Peptic Ulcer Case Wrap Up

Peptic Ulcer Case Wrap Up

The Gastrin Pathway

Protein/amino acids in the stomach → stimulate antral G cells → release gastrin (peptide hormone) → gastrin travels in bloodstream to gastric body → stimulates ECL cells to release histamine → histamine acts on H₂ receptors on parietal cells → activates adenylyl cyclase → ↑ cAMP → protein kinase A activation → H⁺/K⁺-ATPase exocytosed to canalicular membrane → HCl secretion. H₂ receptor antagonists (ranitidine, famotidine = "-tidines") block this H₂-receptor step.

Gastric Emptying Stimulation

Food volume → distension of gastric antrum → myenteric reflexes (local peristalsis) + release of gastrin → increased pyloric pump activity → gastric emptying. The pyloric sphincter prevents too-rapid emptying; its tone is modulated by duodenal feedback (acid/fat slow emptying).

Gastric Mucosal Protection

Aggressive factors (HCl, pepsin, bile salts, H. pylori, NSAIDs, alcohol) must be balanced by protective factors: mucus-bicarbonate layer (secreted by mucous neck cells and surface epithelial cells; traps HCO₃⁻ next to epithelium to neutralise diffused H⁺), prostaglandins (stimulate mucus and HCO₃⁻ secretion + promote mucosal blood flow; NSAIDs inhibit COX → reduce prostaglandins → impair mucosal protection), rapid epithelial cell turnover (surface cells replaced every 3–5 days), and mucosal blood flow (delivers HCO₃⁻ and removes acid).

Helicobacter pylori and Peptic Ulcers

H. pylori is a gram-negative, urease-producing spiral bacterium that colonises the gastric mucus layer. Urease converts urea to ammonia → local pH rise → allows H. pylori to survive the acid environment. H. pylori causes chronic gastritis, impairs mucosal defences, increases gastrin secretion (via antritis inhibiting D cells → less somatostatin → more gastrin) → excessive HCl → imbalance between aggressive and protective factors → duodenal ulcer (most common site) or gastric ulcer. Treatment: triple therapy (PPI + amoxicillin + clarithromycin for 7–14 days).