Long-term use of non-steroidal anti-inflammatory drugs predisposes to gastric ulceration. The protective effect of endogenous prostaglandins (chiefly PGE2) on the gastric mucosa is mediated by:

• A Stimulation of parietal cell H+-K+-ATPase activity, thickening the unstirred layer
• B Acceleration of gastric emptying, reducing contact time between acid and mucosa
• C Direct inhibition of Helicobacter pylori colonization of the antrum
• D Increased secretion of mucus and bicarbonate by surface epithelial cells and enhanced mucosal blood flow ✓

Explanation

Prostaglandins of the E series act on surface mucous cells to increase mucus and bicarbonate secretion and also maintain mucosal blood flow, together forming the gastric mucosal barrier. NSAIDs inhibit cyclooxygenase and abolish this protection, which is why misoprostol, a PGE1 analogue, is used prophylactically. Prostaglandins actually inhibit rather than stimulate acid secretion, so option A is wrong.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.