Peptic Ulcer Disease (PUD) Fitz and Leik Flashcards

(49 cards)

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
Duodenal ulcer
``` Epigastric burning, gnawing pain about 2–3 hr after meals; relief with foods, antacids ```
26
Duodenal ulcer
``` Clusters of symptoms with periods of feeling well; awakening at 1–2 a.m. with symptoms common, morning waking pain rare ```
27
Duodenal ulcer
``` Tender at the epigastrium, left upper quadrant abdomen; slightly hyperactive bowel sounds ```
28
Duodenal ulcer
``` 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
Gastric Ulcer
``` 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
Gastric ulcer
Pain often reported with or immediately after meals
31
Gastric ulcer
Nausea, vomiting, | weight loss common
32
Gastric ulcer
Difficulty distinguishing gastric ulcer from stomach cancer through UGI imaging
33
Gastric ulcer
UGI endoscopy with biopsy vital to rule | out gastric malignancy
34
Gastric ulcer
Need confirmation of presence of H. pylori before treatment, as is present in some of cases
35
Nonerosive gastritis, chronic type B (antral) gastritis
Most likely caused by | H. pylori infection
36
Nonerosive gastritis, chronic type B (antral) gastritis
``` Nausea Burning and pain limited to upper abdomen without reflux symptoms ```
37
Nonerosive gastritis, chronic type B (antral) gastritis
Upper GI endoscopy is helpful diagnostic | test, likely with H. pylori testing
38
Erosive gastritis
Usually secondary to alcohol and NSAID use, ASA use, stress
39
Erosive gastritis
H. pylori infection usually | not a factor
40
Erosive gastritis
``` Nausea Burning and pain limited to upper abdomen without reflux symptoms; bleeding common ```
41
Erosive gastritis
Upper GI endoscopy is helpful diagnostic | test, likely with H. pylori testing
42
H2RAs
have 'tidine' suffix - famotidine (pepcid)
43
H2RAs
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
H2RAs - Cimetidine
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
Proton pump inhibitors (PPIs)
suffix 'azole'
46
Proton pump inhibitors (PPIs)
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
PPI use is indicated
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
373. 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
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
688. 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
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.