消化内科课件-12peptic-ulcer

PepticUlcerDisease(PUD)DepartmentofGastroenterology,theFirstAffiliatedHospitalofChongqingMedicalUniversity1.Definition2.epidemiology3.Etiologyandpathogenesis4.Clinicalpresentations5.Diagnosis6.Complications7.TreatmentMainContents1.DefenitionofPUDPUDisUlcerationofgastrointestinalmucosaresultingfromauto-digestionofgastricacidandpepsin.Stomach(gastriculcer,GU)Duodenum(deodenalucler,DU)esophagusGastro-jejunalanastomosis(postsubtotalgastrectomy)Terminalileumdiverticulum（回肠末段憩室）（回肠末段憩室）(Meckelsdiverticulum，heterotopicgastricmucosa)SitesofpepticulcerSitesofpepticulcerAnastomotic ulcerSitesofpepticulcerSitesofpepticulcerDifferenceofulceranderosionDifferenceofulceranderosion UlcerUlcerisamucosaldefectthatisamucosaldefectthatpenetratesthemuscularispenetratesthemuscularismucosamucosa（粘膜肌层）（粘膜肌层）（粘膜肌层）（粘膜肌层）ErosionErosionisasmall,superficialisasmall,superficialmucosalbreakthatmucosalbreakthatnomorethannomorethanthemuscularismucosathemuscularismucosa（粘膜肌（粘膜肌（粘膜肌（粘膜肌层）层）层）层）2.EpidemiologyllPrevalencerateaPrevalencerateaboutbout1 10 0%overalllifetimeoveralllifetimellTheincidenceofDUwashigherthanGUTheincidenceofDUwashigherthanGUllTheincidenceofwasmalehigherthanfemaleTheincidenceofwasmalehigherthanfemalellThepredominantageofDUisbetween20and50ThepredominantageofDUisbetween20and50yearsold,whereasGUoccursinpatientsmorethanyearsold,whereasGUoccursinpatientsmorethan40yearsold40yearsoldllThediseaseismorecommoninsmokersThediseaseismorecommoninsmokers3.EtiologyandpathogenesisGastricMucosa&SecretionsTheinsideofthestomachisbathedinabout2litersofgastricjuiceeverydayGastricjuiceiscomposedofdigestiveenzymes&concentratedhydrochloricacid,whichcaneasilytearapartthetoughestfoodormicroorganism12pathogenesisofPUDpathogenesisofPUDprotective or defensive factorsdamaging or aggressive factorsAggressivefactorsincreasingorthedefensivefactorsdecreasingwillresultinmucosaldamage,thenleadtoulceration.PathogenesisofUlcersAggressiveFactorsH.pyloriNSAIDsGastricacid,pepsinBilesaltsPancreatinSmokingandalcoholothersDefensiveFactorsMucus-bicarbonatelayer（粘液（粘液-碳酸氢盐）碳酸氢盐）Mucosa（粘膜）（粘膜）Bloodflow,cellrenewalProstaglandinsGrowthfactorsDefensivefacors:1)Mucus-bicarbonatelayer（粘液粘液-HCO3-屏障屏障）:MucosalcellssecretedmucusandHCO3-,whichmixedandformedgel-likelayeronmucosalsurface.（粘膜细胞分泌的粘液和（粘膜细胞分泌的粘液和HCO3-，混合在一起覆盖于粘膜的表面形，混合在一起覆盖于粘膜的表面形 成凝胶状的不流动层）成凝胶状的不流动层）2)mucosalbarrier（粘膜屏障粘膜屏障）Formedbytightjunctionsbetweenmucosalepithelialcells.（粘膜上皮顶部的细胞膜及其细胞之间的紧密连接，称为粘膜屏障粘膜上皮顶部的细胞膜及其细胞之间的紧密连接，称为粘膜屏障）3)mucosalbloodflow（粘膜血流粘膜血流）ProvideoxygenandnutrientstoMucosaandsubmucosaltissues（给予粘膜和粘膜下组织供应氧和营养物质给予粘膜和粘膜下组织供应氧和营养物质）CarryoffH+andmetaboliteintissues（带走组织中的带走组织中的H+和代谢产物和代谢产物）Transportbicarbonatetomucosalsurfaceforpreventingexcessiveacidificationofmucosalcells.（向粘膜表面细胞输送向粘膜表面细胞输送HCO3-，防止细胞过度酸化），防止细胞过度酸化）16Mucus-bicarbonatelayermucosalbarriermucosalbloodflow4)ProstaglandinE(PGE)uPromotemucosalbloodcirculationupromotethesecretionofbicarbonate(HCO3-)uPromoteDNAsynthesisofmucosalcells5)cellfactors:EGF(EpidermalGrowthFactor)FGF(fibroblastGrowthFactor)TGF(transformingGrowthFactor)uimportantregulatoryeffectonmucosalwoundrepairEtiology(AggressiveFactors)1.Helicobacterpylori(H.pylori)2.NSAIDs(non-steroidalanti-inflammatorydrugs)3.Acidandpepsin4.Otherriskfactors:geneticpredisposition,smoking,alcohol,stress,diet,virusinfectionEtiology H.pyloriinfectionSpiralshaped,flagellated,gram-negativebacillus（螺旋状，带有鞭毛，革兰氏阴性杆菌）（螺旋状，带有鞭毛，革兰氏阴性杆菌）H.Pylori:ColonizinginhumanstomachTransmittedfrompersontopersonbyoraloralorfeco-oralspreadNobelPrize2005“fortheirdiscoveryofthebacteriumHelicobacter pylorianditsroleingastritisandpepticulcerdiseaseBarryJ.MarshallBarryJ.MarshallJ.RobinWarrenJ.RobinWarren1.1.MostpepticulcersassociatedwithMostpepticulcersassociatedwithH.H.pyloripyloriinfectioninfection90-100%ofDUand80-90%ofGUare90-100%ofDUand80-90%ofGUareassociatedwithassociatedwithH.PyloriH.PyloriinfectioninfectionClinicalSurveyProvementClinicalSurveyProvement2.2.riskfordevelopmenttopepticulcersinriskfordevelopmenttopepticulcersinpatientswithpatientswithH.pyloriH.pyloriinfectionisinfectionisincreasedincreasedForthepatientswithForthepatientswithH.pyloriH.pyloripositive,positive,about15to20%willdeveloptopepticabout15to20%willdeveloptopepticulcersin10yearsulcersin10yearsClinicalSurveyProvementClinicalSurveyProvement3.3.EradicationofEradicationofH.pyloriH.pyloriisisassociatedwithhigherhealingassociatedwithhigherhealingratesratesthehealingrateofpepticulcerthehealingrateofpepticulcer-OnlyeradicationofOnlyeradicationofH.pyloriH.pylorivshighvshigheffectiveacidsuppressivetherapyeffectiveacidsuppressivetherapy-AftereradicationofAftereradicationofH.pyloriH.pylori,refractoryulcercanbehealedrefractoryulcercanbehealedClinicalSurveyEvidenceClinicalSurveyEvidence4.Eradicationof4.EradicationofH.pylori is H.pylori is associatedwithlowerulcerassociatedwithlowerulcerrecurrenceraterecurrenceratetherecurrencerateofpepticulcertherecurrencerateofpepticulcer(peryear):(peryear):ClinicalSurveyProvementClinicalSurveyProvementnotreatmentofH.pyloriH.pylori eradication50-70%5%WhyHWhyH.pylori.pylori isoneoftheisoneofthemaincausesofPUD?maincausesofPUD?1.Mostpepticulcersassociatedwith1.MostpepticulcersassociatedwithH.pylori H.pylori infectioninfection2.riskfordevelopmenttopepticulcersinpatientswith2.riskfordevelopmenttopepticulcersinpatientswith H.pylori H.pyloriinfectionisincreasedinfectionisincreased3.Eradicationof3.EradicationofH.pyloriH.pyloriisassociatedwithhigherisassociatedwithhigherhealingrateshealingrates4.Eradicationof4.EradicationofH.pylori H.pylori isis associatedwithlowerulcerassociatedwithlowerulcerrecurrenceraterecurrencerateQuestion:Thehighacidityofthestomachkillsmanymicroorganisms.ButhowcanH.pylorisurviveinhighacidenvironment?1.WhyHpcansurviveinthestomach (Hp 在胃内存活的原因在胃内存活的原因)1）UreasesecretedbyH.pyloricanhydrolysisureatoformammoniaand“ammoniaclouds”aroundH.pylori,whichneutralizeorbuffergastricacidandprotectH.pylori.（Hp产生的尿素酶水解尿素产生的氨在产生的尿素酶水解尿素产生的氨在Hp周围形成周围形成“氨云氨云”，中和周围胃酸，从而保护中和周围胃酸，从而保护Hp）2）Theflagellum（鞭毛）makeitmotile,allowingittolivedeepbeneaththemucuslayer（Hp菌体呈螺旋形，一端有鞭毛，提供运动动力，使 其能寄居于最适部位）3)H.pyloricanexcreteadhesive factor,whichmakeH.pyloriadheretogastricepithelium,thenfacilitatethetoxinstodamagegastricepithelialcells.(Hp存在粘附因子，它使Hp特异地粘附于胃粘膜，其 毒素作用上皮细胞)2.HpdamagedDefenseandrepairmechanismofgastricmucosaHpHp损害粘膜的防御修复机制损害粘膜的防御修复机制损害粘膜的防御修复机制损害粘膜的防御修复机制1)Vacuolatingcytotoxin(VacA):thecellsvacuoles空泡毒素（空泡毒素（空泡毒素（空泡毒素（VacAVacA）蛋白：使细胞产生空泡）蛋白：使细胞产生空泡）蛋白：使细胞产生空泡）蛋白：使细胞产生空泡2)Urease:damagemucosaldirectlyorindirectly尿素酶：直接或间接破坏粘膜屏障尿素酶：直接或间接破坏粘膜屏障尿素酶：直接或间接破坏粘膜屏障尿素酶：直接或间接破坏粘膜屏障3)Mucusenzyme:degradatemucus,andpromoteH+dispersion粘液酶：降解粘液，促进粘液酶：降解粘液，促进粘液酶：降解粘液，促进粘液酶：降解粘液，促进H+H+反弥散反弥散反弥散反弥散4)Lipopolysaccharide,esterase,andphospholipase:destructionofmucosalintegrity.脂多糖、酯酶、磷脂酶：破坏粘膜的完整性脂多糖、酯酶、磷脂酶：破坏粘膜的完整性脂多糖、酯酶、磷脂酶：破坏粘膜的完整性脂多糖、酯酶、磷脂酶：破坏粘膜的完整性3.H.pyloristimulatesexcesssecretionofgastrinhormone,whichelevatesacidsecretionandthusincreasesaggressivefactors.EtiologyuNon-SteroidalAnti-inflammatoryDrugs(NSAIDS)Aspirin,Ibuprofen,NaproxenRiskfactor:age,dose,durationoftherapyPU:1030%GUismorethanDUcomplicationsarehigherthangeneralpopulationComplication:15%NSAIDsNSAIDsinhibitprostaglandinsynthesisinhibitprostaglandinsynthesis byblockingbyblockingcyclooxygenase(COX)cyclooxygenase(COX)PathogenesisofNSAIDSCOX-2selectiveinhibitor(celecoxib)preferentiallyinhibitCOX-2,anddecreasetheriskofNSAID-relatedulceration.NSAIDsuAttention:BothNSAIDsandHelicobacterpyloriaretheindependentriskfactorsofpepticulcer.（NSAIDsNSAIDs和幽门螺杆菌是引起消化性溃疡的两个独立因素和幽门螺杆菌是引起消化性溃疡的两个独立因素）EtiologyuGastricacidandpepsinPepsinisthedirectfactorwhichcandamagegastricmucosa,butpepsincanbeactivatedonlywhenPHvaluelessthan4instomachlPUonlyoccursinpositionwhichcontactwithgastricacidlInhibitionacidsecretioncanhealulcerlGastrinomaproducemultiple,atypical,refractoryulcerslPUwontoccurwhenacidiscompletelylackingNoacid,noulcerEtiologyugeneticpredispositionGeneticsusceptibilityorintrafamilialH.pyloriinfectionTheconcordanceofpepticulcerincidenceindizygotictwinshigherthanenzygotictwinsEtiologyEtiologyuu Otherriskfactors:Otherriskfactors:smoking,alcohol,smoking,alcohol,stressstress,diet,virus,diet,virus infectioninfectionSummarySummary PepticulcerisamultiplefactorsdiseasePepticulcerisamultiplefactorsdisease BothHelicobacterpyloriandNSAIDsaremaincausesBothHelicobacterpyloriandNSAIDsaremaincauses ImbalancebetweenMucosalaggressivefactorsandImbalancebetweenMucosalaggressivefactorsanddefensivefactorsdefensivefactors Noacid,noulcerNoacid,noulcer emphasisonthepathogenesisofGUandDUisdifferenceemphasisonthepathogenesisofGUandDUisdifferencePathologyPathology（病理）（病理）（病理）（病理）Location:Location:DUisalwayslocatedintheanteriorwallofDUisalwayslocatedintheanteriorwallofduodenum,GUisalwaysbefoundonthegastricangleduodenum,GUisalwaysbefoundonthegastricangleandlessercurvatureofgastricantrumandlessercurvatureofgastricantrum （部位部位部位部位:DU:DU多在球部前壁，多在球部前壁，多在球部前壁，多在球部前壁，GUGU多在胃角和胃窦小弯多在胃角和胃窦小弯多在胃角和胃窦小弯多在胃角和胃窦小弯）Numbers:Numbers:singleormultiplesingleormultiple Size:Size:DU15mm,GU20mmDU15mm,GU20mm)(diameter20mm)Shape:Shape:round,oval,linear,irregularround,oval,linear,irregularClinicalManifestationsuMainsymptoms:abdominal painProperties:dull,burning,swelling,sharpPosition:vagueuOtherdyspepticsymptoms:anorexia（厌食）,nausea,vomiting,bloating,belchinguCharacteristicsofabdominalpain:1.Chronic,recurrentattacks（慢性过程，反复发作）慢性过程，反复发作）2.periodic,remissionphaseisalternatingwithattacks.（发作呈周期性，与缓解期相互交替）发作呈周期性，与缓解期相互交替）3.seasonal,occurswhenautumnturnsintowinterorwinterturnsintospring（季节性，多在秋冬、冬春之交）季节性，多在秋冬、冬春之交）4.rhythmicity（发作时上腹痛呈节律性）发作时上腹痛呈节律性）5.acidsuppressiontherapyiseffective（抑酸治疗有效）（抑酸治疗有效）ClinicalManifestationsRhythmicityGU:meal-pain-remissionaccentuatedbyeatingDU:pain-meal-remissionhungerpain:manifestsmostlybeforethemeal,relievedbyfoodnocturnalpain:wakesuppatientatmidnightuuSigns:Signs:Activepepticulcer:Activepepticulcer:fixedandlimitedfixedandlimitedtendernesstendernessAlleviatedpepticulcer:Alleviatedpepticulcer:noobvioussignsnoobvioussignsPhysicalExaminationPhysicalExaminationSpecialTypesofPUDSpecialTypesofPUD PostbulbarduodenalulcerPostbulbarduodenalulcer（球后溃疡）（球后溃疡）（球后溃疡）（球后溃疡）SilenceulcerSilenceulcer（无症状性溃疡）（无症状性溃疡）（无症状性溃疡）（无症状性溃疡）PyloricchannelulcerPyloricchannelulcer（幽门管溃疡）（幽门管溃疡）（幽门管溃疡）（幽门管溃疡）UlcerinelderlyUlcerinelderly（老年人溃疡）（老年人溃疡）（老年人溃疡）（老年人溃疡）ComplexulcersComplexulcers（复合溃疡）：（复合溃疡）：（复合溃疡）：（复合溃疡）：GU+DUGU+DUGU+DU RefractoryulcerRefractoryulcer（难治性溃疡）（难治性溃疡）（难治性溃疡）（难治性溃疡）DiagnosisofPUDDiagnosisofPUD HistoryHistory EndoscopyandbiospyEndoscopyandbiospy BariumRadiologyBariumRadiologyUpperEndoscopyUpperEndoscopythemostaccuratetestforPUDUpperEndoscopyUpperEndoscopy RoutinebiopsycanbeusedforRoutinebiopsycanbeusedforexcludegastriccarcinomaexcludegastriccarcinomaUpperEndoscopyUpperEndoscopy Ensureifthereisornoulcer,siteandstageofulcer,Ensureifthereisornoulcer,siteandstageofulcer,themisseddiagnosisrateisbelow510%themisseddiagnosisrateisbelow510%BiopsycanbeusedfordistinguishbenignandBiopsycanbeusedfordistinguishbenignandmalignantulcermalignantulcer MorereliablethantheBariumRadiologyforfindingMorereliablethantheBariumRadiologyforfindinggastricbodyposteriorwallulcergastricbodyposteriorwallulcer（胃体后壁溃疡）（胃体后壁溃疡）andandduodenalulcer.duodenalulcer.EndoscopichemostasisEndoscopichemostasis（止血）（止血）EvaluationoftherapeuticeffectEvaluationoftherapeuticeffectBariumRadiologyuDirectsigns:niche（龛影）（龛影）forestablishingulcerniche isoutsidestomachandduodenumBariumcontourinBenign ulcerniche isinsidestomachandduodenumBariumcontourinmalignant ulceruIndirectsigns:justindicateulcerLocaltenderness（局部压痛）incisuraleadingbyspasmingastricgreatercurvature（胃大弯痉挛切迹）bulbardeformity（球部变形）52BariumRadiologyuAdvantages:nopainuDisadvantages:(1)Noulcerinbariumradiologycannotruledoutulcercompletely(2)CannotbeusedforHpdetection(3)DistinguishingbetweenbenignandmalignantulcerisnotreliableuSelectionprinciple:(1)Nocontraindication,preferredendoscopy(2)Ifpatientscantafford,bariumradiologyisrecommendBariumRadiologyDiagnosisofH.pyloriInfectionNon-invasiveC13 or C14 Urea Breath TestStoolantigentestH.pyloriIgGtiter(serology)Invasivetest(endoscopy)Rapid urease testHistologicalexaminationMicrobialcultureDiagnosisofH.pylori:non-invasive1.C13orC14UreaBreathTestThebestnon-invasivetestforH.pyloriinfectionThepreferredmethodforre-evaluationDiagnosisofH.pylori:non-invasive2.SerologyTestSerumAntibodies(IgG)toH.pyloriNotforactiveinfection3.StoolantigentestFecalantigenofH.pyloripossiblealternativetoureatestDiagnosisofH.pylori:invasive1.RapidureasetestConsideredtheendoscopicdiagnostictestofchoiceGastricbiopsyspecimensareplacedinthetestkit.IfHpyloriarepresent,bacterialureaseconvertsureatoammonia,whichchangespHandproducesaCOLORchangeDiagnosisofH.pylori:invasive2.HistologicalexaminationH.PyloriongastricepithelialcellsDiagnosisofH.pylori:invasive3.Microbialculture-UsedinresearchstudiesandisnotavailableroutinelyforclinicaluseDifferentialDiagnosisofPUDlFunctionaldyspepsia-endoscopylBiliaryorpancreaticdiseases-ultrosonography,-MRCP,ERCPlGastriccancerlGastrinomas(ZollingerEllisonsyndrome)DifferentialDiagnosis:Benigngastriculcer-smooth,regular,roundededges,-flat,smoothulcerbaseGastriccancer-ulceratedmass-nodular,clubbed,-fusedsurroundingfolds-irregularorthickenedmarginsMultiplebiopsiesoptimalnumberofbiopsiesfirstbiopsy-correctdiagnosisin70%fourbiopsy95%Sevenbiopsy98%Follow-upendoscopyDifferentiation:gastriculcervs.cancerDifferentialDiagnosis:Gastrinomas(Zollinger-Ellisonsyndrome)non-betaisletcelltumorofthepancreasleadingtomassiveproductionofgastrinandexcessivesecretionofgastricacidmultiple&refractoryulcersinunusuallocationsoftencompaniedwithdiarrheaGastricsecretorytest-Basicacidoutput15mEq/hourFastingserumgastrin500pg/mlUltrosonography,CTGastrinomas(Zollinger-Ellisonsyndrome)ComplicationsofPUDCommon:1.Hemorrhage2.Perforation3.outletStenosisorpyloricobstruction4.MalignantTransformation1.HemorrhagethemostcommoncomplicationItoccurswhentheulcererodesoneofthebloodvesselsclinicalfeaturesmayappearashematemesisorbloodyvomitus,orthebloodmayappearinstools,whereitgivesthestoolsadark,tarryappearance,whichisreferredtoasmelenaSeverehemorrhagemayleadtoshockhematemesistreatment-Routinemedicaltherapy-Emergencyendoscopytostopbleeding-Surgery69 ForresttypingofpepticulcerbleedingForresttypingofpepticulcerbleeding （消化性溃疡出血的（消化性溃疡出血的（消化性溃疡出血的（消化性溃疡出血的ForrestForrest分型）分型）分型）分型）typecharacteristicsrateofbleedingagaintreatment(类型）类型）（特点）（特点）（再出血率（再出血率%）（治疗策略）（治疗策略）active active bleeding bleeding （活动性动脉出血）（活动性动脉出血）90 PPI+endoscopy+PPI aa Naked blood vessels Naked blood vessels with obvious Errhysis with obvious Errhysis （裸漏血管伴明显渗血）（裸漏血管伴明显渗血）50 PPI+endoscopy+PPI bb blood clot blood clot （血凝块（血凝块 ）25-30 PPI,endoscopy aa a few a few Errhysis Errhysis （少量渗血）（少量渗血）10 PPI bb (only ulcer,no blood)(only ulcer,no blood)仅有溃疡，无血迹仅有溃疡，无血迹 3 PPI2.Perforation:Anulcercanbreakthroughtheentiregastro-intestinalwallBacteriaandpartiallydigestedfoolspillintoperitoneum=peritonitisclinicalfeaturesThefirstsignisoftensuddenintenseabdominalpainSignsofacuteperitonitisBoardlikerigidityofabdomenX-ray mayrevealfreegasunderthediaphragmtreatmentSurgeryisrequiredimmediately3.StenosisScarringandswellingduetoulcerscausesnarrowingintheduodenumandgastricoutletobstructionGastricoutletobstructionclinicalfeaturesRecurrent,large-volumevomiting,unpleasantinnature,totallylackinginbile,containingfoodstufftakenseveraldayspreviously4.MalignantTransformation:DUgenerallybenignGUwithpossibilityofmalignancyBiopsyisveryimportantTreatment1.Lifestylechanges2.Medications3.Surgicalintervention1.Life-styleModificationRegularlifestyle,rest,relaxationDiet:Regularmealsblanddiet（清淡饮食）:avoidspices,coffee,alcohol,ordietsrichinmilkandcreamlSmokingcessationlNSAIDsdiscontinuationifpossible2.Medications1.Acidsuppression2.EradicationofH.pylori3.MucosalProtectantsAcidSuppression1.Protonpumpinhibitors(PPIs)2.H2-recptorantagonists(H2RAs)No acid,no ulcer!ProtonPumpInhibitorsProtonPumpInhibitors(PPIs)(PPIs)MechanismofactionMechanismofaction UncompetitiveandirreversibleinhibitionUncompetitiveandirreversibleinhibitionofprotonpumpofprotonpump(H(H+/K K+-ATPase)-ATPase)thatisthatisresponsibleforfinalstepingastricacidresponsibleforfinalstepingastricacidsecretionfromtheparietalcell.secretionfromtheparietalcell.Mosteffectivedrugsinacidsuppression,Mosteffectivedrugsinacidsuppression,i inhibitnhibitingingover90%over90%of24-houracidof24-houracidsecretionsecretionPPIs include:Omeprazole,Lansoprazole,PantoprazoleRabeprazole,EsomeprazoleMechanismofactionMechanismofaction CompetitivelyandreversiblyblocktoCompetitivelyandreversiblyblocktohistamineHhistamineH22receptorsontheparietalreceptorsontheparietalcellsthusreducegastricsecretioncellsthusreducegastricsecretion LesspotentthanPPIsLesspotentthanPPIsH2RAs include:Cimetidine,Ranitidine,Famotidine,NizatidineH2-recptorAntagonists(H2RAs)EradicationofH.pylori:lH.pyloriissensitivetothefollowingantibiotics:-Amoxicillin（阿莫西林）（阿莫西林）-Tetracyclin（四环素）（四环素）-Clarithromycin（克拉霉素）（克拉霉素）-Metronidazole（甲硝唑）（甲硝唑）lTherapywithoneortwodrugsisineffectivelCombinedtherapyisusuallyused-EradicationofH.pyloriThestandardfirst-linetherapyistripletherapy”-PPIorbismuth+twoantibioticsquadrupletherapy:PPI+bismuth+twoantibioticscourseoftreatmentis10or14daysEradicateH.pyloriinfectionPPIandBismuthTwoAntibiotics +Clarithromycin500mgbidAmoxicillin1000mgbid(Tetracycline)750mgbidMetronidazole400mgbidFurazolidone100mgbidQuadrupletherapy,for10or14daysOmeprazole20mgbidLansoprazole30mgbidPantoprazole40mgbidRabeprazole10mgbidEsomeprazole20mgbidTreatmentcourseofpepticulcerTotalcouseforGU:6-8weeksTotalcourseforDU：4-6weeksAttention:treatmentcourseforPUcourseforeradicatingHPMucosalProtectiveAgentslSucralfate（硫糖铝）（硫糖铝）lMisoprostol（米索前列醇）（米索前列醇）lColloidalBismuthcompounds（胶体铋化合物）（胶体铋化合物）Sucralfate:CoatsulceratlowpH,thuspromotinghealingThemainsideeffectisconstipationColloidalBismuthcompoundsItformsaprecipitatewithmucouscovertheulcerwithaprotectivecoatthatpreventeffectofHClPromotehealingofulcerBactericidaleffectagainstH.pyloriMisoprostolProstaglandinanalogsShouldbeparticularlyeffectiveathealingNSAIDinducedulcersFrequentlycausesdiarrheaanduterinecontraction（子宫收缩）（子宫收缩）GeneralStrategyDeterminetheetiologyofulcerEradicate H.pylori infection DiscontinueNSAIDsuseifpossibleSmokingcessationshouldbeencouragedUseAcidsuppressivetherapyTreatcomplications3.SurgicalTreatmentIndications:itisdifficulttocontrolthebleedingofdigestivetractwithconservativetreatmentacuteperforationandfollowingacutediffuseperitonitiscicatricialpyloricobstruction（瘢痕性幽门梗阻）MalignantulcerCasestudy Case1:Case1:A27-year-oldmanhasa3-monthhistoryofA27-year-oldmanhasa3-monthhistoryofintermittentburningepigastricpainthatismadeworseintermittentburningepigastricpainthatismadeworsebyfastingandimproveswithmeals.Antacidsprovidebyfastingandimproveswithmeals.Antacidsprovidetemporaryrelief.Heisotherwisehealthyandhasnotemporaryrelief.Heisotherwisehealthyandhasnoothersymptoms.Hisonlymedicationisoccasionalothersymptoms.Hisonlymedicationisoccasionalacetaminophenforkneediscomfort.Physicalacetaminophenforkneediscomfort.Physicalexaminationdisclosesonlymildepigastrictendernesstoexaminationdisclosesonlymildepigastrictendernesstopalpation;vitalsignsarenormal.palpation;vitalsignsarenormal.WhichofthefollowingdiagnosticstudiesshouldbeWhichofthefollowingdiagnosticstudiesshouldbedonenext?donenext?A)AbdominalultrasonographyA)Abdominalultrasonography B)SerologictestingforB)SerologictestingforH.pyloriH.pylori C)UpperendoscopyC)Upperendoscopy D)UppergastrointestinalbariumstudyD)Uppergastrointestinalbariumstudy Case2Case2:A65-year-oldwomanwasrecentlydischargedA65-year-oldwomanwasrecentlydischargedfromthehospitalaftertreatmentofuppergastrointestinalfromthehospitalaftertreatmentofuppergastrointestinalbleedingsecondarytoaduodenalulcer.Whilehospitalized,bleedingsecondarytoaduodenalulcer.Whilehospitalized,sheunderwentupperendoscopy,andantralbiopsysheunderwentupperendoscopy,andantralbiopsyspecimensshowedspecimensshowedH.pyloriH.pylori.Thepatientwastreatedwith.Thepatientwastreatedwithappropriateantibioticsandaprotonpumpinhibitor.approp