教案消化病理

ViralViralViralhepatitisis forinfectionofthelivercausedbyagroupof havingaparticularaffinityfortheliver.DegenerationsandnecrosisofliverparenchymaarethepredominantpathologicchangesoftheliverinjuryCausativeHepatitisA isthemostcommoncauseofacuteHAVisnotdirectlycytopathic,andhepaticinjuryhasbeenattributedtoanimmunologicreactiontovirallyinfectedHepatitisB isamajorcauseofacuteandchronicliverdiseaseThehostimmuneresponsetothe isthemaindeterminantofthe eoftheinfection.Hepatocytedamageisbelievedtoresultfromdamagetothe -infectedcellsbyCD8+cytotoxicTcells.

DegenerationofHepaticcells1)Rareficationandballooning2)Fattychange,MicrovesicularMacrovesicular3)AcidophilicchangesFundamentalHepatocyteNecrosisofhepaticcells壞死–FocalnecrosisPiecemealnecrosisBridgingnecrosisSubmassivenecrosisandmassivePiecemealnecrosis碎片狀壞死periportalnecrosisnecrosisofcells,particularlyattheinterfacebetweentheperiportalinfl andadjacenthepaticcords.hepatocytesaredestroyed,whichoftencreatesnecroticzonesbridgingnecrosisconnectingportal-to-portal,central-to-central,orportal-to-centralregionsofadjacentlobulesFundamentalInfiltrationof lymphocytes,macrophages,occasionalsmacells,andrareneutrophilsoreosinophilsReactiveProliferationofInterstitialTissueandRegenerationofHepatocytes間質(zhì)反應(yīng)性增生及 siaand/orhypertrophyofKupfferProliferationofinterstitialcellsandHepatic latecell(Itocell)→myofibroblastlikeAcute ChronicAcuteViralGrossslightly moreandlessAcuteViraldiffuselivercellinjury(rarefication,ballooningdegeneration,rarelyacidophylicbody)spottyreactivechangesinKupffercellsandsinusoidalliningcellsandan toryinfiltrateinportalhepatocyticregenerationmildlyenlargedliverpaininliverregionelevatedlevelofserumglutamatetransaminase(SGPT)ChronicViralChronichepatitisisdefinedassymptomatic,biochemical,orserologicevidenceofcontinuingorrelapsinghepaticdiseaseformorethan6months,withhistologically edinfl tionandMildchronichepatitisModeratechronichepatitisSeverechronichepatitisMildestformSpottynecrosis,occasionallypiecemealSignificantinfl tionislimitedtoportalLymphocytes,macrophages,occasional rareneutrophilsoreosinophilsPeriportalLiverarchitectureisusuallywellpGross:enlargedliver,smoothsurfaceProgressiveliverInterfacehepatitis(piecemealnecrosis)andbridgingnecrosisFibrosisoccursintheGross:enlargedliverwithfinelySeverehepatocytesSeverepiecemealLargeareabridgingIrregularlyregenerationofhepatocytesFibrousseptabetweenlobulesandwithinViableisolatedhepatocytesorclustersofcellshave‘groundglass’,finelygranular,eosinophyliccyto sm(HE)ladenwithEM:spheresandtubulesintheEROrceinstains地衣紅染色:redImmunofluorescenttechniquesandimmunoenzememethods:positiveAcuteseverehepatitisSubacuteseverehepatitisAcutesevereAcuteRedorYellowAtrophyofLiver(MassiveHepaticNecrosis)Theclinicalcourseisextremelyshort,theprogressofdiseaseisveryquickly,generallyabout7-10dayswithearlyGross---theentirelivermaybesizeoflivercapsule:softinloseinweight(600-color:yellowingordarkontransection,necrosisareashaveamuddyred,mushyappearancewithblotchybileMassiveanddiffusenecrosisofliverLeavesonlyacollapsedreticulinframeworkandp portaltractsSinusoidsdistendedwithbloodSurprisinglylittleinfl toryreactionNoregenerationSubacutesevereTheprogressofdiseasetendstobeslower,sothatdeathoccuratalaterstageoronlyafterrepeatedattacks.Characterinsubmassivenecrosis+regenerationwithnodularhyper sia,withprogressofthedisease,itmaydeveloppostnecroticCirrhosisCirrhosisofCirrhosisofCirrhosisisdefinedasadiffuseprocesscharacterizedbyfibrosisandtheconversionofnormalliverarchitectureintostructurallyabnormalnodules.ItsthreemainBridgingfibrousParenchymalDisruptionofthearchitectureoftheentire MicronodularcirrhosisMixnodularcirrhosisplete

PortalcirrhosisBiliarycirrhosisCongestivecirrhosisParasiticcirrhosisEtiologyandViralhepatitisAlcoholicliverdiseaseBiliarydiseaseWilsondiseaseα1-antitrypsindeficiencyCryptogeniccirrhosisPortalLaennecCirrhosisMicronodularCirrhosisEtiologyandChronic Chemicalpoisoningetc.毒物livercellnodulesoflivercellnodulesofoffibroushepaticbloodIndurationanddeformityoftheGrossenlargeliver/atrophicorsmallernormalinshapereducedinweightfirminconsistencyreddishbrownoryellowishinOntheoutersurface:granularorfinelynodular,uniforminsize2-3mm,<1cmOnthecutsurface:thinfibrousseptaaroundsmallernodularThenormalarchitectureoftheliveris yupsetbybandsofconnectivetissuethatredividetheliverintoirregularnoduleshavingnoconstantrelationshiptocentralveinsorportalregions.Clinic-pathological

PortalCongestionofgastro-intestinetractAscites lcirculateformation→肝竇→V→小葉下V→肝Hepaticfailure

iscausedbyinadequateclearanceofbilirubinbytheliverDefectsof

refertoneurologicsignsandsymptomsofliverfailureoftencause

isafactorof

Feminizationinman: GonadalfailureinPalmarThecauseofdeathinportalHepaticcoma (fromesophagealvaricesorgastricerosions)CarcinomaoftheliverAcuteandchronicPostnecroticMacronodularCirrhosisMixedmacro-and-micro-nodularViralhepatitis(submassivenecrosis)DrugandchemicalpoisoningLargernodules,1cmormoreinBroadbandsoffibroticThepseudolobulesofvaryingshapeandthickerfibroustissue,markedinfiltrationof torycells,withoutfattyClinicalThecourseofdiseaseisshortThehepaticdysfunctionismoresevere.ThemalignancyrateishighBiliaryBiliarySecondaryBiliaryPrimaryBiliarySecondaryBiliaryEtiologyextrahepaticbileductobstructionbiliaryatresiacarcinomaofpancreaticFinegranularappearanceonsurfaceofliver,greenorbrownincolormoderatedegreeofreticularnecrosisproliferationoffibroustissuearoundthebileducts,atthelaterst