Gastric Ulcer
Gastric ulcers characteristically worsen with eating, in contrast to duodenal ulcers where food typically provides relief. 1
Clinical Presentation and Pain Pattern
The key distinguishing feature is that gastric ulcer pain is exacerbated by food intake, while duodenal ulcer pain is typically relieved by eating and worsens 2-3 hours after meals or at night when the stomach is empty. 1
- Gastric ulcer patients often experience epigastric discomfort that intensifies during or shortly after meals, leading to food avoidance and weight loss 1
- This pain pattern occurs because food stimulates acid secretion, which directly irritates the gastric ulcer 1
- Patients may present with loss of appetite specifically because eating triggers pain 1
Underlying Etiology in Context
The risk factors you've identified are highly relevant:
- H. pylori infection is responsible for the majority of gastric ulcers (though slightly less commonly than duodenal ulcers), and eradication therapy is essential 2, 3
- NSAID use is a major independent risk factor, with NSAIDs causing gastric ulcers more frequently than duodenal ulcers 2
- The combination of H. pylori and NSAIDs synergistically increases ulcer risk more than sixfold, particularly for bleeding complications 4
- Smoking increases ulcer risk and impairs healing 2
Diagnostic Approach
For patients over 45 years with new dyspeptic symptoms or those with alarm features (weight loss, progressive dysphagia, hematemesis, melena), immediate endoscopy is mandatory to exclude gastric malignancy, which accounts for over 10,000 deaths annually in England and Wales. 2
- Younger patients (<45 years) without alarm symptoms can be managed with H. pylori testing and treatment 2
- All gastric ulcers require endoscopic biopsy to exclude malignancy, unlike duodenal ulcers 5
- Endoscopic follow-up is essential for gastric ulcers to confirm healing 2
Management Priorities
Discontinue NSAIDs immediately if possible—this single intervention heals 95% of NSAID-induced ulcers and reduces recurrence from 40% to 9%. 5
- If NSAIDs cannot be stopped, add PPI therapy indefinitely for gastroprotection 2, 3
- Test for H. pylori and eradicate if positive using triple therapy (PPI + amoxicillin 1000mg twice daily + clarithromycin 500mg twice daily for 14 days) 3, 6
- Standard PPI therapy (omeprazole 20mg daily) for 4-8 weeks is first-line for ulcer healing 6
Critical Pitfall
H2-receptor antagonists are inadequate for gastric ulcers—they reduce duodenal ulcer risk but not gastric ulcer risk, making them inappropriate for this clinical scenario. 2 PPIs are superior and should be used instead. 2