duodenal ulcer

Duodenal ulcers occur in the first part of the duodenum, most commonly on the anterior wall (posterior ulcers risk perforation into gastroduodenal artery causing massive GI bleed, or penetration into pancreas causing pancreatitis). Pathophysiology involves increased acid secretion combined with mucosal defense breakdown - H. pylori infection (present in ~90% of cases) causes chronic gastritis and increases gastrin release by disrupting somatostatin-secreting D cells, while NSAIDs inhibit COX-1, reducing protective prostaglandins (PGE2) that normally stimulate mucus/bicarbonate secretion. Clinically, pain is relieved by food/antacids (unlike gastric ulcers where eating worsens pain) because food buffers acid and duodenal mucosa has less acid-stimulated pain response initially, though rebound acid secretion causes pain 2-3 hours later. Risk factors include H. pylori, NSAIDs, smoking, Zollinger-Ellison syndrome (gastrinoma causing ulcers refractory to therapy, often multiple/distal), and blood group O. Complications include upper GI bleeding (most common complication, presents with melena, hematochezia if brisk), perforation (sudden severe pain, free air under diaphragm on imaging, peritonitis), and gastric outlet obstruction from scarring/edema causing chronic pyloric stenosis-like presentation. Diagnosis involves upper endoscopy (biopsy not routinely needed for benign duodenal ulcers unlike gastric ulcers which require biopsy to rule out malignancy), H. pylori testing (urea breath test, stool antigen, biopsy with rapid urease test), and considering gastrin levels if refractory or atypical presentation to screen for Zollinger-Ellison syndrome. Treatment includes H. pylori eradication (triple therapy: PPI + amoxicillin + clarithromycin, or quadruple therapy with bismuth), PPIs to reduce acid, discontinuing NSAIDs, and surgery reserved for complications (perforation, refractory bleeding, obstruction) - vagotomy and antrectomy historically used to reduce acid secretion.