Drug of choice for NSAID induced peptic ulcer disease is
**Core Concept**
NSAID-induced peptic ulcer disease is a common complication of nonsteroidal anti-inflammatory drug (NSAID) therapy, resulting from the suppression of prostaglandin synthesis, which normally protects the gastric mucosa. This leads to mucosal damage, inflammation, and ulceration. The management of NSAID-induced peptic ulcer disease involves the use of medications that can restore the protective prostaglandin barrier.
**Why the Correct Answer is Right**
The drug of choice for NSAID-induced peptic ulcer disease is a proton pump inhibitor (PPI). PPIs work by irreversibly inhibiting the H+/K+ ATPase enzyme system on the gastric parietal cell surface, thereby reducing gastric acid secretion. This reduction in acid production allows the stomach lining to heal and protects the mucosa from further damage. PPIs are more effective than histamine-2 (H2) receptor antagonists in promoting ulcer healing and preventing recurrence.
**Why Each Wrong Option is Incorrect**
**Option A:** Misoprostol - While misoprostol can protect the gastric mucosa by promoting prostaglandin synthesis, it is not the drug of choice for NSAID-induced peptic ulcer disease due to its limited efficacy compared to PPIs.
**Option B:** Sucralfate - Sucralfate forms a protective barrier over the ulcer site, but it does not reduce gastric acid secretion and is not as effective as PPIs in promoting ulcer healing.
**Option C:** H2 receptor antagonists - While H2 receptor antagonists can reduce gastric acid secretion, they are less effective than PPIs in promoting ulcer healing and preventing recurrence.
**Clinical Pearl / High-Yield Fact**
PPIs are the preferred treatment for NSAID-induced peptic ulcer disease due to their potent acid-suppressive effects and ability to promote ulcer healing. It is essential to also discontinue the offending NSAID whenever possible and consider alternative analgesic or anti-inflammatory agents.
**Correct Answer:** B. Sucralfate is not the correct answer here.