A 45-year-old woman presents to her primary care physician complaining of

fatigue, weight gain, and shortness of breath. She has always

been an active athlete, but in the past 2 weeks, has found it impossible to jog for
more than a few minutes, after which she feels tired and
winded. She feels like her appetite is normal or has even declined, but she
notices that she has gained 15 pounds and her pants and shoes
no longer fit welI. She has very little energy, and is sleeping poorly, with
occasional difficulty breathing at night. She denies any pain, fever, or
chills. Review of her chart reveals an up-to-date health screening including a
normal baseline mammogram, a normaI Pap smear in the last
year, and total cholesterol of 165 mg/dL two years ago. On physical examination,
she appears comfortable, has a temperature of 36.8 C
(98.2. F), blood pressure of 135/68 mm Hg, pulse of 90/min, and respiratory rate
of 24/min. She appears fatigued but not in acute distress,
and her skin appears normaI. Expiratory wheezes are heard at the bases of both
lungs. Her heart has a normaI-sounding S1 and S2, with a
II/IV soft holosystolic murmur heard best at the apex of the heart. Her abdomen
is modestly distended, and her ankles are edematous. A
chest x-ray film reveals cardiomegaly as well as increased vascular markings in
the lung beds and bilateral small pleural effusions.
Laboratory studies show:
Question 1 of 5
Which of the following is the most likely diagnosis?
/ A. Acute leukemia
/ B. Cardiomyopathy
/ C. Fibromyalgia
/ D. Hypothyroidism
/ E. Major depressive disorder
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Explanation - Q: 1.1 Close

The correct answer is B. This woman has many of the classic symptoms of
heart failure, with symptoms of both poor forward cardiac output (fatigue, poor
appetite) and of vascular congestion in both the right and left atria (edema,
abdominal distension that may be ascites, cardiomegaly, pulmonary vascular
congestion and effusions seen on chest x-ray, dyspnea with exertion, and
paroxysmal nocturnal dyspnea.)

Acute leukemia (choice A) is a potential cause of fatigue, poor energy, and

poor nutritional status (which can cause edema and pleural effusion). Usually
some abnormality will be apparent, most commonly pancytopenia, due to
replacement of bone marrow with leukemic cells; the leukocyte count may be
elevated due to the presence of leukemic cells in the peripheral blood. They
often present with bleeding or infectious complications of pancytopenia.
Anemia could potentially cause a murmur due to elevated cardiac output, but
an acute leukemia would not typically cause cardiomegaly or pulmonary
 edema.

Fibromyalgia (choice C) is a potential cause of fatigue, poor energy, and

poor sleep, especially in women ages 25-45: its principal sign, however, is
diffuse musculoskeletal pain and stiffness, with characteristic tender trigger
points. It is not consistent with this patient's chest x-ray abnormalities or
cardiac and lung findings.

Based on examination, this patient could certainly have hypothyroidism

(choice D). Symptoms are usually insidious in onset and include fatigue, poor
appetite with weight gain, poor sleep and possibly, obstructive sleep apnea.
Patients often complain of constipation, cold intolerance, stiffness and muscle
cramping, as well as decreased intellectual activity. Severe hypothyroidism
can result in cardiomegaly, pericardial effusion, and symptoms of cardiac
failure. The skin often appears dry, rough, and doughy in texture. The normal
TSH, however, makes hypothyroidism in this patient very unlikely: The TSH is
nearly always elevated, as most hypothyroidism is primary, which means the
pituitary is secreting maximal TSH in an attempt to stimulate a hypofunctional
thyroid gland. Rarely, TSH may be normal or depressed (even undetectable)
in pituitary or hypothalamic failure. To rule this out, one might test first for T4
and T3 levels. Normal levels of these, in conjunction with the normal TSH,
would rule out hypothyroidism as a cause of this clinical presentation.

Major depression (choice E) should always be in the differential for a patient

who presents with disturbances in sleep, appetite, and energy, and can also
result in weight loss or gain. These "vegetative signs" of depression may be
the presenting abnormality in a depressed patient who does not note a mood
disturbance themselves. One should also ask about depressed mood,
anhedonia (loss of interest in or inability to take pleasure in activities the
person normally enjoys), an inability to concentrate and carry on usual
intellectual activities, feelings of worthlessness or guilt, and suicidal ideation.
Depression cannot, however, on its own, produce the physical findings this
patient has, which taken together, are worrisome for some physiologic
abnormality.
Question 2 of 5
Which of the following is the most likely cause of the patient's murmur?
/ A. Aortic insufficiency
/ B. Aortic stenosis
/ C. High-output flow murmur
/ D. Mitral regurgitation
/ E. Mitral stenosis
/ F. Pulmonic insufficiency
/ G. Pulmonic stenosis
/ H. Tricuspid regurgitation
/ I. Tricuspid stenosis
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Explanation - Q: 1.2 Close

The correct answer is D. Mitral regurgitation is characterized by a

holosystolic murmur heard best at the apex, often with a blowing sound,
which may radiate to the axilla.

The murmur of aortic insufficiency (choice A) is a decrescendo diastolic

murmur. Remember that the aortic valve is open during systole; a systolic
murmur, then, cannot represent regurgitant aortic flow due to an improperly
closed valve.

Aortic stenosis (choice B) does produce a systolic murmur caused by

turbulent flow across a narrowed aortic valve during systole. This murmur is
usually a crescendo-decrescendo murmur, often with a harsh quality, and is
characteristically heard best at the base of the heart; it may radiate to the
carotids as well.

High-output states (choice C) can cause a similar soft systolic murmur to that
described here. However, this patient's history is most consistent with cardiac
failure, which is a low-output state.

Mitral stenosis (choice E) causes a murmur due to turbulent low-velocity flow

during diastolic filling of the left ventricle through a narrowed mitral orifice.
This results in a soft diastolic murmur heard best at the apex. Remember that
the mitral valve is closed during systole, therefore, an abnormal mitral sound
in systole must be the sound of abnormal regurgitant flow through a closed
valve.

The right-sided murmurs are less common, similar in quality, and usually less
loud than the left-sided murmurs (given that pressures on the right are usually
lower):

Pulmonic insufficiency (choice F), when audible, therefore causes a soft

diastolic murmur at the right upper sternal border.

Pulmonic stenosis (choice G) causes a crescendo-decrescendo systolic

murmur also heard at the base of the heart.

Tricuspid regurgitation (choice H) causes a holosystolic murmur at the left

lower or right lower sternal border.

Tricuspid stenosis (choice I) when audible, is a diastolic murmur heard best

at the same location
Question 3 of 5
BIood in the pulmonary veins is at the same pressure (during all phases of the
cardiac cycle) as blood in which of the following?
/ A. Aorta
/ B. Left atrium
/ C. Left ventricle
/ D. Right atrium
/ E. Right ventricle

Explanation - Q: 1.3 Close

The correct answer is B. The pressures in two chambers, which are not
separated by a closed valve, will be equal. The pulmonary vein empties into
the left atrium, and no valve separates the two chambers, therefore the
pressures are equal in all phases of the cardiac cycle. This patient's
pulmonary vascular congestion is likely due to elevated pulmonary venous
pressure, which is, in turn, likely due to elevated left atrial pressures.

Pressures in the aorta (choice A) will be higher than pressures in the

pulmonary veins during the cardiac cycle.

The left ventricle (choice C) is separated from the left atrium and the
pulmonary veins by the mitral valve. The pulmonary veins and the left atrium
are at the same pressure as the left ventricle during diastole, when the mitral
valve is open. With complete mitral insufficiency, the pulmonary veins are
completely exposed to left ventricular pressures during systole, resulting in
severe pulmonary edema.

The right atrium (choice D) is not in communication with the pulmonary veins,
being separated from them by, in sequence, the tricuspid valve, the right
ventricle, the pulmonic valve, the pulmonary arterial system, and the
pulmonary capillary bed.

The right ventricle (choice E), during systole, is at the same pressure as the
pulmonary artery, not the pulmonary veins. During diastole, the pulmonary
arterial pressure exceeds right ventricular pressure, and the valve is closed.

Question 4 of 5
To improve her shortness of breath, the patient is given furosemide. What is the
molecular mechanism and site of action of this drug?
/ A. ADH antagonism of in the collecting ducts
/ B. AIdosterone antagonism in the distal tubule
/ C. BIockade of sodium reabsorption in the proximal tubule
/ D. BIockade of sodium transport in the distal tubule
/ E. Inhibition of carbonic anhydrase in the proximal tubule
/ F. Inhibition of sodium-potassium-chloride cotransport in the loop of Henle
 Explanation - Q: 1.4 Close

The correct answer is F. The Na-K-2Cl cotransporter in the loop of Henle

operates via an ATP-dependent sodium-potassium exchange pump in the cell
that creates a gradient for sodium diffusion from the urine space into the cell.
This maintains the sodium concentration gradient of the renal medulla.
Furosemide is the most commonly used loop diuretic; it acts by blocking the
action of the cotransporter in the thick ascending limb of the loop of Henle.

ADH antagonism (choice A) is not an important diuretic drug mechanism,

however, certain drugs, most notably lithium, inhibit ADH's action, resulting in
nephrogenic diabetes insipidus.

Aldosterone promotes the reabsorption of sodium in the late distal tubule and
collecting system and promotes the excretion of potassium. Aldosterone
receptor antagonism (choice B) is the mechanism of action of potassium-
sparing diuretics such as spironolactone.

Sodium reabsorption in the proximal tubule (choice C) is a largely passive

process, which is coupled to the transport of organic solutes and anions and
also to chloride transport, via both transcellular and paracellular mechanisms.

The thiazide diuretics work primarily by blocking sodium transport in the early
portion of the distal tubule (choice D).

Acetazolamide inhibits carbonic anhydrase (choice E), preventing the luminal

transformation of bicarbonate into CO2, which diffuses back into the cell.
Inhibition of this enzyme increases both bicarbonate and sodium
concentrations in the urine, resulting in high urine pH and metabolic acidosis.
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Question 5 of 5
What important physiologic effect will starting this patient on an angiotensin-
converting-enzyme inhibitor achieve?
/ A. Decrease in arteriolar resistance, resulting in less resistance to forward
cardiac output
/ B. Decrease in cardiac filling pressures, resulting in less pulmonary congestion
/ C. Increase in arteriolar resistance, resulting in improved blood pressure
/ D. Increase in left-ventricular end-diastolic volume, improving stroke volume
via Starling forces
/ E. Increase in myocardial contractility, resulting in improved stroke volume
/ F. Stabilization of myocardial membranes, resulting in reduced risk of
arrhythmia
Explanation - Q: 1.5 Close

The correct answer is A. In cardiac failure, the juxtaglomerular apparatus

releases renin in response to low blood pressure or low flow states. Renin
cleaves angiotensinogen into angiotensin I, which is then cleaved by
angiotensin-converting enzyme (ACE) into angiotensin II. Angiotensin II is a
potent vasoconstrictor and increases blood pressure. This, however,
increases the resistance against which the heart must pump, thereby
reducing cardiac output. By reducing angiotensin II activity, systemic vascular
resistance (normally high in cardiac failure, in an attempt to maintain blood
pressure in the presence of low flow) is reduced, permitting the heart to eject
more volume against a lower aortic pressure. This is often described as
"afterload reduction" and is the mainstay of therapy in congestive heart
failure. Paradoxically, blood pressure may not change: the reduced
resistance, by permitting increased flow, may result in no net change in
pressure. This is most easily understood as a physiologic manifestation of
Ohm's law: V = IR. In electricity, this law means that voltage is equal to
current times resistance. Blood pressure is analogous to voltage, cardiac
output to current flow, and the resistance in this case is the resistance of the
systemic vasculature.

Reduction of cardiac filling pressures (choice B) or "preload," is also an

important aspect of the treatment of heart failure. In heart failure, the heart
operates at high filling pressures and high left ventricular end-diastolic volume
(LVEDV) because both aldosterone and ADH promote the retention of fluid in
response to low forward flow and decreased effective circulating volume. The
result is vascular congestion in the pulmonary veins due to the high LV
diastolic pressure, resulting in symptomatic pulmonary edema. By reducing
this preload, congestive symptoms can be relieved, and LVEDV can be
reduced without significant loss of stroke volume. ACE inhibitors, however, do
not reduce preload: drugs that do this are nitrates (which act as venodilators)
and diuretics.

Increasing arteriolar resistance (choice C) in heart failure increases the

"afterload" against which the heart must eject and does not improve cardiac
output.

Increasing LVEDV (choice D) is usually helpful in hypovolemia or other

states in which inadequate volume is available to the heart, thereby limiting
cardiac output. This happens in the portion of the Starling curve at low
LVEDV, where an increase in LVEDV results in a large increase in stroke
volume. Patients in symptomatic heart failure like this patient operate at very
high LVEDV and benefit from its reduction.

Increasing myocardial contractility (choice E) is beneficial in heart failure, and

is the mechanism of action of inotropic drugs. This is not a mechanism of
ACE inhibitors.

Prevention of arrhythmia (choice F) is also important in heart failure, as the

 dilated heart is vulnerable to both atrial and ventricular arrhythmias. This is
not a direct action of ACE inhibitors, however.

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A 23-year-old man presents to the urgent care clinic complaining of severe throat
pain, fever, chills, and diffuse joint pains. He first developed
symptoms two weeks ago and was evaluated by another physician at the same
clinic. A throat culture was done, and the patient was given a
prescription for antibiotics that he did not filI. He now returns with a worsening of
his symptoms. He has since developed severe joint pain and
swelling, which first affected his right wrist, then spread to both knees, and now
has also affected his left ankle. He also complains of
moderate to severe chest discomfort and shortness of breath. His temperature is
38.7 C (101.6 F), blood pressure is 118/86 mm Hg, pulse
is 104/min, and respirations are 20/min. There is an exudate on his oropharynx
and bilateral anterior cervical lymphadenopathy. On lung
examination, there are bibasilar crackles, and the cardiac examination reveals
tachycardia, but a normal rhythm and no murmurs or rubs.
Examination of his joints reveals synovitis in his right wrist, Ieft ankle, and both
knees. A c `.Í ... . ..Í. 1 .. Í . . ;.. 1
`....`.``-..--.....`..```..`-.-`.--.`
Question 1 of 5
:
Which of the following is the most likely cause of this patient's cardiac findings?
/ A. Acute myocardial infarction
/ B. Aortic dissection
/ C. Mitral regurgitation
/ D. Myocarditis
/ E. Wolff-Parkinson-White (WPW) syndrome

Explanation - Q: 2.1 Close

The correct answer is D. The patient has myocarditis, which is an

inflammation of the cardiac muscle. It is most commonly the result of an
infectious process. Signs and symptoms can range from an asymptomatic
state to arrhythmias, heart failure, and death. The patient often has an
antecedent infection, and in this case, he had an exudative pharyngitis.

Acute myocardial infarction (choice A) usually presents with severe

squeezing left-sided chest pain that can radiate down the left arm. Patients
are generally middle-aged, and can have risk factors for cardiac disease such
as hypertension, diabetes, hypercholesterolemia, or a history of tobacco use.
The electrocardiogram can vary from nonspecific T wave changes to ST
segment elevation.

Aortic dissection (choice B) would 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, or hypertension, which is often a
predisposing factor. Patients can also have unequal pulses in their
extremities, if the dissection affects one of the major arteries branching off the
aortic arch.

Mitral regurgitation (choice C) is a result of mitral valve insufficiency, in which

there is a regurgitant flow of blood across the mitral valve, from the left
ventricle, into the left atrium, during systole. It is often due to rheumatic heart
disease, but can also result from mitral valve prolapse, or papillary muscle
rupture. Physical examination should reveal a holosystolic murmur, heard
best at the apex.

Wolff-Parkinson-White (WPW) syndrome (choice E) is a ventricular

preexcitation syndrome associated with an atrioventricular bypass track.
Patients often have paroxysmal tachycardias, and an electrocardiogram will
often reveal a shortened PR interval, a delta wave, and a wide QRS complex.
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Question 2 of 5
What underlying condition can explain the patient's upper respiratory as well as
cardiac and joint signs and symptoms?
/ A. Acute rheumatic fever
/ B. Budd-Chiari syndrome
/ C. Ebstein's anomaly
/ D. Sjögren syndrome
/ E. Takayasu arteritis

Explanation - Q: 2.2 Close

The correct answer is A. Acute rheumatic fever is an inflammatory disorder

that affects multiple systems. There are five major criteria for rheumatic fever:
carditis, migratory polyarthritis, subcutaneous nodules, Sydenham chorea,
and erythema marginatum. There are also minor criteria: fever, arthralgia,
elevated acute phase reactants, and a prolonged PR interval.

Budd-Chiari syndrome (choice B) is an occlusion of the major hepatic veins,

which leads to congestive liver disease. Patients often have abdominal pain,
jaundice, and hepatomegaly.

Ebstein's anomaly (choice C) is due to an anomalous attachment of the

tricuspid leaflets, and results in downward displacement of the tricuspid valve
into the right ventricle. This results in tricuspid regurgitation. Symptoms can
vary from cyanosis to arrhythmias.

Sjögren syndrome (choice D) is an autoimmune disorder characterized by

 inflammatory changes in glands, producing dry eyes and dry mouth.

Takayasu arteritis (choice E) is a vasculitis syndrome that affects medium to

large arteries, in particular, the aortic arch and its branches. It is also known
as "pulseless disease" because patients have weak or absent pulses in their
upper extremities. It primarily affects young Asian females.

Question 3 of 5
Which of the following test results would help confirm the most likely diagnosis?
/ A. EIevated antinuclear antibody
/ B. Low anti-deoxyribonuclease B titer
/ C. Low anti-hyaluronidase titer
/ D. Low anti-streptolysin O titer
/ E. Throat culture positive for group A streptococci

Explanation - Q: 2.3 Close

The correct answer is E. To meet criteria for the diagnosis of rheumatic

fever, patients must have either two major, or 1 major and 2 minor criteria,
plus evidence of an antecedent streptococcal infection. A throat culture
positive for group A streptococci would fulfill the criteria in the presence of
myocarditis and migratory polyarthritis.

Elevated antinuclear antibody (choice A) is not associated with rheumatic

fever. In the appropriate clinical setting, it is helpful in the diagnosis of
rheumatologic disorders such as systemic lupus erythematous.

Anti-streptolysin O (choice D), anti-deoxyribonuclease B (choice B), and

anti-hyaluronidase (choice C) are all streptococcal antibody tests. In the
setting of rheumatic fever associated with a recent group A streptococcal
infection, the titers for these antibody tests would be elevated (in the absence
of infection, they may actually be undetectable). A significant titer of any of
these antibody tests would meet criteria for the documentation of an
antecedent streptococcal infection.
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Question 4 of 5
A biopsy of the affected cardiac tissue would most likely show which of the
following?
/ A. Angiosarcoma
/ B. Aschoff body
/ C. Atheromas
/ D. Hyperplastic arteriolosclerosis
/ E. Libman-Sacks lesions
Explanation - Q: 2.4 Close
 The correct answer is B. The Aschoff body is the classic lesion of rheumatic
fever. It is an area of focal interstitial myocardial inflammation. It is
characterized by large cells, known as Anitschkow myocytes, and Aschoff
cells, which are multinucleated giant cells.

Angiosarcoma (choice A), a rare malignant tumor affecting the vascular

tissue, can occur in the skin, breast, liver, or musculoskeletal system.

Atheromas (choice C) are fibrous plaques within the intima of arteries. They
are a finding of atherosclerosis.

Hyperplastic arteriolosclerosis (choice D) is characterized by concentric,

laminated thickening of arteriolar walls. It often occurs in the kidneys, and
may lead to malignant nephrosclerosis.

Libman-Sacks lesions (choice E) are small vegetations that occur on valvular

heart tissue. They can occur on either side of the valve, and are associated
with endocarditis in systemic lupus erythematous.
uest|on 0
The patient continues to deteriorate, he develops worsening heart failure, and
requires transfer to the intensive care unit for use of an
inotropic agent to increase his cardiac output. Which of the following agents
would most likely be used?
/ A. Benazepril
/ B. Diltiazem
/ C. Dobutamine
/ D. Metoprolol
/ E. Phenylephrine
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Explanation - Q: 2.5 Close

The correct answer is C. Dobutamine is a positive inotropic agent used in

severe cases of heart failure that require inotropic support.

Benazepril (choice A) is an angiotensin converting enzyme inhibitor.

Medications in this class can be used in heart failure to decrease afterload,
but they do not have any direct affect on cardiac tissue.

Diltiazem (choice B) and metoprolol (choice D) are both negative inotropic

agents. When used in the setting of acute heart failure, the patient's course
can worsen, although beta blockers such as metoprolol and carvedilol (mixed
alpha and beta blocker) are sometimes cautiously used in some patients with
CHF.

Phenylephrine (choice E) is an alpha-receptor agonist. It causes

 vasoconstriction, and is used in severe cases of hypotension.

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A 78-year-old man had been previously active, but found that his health was
declining. Over a four-month period, his ability to perform even
very minimal exercise, such as walking around his yard, declined precipitously.
The family took him from doctor to doctor, none of whom were
initially able to figure out what was wrong with him. Because of the patient's age,
most of the physicians that the family consulted were
unwilling to do much other than to listen to the family's story and then run a few
screening tests. In some ways, he acted as if he were in
congestive heart failure, but he initially had no evidence of fluid overload and his
lungs were clear. The cardiac profile on chest X-ray was
slightly enlarged. His ECG studies were interpreted as within the normal range
for his age. Angiography studies showed no evidence of
significant coronary artery occlusion. Pulmonary function studies were
unrevealing.
Question 1 of 6
Following a Thanksgiving meaI, the patient's condition worsened markedly over
the next few hours, and he was taken to an emergency
department. At that point, the patient was in obvious, severe, congestive heart
failure with evidence of fluid overload and pulmonary edema.
Intravenous furosemide was started, which over the next few hours markedly
improved his clinical condition. Furosemide is classified as
which of the following?
/ A. Carbonic anhydrase inhibitor
/ B. Loop diuretic
/ C. Osmotic diuretic
/ D. Potassium-sparing diuretic
/ E. Thiazide diuretic

Explanation - Q: 3.1 Close

The correct answer is B. Large, salty, holiday meals are notorious for
setting off (potentially fatal) exacerbations of what might have been previously
mild congestive failure. There are a number of drugs with diuretic activity that
can increase the amount of urine that is produced. Pharmacologists
subclassify these drugs based on the mechanisms by which they act.
Furosemide is a diuretic that is commonly used in the hospital setting in
intravenous form to rapidly reduce the degree of fluid overload present in a
patient in severe congestive heart failure. This diuretic acts by inhibiting the
Na/K/2Cl cotransporter on the luminal membrane of the thick ascending
portion of the loop of Henle. It is consequently classified as a loop diuretic, as
is ethacrynic acid, which has a similar mechanism of action.
 Carbonic anhydrase inhibitors (choice A), such as acetazolamide and
dorzolamide, act on the proximal convoluted tubule to reduce Na+ resorption
secondary to an inhibition of CO2 formation with resulting decreased
intracellular bicarbonate and H+ levels.

Osmotic diuretics (choice C), such as mannitol, inhibit water reabsorption

throughout the nephron.

Potassium-sparing diuretics (choice D), such as spironolactone, amiloride,

and triamterene, act at the level of the collecting tubules and ducts by acting
as aldosterone receptor antagonists.

Thiazide diuretics (choice E), such as hydrochlorothiazide, indapamide, and

metolazone, inhibit the Na/Cl cotransporter in the distal convoluted tubule.
Question 2 of 6
The patient is seen the following morning by a cardiologist. The cardiologist does
a very careful physical examination. He notes that the heart
sounds appear distant. He then has the patient lie at an angle of 30 to 45
degrees, and does a careful examination of the right jugular pulse,
which he finds very worrisome. The pulse is both very elevated and shows
dramatic x and y descents. Further, he notes that the venous
distention paradoxically increases during inspiration. This last finding is
sometimes called which of the following?
/ A. Chvostek's sign
/ B. Corrigan's sign
/ C. Homans' sign
/ D. KussmauI's sign
/ E. Murphy's sign
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Explanation - Q: 3.2 Close

The correct answer is D. The sign described is Kussmaul's sign. The act of
inflating the lungs during inspiration lowers the pressure in the chest while
increasing that in the abdomen, drawing blood from the abdomen into the
chest (and increased abdominal pressure helps to directly drive blood toward
the chest). If the right atrium cannot fill, then the jugular venous pressure
rises paradoxically (not so much from blood flow from the head as from the
abdomen, because the inferior vena cava and superior vena cava are
functionally connected through the right atrium). Kussmaul's sign is seen in
patients who have non-compliant right ventricles. It can also be seen in
patients with severe ascites (which increases the intra-abdominal pressure).
This case illustrates the importance of considering the jugular venous pulse
as well as the arterial pulse, since the cardiologist was able to find a number
of significant findings pertaining to the jugular venous pulse, which other
physicians had missed. The jugular venous pressure can be used at the
 bedside to estimate the right atrial filling pressure. The jugular venous
pressure is estimated by measuring the height of the visible venous pulse
above the sternal angle, and then adding 5 cm (corresponding to how far
below the sternum the right atrium is located). The jugular venous waveform
has an A wave, which is followed by an X descent, then a V wave, and finally
a Y descent. The A wave (first rise in pressure) reflects the right atrial
contraction, while the X-descent reflects right atrial diastole, and then early
right ventricular systole. The V wave is the second major positive wave, and
reflects continued venous inflow into the right atrium in opposition to a closed
mitral valve. The following Y-descent is the negative deflection that occurs
when the tricuspid valve opens in early diastole.

Chvostek's sign (choice A) is seen in tetany, and is a facial muscle spasm

occurring when the facial nerve is tapped anterior to the external auditory
meatus.

Corrigan's sign (choice B), which suggests aortic regurgitation, is a full, hard
arterial pulse, which is followed by a sudden collapse.

Homans' sign (choice C) is pain at the back of the knee or calf when the
ankle is dorsiflexed, and suggests venous thrombosis of the leg.

Murphy's sign (choice E) is pain on palpation of the right subcostal area

during inspiration, and is frequently seen in acute cholecystitis.
Question 3 of 6
This patient most likely has which of the following?
/ A. Acute myocarditis
/ B. Congestive cardiomyopathy
/ C. OId left ventricle myocardial infarction
/ D. Recent left ventricle myocardial infarction
/ E. Restrictive cardiomyopathy
Explanation - Q: 3.3 Close

The correct answer is E. The "distant" heart sounds and jugular venous
pulse findings both suggest that this patient has restrictive cardiomyopathy
that is limiting the heart's ability to fill during diastole and is also impairing
ventricular contraction. Other findings that may be encountered on physical
examination in patients with restrictive cardiomyopathy include S3 and/or S4
heart sounds, occasional mitral or tricuspid regurgitation murmurs, and, if the
patient is in secondary congestive failure, peripheral edema and pulmonary
rales. Restrictive cardiomyopathy is relatively rare and the findings on
physical examination are subtle, and consequently this patient's history of
missed diagnosis is unfortunately not all that uncommon. Underlying causes
of restrictive cardiomyopathy include endomyocardial fibrosis, Loeffler
eosinophilic endomyocardial disease, hemochromatosis, amyloidosis,
sarcoidosis, scleroderma, carcinoid heart disease, and glycogen storage
 disease. Patients typically present at an advanced stage of the disease, and
may have symptoms of angina, shortness of breath, peripheral edema, and
ascites with abdominal discomfort (related to pooling of blood in the liver and
other abdominal organs). Once the diagnosis is suspected, echocardiography
typically demonstrates normal to symmetrically thickened heart chamber
walls with rapid early-diastolic filling and slow late-diastolic filling (the cardiac
chambers are acting more or less like poorly distensible plastic bags).
Cardiac catheterization will more or less repeat the observations seen in the
analysis of the jugular venous pulse, typically showing elevated ventricular
end-diastolic pressure, normal to slightly decreased ejection fraction, and
prominent x and y descents.

Acute myocarditis (choice A) can cause congestive cardiomyopathy (choice

B), but the heart is usually larger and the constrictive findings seen in this
case would not be present.

While recent and old myocardial infarctions affecting the right ventricle may
produce similar jugular venous findings to those seen in this case, left
ventricular infarction (choices C and D) would not impair right ventricular
filling and contraction.

Question 4 of 6
An endomyocardial biopsy is performed, which demonstrates eosinophilic
acellular deposits within the myocardial biopsy. When recut,
histological sections are stained with Congo red and viewed under polarized
light, and the deposits appear bright green. These deposits are
most likely to be composed of which of the following?
/ A. Amyloid
/ B. Fibrin
/ C. Hemosiderin
/ D. Melanin
/ E. Uric acid
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Explanation - Q: 3.4 Close

The correct answer is A. Amyloid deposits are suspected when hematoxylin

and eosin-stained histological sections show extracellular eosinophilic
deposits. The presence of amyloidosis is confirmed when the characteristic
"apple-green birefringence" on Congo red stain is demonstrated.

Fibrin deposits (choice B) are also red on hematoxylin and eosin stain, but
show no fluorescence with Congo red stain.

Hemosiderin (choice C) causes yellow brown deposits; melanin (choice D)

causes brown-black deposits; and uric acid (choice E) causes yellow
crystalline deposits.
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Question 5 of 6
Which of the following features of proteins is most likely responsible for the bright
green appearance of the Congo red-stained materiaI?
/ A. Beta pleated sheet configuration
/ B. Calcium binding
/ C. Iron containing heme moiety
/ D. Multiple alpha helices
/ E. Presence of multiple subunits

Explanation - Q: 3.5 Close

The correct answer A. It was originally assumed by biochemists that

amyloid was always composed of the same material. It came as something of
a shock when antibody techniques were developed that demonstrated that
the antigenicity of amyloid in different clinical settings varied markedly. The
common feature these proteins shared that accounted for both the affinity for
Congo red and their characteristic regular fibrillar structure on electron
microscopy turned out to be that the proteins all have a beta pleated sheet
tertiary (secondary according to some biochemical purists) configuration, best
demonstrated by X-ray diffraction.

Selective or non-selective binding to calcium (choice B) is common in

proteins.

Heme moieties containing iron (choice C) are a part of myoglobin and

hemoglobin.

Alpha helices (choice D) are a common secondary structure in proteins, but

do not contribute to the protein forming amyloid.

The presence of multiple subunits (choice E) is also common in proteins, but

does not contribute to a protein forming amyloid.
Question 6 of 6
Which of the following would most likely be found in the Congo red-stained
extracellular deposits with the bright green appearance under
polarized light?
/ A. Amyloid AA
/ B. Beta-2-microglobulin
/ C. Beta protein precursor
/ D. Immunoglobulin light chains
/ E. Transthyretin

Explanation - Q: 3.6 Close

The correct answer is D. Amyloidosis occurs in a large variety of forms.

Primary amyloidosis is one of the more common forms of systemic
 amyloidosis, and can affect a variety of organs, including the heart, kidney,
peripheral nerve, gastrointestinal tract, and respiratory tract. In primary
amyloidosis, the amyloid is composed of immunoglobulin light chains, and the
disease is now interpreted as a plasma cell disorder closely related to
multiple myeloma. This interpretation is clinically significant, as it has led to
modern treatments of primary amyloidosis (which formerly had a dismal
prognosis) with the chemotherapies designed for multiple myeloma. The
treatments are affective only if the disease is recognized and passed to the
appropriate specialists as early as possible in the clinical course.

Amyloid AA (choice A) is seen in inflammation-associated amyloidosis and

familial Mediterranean fever.

Beta-2-microglobulin (choice B) comprises the amyloid of dialysis-associated

amyloidosis.

Beta protein precursor (choice C) comprises the amyloid seen in the brains
of patients with Alzheimer's disease and Down syndrome.

Transthyretin (choice E) comprises the amyloid seen in familial amyloidosis

and senile cardiac amyloidosis.

A 40-year-old man presents to the emergency department complaining of severe

shortness of breath. The breathlessness has been
worsening over the past few years, and the patient reports growing tachypneic
with mild exertion, and sometimes even at night. On
examination, he has generalized edema, jugular venous distention, and hepatic
distention. Cardiac examination shows a right ventricular
heave, a right-sided S3, and S4 with a pulmonary ejection click. A chest x-ray
film shows cardiomegaly and widening of the hilar vessels,
including the pulmonary arteries. An electrocardiogram shows talI, peaked P
waves in leads lI, III, and aVF, right axis deviation, and right
ventricular hypertrophy.
Question 1 of 5
Which of the following is the most likely diagnosis?
/ A. Cor pulmonale
/ B. Hypertrophic cardiomyopathy
/ C. Left ventricular failure
/ D. Myocardial infarction
/ E. Pulmonary embolus (acute)
Explanation - Q: 4.1 Close

The correct answer is A. This patient has cor pulmonale, which is defined
as enlargement of the right ventricle secondary to diseases of the lung,
thorax, or pulmonary circulation. In this case, it is chronic, given the duration
of the patient's symptoms and the presence of many clinical sequelae of the
 condition: edema, jugular venous distention, hepatic distention, and right
ventricular heave. The electrocardiogram also supports the diagnosis of
enlargement of the right ventricle showing right axis deviation due to the
increase in the mass of the right heart. Evidence of right atrial enlargement is
also present, i.e., the tall peaked P waves in leads II, III, and aVF (P
pulmonale).

Hypertrophic cardiomyopathy (choice B) is an anomaly in which the

myocardium hypertrophies. The fibers are erratic and conduction
abnormalities and outflow obstruction may result. Typically, this disorder
presents in the second decade of life, and will manifest as dysrhythmia and/or
shortness of breath. In addition, a right axis deviation would be inconsistent
with this cardiomyopathy because the left ventricle hypertrophies, as well as
the right. Thus, this diagnosis is unlikely.

Left ventricular failure (choice C) often accompanies right ventricular failure,

but in this case, the right-sided symptoms, such as systemic edema, jugular
venous distention, and hepatic congestion, are more pronounced. Left-sided
failure shows engorgement of the entire pulmonary tree in conjunction with
pulmonary edema.

Myocardial infarction (choice D) is unlikely. The ECG findings are not

consistent with the pattern typically seen in MI. In addition, this patient does
not suffer from the symptoms of myocardial infarction, such as chest pain,
pressure, jaw numbness, and diaphoresis.

Pulmonary embolus (choice E) may cause acute right heart strain and
failure, but this patient has a chronic condition. Chronic emboli may produce
increased resistance in the pulmonary tree and a picture similar to this.

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Question 2 of 5
Pulmonary hypertension is suspected in the patient, and a Swan-Ganz catheter
is placed. Which of the following denotes the correct
anatomic sequence of vessels that would be traversed by the catheter if it was
introduced into the left subclavian vein?
/ A. Left subclavian vein, Ieft brachiocephalic vein, superior vena cava, right
atrium, right ventricle, pulmonary artery
/ B. Left subclavian vein, Ieft common carotid, superior vena cava, right atrium,
right ventricle, pulmonary artery
/ C. Left subclavian vein, Ieft jugular vein, Ieft atrium, Ieft ventricle, aorta
/ D. Left subclavian vein, Ieft jugular vein, superior vena cava, right atrium, right
ventricle, pulmonary artery
/ E. Left subclavian vein, superior vena cava, right atrium, right ventricle,
pulmonary artery
 Explanation - Q: 4.2 Close

The correct answer is A. The correct sequence for a catheter inserted into
the left subclavian vein is as follows: left subclavian vein, left brachiocephalic
vein, superior vena cava, right atrium, right ventricle, pulmonary artery. With
this catheter in place, a variety of cardiac parameters can be measured,
including pressures in the pulmonary artery. Thus, this catheter can aid in
establishing the diagnosis of pulmonary hypertension.

Calcium channel blockers can be used in this setting to decrease pulmonary

vascular resistance. Which of the following is the calcium
channel blocker that will have the most predominant effect on vascular smooth
muscle?
/ A. Diltiazem
/ B. Hydrochlorothiazide
/ C. Nifedipine
/ D. Pseudoephedrine
/ E. Verapamil

Explanation - Q: 4.3 Close

The correct answer is C. The calcium channel blockers vary in the

propensity to affect vascular smooth muscle versus their effect on cardiac
muscle. Thus, in this case, it is important to select an agent that has
maximum ability to relax the smooth muscle in the pulmonary vessels. The
effect on smooth muscle is as follows: nifedipine>diltiazem (choice A)
>verapamil (choice E). The effect on cardiac muscle is as follows:
verapamil>diltiazem>nifedipine. Thus nifedipine is the agent of choice.

Hydrochlorothiazide (choice B) is a diuretic, and thus would have no effect

on the vascular smooth muscle.

Pseudoephedrine (choice D) is an alpha agonist, and therefore would cause

vasoconstriction.

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Question 4 of 5
Which of the following physiologic stimuli will result in decreased pulmonary
vascular resistance?
/ A. Decreased cardiac output
/ B. Increased cardiac output
/ C. Low O2 tension
/ D. Lung volumes near residual volume (RV)
/ E. Lung volumes near total lung capacity (TLC)

Explanation - Q: 4.4 Close

The correct answer is B. A unique feature of the pulmonary circulation is

that it maintains itself as a low-pressure system. Many of the mechanisms
that control pulmonary vasculature differ from those of the systemic
circulation. One of these features is that pulmonary vasculature resistance is
decreased in response to increased cardiac output. This is accomplished
through distention of open capillaries and the recruitment of collapsed
capillaries. Thus, the resistance in the pulmonary tree decreases in response
to increased right ventricular output. In the pathologic state of pulmonary
hypertension, in which the resistance is elevated and the ventricle fails, this
decreased cardiac output (choice A) may compound the problem and trigger
increased resistance in spite of the primary elevation.

Low O2 tension (choice C) in the pulmonary vessels initiates

vasoconstriction. In the systemic circulation, low O2 tension initiates
vasodilation.

Lung volume also affects pulmonary vascular resistance. The curve of lung
volume versus pulmonary vascular resistance is U-shaped. This effect is due
to the fact alveolar and extra-alveolar vessels act as resistors in series
(additive), and these vessels have little intrinsic support. Thus, resistance in
these vessels is affected by pleural pressures. At low lung volumes (choice
D), the alveolar vessels are open, but extra-alveolar vessels are compressed.
At high lung volumes (choice E), the alveolar vessels are compressed by
distended alveoli, but the extra-alveolar vessels become distended due to the
increase in transmural pressure. Thus a U-shaped curve describes this
relationship.
Question 5 of 5
Some of the examination findings indicate hepatic congestion. Which of the
following terms is commonly used to identify the macroscopic
pattern of red, depressed hepatic nodules with pale periphery that accompanies
the chronic hepatic congestion seen in this condition?
/ A. Centrilobular hemorrhage
/ B. Cirrhosis
/ C. Fatty change
/ D. Nutmeg liver
/ E. Piecemeal necrosis

Explanation - Q: 4.5 Close

The correct answer is D. Chronic passive congestion of the liver leads to a

macroscopic pattern known as nutmeg liver. This is due to the congestion of
blood in the centrilobular region (dark) with hypoxia and fatty change in the
more peripheral hepatocytes. When viewed macroscopically, this pattern
resembles that seen in a cross section of a nutmeg, hence the name.

In this condition, centrilobular hemorrhage (choice A) usually only occurs in

severe acute ischemia. This patient has a chronic condition, and thus most
likely will have nutmeg liver instead.

Cirrhosis (choice B) of the liver may result from chronic damage caused by
chronic congestion. It however produces a scarred, whitish, shrunken liver,
and not the pattern seen here.

Fatty liver (choice C) would produce a large, smooth yellow liver and would
not resemble the pattern seen here.

Piecemeal necrosis (choice E) is a microscopic finding of scattered

hepatocellular necrosis. This diagnosis cannot be made macroscopically.