Which mechanism describes how NSAIDs contribute to peptic ulcer disease?

• A. They inhibit COX-2, reducing inflammation
• B. They stimulate prostaglandin synthesis
• C. They inhibit COX-1, reducing protective prostaglandins in the gastric mucosa
• D. They increase mucous viscosity

Answer: (C)

NSAIDs can cause peptic ulcers mainly by blocking COX-1 in the gastric mucosa, which lowers the production of protective prostaglandins (such as PGE2 and prostacyclin). Those prostaglandins help maintain the mucous layer and bicarbonate secretion, and they support blood flow to the lining. When COX-1 is inhibited, these protective factors decrease, making the stomach lining more vulnerable to acid injury and ulcer formation. COX-2 inhibition reduces inflammation but spares COX-1, so it has less impact on mucosal protection. The option about increasing mucus viscosity isn’t how NSAIDs work. Inhibiting COX-1 to reduce protective prostaglandins in the gastric mucosa best explains NSAID-related ulcers.