Gastritis

Gastritis is a topic covered in the 5-Minute Clinical Consult.

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5-Minute Clinical Consult

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Basics

Description

  • 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 certain medications (e.g., dabigatran, an oral thrombin inhibitor)
  • Infectious gastritis
    • Acute and/or chronic Helicobacter pylori infection
    • Viral infection (reaction to systemic infection)
  • Atrophic gastritis
    • Autoimmune versus environmental
    • Frequent in the elderly
    • Primarily from long-standing H. pylori infections
    • Prolonged proton pump inhibitor (PPI) use
    • Major risk factor for gastric cancer
    • Associated with primary (pernicious) anemia

Geriatric Considerations
Persons age >60 years often harbor H. pylori infection.

Pediatric Considerations
Gastritis rarely occurs in infants or children; increases in prevalence with age

Epidemiology

  • 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 infections
  • Alcohol
  • Aspirin and other NSAIDs
  • Bile reflux
  • Pancreatic enzyme reflux
  • Portal hypertensive gastropathy
  • Emotional stress

Genetics
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.

Risk Factors

  • 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
  • Radiation
  • Ischemia
  • Pernicious anemia
  • Gastric mucosal atrophy

General Prevention

  • Avoid injurious drugs or chemical agents.
  • Patients with hypovolemia or hypoxia (especially ICU patients) should receive prophylaxis with H2 receptor antagonists, prostaglandins, or sucralfate.
  • 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

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