Pathology of the Stomach - Part 1

Overview of Gastric Diseases

• Includes acute gastritis, chronic gastritis, acute gastric ulcer, and chronic peptic ulcers.
• Understanding normal anatomy and histology is essential before discussing pathology.

Normal Anatomy & Histology of the Stomach

• Four main parts: cardia, fundus, body, and antrum (pylorus).
• Cardia: Features mucin-secreting foveolar cells that protect the stomach lining.
• Body and Fundus: Contains parietal cells (secrete HCl) and chief cells (secrete pepsin).
• Antrum: Houses neuroendocrine G cells that stimulate parietal cells to produce acid.

Histological Features

• Histology varies across stomach regions; thickness differs as well.
• In H&E stain, parietal cells appear pink due to acid production.
• The antrum appears bluish with antrum-type epithelium lacking parietal cells.

Inflammatory Conditions of the Stomach

• Acute gastritis and gastropathy often used interchangeably; both involve mucosal injury.
• Acute Gastritis: Characterized by neutrophilic infiltration.
• Gastropathy: Damage and regeneration with minimal to no inflammation; often related to NSAIDs and stress.

Causes and Clinical Features of Acute Gastritis

• NSAIDs are the primary cause; symptoms may remain asymptomatic or present as:
  • Epigastric pain
  • Nausea and vomiting
  • Severe cases may lead to erosions, ulcers, hematemesis, and melena.

Pathogenesis of Gastritis

• Similar mechanisms underlie acute and chronic gastritis.
• Protective mechanisms counteract damaging factors like HCl and peptic enzymes:
  • Surface mucus secretion forms a barrier against acidity.
  • Bicarbonate maintains alkaline pH to protect the stomach lining.
  • Profuse mucosal blood flow aids in rapid regeneration of gastric mucosa and buffers acidity.
  • Epithelial regenerative capacity and prostaglandin synthesis play vital roles.

Injurious Stimuli Leading to Gastritis

• Common injurious factors include:
  • Helicobacter pylori infection
  • Use of NSAIDs and aspirin (reduce prostaglandin levels)
  • Tobacco and smoking
  • Alcohol consumption
  • Conditions causing gastric hyperacidity.