Peptic ulcer disease is a condition in which discrete breaks in the mucosa of the stomach or proximal duodenum extend through the muscularis mucosae, produced when aggressive luminal factors, chiefly gastric acid and pepsin, overwhelm mucosal defense. The two dominant causes are infection with Helicobacter pylori, w…
Peptic ulcer disease is a condition in which discrete breaks in the mucosa of the stomach or proximal duodenum extend through the muscularis mucosae, produced when aggressive luminal factors, chiefly gastric acid and pepsin, overwhelm mucosal defense. The two dominant causes are infection with Helicobacter pylori, which incites chronic gastritis and impairs mucosal integrity, and the use of nonsteroidal anti-inflammatory drugs, which suppress protective prostaglandin synthesis; hypersecretory states such as Zollinger–Ellison syndrome account for a minority. Duodenal and gastric ulcers differ in their typical relationship to meals and in the balance of underlying mechanisms. Characteristic features include epigastric pain, dyspepsia, nausea, and, when complications arise, gastrointestinal bleeding presenting as iron-deficiency anemia, melena, or hematemesis, as well as perforation and gastric outlet obstruction. Because gastric ulcers may harbor or progress to malignancy, persistent or atypical lesions warrant endoscopic evaluation with biopsy, and unexplained iron deficiency prompts assessment of the digestive tract. Diagnosis rests on endoscopy together with testing for H. pylori, and management combines acid suppression, typically with proton pump inhibitors, eradication of H. pylori when present, and withdrawal of injurious drugs. Endoscopic and occasionally surgical intervention controls bleeding and treats complications, while prevention focuses on judicious NSAID use and timely infection treatment to restore the balance between mucosal injury and repair.
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