I. Diet and removal of unfavorable factors.
Eat a light diet, avoid irritating foods, rough foods, overheated drinks, alcoholism, salty foods, etc. Discover and get rid of all the causes of chronic gastritis as much as possible, stop medication, alcohol, smoking, etc.
Second, spiritual and comfort treatment.
People’s fear of chronic gastritis is more biased towards the fear that gastritis will become cancerous. Some clinical observations have found that neuroendocrine dysfunction and imbalance in the release of gastrointestinal hormones play a role in the pathogenesis of chronic gastritis. The lifestyle of patients with autonomic dysfunction manifested by stress, anxiety, agitation, irritability, and sadness should be given adequate attention in the treatment. At present, only atrophic gastritis is related to gastric cancer, so patients should be given proper health education to maintain an optimistic attitude towards life and avoid aggravating their mental burden.
III. Drug treatment.
1.Gastric mucosa protective drugs.
The main function of gastric mucosa protective drugs is to enhance the barrier function of gastric mucosa and strengthen the ability of gastric mucosa to resist damage factors. For those who have acid reflux, heartburn, stomach pain and gastroscopy suggesting mucosal erosion and bleeding, mucosal protective agents can be given.
(1) Aluminum sulfate.
The aluminum salt of sucrose sulfate containing 8 sulfates can dissociate sucrose sulfate complex ions under acidic environment, and the complex ions polymerize into insoluble negatively charged colloids, which can combine with positively charged protein exudates at the ulcer or inflammation to form a protective film covering the surface of the lesion, preventing further invasion by gastric acid, pepsin and other damaging factors, and promoting the healing of the broken mucosa; aluminum thioglycollate also has the ability to It can also adsorb pepsin, neutralize gastric acid and bile acid, and promote the synthesis of endogenous prostaglandin E as well as adsorb epidermal growth factor to concentrate at the ulcer or inflammation, which is conducive to mucosal regeneration.
Dosage and precautions: Thioglycollate 1g, 3-4 times daily, chewed and taken 1 hour before meals and at bedtime on an empty stomach. Adverse reactions are commonly constipation, individual patients may experience dry mouth, nausea, rash, stomach cramps, etc. It should not be applied continuously for more than 8 weeks. Long-term high doses may cause phosphorus deficiency in body fluids, so it should not be taken for a long time by patients with hypophosphatemia such as hyperthyroidism and rickets. Complexation with pepsin in multi-enzyme tablets and pancreatic enzymes reduces their efficacy, so they should not be used together.
(2) Bismuth.
It forms a diffuse protective layer in the gastric acid environment, covering the mucosal surface, isolating the erosion surface and ulcer foci from gastric acid and pepsin, playing a protective role for the damaged mucosa and promoting the repair and healing of damaged mucosal tissues; reducing pepsin activity and increasing mucin secretion; stimulating the production of endogenous prostaglandins and epidermal growth factor, accelerating the healing of trauma and the disappearance of inflammation, and also having a certain Hemostatic effect. It has a killing effect on Helicobacter pylori.
Dosage and precautions: Bismuth potassium citrate 110g, 4 times a day, the first 3 times half an hour before 3 meals, the 4th time 2 hours after dinner; or 2 times a day, 220mg in the morning and 220mg in the evening. bismuth pectin 150-200mg, 4 times a day. It may cause ammonia taste in the mouth and make the tongue and stool grayish-black, which will disappear on its own after stopping the medication. Continuous use should not exceed 8 weeks.
(3) Teprenone.
Animal tests have proved that tiopresidone has strong anti-ulcer effect and improvement of gastric mucosal lesions, and can promote the role of mucus synthesis and secretion; by increasing prostaglandin biosynthetic enzyme activity to increase the role of prostaglandins in the gastric mucosa, which in turn increases and improves the role of gastric mucosal blood flow; it also has the role of maintaining the in vivo equilibrium of cells in the proliferative zone of the gastric mucosa and inhibiting lipid peroxidation.
Dosage and Precautions: Teprenone 50mg Tid. side effects include: constipation, diarrhea, vomiting, thirst, abdominal pain, abdominal distension. Transient elevation of transaminases. Other rare headache, rash, phlegm itch.
2. Gastric stimulants.
For fullness and discomfort, belching can be given gastrointestinal dynamics drugs.
(1) morbutrin.
It is a peripheral dopamine receptor blocker that acts directly on the gastrointestinal wall to increase the tone of the lower esophageal sphincter, prevent gastro-esophageal reflux, enhance gastric motility, promote gastric emptying, coordinate gastric and duodenal motility, inhibit nausea and vomiting, and effectively prevent bile reflux without affecting gastric juice secretion.
Dosage and precautions: Morindarene 10mg Tid or Qid. Since it does not easily pass the blood-cerebrospinal fluid barrier and has no inhibitory effect on dopamine receptors in the brain, there are no neurological or psychiatric adverse effects such as extrapyramidal, but it should be used with caution in children because of their imperfectly developed blood-cerebrospinal fluid barrier. Sometimes serum prolactin levels may be elevated.
(2) Mosapride.
It is a selective 5-hydroxytryptamine 4 (5-HT4) receptor agonist, which promotes the release of acetylcholine through excitation of 5-HT4 receptors in cholinergic interneurons and intermuscular plexus in the gastrointestinal tract, thereby increasing gastrointestinal motility and improving gastrointestinal symptoms in patients with functional dyspepsia, without affecting gastric acid secretion.
Dosage and precautions: Mosapride 5mg Tid . Mosapride has no affinity for dopamine D2, 5-HT4 and 5-HT2 receptors on the synaptic membrane of the brain, and thus has no extrapyramidal side effects caused by the blockade of these receptors. Adverse effects are mainly manifested as diarrhea, abdominal pain, dry mouth, rash and lethargy, dizziness, etc. Occasionally, eosinophilia, elevated triglycerides and elevated glutathione aminotransferase (GOT), glutamate aminotransferase (GPT), alkaline phosphatase (AKP), gamma-glutamyl phalloidin transpeptidase (GGT) are seen.
3. Acid-suppressing drugs.
Chronic gastritis patients can have high or low gastric acid. The application of acid-suppressing drugs can improve the PH value in the stomach, reduce the damage of H+ to the gastric mucosa, i.e. the degree of H+ counter-dispersion, and create a strong local environment for the inflammatory repair of the gastric mucosa.
(1) H2 receptor antagonists: including cimetidine, ranitidine, famotidine, nizatidine, etc.. All of them can inhibit gastric acid secretion by mural cells through competitive antagonism of histamine binding to H2 receptors. Cimetidine, ranitidine and famotidine have strong inhibition of pepsin secretion and increase the blood flow in gastric mucosa.
Usage: Cimetidine 400mg Bid; Ranitidine 150mg Bid; Famotidine 20mg Bid; Nizatidine 150mg Bid.
(2) Proton pump inhibitor: PPI irreversibly binds to the sulfhydryl group of H+-K+-ATPase (also known as proton pump) in the secretory membrane of wall cells through disulfide bond, generating a complex of sulfenamide and proton pump, thus inhibiting the activity of the enzyme and blocking the last link of gastric acid secretion, thus having strong and long-lasting inhibitory effect on gastric acid secretion caused by various reasons. The inhibitory effect is dose-dependent and has an effect on both basal and post-stimulated gastric acid secretion. On the other hand, PPI inhibits the growth of Helicobacter pylori. Therefore, for patients with severe gastric acidity or gastritis with erosion and bleeding, the use of proton to print preparation can be considered. Commonly used representative drugs: omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole. Generally use standard dose, once a day more can achieve better therapeutic effect.
4. Hp eradication therapy.
Hp-positive active gastritis, Hp should be eradicated.
5, other treatments.
(1) age-related atrophy and intestinalization; nutritive drugs for gastric mucosa, such as: carotene, folic acid, zinc, VitE, etc.
(2) For gastric mucosal intestinal and atypical hyperplasia, give vitamin C, E and folic acid, regular endoscopic follow-up, chronic atrophic gastritis with severe heterogeneous hyperplasia in the current mostly considered precancerous lesions, advocating that surgical treatment should be considered.
(3) Treatment of autoimmune gastritis: no special, pernicious anemia can be injected VitB12. dilute hydrochloric acid, digestive enzymes can be given to patients with poor digestive function.