gastric ulcers
Summary
Gastric ulcers are mucosal defects extending through the muscularis mucosae into the submucosa, occurring in the stomach, most commonly at the lesser curvature of the antrum. Major causes are H. pylori infection and NSAID use, which disrupt the mucosal defense barrier. Pain classically worsens with eating, distinguishing them from duodenal ulcers.
Detail
Pathophysiology: Gastric ulcers result from an imbalance between mucosal protective factors (mucus-bicarbonate layer, prostaglandins, blood flow) and damaging factors (acid, pepsin, H. pylori, NSAIDs). H. pylori causes chronic gastritis by inducing inflammation and reducing mucosal defenses; NSAIDs inhibit COX-1, decreasing protective prostaglandin synthesis, impairing mucus/bicarbonate secretion and mucosal blood flow. Unlike duodenal ulcers, gastric ulcers are NOT always associated with increased acid secretion—acid levels may be normal or even low due to mucosal damage.
Clinical features: Epigastric pain that worsens with meals (food-provoked pain) is classic, leading to weight loss due to fear of eating. Nausea and early satiety may occur. Complications include hemorrhage (most common complication overall for PUD), perforation (sudden severe pain, free air under diaphragm on imaging), and gastric outlet obstruction if near pylorus.
Malignancy risk: Gastric ulcers, unlike duodenal ulcers, have malignant potential (associated with intestinal-type gastric adenocarcinoma) and require biopsy of the ulcer margins to rule out cancer, along with follow-up endoscopy to confirm healing. Ulcers on the greater curvature or with irregular, heaped-up margins raise more suspicion for malignancy.
Risk factors: H. pylori infection (~70-90% of gastric ulcers), NSAID/aspirin use, smoking, stress (Cushing ulcers from increased intracranial pressure, Curling ulcers from severe burns), Zollinger-Ellison syndrome (gastrinoma causing acid hypersecretion, though more commonly causes duodenal ulcers).
Diagnosis: Upper endoscopy (EGD) with biopsy is gold standard, especially to exclude malignancy. Testing for H. pylori via urea breath test, stool antigen, or biopsy-based tests (rapid urease test, histology).
Treatment: Triple/quadruple therapy for H. pylori eradication (e.g., PPI + amoxicillin + clarithromycin, or bismuth quadruple therapy), discontinuation of NSAIDs, PPIs to promote healing, and misoprostol (prostaglandin E1 analog) for prevention in patients requiring continued NSAID use. Surgical intervention reserved for perforation, refractory bleeding, or obstruction.
Sources
- First Aid for the USMLE Step 1
- Robbins and Cotran Pathologic Basis of Disease
- UpToDate: Peptic Ulcer Disease
- Harrison's Principles of Internal Medicine
Reviewed by AnkiBoss editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.