A patient taking aspirin for secondary prevention of MI develops sudden-onset hematemesis. Aspirin-induced gastric mucosal damage occurs via which MAIN mechanism beyond direct irritation?
- A Inhibition of COX-1, reducing prostaglandin E2 and I2 synthesis required for mucosal cytoprotection ✓
- B Inhibition of COX-2, reducing anti-inflammatory prostaglandins in the gastric wall
- C Direct chelation of mucus glycoproteins, dissolving the protective mucus layer
- D Activation of H. pylori virulence factors by an acidic environment created by aspirin
Correct answer: A. Inhibition of COX-1, reducing prostaglandin E2 and I2 synthesis required for mucosal cytoprotection
Explanation
Aspirin irreversibly acetylates and inhibits both COX-1 and COX-2. COX-1 is the constitutive isoform responsible for producing cytoprotective prostaglandins (PGE2 and PGI2) in the gastric mucosa; these prostaglandins stimulate mucus and bicarbonate secretion, maintain mucosal blood flow, and inhibit acid secretion. Their depletion by COX-1 inhibition compromises mucosal defence, leading to erosions, ulcers, and bleeding. This is the systemic mechanism that occurs even with enteric-coated or parenteral aspirin.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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