Gastric Ulcers and Gastric Fluid: Pathophysiology and Treatment

Gastric ulcers are mucosal breaks >3 mm in the stomach lining. Gastric fluid (acid, pepsin, bile reflux) contributes to mucosal injury when defense mechanisms fail.

Key Pathogenic Factors

• Helicobacter pylori infection: disrupts mucosal barrier, induces inflammation, alters acid secretion.
• NSAIDs: inhibit COX‑1 → reduce prostaglandins → impair mucus/bicarbonate secretion and mucosal blood flow.
• Smoking: reduces mucosal blood flow, increases acid, impairs healing.
• Stress (critical illness): ischemia‑reperfusion injury (stress ulcers).

Role of Gastric Fluid

Acid (HCl) and pepsin digest the mucosa when the protective mucus‑bicarbonate layer is compromised. Bile acids from duodenogastric reflux further damage cell membranes.

Treatment

• PPIs (omeprazole, pantoprazole) – suppress acid, promote healing.
• H. pylori eradication (triple/quadruple therapy).
• NSAID discontinuation or co‑therapy with PPI/misoprostol.
• Mucosal protectants (sucralfate, bismuth).
• Lifestyle: smoking cessation, alcohol moderation.

Most ulcers heal within 4–8 weeks with appropriate therapy.