gastric ulcer
Summary
A gastric ulcer is a break in the mucosal lining of the stomach extending through the muscularis mucosa, most commonly caused by H. pylori infection or NSAID use. Pain classically worsens with eating (unlike duodenal ulcers, which improve with food). Requires evaluation for malignancy since gastric ulcers can be cancerous.
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 predominantly in the antrum, impairing mucosal defenses; it accounts for a large majority of gastric ulcers. NSAIDs inhibit COX-1, reducing protective prostaglandin synthesis, decreasing mucus/bicarbonate secretion and mucosal blood flow. Other risk factors include smoking, alcohol, stress (Curling ulcer in burns, Cushing ulcer in CNS injury), and Zollinger-Ellison syndrome (gastrinoma causing acid hypersecretion, though more classically duodenal/multiple ulcers).
Clinical features: Epigastric pain that classically worsens with meals (food stimulates acid secretion, exacerbating mucosal damage), weight loss (due to pain-associated food avoidance), nausea. Can present with complications: hemorrhage (hematemesis, melena), perforation (acute abdomen, free air under diaphragm), gastric outlet obstruction, and rarely penetration into adjacent organs (e.g., pancreas causing referred back pain).
Location: Most commonly found on the lesser curvature of the antrum/body junction. Ulcers on the greater curvature or elsewhere raise higher suspicion for malignancy.
Malignancy risk: Unlike duodenal ulcers (almost always benign), gastric ulcers require biopsy of the ulcer margins to rule out gastric adenocarcinoma. Malignant ulcers often have irregular, heaped-up margins, while benign ulcers have smooth, punched-out edges with radiating folds.
Diagnosis: Upper endoscopy (EGD) is gold standard, allowing direct visualization and biopsy. Testing for H. pylori via urea breath test, stool antigen, or biopsy-based tests (rapid urease test, histology).
Treatment: Eradicate H. pylori if present (triple/quadruple therapy: PPI + clarithromycin + amoxicillin/metronidazole, or bismuth-based quadruple therapy). Discontinue NSAIDs if possible. PPIs are first-line for acid suppression and healing. Repeat endoscopy typically performed in gastric ulcers to confirm healing and rule out malignancy, unlike duodenal ulcers.
High-yield boards points: Gastric ulcer pain worsens with food (weight loss) vs. duodenal ulcer pain improves with food (weight gain). Gastric ulcers require biopsy to exclude malignancy; duodenal ulcers rarely require biopsy. H. pylori is present in ~70% of gastric ulcers and ~90% of duodenal ulcers.
Sources
- First Aid for the USMLE Step 1
- Robbins and Cotran Pathologic Basis of Disease
- UpToDate: Peptic ulcer disease
- Goldman-Cecil 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.