1、1Gastritis Zhirou Tan Department of Gastroenterology of the First Affiliated Hospital2DefinitionGastritis is the inflammation of various factors stimulate the gastric mucosa.Categories Acute gastritis Chronic gastritis Special type of gastritis 3 Section I Acute Gastritis4 Summarize acute gastritis
2、also called erosive gastritis,hemorrhagic gastritis,acute gastric mucosa lesion.Gastroscope examination:gastric mucosa erosion,bleedingHistology:acute inflammation of the gastric mucosa5 etiology and pathogenesis1.Stress In the stress state,it can cause gastric mucosal erosion and bleeding,such as s
3、evere trauma,major surgery,large area burn and intracranial lesion,shock,sepsis and multiple organ failure(MOF).6mechanism：gastric mucosa microcirculation dysfunction,hypoxia,mucus secretion decreased,local lack of prostaglandin synthesis,barrier function is damaged,gastric acid secrete increased.7
4、etiology and pathogenesis2.Drug non-steroid anti-inflammatory drug(NSAID),such as aspirin,acetaminophen(对乙酰氨基酚对乙酰氨基酚),etc.Some anti-tumor medicine,potassium chloride liquid,chalybeate,etc.NSAID blocks prostaglandin synthesis by inhibiting the cyclooxygenase(COX).COX-1 help to epithelial cells to rep
5、air.COX-2 promotes inflammation medium.8 etiology and pathogenesis3.Alcohol Alcohol with lipotropy and fat soluble,can destroy the barrier of gastric mucosa directly.4.Trauma and physical factors placed stomach tube,vomiting,stomach eyewinker(异物异物),polyp（息肉（息肉）excision under gastroscope,etc.95.Duode
6、nogastric refluxAbnormal gastric dynamics,Pyloric sphincter dysfunction,billrothoperation6.Gastric mucosa blood circulation obstacleportal hypertensive gastropathy(PHG)10 clinical featureMost patients is asymptomatic.A few patients have epigastric discomfort,nausea and vomiting.It can occur suddenly
7、 hematemesis and(or melaena),even massive hemorrhage of the upper alimentary tract,which accounts for about 10%25%cases of upper gastrointestinal bleeding.sign:slight11 Diagnosis Diagnosis depends on the history and clinical feature，and confirmed diagnosis depends on endoscopic examination.12 Asking
8、 medical history to determine the cause.Many stresses caused by the stress history,which is the main performance of upper gastrointestinal bleeding.Endoscopic examination showed multiple erosions,acute superficial ulcer,hemorrhage and mucosal edema,etc.1314Acute Gastric Mucosal Lesions15 Differentia
9、l diagnosis1.peptic ulcer2.esophogeal varices3.gastric carcinoma16 Treatment1.1.Remove the cause2.2.Drugs inhibiting gastric acid secretion：proton pump inhibitors(PPI)or H2 receptor antagonist.3.3.Gastric mucosa protective agent:sucralfate,misoprostol,bismuth agent,etc.17 Prognosis Most of the gastr
10、ic mucosal erosion and bleeding can heal itself,and a few develop into ulcers.18Preventionv1.stopping NSAIDv2.If under the stress state or need long-term taking aspirin or clopidogrel，it had better to give PPI，H2RA preventively.v3.The use of selective cox-2 inhibitors，such as celecoxib to reduce the
11、 inhibition of cox-1.19It is chronic inflammation of gastric mucosa that caused by a variety of causes.Endoscopy:mucosal uneven color,granular proliferation(增生增生),abnormal plica.Histology:inflammatory cell infiltration,epitheliosis(上皮增殖上皮增殖),gastric gland atrophy.Section II Chronic Gastritis20 etiol
12、ogy and pathogenesis1.H.pylori infection It is the main cause of chronic active gastritis.A.Among the chronic active gastritis patients,Hp detection rate is high.B.H.pyloris distribution in the stomach and the stomach inflammation distribution is consistent.C.After the eradication of Hp,gastric muco
13、sal inflammation is gone.D.Infection model can be cloned in person or animals.21 The 2005 Nobel Prize winner in medicineJ.Robin Warren（older)Barry J.MarshallHelicobacter pylori(silver staining)22 etiology and pathogenesisH.pyloris pathogenic factors:flagella,adhesin,urea enzymes,the empty cell toxin
14、,cytotoxin associated protein and H.pylori thallus,etc.23 etiology and athogenesis2.duodenogastric reflux3.autoimmunity Positive reaction of parietal cell antibody(PCA)and intrinsic factor antibody(IFA)can reduce parietal cells.2425etiology and pathogenesis4.Age and gastric mucosa lack of nutritiona
15、l factors agedness gastric arteriole hyaline change mucosal malnutrition.nutrition deficiency abnormal gastric mucosa epithelial proliferation and gastric gland atrophy26 Gastroscope chronic non-atrophic gastritis：mucous membrane red and white,plica(皱皱襞襞)swelling and enlargementchronic atrophic gast
16、ritis：colour is pale，plica flatten，mucus reduce，mucous membrane thinning，submucosal stria vascularis can be seen.27 Classification1.antral gastritis：caused by Hp infection2.body gastritis：related to autoimmunity3.all gastritis：caused by Hp infection extension 28 Pathology 1.1.InflammationThe main ch
17、ronic inflammatory cells are lymphocyte and plasmocyte.superficial layer mucous membranesuperficial gastritis;disease development spread to the whole layerInflammatory activity:neutrophil appear 292.Metaplasia（化生）（化生）Long-term chronic inflammation can make gastric mucosa surface epithelium and gland
18、ular epithelium be replaced by goblet cell and pyloric gland cell.intestinal metaplasiaIntestinal gland which with goblet cell replaces inherent gastric glands pseudopyloric metaplasiaThe hyperplasia of mucous neck cells of oxyntic(泌酸泌酸)gland form pseudopyloric gland303.atrophy(萎缩萎缩)Inflammation ext
19、ends to the deep of the glandsgland damage depletion in numbers mucous membrane thinningnon-metaplasia atrophymetaplasia atrophy314.Dysplasia（异型增生异型增生）Cells are hyperplasia and differentiation（分（分化）化）on the regenerative process,shows cell atypia and disorder of the structure of glands.Dysplasia is p
20、recancerous lesions of gastric carcinoma.It can divide into mild,moderate and severe,and mild dysplasia is reversible.3233Most patients is asymptomatic.symptoms of dyspepsia：abdominal distension which become worse after taking meals,dull pain,belching,acid regurgitation,vomiting,etc.constitutional s
21、ymptom:pernicious anemia,systemic failure,loss of weight.clinical feature34 Diagnosis 1.Endoscopy and biopsy The most reliable diagnostic method.353637 chronic superficial gastritis38Mild atrophySerious atrophy 39 2.H.pylori test invasive method：rapid urease test,micro-aerobic environment cultivatio
22、n,Giemsa staining or Warthin-Starry silver staining.non-invasive method：serum Hp antibody,13C-or 14C-urea breath test,faeces Hp antigen.4041 3.3.Autoimmune gastritis serum gastrin anti-parietal cell anti-body(APCA)（+）anti-intrinsic factor anti-body(AIFA)（+)vitamin B12 42 Differential diagnosis1.pept
23、ic ulcer2.chronic hepatitis3.chronic cholecystitis4.gastric carcinoma43 Treatment1.etiological treatmentA.A.Hp related gastritisbismuth:unite two kinds of antibacterial drugsPPI:PPI:unite two kinds of antibacterial drugs The treatment course is 7 to 14 days.44 B.duodenogastric reflux:gastrointestina
24、l excitomotor C.autoimmunity:glucocorticoidD.deficiency of nutritional factors：supplement multivitamins45 Treatment2.symptomatic treatmentInhibit or neutralize acid:PPI,H2RA protecting gastric mucosa:sucralfate,etcpernicious anemia:VitB12 i.m.463.dispose of precancerous conditions oral cox-2 inhibit
25、or celecoxib,supplement multivitamins and selenium severe dysplasia endoscopic mucosal resection or surgical treatmentTreatment474849 PrognosisChronic non-atrophic gastritis:good prognosisIntestinal metaplasia is usually difficult to reverse.Mild and moderate dysplasia can reverse.Severe dysplasia e
26、asily turn into cancer.50Section III Special type gastritis 1.corrosive gastritisswallow strong acid and strong alkali mucosal burn,serious case gastrointestinal bleeding,perforation.abrosia,parenteral nutrition,early stage should not do gastroscope exam.512.infectious gastritisA.bacterial infection
27、：staphylococcus（葡萄球菌（葡萄球菌）,streptococcus（链球菌）（链球菌）,escherichia coli（大肠杆菌）（大肠杆菌）purulent inflammation abdominal pain,vomiting,necrosis,perforation.B.virus infection：cytomegalovirus（巨细（巨细胞病毒胞病毒）523.Crohns disease4.Eosinophils gastritisThe main inflammatory cells in gastric wall inflammation is eosinop
28、hilic granulocyte.clinical feature:upper abdominal pain,nausea and vomiting，blood eosinophilic granulocyte increase，glucocorticoid useful53 5.Mntrir disease Plica mucosa of the gastric body and fundus became hypertrophy，mucous membrane presents gyrus（脑回脑回）shape，parietal cell and chief cell decrease；hypoproteinemia（低蛋白血症低蛋白血症），），gastric acid secretion decrease，with ulceration.5455 thank you
