stomach

Stomach L.3

Acute Gastritis
Acute gastritis is a transient mucosal inflammatory process that may be asymptomatic or cause variable degrees of epigastric pain, nausea, and vomiting. In more severe cases there may be mucosal erosion, ulceration, hemorrhage, hematemesis, melena, or, rarely, massive blood loss.

Pathogenesis
Multiple mechanisms have evolved to protect the gastric mucosa from digestions by acid:
1. Mucin secreted by surface foveolar cells forms a thin layer of mucus that prevents large food particles from directly touching the epithelium.
2. The mucus layer also promotes formation of an “unstirred” layer of fluid over the epithelium that protects the mucosa and has a neutral pH as a result of bicarbonate ion secretion by surface epithelial cells.
3. the rich vascular supply to the gastric mucosa delivers oxygen, bicarbonate, and nutrients while washing away acid that has back-diffused into the lamina propria.
Acute or chronic gastritis can occur after disruption of any of these protective mechanisms. For example, reduced mucin synthesis in elderly persons is suggested to be one factor that explains their increased susceptibility to gastritis. Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with cytoprotection normally provided by prostaglandins or reduce bicarbonate secretion, both of which increase the susceptibility of the gastric mucosa to injury.

Acute Peptic Ulceration
Focal, acute peptic injury is a well-known complication of therapy with NSAIDs as well as severe physiologic stress. Such lesions include
• Stress ulcers, most commonly affecting critically ill patients with shock, sepsis, or severe trauma