What does gastric mucosal lesions mean

As the name suggests, gastric mucosa is a kind of mucous membrane in the stomach. It is located on the inner wall of our stomach. This layer of mucosa is very thin and fragile and has the function of protecting the stomach wall. Gastric mucosal lesions are lesions that occur on this layer of mucosa, usually referring to acute gastric mucosal lesions. There are many pathogenic factors, and the important function of the stomach determines that the impact of this disease is great. Mucosa, what does gastric mucosal lesions mean? Let’s take a look below.

Causes and pathogenesis

1. Drugs: There are many kinds of drugs, the most common ones are non-steroidal anti-inflammatory drugs such as aspirin, indomethacin, phenylbutazone, etc. and adrenal corticosteroids. Aspirin is non-ionic and relatively fat-soluble in an acidic environment. It can destroy the lipoprotein layer of the gastric mucosal epithelial cells, weaken the mucosal barrier and cause hydrogen ions to osmosis into the mucosa, causing inflammatory exudation, edema, erosion, bleeding or shallow ulcers. Adrenal cortical hormones can cause "steroid ulcers" or even perforation, which is related to increased secretion of gastric acid and protease, decreased secretion of gastric mucus, weakening of the mucosal barrier and inhibition of gastric epithelial cell regeneration. Other drugs such as snakeroot preparations, digitalis, antibiotics, potassium salts, caffeine, etc. can also cause this disease.

2. Alcohol poisoning is also a common cause of this disease. Excessive drinking can cause acute gastric mucosal erosion and bleeding. Ethanol can dissolve the epithelial lipoprotein layer on the gastric mucosa, or ethanol can damage the mucous neck cells of the glands through the bloodstream, reducing gastric mucus. These can cause damage to the gastric mucosal barrier, leading to hydrogen ion reverse osmosis causing inflammatory exudation, bleeding, and ulcers, collectively referred to as stress ulcers. Under stressful conditions, ACTH and adrenal cortex hormones are released in large quantities, gastric secretion increases significantly, gastric mucus decreases, and DNA synthesis in mucus cells decreases. On the other hand, the autonomic nerves cause mucosal vasospasm, and coupled with insufficient blood volume, the gastric mucosal blood flow decreases, causing hypoxia and energy metabolism. Mast cells in the lesions release active substances such as histamine and 5-hydroxytryptamine, causing local vasodilation, exudation, and edema, which further excite the H2 receptors of the parietal cells to secrete a large amount of gastric acid, leading to erosion of the gastric mucosa and the formation of ulcers.

pathology

The lesions mainly invade the mucosal layer, causing congestion, multiple erosions, punctate or linear bleeding and shallow ulcers, invading part or all of the gastric mucosa. In severe cases, the duodenum and even the esophagus may be affected. The ulcers are superficial and do not invade the muscularis mucosa. Only a few ulcers may be deeper or even perforated. Histological manifestations include desquamation of the mucosal epithelium, focal necrosis, congestion, edema, and bleeding. They are unlike peptic ulcers, which show an increase in inflammatory cells and hyperplasia of fibrous tissue. The blood vessels at the site of the disease often do not form thrombi, so bleeding is common clinically.

Clinical manifestations

Upper gastrointestinal bleeding is its most prominent symptom, which can manifest as vomiting blood or black stools. Its characteristics are: 1. There is a history of taking related drugs, alcoholism, or diseases that can cause stress. ② The onset is sudden, with sudden vomiting of blood and black stools. It may occur hours or days after a stressful event. ③ The amount of bleeding is large and may be intermittent and repeated, often leading to hemorrhagic shock. The onset of the disease may also be accompanied by upper abdominal discomfort, burning sensation, pain, nausea, vomiting and acid reflux.

treat

1. General treatment: Eliminate the cause, actively treat the primary disease that causes the stress state, rest in bed, eat liquid food, and fast if necessary.

2. Replenish blood volume by intravenous infusion of 5% glucose saline and blood transfusion if necessary.

3. To stop bleeding, take oral hemostatic drugs such as Baiyao, Panax notoginseng powder, or aspirate acidic gastric juice through a gastric tube, and add 8 mg of norepinephrine to 100 ml of cold saline. Once every 2-4 hours. You can also stop bleeding under gastroscopy, spray hemostatics (such as Meng's solution, Baiyao, etc.) or use electrocoagulation, laser hemostasis, or microwave hemostasis.

4. To inhibit gastric acid secretion, take 200 mg of cimetidine 4 times a day or 800-1200 mg daily by intravenous drip in divided doses, and 150 mg of furanitide twice a day or by intravenous drip.

Recently, sucralfate or prostaglandin E2 have been used and good results have been achieved.