Pain after meal

Introduction Post-meal mouth is a clinical symptom of chronic atrophic gastritis. Chronic atrophic gastritis is mainly characterized by abdominal distension, increased abdominal distension after meals, pale and tasteless, and painful discomfort in the stomach. It is a common digestive system disease characterized by atrophy of gastric mucosa gland, which belongs to the range of Chinese medicine, pain, stomach cramps and bloating.

Cause

The etiology 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, the gastric antrum excretion of gastrin, resulting in the stomach Mucosal dystrophies, etc., are likely to cause damage to the gastric mucosa and atrophy and inflammatory changes.

an examination

Laboratory examination

1 gastric juice analysis: patients with type A CAG are mostly acid-free or low-acid, and patients with type B CAG can be normal or low in acid.

2 Pepsinogen assay: Pepsinogen is secreted by the main cell, and the content of pepsinogen in blood and urine is reduced in chronic atrophic gastritis.

3 serum gastrin assay: G cells of the gastric antrum mucosa secrete gastrin. In patients with type A CAG, serum gastrin is often significantly increased; gastric mucosa atrophy in patients with type B CAG directly affects the secretion of gastrin by G cells, and serum gastrin is lower than normal.

4 immunological examination: wall cell antibody (PCA), internal factor antibody (IFA), gastrin secretion cell antibody (GCA) determination, can be used as a secondary diagnosis of chronic atrophic gastritis and its classification.

2. Gastroscopic examination and biopsy are the most reliable diagnostic methods.

Gastroscopic diagnosis should include the extent of the lesion, degree of atrophy, intestinal metaplasia and degree of dysplasia. Gastric mucosal biopsy is mainly caused by different degrees of atrophy of the intrinsic glands, thickening of mucosal muscle layer, inflammation of the lamina propria, formation of lymphoid follicles, and replacement of pseudo-pyloric gland metaplasia or intestinal gland metaplasia.

Differential diagnosis

Differential diagnosis after a meal:

1. Loss of taste: Taste refers to the feeling that food stimulates and produces a chemosensory system in the mouth of a person's mouth. People in different regions have different classifications of taste. There are many factors that reduce the taste of the elderly, because the taste of food comes not only from the basic taste of the tongue, but also closely related to the effects of smell, vision and nerves.

2, the mouth is light and tasteless: taste abnormality means that when someone is eating, there is a smell in the mouth, or there is an abnormal taste in the mouth. This often suggests that a disease may have been acquired. In Chinese medicine, because the spleen is open to the mouth, stomach, heart, kidney, etc., the visceral gas also follows the mouth to the mouth, so the abnormal smell in the mouth is the reflection of the above-mentioned visceral dysfunction or other visceral lesions. A light mouth means that the taste in the mouth is diminished, it is light and tasteless, or the taste of food cannot be tasted. Many diseases can cause a dullness.

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