A 60-year-old man comes to the emergency department complaining of bright red

blood per rectum. The bleeding began abruptly several

hours prior to his visit. He has light-headedness when he stands up rapidly, but
has no abdominal pain, cramping, fever, nausea, or vomiting.
He has no history of previous episodes of bleeding or abdominal pain, but has a
history of coronary artery disease and takes aspirin as a
"blood thinner." He is afebrile, slightly hypotensive and tachycardic, but stable.
On examination, he has decreased skin turgor, and dry mucous
membranes. He has no abdominal tenderness. Rectal examination is positive for
gross blood.
Question 1 of 5

Which of the following is the most likely diagnosis?

/A. Arteriovenous malformation
/B. Diverticulitis
/C. Infectious colitis
/D. Ischemic colitis
/E. UIcerative colitis
Explanation - Q: 1.1

Close

The correct answer is A. Painless hematochezia or bright red lower GI

bleeding can come from many sources. While bright red lower GI bleeding
tends to indicate lower GI bleeding (bleeding distal to the ligament of Treitz),
brisk upper GI bleeding can also be the source. The clinical manifestations of
such bleeding range from negligible to hemodynamic instability, depending
upon the rate of bleeding. The differential diagnosis for painless
hematochezia includes AV malformations, gastric erosions, esophageal
varices, esophagitis, duodenal or gastric ulcer, hemorrhoids, diverticulosis,
and colonic neoplasm.
Diverticulitis (choice B) occurs when a colonic outpouching or diverticulum
becomes inflamed. Patients tend to be elderly and present with fever,
abdominal pain, and abdominal tenderness on examination. While painful,
these lesions do not bleed significantly (unlike their uninflamed counterparts
in diverticulosis).
Infectious colitis (choice C) may present as rectal bleeding, but this bleeding
is typically accompanied by pain, cramping, and fever. Causative organisms
may include Salmonella, Shigella, Campylobacter jejuni, E. coli, and
Entamoeba histolytica.
Ischemic colitis (choice D) may have rectal bleeding, but the hallmark of
ischemic colitis is severe abdominal pain out of proportion to examination
findings.
Ulcerative colitis (choice E) presents as abdominal pain and diarrhea, which

may be bloody or nonbloody. In addition, the onset of the disease tends to be

earlier, so this patient would likely have had previous episodes of pain.
Question 2 of 5

After the patient has stabilized, a colonoscopy is performed to elucidate the origin
of the bleeding. Several star-shaped branching vessels
measuring 0.2 to 1.0 cm are seen in the colonic submucosa. BIeeding is stopped
by electrocoagulation. A diagnosis of lower gastrointestinal
bleeding is given. Which anatomic landmark demarcates upper gastrointestinal
bleeding from lower gastrointestinal bleeding?
/A. IIeocecal valve
/B. Ligament of Treitz
/C. Papilla of Vater
/D. Pylorus
/E. Splenic flexure of the colon
Explanation - Q: 1.2

Close

The correct answer is B. The ligament of Treitz, or the peritoneal ligament,

which separates the third (retroperitoneal) portion of the duodenum from the
fourth (peritoneal) portion of the duodenum, traditionally demarcates upper GI
bleeding from lower GI bleeding. Bleeding proximal to this landmark tends to
produce melena or black tarry stools. Bleeding distal to this landmark tends to
produce hematochezia or red blood per rectum.
The ileocecal valve (choice A) separates the terminal ileum from the cecum.
The papilla of Vater (choice C) is where the pancreatic duct and common bile
duct empty into the duodenum.
The pylorus (choice D) is the sphincter separating the stomach from the
duodenum.
The splenic flexure of the colon (choice E) marks the transition from
transverse colon to the descending colon.
Question 3 of 5

The aspirin taken by this patient represents a contributor to his condition. Which
of the following best describes the mechanism of action of
aspirin?
/A. Aspirin decreases the serum level of factor VIII
/B. Aspirin decreases the serum level of factor IX
/C. Aspirin irreversibly inhibits platelets
/D. Aspirin irreversibly inhibits thrombin

/E. Aspirin reversibly inhibits platelets

/F. Aspirin reversibly inhibits thrombin

Explanation - Q: 1.3

Close

The correct answer is C. Patients with gastrointestinal bleeding must be

assessed for anatomic as well as physiologic and pharmacologic sources of
bleeding. Aspirin acts as an anticoagulant by irreversibly inhibiting platelets,
preventing the formation of a clot by blocking platelet adhesion and
aggregation. Since this platelet mass acts as a matrix for fibrin clot formation,
blocking platelets prevents clot formation. This mechanism has been utilized
in patients with atherosclerotic disease to prevent intravascular clot formation,
but may aggravate bleeding conditions such as this.
Aspirin does not decrease the serum level of factor VIII (choice A). Factor VIII
deficiency is the pathophysiology behind hemophilia A.
Factor IX deficiency (choice B) is associated with hemophilia.
Aspirin does not inhibit thrombin (choices D and F). Thrombin is the enzyme
responsible for cleaving fibrinogen to fibrin.
Aspirin's effects on platelets are not reversible (choice E), and a new
population of functional platelets must replace the inhibited platelets before
coagulation is fully restored.
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Question 4 of 5

Which of the following is an important mechanism in short-term blood pressure

maintenance?
/A. BIood pressure regulation occurs slowly by endocrine mechanisms only
/B. Decreased stretch in the carotid bodies decreases sympathetic and
increases parasympathetic discharge to the heart
/C. Decreased stretch in the carotid bodies increases sympathetic and
decreases parasympathetic discharge to the heart
/D. Decreased stretch in the carotid sinus decreases sympathetic and
increases parasympathetic discharge to the heart
/E. Decreased stretch in the carotid sinus increases sympathetic and decreases
parasympathetic discharge to the heart
Explanation - Q: 1.4

Close

The correct answer is E. As blood pressure falls in this patient with

hypovolemia, many short term and long term mechanisms work to raise the
falling pressure. In the short term, the baroreceptors found in the carotid sinus
and aortic arch regulate blood pressure by modulating the autonomic nervous
system. As pressure falls in this patient, the baroreceptors sense this change

as a decrease in stretch in the vessel walls. Afferent fibers from the

baroreceptors then "report" this change to the medullary cardiovascular
center. This center responds by increasing sympathetic discharge and
decreasing parasympathetic discharge to the heart and resistance vessels.
This acts to restore the blood pressure by increasing heart rate, stroke
volume, and vascular resistance.
While endocrine mechanisms (choice A) restore mean arterial pressure for
the long term, the sympathetic mechanisms outlined above restore pressure
toward baseline much more rapidly.
Choices B and C are incorrect. The carotid bodies contain chemoreceptors
(not stretch receptors) that detect changes in PO 2, PCO2, and pH. They
restore these parameters to normal by acting through the medullary centers to
change heart rate, stroke volume, vascular resistance, and ventilatory
parameters.
The decrease in pressure triggers an increase in sympathetic discharge and
decrease in parasympathetic discharge (compare with choice D).
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Question 5 of 5

Normal saline is administered to this patient and his blood pressure and heart
rate normalize. One of the goals in fluid resuscitation is to
optimize cardiac parameters according to Starling's Law. Starling's Law
describes which of the following?
/A. The relationship between end diastolic volume and contractility
/B. The relationship between heart rate and stroke volume
/C. The relationship between preload and afterload
/D. The relationship between stroke volume and end systolic volume
/E. The relationship between systemic vascular resistance and cardiac output
Explanation - Q: 1.5

Close

The correct answer is A. Starling's law of the heart describes the

relationship between end diastolic volume or preload and cardiac contractility.
It states that cardiac contractility is maximized at a particular preload. It also
states that cardiac contractility declines as the preload is increased or
decreased from this optimum. The basis for this principle is that at a particular
preload, the myocardium is "stretched" to a point that maximizes the number
of actin and myosin units that may interact in a given contraction.
Choice B is incorrect. Heart rate x stroke volume = cardiac output
Choice C is incorrect. Preload is related to end diastolic volume and passive

wall tension exerted on the diastolic ventricle.

Choice D is incorrect. End diastolic volume - end systolic volume = stroke
volume
Choice E is incorrect. Mean arterial pressure = cardiac output x total
peripheral resistance.

A 9-day-old baby is noted to be lethargic and has been feeding poorly. Over the
next day, the baby develops bilious vomiting, a distended
tender abdomen, and bloody stools.
Question 1 of 5

Which of the following diseases would most likely cause gastrointestinal bleeding
in a neonate?
/A. Crohn disease
/B. Cystic fibrosis
/C. Diverticulitis
/D. Necrotizing enterocolitis
/E. UIcerative colitis
Explanation - Q: 2.1

Close

The correct answer is D. Necrotizing enterocolitis is a feared complication of

infancy. It has an incidence of 1 to 5% in neonatal intensive care unit
admissions. The condition is a necrotizing disease of the small intestine, and
sometimes, the colon. The pathogenesis is still not clear, but may involve an
ischemic insult leaving the bowel susceptible to bacterial overgrowth.
Necrotizing enterocolitis may develop suddenly, with features suggesting
neonatal sepsis, or more slowly, over a period of one or two days. The case
description illustrates typical features.
Crohn disease (choice A) and ulcerative colitis (choice E) may present as
early as in the teenage years, but not usually in infancy.
Cystic fibrosis (choice B) is a cause of meconium ileus and later
malabsorption, but does not typically present with gastrointestinal bleeding.
Diverticulitis (choice C) is usually a disease of middle-aged to older adults.

Question 2 of 5

Which of the following is considered the most important risk factor for this
patient's disease?
/A. Perinatal asphyxia
/B. Polycythemia
/C. Prematurity
/D. Respiratory distress syndrome
/E. Shock
Explanation - Q: 2.2

Close

The correct answer is C. Prematurity is the most important risk factor for
necrotizing enterocolitis, although term infants also sometimes develop the
condition. Clinical series have reported that between 60 and 95% of affected
babies are premature, and the incidence is markedly increased in babies born
at lower gestational ages.
Many other purported risk factors have also been cited but seem to have a
lesser effect, including perinatal asphyxia (choice A), respiratory distress
syndrome (choice D), umbilical catheterization, hypothermia, shock (choice
E), patent ductus arteriosus, cyanotic congenital heart disease, polycythemia
(choice B), thrombocytosis, anemia, exchange transfusion, congenital GI
anomalies, chronic diarrhea, non-breast milk formula, nasojejunal feedings,
hypertonic formula, and colonization with necrogenic bacteria. It may simply
be that any already fragile baby, particularly if premature, who has other
significant underlying disease, is at increased risk for developing necrotizing
enterocolitis.
Question 3 of 5

A plain radiograph of the abdomen demonstrates gas within the bowel walI
(pneumatosis). Which of the following would most likely be
associated with this finding?
/A. Air in the biliary tract
/B. BIood in the biliary tract
/C. Gas in the hepatic veins
/D. Gas in the mediastinum
/E. Gas in the portal vein
Explanation - Q: 2.3

Close

The correct answer is E. Portal venous gas is seen in association with

pneumatosis intestinalis, most commonly with necrotizing enterocolitis. The
physiology of this is that the portal vein, via the mesenteric veins, drains
nutrient-rich blood from the gut to the liver. In the case of necrosis with air in

the bowel wall, air migrates into the portal venous system and to the liver. On
CT, this has the characteristic appearance of peripheral lucencies following
the portal venous system intrahepatically. In cases of more severe
pneumatosis, the bowel may rupture and lead to pneumoperitoneum.
Note: Although this item may have seemed difficult, it was, in essence, a
straightforward pathophysiology question, i.e., "Where would gas in the wall of
the intestine go?" The distracter explanations give additional information
concerning the radiographic appearance of the other conditions (the following
will most likely NOT be tested on Step I of the USMLE).
Pneumobilia, or air in the biliary tract (choice A), would be seen after
instrumentation of the biliary system, such as after an endoscopic retrograde
cholangiopancreatogram (ERCP). Other causes include a gas-forming
infection within the biliary tree or previous sphincterotomy (endoscopic
opening of the sphincter of Oddi). Pneumobilia has a distinct appearance on
CT: there is gas located centrally in the liver within the ducts.
Hemobilia, or blood in the biliary tract (choice B), would be seen after
instrumentation of the biliary system, such as after an endoscopic retrograde
cholangiopancreatogram (ERCP), from a biliary or hepatic tumor, or
secondary to a hypocoagulable state. Hemobilia is found at endoscopy, and is
generally not visible on plain radiographs. High attenuation material may be
seen within the bile ducts on a CT scan, suggesting hemobilia.
Hepatic venous gas (choice C) would not be seen with pneumatosis because
the hepatic veins drain the liver into the inferior vena cava (IVC). Gas from the
bowel wall gets trapped in the portal veins and does not traverse the liver to
get into the hepatic veins.
Pneumomediastinum (choice D) is usually from thoracic trauma causing
rupture of the esophagus or pneumothorax. Gas within the soft tissues of the
head and neck may dissect to the mediastinum. Rarely, pneumoperitoneum
may lead to secondary pneumomediastinum. Pneumatosis without
pneumoperitoneum would not lead to pneumomediastinum.
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Question 4 of 5

The baby's condition continues to deteriorate, and the decision is made to

surgically resect the affected GI segment. Resection of which of the
following areas of the gastrointestinal tract would most likely produce severe
long-term malabsorption?
/A. Ascending colon
/B. Duodenum
/C. Jejunum
/D. Stomach

/E.

Terminal ileum
Explanation - Q: 2.4

Close

The correct answer is E. Babies with early necrotizing enterocolitis are

sometimes successfully managed medically with fluids, bowel rest, and
correction of anemia and thrombocytopenia that may have developed
secondary to the gastrointestinal bleeding. Surgical resection may be
necessary in more severe cases of necrotizing enterocolitis, but may have a
mortality of 30-40% in these deathly ill infants. Unfortunately, necrotizing
enterocolitis most often affects the terminal ileum, which is also the site most
necessary to prevent long-term malnutrition. In practice, more than 50% of the
bowel must usually be removed before substantial malabsorption occurs. The
ileum is the site that is most active in nutrient (particularly fats) absorption,
vitamin B12 absorption, and conjugated bile salt absorption.
The ascending colon (choice A) is good at absorbing water and has a small
capacity for absorbing carbohydrates.
The duodenum (choice B) and jejunum (choice C) are also important
absorptive sites, but are less of a long-term problem because the ileum
appears to usually have the capacity to replace their absorptive function after
proximal small intestine resection.
Nutrient absorption does not usually occur in the stomach (choice D).
Question 5 of 5

The baby's resected gastrointestinal segment would be most likely to show which
of the following on pathologic examination?
/A. Distended macrophages with PAS-positive granules in the submucosa
/B. Gangrenous intestinal wall
/C. Granuloma formation
/D. Neoplastic epithelial proliferation
/E. Outpouching of intestinal mucosa through the muscular layer
Explanation - Q: 2.5

Close

The correct answer is B. The intestinal wall in early necrotizing enterocolitis

shows edema, hemorrhage, and necrosis. In more advanced disease,
gangrenous necrosis of the full bowel thickness is seen, and necrotic
inflammatory debris may adhere to the mucosal surface. Some cases show
evidence of reparative change, such as epithelial regeneration and
granulation tissue formation, suggesting that the lesion may have evolved
over several days before becoming clinically obvious.

Choice A is a feature of Whipple disease.

Choice C is a feature of Crohn disease.
Choice D is a feature of colonic polyps and cancers.
Choice E is a feature of diverticulitis.
A 55-year-old man with a history of coronary artery disease and alcoholism
presents to the emergency department complaining that he
vomited bright red blood twice this morning. He denies previous episodes of
bleeding or abdominal pain. On examination, he is a
malnourished man in acute distress. His blood pressure is 90/50 mm Hg and his
pulse is 110/min. His mucous membranes are dry and his
sclera are icteric. Abdominal examination reveals a distended abdomen with an
enlarged, palpable spleen. Purplish striae are seen around
the umbilicus. On rectal examination, Iarge hemorrhoids are seen, but the stool is
negative for blood.
Question 1 of 4

Which of the following is the most likely diagnosis?

/A. Erosive gastritis
/B. Esophageal varices
/C. Infectious enteritis
/D. Mallory Weiss tear
/E. Peptic ulcer disease
Explanation - Q: 3.1

Close

The correct answer is B. While all of the answer choices listed must be
considered in the differential, upper gastrointestinal bleeding from esophageal
varices is most likely. This patient displays many of the stigmata of hepatic
disease and portal hypertension: icteric sclera, hemorrhoids, distended
umbilical veins (caput medusae), and a history of alcoholism. In this setting,
esophageal varices would be the most likely. To make this diagnosis
definitively, however, one needs to examine the gastrointestinal tract
endoscopically.
Erosive gastritis (choice A) is a source of upper gastrointestinal hemorrhage,
but it seldom bleeds so profusely that the patient becomes hemodynamically
unstable.
Infectious disease in the gastrointestinal tract (choice C) may produce
hemorrhage, but it tends to produce lower GI bleeding.

Mallory Weiss tears (choice D) produce upper GI bleeding. This tearing of the
gastroesophageal junction occurs in alcoholics, but usually a history of
retching precedes bleeding. No such history is elicited here.
Peptic ulcer disease (choice E) can produce brisk upper GI bleeding. It is
less likely in this case because this patient has no history of GI pain.
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Question 2 of 4

Which of the following coagulation factors would most likely be unaffected in this
patient?
/A. Factor ll
/B. Factor VII
/C. Factor IX
/D. Factor XIII
/E. Von Willebrand's factor
Explanation - Q: 3.2

Close

The correct answer is E. Von Willebrand's factor is a coagulation factor

produced by the vascular endothelium and megakaryocytes. It is the only
protein in the cascade that is not synthesized in the liver. vWF mediates the
adhesion of platelets to the vessel wall basement membrane after vascular
injury. Patients with a deficiency of von Willebrand's factor have a tendency to
bleed. It is an autosomal dominant disease, and the ristocetin cofactor activity
test is the best way to clinically assess vWF function.
Factor II (choice A) is produced in the liver. Deficiency is very rare, but can
produce spontaneous or posttraumatic bleeding.
Factor VII (choice B) is produced in the liver.Severe factor VII deficiency is a
very rare cause of bleeding.
Factor IX (choice C) is produced in the liver. A factor IX deficiency is known
as hemophilia B, which is an X-linked disease.
Factor XIII (choice D) is produced in the liver. A deficiency of factor XIII
produces delayed bleeding and poor wound healing.
Question 3 of 4

Which of the following anatomic relationships provides the basis for the patient's
hemorrhoids?

/A. Coronary vein anastomosis with the esophageal plexus

/B. Inferior rectal vein anastomosis with the iliac vein
/C. Paraumbilical vein anastomosis with the inferior epigastric vein
/D. Superior mesenteric vein anastomosis with the splenic vein
/E. Superior rectal vein anastomosis with the inferior and middle rectal

Explanation - Q: 3.3

vein
Close

The correct answer is E. The patient's hemorrhoids are a consequence of

his portal hypertension. The patient has a cirrhotic liver, which impedes
circulation in the portal system. As the pressure rises in the portal system,
blood in the portal circulation begins to backflow into the caval circulation. At
the sites at which the portal system anastomoses with the caval circulation,
venous engorgement occurs. At one such site, the confluence of the superior
rectal vein (portal) with the middle and inferior rectal vein (caval), this venous
engorgement leads to hemorrhoids.
The coronary vein anastomosis with the esophageal venous plexus (choice
A) provides the anatomic basis for the esophageal varices seen in portal
hypertension. As pressure builds in the portal system, venous engorgement
occurs, and varices are produced in the distal esophagus. These varices can
be the site of life-threatening upper GI bleeding.
The anastomosis of the inferior rectal vein with the iliac vein (choice B) is a
caval-caval anastomosis and would not be affected by portal hypertension.
The anastomosis of the paraumbilical vein and the inferior epigastric vein
(choice C) is the portal-caval anastomosis responsible for the purplish striae
or caput medusae seen on this patient's abdomen. This circulatory route is an
embryologic remnant, and is only patent when portal pressure rises high
enough to re-open this pathway.
The anastomosis of the superior mesenteric vein and the splenic vein (choice
D) marks the origin of the portal vein. It may have an elevated pressure, but it
is not the basis for hemorrhoids.

Question 3 of 4

Which of the following anatomic relationships provides the basis for the patient's
hemorrhoids?
/A. Coronary vein anastomosis with the esophageal plexus
/B. Inferior rectal vein anastomosis with the iliac vein
/C. Paraumbilical vein anastomosis with the inferior epigastric vein
/D. Superior mesenteric vein anastomosis with the splenic vein
/E. Superior rectal vein anastomosis with the inferior and middle rectal vein

Explanation - Q: 3.3

Close

The correct answer is E. The patient's hemorrhoids are a consequence of

his portal hypertension. The patient has a cirrhotic liver, which impedes
circulation in the portal system. As the pressure rises in the portal system,
blood in the portal circulation begins to backflow into the caval circulation. At
the sites at which the portal system anastomoses with the caval circulation,
venous engorgement occurs. At one such site, the confluence of the superior
rectal vein (portal) with the middle and inferior rectal vein (caval), this venous
engorgement leads to hemorrhoids.
The coronary vein anastomosis with the esophageal venous plexus (choice
A) provides the anatomic basis for the esophageal varices seen in portal
hypertension. As pressure builds in the portal system, venous engorgement
occurs, and varices are produced in the distal esophagus. These varices can
be the site of life-threatening upper GI bleeding.
The anastomosis of the inferior rectal vein with the iliac vein (choice B) is a
caval-caval anastomosis and would not be affected by portal hypertension.
The anastomosis of the paraumbilical vein and the inferior epigastric vein
(choice C) is the portal-caval anastomosis responsible for the purplish striae
or caput medusae seen on this patient's abdomen. This circulatory route is an
embryologic remnant, and is only patent when portal pressure rises high
enough to re-open this pathway.
The anastomosis of the superior mesenteric vein and the splenic vein (choice
D) marks the origin of the portal vein. It may have an elevated pressure, but it
is not the basis for hemorrhoids.
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Question 4 of 4

Which of the following structures are found in the portal triad?

/A. Hepatic vein, common hepatic artery, common bile duct
/B. Portal vein, celiac artery, common bile duct
/C. Portal vein, common hepatic artery, common bile duct
/D. Portal vein, falciform ligament, common bile duct
/E. Portal vein, sinusoids, bile canaliculi
Explanation - Q: 3.4

Close

The correct answer is C. The portal triad contains the portal vein, common
hepatic artery, and common bile duct. It is found in the fold of peritoneum,
called the hepatoduodenal ligament, that separates the greater and lesser

abdominal sacs.
None of the other choices offer a complete answer:
The hepatic vein (choice A) drains the liver into the inferior vena cava (IVC).
The celiac artery (choice B) supplies blood to the anatomic foregut. One of its
branches, the common hepatic artery, travels in the porta hepatis.
The falciform ligament (choice D) is the remnant of the umbilical vein that
passes from the anterior abdominal wall to the superior surface of the liver.
Bile canaliculi (choice E) are microscopic channels that drain bile from the
hepatocytes.
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A 25-year-old man presents to the emergency department complaining of

passing bright red blood per rectum. He reports no prior episodes
of gastrointestinal bleeding, but he has had occasional lower abdominal pain and
diarrhea for the past ten months. He reports a 7 kg weight
Ioss since the onset of these symptoms. He denies sick contacts. On
examination, he is febrile with moderate, diffuse abdominal pain to
palpation and percussion. Rectal examination is positive for blood.
Question 1 of 4

Which of the following is the most likely diagnosis?

/A. Chronic pancreatitis
/B. Duodenal ulcer
/C. Infectious colitis
/D. Inflammatory bowel disease
/E. Ischemic colitis
Explanation - Q: 4.1

Close

The correct answer is D. Patients with inflammatory bowel disease can

present with a variety of symptoms. While ulcerative colitis and Crohn disease
patients may have distinct presentations, mixed presentations are common.
Distinguishing Crohn disease and ulcerative colitis is difficult, based on
clinical findings. Symptoms typical for Crohn disease include: abdominal pain,
fever, diarrhea, weight loss, and anal disease. Symptoms typical for ulcerative
colitis include: bloody diarrhea, fever, and weight loss.
Chronic pancreatitis (choice A) presents as epigastric pain that radiates to
the back, weight loss, and steatorrhea. In many cases, a history of alcoholism
is present. Thus the location of this patient's pain and his lower GI bleeding

are not consistent with chronic pancreatitis.

Duodenal ulcer (choice B) may present as epigastric pain, and with severe
disease, severe bleeding may be present. Patients with duodenal ulcer rarely
have diarrhea and weight loss. Thus this diagnosis is unlikely.
Infectious colitis (choice C) presents as abdominal pain and bleeding. Many
infectious agents may cause GI bleeding, including Salmonella, Shigella,
Campylobacter jejuni, and E. coli. The chronic nature of this patient's
complaints and the lack of sick contacts suggests a different diagnosis.
Ischemic colitis (choice E) presents as acute onset of severe abdominal pain
often with copious bright red blood per rectum. On examination, they display
the classic finding of "pain out of proportion to examination." They are typically
elderly patients with a history of atherosclerotic or embolic disease.
Question 2 of 4

A colonoscopy is performed and mucosal ulceration with bleeding extending

continuously from the rectum to the cecum is seen. The terminal
ileum is spared. Had the terminal ileum been affected, the patient would have
been at risk for which of the following conditions?
/A. Diabetes mellitus
/B. Folate deficiency
/C. Iron deficiency anemia
/D. Kwashiorkor
/E. Pernicious anemia
Explanation - Q: 4.2

Close

The correct answer is E. Pernicious anemia is a hypochromic, megaloblastic

anemia that may be associated with neurologic complications. It occurs as a
result of a lack of vitamin B 12. The B12/intrinsic factor complex is absorbed
in the terminal ileum by active transport. If this patient's ulcerative colitis
extended into the terminal ileum, this condition could complicate his disease.
Crohn disease almost invariably affects the terminal ileum, and this
malabsorptive condition is more common in that setting. Ulcerative colitis
usually affects only the colon, but ileal extension has been observed.
Diabetes mellitus (choice A) is an endocrine condition, and is unrelated to the
absorptive capacity of the terminal ileum.
Folate (choice B) is absorbed in the proximal small intestine. Ileal
involvement would not affect its absorption.

Iron (choice C) is also absorbed in the proximal small intestine. Ileal

involvement would not affect its absorption.
Kwashiorkor (choice D) is protein malnutrition. Protein is absorbed
throughout the small intestine. Ileal involvement would not affect its
absorption.
Question 3 of 4

At colonoscopy the colonic mucosa appears granular, and is ulcerated.

Numerous crypt abscesses and pseudopolyps are observed. Which of
the following is the most likely diagnosis?

Explanation - Q: 4.3

Close

The correct answer is E. Granular, flat mucosa with ulcers, crypt abscesses,
and pseudopolyps are characteristic findings in ulcerative colitis.
Celiac disease (choice A) is a disease of the intestine resulting from a
hypersensitivity to the protein gluten. The intestinal mucosa is smooth and
atrophic.
Clostridium difficile colitis (choice B) or "pseudomembranous colitis" is a
colonic infection seen after extensive antibiotic use, which disturbs the colonic
flora, promoting overgrowth of C. difficile. Fibrinous pseudomembranes are
seen in the colon at colonoscopy.
Endoscopic evaluation of Crohn disease (choice C) reveals swollen mucosa
with transverse fissures and linear ulcers. Biopsy findings demonstrate
transmural involvement with granuloma formation.
Diverticula are outpouchings of the intestinal mucosa. They may bleed, or
they may become infected, leading to a painful condition, diverticulitis. The
findings here do not suggest diverticulosis (choice D).
Question 4 of 4

Several months pass and this patient's symptoms progress. He continues to

have frequent bloody diarrhea and abdominal pain. Abruptly, this

patient experiences the acute onset of severe abdominal pain and is taken to the
emergency department by friends. In the emergency
department, he is febrile, and his abdomen is rigid, with severe pain to palpation
and percussion. Laboratory findings are consistent with
dehydration. Amylase and lipase are normaI. Which of the following most likely
explains this patient's new findings?
/A. Abdominal aortic aneurysm rupture
/B. Acute pancreatitis
/C. Bowel perforation and peritonitis
/D. Sepsis from fulminant infectious colitis
/E. Severe ischemic colitis
Explanation - Q: 4.4

Close

The correct answer is C. This patient's chronic course with acute

exacerbation suggests that this patient has viscus perforation with peritonitis
secondary to exacerbation of his ulcerative colitis. The inflammatory
processes in ulcerative colitis can be so severe that erosion from
inflammation can cause colonic perforation. Bowel contents then leak into the
peritoneal cavity, causing peritonitis. Peritonitis is characterized by fever,
severe abdominal pain, abdominal tenderness to palpation and percussion,
and rigidity of the abdominal wall.
Abdominal aortic aneurysm rupture (choice A) presents as abdominal pain
that radiates to the back. It is accompanied by hemodynamic instability that
may deteriorate to shock. This presentation is not consistent with findings in
this patient.
Acute pancreatitis (choice B) can cause severe abdominal pain and fever.
The pain, however is usually epigastric and radiating to the back. Typically
nausea and vomiting accompany pancreatitis. Amylase and lipase are
elevated.
This patient does not display the symptoms of sepsis (choice D). In sepsis,
patients are febrile with hemodynamic instability.
Ischemic colitis (choice E) can lead to perforation and peritonitis, and if the
patient had symptomatology consistent with ischemic colitis, it could be the
source of this patient's peritonitis. This patient did not report bright red blood
per rectum, or "pain out of proportion to examination," making ischemic colitis
less likely.

A 47-year-old, darkly pigmented man with a known history of alcohol abuse

begins vomiting large quantities of blood and is brought by
ambulance to the emergency department.
Question 1 of 6

In the emergency department, the man is found to have a temperature of 36.7 C

(98.1 F), blood pressure of 65/40 mm Hg and dropping
rapidly, a weak pulse of 130/min, and respirations of 29/min. These vital signs
suggest that which of the following is developing?
/A. Congestive heart failure
/B. Meningitis
/C. Pneumonia
/D. Septicemia
/E. Shock
Explanation - Q: 5.1

Close

The correct answer is E. The patient's low and dropping blood pressure,
tachycardia, high respiratory rate, and slightly below normal body temperature
are all consistent with impending shock. At this point, the other conditions
listed in the choices have not yet been ruled out, but clinically, the patient
should begin to be immediately treated for the shock, even if the therapeutic
workup for underlying conditions must be temporarily deferred.
Question 2 of 6

A blood sample is drawn and an IV Iine is started. While the patient is being
cross-matched, the physical examination is continued. The
patient's sclerae are noted to be icteric and his nail beds and palms have a
yellowish hue. A caput medusa is noted. Which of the following is
the most accurate description of a caput medusa?
/A. Ecchymoses over the mastoid process
/B. Paradoxical increase in venous distension and pressure during inspiration
/C. Reflex movement of the eyes in the opposite direction to that in which the
head is moved
/D. Small bony masses found on the terminal phalanges
/E. Varicose veins radiating from the area of the umbilicus
Explanation - Q: 5.2

Close

The correct answer is E. Medusa was a goddess with snakes instead of hair
on her head. The caput medusa (Medusa's head) is an old term still in fairly

common use for numerous varicose veins radiating over the abdomen from
the area of the umbilicus.
Choice A describes Battle's sign, which is suggestive of basal skull fracture.
Choice B describes Kussmaul's sign, which is seen in constrictive
pericarditis.
Choice C describes the doll's eye sign, which is looked for in the evaluation of
comatose patients and suggests functional integrity of the brainstem
tegmental pathways and cranial nerves involved in eye movement.
Choice D describes Heberden's nodules, which are seen in osteoarthritis.
Question 3 of 6

Caput medusa specifically suggests which of the following diagnoses?

/A. BIadder infection
/B. Duodenal ulcer
/C. Gastric ulcer
/D. Pancreatitis
/E. Portal hypertension
Explanation - Q: 5.3

Close

The correct answer is E. The caput medusa develops when severe portal
hypertension induces dilation of the anastomotic channels between the portal
venous system and the systemic venous system, some of which involve the
superficial veins near the umbilicus. The other answers are distracters.
Question 4 of 6

Which of the following is the most common cause of this patient's disorder in the
United States?
/A. Hepatic cirrhosis
/B. Hepatic vein thrombosis
/C. Hepatocellular carcinoma
/D. Metastatic disease to the liver
/E. Portal vein thrombosis
Explanation - Q: 5.4

Close

The correct answer is A. The overwhelmingly most common cause of portal

hypertension in the United States is hepatic cirrhosis, which is usually due to

either alcoholism or hepatitis viral infection. In this patient's case, the
diagnosis of cirrhosis is further clinically substantiated by his jaundice, as
evidenced by his sclera, nail beds, and palms. (Look in these areas on
individuals in whom dark skin pigmentation may mask the jaundice generally.)
The other entities listed are occasional causes of portal hypertension.
Question 5 of 6

Endoscopic studies demonstrate that this patient has bleeding esophageal

varices, and the bleeding is successfully stopped with
sclerotherapy. What percentage of patients with bleeding esophageal varices
have another episode of variceal bleeding at a subsequent
time?
/A. 5%
/B. 25%
/C. 40%
/D. 70%
/E. 95%
Explanation - Q: 5.5

Close

The correct answer is D. Patients who have had one episode of bleeding
from esophageal varices have an approximately 70% chance of developing a
second incident of bleeding, and one third of these episodes of rebleeding is
fatal.
Question 6 of 6

Following blood transfusions and sclerotherapy, the patient initially feels

reasonably well and is able to converse with medical personneI. Over
the next 12 hours, while he does not begin to rebleed, his mental status
deteriorates. Arterial blood levels of which of the following would be
most helpful in confirming the likely diagnosis?
/A. Ammonia
/B. Angiotensin l
/C. Calcitonin
/D. Carbon monoxide
/E. Ceruloplasmin
Explanation - Q: 5.6
The correct answer is A. Hepatic encephalopathy is seen in end-stage

Close

cirrhosis patients, and can either present or worsen in the presence of

gastrointestinal bleeding. The blood in the upper gastrointestinal tract
behaves essentially as a high protein load, and increases the absorption of
ammonia and nitrogen, which cannot be appropriately metabolized by the
liver. GI bleeding may also predispose for inadequate renal function
secondary to hypotension.
Angiotensin I (choice B) is part of the renin-angiotensin-aldosterone system
for blood pressure and sodium ion control.
Calcitonin (choice C) is a hormone secreted by the thyroid, which may be
increased in medullary carcinoma of the thyroid.
Carbon monoxide (choice D) increases in the blood in smokers.
Ceruloplasmin (choice E) is a copper-carrying protein monitored in patients
with Wilson disease.
A 2-year-old child is seen in the emergency department because of bright red
blood per rectum. This is the third time this has happened, and
on the previous episode, no lesion was identified on colonoscopy. During this
visit, the child is scheduled for small bowel barium studies,
which show an outpouching of the distal ileum about 2 feet proximal to the
cecum.
Question 1 of 7

Which of the following is the most likely diagnosis?

/A. Abnormally located appendix
/B. Crohn disease
/C. Diverticulosis
/D. Meckel diverticulum
/E. Potter syndrome
Explanation - Q: 6.1

Close

The correct answer is D. This patient has a Meckel diverticulum. Meckel

diverticula can be asymptomatic through life, or may come to medical
attention because of a bleeding peptic ulcer, acute inflammation, rupture,
strangulation, or intussusception of the Meckel diverticulum. Diagnosis, as in
this case, may be difficult because the ileum is difficult to visualize. In some
cases, small bowel barium studies may successfully identify the lesion.
While the appendix (choice A) can have variations in location, these tend to
involve the side of the cecum into which it opens. Also, the appendiceal lumen
remains narrow in aberrant locations.

Crohn disease (choice B) can involve the distal ileum and cause
gastrointestinal bleeding, but would not cause an isolated outpouching of the
ileum.
Diverticulosis (choice C) refers to acquired diverticula, and is usually a
disease of older individuals.
Potter syndrome (choice E) refers to the cluster of bilateral renal agenesis,
oligohydramnios, limb deformities, facial deformities, and pulmonary
hypoplasia.
Question 2 of 7

The prevalence of this patient's anatomic anomaly in the US population is which

of the following?
/A. 2%
/B. 6%
/C. 15%
/D. 40%
/E. 80%
Explanation - Q: 6.2

Close

The correct answer is A. The usually cited prevalence for Meckel

diverticulum is 2%, although it actually varies from 0.2% to 4%. Many medical
students remember five "2s" associated with Meckel diverticulum: 2 inches
long, 2 feet from the ileocecal valve, 2% of the population, commonly
presents in the first 2 years of life, and may have 2 types of epithelium.
Question 3 of 7

This patient's anatomic anomaly is thought to be embryologically derived from

which of the following?
/A. Mesonephric duct
/B. Mullerian duct
/C. Paramesonephric duct
/D. Vitelline duct
/E. Wolffian duct
Explanation - Q: 6.3

Close

The correct answer is D. The vitelline duct or yolk stalk embryologically

connects the midgut to the yolk sac. The duct usually disappears by the
seventh gestational week, but if it fails to obliterate, several lesions can be
produced, including Meckel diverticulum, a persistent vitelline duct that drains

as a fistula through the anterior abdominal wall at the umbilicus, a fibrous

band, or a vitelline duct cyst. The other ducts are genital ducts.
The mesonephric (wolffian) duct (choices A and E) develops into seminal
vesicles, epididymis, ejaculatory duct, and ductus deferens; the
paramesonephric (mullerian) duct (choices B and C) develops into the
fallopian tube, uterus, and part of the vagina.

Question 4 of 7

Which of the following is the most common type of ectopic tissue seen in this
patient's anatomic anomaly?
/A. Endometrial tissues
/B. Gastric mucosa
/C. Jejunal mucosa
/D. Pancreatic tissue
/E. Rectal mucosa
Explanation - Q: 6.4

Close

The correct answer is B. Meckel diverticula often have ectopic tissues in

them, the most common of which is heterotopic gastric mucosa. The tissues
listed in the other choices can also be seen, as well as colonic mucosa.
Question 5 of 7

The ulceration that was the source of bleeding in this patient is most likely related
to acid secretion by which of the following cell types?
/A. Chief cells
/B. Mucous neck cells
/C. Parietal cells
/D. Surface epithelial cells
/E. Zymogenic cells
Explanation - Q: 6.5

Close

The correct answer is C. In gastric mucosa, whether in the stomach, or in an

ectopic location, it is the parietal cells that secrete acid. This acid secretion is
particularly likely to cause peptic ulceration in a Meckel diverticulum or the
adjacent ileum, because the secretion of protective mucus is likely to be
markedly inadequate in this setting, and the distal small intestinal mucosa is
not equipped to handle an acid environment.
The chief cells, also called zymogenic cells (choices A and E) secrete

pepsinogen.
The mucous neck cells and surface epithelial cells (choices B and D) secrete
mucus.
Question 6 of 7

The acid-secreting cells are stimulated by which of the following hormones?

/A. Cholecystokinin
/B. Gastric inhibitory peptide
/C. Gastrin
/D. Secretin
/E. Vasoactive intestinal polypeptide
Explanation - Q: 6.6

Close

The correct answer is C. The polypeptide hormone gastrin is secreted by

the duodenum and pyloric antrum. Its release is stimulated by the presence of
digested protein in the stomach and duodenum. Gastrin stimulates acid
secretion from the parietal cells of the gastric glands and pepsinogen
secretion from the chief cells.
Cholecystokinin (choice A) is secreted by the endocrine cells of the
duodenum and proximal jejunum, and stimulates pancreatic enzyme
synthesis and secretion, increases gall bladder emptying, and decreases
gastric emptying.
Gastric inhibitory peptide (choice B) inhibits gastrin release and gastric acid
secretion, and causes insulin release from the endocrine pancreas.
Secretin (choice D) is produced in the crypts of Lieberkhn of the duodenum,
and stimulates pepsinogen secretion from the stomach, and fluid and
bicarbonate release from the pancreas.
Vasoactive intestinal polypeptide (choice E) induces smooth muscle
relaxation, modifies the composition of pancreatic juice and bile, and inhibits
gastric acid secretion and absorption from the intestinal lumen.
Question 7 of 7

Stimulation of which receptor on the acid-secreting cell leads to increased acid

secretion?
/A. Epinephrine receptor
/B. Histamine-1 receptor
/C. Histamine-2 receptor
/D. Prostaglandin E2 receptor

/E.

Somatostatin receptor
Explanation - Q: 6.7

Close

The correct answer is C. Acid secretion by parietal cells can be stimulated

by the gastrin receptor, the histamine-2 (H2) receptor, and the acetylcholine
receptor. Drugs with anti-H2 receptor activity are used to treat peptic ulcer
disease. The histamine that stimulates the H2 receptors is probably derived
from enterochromaffin cells.
Epinephrine and histamine-1 receptors (choices A and B) do not appear to
have a physiologic role in gastric acid secretion.
Substances capable of reducing gastric acid secretion include prostaglandin
E2(choice D), secretin, and somatostatin (choice E).