Chronic erosive gastritis

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

　　1. Etiology

　　1. Endogenous factors:Including severe infection, severe trauma, intracranial hypertension, severe burns, major surgery, shock, excessive tension and fatigue, etc. Under stress conditions, it can excite the sympathetic and vagus nerves, the former causing vasoconstriction of the gastric mucosal blood vessels and a decrease in blood flow, and the latter causing the short-circuit opening of submucosal arteries and veins, promoting the aggravation of mucosal ischemia and hypoxia, leading to damage to the gastric mucosal epithelium, causing erosion and bleeding. Severe shock can lead to the release of serotonin and histamine, the former stimulating the release of lysosomes by gastric wall cells, directly damaging the gastric mucosa, and the latter increasing the secretion of pepsin and gastric acid, damaging the gastric mucosal barrier.

　　2. Exogenous factors:Certain drugs such as non-steroidal anti-inflammatory drugs, certain antibiotics, alcohol, etc., can damage the gastric mucosal barrier, leading to increased mucosal permeability, backflow of hydrogen ions from gastric juice into the gastric mucosa, causing erosion and bleeding of the gastric mucosa. Adrenal cortical steroids can increase the secretion of hydrochloric acid and pepsin, reduce the secretion of gastric mucus, and slow down the renewal rate of gastric mucosal epithelial cells, leading to the disease.

　　3. Pathophysiology:During the stress state, the secretion of norepinephrine and adrenal cortical hormones increases, visceral blood vessels constrict, and blood flow to the stomach decreases, making it unable to clear the reverse diffusion of H+; hypoxia and norepinephrine reduce the synthesis of prostaglandins, insufficient mucus secretion, and a decrease in HCO3- secretion; during the stress state, gastrointestinal motility is slow, pyloric function is dysregulated, causing bile reflux, and further damage to the ischemic gastric mucosal epithelium by bile salts, leading to the destruction of the gastric mucosal barrier, ultimately resulting in erosion and bleeding of the mucosa. Lesions are often seen in the fundus and body of the stomach, sometimes involving the antrum, with multiple erosions of the gastric mucosa, accompanied by patchy hemorrhage, and sometimes shallow small ulcers covered with white or yellow fur. Histological examination shows focal desquamation of superficial epithelial cells in the erosion, twisted glands due to edema and hemorrhage, and infiltration of neutrophils and monocytes in the lamina propria.

　　Two, Pathogenesis

　　The specific pathogenesis is as follows:

　　1, Drugs

　　(1) Non-steroidal anti-inflammatory drugs, including aspirin, indomethacin (消炎痛), and so on. This class of drugs can directly damage the gastric mucosa and inhibit the damage of cyclooxygenase.

　　(2) Antitumor drugs.

　　2, Stress:Severe trauma, major surgery, large-area burns, intracranial lesions, sepsis, severe organ damage, and multiple organ failure can all lead to this disease.

　　(1) Increased release of adrenaline and norepinephrine leads to vasoconstriction of the gastric mucosal blood vessels and reduced blood flow, resulting in mucosal ischemia, insufficient secretion of mucus and sodium bicarbonate, decreased local prostaglandin synthesis and regeneration capacity, reduced mucosal barrier function, and mucosal damage;

　　(2) Increased secretion of adrenal cortical hormones leads to increased gastric acid secretion and enhanced mucosal invasive factors;

　　(3) Weakening of gastrointestinal motility and pyloric dysfunction can lead to bile and pancreatic juice reflux, causing the destruction of the gastric mucosal barrier.

　　3, Alcohol:The lipophilicity and solubilizing property of alcohol lead to the destruction of the gastric mucosal barrier, damage to epithelial cells, and mucosal hemorrhage and edema can also cause increased gastric acid secretion and mucosal damage.

　　This disease has a sudden onset, and clinically, upper gastrointestinal bleeding is the main manifestation of the disease, with an incidence rate of more than 1/4 of upper gastrointestinal bleeding etiologies, second only to bleeding from peptic ulcers. The mild cases may only have positive occult blood in the stool, while most patients have hematemesis and melena. The bleeding presents intermittently with the recurrence of the condition. Generally, the condition of this disease is more severe than that of bleeding from peptic ulcers, and even after a large amount of blood transfusion, it is difficult to increase the hemoglobin level.

　　1, Inducing other diseases:If erosive gastritis is not treated in a timely manner, or treated, it may induce the occurrence of atrophic gastritis, weaken the patient's self-healing ability, and lead to exacerbation of the patient's condition.

　　2, Gastric cancer:If erosive gastritis is not treated in a timely manner, it may lead to more bacterial proliferation, which may transform into gastric cancer, causing greater harm to the patient, and at the same time, the difficulty of treatment will also increase.

　　3, Gastric ulcer:If erosive gastritis is not treated actively, the erosion site may worsen, causing gastric ulceration to appear, leading to further expansion of the erosion area and exacerbation of the condition.

　　4, Gastric perforation:If erosive gastritis has deep erosion, there may be a risk of gastric perforation, which may even threaten the patient's life and health.

　　One, Symptoms

　　1, The symptoms of chronic erosive gastritis are mostly non-specific, mainly including nausea, vomiting, and discomfort in the upper abdomen.

　　2, Most patients are asymptomatic or have varying degrees of dyspeptic symptoms such as epigastric pain, acid regurgitation, postprandial fullness, decreased appetite, and so on. When the disease develops into chronic atrophic gastritis, patients may have symptoms such as anemia, diarrhea, glossitis, and emaciation. In some patients with mucosal erosion, epigastric pain is more obvious, and bleeding may occur.

　　3. Sudden upper gastrointestinal bleeding may occur during the course of the primary disease, manifested as hematemesis and melena, with melena alone being rare. Bleeding is often intermittent. Massive bleeding can cause syncope or shock, accompanied by anemia. There may be upper abdominal dull pain or tenderness during bleeding.

　　4. Patients with secondary atrophic gastritis due to erosive gastritis may have anemia, emaciation, glossitis, diarrhea, etc. Some patients with mucosal erosion have more obvious upper abdominal pain and may have bleeding.

　　Second, signs

　　1. Abdominal distension. It is mainly caused by gastric retention, delayed emptying, and poor digestion. In addition, there may be loss of appetite, acid regurgitation, nausea and vomiting, fatigue, constipation, or diarrhea.

　　2. Upper abdominal pain. This is the most common symptom of chronic superficial gastritis. It is generally manifested as diffused upper abdominal burning pain, hidden pain, or distension. If one eats cold, hot, hard, spicy, or other刺激性 food, the condition may worsen.

　　3. Belching. Patients show an increase in gastric gas, which is expelled through the esophagus, which can relieve the symptoms of upper abdominal fullness.

　　4. Recurrent bleeding. Bleeding is due to the acute inflammatory change of gastric mucosa on the basis of chronic superficial gastritis.

　　The gastric mucosa may appear multiple warty, enlarged fold-like, or papillary elevations, with a diameter of 5-10mm, with mucosal defects or umbilical-like indentations at the top, with erosions in the center, and no erythema around the elevations, but often accompanied by similar-sized erythemas, more common in the antrum. In the Sydney system classification of chronic gastritis, it belongs to a special type of gastritis, and the endoscopic classification is elevated erosive gastritis and flat erosive gastritis. Chronic gastritis lacks specific symptoms, and the severity of symptoms is not consistent with the degree of mucosal lesions.

　　Endoscopy often shows multiple nodular or aphthous ulcers. Chronic non-erosive gastritis can be idiopathic or caused by drugs (especially aspirin and non-steroidal anti-inflammatory drugs, see the treatment section of peptic ulcer), Crohn's disease, or viral infection. Helicobacter pylori may not play an important role in this.

　　Symptoms are mostly non-specific, including nausea, vomiting, and discomfort in the upper abdomen. Under endoscopy, the thickened folds have nodular erosions at the edges, with white spots or indentations in the center. The histological changes are diverse.

　　1. Relax your mood

　　Stress is a promoting factor for chronic gastritis and should be avoided. Emotional unrest and impatience are easy to cause mucosal disorders and gastrointestinal dysfunction. Therefore, it is best to avoid emotional stress responses and relieve tension. In daily life, do not get angry when encountering things, do not rush in the middle, do not worry in a hurry, and keep a pleasant mood, which is very beneficial for the recovery of gastritis.

　　2. Take antibiotics

　　Helicobacter pylori can cause gastritis and other digestive tract problems. Taking antibiotics for two weeks can defeat these bacteria. Helicobacter pylori can be detected through blood and saliva tests.

　　3. Use of antacids

　　For the treatment of mild gastritis, it is best to take antacids about 1-2 hours after eating, as this is when the stomach acid is at its peak, which is exactly the time for antacid action. It is even better if you can take another dose around 9-10 PM before going to bed.

　　4. Use medication cautiously

　　It should be avoided to take drugs such as aspirin, acetaminophen, phenylbutazone, indole drugs, tetracycline, erythromycin, prednisone, etc., especially during the active phase of chronic gastritis.

　　5. Appropriate exercise

　　Appropriate exercise is a good way to increase gastrointestinal motility, which can effectively promote gastric emptying, enhance gastrointestinal secretion function, improve digestion, and help the recovery of gastritis.

　　6. Quit smoking

　　Smoking can promote the onset of stomach pain. After smoking, nicotine (i.e., nicotine) can stimulate the gastric mucosa, causing an increase in gastric acid secretion, exerting harmful stimulatory effects on the gastric mucosa. Excessive smoking can lead to dysfunction of the pyloric sphincter, causing bile reflux, damaging the gastric mucosa, and affecting the blood supply to the gastric mucosa and the repair and regeneration of gastric mucosal cells, so it is necessary to quit smoking.

　　7. Abstain from alcohol

　　Alcohol can directly destroy the gastric mucosal barrier, invade the gastric mucosa, causing mucosal congestion, edema, and erosion.

　　Firstly, laboratory examination

　　Patients present with vomiting and (or) black tarry stools, and in some cases, acute massive hemorrhage, the total hemoglobin level decreases, and the occult blood test in feces and vomit is positive.

　　Secondly, other auxiliary examinations

　　1. X-ray examination:Barium meal examination of the gastrointestinal tract often cannot detect erosive lesions and is not suitable for patients with acute active bleeding because barium can be deposited on the mucosal surface, making it impossible to perform endoscopy or angiography in the near future; in acute hemorrhage, superselective mesenteric angiography can be used for localization diagnosis of hemorrhage, and it is often negative during the interval of hemorrhage.

　　2. Emergency endoscopic examination:Emergency endoscopic examination within 24-48 hours after bleeding shows acute mucosal lesions characterized by multiple erosions and hemorrhagic foci, which have diagnostic value.

　　3. Endoscopic observation:The gastric mucosa shows multiple warty, dilated fold-like or papillary elevations, with a diameter of 5-10mm. At the top, there may be mucosal defects or umbilical-like indentations, with erosion in the center. There is usually no erythema around the elevations, but there are often similar-sized erythemas, most commonly in the antrum. They can be classified into persistent and disappearing types. In the Sydney system classification of chronic gastritis, it belongs to a special type of gastritis, and the endoscopic classification is elevated erosive gastritis and flat erosive gastritis. Chronic gastritis lacks specific symptoms, and the severity of symptoms is not consistent with the degree of mucosal lesions. Most patients are asymptomatic or have varying degrees of dyspeptic symptoms such as upper abdominal pain, decreased appetite, postprandial fullness, and acid regurgitation. Patients with atrophic gastritis may have anemia, weight loss, glossitis, diarrhea, etc. Some patients with mucosal erosion may have more pronounced upper abdominal pain and may have bleeding.

　　Endoscopic manifestations are often multiple punctate or aphthous ulcers. Chronic nonerosive gastritis can be idiopathic or caused by drugs (especially aspirin and nonsteroidal anti-inflammatory drugs, see the section on the treatment of peptic ulcers), Crohn's disease, or viral infection. Helicobacter pylori may not play a significant role here. Symptoms are mostly non-specific, and may include nausea, vomiting, and upper abdominal discomfort. Endoscopically, there are punctate erosions at the raised edges of thickened folds, with white spots or depressions in the center. Histological changes are diverse.

　　First, What to Eat Best for Chronic Gastritis

　　1. Pay Attention to Soft, Rotten, and Digestible:Main foods, vegetables, and meat dishes such as fish, especially beans, peanuts, and other hard nuts, should be cooked thoroughly and well-cooked to make them soft and easy to digest. Eat less rough and fibrous foods. The food should be well-prepared and nutritious.

　　2. Keep Fresh and Light:All kinds of food should be fresh and not stored for a long time. Eat fresh vegetables and fruits with little fiber, such as winter melon, cucumber, tomato, potato, spinach leaves, Chinese cabbage, apple, pear, banana, orange, etc. Eat light and low-fat dishes. Light dishes are easy to digest and absorb and are beneficial to the recovery of gastric diseases.

　　Second, What Not to Eat for Chronic Gastritis

　　Patients with chronic gastritis should avoid drinking strong alcohol (other types of alcohol should be drunk less or not at all), cigarettes, strong tea, coffee, chili, wasabi, and other strong spices. It is not advisable to eat sweet, salty, strong, cold, hot, or sour soups and dishes to prevent injury to the gastric mucosa. Excessive drinking of carbonated beverages can also cause varying degrees of damage to the gastric mucosa.

　　First, Inhibit Gastric Acid Secretion

　　1. H2 Receptor Antagonists:For example, Cimetidine, Ranitidine, Famotidine, etc., 20mg, twice a day.

　　2. Proton Pump Inhibitors:For example, Omeprazole tablets 20mg, taken half an hour before breakfast and dinner, or Lansoprazole tablets 15mg, taken half an hour before breakfast and dinner each day.

　　3. Protect the gastric mucosa:Take 3 capsules of Pectin Bismuth Capsules half an hour before each meal, or 10ml of Gastrodin Oral Solution half an hour before each meal.

　　Select the above two drugs, the course of treatment is one and a half to two months.

　　Second, Eradicate Helicobacter pylori

　　Take 2 tablets of Clarithromycin tablets three times a day, and 2 tablets of Metronidazole tablets three times a day (after meals) for half a month. The four-drug therapy can be used: Lansoprazole tablets, Pectin Bismuth Capsules, Metronidazole tablets, Clarithromycin tablets. (If Helicobacter pylori is negative, Metronidazole tablets and Clarithromycin tablets do not need to be taken.) Famotidine 20mg can be taken orally twice a day.