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  • Peptic ulcer disease (PUD) refers to ulcerative disorders of the upper gastrointestinal (GI) tract that require acid and pepsin for their formation. The three common etiologies include (1) Helicobacter pylori infection, (2) nonsteroidal anti-inflammatory drug (NSAID) use, and (3) stress-related mucosal damage (SRMD).


  • Benign gastric ulcers, erosions, and gastritis can occur anywhere in the stomach, but the antrum and lesser curvature are the most common locations. Most duodenal ulcers occur in the first part of the duodenum (duodenal bulb).

  • Pathophysiology is determined by the balance between aggressive factors (gastric acid and pepsin) and protective factors (mucosal defense and repair). Gastric acid, H. pylori infection, and NSAID use are independent factors that contribute to disruption of mucosal integrity. Increased acid secretion may be involved in duodenal ulcers, but patients with gastric ulcers usually have normal or reduced acid secretion (hypochlorhydria).

  • Mucus and bicarbonate secretion, intrinsic epithelial cell defense, and mucosal blood flow normally protect the gastroduodenal mucosa from noxious endogenous and exogenous substances. Endogenous prostaglandins (PGs) facilitate mucosal integrity and repair. Disruptions in normal mucosal defense and healing mechanisms allow acid and pepsin to reach the gastric epithelium.

  • H. pylori infection causes gastric mucosal inflammation in all infected individuals, but only a minority develops an ulcer or gastric cancer. Bacterial enzymes (urease, lipases, and proteases), bacterial adherence, and H. pylori virulence factors produce gastric mucosal injury. H. pylori induces gastric inflammation by altering the host inflammatory response and damaging epithelial cells.

  • Nonselective NSAIDs (including aspirin) cause gastric mucosal damage by two mechanisms: (1) direct or topical irritation of the gastric epithelium, and (2) systemic inhibition of endogenous mucosal PG synthesis (the primary mechanism). COX-2 selective inhibitors have a lower risk of ulcers and related GI complications than nonselective NSAIDs. Addition of aspirin to a selective COX-2 inhibitor reduces its ulcer-sparing benefit and increases ulcer risk.

  • Use of corticosteroids alone does not increase risk of ulcer or complications, but ulcer risk is doubled in corticosteroid users taking NSAIDs concurrently.

  • Cigarette smoking has been linked to PUD, impaired ulcer healing, and ulcer recurrence. Risk is proportional to amount smoked per day.

  • Psychological stress has not been shown to cause PUD, but ulcer patients may be adversely affected by stressful life events.

  • Carbonated beverages, coffee, tea, beer, milk, and spices may cause dyspepsia but do not appear to increase PUD risk. Ethanol ingestion in high concentrations is associated with acute gastric mucosal damage and upper GI bleeding but is not clearly the cause of ulcers.


  • Abdominal pain is the most frequent PUD symptom. Pain is often epigastric and described as burning but can present as vague discomfort, abdominal fullness, or cramping. Nocturnal pain may awaken patients from sleep, especially between 12 AM and 3 AM.

  • Pain from duodenal ulcers often occurs 1–3 hours after meals and is usually relieved by food, whereas food may precipitate ...

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