Peptic Ulcer

Definition

Peptic ulcer is a full-thickness mucosal defect that penetrates through the muscularis mucosae, occurring in areas exposed to acid-pepsin digestion. Classic sites are the gastric antrum and the first part of the duodenum (duodenal ulcer). H. pylori and NSAIDs are the two principal aetiological factors.

General / Essential Features

• Sharply demarcated, punched-out ulcer edges (unlike malignant ulcer with heaped-up edges)
• Degeneration / necrosis of mucosal epithelium at ulcer base
• Four-zone histology: fibrinous exudate → coagulation necrosis → granulation tissue → fibrous scar
• Blood vessels at the ulcer base — erosion causes haemorrhage
• Inflammatory cells: lymphocytes, plasma cells, eosinophils in ulcer margin
• Perforation of ulcer leads to acute peritonitis

Sites

• Duodenal ulcer (DU): anterior wall of first part of duodenum — most common
• Gastric ulcer (GU): lesser curvature of the antrum
• Stomal ulcer: at gastroenterostomy anastomosis
• Zollinger–Ellison syndrome: multiple ulcers in atypical sites (jejunum)

Pathophysiology

Imbalance between aggressive factors (acid, pepsin, H. pylori, NSAIDs) and defensive factors (mucus, bicarbonate, prostaglandins, epithelial renewal). NSAIDs inhibit COX-1, reducing mucoprotective prostaglandin synthesis. H. pylori undermines the mucus layer and impairs bicarbonate secretion. Acid contact with exposed lamina propria causes progressive tissue necrosis.

Etiology

• H. pylori infection: ~80% of duodenal ulcers, ~70% of gastric ulcers
• NSAIDs / aspirin: second commonest cause — especially in elderly
• Zollinger–Ellison syndrome: gastrinoma causing massive acid hypersecretion
• Stress ulcers: Curling (burns), Cushing (raised ICP) ulcers
• Smoking: delays healing, increases recurrence

Clinical Features

• DU: epigastric pain relieved by food and antacids; nocturnal waking pain
• GU: epigastric pain precipitated or worsened by food
• Haematemesis or melaena (bleeding — most common complication)
• Sudden severe abdominal pain: perforation → peritonitis
• Pyloric obstruction: projectile vomiting, succussion splash

Diagnosis

• Upper GI endoscopy (OGD): visualises ulcer; biopsy GU to exclude malignancy
• H. pylori testing: CLO test, breath test, stool antigen
• Barium meal: filling defect (rarely used now)
• Fasting serum gastrin: if ZES suspected (>1000 pg/mL diagnostic)

Treatment

• H. pylori eradication: 7-day triple therapy (PPI + amoxicillin + clarithromycin)
• PPI (omeprazole 20 mg BD) for 4–8 weeks
• Stop NSAIDs; use selective COX-2 inhibitors with PPI if unavoidable
• Emergency: endoscopic haemostasis (adrenaline injection, clips) for bleeding
• Surgery: rarely — perforated ulcer repair (Graham patch), vagotomy