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Acute Gastritis

  • Acute Gastritis does not refer to a unique pathophysiological entity but is rather a histological description of acute inflammation occurring in the gastric mucosa. Bouts of acute gastritis are typically transient; however, the pathogenesis is poorly understood. Several general mechanisms may contribute to the development of acute gastritis including increased stomach acid production and reduced bicarbonate production along with reduced blood flow or direct injury to the gastric mucosa.
  • Heavy use of certain exogenous chemicals may result in acute gastritis including NSAIDs, especially aspirin, along with heavy smoking or alcohol consumption. Reduced blood flow to the stomach or the gastric mucosa, resulting in their ischemia, can give rise to acute gastritis. Uremia is also a cause via cryptic mechanisms. Gastric infections with certain microorganisms such as Salmonella can also give rise to acute gastritis.
  • Depending on the etiology, histological signs of acute gastritis may be focal or diffuse and are characterized by a neutrophilic infiltration of the gastric mucosa. Frequently, the gastric epithelium, and in more severe cases the gastric mucosa, is eroded. Although technically this would be considered an ulceration, the term acute gastric ulceration is reserved for a distinct pathological entity which is defined as ulceration past the gastric mucosa and into the gastric submucosa.
Clinical Consequences
  • Acute Gastritis is frequently subclinical but may manifest with epigastric pain, nausea, or vomiting. Signs of mild to massive upper GI bleeding, including melena or 'coffee ground' hematemesis, may also arise.