Pathology

Pathology/C/34

Peptic ulcers

消化性潰瘍

タグ
High-yield / ポイント

Definitions

  • Erosion: circumscribed necrosis-induced defect of mucosa that does not cross the muscularis mucosae
  • Ulcer: defect that extends beyond the mucosa

Peptic Ulcers — Overview

  • Most common ulcers of the alimentary tract
  • Chronic, usually solitary; occur wherever GI tract is exposed to acidic peptic juices
  • 98% occur in the first part of the duodenum or in the stomach

Pathogenesis

Imbalance between gastroduodenal defense and damaging forces:

  • Defense: surface mucus secretion, mucosal blood supply, HCO₃⁻ secretion, PGI synthesis
  • Damaging forces (↑): H. pylori infection, NSAIDs, cigarette smoking, alcohol, gastric hyperacidity
  • Impaired defense (↓): stress situations (shock, burns), delayed gastric emptying

H. pylori Mechanisms:

  • ↑ pro-inflammatory cytokines
  • Toxins → epithelial injury
  • Urease → breakdown of urea → toxic compounds
  • Phospholipase + protease → breakdown of glycoprotein-rich mucous layer → ↓ mucosal defense
  • Enhances gastric acid secretion + impairs duodenal HCO₃⁻ production → ↓ luminal pH in duodenum

NSAIDs Mechanisms:

  • Suppress mucosal prostaglandin synthesis → ↑ HCl secretion + ↓ HCO₃⁻ + ↓ mucin production
  • Major cause of peptic ulcers in H. pylori-negative patients

Morphology

Macroscopic:

  • Single, sharply demarcated, round ulcers 1–2.5 cm in diameter
  • Surrounding mucosal folds radiate → star-like appearance
  • Chronic ulcer: necrosis reaches muscular layer or serosa

Microscopic — 4 layers:

  1. Cell debris and neutrophils
  2. Fibrinoid necrosis
  3. Granulation tissue (PMNLs)
  4. Scar tissue

Clinical Features

  • Epigastric pain = burning sensation
  • Nausea, vomiting, bloating, weight loss

Complications:

  • Hemorrhage: mild to severe; from eroded vessels
  • Perforation: entire wall thickness destroyed → peritonitis
  • Penetration: necrosis of wall enters surrounding structures
  • Pyloric stenosis: progressive shrinkage of fibrotic/scar tissue
  • Malignant transformation (preneoplastic condition)

Therapy: Antibiotics against H. pylori + PPIs + H₂ receptor antagonists

Duodenal Ulcer (specific features)

  • Penetration into the pancreas
  • Profuse bleeding from erosion of superior pancreaticoduodenal artery → hemorrhagic shock
  • No risk of malignant transformation

💡 High-yield: Erosion = doesn’t cross muscularis mucosae; ulcer = extends beyond mucosa. 98% in duodenum or stomach. H. pylori = urease + toxins + ↓ mucus. NSAIDs = ↓ prostaglandins → ↑ HCl + ↓ mucus. 4 microscopic layers: debris → fibrinoid necrosis → granulation → scar. Complications: hemorrhage, perforation (peritonitis), pyloric stenosis. Duodenal ulcer: NO malignant transformation.