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luid 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。 intrinsic factor antibody, IFA?autoimmune disease: acpaniment Hashimoto thyroiditis。 vitiligo?Other factors : ?duodenal juice(Bile and pancreatic juice) reflux?damage gastric mucosa factors: NSAID, alcohol abusepathology? infection ?inflammation :The inflammation cells in chronic gastritis are mainly lymphocytes and plasma cells?activity: Classified phase?static phase:?the predominant inflammatory cells in chronic gastritis are lymphocytes and plasma cells ,and this kind of inflammatory conditions is called “static phase”?active phase: ?there are predominant collections of neutrophils and eosinaphils free in the lamina propria and in the lining epithelium ,this condition is called “active phase” ?atrophic gastritis?atrophic gastritis is characterized by a variable glands loss and encroachment of inflammatory cells into the gland zones.?Metaplasia ?intestinal metaplasia : goblet cell?pseudopyloric gland metaplasia ?dysplasia ?moderate and severe dysplasia is considered to be possible precancerous conditions4 / 24atrophiainflammationmetaplasiaClinical manifestationsymptoms : dyspepsia signs : without。 or lightly tenderness in epigastrium Others: anorexia , weight lose , anaemia , glossitis, upper gastrointestinal hemorrhage . symptoacid secrtion BAOtuy Mserm gasrtinseru APCm IFtype B type Asimlar oulcer canr~ or elvate lower o absent r lwer elvate_ +(90%)_ (75)Laboratory test?Identify ?gastric juice analysis ?gastrin?autoantibody?vitamin B12 detection (identification)?Urease test?culture ?Giemsa stain?WarthinStarry stain?14Cbreath test?serum antibody detectionDiagnosis?Endoscopy: endoscopic examination supplemented by biopsy is of definitive diagnostic value for chronic gastritis superficial gastritis:?patchy mucosal congestion ?hypersecretion of mucus Atrophic gastritis?pale ?red alternate with white(pale alternate with patch congestion) ?the folds are narrow and flat ?submucosal blood vessels can be seen through the thinned mucosaatrophic gastritis?Red alternate with white?mucosa bee thin?submucosal blood vessels can be seen through the mucosadifferential diagnosis⒈ functional dyspepsia⒉ peptic ulcer⒊ gastric cancer⒋ biliary tract diseases⒌ chronic pancreatitis Treatment?removal of the causes?eradicate ?triple regimen CBS(colloridal bismuth subcitrate) 110~120mg qidTetracyclin 200mg qid or Tinidazol 400mg tid Amoxycillin 500mg qid ?course of treatment?two weeks or one week?eradication rate above 90%?Type A gastritis :injection vitamin B12?expectant treatment:?metoclopramide, domperidone, cisapride ,mosapride ?H2receptor antagonist:cimetidin,famotidin,nezatidin?ppI: losic?vitamin C, ?carotene ,folic acid , 病例男性,35 歲,因大面積燒傷而入院,入院后處于休克狀態(tài),一日前突然嘔出咖啡樣 液體,即之黑便。既往無(wú)胃病及肝病史。查體:上腹劍突下輕壓痛,肝脾未觸及。 ⒈可能的診斷是什么?請(qǐng)寫(xiě)出診斷依據(jù) ⒉確診應(yīng)選用哪項(xiàng)檢查? ⒊請(qǐng)寫(xiě)出治療原則Peptic UlcerContents?Introduction?Atiology and Pathogenesis?Pathology ?Clinical Presentation?Laboratory Evaluation?Diagnosis and Differential Diagnosis?Medical ManagementI. Introduction(1 )definition of PU? Ulcers are defects in the gastrointestinal mucosa that perate the muscularis mucosae.? Peptic Ulcer ? gastric ulcer, GU, duodenal ulcer, DU ? Low esophagus, Distal duodenum and jejunum, ileum in or near Meckel’s diverticula.(2)Epidemiology⒈ Case rate?A mon disease(10% individuals)?The most mon PU: DU amp。 GU?DU>GU,about 3:1⒉ Sex: Men>W(wǎng)omen⒊ Onset age:DU:40 GU:50⒋ Attack season:spring amp。 fallII. Etiology and pathogenesis(I)Causes?Helicobacter Pylori(Hp)?Acid amp。 Peptic?Nonsteroidal antiinflammatory drugs(NSAIDs )?Geic factors?Abnormal motor func