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Alcohol-induced gastric mucosal injury

Introduction
Cause
Examine
Diagnosis

Introduction

Introduction Gastric mucosal damage can be induced when the internal and external damage factors such as ethanol, non-steroidal anti-inflammatory drugs (NSAID), acid, and bile reach a certain concentration or dose. Gastric mucosal injury is manifested as a programmed injury response. First, the superficial mucosal damage is caused by the exfoliation of the epithelial epithelium; the damage is further developed, and the microvascular endothelial cell injury will lead to mucosal ischemia, hypoxia, tissue necrosis, and deep mucosa Injury (smashed or ulcerated).

Cause

Cause

Oral intake of alcohol can directly damage the lipoprotein layer of the gastric mucosal epithelium, damage the gastric mucosal barrier, and the hydrogen ions in the gastric juice can be oozing back into the mucosal epithelial cells, resulting in the release of histamine, serotonin and heparin, causing submucosal artery. Short circuit, increased capillary pressure and permeability, eventually mucosal congestion, red blood cell exudation, gastric mucosal erosion, and even superficial ulcers; excessive drinking can cause pyloric spasm, prolong gastric emptying time, easily cause nausea Vomiting, often manifested as acute bleeding and gastritis under gastroscope. Recent studies have shown that gastric mucosal damage and tissue prostaglandin E2 (PGE2), nitric oxide (NO) reduction, tumor necrosis factor (TNF-) Increase related.

Examine

an examination

Related inspection

Pepsin gastric ultrasound examination of gastric occult blood test fungal isolation and identification of fiber endoscopy

Contrast-enhanced ultrasonography has a certain diagnostic value for acute gastric mucosal injury. A gastroscope can also be used to check the diagnosis.

Gastroscopic examination, to observe the color of the gastric mucosa, bleeding points, congestion and erosion damage, compared before and after changes, according to the degree of disease is divided into light, moderate and severe damage.

Gastrointestinal contrast-enhanced ultrasonography can clearly show the structural level of the stomach wall and has a certain diagnostic value for acute gastric mucosal injury.

Regardless of the invasive factors, the gastric mucosal damage caused by it is a programmed injury response: firstly, the superficial mucosal damage is caused by the exfoliation of the epithelial epithelium; the damage is further developed, and the microvascular endothelial cell injury will lead to mucosal ischemia and deficiency. Oxygen, tissue necrosis, resulting in deep mucosal damage (erosive or ulceration).

Diagnosis

Differential diagnosis

Differential diagnosis of alcoholic gastric mucosal injury:

1, gastric mucosal congestion: gastroscopy of acute gastritis can be seen mucosal extensive congestion, edema, erosion, bleeding, sometimes visible mucus spots on the mucosal surface or reflux bile. When Hp is infected with gastritis, micronodular formation of gastric mucosa can also be seen.

2, gastric mucosal injury: the entire inner surface of the stomach is covered with a layer of mucosal tissue, which can secrete mucus, forming a mucous membrane-mucosal barrier of the stomach to protect the stomach tissue. Gastric mucosal injury is more common in gastritis and gastric ulcer.

3, gastric mucosal shedding: gastric mucosa shedding is more relaxed gastric mucosa, when the stomach contraction, the gastric mucosa near the pylorus part is into the duodenal bulb cavity. The clinical symptoms are symptoms of gastritis.

4, gastric mucosal thickening: "stomach mucosa thickening" is one of the clinical manifestations of "chronic atrophic gastritis" (intestinal, atypical hyperplasia), chronic atrophic gastritis is a common stomach disease. Arteriosclerosis, insufficient blood flow to the stomach, and hobby of tobacco and tea are all likely to impair the barrier function of the gastric mucosa and cause chronic atrophic gastritis. In atrophic gastritis, the gastric mucosa is atrophied and replaced by intestinal epithelial cells, ie intestinal metaplasia; inflammation continues to evolve, cell growth is atypical, ie, metastasis; even cell proliferation and carcinogenesis.