A 59-year-old woman with a 10-year history of type 2 diabetes mellitus is noted

by her physician to have bilateral pitting edema of the ankles

and feet. No erythema is noted. On questioning, the patient also reports
shortness of breath on exertion and states that she has been using 3
pillows at night in order to sleep comfortably.
Question 1 of 6
This patient's symptoms are most suggestive of which of the following?
/A. Cellulitis
/B. Congestive heart failure
/C. Gynecologic cancer
/D. Lipedema
/E. Thrombophlebitis

Explanation - Q: 1.1 Close

The correct answer is B. The combination of leg edema and pulmonary edema (as
indicated by shortness of breath and sleeping on multiple pillows) strongly suggests
that the patient has congestive heart failure involving both ventricles. Heart failure is
a pathologic state in which an abnormality of cardiac function leads to failure of the
heart to pump blood throughout the body at a rate sufficient to meet the body's
requirements. Some of the adaptive mechanisms that compensate for the failing
heart include increasing preload (through the Frank-Starling mechanism), myocardial
hypertrophy (to restore elevated ventricular wall stress to within normal limits),
redistribution of cardiac output from non-vital organs to vital organs, and
neurohumoral adjustments. Congestion develops behind the failing ventricle, with left
ventricular failure causing signs and symptoms of pulmonary congestion, and right
ventricular failure causing signs and symptoms of systemic congestion.

Cellulitis (choice A) is usually markedly erythematous.

Gynecologic cancer (choice C) and thrombophlebitis (choice E) are causes of

unilateral leg edema.

Lipedema (choice D) is not a true edema (and would not show pitting), but is instead
the deposition of fatty tissues around the ankles of obese individuals.

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Question 2 of 6
A chest x-ray film demonstrates pulmonary venous congestion and interstitial
edema indicative of pulmonary edema. Which of the following
physiologic mechanisms is most likely the immediate cause of the pulmonary
edema?
/A. Damage to endothelial cells
/B. Damage to the epithelial lining of the alveoli
/C. EIevated pulmonary capillary pressure
/D. Low serum albumin
/E. Poor lymphatic drainage of fluid

Explanation - Q: 1.2 Close

The correct answer is C. The cause of pulmonary edema in congestive

heart failure is an increase in the hydrostatic pressure at the level of the
capillaries of the lung. This increased pressure serves to drive fluid out of the
capillaries and into the alveoli. The other reasons cited in the choices can
also cause pulmonary edema, but occur in other clinical settings.

Damage to endothelial cells (choice A) can occur in vasculitis.

Damage to the epithelial lining of the alveoli (choice B) can occur in

pneumonia and respiratory distress syndrome.

Low serum albumin (choice D) can be seen in liver and kidney disease.

Poor lymphatic drainage (choice E) can be seen in lungs with chronic

damage due to severe emphysema or fibrosis.

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Question 3 of 6
A chest x-ray film additionally demonstrates a markedly enlarged cardiac shadow
with dilation of both the right and left ventricles.
Echocardiography shows dilated, hypokinetic ventricles. The physician
prescribes several medications, including captopriI. Which of the
following best characterizes captopriI?
/A. ACE inhibitor
/B. AIpha blocker
/C. Beta blocker
/D. Diuretic
/E. Positive inotrope

Explanation - Q: 1.3 Close

The correct answer is A. ACE inhibitors, including captopril, enalapril, and

lisinopril, are becoming mainstays in the treatment of congestive heart failure,
more formally known as dilated congestive cardiomyopathy. These agents
inhibit the conversion of angiotensin I to angiotensin II, thereby interrupting
the renin-angiotensin-aldosterone loop. The functional result is vasodilation,
with a reduction in both cardiac afterload and cardiac preload. Furthermore,
the ACE inhibitors, such as captopril and enalapril, are proven to delay the
progression of this condition by protecting the ventricles from deleterious
remodeling.

Alpha-blockers (choice B) are not commonly used in CHF, although

carvedilol has some alpha-blocking activity.

Carvedilol is a non-cardioselective alpha- and beta-blocker (choice C)

approved by the FDA for the treatment of both ischemic and non-ischemic
heart failure; its alpha blocking effects confer vasodilatory activity.
Catecholamine production is enhanced in the early development of CHF to
compensate for decreasing cardiac output. Beta-blockers are beneficial in
heart failure, since they diminish the chronic sympathetic nervous system
stimulation; they may also be beneficial through the following mechanisms:
improving cardiac output, increasing diastolic filling time, and decreasing
arrhythmias.

Loop diuretics (choice D), such as bumetanide and furosemide, are also
considered to be first-line agents in the treatment of heart failure. These
agents are indicated for the treatment of edema associated with CHF, hepatic
cirrhosis, and renal disease, as well as treatment of hypertension (furosemide
and torsemide).

Digoxin (choice E) causes a positive inotropic effect by inhibiting the Na +/K+

ATPase in cardiac cell membranes. This inhibition leads to increased
intracellular sodium, which alters the driving force for the Na +/Ca2+ exchange
mechanism, leading to a decrease of calcium removal from the cell. This
results in increased calcium storage in the sarcoplasmic reticulum, which
when released, increases contractile force. Digitalis also modifies autonomic
outflow.

Question 4 of 6
An increase in which of the following is the most likely explanation for the edema
in her legs?
/A. Interstitial colloid osmotic pressure
/B. Lymph flow
/C. PIasma colloid osmotic pressure
/D. Right atrial pressure
/ E. Stroke volume
Explanation - Q: 1.4 Close

The correct answer is D. Right atrial pressure rises in congestive heart

failure, which elevates venous pressure throughout the body. This increase in
venous pressure can cause excessive fluid loss from the microcirculation and
the development of peripheral edema.

Fluid loss from the capillaries washes protein molecules from the interstitial
compartment and thereby decreases interstitial colloid osmotic pressure
(choice A).

Increased lymph flow (choice B) is a consequence rather than a cause of the

edema.

Increased plasma colloid osmotic pressure (choice C) would tend to

decrease the development of edema.

Stroke volume (choice E) has no effect on the formation of peripheral edema.

Question 5 of 6

As this patient's condition progresses, she is started on digoxin. Her most recent
digoxin blood level was 2.0 ng/mL. She will be at the highest
risk for developing digoxin toxicity if she has which of the following conditions?
/A. Hypokalemia
/B. Hyponatremia
/C. Hypophosphatemia
/D. Vitamin B12 deficiency
/E. Vitamin K deficiency

Explanation - Q: 1.5 Close

The correct answer is A. Digoxin is a cardiac glycoside indicated for the

treatment of congestive heart failure, atrial fibrillation, and atrial flutter. The
therapeutic drug serum levels for digoxin are 0.5 to 2.2 ng/mL. Toxicity
typically occurs when digoxin levels are > 2.5 ng/mL, unless the patient is
hypokalemic, then toxicity can occur at any therapeutic concentration.
Hypokalemia sensitizes the myocardium to digoxin and may reduce the
positive inotropic effects of the medication. Other signs and symptoms of
digoxin toxicity include nausea, vomiting, anorexia, and appearance of
yellow-green halos in the visual field, as well as the development of cardiac
arrhythmias.
 Although hyponatremia (choice B) and hypophosphatemia (choice C) can
result in the development of other pathological disturbances, they do not
potentiate digoxin toxicity.

Vitamin B12 deficiency (choice D) is associated with the development of

pernicious anemia.

Vitamin K deficiency (choice E) is associated with the development of clotting

disorders. Furthermore, vitamin K deficiency is known to potentiate warfarin
toxicity.
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Question 6 of 6
This patient's condition is associated with which of the following 5-year mortality
rates?
/A. 5%
/B. 30%
/C. 50%
/D. 70%
/E. 95%

Explanation - Q: 1.6 Close

The correct answer is D. In temperate zones, dilated congestive

cardiomyopathy is most commonly the result of diffuse coronary artery
disease with diffuse ischemic myopathy, which produces chronic myocardial
fibrosis with diffuse loss of myocytes. Other causes are very diverse and can
include a wide variety of infections, granulomatous disease, metabolic
disorders, drugs and toxins, cancers, connective tissue disorders, familial
neuromuscular disorders, and pregnancy. The dilated chambers usually
function poorly, leading to a low ejection fraction. Tachycardia and increased
end-diastolic volume initially maintain cardiac output, but often eventually fail
with disease progression to adequately supply the tissues with oxygenated
blood. Overall, dilated congestive cardiomyopathy is more often fatal than
many cancers, with a 5-year mortality rate of 70%.

A 55-year-old woman consults a physician because of edema involving her lower

legs. While both of her ankles are swollen, the left one is
much more swollen than the right. Physical examination additionally
demonstrates a swollen, tender, bluish, cord-Iike structure immediately
below the skin on her left lower leg extending from her ankle to near her knee.
Edema at sites other than the ankles is not apparent on physical
examination. The patient has not been having any other symptoms. The woman
works as a nurse and had a long airplane trip during the
previous week.
Question 1 of 5
The tender cord-Iike structure is most likely which of the following?
/A. Artery
/B. Ligament
/C. Lymphatic channel
/D. Tendon
/E. Vein

Explanation - Q: 2.1 Close

The correct answer is E. The structure is most likely an inflamed vein. Large
superficial veins are common on the legs.

The superficial arteries (choice A) of the legs are usually much less apparent
and located deeper than are the veins.

Ligaments (choice B) attach bone to bone, and can be palpated, but not
usually seen, in the feet and at the knee.

Lymphatic channels (choice C) are usually invisible on surface examination,

unless they are markedly inflamed and accompanied by skin erythema. Then
they appear as red lines.

Tendons (choice D) also produce cord-like structures, but they are pale in
color and do not appear blue through the skin.
A 55-year-old woman consults a physician because of edema involving her lower
legs. While both of her ankles are swollen, the left one is
much more swollen than the right. Physical examination additionally
demonstrates a swollen, tender, bluish, cord-Iike structure immediately
below the skin on her left lower leg extending from her ankle to near her knee.
Edema at sites other than the ankles is not apparent on physical
examination. The patient has not been having any other symptoms. The woman
works as a nurse and had a long airplane trip during the
previous week.
Question 2 of 5

Which of the following is the most likely cause of the increased edema in the
patient's left lower leg?
/A. Congestive heart failure
/B. Lymphatic obstruction
/C. Pulmonary failure
/D. Renal failure
/E. Venous obstruction

Explanation - Q: 2.2 Close

 The correct answer is E. While on paper, leg edema can have a very large
number of potential causes, an acute exacerbation of leg edema limited to
one leg and accompanied by an obviously damaged vein should make you
think of superficial thrombophlebitis. This condition occurs when thrombosis
of a vein induces an accompanying inflammation of the vein (which
essentially always happens). Superficial thrombophlebitis that occurs in
previously healthy legs does not always induce ankle edema because the
venous return via other routes is usually adequate. However, exacerbation of
ankle edema can, as in this case, be the presenting complaint if a patient's
legs are already damaged. In this case, the working history of being a nurse
implies that the patient may have a history of long periods of walking and
standing, which may lead to dependent edema in the ankles. Superimposed
on this is a recent history of a long airline flight, which can act as a trigger for
thrombophlebitis secondary to the prolonged immobilization experienced on
the flight.

Congestive heart failure (choice A) and renal failure (choice D) would

produce bilateral ankle edema, and possibly edema visible in other sites.

Lymphatic obstruction (choice B) can also produce localized edema, but this
woman has an obviously inflamed vein, and that is the more likely cause.

Pulmonary failure (choice C), unless due to pulmonary edema secondary to

congestive heart failure, would be unlikely to be associated with ankle edema.

Question 3 of 5
Which of the following is the most serious complication of this condition?
/A. Focal arterial obstruction
/B. Involvement of deep leg veins
/C. Obstruction of a joint space
/D. Rupture of an involved tendon
/E. Secondary lymphangiosarcoma

Explanation - Q: 2.3 Close

The correct answer is B. Superficial thrombophlebitis often resolves

spontaneously without sequelae, but should always be taken very seriously
because the same patients who develop superficial thrombophlebitis may
either have an extension of the clot into the deep veins (with increased risk of
potentially fatal pulmonary embolism) or may develop a separate deep
venous clot concurrently or at a later date. In hospitalized patients with
superficial thrombophlebitis, it is thought that as many as 10% eventually
develop pulmonary embolus (typically from an undiagnosed or later deep vein
thrombosis), and of this subset of patients with pulmonary embolus, 20% die.

The artery (choice A), joint space (choice C), and tendons (choice D) are
 not directly involved by this disease process.

Lymphangiosarcoma (choice E) is a rare complication of chronic lymphatic

obstruction.

Question 4 of 5
Which of the following techniques is most useful for initial evaluation of the
presence of this complication?
/A. Computed tomography
/B. D-dimer levels in serum
/C. Duplex ultrasonography
/D. Magnetic resonance imaging
/E. Prothrombin time

Explanation - Q: 2.4 Close

The correct answer is C. The accurate diagnosis of deep vein thromboses is

a problematic area of medicine, because no completely reliable diagnostic
technique is easily available. Various techniques of physical diagnosis have
been proposed, but can be misleading in most people's hands, and leave an
erroneous impression that the patient does not have deep vein involvement
when it is actually present. Both Duplex ultrasound (a combination of real-
time and Doppler ultrasound techniques) and plethysmography (using volume
and pressure changes to look at venous filling) can be used to diagnose deep
vein thromboses, and are often used in conjunction as they tend to miss and
pick up slightly different cases.

Computed tomography (choice A) and magnetic resonance venography

(choice D) can also be used, but are very expensive and not warranted in
most cases.

Serum indicators of clotting problems, such as D-dimers (choice B) and

prothrombin time (choice E) are too nonspecific to be helpful in diagnosing
deep vein thrombosis.

Question 5 of 5
Following the appropriate studies, which demonstrated the most serious
complication of this condition, the decision is made to anticoagulate
the patient. Which of the following is the most appropriate initial choice of
medications?
/A. Intravenous Coumadin
/B. Intravenous heparin
/C. Oral aspirin
/D. OraI Coumadin
/E. Oral heparin

Explanation - Q: 2.5 Close

The correct answer is B. A patient with a known deep venous thrombosis is

usually initially anticoagulated with intravenous heparin, then switched over
the next days to weeks to oral Coumadin (choice D). These patients may
also be treated with fibrinolytic agents, particularly if the deep vein clot is
extending or has recently developed.

Heparin is not available orally (choice E), and Coumadin is not usually given
intravenously (choice A).

Aspirin (choice C) is not effective in preventing venous clots (which are

triggered predominantly by stasis).

A fifty-year-old alcoholic man presents to the emergency department complaining

of shortness of breath and ankle swelling. He has a history of
intravenous drug use and had a previous episode of upper GI bleeding. On
examination, he is a malnourished man in mild distress. His sclera
are icteric, and his abdomen is distended. He has moderate pretibial edema, and
his mentation is slightly impaired. Laboratory studies show
a conjugated hyperbilirubinemia.
Question 1 of 5
Which of the following is the most likely diagnosis?
/A. Choledocholithiasis
/B. Congestive heart failure
/C. Hemolytic anemia
/D. Hepatic cirrhosis
/E. Renal failure

Explanation - Q: 3.1 Close

The correct answer is D. This patient's constellation of symptoms and signs

can be explained by cirrhosis of the liver with portal hypertension. His
shortness of breath and distended abdomen are a product of ascites from
portal hypertension and liver cirrhosis. As ascites fluid accumulates, intra-
abdominal pressure increases. This can lead to decreased diaphragmatic
excursion, atelectasis, and shortness of breath. His history of GI bleeding
suggests varices, which are a result of portal hypertension. The jaundice
 results from decreased flow of bile out of the cirrhotic liver. His altered
mentation is from the liver's decreased ability to detoxify nitrogenous
metabolites.

Choledocholithiasis (choice A), or stones in the common bile duct, can cause
a conjugated hyperbilirubinemia, but it is typically accompanied by severe
right upper quadrant pain and it does not cause ascites.

Congestive heart failure (choice B) would cause edema and shortness of

breath, but it would not cause jaundice. Severe heart failure (especially right
heart failure) can cause hepatic congestion, and mild ascites, but given the
patient's history and symptoms, the CHF diagnosis can be excluded.

Hemolytic anemia (choice C) causes an unconjugated hyperbilirubinemia.

Hemolysis liberates free heme, which is a precursor to bilirubin. The rate of
production of bilirubin from this heme exceeds the liver's conjugating capacity
and unconjugated hyperbilirubinemia with jaundice results. It does not
produce ascites.

The patient's edema could be the result of renal failure (choice E), but renal
failure would fail to explain the rest of his symptoms. Renal failure does not
cause jaundice or GI bleeding.
Question 2 of 5
A serum analysis is performed and it is found that the patient is infected with
Hepatitis C. Which of the following best describes the Hepatitis C
virus?
/A. FIavivirus
/B. Picornavirus
/C. Poxvirus
/D. Reovirus
/E. Rhinovirus

Explanation - Q: 3.2 Close

The correct answer is A. The hepatitis C virus is a Flavivirus-like organism.

It is less likely than hepatitis B to cause a fulminant infection, but it is more
likely to cause a chronic infection. 60-90% of cases become chronic, and
ultimately 40% progress to cirrhosis. The synergy of hepatitis C and alcohol is
particularly damaging, and this certainly contributed to this patient's
pathology.

The picornavirus is a small RNA virus ( "pico" + RNA) (choice B). The most
well known virus in this group causes polio.

Poxviruses (choice C) do not cause hepatitis. They are known to cause

 molluscum contagiosum and smallpox.

The reovirus (choice D) family consists of two distinct classes of virus; the
rotavirus and the enteric calicivirus. Rotavirus can cause diarrheal illness,
particularly in children. The enteric caliciviruses cause gastroenteritis in adults
and children. Neither causes hepatitis C.

Rhinoviruses (choice E) are a cause of " the common cold."

Question 3 of 5

Which of the following best describes the pathophysiology underlying this

patient's distended abdomen?
/A. Decreased intra-abdominal pressure, decreased plasma oncotic pressure
/B. Decreased portal hydrostatic pressure, decreased plasma oncotic pressure
/C. Decreased portal hydrostatic pressure, increased plasma oncotic pressure
/D. Increased portal hydrostatic pressure, decreased plasma oncotic pressure
/E. Increased portal hydrostatic pressure, increased plasma oncotic pressure

Explanation - Q: 3.3 Close

The correct answer is D. Many things contribute to the accumulation of

ascites fluid, but the exact mechanism is not completely understood. Known
contributors include: increased portal hydrostatic pressure (from portal
hypertension secondary to obstructed portal flow), decreased plasma oncotic
pressure (from hypoalbuminemia secondary to failing hepatic synthesis), and
a renal retention of sodium (secondary to a perceived hypovolemia from
splanchnic sequestration of fluid).

None of the other answer combinations occur in ascites.

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Question 4 of 5
During the patient's hospitalization, his mental status deteriorates. He becomes
unconscious and a flapping tremor is elicited at the wrist.
Scant blood is passed per rectum. His vital signs remain stable, and his
hemoglobin falls 1g/dL. EIectrolytes are normaI. Which of the following
explains his altered mental state?
/A. Encephalopathy secondary to gastrointestinal bleeding
/B. Hypovolemia secondary to rapid accumulation of ascites fluid
/C. Hypoxia secondary to gastrointestinal bleeding
/D. Poor cerebral perfusion secondary to gastrointestinal bleeding.
/E. Severe azotemia secondary to renal failure

Explanation - Q: 3.4 Close

 The correct answer is A. This patient suffers from hepatic encephalopathy
precipitated by gastrointestinal bleeding. In this patient, the gastrointestinal
bleeding increased the amount of nitrogenous substrate available to colonic
flora. These flora metabolize nitrogenous compounds into amines, which may
act as neuromodulators. In patients with normal portal circulation, the liver
would metabolize these compounds into nontoxic substances. In this patient,
the portal hypertension causes shunting of blood into the systemic circulation
without passing through the liver, producing hepatic encephalopathy. The
asterixis, or flapping tremor, confirms this diagnosis.

The fluid shifts in ascites are slow (compare with choice B), and would not
cause altered mental status. The kidneys "sense" this fluid shift as
hypovolemia and retain fluid accordingly.

Hypoxia (choice C) is a common cause of altered mental status. It is unlikely

that a drop in hemoglobin of only 1g/dL would cause hypoxia in the absence
of any other catastrophic event.

This patient has suffered a minor GI bleed. Given that the vitals are stable
and the hemoglobin has fallen only slightly, it is unlikely that there is
hemodynamic instability that would cause an altered level of consciousness
(choice D).

There is no evidence of renal failure in this scenario. The electrolytes are

normal, and thus azotemia from renal failure (choice E) is an unlikely cause
for this patient's altered mental status

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Question 5 of 5
Lactulose syrup is administered to this patient after he developed altered mental
status. Which of the following best describes how lactulose
will help restore mental function?
/A. Lactulose acts as an osmotic diuretic to decrease intracranial pressure
/B. Lactulose acts as an osmotic laxative to aid in evacuation of gastrointestinal
blood
/C. Lactulose is bactericidal to intestinal flora
/D. Lactulose restores the integrity of the blood-brain barrier
/E. Lactulose stabilizes axonal transmission of neural impulses

Explanation - Q: 3.5 Close

The correct answer is B. Lactulose is administered to patients with hepatic

encephalopathy for several reasons. Following a GI bleed, removal of protein
(and thus nitrogenous toxins) from the colonic lumen is paramount. Lactulose
is a non-absorbable disaccharide that acts as an osmotic laxative to remove
nitrogenous toxins (and their proteinaceous precursors) from the colon. In
addition, bacterial metabolism of lactulose decreases the gut pH, which
protonates the amines to the less absorbable ammonium form.

Lactulose is not absorbed from the gut so it could not act as an osmotic
diuretic (choice A). Mannitol is an osmotic diuretic used to decrease
intracranial pressure.

Lactulose is not bactericidal to intestinal flora (choice C).

Lactulose is not absorbed from the gut and thus cannot act on the blood-brain
barrier (choice D).

Lactulose is not absorbed from the gut and thus cannot affect axonal
transmission (choice E).