gastritis-s.ppt

GastritisGastritisProf.Chengwei Tang Dept.Gastroenterology West China Hospital Sichuan UniversityMucosal defenseFirst line of defensemucus,phospholipids and bicarbonateSecond line of defenseApical barrierExtrusion of back-diffusedhydrogen ions Intrinsic mechanisms for antioxidant stress Epithelium cell growthThird line of defenseMucosal blood flowProsglandinsGastritis represents a nonspecific inflammation of the stomach.Gastropathy refers to a pattern of mucosal injury in which inflammatory infiltrates are minimal or absent and the dominant abnormality is either epithelial or vascular.Endoscopic appearances of gastritis Hyperemia Subepithelial hemorrhage (Discrete petechiae or bright red streaks and patchs)Superficial erosions Nodules AtrophyHistology Hyperemia Inflammatory cells:neutrophils lymphocytes mononuclear cells Glands loss,hyperplasia,metaplasia Overview of gastritis and gastropathyErosive and hemorragicNonerosiveDistinctiveAssociations with erosive/hemorrhagic gastritis and gastropathyStress lesions in seriously ill patientsDrugsTrauma and physical agentsVascularReflux injuryidiopathic Stress gastropathy Subepithelial hemorrhages or erosions are found in:most patients hours after major operationwithin 24 hours of the onset of major multisystem illness The mortality rate depends if the underlying illnesses are serious.PreventionBetter intensive care of critically ill patientsPharmacolgic prophylaxis antacids H2 receptor antagonists sucralfateDrugs Nonsteroidal anti-inflammatory drugs (NSAIDs)Alcohol Corrosive ingestion Others:potassium chloride iron chemotherapy Cyclooxygenase(COX)inhibitionTopical effectsOther multifactorial mechanismsMechanismsPGE2 I2 F2 Arachidonic acidMembrane phospholipidsPhospholipase A2Thromboxane A2COX-1 (constitutive)COX-2 (inducible)NSAIDsCOX-2 inhibitorsDirect topical effectDenudation of surface epithelial cellsIncrease mucosal permeability to sodium and hydrogen ionsMechanismsDirect topical effectDenudation of surface epithelial cellsIncrease mucosal permeability to sodium and hydrogen ionsMechanismsClassification 1st degree Superficial and produce edema and erythema of only the mucosa.Without scar or stricture formationClassification 2nd degree Penetration occurs through the submucosa into the muscular.deep ulceration scar formation3rd degree perforationInfection and additional traumaClinical featuresAcute manifestations(1)Persistent salivation Inability to swallow Edema,ulceration,white membrane of palate uvula pharynx The lesions bleed easily and painfulClinical featuresAcute manifestations(2)Dysphagia Odynophagia Hematemesis Epigastric pain Retching Emesis of tissue,bloodClinical featuresAcute manifestations(3)3rd degree Tachypnea Dyspnea Stridor Shock Acute peritonitis Clinical featuresLate manifestations Dysphagia Gastric outlet obstruction early satiety weight loss progressive emesisDiagnosisHistory of caustic ingestionEndoscopyUpright chest and abdominal roentgenogramsTreatment Dilution of causticsAntibiotics NutritionEarly esophageal dilationSurgery Vascular Ischemia Congestive gastropathy Portal hypertensive gastropathy Characterized as venous and capillary ectasia in the gastric mucosa and submucosa with little associated inflammatory activity.PHG is a common finding in patients with portal hypertension.It accounts for 8%20%of all acute bleeding in patients with PHG.Portal hypertensive gastropathy Endoscopic appearance mild:“mosaic”or“snakeskin”pattern of erythema severe:bright-red punctate erythema diffuse hemorrhagic lesions black or brown spotsOverview of gastritis and gastropathyErosive and hemorragicNonerosiveDistinctiveNonerosive gastritis typesH.pylori gastritisReactive gastropathyLymphocytic gastritisSevere atrophic gastritis with withoutPernicious anemiaAutoimmune basisNonerosive gastritis The most important and common cause of nonerosive gastritis is Helico-bacter pylori(H.pylori).H.pyloriMicroaerophilic Highly motileGram-negative spiral organismIts most striking biochemical characteristic is the abundant production of urease.It usually colonizes between mucus and epithelium of antrum.Virulence factors possessed by H.pylori that promote colonization and induce tissue injuryPromote colonization Motility Urease Adherence Induction of hypochlorhydriaInduce tissue injuryLipopolysaccharide(LPS)Leukocyte recruitment and activating factorsCag A and Vac A proteinsHeat shock proteinNatural history of chronic infectionAcute gastritisChronic active gastritisAntral predominant gastritisDuodenal ulcerMultifocal atrophic gastritisGastric cancerGastric ulcerLymphomaEnvironmental factorsLymphoma Although the organism is spon-taneously cleared in some individuals,infection in most adults appears to be long term.Most individuals with H.pylori infection remain asymptomatic through-out their lives.H.pylori usually colonizes between mucus and epithelium of antrum and results in antral gastritis.Type B gastritisMost commonGenerally diffuseSuperficial gastritis The inflammatory cells are confined to the pit region.In some individuals,chronic superficial H.pylori gastritis progresses over time to atrophic gastritis.Atrophic gastritis There is variable gland loss,which is often accompanied by intestinal metaplasiaIntestinal metaplasia Epithelial cells acquire the features of intestinal epithe-lium.Three patterns:Oxyntic(type A)Antral(type B)Multifocal atrophic gastritisHistologic patterns of nonerosive gastritis Type of gastritisInflammatory cellsGlandsSpecial featuresSuperficialConfined to pit regionsIntact H.pylori presentAtrophicExtension into gland zonesVariable gland lossMetaplasia:intestinal or mucous gland(pseudopyloric)Epithelial or vascular changes dominantClinical manifestationsRemaining asymptomatic through-out their livesNausea,anorexia,bloating,fullness,gnawing vomiting DiagnosisClinical manifestationsEndoscopyBiopsy histology H.pylori testTreatmentH.pylori eradication therapy Treatment of dyspepsiaH.pylori eradication therapyTreatment of patients with H.pylori gastritis is controversial.There is evidence for a small benefit of eradicating H.pylori in gastritis.What is the aim for H.pylori eradication therapy?(1)H.pylori is an important cause of gastric cancer.To prevent gastric carcinoma in average-risk populations.Indication?A patient has a family history of gastric cancer.H.pylori gastritis with premalignant conditionsAtrophy Metaplasia DysplasiaWhat is the aim for H.pylori eradication therapy (2)H.pylori is a major cause of peptic ulcer.H.pylori eradication therapy reduces the recurrence of peptic ulcer disease and is cost-effective.Indication?Indication?The patients with H.pylori gastritis have the history of peptic ulcer.H.pylori gastritis with erosive duodenitis.What is the aim for H.pylori eradication therapy (3)H.pylori is a common cause of nonerosive gastritis.To alleviate the symptoms of dyspepsia It is not cost-effective.Indication?Indication?Erosive mucosa recommendedNonerosive mucosa recommended?Antibiotics used in regimens to eradicate H.pylori AmoxicillinClarithromycinMetronidazoleTetracycline It is contraindicated in children because of the staining of teeth.Adjunctive agents used in regimens to treat H.pylori infectionBismuth colloidal bismuth subcitrateH,K-ATPase(proton-pump)inhibitors omeprazole,esomeprazole H2 receptor antagonists famotidine,ranitidineFirst-line management issuesSpecific concerns of the patients about their symptoms should be addressed.Identification of potential precipitating factors for symptoms.Patients should be advised to avoid these factors(eg.Alcohol,smoking,aspirin).First-line drug therapyProkinetics Domperidone(MOTILIUM)If dysmotility-likeAntisecretory therapy H2 RA,PPI Antiacid Hydrotalcite(TALCID)If ulcer-like