Peptic Ulcer Disease (PUD) Fitz and Leik Flashcards

1
Q
55. The gastric parietal cells produce:
A. hydrochloric acid.
B. a protective mucosal layer.
C. prostaglandins.
D. prokinetic hormones.
A

A. hydrochloric acid.

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2
Q
  1. Antiprostaglandin drugs cause stomach mucosal injury primarily by:

A. a direct irritative effect.
B. altering the thickness of the protective mucosal layer.
C. decreasing peristalsis.
D. modifying stomach pH level.

A

B. altering the thickness of the protective mucosal layer.

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3
Q
  1. A 24-year-old man presents with a 3-month history of upper abdominal pain. He describes it as an intermittent,
    centrally located “burning” feeling in his upper abdomen, most often occurring 2 to 3 hours after meals. His presentation is most consistent with the clinical presentation of:
    A. acute gastritis.
    B. gastric ulcer.
    C. duodenal ulcer.
    D. cholecystitis
A

C. duodenal ulcer.

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4
Q
  1. When choosing pharmacological intervention to prevent recurrence of duodenal ulcer in a middle-aged
    man, you prescribe:
    A. a proton pump inhibitor (PPI).
    B. timed antacid use.
    C. antimicrobial therapy.
    D. a histamine2-receptor antagonist (H2RA).
A

C. antimicrobial therapy.

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5
Q
  1. The H2RA most likely to cause drug interactions with phenytoin and theophylline is:

A. cimetidine.
B. famotidine.
C. nizatidine.
D. ranitidine.

A

A. cimetidine

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6
Q
60. Which of the following is least likely to be found in a patient with gastric ulcer?
A. history of long-term naproxen use
B. age younger than 50 years
C. previous use of H2RA or antacids
D. cigarette smoking
A

B. age younger than 50 years

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7
Q
61. Nonsteroidal anti-inflammatory drug (NSAID)-induced peptic ulcer can be best limited by the use of:
A. timed antacid doses.
B. an H2RA.
C. an appropriate antimicrobial.
D. misoprostol.
A

D. misoprostol.

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8
Q
  1. Cyclooxygenase-1 (COX-1) contributes to:
    A. the inflammatory response.
    B. pain transmission.
    C. maintenance of gastric protective mucosal layer.
    D. renal arteriole constriction.
A

C. maintenance of gastric protective mucosal layer.

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9
Q
  1. Cyclooxygenase-2 (COX-2) contributes to:
    A. the inflammatory response.
    B. pain transmission inhibition.
    C. maintenance of gastric protective mucosal layer.
    D. renal arteriole dilation.
A

A. the inflammatory response.

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10
Q
  1. You see a 48-year-old woman who has been taking a COX-2 inhibitor for the past 3 years. In counseling her,
    you mention that long-term use of COX-2 inhibitors is associated with all of the following except:
    A. hepatic dysfunction.
    B. gastropathy.
    C. cardiovascular events.
    D. cerebrovascular events.
A

A. hepatic dysfunction.

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11
Q
  1. A 64-year-old woman presents with a 3-month history of upper abdominal pain. She describes the discomfort
    as an intermittent, centrally located “burning” feeling in the upper abdomen, most often with meals and
    often accompanied by mild nausea. Use of an over-thecounter H2RA affords partial symptom relief. She also uses diclofenac on a regular basis for the control of osteoarthritis pain. Her clinical presentation is most consistent with:
    A. acute gastroenteritis.
    B. gastric ulcer.
    C. duodenal ulcer.
    D. chronic cholecystitis.
A

B. gastric ulcer.

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12
Q
  1. Which of the following statements about Helicobacter pylori is false?
    A. H. pylori is a gram-negative, spiral-shaped
    bacterium.
    B. Infection with H. pylori is the most potent risk factor
    for duodenal ulcer.
    C. The organism is often resistant due to the production of beta-lactamase.
    D. H. pylori is transmitted via the oral-fecal or oral-oral
    route.
A

C. The organism is often resistant due to the production of beta-lactamase.

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13
Q
  1. The most sensitive and specific test for H. pylori infection from the following list is:
    A. stool Gram stain, looking for the offending organism.
    B. serological testing for antigen related to the infection.
    C. organism-specific stool antigen testing.
    D. fecal DNA testing.
A

C. organism-specific stool antigen testing.

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14
Q
68. Which of the following medications is a PPI?
A. loperamide
B. metoclopramide
C. nizatidine
D. lansoprazole
A

D. lansoprazole

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15
Q
69. Peptic ulcer disease can occur in any of the following locations except:
A. duodenum.
B. stomach.
C. esophagus.
D. large intestine.
A

D. large intestine.

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16
Q
  1. An ulcer that is noted to be located in the region below the lower esophageal sphincter and before the pylorus
    is usually referred to as a(n) ________ ulcer.
    A. duodenal
    B. esophageal
    C. gastric
    D. stomach
A

C. gastric

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17
Q
  1. A 56-year-old man with a 60 pack-year cigarette smoking history, recent 5-lb unintended weight loss, and a
    3-month history of new-onset symptoms of peptic disease presents for care. He is taking no medications on a regular basis and reports drinking approximately
    six 12-oz beers per week with no more than three beers per day. Physical examination is unremarkable except
    for mild pharyngeal erythema and moderate epigastric
    tenderness without rebound. The most helpful diagnostic
    test at this point in his evaluation is:
    A. an upper endoscopy.
    B. a barium swallow.
    C. an evaluation of H. pylori status.
    D. an esophageal pH monitoring.
A

A. an upper endoscopy.

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18
Q
72. Which of the following medications is a prostaglandin analogue?
A. sucralfate
B. misoprostol
C. esomeprazole
D. metoclopramide
A

B. misoprostol

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19
Q
  1. Long-term PPI use is associated with all of the following except:
    A. increased risk of pneumonia in hospitalized patients.
    B. increased risk of C. difficile colitis in hospitalized
    patients.
    C. reduced absorption of calcium and magnesium.
    D. reduced absorption of dietary carbohydrates.
A

D. reduced absorption of dietary carbohydrates.

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20
Q
  1. To avoid rebound gastric hyperacidity following discontinuation of long-term PPI use, all of the following methods can be used except:
    A. gradually tapering the PPI dose with supplemental antacid.
    B. switching to every-other-day dosing of PPI with supplemental antacid.
    C. switching to a low-dose H2RA therapy with supplemental antacid.
    D. empiric H. pylori therapy.
A

D. empiric H. pylori therapy.

21
Q

Helicobaceter Pylori Infection associated with duodonal/gastric ulcer - treatment - shorter course

A

Sequential therapy with rabeprazole 20 mg BID plus amoxicillin 1 g BID × 5 days

then

rabeprazole 20 mg BID plus clarithromycin 500 mg plus tinidazole 500 mg BID × additional 5 days

22
Q

Helicobaceter Pylori Infection associated with duodonal/gastric ulcer - treatment - longer course

A

Bismuth subsalicylate 2 tabs QID plus

metronidazole 500 mg TID plus tetracycline 500 mg QID plus omeprazole 20 mg BID for 10-14 days

23
Q

diagnose H. pylori

A

stool antigen testing is the most cost-effective method of diagnosing H. pylori infection

24
Q

Duodenal ulcer

A
Helicobacter pylori infection
(most common),
NSAID use, cortico -
steroid use (much less
common)
25
Q

Duodenal ulcer

A
Epigastric burning,
gnawing pain about
2–3 hr after meals;
relief with foods,
antacids
26
Q

Duodenal ulcer

A
Clusters of symptoms
with periods of
feeling well; awakening
at 1–2 a.m. with
symptoms common,
morning waking
pain rare
27
Q

Duodenal ulcer

A
Tender at the epigastrium,
left upper
quadrant abdomen;
slightly hyperactive
bowel sounds
28
Q

Duodenal ulcer

A
Stool antigen testing ≥90% sensitive
and specific
If H. pylori stool antigen test is positive
and PUD history, assume active infection
and treat because cost of treatment
less than that of confirmatory
endoscopy. Repeat stool antigen
test ≥8 wk post-treatment.
29
Q

Gastric Ulcer

A
NSAID and corticosteroid
use (potent risk factor)
Cigarette smoking
Male:female ratio equal
Peak incidence in fifth
and sixth decades of
life; nearly all found
in patients without
H. pylori infection are
a result of chronic NSAID
or long-term systemic
corticosteroid use
30
Q

Gastric ulcer

A

Pain often reported
with or immediately
after meals

31
Q

Gastric ulcer

A

Nausea, vomiting,

weight loss common

32
Q

Gastric ulcer

A

Difficulty distinguishing gastric ulcer
from stomach cancer through UGI
imaging

33
Q

Gastric ulcer

A

UGI endoscopy with biopsy vital to rule

out gastric malignancy

34
Q

Gastric ulcer

A

Need confirmation of presence of
H. pylori before treatment, as is present
in some of cases

35
Q

Nonerosive
gastritis,
chronic type B
(antral) gastritis

A

Most likely caused by

H. pylori infection

36
Q

Nonerosive
gastritis,
chronic type B
(antral) gastritis

A
Nausea
Burning and pain
limited to upper
abdomen without
reflux symptoms
37
Q

Nonerosive
gastritis,
chronic type B
(antral) gastritis

A

Upper GI endoscopy is helpful diagnostic

test, likely with H. pylori testing

38
Q

Erosive gastritis

A

Usually secondary to
alcohol and NSAID use,
ASA use, stress

39
Q

Erosive gastritis

A

H. pylori infection usually

not a factor

40
Q

Erosive gastritis

A
Nausea
Burning and pain
limited to upper
abdomen without
reflux symptoms;
bleeding common
41
Q

Erosive gastritis

A

Upper GI endoscopy is helpful diagnostic

test, likely with H. pylori testing

42
Q

H2RAs

A

have ‘tidine’ suffix - famotidine (pepcid)

43
Q

H2RAs

A

competitively block the binding of histamine to the H2-receptor site, reducing the secretion of gastric acid. In prescription dosages, these products suppress approximately 90% of hydrochloric acid production, whereas
over-the-counter dosages suppress about 80%.

44
Q

H2RAs - Cimetidine

A

inhibits cytochrome P-450, slowing metabolism of many drugs. As a result, drug interactions between cimetidine and warfarin, diazepam,
phenytoin, quinidine, carbamazepine, theophylline, imipramine,
and other medications can occur

45
Q

Proton pump inhibitors (PPIs)

A

suffix ‘azole’

46
Q

Proton pump inhibitors (PPIs)

A

These drugs inhibit gastric acid secretion by inhibiting the final step in acid secretion by altering the activity of
the “proton pump” (H+, K+-ATPase). As a result, there is a virtual cessation of stomach hydrochloric acid production

47
Q

PPI use is indicated

A

in the treatment of peptic ulcer disease and gastroesophageal reflux disease
(GERD) particularly when an H2RA is ineffective, and in refractory
erosive esophagitis and Zollinger-Ellison syndrome

48
Q
  1. Which of the following drug classes is indicated for initial treatment of an
    uncomplicated case of Helicobacter pylori-negative peptic ulcer disease?
    A) Proton-pump inhibitors
    B) H2 receptor antagonists
    C) Antibiotics
    D) Antacids
A

B) H2 receptor antagonists

Because the ulcer is not infected with Helicobacter
pylori, antibiotics are not recommended. The first-line treatment option are H2
receptor antagonists (also known as H2 blockers) such as ranitidine (Zantac),
famotidine (Pepcid), or nizatidine (Axid). Other causes of peptic ulcer disease are
nonsteroidal anti-inflammatory drugs (NSAIDs); the patient should be educated to
avoid use of these agents.

49
Q
  1. Which of the following regimens is known as “triple therapy” for treating a
    Helicobacter pylori infection?
    A) Metronidazole (Flagyl) BID, doxycycline BID, and omeprazole (Prilosec) daily

B) Bismuth subsalicylate (Pepto-Bismol) tablets QID, metronidazole (Flagyl) QID,
azithromycin (Zithromax), and cimetidine (Tagamet) daily

C) Amoxicillin BID, sulfamethoxazole–trimethoprim (Bactrim DS) BID, and
ranitidine (Zantac) daily

D) Clarithromycin (Biaxin) BID, amoxicillin BID, and omeprazole (Prilosec) daily

A

D) Clarithromycin (Biaxin) BID, amoxicillin BID, and omeprazole
(Prilosec) daily This combination is known as “triple therapy” for the
treatment of peptic ulcer disease caused by the bacterium Helicobacter pylori. The
original quadruple therapy consists of bismuth subcitrate (Pepto Bismol),
metronidazole, and tetracycline with a proton-pump inhibitor (PPI) or H2 blocker.
The antibiotics are taken for 14 days with a PPI or an H2 blocker, and then the PPI
or H2 blocker is continued for 2 to 4 weeks after.

Currently, there are several
regimens for treating H. pylori infection.

To confirm eradication, order a urea breath test or fecal antigen test.