GASTROENTEROLOGY LITERATURE REVIEW SESSION
October 21, 1999
| Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal Toxicity of Nonsteroidal Antiinflammatory Drugs. N Engl J Med 1999;340:1888-1899. |
1. The use of H2RA to prevent NSAID-related ulcers:
a. effectively prevents the occurrence of gastric and duodenal ulcers
b. decreases the symptoms of dyspepsia
c. decreases the incidence of duodenal ulcers
d. was ineffective in preventing most gastric ulcers
2. Potential effects of NSAID use in the GI tract include
a. colonic strictures
b. pill-induced esophagitis
c. improvement of inflammatory bowel disease
d. small bowel strictures
e. acute diffuse jejunitis3. Established risk factors associated with increased risk for NSAID-related complications include
a. advanced age
b. the longer the NSAID is taken, the higher the risk
c. concomitant use of corticosteroids
e. Helicobacter pylori infection
f. cigarette smoking
4. Inhibition of prostaglandin formation by NSAID's results in:
a. increased gastric mucus production
b. increased mucosal blood flow, leading to hyperemia and bleeding
c. decreased bicarbonate secretion
d. decreased mucosal resistance
e. decreased gastrin production
True or False
5. Helicobacter pylori infection should be looked for and treated in patients prior to initiating therapy with NSAID's
6. NSAID-related ulcers heal as well with PPI as with H2RA in patients who continue to take NSAID's
7. While selective COX-2 inhibitors are more than 100X as selective in their ability to suppress COX-2 than non-selective agents, this selectivity may change from person to person based on genetic differences
8. Over 80% of patients with endoscopic evidence of NSAID gastritis are symptomatic
9. Cyclooxygenase-1 (COX-1) is present in most normal tissues, and serves as a "housekeeping enzyme", its inhibition leads to potential disruptions in tissue function.
10. Patients who develop an NSAID-related ulcer, and then discontinue the use of NSAID upon diagnosis of the ulcer, must be treated with PPI to heal the ulcer.
11. Dyspeptic symptoms are a reliable marker for significant NSAID toxicity
12. COX-1 inhibition is felt to be responsible for the deleterious effects of NSAID's, while COX-2 inhibition mediates the anti-inflammatory properties of NSAID's.
13. Nabumetone (Relafen) and etodolac (Lodine) have a lower incidence of peptic ulceration when used in low doses, this benefit disappears with higher doses
14. The use of rectal or parenteral use of NSAID has led to a decrease in the gastroduodenal complications of NSAID use
15. Sucralfate is an effective alternative for the prevention of NSAID-related ulcers
16. H-2 receptor antagonists are ineffective in treating symptoms of dyspepsia related to NSAID use.
17. Misoprostol, taken as 200ug bid is an effective form of prophylaxis against NSAID-related ulcerations
18. NSAID-related duodenal ulcer is more common that NSAID-related gastric ulcer
19. Low dose aspirin (30mg) has no effect on gastric mucosal prostaglandin synthesis
20. Cyclooxygenase-2 (COX-2) is nearly undetectable in most tissues under physiologic conditions
21. Most patients with NSAID-related dyspepsia have abnormal findings on upper endoscopic examination
22. As inhibition of COX-1 is the only mechanism for ulcer production during the use of NSAID's, the use of selective COX-2 inhibitors should not be associated with any risk of peptic ulcer.
23. Misoprostol has been shown to be as effective as PPI in the prevention as well as the treatment of NSAID-related ulcers.
24. Regarding the epidemiology of NSAID-related gastrointestinal complications, which statement(s) is (are) true
a. Serious complications are more common in patients taking NSAID's for osteoarthritis
b. dyspepsia occurs in 10 to 20% of patients taking NSAID's
c. 13 of every 1000 patients with R.A. taking NSAID's for one year have a serious GI complication
d. the rate of serious NSAID-related complications is increasing at present
e. mortality rate among patients hospitalized with NSAID-related GI bleeding is 5%-10%