Atrophic changes in gastric mucosa
Introduction
Introduction The atrophic change of gastric mucosa is a clinical manifestation of inflammatory lesions of the gastric mucosa and chronic atrophic gastritis.
Cause
Cause
Etiology: The cause of chronic atrophic gastritis has not been known so far and may be related to the following factors:
(1) Continuation of chronic superficial gastritis: Chronic atrophic gastritis can be developed from chronic superficial gastritis. Six hospitals including the General Hospital of the People's Liberation Army reported 164 cases of superficial gastritis after 5 to 8 years of follow-up, of which 34 cases were converted into chronic atrophic gastritis (20.7%). The cause of chronic superficial gastritis can become a causative and aggravating factor of chronic atrophic gastritis.
(2) Genetic factors: According to the Varis survey, the incidence of chronic atrophic gastritis was significantly increased among the first generation of relatives of patients with chronic atrophic gastritis, and the genetic factors of pernicious anemia were also obvious. The incidence of relative relationships was 20 times greater than that of the control group, indicating that chronic atrophic gastritis may be related to genetic factors.
(3) Metal contact: The incidence of gastric ulcer in lead workers is high, and the incidence of atrophic gastritis is also increased in gastric mucosa biopsy. Polmer calls it excretory gastritis. In addition to lead, many heavy metals such as mercury, strontium, copper and zinc have certain damage to the gastric mucosa.
(4) Radiation: Radiation treatment of ulcer disease or other tumors can cause damage or even atrophy of the gastric mucosa.
(5) Iron deficiency anemia: Many facts indicate that iron deficiency anemia is closely related to atrophic gastritis. Badanoch reported 50 cases of iron deficiency anemia, normal gastric mucosa, superficial gastritis and atrophic gastritis accounted for 14% and 46% respectively. And 40%. However, the mechanism of anemia caused by gastritis is still unclear. Some scholars believe that gastritis is the primary disease, because gastritis is low in stomach acid, iron can not be absorbed, or due to gastric bleeding, resulting in anemia; another opinion is that there is anemia first, because the iron deficiency in the body makes the gastric mucosal renewal rate affected and easily occurs. Inflammation.
(6) Biological factors: The effects of chronic infectious diseases such as hepatitis and tuberculosis on the stomach have also attracted people's attention. Chronic liver disease patients often have symptoms and signs of chronic gastritis. Gastric mucosal staining also confirmed the presence of hepatitis B virus antigen-antibody complex in the gastric mucosa of patients with hepatitis B. Ruijin Hospital reported 91 patients with atrophic gastritis, and 24 patients (26.4%) had chronic hepatitis. Therefore, the impact of chronic infectious diseases, especially chronic liver diseases, on the stomach is worth noting.
(7) Constitutional factors: Clinical statistics show that the incidence of this disease is significantly positively correlated with age. The older the age, the worse the "resistance" of the gastric mucosal function is, and it is easily damaged by external adverse factors.
(8) bile or duodenal reflux: due to pyloric sphincter dysfunction or gastrojejunostomy, bile or duodenal juice can reflux to the stomach, and destroy the gastric mucosal barrier, promote H? + and pepsin Dissemination into the mucosa causes a series of pathological changes leading to chronic superficial gastritis and can develop into chronic atrophic gastritis.
(9) Immune factors: In atrophic gastritis, especially in the blood, gastric juice or plasma cells of atrophic mucosa in patients with atrophic gastritis, wall cell antibodies or internal factor antibodies are often found, so the autoimmune response is considered to be chronic atrophy. The cause of gastritis. In recent years, a small number of patients with gastric antrum gastritis have been found to have gastrin-secreting cell antibodies, which are special autoimmune antibodies of cells, belonging to the Ig G line. Some patients with atrophic gastritis have abnormal lymphocyte transformation test and leukocyte migration inhibition test, suggesting that cellular immune response is also important in the occurrence of atrophic gastritis.
(10) Helicobacter pylori (HP) infection: In 1983, Australian scholars Marshall and Warren first isolated HP from the gastric mucosal layer and epithelial cells of patients with chronic gastritis. Since then, many scholars have carried out a large number of experimental studies on patients with chronic gastritis, and HP is cultured in the gastric mucosa of 60% to 90% of patients with chronic gastritis, and then it is found that the degree of HP infection is positively correlated with the degree of gastric mucosal inflammation. At the eighth session of the World Gastroenterology Society in 1986, HP infection was one of the important causes of chronic gastritis.
In addition; such as improper diet, long-term tobacco and alcohol, drug abuse, chronic inflammation of the upper respiratory tract, central nervous system dysfunction, damage to the gastric mucosa, and gastric resection after gastrectomy, gastric antrum excision, resulting in the stomach Mucosal dystrophies, etc., are likely to cause damage to the gastric mucosa and atrophy and inflammatory changes.
Examine
an examination
Related inspection
Electronic gastroscope fiber endoscope
Diagnosis: Clinical manifestations of loss of appetite, nausea, belching, upper abdominal fullness or dull pain, a small number of patients may have upper gastrointestinal bleeding, weight loss, anemia, crisp nails, glossitis or tongue nipple atrophy.
Diagnosis
Differential diagnosis
Gastric mucosal damage: The entire inner surface of the stomach is covered with a layer of mucosal tissue that secretes mucus, forming a mucous-mucosal barrier of the stomach to protect the stomach tissue. Gastric mucosal injury is more common in gastritis and gastric ulcer. 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).
Thickening of gastric mucosa: 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.
Gastric mucosa shedding: The gastric mucosa is relatively relaxed. When the stomach contracts, the gastric mucosa near the pylorus is removed into the duodenal bulb. The clinical symptoms are symptoms of gastritis.
Diagnosis: Clinical manifestations of loss of appetite, nausea, belching, upper abdominal fullness or dull pain, a small number of patients may have upper gastrointestinal bleeding, weight loss, anemia, crisp nails, glossitis or tongue nipple atrophy.
