Gastritis
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Basics
Description
- 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”
Etiology
- 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
- Stress (sepsis, burns, trauma):
- 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
-- To view the remaining sections of this topic, please log in or purchase a subscription --
Basics
Description
- 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”
Etiology
- 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
- Stress (sepsis, burns, trauma):
- 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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