肝性腦病英文課件培訓(xùn)講學(xué)

肝性腦病英文課件肝性腦病英文課件PARTIIntroductionandConceptionLiverThelargestandmostmetabolicallycomplexorgan1.TheliverPARTIIntroductionandConc2.TheliveranatomyTheliverisdividedinto2mainlobes,eachconsistingofmanylobules.Theselobulesaresurroundedbybranchesofthehepaticartery,whichsuppliestheliverwithoxygenatedblood.Theportalveinsuppliesnutrient-richblood.Deoxygenatedbloodfromtheliverdrainsintothehepaticveins.

Anetworkofductscarriesbilefromthelivertothegallbladderandthesmallintestine2.TheliveranatomyTheliver3.Thefunctionsoftheliver☆Substancemetabolism☆immunefunction☆Hemostasisregulation☆productionandsecretionofbile☆Bio-transformation(detoxification)

3.Thefunctionsoftheliver4.HepaticinsufficiencySeveredamageinlivercellswillresultinseriouscondition,manifestingasjaundice,bleeding,infection,renaldysfunctionorencephalopathy,termedalltogetherthesesyndromesofhepaticinsufficiency.AcuteHepaticinsufficiencyChronicHepaticinsufficiency4.HepaticinsufficiencySever5.HepaticfailureTerminalstageofhepaticinsufficiencyHepaticencephalopathy(focalpoint)HepatorenalsyndromePrimaryclinicalmanifestations5.HepaticfailureTerminalstPARTIIEtiology1.Biological2.Physicalandchemical3.Inheritedconditions4.Immune5.NutritionalcausesHepatitisvirus(suchasHBV),bacteria,parasites,etc.Industrialtoxins,somedrugs,alcohol,etc.Idiopathichemochromatosis,Wilson’sdisease,etc.ExtentofinflammationandnecrosisPARTIIEtiology1.BiologicaPARTIIIHepaticinsufficiencyLiverVariousetiologycauseshepatocytesNon-parenchymalcellsdamagedamageKupffercells,hepaticsatellitecells,lipocytes,liverassociatedlymphocytes,hepaticsinusoidendothelialcellsHepaticinsufficiencyPARTIIIHepaticinsufficienSyndromesofHepaticinsufficiency1.Metabolicdisorders2.Waterandelectrolytesimbalance3.Disordersinproductionofbilesaltsandeliminationofbilirubin4.ImpairedkupffercellsfunctionCarbohydrateMetabolicDisordersLipidMetabolicDisordersProteinMetabolicDisordersHepaticAscitesElectrolyticMetabolicDisordersSyndromesofHepaticinsuffici1.Metabolicdisorders1)CarbohydrateMetabolicDisordersCarbohydrateMetabolismofliverTomaintainconcentrations

ofglucoseinbloodwithinanarrow,normalrange.

insulinAhormoneproducedbythepancreasthatregulatesglucoselevelsintheblood.Itisnormallyproducedinresponsetoraisedglucoselevelsfollowingamealandpromotesglucoseabsorptionintotheliver

andmusclecells(whereitisconvertedintoenergy).Excessglucoseenteringthebloodafteramealisrapidlytakenupbytheliverandsequesteredasthelargepolymer,glycogenglycogenesis1.Metabolicdisorders1)Carbglyconeogenesisglycogenolysiswhenbloodconcentrationsofglucosebegintodecline,theliveractivatesotherpathwayswhichleadtodepolymerizationofglycogenWhenhepaticglycogenreservesbecomeexhaused,asoccurswhenananimalhasnoteatenforseveralhours,thehepatocytes,recognizetheproblemandactivateadditionalgroupsofenzymesthatbeginsynthesizingglucoseoutofsuchthingsasaminoacidsandnon-hexosecarbohydrates.glyconeogenesisglycogenolysiswSevereliverdiseaseHypoglycemiaHyperglycemiaCausedbyadecreaseinfunctionalhepatocytemass.Whenglucogenreservesaredepleted:gluconeogenensisimpared;

inactivationof

insulinweakenCausedbyportal-to-systemicshuntingDecreasethepostprandialextractionofglucosefromprotalbloodSomepatientsmaysufferabnormalglucosetoleranceSevereliverdiseaseHypoglycem1.Metabolicdisorders2)LipidMetabolicDisordersLiveristhecenteroflipidmetabolismManufacturing80%ofthecholesterolSynthesizing,storingandexportingtriglyceridesAssembling,secretingandtakinguplipoproteinparticle,suchasVLDL,LDL,andHDL.1.Metabolicdisorders2)LipiSevereliverdiseaseDisturbanceoflipidmetabolismSyndromesoffataccumulation(fattyliver)IncertainchronicliverdiseasePrimarybiliarycirrhosisDestructionofbileductsBileflowdecreaseDecreaselipidclearanceviabilehyperlipidemiaThesepatientsoftendevelop

xanthomas——accumulationofcholesterol

SevereliverdiseaseDisturbanc1.Metabolicdisorders3)ProteinMetabolicDisordersThelivermanufacturesandsecretesmanyoftheproteinfoundinplasmaalbuminSomeclottingfactorsSomebindingproteinsSomehormoneprecursorsTomaintainplasmaoncoticpressureToregulatehemostasisSteroidandthyroidhormone-bindingproteintoregulatemetabolismangiotensinogen——toregulatebloodpressureInsulinlikegrowthfactor-1——toregulategrowth1.Metabolicdisorders3)ProtOtherrolesoftheliverinproteinmetabolismProcessesofoxidativedeaminationandtransaminationTheureacycleallowsnitrogentobeexcretedintheformofureaOtherrolesoftheliverinpSevereliverdiseaseDisturbanceofproteinmetabolismDecreasedconversionofammoniatoureaPlasmaproteinsdecreaseElevatedammonialevelalbuminClottingfactorsHepaticencephalopathyEdemaandascitesBleedingtendancySevereliverdiseaseDisturbanc2.Waterandelectrolytesimbalance1)HepaticAscitesAsctiesisthepresenceoftheexcessfluidintheperitonealcavityItisalate-stagedmanifestationoftheliverdisease.2.WaterandelectrolytesimbaMechanismsofHepaticAscites1)AnincreaseincapillarypressureCauses:portalhypertension;obstructionofvenousandlymphflow2)DecreaseincolloidalosmoticpressureCause:impairedsynthesisofalbumin3)SaltandwaterretentionbythekidneyCause:

effectivebloodvolumeisreducedbecauseoffluidshiftandvasodilation

glomerularfiltrationrate(GFR)rennin-angiotension-aldosteronesystem(+)metabolismofaldosterone

portal-to-systemicshunting

vasodilatoryproductsaredilveredtothesystemiccirculation

MechanismsofHepaticAscites12.Waterandelectrolytesimbalance2)ElectrolyticMetabolicDisorders1)Hypokalemia2)Hyponatremia2.Waterandelectrolytesimba3.DisordersinproductionofbilesaltsandEliminationofbilirubinSevereliverdiseaseAfailuretosecretebileAFailuretosolubilizesubstancesMalabsorptionanddeficiencystatesDecreasedeliminationofbilirubinElevationofserumbilirubinandjaundiceJaundice:Yellowingoftheskinandthewhitesoftheeyes,causedbyanaccumulationofbilirubinintheblood.3.Disordersinproductionof4.ImpairedkupffercellsfunctionKupffercellsfunction1)Removingandphagocytizingoldanddefectivebloodcells,bacteria,etc.2)Producingavarietyofbioactivesubstancesandcytokines,suchasIL-1,IL-6etc.4.ImpairedkupffercellsfuncdysfunctionofKupffercellsLossofclearancefunctiontobacteriaPortal-systemicshuntingEnterictoxinsenterthesystemiccirculationEntericendotoxemiadysfunctionofKupffercellsLoBriefSymptomsofhepaticfailureWaterandelectrolytesimbalanceHypoorhyper-glycemiaHyperlipidemiaandxanthomasPlasmaproteinsdecreaseedema,bleedingMetabolicdisordersHepaticAscitesHypokalemiaandHyponatremiaDisordersinproductionofbilesaltsandEliminationofbilirubinMalabsorptionanddeficiencystatesElevationofserumbilirubinandjaundiceImpairedkupffercellsfunctionEntericendotoxemiaBriefSymptomsofhepaticfailuHepaticencephalopathy(HE)isaprimaryclinicalmanifestationofhepaticfailure.PARTIVHepaticencephalopathyIntroductionandConceptionEtiologyandclassificationPathogenesisPrecipitatingfactorsofHEPrinciplesoftreatmentHepaticencephalopathy(HE)is1.IntroductionandConceptionConceptionofhepaticencephalopathyHEisacomplex,potentiallyreversibledisturbanceincentralnervoussystemthatoccursasaconsequenceofsevereliverdiseases.FourstagesofhepaticencephalopathySlightlyalteredmoodorbehaviourSomnipathyandinappropriatebehaviorsDrowsyandpsychopathyDeepcoma1.IntroductionandConception2.EtiologyandclassificationEtiologyChronicliverdiseasesFulminanthepaticfailure(FHF)ViralinfectionDrugreactionPoisoningwithcarbontetrachlorideorphosphorusCirrhosisofanyorigin2.EtiologyandclassificationClassificationEndogenousHEHavenoapparentprecipitatingfactorsOftencausedbyextensivelivercelldestructionExogenousHEPrecipitatedbysomeknownagentsorabnormalities

suchas:gastrointestinalbleedingingestionmanyproteinsOftencausedbyportal-systemicshuntsAccordingtooriginClassificationEndogenousHEExoAccordingtoclinicalcharacteristicAcuteorsubacuteencephalopathyAcuteorsubacuterecurrentencephalopathyChronicrecurrentencephalopathyChronicpermanentencephalopathyAccordingtoclinicalcharacte3.Pathogenesis◎AmmoniaIntoxication◎FalseNeurotransmitters◎

AminoAcidimbalance◎

TheGamma-AminobutyricAcidhypothesisSeveralhypotheses3.Pathogenesis◎AmmoniaInto◎AmmoniaIntoxicationBasis1.HealthydogCreatingaportal-systemicshuntingFedbymeatcomatose2.80%patientswithHEBloodammonialevels3.CirrhosispatientsingestionofalargeamountsofproteinHepaticcoma4.HEpatientswithcirrhosisTherapiestoreduceammoniaabsorptionAmeliorationsofHE◎AmmoniaIntoxicationBasis1.HCauseforelevatedammoniaInnormalconditionsUreaAmmoniaKidneyAmmoniaProteins,aminesUrea,purinesAmmoniaismainlyproducedingastrointestinaltractAmmoniaisdetoxifiedinliverbyconversiontoureathroughKrebs-Henseleitureacycle.CauseforelevatedammoniaInnInHepaticfailureKrebs-HenseleitureacyclefunctionisimpairedBloodammonialevelincreased(endogenous)OrnithineCitrullineargininearginase

NH3NH3Urea

Inhepaticfailure：

substrates

enzymeATPPortal-systemicshuntingalsoreducestheureaproduction(exogenous)InHepaticfailureKrebs-HenselAmmoniaproductionincreasedBloodammonialevelincreased1)Productionofammoniainintestinelumenincreased2)ProductionofammoniainkidneyincreasedProtein,urea,purinedegradedEnzymeofbacteriaammoniaglutamineglutaminaseammonia3)ProductionofammoniainskeletalmuscleincreasedAmmoniaproductionincreasedBEndogenousHEKidneyBloodNH3NH3Urea×NH3NH3proteinureaAmmoniaproductionUreaCyclefunctionimpairedLivercellmassdamagedHyperammonemiaIntoxicationofammoniaonbrainEndogenousHEKidneyBloodNH3NExogenousHEAmmoniaproductionPortal-systemicshuntingHepaticcirrhosisHyperammonemiaIntoxicationofammoniaonbrainExogenousHEAmmoniaproductionIntoxicationofammoniaonbrainAmmoniaproductionPortal-systemicshunting(exogenous)UreaCyclefunctionimpaired(endogenous)Hyper-ammonemiaHE?Intoxicationofammoniaonbrain1)Impairmentofenergymetabolisminbrain2)Alternationoftheneurotransmitters3)InhibitingactiononnervecellsmembraneMitochondrialpermeabilitytransitioninducedbyOxidativestressIntoxicationofammoniaonbra1)ImpairmentofenergymetabolisminbrainGlucoseisthemostimportantfuelforcerebralenergy.HyperammonemiaDepressionincerebralglucosemetabolismATPoutputreductiontricarboxylicacidcycle1)Impairmentofenergymetab2)AlternationoftheneurotransmittersHyperammonemiaDominantneurochemicallesions2)Alternationoftheneurotr3)InhibitingactiononnervecellsmembraneHyperammonemiaInhibitingbrainNa+-K+ATPaseIncreaseofintracellularsodiumImpairmentofNeurotransmission3)InhibitingactiononnerveMitochondrialpermeabilitytransition(MPT)inducedbyOxidativestressHyperammonemiaDysfunctionofastrocytes1)Inculturedastrocytes,ammoniainducesMPT,frequentlycausedbyoxidativestressIncreasedfreeradicalproductioninculturedastrocytesexposedtoammonia3)AntioxidantscaninhibittheMPTinammonia-treatedculturedastrocytesMitochondrialpermeabilitytraTherearesomeargumentagainstAmmoniaintoxicationhypothesis?10%ofHEpatientshavenormalserumammonialevels?somepatientswithhyperammonemiahavenoHEsignsSotherearesynergisticactionofmultipletoxinsontheCNS.Therearesomeargumentagains◎FalseNeurotransmittersBasisHEpatientswithfulminanthepatitisL-dopatreatmentRecoverquicklyL-dopaisaprecursorofnormalneurotransmittersnormalneurotransmitters,suchasdopamineandnorepinephrine,areendogenoussingnalingmoleculessecretedbyneuronsthatcanalterthebehaviorofneuronsoreffectorcells.◎FalseNeurotransmittersBasisConceptionFalseNeurotransmitters(FNT)isakindofchemicalsubstance,whichhavesimilarstructuresoftrueneurotransmitters(NNT),butmuchweakeractivitythantrueneurotransmitters.ConceptionFalseNeurotransmitHOHOCHOHCH2NH2HOCHOHCH2NH2HOHOCH2CH2NH2NorepinephinedopamineCHOHCH2NH2phenolethanolamineoctopamineNormalNeurotransmittersFalseNeurotransmittersHOHOCHOHCH2NH2HOCHOHCH2NH2HOHO◎

AminoAcidimbalanceSynthesisofneurotransmitterisdependentontherateofprecursoraminoacidsBranchchainaminoacids(BCAA)Aromaticaminoacids(AAA)Valine,leucineandisoleucinePrecursorsofNNTTyrosine,phenylalanineandtryptophanPrecursorsofFNTNormally,plasmaBCAAtoAAArateis3-3.5InHEpatients,plasmaBCAAtoAAArateis0.6-1.2◎AminoAcidimbalanceSynthesiDecreasedplasmaBCAAlevelsMechanisms1)AmmoniaInHEpatients,BCAAmightbeutilizedfordetoxificationofammonia.2)hyperinsulinismmetabolismofinsulinhyperinsulinismPortal-systemicshuntingUptakeofBCAAintomuscle3)InflammationcytokineTumornecrosisfactor-αDecreasedplasmaBCAAlevelsDecreasedplasmaBCAAlevelsMeIncreasedplasmaAAAlevelsMechanisms1)Dysfunctionofhepaticdeamination2)ReleaseofAAAfromthenecrotichepatocytesIncreasedplasmaAAAlevelsMecphenethylaminephenolethanolaminetyrosameinoctopamineAAA↑BCAA↓Blood-brainbarrier5-hydroxytryptophanserotoninDopa×phenylalaninetyrosinetryptophanvector多巴胺NE××dopamineNE↓InhibitoryFNTFNTNNTDysfunctionofsynthesisofneurotransmittersinbrainphenethylaminephenolethanolamiDecreasedplasmaBCAAlevelsIncreasedplasmaAAAlevelsInHEpatients,plasmaBCAAtoAAAratedecreasedNeuronalcontentsofNNT

FNTReducedneuralexitationIncreasedneuralinhibitonBRIEFFNTandaminoacidimbalanceDecreasedplasmaBCAAlevelsIn◎

TheGamma-AminobutyricAcidhypothesisBasisTheGamma-AminobutyricAcid(GABA)isainhibitoryneurotransmitterinCNS,asacauseofHE.2)IncreasedGABA-ergictoneisobservedinpatientswithcirrhosis3)Flumazenil,abenzodiazepineantagonist,cantransientlyreverseHEinpatientswithcirrhosis◎TheGamma-AminobutyricAcidIncreasedplasmaGABAlevelsHepaticfailureDecreasedhepaticmetabolismofGABAGutabsorption(intestinalbacteriaandtheintestinalwall)BloodGABAlevelsThepermeabilityoftheblood-brainbarriertoGABASomeGABAreachesGABAreceptorsandaugmentGABA-ergicneurotransmissionIncreasedplasmaGABAlevelsHMechanism1.Increaseddensityand/oraffinityofreceptorsforGABAonthesupramolecularcomplex.GABA/BZreceptor/chlorideionophorecomplexAGABAreceptoraBZreceptorachlorideionophore(thatcontainsreceptorforbarbiturates)Notes:AdministrationofbenzodiazepinesandbarbituratestopatientswithcirrhosisincreasesGABA-ergictoneandpredisposesdepressionMechanism1.Increaseddensit2.MechanismofGABA-ergicinhibitoryneurotransmissionGABAreceptor(+)NeuronalmembranepermeabilitytoCl-Cl-restingpotentialoftheneuronsismorenegativethannormal.Cl-ionophoreopeningNeuralMembranehyperpolarizationLeadingtoconsciousnessandmotorcontrolimpaired2.MechanismofGABA-ergicinh4.PrecipitatingfactorsofHE1)GastrointestinalBleedingThemostimportantisNitrogenousoverloadHypovolemia,shock,hypoxiaAmmoniaproduction2)Abuseofsedativesandnarcotic3)MassiveparacentesisandexcessivediuresisbenzodiazepinesandbarbituratesFluidorelectrolyteabnormalitiesandacidbasedisturbance4)Infectionstissuebreakdown4)InfectionsProteinbreakdown4.PrecipitatingfactorsofHE5.TreatmentofHEPrinciples1)Eliminatingorcorrectingprecipitatingfactors2)Reducingplasmaammoniaandothertoxin3)Correctingplasmaaminoacidimbalanceandsupplyingnormalneurotransmitters4)Improvinghepatocytefunctions5)Livertransplantation5.TreatmentofHEPrinciples1ConceptionThedefinitionofhepatorenalsyndrome(HRS)isreferedtothedevelopmentofareversibleandfunctionalrenalfailureinpatientswithseverliverdiseases(acuteorchronicinabsenceofanyotheridentifiedcauseofrenalpathology.PARTIVhepatorenalsyndromeConceptionThedefinitionofheMechanismRenalbloodsupplyGlomerularfiltrationrate(GFR)AcutefunctionalrenalfailureHepaticfailureRenalvasoconstriction？MechanismRenalbloodsupplyGlFactorsinvolvedinrenalvasoconstriction1)Stimulatedsympatheticnervoussystem2)Renin-Angiotension-Aldosteronesystem(+)3)Increasevasopressinrelease4)OtherhumoralfactorsSuchasendothelin,NO,PGs,ets.FactorsinvolvedinrenalvasoThanksThanks此課件下載可自行編輯修改，僅供參考！

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感謝您的支持，我們努力肝性腦病英文課件肝性腦病英文課件PARTIIntroductionandConceptionLiverThelargestandmostmetabolicallycomplexorgan1.TheliverPARTIIntroductionandConc2.TheliveranatomyTheliverisdividedinto2mainlobes,eachconsistingofmanylobules.Theselobulesaresurroundedbybranchesofthehepaticartery,whichsuppliestheliverwithoxygenatedblood.Theportalveinsuppliesnutrient-richblood.Deoxygenatedbloodfromtheliverdrainsintothehepaticveins.

Anetworkofductscarriesbilefromthelivertothegallbladderandthesmallintestine2.TheliveranatomyTheliver3.Thefunctionsoftheliver☆Substancemetabolism☆immunefunction☆Hemostasisregulation☆productionandsecretionofbile☆Bio-transformation(detoxification)

3.Thefunctionsoftheliver4.HepaticinsufficiencySeveredamageinlivercellswillresultinseriouscondition,manifestingasjaundice,bleeding,infection,renaldysfunctionorencephalopathy,termedalltogetherthesesyndromesofhepaticinsufficiency.AcuteHepaticinsufficiencyChronicHepaticinsufficiency4.HepaticinsufficiencySever5.HepaticfailureTerminalstageofhepaticinsufficiencyHepaticencephalopathy(focalpoint)HepatorenalsyndromePrimaryclinicalmanifestations5.HepaticfailureTerminalstPARTIIEtiology1.Biological2.Physicalandchemical3.Inheritedconditions4.Immune5.NutritionalcausesHepatitisvirus(suchasHBV),bacteria,parasites,etc.Industrialtoxins,somedrugs,alcohol,etc.Idiopathichemochromatosis,Wilson’sdisease,etc.ExtentofinflammationandnecrosisPARTIIEtiology1.BiologicaPARTIIIHepaticinsufficiencyLiverVariousetiologycauseshepatocytesNon-parenchymalcellsdamagedamageKupffercells,hepaticsatellitecells,lipocytes,liverassociatedlymphocytes,hepaticsinusoidendothelialcellsHepaticinsufficiencyPARTIIIHepaticinsufficienSyndromesofHepaticinsufficiency1.Metabolicdisorders2.Waterandelectrolytesimbalance3.Disordersinproductionofbilesaltsandeliminationofbilirubin4.ImpairedkupffercellsfunctionCarbohydrateMetabolicDisordersLipidMetabolicDisordersProteinMetabolicDisordersHepaticAscitesElectrolyticMetabolicDisordersSyndromesofHepaticinsuffici1.Metabolicdisorders1)CarbohydrateMetabolicDisordersCarbohydrateMetabolismofliverTomaintainconcentrations

ofglucoseinbloodwithinanarrow,normalrange.

insulinAhormoneproducedbythepancreasthatregulatesglucoselevelsintheblood.Itisnormallyproducedinresponsetoraisedglucoselevelsfollowingamealandpromotesglucoseabsorptionintotheliver

andmusclecells(whereitisconvertedintoenergy).Excessglucoseenteringthebloodafteramealisrapidlytakenupbytheliverandsequesteredasthelargepolymer,glycogenglycogenesis1.Metabolicdisorders1)Carbglyconeogenesisglycogenolysiswhenbloodconcentrationsofglucosebegintodecline,theliveractivatesotherpathwayswhichleadtodepolymerizationofglycogenWhenhepaticglycogenreservesbecomeexhaused,asoccurswhenananimalhasnoteatenforseveralhours,thehepatocytes,recognizetheproblemandactivateadditionalgroupsofenzymesthatbeginsynthesizingglucoseoutofsuchthingsasaminoacidsandnon-hexosecarbohydrates.glyconeogenesisglycogenolysiswSevereliverdiseaseHypoglycemiaHyperglycemiaCausedbyadecreaseinfunctionalhepatocytemass.Whenglucogenreservesaredepleted:gluconeogenensisimpared;

inactivationof

insulinweakenCausedbyportal-to-systemicshuntingDecreasethepostprandialextractionofglucosefromprotalbloodSomepatientsmaysufferabnormalglucosetoleranceSevereliverdiseaseHypoglycem1.Metabolicdisorders2)LipidMetabolicDisordersLiveristhecenteroflipidmetabolismManufacturing80%ofthecholesterolSynthesizing,storingandexportingtriglyceridesAssembling,secretingandtakinguplipoproteinparticle,suchasVLDL,LDL,andHDL.1.Metabolicdisorders2)LipiSevereliverdiseaseDisturbanceoflipidmetabolismSyndromesoffataccumulation(fattyliver)IncertainchronicliverdiseasePrimarybiliarycirrhosisDestructionofbileductsBileflowdecreaseDecreaselipidclearanceviabilehyperlipidemiaThesepatientsoftendevelop

xanthomas——accumulationofcholesterol

SevereliverdiseaseDisturbanc1.Metabolicdisorders3)ProteinMetabolicDisordersThelivermanufacturesandsecretesmanyoftheproteinfoundinplasmaalbuminSomeclottingfactorsSomebindingproteinsSomehormoneprecursorsTomaintainplasmaoncoticpressureToregulatehemostasisSteroidandthyroidhormone-bindingproteintoregulatemetabolismangiotensinogen——toregulatebloodpressureInsulinlikegrowthfactor-1——toregulategrowth1.Metabolicdisorders3)ProtOtherrolesoftheliverinproteinmetabolismProcessesofoxidativedeaminationandtransaminationTheureacycleallowsnitrogentobeexcretedintheformofureaOtherrolesoftheliverinpSevereliverdiseaseDisturbanceofproteinmetabolismDecreasedconversionofammoniatoureaPlasmaproteinsdecreaseElevatedammonialevelalbuminClottingfactorsHepaticencephalopathyEdemaandascitesBleedingtendancySevereliverdiseaseDisturbanc2.Waterandelectrolytesimbalance1)HepaticAscitesAsctiesisthepresenceoftheexcessfluidintheperitonealcavityItisalate-stagedmanifestationoftheliverdisease.2.WaterandelectrolytesimbaMechanismsofHepaticAscites1)AnincreaseincapillarypressureCauses:portalhypertension;obstructionofvenousandlymphflow2)DecreaseincolloidalosmoticpressureCause:impairedsynthesisofalbumin3)SaltandwaterretentionbythekidneyCause:

effectivebloodvolumeisreducedbecauseoffluidshiftandvasodilation

glomerularfiltrationrate(GFR)rennin-angiotension-aldosteronesystem(+)metabolismofaldosterone

portal-to-systemicshunting

vasodilatoryproductsaredilveredtothesystemiccirculation

MechanismsofHepaticAscites12.Waterandelectrolytesimbalance2)ElectrolyticMetabolicDisorders1)Hypokalemia2)Hyponatremia2.Waterandelectrolytesimba3.DisordersinproductionofbilesaltsandEliminationofbilirubinSevereliverdiseaseAfailuretosecretebileAFailuretosolubilizesubstancesMalabsorptionanddeficiencystatesDecreasedeliminationofbilirubinElevationofserumbilirubinandjaundiceJaundice:Yellowingoftheskinandthewhitesoftheeyes,causedbyanaccumulationofbilirubinintheblood.3.Disordersinproductionof4.ImpairedkupffercellsfunctionKupffercellsfunction1)Removingandphagocytizingoldanddefectivebloodcells,bacteria,etc.2)Producingavarietyofbioactivesubstancesandcytokines,suchasIL-1,IL-6etc.4.ImpairedkupffercellsfuncdysfunctionofKupffercellsLossofclearancefunctiontobacteriaPortal-systemicshuntingEnterictoxinsenterthesystemiccirculationEntericendotoxemiadysfunctionofKupffercellsLoBriefSymptomsofhepaticfailureWaterandelectrolytesimbalanceHypoorhyper-glycemiaHyperlipidemiaandxanthomasPlasmaproteinsdecreaseedema,bleedingMetabolicdisordersHepaticAscitesHypokalemiaandHyponatremiaDisordersinproductionofbilesaltsandEliminationofbilirubinMalabsorptionanddeficiencystatesElevationofserumbilirubinandjaundiceImpairedkupffercellsfunctionEntericendotoxemiaBriefSymptomsofhepaticfailuHepaticencephalopathy(HE)isaprimaryclinicalmanifestationofhepaticfailure.PARTIVHepaticencephalopathyIntroductionandConceptionEtiologyandclassificationPathogenesisPrecipitatingfactorsofHEPrinciplesoftreatmentHepaticencephalopathy(HE)is1.IntroductionandConceptionConceptionofhepaticencephalopathyHEisacomplex,potentiallyreversibledisturbanceincentralnervoussystemthatoccursasaconsequenceofsevereliverdiseases.FourstagesofhepaticencephalopathySlightlyalteredmoodorbehaviourSomnipathyandinappropriatebehaviorsDrowsyandpsychopathyDeepcoma1.IntroductionandConception2.EtiologyandclassificationEtiologyChronicliverdiseasesFulminanthepaticfailure(FHF)ViralinfectionDrugreactionPoisoningwithcarbontetrachlorideorphosphorusCirrhosisofanyorigin2.EtiologyandclassificationClassificationEndogenousHEHavenoapparentprecipitatingfactorsOftencausedbyextensivelivercelldestructionExogenousHEPrecipitatedbysomeknownagentsorabnormalities

suchas:gastrointestinal