Gastritis

　　Etiology of acute gastritis

　　Can be caused by chemical factors, physical factors, microbial infection, or bacterial toxins, etc. In addition, dysfunction of the mental and nervous system, stress state, or body's变态 reactions caused by various factors can also act as endogenous stimuli, causing acute inflammatory damage to the gastric mucosa.

　　Etiology of chronic gastritis

　　Chronic gastritis is caused by a variety of factors. It is now clear that Helicobacter pylori infection is the most common cause of chronic gastritis, and some people call it Helicobacter pylori-associated gastritis. However, other physical, chemical, and biological harmful factors that act repeatedly and continuously on susceptible individuals can also cause this disease. The persistence or recurrence of the cause can lead to chronic lesions. Chronic atrophic gastritis is a chronic progressive lesion that starts with superficial inflammation and finally becomes irreversible atrophic inflammation. The etiology of chronic gastritis has not been fully elucidated in medical clinical practice, and it is generally believed to be related to harmful factors in the surrounding environment and susceptible constitution. Physical, chemical, and biological harmful factors that act repeatedly and continuously on susceptible individuals can cause this disease. The persistent and recurrent occurrence of chronic gastritis can lead to chronic lesions.

　　1. Long-term use of drugs, foods, and rough foods that irritate the stomach, as well as smoking. These factors repeatedly act on the gastric mucosa, causing congestion and edema.

　　2. Long-term congestion and hypoxia of the gastric mucosa. Patients with conditions such as congestive heart failure or portal hypertension have their gastric mucosa in a state of congestion and hypoxia for a long time, which leads to nutritional disorders and gastritis.

　　3. If acute gastritis is not treated properly and does not heal, it may transform into chronic gastritis.

　　4. Lack of gastric acid, which makes bacteria easy to reproduce in the stomach, can also cause chronic gastritis.

　　5. Nutritional deficiency, endocrine dysfunction, and immune function abnormalities can cause chronic gastritis.

　　6. Infections by Campylobacter jejuni and other factors may be pathogenic factors for chronic gastritis.

　　7. The action of bacteria and their toxins. Due to the continuous ingestion of bacteria or toxins from infection foci in the nose, mouth, throat, and other parts; or the lack of gastric acid in the stomach, bacteria are prone to reproduce in the stomach, leading to chronic gastritis through long-term action.

　　8. Mental factors. Excessive mental stimulation, depression, and other mental factors repeatedly acting on the cerebral cortex cause functional disorders of the cerebral cortex, leading to spasmodic contraction of the gastric wall vessels and inflammation or ulceration of the gastric mucosa.

　　Complications of acute gastritis are rare and mild, while the complications of chronic gastritis include:
　　1. Gastric hemorrhage: Hemorrhage in chronic gastritis is not uncommon: mucosal atrophy and thinning, visible vessels, abrasion of coarse food, erosion and hemorrhage of the mucosa, mainly manifested as melena. If the amount of bleeding is large, hematemesis may occur suddenly, with severe cases presenting with dizziness, palpitations, dark vision, profuse sweating, and even shock.
　　2. Anemia: After a large amount of bleeding in chronic gastritis, two types of anemia may occur: megaloblastic anemia, also known as pernicious anemia, with symptoms of anemia such as dizziness, fatigue, palpitations, and pale complexion; iron deficiency anemia is caused by chronic bleeding and is also related to insufficient eating and malnutrition in chronic gastritis patients, as well as the lack of gastric acid affecting the digestion and absorption of hematopoietic raw materials.
　　3. Gastric ulcer: Gastric ulcer coexists with superficial gastritis and erosive gastritis, with obvious inflammatory stimulation, atrophy and thinning of the gastric mucosa, and concurrent erosion and ulceration. It is necessary to undergo gastroscopy in a timely manner to avoid delay in diagnosis and treatment.
　　4. Precancerous stage of gastric cancer: The canceration of chronic gastritis is closely related to gastritis hyperplasia. There are two types of chronic gastritis that are prone to canceration: chronic gastritis with pernicious anemia, where the incidence of canceration is more than 20 times higher than that of other gastrointestinal diseases, which should be paid attention to by gastrointestinal disease patients; atrophic gastritis with intestinal metaplasia and severe atypical hyperplasia.

　　Symptoms of acute gastritis

　　The clinical manifestations of acute gastritis are often of varying degrees of severity, but the onset is always acute. Mild cases may only have abdominal pain, nausea, vomiting, and indigestion; severe cases may have hematemesis, melena, even dehydration, and poisoning and shock.

　　Acute simple gastritis has a short course and is self-limiting; other types of acute gastritis, after treatment, do not leave any residual lesions, but acute corrosive gastritis has a severe course, and stenosis may occur in the esophagus, pylorus, and other parts in the later stage.

　　(1) There is often fever, headache, general discomfort, and varying degrees of poisoning symptoms.

　　(2) In severe cases of vomiting and diarrhea, dehydration, acidosis, and even shock may occur.

　　(3) Signs are not prominent, with tenderness in the upper abdomen and around the umbilicus, without muscle tension or rebound pain, and intestinal sounds are often hyperactive.

　　(4) A history of overeating or eating unclean, decayed, or spoiled food.

　　(5) The onset is acute, with frequent nausea and vomiting, severe abdominal pain, frequent diarrhea, mostly watery stools, which may contain undigested food, a small amount of mucus, and even blood.

　　Symptoms of chronic gastritis

　　Chronic gastritis is a chronic gastric disease with non-specific chronic inflammation of the gastric mucosa as the main pathological change. The lesions can be limited to a part of the stomach or spread to the entire stomach. The clinical manifestations are non-specific, and the severity of symptoms is not consistent with the degree of mucosal lesions. Most patients are asymptomatic or have varying degrees of dyspepsia, such as discomfort and pain in the upper abdomen, nausea and vomiting, decreased appetite, postprandial fullness, acid regurgitation, and belching. Gastric mucosal erosion and hemorrhage may be accompanied by hematemesis and melena. Chronic atrophic gastritis patients may have reduced gastric acid, dyspepsia, anemia, weight loss, glossitis, diarrhea, etc. Some patients with mucosal erosion may have more obvious upper abdominal pain and may have hemorrhage.

　　Gastritis is often caused by unreasonable diet and living habits. To prevent the disease, it is necessary to pay attention to avoiding risk factors for gastritis in daily life. Specific measures include:

　　1. Stay away from chemical stimulation

　　Oral intake of certain drugs such as salicylates, reserpine, and adrenal cortical hormones, excessive drinking of strong alcohol, strong tea, coffee, etc., can stimulate and damage the gastric mucosa, causing congestion, edema of the gastric mucosa, and even bleeding and erosion, leading to the occurrence of acute simple gastritis.

　　2. Avoid pathogenic factors

　　The common causes of acute gastritis are usually acute gastritis caused by unclean diet, common bacterial infections include staphylococcal exotoxin, botulinum toxin, Salmonella enterotoxin, and acidophilus. Helicobacter pylori also causes acute gastritis during the acute infection period, and if it is not eliminated, it may transform into chronic active gastritis. Common viral infection factors include influenza virus, enterovirus, etc.

　　3. Other factors:

　　Dysfunction of the mental and nervous system, stress state, body变态 reactions caused by various factors, and certain systemic diseases. Chronic pulmonary heart disease, respiratory failure, vitamin deficiency disease, malabsorption of the small intestine, and advanced cancer can all act as endogenous stimuli, causing acute inflammation of the gastric mucosa.

　　Common laboratory examination items for gastritis include:

　　Gastroscopy and biopsy

　　Gastroscopy is the best method for diagnosing gastritis, as it can observe changes in the gastric mucosa. During gastroscopy, it is also possible to take gastric mucosal tissue for tissue sections, observe the condition of the tissue under a microscope, and determine the diagnosis by integrating the results of gastroscopy and pathological examination.

　　Gastroscopy precautions:

　　(1) Perform gastroscopy in the morning:

　　After 8:00 p.m. the night before, no food or drinks should be consumed, and smoking is prohibited.

　　Eat less fiber and easily digestible food the night before. Because even a small amount of water can change the color of the gastric mucosa, such as the natural lesion of marked atrophic gastritis, the gastric mucosa can turn red after drinking water, leading to incorrect diagnosis.

　　(2) Perform gastroscopy in the afternoon:

　　The patient can drink some sugar water before 8:00 a.m. on the same day, but should not eat anything else, and should not eat anything at noon. For patients with pyloric stenosis, it is necessary to perform lavage the night before the examination, thoroughly cleaning the contents of the stomach until the回流液 is clear.

　　Before the gastric tube is removed after lavage, the patient assumes a head-down, feet-up supine position to ensure complete expulsion of residual fluid in the stomach.

　　Gastric lavage cannot be performed on the same day, as it can change the color of the gastric mucosa after lavage.

　　(2) Helicobacter pylori detection

　　It is possible to take another piece of living tissue for rapid urease test during endoscopic examination to increase the reliability of the diagnosis of Helicobacter pylori infection. The detection of Helicobacter pylori antibodies is a qualitative detection using colloidal gold technology for human serum, plasma, or whole blood. When the patient's sample contains specific antibodies against Helicobacter pylori, they form an antigen-antibody-antigen colloidal gold particle complex with the antigen on the detection line (T line) and show a red line. The breath test for Helicobacter pylori using a breath testing instrument is simple, has no adverse reactions, and is one of the ideal detection methods at present. The sensitivity of the test results is over 95%, and it is currently the gold standard in the medical field for detecting HP.

　　(3) Upper gastrointestinal contrast

　　Upper gastrointestinal contrast is one of the commonly used examination methods, and this examination has certain value for the diagnosis of ulcer disease and tumor, but due to the limitation that this examination can only observe changes in the shape of the stomach and cannot observe the changes in the gastric mucosa, it has limitations.

　　(4) Related examinations for autoimmune gastritis

　　Patients suspected of having autoimmune gastritis should be tested for blood PCA and IFA. Positive results suggest the presence of autoimmune factors. The determination of serum vitamin B12 concentration and vitamin B12 absorption test is helpful in diagnosing pernicious anemia.

　　(5) Determination of serum gastrin G17, pepsinogen I, and II

　　Serum gastrin and pepsinogen detection are non-invasive examinations that help determine the presence, distribution, and extent of gastric mucosal atrophy.

　　Acute gastritis is an acute, reversible change in the gastric mucosa, which can be caused by chemical (tobacco, strong alcohol, strong tea, coffee, drugs, etc.), physical (overheated, overcooled, rough food, X-ray irradiation, etc.) stimulation, or contact with bacteria or their toxins. The course of the disease is generally short, with improvement in 1 to 2 days and a good prognosis. It is generally divided into five types: simple, corrosive, infectious, suppurative, and hemorrhagic erosive gastritis.

　　The principles of diet and health care for patients with acute gastritis are as follows:

　　① Patients often have symptoms such as vomiting and diarrhea during the acute phase. Due to significant fluid loss, attention should be paid to the supplementation of a large amount of fluid in the diet, and liquid foods such as fresh fruit juice, lotus root starch, rice gruel, and egg soup can be provided, and a large amount of water should be consumed to relieve dehydration and accelerate the excretion of toxins.

　　② After the condition improves, patients can be given semi-liquid food with less residue, gradually transitioning to soft rice with less residue. The diet should be non-irritating and low in fiber, such as congee, noodles, and can also include steamed bread as needed.

　　③ Supplement an appropriate amount of protein.

　　④ To reduce the burden on the gastrointestinal tract, it is advisable to eat less and more often, with 5 to 6 meals a day being more appropriate.

　　Chronic gastritis refers to inflammatory or atrophic changes in the gastric mucosa and is a common disease. Modern medicine divides the disease into four types: chronic superficial gastritis, chronic atrophic gastritis, chronic erosive gastritis, and chronic hypertrophic gastritis.

　　It is generally believed that the pathogenic factors causing chronic gastritis include: persistent acute gastritis, bacterial infection, drug stimulation, improper diet, chronic foci in the nasal pharynx and oral cavity, lack of gastric acid, and so on.

　　Principles of dietary health care treatment for chronic gastritis patients:

　　① Try to eliminate triggering factors. For example, thoroughly treating chronic gastritis, avoiding spicy, hard foods, and drugs that irritate the stomach, treating chronic infections in the mouth and throat, etc.

　　② Eat easily digestible and non-irritating foods, such as semi-liquid or low-fiber diets.

　　③ Eat in small portions and avoid mechanical and chemical stimulation from foods and cold foods.

　　④ It is advisable to provide a rich diet of protein and various vitamins, such as fresh tender green vegetables.

　　⑤ Patients with excessive gastric acid should avoid concentrated fresh soups such as chicken soup, acidic foods, and large amounts of protein to prevent increased secretion of gastric acid. It is advisable to eat soy milk, mashed vegetables, congee, and other foods.

　　Common methods for Western medicine to treat gastritis include:

　　(1) Eradication of Helicobacter Pylori

　　Although there is currently a lack of unified opinion on whether helicobacter pylori-induced chronic gastritis should be routinely eradicated, successful eradication of helicobacter pylori can improve the histology of the gastric mucosa, prevent peptic ulcers, and possibly reduce the risk of gastric cancer. In some patients, dyspepsia symptoms can also be improved. The consensus of Chinese chronic gastritis suggests that eradication of helicobacter pylori is particularly suitable for: ① Patients with gastric mucosal erosion, atrophy, intestinal metaplasia, and atypical hyperplasia; ② Patients with dyspepsia symptoms; ③ Patients with a family history of gastric cancer.

　　(2) Treatment for Improving Dyspepsia Symptoms

　　For patients with dyspepsia symptoms accompanied by chronic gastritis, there is no clear relationship between the symptoms and chronic gastritis. Therefore, the symptom treatment in fact belongs to empirical treatment for functional dyspepsia. Acid-suppressing or antacid drugs, gastrointestinal motility drugs, and gastric mucosal protective drugs can all be tried. In addition to the therapeutic effects on symptoms, these drugs may also have certain effects on the repair of gastric mucosal epithelium and inflammation.

　　(3) Treatment of Autoimmune Gastritis

　　There is currently no specific treatment, and anemia can be corrected after the injection of vitamin B12 when there is malignant anemia.

　　(4) Treatment of Atypical Hyperplasia

　　Atypical hyperplasia is a precancerous lesion of gastric cancer and should be highly valued. In addition to the above active treatment for mild atypical hyperplasia, the key is regular follow-up. For confirmed severe atypical hyperplasia, prophylactic surgery is recommended, and endoscopic submucosal resection of the gastric mucosa is commonly used at present.