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- Inflammation of the gastric mucosa
- Patchy erythema of gastric mucosa
- Common on endoscopy; usually insignificant
- Erosive gastritis or reactive gastropathy
- A reaction to mucosal injury by a noxious agent (especially NSAIDs or alcohol)
- Damage to the surface epithelium caused by mucosal hypoxia or the direct action of NSAIDs
- Reflux gastritis
- A reaction to protracted reflux exposure to biliary and pancreatic fluid
- Typically limited to the prepyloric antrum
- Hemorrhagic gastritis (stress ulceration)
- A reaction to hemodynamic disorder (e.g., hypovolemia or hypoxia [shock])
- Common in ICU patients, particularly after severe burns and trauma
- Seen rarely with dabigatran (oral thrombin inhibitor)
- Infectious gastritis
- Acute and/or chronic Helicobacter pylori infection
- Viral infection, usually as a component of systemic infection.
- Atrophic gastritis
- Autoimmune versus environmental
- Frequent in the elderly
- Primarily from long-standing H. pylori infections
- May be caused by prolonged proton pump inhibitor (PPI) use
- Major risk factor for gastric cancer
- Associated with primary (pernicious) anemia
Persons age >60 years often harbor H. pylori infection.
Gastritis rarely occurs in infants or children; increasing prevalence with age
- Predominant age: all ages (more common in elderly)
- Predominant sex: male = female
Etiology and Pathophysiology
- Noxious agents cause a breakdown in the gastric mucosal barrier, exposing epithelium to injury.
- Infection: H. pylori (most common cause), Staphylococcus aureus exotoxins, and viral infection
- Aspirin and other NSAIDs
- Bile reflux
- Pancreatic enzyme reflux
- Portal hypertensive gastropathy
- Emotional stress
Unknown, but observational studies show that 10% of a given population is never colonized with H. pylori, regardless of exposure. Genetic variations in TLR1 may help explain some of this observed variation in individual risk for H. pylori infection.
- Age >60 years—prevalence of 50–60% by age 60 years
- Exposure to potentially noxious drugs or chemicals (e.g., alcohol or NSAIDs)
- Hypovolemia, hypoxia (shock), burns, head injury, complicated postoperative course
- Autoimmune diseases (thyroid disease and diabetes)
- Family history of H. pylori and/or gastric cancer
- Stress (hypovolemia or hypoxia)
- Tobacco use
- Pernicious anemia
- Gastric mucosal atrophy
- Avoid injurious drugs or chemical agents.
- Patients with hypovolemia or hypoxia (especially ICU patients) should receive prophylactic therapy. H2 receptor antagonists, prostaglandins, or sucralfate are commonly used for gastric mucosal protection.
- Consider testing for H. pylori (and eradicating if present) in patients on long-term NSAID therapy.
Commonly Associated Conditions
- Gastric or duodenal peptic ulcer
- Primary (pernicious) anemia—atrophic gastritis
- Portal hypertension (HTN), hepatic failure
- Mucosa-associated lymphoid tissue (MALT) lymphoma