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Prostaglandin synthesis in the gastric mucosa is a vital process for maintaining mucosal integrity and protecting against damage from acid and other irritants. It involves the conversion of arachidonic acid to prostaglandins (primarily PGE2 and PGI2) via COX enzymes and terminal synthases. These prostaglandins then exert protective effects by inhibiting acid secretion, stimulating mucus/bicarbonate production, and enhancing blood flow. Disruption of this pathway, especially by NSAIDs, increases the risk of peptic ulcers.
NSAIDs inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis. Prostaglandin analogs supplement endogenous prostaglandin levels.
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