Stress-Induced Gastritis
- PMID: 29763101
- Bookshelf ID: NBK499926
Stress-Induced Gastritis
Excerpt
Gastric acid production is necessary for the body to digest food and break down nutritional components into absorbable amino acids, carbohydrates, and fats. Most of the acid is produced when gastric pH stimulates the release and activation of various digestive enzymes. The stomach is a relatively acidic environment with a pH of less than 4.0, which can drop to 2.0 with parietal cells. Parietal cells live in the fundus and the body of the stomach and secrete hydrogen ions. Three predominant substances stimulate hydrogen ion secretion.
Neurotransmitter acetylcholine (ACH) stimulates parietal cells via the phospholipase pathway to secrete hydrogen. Phospholipase is stimulated on the cellular wall, cleaving PIP into IP3 and DAG, releasing calcium ions into the cytoplasm. These calcium ions bind calmodulin and stimulate protein kinase C (PKC). PKC leads to the phosphorylation and activation of the hydrogen/potassium ATPase (H/K ATPase), resulting in acid secretion. The source of ACH is from the vagus nerve (cranial nerve X).
Gastrin is a hormone known to stimulate hydrogen ion secretion via the same mechanism of ACH, resulting in the activation of the H/K ATPase. Gastrin is predominantly secreted via the G cells, located in the antrum of the stomach, which are stimulated by the presence of amino acids and ACH in the gastric lumen.
Histamine stimulates parietal cells to secrete hydrogen ions via the cAMP pathway via the activation of protein kinase A and activate the H/K ATPase. Histamine is predominantly secreted via the mast cells from the surrounding gastric tissues.
The dysregulation of the above-mentioned mechanisms can result in hemorrhagic or erosive gastropathy, also known as stress gastritis. The mucosal barrier is disrupted secondary to an acute illness. This article aims to discuss the etiology and methods of preventing and identifying stress gastritis.
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Sections
- Continuing Education Activity
- Introduction
- Etiology
- Epidemiology
- Pathophysiology
- Histopathology
- History and Physical
- Evaluation
- Treatment / Management
- Differential Diagnosis
- Pertinent Studies and Ongoing Trials
- Staging
- Prognosis
- Complications
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- Deterrence and Patient Education
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