胃十二指肠疾病英文课件(2010年修订版)

1Stomach&DuodenumByChenJun-qiangM.D.&Ph.D.PepticulcerDefinitionofulcer•Fromahistologicperspectiveanulcerisalossofthesurfaceepitheliumthatextendsdeeplyenoughtoreachorpenetratethemuscularismucosae•Fromaclinicalperspectiveanulcerisalossofthemucosalsurface,visiblebyendoscopyorradiography,which,inadditiontohavingdepth,isgreaterthan5mmindiameterThreedifferenttypesofpepticulcerDependingontheiretiology,ulcerscanbeclassifiedintothreegroups:①H.pylori-associatedulcers②NSAID-inducedulcers③Idiopathic(non-H.pylori,non-NSAIDulcers)OtherlesscommoncausesincludeulcerssecondarytodrugsotherthanNSAIDs(forexample,potassiumchloride,bisphosphonates),stressulcersduetoacriticalillness,ulcersofCrohn’sdisease,andinfectiouscauses(forexample,cytomegalovirusulcersinHIVpatients,orherpessimplexvirus)PATHOGENESISpepticulcermaybebestviewedasrepresentingacomplexscenarioinvolvinganimbalancebetweendefensiveandaggressivefactorsDefensivefactors①mucus-bicarbonatelayer②Prostaglandinsenhancethelayerofmucus③cellularrenovation④bloodflow2Aggressivefactors①hydrochloricacid②Pepsin③Ethanol④bilesalts⑤somemedications:nonsteroidalanti-inflammatorydrugs(NSAIDs)(occuringin10–30%ofusers)⑥Helicobacterpyloriinfection③④⑤caninhibitthesecretionofHCO3-Evidence①HighdetectionrateofH.pyloriinpepticulcerduodenalulcer90%~95%gastriculcer70%②Itseradicationcanfacilitatethehealofulcer③EradicationofH.pyloricanpreventtherecurrenceordecreasetherecurrentrateofulcerH.pyloriinfectionisthemajorcauseofpepticulcerHowdoesH.pyloriinfluenceacidsecretion?•Theprecisepathwayisnotknown•onepossiblemechanismItdecreasesantralsomatostatinsecretion(whichinhibitsgastrinrelease),leadingtoprolongedhypergastrinaemiaHowdoesH.pyloriinfluencemucosaldefence?•InfluencemicrocirculationExtractsofH.pylorifromhumaninfectionproduceplateletactivationandaggregationinthemucosalmicrocirculationofrats,withleakageofalbumin.Thesechangeswouldpredisposetoulcerationanddelayhealing.•Itisnotyetclearinwhatotherways,ifany,H.pyloriinhibitsdefencemechanismsThemostimportantmechanismbywhichNSAIDscauseulcers•byindirectlydecreasingprostaglandinproductionviatheinhibitionoftheCOX-1enzyme•Prostaglandinsareimportantinmaintainingmucosalintegrityby①producingmucus②stimulatingbicarbonateproduction③decreasingacidproduction④maintainingmucosalbloodflowPathogenicmechanismcausesidiopathiculcer•remainsunknown•Postulatingtheory①Geneticpredisposition②defectivemucosaldefensemechanisms③andincreasedacidproduction3Currentconceptofpathogenesis•Noacid,noulcer•NoH.pyroli,noulcerrecurrence•Noimpairmentofmucosaldefense,nopepticulcerationTableUncommoncausesofnon-Helicobacterpylorinon-NSAIDpepticulcerdiseaseHerpessimplexinfectionPortalhypertensionSystemicmastocytosisCMVinfectionLymphomaCarcinomaHelicobacterheilmanniiinfectionCrohn’sdiseaseTuberculosisHypercalcemiaZollinger-EllisonsyndromeClassificationofgastroduodenalpepticulcersbysiteAnastomoticZollinger-EllisonsyndromeGastrictypeⅡCombinedPostbulbarbulbarDuodenalGastricGastriculcerclassificationaccordingtolocationagastriccardiaulcerTypeIVaprepyloriculcerTypeIIIgastriculcerisassociatedwithasimultaneousduodenalulcerTypeIIanulcerattheincisuraangularisonthelessercurvatureTypeIⅠⅢⅣⅡgastricacidoutputcharacteristicsTypeIVTypeIIITypeIITypeIlowPenetrateandbleedeasily,“O”bloodtypepatientsnormalorlowresultofchronicuseofnonsteroidalanti-inflammatoryagentsintherangeassociatedwithduodenalulcerLesschanceformalignantchangenormalorlowAtypicalclinicalsymptomsClinicalFindings①SymptomsandSigns②DiagnosticTests③ImagingStudies④EndoscopyandBiopsy4SymptomsandSigns•epigastricpainordyspepsiaoftendescribedasgnawing,burning,aching,orlikeahungerpain•Varyingdegreesofnausea,anorexiaandvomiting•localizedepigastrictendernesstotheleftofthemidline,usuallyisavariablefindingtotherightofthemidlineinmanyinstancesnotendernesscanbeelicitedGastriculcerDuodenalulcerCharacteristicsofthepainrecuratintervalsofweeksormonthsDuringperiodsofexacerbation,thepainoccursdailyforaperiodofweeksandthenremitsuntilthenextrecurrenceperiodicityregularlyrelievedbyfood,milk,orantacidsbutreturns1.5–4hoursaftereatingItmayawakenthepatientfromsleepbetween1:00and3:00AM,especiallyifasnackatbedtimewastakenDuodenalulcerthepainisleastorabsentduringfastingbutoccursshortlyaftereating(5–15minutes)remainsuntilthestomachempties,eithernaturallyorbyvomitingrhythmicityGastriculcerDiagnosticTests•Gastricanalysis①basalacidoutput(BAO)acidproductionbytheunstimulatedstomachunderbasalfastingconditionstheresultisexpressedasH+secretioninmeq/h②maximalacidoutput(MAO)acidproductionduringstimulationbyhistamineorpentagastringiveninadosemaximalforthiseffect40303020MFMaximal(pentagastrin)5.532.51.5MFBasalDuodenalulcerNormalsexMeanAcidOutput(meq/h)Theupperlimitsofnormalare:Basal,5meq/h;maximal,30meq/h.Achlorhydria•Definitionnoacid(pH6.00)afterpentagastrinstimulation•ClinicalsignificanceitisincompatiblewiththediagnosisofbenignpepticulcerandsuggestsamalignantgastriculcerAbout5%ofmalignantgastriculcerswillbeassociatedwiththisfindingSerumgastrin200pg/mLHigh50-100pg/mLNormal(average)Normalbasalgastrinlev