• Inflammatory response of gastric mucosa to injury – “gastritis”
  • 3 lines of defense of gastric mucosa:
    • Mucous layer that forms protective pH gradient
    • Surface epithelial cells that can repair small defects
    • Postepithelial barrier that neutralizes any acid that has traversed first 2 layers
  • No definite link between histologic gastritis and dyspeptic symptoms
  • Epithelial cell damage with no associated inflammation – “gastropathy”


  • Common causes of gastritis: Infections, autoimmune, drugs (i.e., cocaine), hypersensitivity, stress
  • Common causes of gastropathy: Endogenous or exogenous irritants, such as bile reflux, alcohol, or aspirin and NSAIDs, ischemia, stress, chronic congestion
  • Acute gastritis:
    • Stress (sepsis, burns, trauma):
      • Decrease in splanchnic blood flow leading to decreased mucus production, bicarbonate secretion, and prostaglandin synthesis
      • Results in mucosal erosions and hemorrhage
    • Alcohol:
      • Induces production of leukotrienes that cause microvascular stasis, engorgement, and increased vascular permeability
      • Leads to hemorrhage
    • NSAIDs, including aspirin:
      • Interfere with prostaglandin synthesis, leading to similar cascade as induced by alcohol
      • Results in mucosal erosions
    • Steroids
  • Chronic gastritis:
    • Produced by Helicobacter pylori
    • Mechanism of H. pylori unclear:
      • Gram-negative spiral bacteria found in gastric mucous layer
      • Contains enzyme urease that allows it to change pH level (alkaline) of its microenvironment

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