Gastroenterology and Hepatology Exam
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Gastro 1
A 38-year-old man is evaluated for persistent dyspepsia 2 months after a duodenal
ulcer was detected and treated. He originally presented with new-onset epigastric pain,
and esophagogastroduodenoscopy showed a duodenal ulcer; biopsy specimens
showed the presence of Helicobacter pylori. The patient, who does not use NSAIDs and
is penicillin-allergic, completed a 10-day course of therapy with omeprazole,
metronidazole, and clarithromycin.
At this time, urea breath testing for H. pylori shows persistent infection.
In addition to a proton pump inhibitor, which of the following regimens is indicated for
this patient?
A Amoxicillin and levofloxacin
B Bismuth subsalicylate, metronidazole, and tetracycline
C Clarithromycin and amoxicillin
D Clarithromycin and metronidazole
E Trimethoprim-sulfamethoxazole and erythromycin - Answer-B
Bismuth-based quadruple therapy should be considered in a patient in whom initial
proton pump inhibitor-based triple therapy has failed to eradicate Helicobacter pylori.
This patient has persistent Helicobacter pylori infection despite initial therapy with a
proton pump inhibitor, clarithromycin, and metronidazole, an appropriate regimen for
this patient with penicillin allergy. The most likely reason for failure of treatment in most
patients is either noncompliance with therapy or antibiotic resistance; antibiotic
resistance (probably to clarithromycin) is a likely cause of treatment failure in this
patient. Therefore, an additional treatment regimen, one that does not contain
clarithromycin, needs to be given. In the United States, bismuth-based quadruple
therapy is indicated in a patient whose infection has failed to respond to proton pump
inhibitor-based triple therapy. Levofloxacin-based triple therapy is also used in patients
with persistent infection, but this regimen has not been validated in the United States.
Regimens containing amoxicillin would not be indicated in this patient with penicillin
allergy. Therapy with the same regimen that failed initially to eradicate the organism
because of likely antibiotic resistance would not be appropriate. H. pylori is naturally
resistant to trimethoprim, and the regimen of trimethroprim-sulfamethoxazole and
erythromycin is not an approved regimen for eradication of the organism.
,Gastro 2
A 19-year-old woman is evaluated for a 2-week history of nausea and new-onset
jaundice. Six weeks ago she had an uncomplicated cystitis, which resolved after a 3-
day course of therapy with trimethoprim-sulfamethoxazole.
On physical examination, the temperature is 37.3 °C (99.2 °F), the blood pressure is
120/85 mm Hg, the pulse rate is 88/min, and the respiration rate is 14/min; the BMI is
31. There is conjunctival icterus, jaundice, and right upper quadrant tenderness on deep
palpation. Murphy sign is not elicited, and there is no asterixis or stigmata of chronic
liver disease. Stool is negative for occult blood.
Laboratory studies:
Leukocyte count 7800/µL (7.8 × 109/L) with normal differential
Bilirubin (total) 12.0 mg/dL (205.2 µmol/L)
Bilirubin (direct) 5.6 mg/dL (95.6 µmol/L)
Aspartate aminotransferase 23 U/L
Alanine aminotransferase 35 U/L
Alkaline phosphatase 464 U/L
Antinuclear antibody titer Negat - Answer-D
Liver test elevations in the setting of a recently started medication should raise the
suspicion of a possible drug induced liver injury.
This patient has drug-induced liver injury secondary to trimethoprim-sulfamethoxazole
therapy. Antibiotics are common causes of drug-induced liver injury, which can cause
either an elevation in the aminotransferases or, as in this patient, a cholestatic form of
liver injury. Some drugs have their own particular fingerprint of injury. For example,
acetaminophen causes a predominant hepatocellular injury, whereas trimethoprim-
sulfamethoxazole often produces a cholestatic form characterized by an alkaline
phosphatase level more than twice normal. If a mixed pattern injury occurs in
combination with an elevated alkaline phosphatase level, the patient is at increased risk
of progressive liver injury. Phenytoin is an example of a drug that characteristically
produces a mixed pattern. Drug-induced liver injury is often difficult to diagnose
because there is no gold standard for diagnosis. Some drugs causing hepatic injury
may be associated with the more familiar hypersensitivity syndrome characterized by
fever, rash, and peripheral eosinophilia, but many drug reactions are characterized only
by hepatic injury. Therefore, it is often a diagnosis of exclusion of other causes of liver
injury in the presence of a potential offending agent taken within a recent period of time,
usually weeks. Most patients can be monitored conservatively because discontinuation
of the offending drug usually leads to eventual recovery, which can, however, take
months. It is important to monitor for signs of progressive liver injury by monitoring
prothrombin time and clinical status of the patient.
Cholecystectomy is incorrect because the patient has no radiographic evidence to
suggest cholecystitis, her gallb
,Gastro 3
A 35-year-old woman is evaluated for symptomatic ulcerative colitis. One year ago, she
was diagnosed with pan-ulcerative colitis and responded well to initial and maintenance
therapy with balsalazide. However, 2 months ago she developed urgent bloody diarrhea
several times a day and lower abdominal cramping; prednisone, 40 mg/d, alleviated her
acute symptoms, but her symptoms have returned with prednisone tapering. The patient
is otherwise healthy, and her medications are balsalazide, 750 mg three times a day,
prednisone, 15 mg/d, and calcium with vitamin D.
On physical examination, vital signs and other findings are normal. Laboratory studies
reveal hemoglobin 11.4 g/dL (114 g/L) and plasma glucose 140 mg/dL (7.77 mmol/L).
Stool analysis for Clostridium difficile toxin A and B is negative.
Which of the following is the most appropriate next step in the treatment of this patient?
A Add olsalazine
B Add bu - Answer-D
Patients with ulcerative colitis who become corticosteroid-dependent should be started
on therapy with an immunomodulator, such as azathioprine or 6-mercaptopurine with a
steroid taper.
5-Aminosalicylates (5-ASA) are the first-line therapy for ulcerative colitis, and remission
can often be induced and maintained with a 5-ASA only. When 5-ASA therapy is not
effective initially or patients develop a flare while in remission on 5-ASAs, often a short
course of corticosteroids is required to induce or re-induce remission. However,
corticosteroids are not effective as maintenance therapy and have many potential side
effects, including hyperglycemia, osteoporosis, hypertension, mood instability, acne,
infection, and osteonecrosis. Although some patients may maintain remission with
continued 5-ASA therapy after corticosteroid taper, other patients become
corticosteroid-dependent or -resistant, as did this patient, and therapy with an
immunomodulator such as 6-mercaptopurine or azathioprine should be started. These
agents are nucleotide analogues that interfere with DNA synthesis and induce
apoptosis. Therapy with these agents may be required for up to 3 months before
providing clinical benefit, and therefore, they are generally started with corticosteroids,
which are then tapered.
Because corticosteroids are not effective maintenance therapy, simply increasing the
dose of prednisone without adding an immunomodulator would not be appropriate in
this patient. The addition of another 5-ASA, such as olsalazine, will not provide any
greater benefit. Antibiotic therapy has not been shown to be effective in the treatment of
ulcerative colitis, and the patient's stool was negative for Clostridium difficile.
Budesonide is a nonsystemic corticosteroid that is useful in the induction of remission in
patients with ulcerative colitis
, Endo 4
A 27-year-old woman with an 8-year history of ulcerative colitis is evaluated during a
follow-up examination. The initial colonoscopy after diagnosis showed pancolitis. She
has been treated with mesalamine since diagnosis and has had episodes of bloody
diarrhea two or three times a year but has otherwise done well. Her most recent
colonoscopy 1 year ago when she had increased diarrhea and bleeding showed no
progression of disease. Since then she has been clinically stable. The patient's medical
history includes nephrolithiasis, and her only medications are mesalamine, 2.4 g/d, and
a multivitamin. There is no family history of inflammatory bowel disease or colorectal
cancer.
On physical examination, vital signs are normal; BMI is 20.5. There is mild abdominal
tenderness in the right lower quadrant without rebound or guarding. The rest of the
physical examination is normal. Laboratory studies reveal a normal c - Answer-C
Patients with inflammatory bowel disease should initiate screening for colorectal cancer
after 8 years of duration of disease.
This patient has pancolitis of 8 years' duration. The inflammation involves the ileum and
proximal colon. The colon cancer risk in patients with ulcerative colitis or Crohn disease
reaches a significant level after 8 years of inflammation; the annual cancer risk is
estimated to be 1% to 2% per year after 8 years. The cancer risk is slightly delayed for
patients with inflammation limited to the distal colon. The recommendation is to initiate a
surveillance program with colonoscopy 8 years after onset of her disease, with follow-up
colonoscopy every 1 to 2 years thereafter. Biopsies are performed in four-quadrant
fashion throughout the entire colon.
The patient's disease is reasonably well controlled on her current dose of mesalamine,
and treatment with mesalamine does not in itself prevent colon cancer. There is no
recommendation for standard screening for small-bowel carcinoma in the setting of
ulcerative colitis or Crohn disease, and therefore, capsule endoscopy is not indicated.
Flexible sigmoidoscopy would not reach the at-risk colonic mucosa in the proximal colon
beyond the reach of the sigmoidoscope.
Gastro 5
A 71-year-old man is evaluated for chronic epigastric discomfort, heartburn, and
diarrhea of 4 years' duration. His weight has been stable during this time period. The
patient has no significant medical history and takes no medications.
On physical examination, there is mild epigastric tenderness but no rebound or
guarding. Rectal examination reveals brown stool that is positive for occult blood.
Laboratory studies reveal hemoglobin of 12.3 g/dL (123 g/L) with a mean corpuscular
volume of 75 fL. Test for serum Helicobacter pylori antibody is negative.
