【正文】 ancreatic enzymes depose mucus and break biological membrane. These mechanism can all result in mucosal injury and erosion.3 / 24Drugs,ethanol stresblod flow acid outptmucs ecrtionHCO3rtiPGs ynthesiDamge of mucosal brier acid back difusionErosin, hemorhagePathology⒈diseased region：gastric antrum、gastric body or to fill with whole stomach.⒉pathological changes：hyperemia 、oedema 、erosio、hemorrhage、superficial ulceration with gastric mucosa .Characteristics of histology⒈Inflammatory cell infiltrate of lamina propria mucosae；⒉Deprivation and hemorrhage of epithelial cells；⒊ Distort and effusion of gland in mucosa.Clinical feature?Bleeding?many cases of acute gastritis are insidious (asymptomatic or be covered up by other medical conditions ), so lead to escape diagnosis?in some cases, massive bleeding occurs and some times the bleeding may be vital?generally,the bleeding is selflimited?Other symptoms : apigastric pain nausea vomiting indigestion diarrhea ?Signs: slight tenderness in epigastriumDiagnosis?History: ?Symptoms:?definitive diagnosis: endoscopic exam . generally, the acute endoscopic examination should be performed within 24~48 hours after the bleeding. ?Endocopy: hyperemia petechia hemorrhage erosions superficial ulceration ?These changes may be diffuse or limited to the antrum , fundus or body.?In the strictest sense, the diagnosis of acute gastritis should be made by pathologists from the histopathologic findings of the biopsy specimen. ?Inflammatory cells(usually neutrophils and mononuclear cells) infiltrate the lamina propria, where the glandular areas are distorted by edema and hemorrhage. Differential diagnosis?Peptic ulcer disease?hepatic cirrhosis ?gastric carcinoma Treatment1. Removal of the causes?avoidance and discontinuance of the administration of NSAIDs and ethanol ?effective treatment of severe diseases 2. prevention and treatment ?reduce gastric acid . ?Neutralizing gastric acid(antacids)–colloidal alumiun hydroxid, NaHCO3?reducing gastric acid secretion H2RA PPI?Protect mucose : prostaglandin 3. management of gastric bleeding : ①general treatment：bed rest liquid diet overview and surveille②blood volume supplement：fluid infusion、blood transfusion—first elect③stop bleeding：anti acid medicine endoscopic hemostasis surgeryCHRONIC GASTRITISIntroduction?Chronic gastritis main refer to chronic inflammation of gastric mucosa caused by and involves inflammatory changes in the mucosa ?Is a very mon disease.?The inflammation cells in chronic gastritis are mainly lymphocytes and plasma cells,and there may be a few of neutrophils and eosinophils.?The inflammatory changes are usually patchily distributed . In late stage atrophy and metaplasia can be found in the gastric mucosa .Epidemiology ?Prevalence : 50%?: in population ,the infection rate is 40%70% in chronic gastritis, the infection rate is 87%Classification ?There are many classifications:?Whitehead(1972):?superficial gastritis?atrophic gastritis?Strikland (1973) :According to the anatomic portion predominantly involved , atrophic gastritis is classified :?type A( body gastritis) ?type B( antral gastritis)positncaueType Bgastris Type Agatrisntrumfundsnd (90%) imolgical isrdebile rfluxNSAIDssmokingalchl?Misiewicz and Tytgat (1990): Sydney System?1996: Updated Sydney System?nonatrophic gastritisatrophic gastritis special gastritis etiology and mechanism ? infection?A gramnegative bacterium?a quite strong infective ability?incidence is very high.?It is estimated that 50% of the population over the age of 50 years are infected with in developed countries.?The infective rate is 80%95% in the chronic gastritis H. pylori?Stay in gastric antrum, lives in the gastric crypts, gastric metaplasia (duodenal bulb)?Mechanism?H. pylori have the ability to produce a wide variety of virulence factors.?Most associated gastritis dose not develop to erosions,but the inflammation can progress to depth of the mucosa and lead to atrophy. ?Autoimmunity and heredity ?autoantibody in the blood : parietal cell antibody, PCA。 fallII. Etiology and pathogenesis（I）Causes?Helicobacter Pylori（Hp）?Acid amp。 Tissue regenerate to fill the ulcer crater.S（scar stage） Granulation tissue converts to fibrous tissue. Contraction of the scar. V. Complications1． bleeding The most mon causes of UGIH（50%）⑴ DU: 1520%, GU: 1015%.⑵ Being the initial symptom in 1020% PU patients.⑶From occult blood loss to massive bleeding.(4) Easily to be induced by NSAIDs.(5) 3050% patients will bleed again. 2．Perforation① Acute perforation (Free perforation) Rupture into the peritoneal cavity。⑵ Antimuscarine drugs?Affect： Block gastric muscarinic receptorsreduce fast and food stimulated acid secretion.?Drugs ： Pirenzipine?Side effects :Block other muscarinic receptors. Delay gastric emptying, GU can not be used.⑶ H2 Receptor antagonists (H2RA) Drugs Intensity Direction Cimetidine 1 400mg bid( 800mg hs ) Ranitidine 410 150mg bid ( 300mg hs )Famotidine 2050 20mg bid ( 40mg hs )Nizatidine 410 150mg bid( 300mg hs ) Course：DU 68 weeks ，GU 812 weeks⑷ Proton pump inhibitor（PPI ） Drugs DirectionOmeprazole 20 mg qdLansoprazole 30 mg qdPantoprazole 40 mg qdRabeprazole 10 mg qd唉索美拉唑 40mg qd2．Enhancing Mucosal Defense Drugs⑴ sucralfate ① Affect：Form