## NSAID-Induced Gastrointestinal Ulceration Sites **Key Point:** The gastric body along the lesser curvature is the most common site of NSAID-induced ulceration, accounting for approximately 60–70% of cases. ### Pathophysiology NSAIDs inhibit COX-1 and COX-2, reducing prostaglandin synthesis. Prostaglandins normally protect gastric mucosa by: 1. Stimulating mucus and bicarbonate secretion 2. Maintaining mucosal blood flow 3. Promoting epithelial cell proliferation Without this protection, NSAIDs directly damage the mucosa and inhibit healing. ### Distribution of NSAID-Induced Ulcers | Site | Frequency | Notes | |------|-----------|-------| | **Gastric body (lesser curvature)** | **60–70%** | **Most common; NSAID-specific** | | Duodenum | 20–30% | More common with H. pylori or acid hypersecretion | | Gastric antrum | 5–10% | Less common with NSAIDs alone | | Pyloric channel | Rare | Unusual location | **Clinical Pearl:** Gastric ulcers from NSAIDs typically occur along the lesser curvature because this area has reduced blood flow and is more vulnerable to direct mucosal injury. **High-Yield:** In contrast, duodenal ulcers are more common in H. pylori infection and Zollinger–Ellison syndrome (acid hypersecretion states), not NSAIDs. ### Risk Factors for NSAID Ulceration - Age > 65 years - H. pylori co-infection - High-dose or prolonged NSAID use - Concurrent corticosteroid or anticoagulant use - History of peptic ulcer disease **Tip:** When an older patient on NSAIDs presents with GI bleeding, suspect a gastric ulcer on the lesser curvature until proven otherwise.
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.