Higher acid delivery to the duodenum: Patients with duodenal ulcer disease tend to have higher basal and maximal gastric acid output. In contrast, gastric-ulcer patients as a group often have normal or reduced acid production. This makes the duodenal bulb particularly susceptible to acid-peptic injury. - Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 4177; Mulholland and Greenfield's Surgery, p. 3255

Typical pattern of H. pylori infection: Antral-predominant H. pylori gastritis reduces somatostatin, increases gastrin, and therefore increases acid secretion. The resulting acid load causes gastric metaplasia in the duodenal bulb, which can become colonized by H. pylori, inflamed, and ulcerated. Eradication reverses the raised gastrin and acid secretion in many patients with duodenal ulcers. - Bailey and Love's Short Practice of Surgery, p. 8503; Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 4177

The duodenal bulb has comparatively less reserve against repeated acid exposure: It must neutralize acidic chyme rapidly using bicarbonate-rich pancreatic and biliary secretions. When acid delivery exceeds this buffering and mucosal-defense capacity, ulceration develops.

Gastric ulcer needs a different balance of injury: Gastric ulcers more often occur when protective factors fail, such as from NSAID-related prostaglandin depletion, mucosal inflammation/atrophy, bile reflux, smoking, or impaired blood flow. Acid can be normal or low, so excessive acid is not as central as in duodenal ulcer disease.