What are the factors of acute gastric mucosal lesions?

Acute gastric mucosal lesions are a common stomach disease. The main cause is erosion or bleeding of the gastric mucosa, or shallow ulcers. At this time, the patient's condition becomes more acute, often leading to some acute hemorrhagic gastritis. There are many causes of acute gastric mucosal lesions, such as frequent drinking, serious infection, excessive fatigue and so on.

1. Exogenous factors

Certain drugs, such as non-steroidal anti-inflammatory drugs aspirin, phenylbutazone, indomethacin, corticosteroids, certain antibiotics, alcohol, etc., can damage the gastric mucosal barrier, leading to increased mucosal permeability, and the hydrogen ions of gastric juice back-penetrating into the gastric mucosa, causing gastric mucosal erosion and bleeding. This disease is caused by decreased renal mucus secretion and slower renewal of gastric mucosal epithelial cells.

2. Endogenous factors

Including severe infection, severe trauma, intracranial hypertension, severe burns, major surgery, shock, excessive stress and fatigue, etc. Under stress, the sympathetic nerves and vagus nerves can be excited. The former causes spasm and contraction of the gastric mucosal blood vessels, reducing blood flow, while the latter causes submucosal arteriovenous shunts, aggravating mucosal ischemia and hypoxia, leading to damage to the gastric mucosal epithelium, erosion and bleeding. Severe shock can lead to the release of ECTkey=5-hydroxytryptamine target=_blank>5-hydroxytryptamine and histamine. The former stimulates the gastric parietal cells to release lysosomes, directly damaging the gastric mucosa, while the latter increases the secretion of pepsin and gastric acid and damages the gastric mucosal barrier.

The etiology and pathogenesis of this disease have not yet been fully elucidated. It is generally believed that it may be due to various exogenous or endogenous pathogenic factors that cause a decrease in mucosal blood flow or the destruction of normal mucosal defense mechanisms, coupled with the damaging effects of gastric acid and pepsin on the gastric mucosa.