肝性脑病英文课件.ppt

肝性脑病英文课件.ppt

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HepaticFailureTaoWang,PH.D.,AssociatedprofessorPathophysiologydepartmentAnhuiMedicalUniversity1nIntroductionandConceptionnEtiologynHepaticinsufficiencynHepaticfailureHepaticencephalopathy（focalpoint）HepatorenalsyndromeHepaticFailure2PARTIIntroductionandConceptionLiverThelargestandmostmetabolicallycomplexorgan1.Theliver32.TheliveranatomyTheliverisdividedinto2mainlobes,eachconsistingofmanylobules.Theselobulesaresurroundedbybranchesofthehepaticartery,whichsuppliestheliverwithoxygenatedblood.Theportalveinsuppliesnutrient-richblood.Deoxygenatedbloodfromtheliverdrainsintothehepaticveins.Anetworkofductscarriesbilefromthelivertothegallbladderandthesmallintestine43.ThefunctionsoftheliverSubstancemetabolismimmunefunctionHemostasisregulationproductionandsecretionofbileBio-transformation（detoxification）54.HepaticinsufficiencySeveredamageinlivercellswillresultinseriouscondition,manifestingasjaundice,bleeding,infection,renaldysfunctionorencephalopathy,termedalltogetherthesesyndromesofhepaticinsufficiency.AcuteHepaticinsufficiencyChronicHepaticinsufficiency65.HepaticfailureTerminalstageofhepaticinsufficiencyHepaticencephalopathy（focalpoint）HepatorenalsyndromePrimaryclinicalmanifestations7PARTIIEtiology1.Biological2.Physicalandchemical3.Inheritedconditions4.Immune5.NutritionalcausesHepatitisvirus（suchasHBV）,bacteria,parasites,etc.Industrialtoxins,somedrugs,alcohol,etc.Idiopathichemochromatosis,Wilsonsdisease,etc.Extentofinflammationandnecrosis8PARTIIIHepaticinsufficiencyLiverVariousetiologycauseshepatocytesNon-parenchymalcellsdamagedamageKupffercells,hepaticsatellitecells,lipocytes,liverassociatedlymphocytes,hepaticsinusoidendothelialcellsHepaticinsufficiency9SyndromesofHepaticinsufficiency1.Metabolicdisorders2.Waterandelectrolytesimbalance3.Disordersinproductionofbilesaltsandeliminationofbilirubin4.ImpairedkupffercellsfunctionCarbohydrateMetabolicDisordersLipidMetabolicDisordersProteinMetabolicDisordersHepaticAscitesElectrolyticMetabolicDisorders101.Metabolicdisorders1）CarbohydrateMetabolicDisordersCarbohydrateMetabolismofliverTomaintainconcentrationsofglucoseinbloodwithinanarrow,normalrange.insulinAhormoneproducedbythepancreasthatregulatesglucoselevelsintheblood.Itisnormallyproducedinresponsetoraisedglucoselevelsfollowingamealandpromotesglucoseabsorptionintotheliverandmusclecells（whereitisconvertedintoenergy）.Excessglucoseenteringthebloodafteramealisrapidlytakenupbytheliverandsequesteredasthelargepolymer,glycogenglycogenesis11glyconeogenesisglycogenolysiswhenbloodconcentrationsofglucosebegintodecline,theliveractivatesotherpathwayswhichleadtodepolymerizationofglycogenWhenhepaticglycogenreservesbecomeexhaused,asoccurswhenananimalhasnoteatenforseveralhours,thehepatocytes,recognizetheproblemandactivateadditionalgroupsofenzymesthatbeginsynthesizingglucoseoutofsuchthingsasaminoacidsandnon-hexosecarbohydrates.12SevereliverdiseaseHypoglycemiaHyperglycemiaCausedbyadecreaseinfunctionalhepatocytemass.Whenglucogenreservesaredepleted:

gluconeogenensisimpared;inactivationofinsulinweakenCausedbyportal-to-systemicshuntingDecreasethepostprandialextractionofglucosefromprotalbloodSomepatientsmaysufferabnormalglucosetolerance131.Metabolicdisorders2）LipidMetabolicDisordersLiveristhecenteroflipidmetabolismManufacturing80%ofthecholesterolSynthesizing,storingandexportingtriglyceridesAssembling,secretingandtakinguplipoproteinparticle,suchasVLDL,LDL,andHDL.14SevereliverdiseaseDisturbanceoflipidmetabolismSyndromesoffataccumulation（fattyliver）IncertainchronicliverdiseasePrimarybiliarycirrhosisDestructionofbileductsBileflowdecreaseDecreaselipidclearanceviabilehyperlipidemiaThesepatientsoftendevelopxanthomasaccumulationofcholesterol151.Metabolicdisorders3）ProteinMetabolicDisordersThelivermanufacturesandsecretesmanyoftheproteinfoundinplasmaalbuminSomeclottingfactorsSomebindingproteinsSomehormoneprecursorsTomaintainplasmaoncoticpressureToregulatehemostasisSteroidandthyroidhormone-bindingproteintoregulatemetabolismangiotensinogentoregulatebloodpressureInsulinlikegrowthfactor-1toregulategrowth16OtherrolesoftheliverinproteinmetabolismProcessesofoxidativedeaminationandtransaminationTheureacycleallowsnitrogentobeexcretedintheformofurea17SevereliverdiseaseDisturbanceofproteinmetabolismDecreasedconversionofammoniatoureaPlasmaproteinsdecreaseElevatedammonialevelalbuminClottingfactorsHepaticencephalopathyEdemaandascitesBleedingtendancy182.Waterandelectrolytesimbalance1）HepaticAscitesAsctiesisthepresenceoftheexcessfluidintheperitonealcavityItisalate