Gastritis

Basics

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

There's more to see -- the rest of this topic is available only to subscribers.