limits.
Question 1 of 5

Which of the following is the most likely diagnosis?

/A. Angina
/B. Gastroesophageal reflux disease
/C. Myocardial infarction
/D. Pulmonary embolism
/E. Thoracic aortic aneurysm rupture

Explanation - Q: 5.1 Close

The correct answer is A. The patient has four independent cardiac risk
factors (male sex, smoker, hypertensive, inactivity). He presented with typical
cardiac chest pain on exertion, accompanied by diaphoresis, which was
relieved with nitroglycerin. This is typical of angina. T-wave inversion is also
consistent with ischemia. However, this is unlikely to be a myocardial
infarction (choice C) because there were no raised ST segments on the
electrocardiogram and his cardiac enzymes (e.g., troponin) were not
elevated. He would probably require a cardiac stress test to see if the EKG
changes could be reproduced in a controlled stressful environment (e.g.,
treadmill). On this visit, his symptoms are better described as being anginal
with ischemic EKG findings on the anterior cardiac wall.

Gastroesophageal reflux disease (choice B) would present with a

longitudinal burning sensation in the epigastric area, usually after the
consumption of large meals, caffeinated products, exercising, or lying flat
after eating. It is treated with H2-blockers and proton pump inhibitors, along
with eating smaller meals and the avoidance of caffeine. It is an important
part of the differential diagnosis of chest pain.

The patient has risks for thromboembolism, including smoking and inactivity,
which could lead to pulmonary embolism. Pulmonary embolism (choice D)
would be suggested if the patient had a sudden onset of shortness of breath
and chest pain. In addition, on examination, one would look for tachycardia,
tachypnea, and diaphoresis. The work-up includes D-dimers, a lower leg
Doppler, prothrombin time (PT), partial thromboplastin time (PTT), and a
ventilation/perfusion scan. Treatment would be anticoagulation with heparin,
and then eventually with Coumadin.

Rupture of a thoracic aortic aneurysm (choice E) would present as severe

chest pain radiating to the back. The patient would typically be elderly. The
blood pressure may drop and there will sometimes be a discrepancy in arm-
to-arm blood pressure readings.
Question 2 of 5
Which of the following vessels is most likely affected in this patient?
/A. Circumflex coronary artery
/B. Left anterior descending artery
/C. Marginal artery
/D. Posterior descending artery
/E. Right coronary artery

Explanation - Q: 5.2 Close

 The correct answer is B. The electrocardiogram revealed inverted T-waves
(suggestive of ischemia) in leads V2 and V3. These leads correspond mainly
to the anterior wall of the left ventricle, where the ischemia is likely to have
taken place. The left anterior descending artery is a terminal branch of the left
coronary artery (the other branch being the circumflex artery). It passes
posterior to the pulmonary artery, then anteriorly between this vessel and the
left auricle to reach the anterior longitudinal sulcus. Since it supplies blood to
the anterior walls of both ventricles, ischemia in this location would manifest
as T-wave inversion in leads V1 to V4.

The circumflex artery (choice A) supplies the lateral wall of the heart (atrium
and ventricle). Ischemia with this artery would manifest as T-wave inversion
of leads I, aVL, and leads V5 and V6. The circumflex artery branches off the
left coronary artery and follows the left part of the coronary sulcus giving
branches to the left atrium and ventricle.

The marginal artery (choice C) is a branch of the right coronary artery, and it
supplies branches to both surfaces of the right ventricle. Disease in this
vessel is not associated with specific EKG changes.

Inverted T-waves in leads II, III, and aVF would correspond mainly to
ischemia of the inferior wall of the left ventricle. The main artery supply to this
area is the right coronary artery (choice E). It arises from the anterior aortic
sinus, then passes between the conus arteriosus and the right auricle, and
then runs in the right portion of the coronary sulcus. From there it continues
on the diaphragmatic surface of the heart from the right to left, as far as the
posterior longitudinal sulcus. It eventually arrives at the apex of the heart in
the form of the posterior descending artery (choice D).

Question 3 of 5

Which of the following is most likely responsible for this patient's symptoms?
/A. Atheromatous plaque rupture
/B. Hyaline arteriosclerosis
/C. Hyperplastic arteriosclerosis
/D. Thrombus embolization
/E. Vasospasm of the coronary vessels.

Explanation - Q: 5.3 Close

The correct answer is A. Several hypotheses have been formulated about

atheromatous plaque formation. One hypothesis involves endothelial wall
damage, resulting in monocyte and platelet adhesion and migration of
monocytes into the intima from the lumen and smooth muscle media. Another
hypothesis involves hyperlipidemia causing an increased rate of LDL (low
 density lipoprotein) penetration into the artery wall, causing endothelial injury
and the promotion of foam cells. Once the atheromatous plaque is formed,
any rupture (e.g., with vasospasm) will expose subendothelial collagen,
promoting platelet adherence, and the eventual aggregation of platelets. This
may cause a total occlusion of the coronary vessel (as in the case of an
infarction) or a transient subocclusion (that leads to angina due to ischemia).

Arteriosclerosis typically produces less acute effects than the occlusion seen
with atheromatous plaque formation. Hyaline arteriosclerosis (choice B) is
microangiopathy seen in hypertensive and diabetic patients. It is due to
leakage of plasma components across the vascular endothelium and
increasing extracellular matrix production by smooth muscle walls. This
eventually narrows the arteriolar lumina causing reduced blood flow for that
organ e.g., the kidney.

Hyperplastic arteriosclerosis (choice C) is usually seen in "malignant" or

severe hypertension and is characterized by laminated thickenings of the wall
of the lumina. The most commonly affected sites are the kidney, gallbladder,
pancreas, and intestines.

An embolus is a detached intravascular solid, liquid, or gaseous mass carried

by the blood to a site distal to the point of origin. Thrombus embolization
(choice D) represents 99% of all emboli. An example is a pulmonary
(thrombo)embolism. Although atherosclerosis may provide a site for thrombus
formation and embolization, this is not the most common mechanism for
angina.

Vasospasm (choice E) may cause angina more rarely; this is called

Prinzmetal's angina. There may be essentially no major atheromatous
changes in the coronary vessels. Prinzmetal's angina is often treated with
calcium channel blockers.

*** Font Exploring versus font guessing ***

Question 4 of 5
The cardiac enzyme marker troponin is normally found predominantly in which of
the following sites?
/A. Cell membranes of myocardial cells
/B. Endoplasmic reticulum
/C. Mitochondria
/D. Myofibrils
/E. Nuclei
/F. Ribosomes

Explanation - Q: 5.4 Close

The correct answer is D. Troponins are tightly bound structural proteins that
 regulate the calcium-mediated interaction of actin and myosin in striated
muscle (myofibrils). Troponin release would indicate cell death, such as that
seen in infarction. The rise of this marker after cardiac injury parallels that of
creatine kinase (CK) (another cardiac enzyme marker). However, in contrast
to CK, baseline levels of troponin are undetectable in normal volunteers.

Neither troponin nor creatine kinase are found in cell membranes (choice A)
of the myocardium.

Creatine kinase is a cardiac marker that resides in the cytoplasm and

mitochondria (choice C). During cardiac injury, destruction of the cell walls
and sarcolemma of the myocardial cells causes rapid release of the CK into
the bloodstream. It is also released in noninfarction cardiac injuries (e.g.,
blunt chest trauma).

The nucleus (choice E), ribosomes (choice F), and endoplasmic reticulum
(choice B) are sites of transcription, translation and post-translational
modification of troponin. Troponin is then incorporated into the myofibril
structure via covalent attachment.

Question 5 of 5

Which of the following is the mechanism of action of nitroglycerin?

/A. Increases stroke-work index of the heart
/B. Maintains coronary perfusion despite fluctuations in blood pressure
/C. Relaxes bronchial smooth muscle
/D. Relaxes vascular smooth muscle
/E. Unblocks coronary vessels by fibrinolysis

Explanation - Q: 5.5 Close

The correct answer is D. Relaxation of vascular smooth muscle is the

principal pharmacologic action of nitroglycerin. Nitroglycerin (glyceryl
trinitrate) is a therapeutically active member of the nitrate group of drugs.
Nitrates improve oxygen supply to the myocardium (dilation of the coronary
artery, reduction of the end-diastolic pressure in the left ventricle) and
reduces myocardial oxygen requirements (dilation of the peripheral arteries,
lowering of the systemic blood pressure). Reduction of venous return is a
particular benefit (reduction of preload) in the event of heart failure. In smooth
muscle cells, nitrates increase the intracellular concentration of nitric oxide
(NO). NO stimulates guanylate cyclase, forming cGMP, which probably
dephosphorylates the phosphorylated form of myosin light chain, leading to
smooth muscle relaxation.

Myocardial oxygen consumption or demand (as measured by the pressure-

rate product, tension-time index, and stroke-work index, choice A) is
decreased by both the arterial and venous effects of nitroglycerin, and a more
 favorable supply-demand ratio can be achieved. Therapeutic doses of
intravenous nitroglycerin reduce systolic, diastolic, and mean arterial blood
pressures.

Effective coronary perfusion pressure (choice B) is usually maintained, but

can be compromised if blood pressure falls excessively or increased heart
rate decreases diastolic filling time.

The bronchial smooth muscle is unaffected by nitrates. Bronchodilation

(choice C) can be achieved by stimulation of beta-2 adrenergic receptors.
Inhalation of beta-agonists, such as albuterol, can help reduce wheezing
during asthmatic episodes.

Reperfusion of coronary vessels through fibrinolysis (choice E) is the action

of fibrinolytic agents like alteplase or streptokinase. They are used primarily in
myocardial infarctions. If the agent is administered done quickly enough, the
infarct size is reduced and left ventricular function is preserved, thereby
reducing mortality.

A 19-year-old college student is referred to a family medicine physician for an

abnormal heart sound heard on a routine school physical
examination. On questioning, he denies chest pain or shortness of breath, but
says he does occasionally experience palpitations. He is
adopted and does not know his family history. On physical examination, he is 201
cm (79 inches) talI, weighs 73 kg (160 Ib), and has long
arms and legs. On examination, there is a mid-systolic click, heard best at the
apex. The click also occurs earlier when the patient stands or
performs a Valsalva maneuver.
Question 1 of 6
Which of the following cardiac abnormalities does this patient most likely have?
/A. Aortic regurgitation
/B. Aortic stenosis
/C. Mitral stenosis
/D. Mitral valve prolapse
/E. Tricuspid regurgitation

Explanation - Q: 6.1 Close

The correct answer is D. Mitral valve prolapse is a common valvular

abnormality that can be benign and asymptomatic, but it can also cause
palpitations, chest pain, and shortness of breath. It is due to stretching of the
posterior mitral valve leaflets, resulting in prolapse of the valve. This change
produces the classic midsystolic click, that is sometimes is followed by a
 murmur.

Aortic regurgitation (choice A) would result in a blowing, diastolic murmur

heard best at the left second intercostal space.

Aortic stenosis (choice B) would result in a systolic ejection murmur heard

best at the right second intercostal space.

Mitral stenosis (choice C) produces a low-pitched diastolic murmur heard

best over the apex. It is often preceded by an opening snap.

Tricuspid regurgitation (choice E) produces a blowing systolic murmur heard

best at the left lower sternal border.
*** Klepting everything! ***
Question 2 of 6
An echocardiogram is performed. Which of the following would likely be observed
during the study?
/A. Ballooning of the aortic valve into the ventricle during diastole
/B. Ballooning of the mitral valve into the atrium during diastole
/C. Rupture of the aortic valve
/D. Rupture of the tricuspid valve
/E. Stenotic mitral valve

Explanation - Q: 6.2 Close

The correct answer is B. Ballooning of the mitral valve into the atrium during
diastole is diagnostic of mitral valve prolapse.

Ballooning of the aortic valve into the ventricle during diastole (choice A)
does not occur in mitral valve prolapse. In addition, this would not result in a
mid-systolic click.

Rupture of the aortic valve (choice C) could result in severe hemodynamic

compromise, especially if it were acute, due to a large regurgitant flow of
blood. A harsh diastolic murmur would be heard on examination.

Rupture of the tricuspid valve (choice D) would cause a blowing systolic

murmur heard over the left lower sternal border.

A stenotic mitral valve (choice E) is not associated with mitral valve prolapse.
In mitral stenosis, the valve is thick and stiff. There is a low-pitched diastolic
murmur, which is often preceded by an opening snap.

Question 3 of 6
Which of the following genetic disorders can be associated with this abnormality?
/A. KIinefelter syndrome
/B. Marfan syndrome
/C. Osler-Weber-Rendu syndrome
/D. Tay-Sachs disease
/E. Wilson disease
*** Sum the numbers in Notepad, MS Word and e-mail! ***
Explanation - Q: 6.3 Close

The correct answer is B. Marfan syndrome is a connective tissue defect due

to a deficiency in fibrillin. This results in defects in skeletal, visual, and
cardiovascular structures, such as mitral valve prolapse and/or aortic
aneurysms.

Klinefelter syndrome (choice A) is chromosomal disorder, most often

characterized by the karyotype 47,XXY. It results in hypogonadism, and in
some cases, mild mental retardation.

Osler-Weber-Rendu syndrome (choice C) is also known as hereditary

hemorrhagic telangiectasia. It is characterized by telangiectasias of the skin
and mucous membranes and hemorrhage at these sites.

Tay-Sachs disease (choice D) is a lysosomal storage disease caused by a

deficiency of hexosaminidase A. It results in central nervous system
degeneration, mental retardation, motor deterioration, and blindness.

Wilson disease (choice E) is a disorder of copper metabolism. It is

characterized by decreased serum ceruloplasmin and results in accumulation
of copper in the liver, kidney, brain, and cornea.

*** More klepting in less time ***

Question 4 of 6
This patient is diagnosed with a genetic disorder associated with the valvular
abnormality. Which of the following modes of inheritance does
this disease follow?
/A. Autosomal dominant inheritance
/B. Autosomal recessive inheritance
/C. Mitochondrial inheritance
/D. X-Iinked dominant inheritance
/E. X-Iinked recessive inheritance

Explanation - Q: 6.4 Close

The correct answer is A. Marfan syndrome is inherited in an autosomal

dominant manner. Usually, in diseases with this pattern of inheritance, one
heterozygous parent carries a gene with the phenotypic expression of the
disorder, and the other parent is normal.
 Autosomal recessive inheritance (choice B) usually occurs when both
parents are heterozygotes and do not phenotypically manifest the disorder.
Cystic fibrosis is an example of an autosomal recessive disease.

Mitochondrial inheritance (choice C) is due to the maternal transmission of

mitochondrial genes. Mitochondrial myopathies are inherited in this pattern.

X-linked dominant inheritance (choice D) is a rarity. The heterozygous female

and the hemizygous male will manifest the phenotype.

X-linked recessive inheritance (choice E) is most often the result of a

heterozygous female parent and a genotypically and phenotypically normal
male parent. Male children who inherit the affected X chromosome will
manifest the disorder, but the female children will only be carriers.
Question 5 of 6
Over the next year the patient develops chest pain, shortness of breath, and
progressive fatigue. On auscultation, he has a midsystolic click,
which is now followed by a high-pitched, blowing systolic murmur. Which of the
following is the most likely cause of this new development?
/A. Aortic aneurysm
/B. Aortic stenosis
/C. Mitral regurgitation
/D. Mitral stenosis
/E. Myocardial infarction

Explanation - Q: 6.5 Close

The correct answer is C. In severe cases of mitral valve prolapse, patients

can develop mitral regurgitation, which may require surgical treatment if the
symptoms are severe.

Aortic aneurysm (choice A) can occur in Marfan disease, but it is not

associated with mitral prolapse or a systolic murmur.

Aortic stenosis (choice B) causes a systolic ejection murmur heard best at

the right second intercostal space, which often radiates to the carotid arteries.
It is not associated with extra heart sounds.

Mitral stenosis (choice D) is not a complication of mitral valve prolapse.

Furthermore, it causes a diastolic murmur, which can be preceded by an
opening snap.

Myocardial infarction (choice E) is not associated with mitral valve prolapse.

Question 6 of 6
The patient is treated with propanoloI. What is the mechanism of action of this
medication?
/A. AIpha-1 selective adrenergic blockade
/B. Beta-1 selective adrenergic blockade
/C. Calcium channel blockade
/D. Nonselective beta adrenergic blockade
/E. Nonselective alpha adrenergic blockade

Explanation - Q: 6.6 Close

The correct answer is D. Propanolol, as well as timolol, pindolol, nadolol,

and labetalol, all exhibit nonselective beta-adrenergic blockade. They are
generally used in the treatment of hypertension, angina, and arrhythmias.

Alpha-1 selective adrenergic blockade (choice A) is a mechanism used by

prazosin, terazosin, and doxazosin. These agents can be used to treat
hypertension or urinary retention due to benign prostatic hypertrophy.

Beta-1 selective adrenergic blockade (choice B) is a mechanism used by

metoprolol, atenolol, and esmolol. Unlike the nonselective beta-adrenergic
blockers, these medications selectively block beta 1 receptors over beta 2
receptors.

Calcium channel blockade (choice C) is a mechanism used by nifedipine,

diltiazem, and verapamil. They can also be used to treat hypertension and
angina. Verapamil and diltiazem can also be effective in the treatment of
arrhythmias.

Nonselective alpha-adrenergic blockade (choice E) is a mechanism used by

phenoxybenzamine and phentolamine. They can be used in the treatment of
pheochromocytoma.

*** Sum the numbers in Notepad, MS Word and e-mail! ***

A 21-year-old woman presents to an urgent care clinic with complaints of sharp,
knife-Iike chest pain and shortness of breath for the past 4
days. She states that the pain is worse with inspiration, coughing, and
movement. However, it is not related to position. She also complains
of fever, chills, and a dry cough. She has a history of some type of rheumatologic
disease, but she does not know which one. She was
previously seen by a rheumatologist, but was lost to follow up, and stopped
taking her medications 6 months ago. Her physical examination is
notable for a temperature of 37.8 C (100 F), tachycardia, decreased breath
sounds at both lung bases, and a friction rub. There is no pinpoint
chest wall tenderness.
Question 1 of 6
Which of the following is the most likely cause of this patient's chest pain?
/A. Angina pectoris
/B. Anxiety
/C. Esophageal spasm
/D. PIeuritis
/E. Rib fracture

Explanation - Q: 7.1 Close

The correct answer is D. Pleuritis is inflammation of the parietal pleura of

the lung, which can often result in a friction rub heard on auscultation.
Patients can also have pleural effusions. Pleuritis is associated with many
different disease processes, including collagen vascular diseases and
infections.

Angina pectoris (choice A) is chest pain related to underlying coronary artery

disease. The pain is usually substernal, worse with exertion, and relieved by
rest. It is not associated with fever or chills, nor is it pleuritic in nature.

Anxiety (choice B) can often be a cause of chest pain. It is a clinical

diagnosis and should be associated with other symptoms of anxiety. It is not
pleuritic in nature, and is not associated with a cough, fever, or chills.

Esophageal spasm (choice C) is due to uncoordinated contractions of the

esophagus. It is generally associated with dysphagia.

Rib fracture (choice E) should result in well-localized chest pain. There is

pinpoint chest wall tenderness, and bone crepitus can be noted on palpation.
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Question 2 of 6
On a chest radiograph, the patient is noted to have bilateral pleural effusions.
Evaluation of the fluid would most likely reveal which of the
following?
/A. Exudative effusion
/B. Low pleural fluid LDH
/C. PIeural fluid to serum lactate dehydrogenase (LDH) ratio <0.6
/D. PIeural fluid to serum protein ratio <0.5
/E. Transudative effusion

Explanation - Q: 7.2 Close

The correct answer is A. This patient has an exudative pleural effusion

associated with an underlying rheumatologic condition.

Pleural fluid to serum protein ratio <0.5 (choice D), pleural fluid to serum
 lactate dehydrogenase (LDH) ratio <0.6 (choice C), and low pleural fluid LDH
(choice B) are all diagnostic of a transudative effusion.

A transudative effusion (choice E) occurs when systemic factors that affect

the formation of pleural fluid are altered. It is associated with heart failure,
cirrhosis, and nephrotic syndrome.
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Question 3 of 6
The patient also gives a history of symmetric joint pain and swelling as well as a
malar rash and photosensitivity. Which of the following is the
most likely diagnosis?
/A. Ankylosing spondylitis
/B. Polyarteritis nodosa
/C. Psoriatic arthritis
/D. Rheumatoid arthritis
/E. Systemic lupus erythematous (SLE)

Explanation - Q: 7.3 Close

The correct answer is E. Systemic lupus erythematous (SLE) is an

autoimmune disorder that can affect multiple organ systems, especially joints,
serous membranes, lungs, skin, and kidneys. It is characterized by the
presence of pathogenic autoantibodies and immune complexes, which cause
cellular and tissue damage.

Ankylosing spondylitis (choice A) is a chronic disease in which inflammatory

changes and new bone formation occur at the attachment of tendons and
ligaments to bone. It often affects the spine and sacroiliac joints, and may
result in rigidity and fixation of the spine.

Polyarteritis nodosa (choice B) is an immune complex vasculitis, which

involves small and medium sized arteries. It can affect any organ system, and
predominantly occurs in men.

Psoriatic arthritis (choice C) is an arthritis associated with psoriasis. It can

present in many different ways, including a monoarthritis or a polyarthritis,
which can be symmetrical or asymmetrical.

Rheumatoid arthritis (choice D) is a chronic inflammatory disorder that

primarily affects the joints. It can produce extra-articular manifestations
including arteritis, scleritis, and pleural involvement, but it is not associated
with a malar rash or photosensitivity.
Question 4 of 6
Evaluation of the malar rash would most likely reveal which of the following?
/A. Coral red fluorescence under Wood's lamp
/B. Hyperplasia of all components of the epidermis
/C. IgG autoantibodies directed against the epidermal basement membrane
/D. Immune complex deposits at the dermaI-epidermal junction
/E. Proliferation of the epidermis and parakeratosis
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Explanation - Q: 7.4 Close

The correct answer is D. Immune complex deposits at the dermal-epidermal

junction are classically associated with the malar rash of SLE.

Coral red fluorescence under Wood's lamp (choice A) evaluation occurs in

erythrasma, which is a chronic bacterial infection caused by Corynebacterium
minutissimum.

Hyperplasia of all components of the epidermis (choice B) occurs in lichen

simplex chronicus, which is a well-circumscribed area of lichenification due to
repeated physical trauma such as scratching or rubbing.

IgG autoantibodies directed against the epidermal basement membrane

(choice C) cause a disease known as bullous pemphigoid. It is an
autoimmune disorder, which presents as chronic bullous eruptions.

Proliferation of the epidermis and parakeratosis (choice E) are associated

with psoriasis, which is a chronic inflammatory process characterized by
erythematous papules and plaques with silvery scaling.

Question 5 of 6
Which of the following laboratory tests would help confirm the diagnosis of the
underlying rheumatologic disorder?
/A. Antibodies to single-stranded DNA
/B. Antibodies to Sm antigen
/C. EIevated C reactive protein
/D. EIevated sedimentation rate
/E. Rheumatoid factor

Explanation - Q: 7.5 Close

The correct answer is B. Antibodies to Sm antigen as well as antibodies to

double-stranded DNA are highly specific for systemic lupus erythematous.

Antibodies to single-stranded DNA (choice A) can be found in drug drug-

induced lupus, but not in idiopathic SLE.

Elevated C reactive protein (choice C) and elevated sedimentation rate

 (choice D) often occur in SLE, especially when it is active. However, these
tests are nonspecific and can be elevated whenever there is inflammation or
infection. They do not confirm the diagnosis of SLE.

Rheumatoid factor (choice E) is often positive in patients with rheumatoid

arthritis. It is not associated with SLE.
Question 6 of 6
The patient is treated empirically with levofloxacin for a possible pneumonia.
Which of the following is the mechanism of action of this drug?
/A. Inhibition of cell wall synthesis
/B. Inhibition of DNA gyrase and topoisomerase IV
/C. Inhibition of ergosterol synthesis
/D. Inhibition of protein synthesis by blocking translocation
/E. Inhibition of squalene epoxidase

Explanation - Q: 7.6 Close

The correct answer is B. Levofloxacin is a bactericidal antibiotic that inhibits

DNA gyrase and topoisomerase IV. It belongs to the group of antibiotics
known as fluoroquinolones, which also includes ciprofloxacin and norfloxacin.

Penicillin is an example of an antibiotic that inhibits cell wall synthesis

(choice A).

Fluconazole is an example of an antifungal agent that inhibits ergosterol

synthesis (choice C).

Macrolides inhibit protein synthesis by blocking translocation (choice D). The

macrolides include erythromycin, clarithromycin, and azithromycin.

Inhibition of squalene epoxidase (choice E) results in decreased cell

membrane ergosterol synthesis. This is a mechanism of action used by
antifungal agents, including terbinafine.