病理生理英文课件

PartⅠPotassiumBalanceⅠContentandDistributionofPotassiumintheBody

ⅡIntakeandExcretionofPotassiumDietaryKintake70~100mmol/dayECF2%Serum[K+]round4.5mmol/LK+SkintrivialnormallyColon10%Kidneys>80%Moreingested,moreexcretedLessingested,lessexcretedNotingested,excretiongoeson

Content,distribution,intakeandexcretionofKExcretionICF[K+]160mmol/L98%ofthetotalbodypotassiumTotalbodyKcontent31~57mmol/Kgbodyweight1.Hormones—insulin,glucagon,catecholamines,thyroidhormone2.Serum[K+]3.pHofECFandplasmaosmolality4.Others—rateofcellbreakdown,hypoxia,hypothermia,exerciseInfluencingFactors[K+]↑Na+Na+/K+-ATPaseK+K+H+Catecholamine

InsulinRegulationofRenalPotassiumExcretionFiltration,reabsorptionandsecretion

ofpotassium

ThenephronandcollectingtubuleCl-Na+/K+ATPase(Mg2+activated)Na+/K+ATPaseH+-

K+ATPaseAfferentEfferentarterioleBowman’scapsuleglomerulusProximaltubuleReabsorptionGlucoseSodiumWaterBicarbonate(HCO3-)Henle’sloop(thickandthinsegment)PrimerUrine180L/day(ultrafiltrate)JuxtaglomerularcellsReninAngiotensinIIIIIIAldosterone(Adrenalcortex)RAAS(+)MaculadensaReabsorptionSodium>WaterdiluteReabsorptionWater>SodiumExchangeofionHydrogen-SodiumPotassium-SodiumReabsorbwaterADHcanincreasethepermeabilityofthetubularmembranewallstoreabsorbmorewater.CollectingtubulecondenseUrine1.5~2.0L/dayAdlosteronecanenhancetheexchangeofpotassium-sodium(increasesthereabsorptionofsodium)(enhancestheexcretionofpotassium)(1)Reabsorbsodium(water)andexcretepotassium.(2)ExcretehydrogenandreabsorbbicarbonateDistalconvolutedtubuleRegulationofRenalPotassiumExcretionFiltration,reabsorptionandsecretion

ofpotassiumSecretionofpotassiuminthedistalandcollectingtubulesprincipalcells,withNa+/K+ATPasemembranepump,forsecretionofK+lumenPrincipalCellbloodK+Na+Na+K+Cl-Cl-K+CO2HCO3-Cl-Cl-H+K+CO2IntercalatedCellRegulationofRenalPotassiumExcretionFiltration,reabsorptionandsecretion

ofpotassiumSecretionofpotassiuminthedistalandcollectingtubules

ReabsorptionofKinthedistalandcollectingtubules,intercalatedcells,withH+/K+-ATPase(protonpump)forreabsorptionofK+RegulationofRenalPotassiumExcretionFiltration,reabsorptionandsecretionofpotassiumSecretionofpotassiuminthedistalandcollectingtubulesReabsorptionofKinthedistalandcollectingtubulesintercalatedcells,withH+/K+-ATPase(protonpump)forreabsorptionofK+FactorsinfluencingexcretionofK+bythedistalandcollectingtubules

FactorsInfluencingExcretionofK+bytheDistalandCollectingTubules

Aldosterone—activatesNa+/K+ATPase,increasemembranepermeabilitytoK[K+]intheECFFlowrateoftubularfluidinthedistaltubulepHofECF—↓pHinhibitsNa+/K+ATPase+lumenbloodPrincipalCellK+Na+Na+K+Cl-Cl-K+[K+]↑②③CO2HCO3-Cl-Cl-H+K+CO2IntercalatedCell[H+]↑①flowrateFactorsInfluencingExcretionofK+bythe

DistalandCollectingTubules

++Ald+++++-MaintenanceofPotassiumHomeostasisDistributionofpotassiumacrossthecellmembraneRegulationofrenalpotassiumexcretionExcretionofKbytheColonalsocontrolledbyaldosterone

FunctionofPotassiumintheBody

ⅣFunctionofPotassiumintheBodyThepartK+playsinmetabolismMaintenanceoftherestingmembranepotentialofexcitablecellsMaintenanceandregulationofosmoticpressureandacid-basebalancebothinICFandECFPartⅡPotassiumImbalance---abnormalchangesin[K+]inECFHypokalemiaSerum[K+]<3.5mmol/L,mayormaynotbe

associatedwithKdeficitECF2%Dietaryintake

Serum[K+]<3.5mmol/LG.Ilosses---diarrhea,vomitingRenallosses---diuretics,somediseasesofthekidney

Lossesfromtheskin---profusesweating,burnsExcessivelossesICF[K+]mayormaynotbedecreasedTotalbodyKcontent—decreased(Kdeficit)shifting—normalCrudecottonseedoilpoisoningorEtiologyandPathogenesisEtiologyandPathogenesisⅠ.InadequateIntakeFasting,anorexia,inabilitytoeat,prolongedIValimentationwithoutKsupplementation,alcoholism

Ⅱ.ExcessiveLosses1.GastrointestinallossesDiarrhea→extrusionoflargeamountofalkalineliquidstoolwithahighcontentofK→Kdepletion,acidosis,ECFvolumecontraction→↑secretionofaldosterone

Vomiting→mainlyincreasedrenalexcretionofK+duetometabolicalkalosiscausedbylossofgastricacid,contractionofECFvolumeEtiologyandPathogenesis

Ⅰ.InadequateIntakeⅡ.ExcessiveLosses1.Gastrointestinallosses

2.Excessiverenallosses(1)Diuretics→increasedflowrateanddeliveryofNa+,Cl-andwatertothedistaltubule→increasedNa+-K+exchange;volumecontraction→increasedaldosterone→renalKexcretion↑

RegulationofRenalPotassiumExcretionThenephronandcollectingtubuleCl-Na+/K+ATPase(Mg2+activated)Na+/K+ATPaseH+-

K+ATPaseEtiologyandPathogenesisⅠ.InadequateIntakeⅡ.ExcessiveLosses1.Gastrointestinallosses

2.Excessiverenallosses(1)Diuretics(2)SomediseasesofthekidneyRenaltubularacidosisExcessiveRenalLosses(1)Diuretics(2)SomediseasesofthekidneyRenaltubularacidosisDiureticrecoveryphaseofacuterenalfailure(3)Antibiotics(4)ExcessofadrenocorticalhormonesAldosteronism,Cushing’ssyndrome(5)Magnesiumdeficiency

DiureticrecoveryphaseofacuterenalfailureRegulationofRenalPotassiumExcretionThenephronandcollectingtubuleCl-Na+/K+ATPase(Mg2+activated)Na+/K+ATPaseH+-

K+ATPaseExcessiveRenalLosses(1)Diuretics(2)SomediseasesofthekidneyRenaltubularacidosisDiureticrecoveryphaseofacuterenalfailure(3)Antibiotics(4)ExcessofadrenocorticalhormonesAldosteronism,Cushing’ssyndrome(5)Magnesiumdeficiency(6)AlkalosisEtiologyandPathogenesisⅠ.InadequateIntakeⅡ.ExcessiveLosses1.Gastrointestinallosses

2.Excessiverenallosses3.ExcessivelossesfromtheskinProfusesweatings,burnsorscaldsEtiologyandPathogenesisⅠ.InadequateIntakeⅡ.ExcessiveLossesⅢ.ShiftingofK+fromtheECFtoICF1.Overdoseofinsulin2.-adrenergicagonistoverdose

Na+Na+/K+-ATPaseK+K+H+AlbuterolInsulinEtiologyandPathogenesisⅠ.InadequateIntakeⅡ.ExcessiveLossesⅢ.ShiftingofK+fromtheECFtoICF

1.Overdoseofinsulin2.-adrenergicagonistoverdose3.Alkalosis4.Bariumpoisoning5.Familialhypokalemicperiodicparalysis

Na+Na+/K+-ATPaseK+K+H+AlbuterolInsulinEtiologyandPathogenesisⅠ.InadequateIntakeⅡ.ExcessiveLossesⅢ.ShiftingofK+fromtheECFtoICF

CrudeCottonSeedOilpoisoningEffectsontheBody—factorsinfluencingtheeffects:theunderlyingdiseases,thedegreeofhypokalemiaandrapidityofitsdevelopment,theratioof[K+]i/[K+]eEffectsonNeuromuscularExcitability

TheRestingMembranePotential(RMP)andActionPotential(AP)ofaskeletalmusclecellinthenormalstate

+350-60-90Millivolts

MillisecondsThreshold

NernstequationEm=-60lg[K+]icf/[K+]ecf(mv)AcuteHypokalemia[K+]i/[K+]e↑RMPmorenegativethannormalhyperdepolarizationblock,excitability↓muscleweakness,flaccidparalysis,smoothmusclesymptoms-120-90-60-30030NormalLow[K+]High[K+]TMPRMPActionpotential(AP)TheeffectsofserumK+concentrationoncellularmembraneexcitability

mv

ratioof[K+]i

to

[K+]emaybenormal,RMPandexcitabilityunchanged,interferingwithcellularmetabolismandvasodilationofmusclesduringexerciseChronicHypokalemiaEffectsontheHeart

ABriefReviewoftheBioelectricPhenomenaoftheHeart

a:effectiverefractoryperiod;b:relativerefractoryperiod

c:supranormalperiodRMPandAPofaVentricularMuscleCelloftheHeart40+200-20406080100401234340124RMPmax.diast.potentialAtrialmusclePurkinje’sfiberTheMembranePotentialofAtrialMuscle,

andPurkinje’sFiber1.Effectsonexcitability

RMP<-90mv,excitabilityCa2+inflowplateau,ERPshortenedPhase3,SNPprolongedAPprolongedEffectsoflowserum[K+]ontheactionpotentialofthemyocardialcellnormal

normal

low[K+]eThresholdpotentialrepolarizationprolongeda.mus.v.mus.2.Effectsonautorhythmicity

Kchannelconductanceofthecellmembraneofthefastresponseautonomiccellsaccelerationofspontaneousdiastolicdepolarization,autorhythmicityTheMembranePotentialofPurkinje’sFiber340124max.diast.potentialnormalhypokalemia3.Effectsonconductivity

Amplitudeandrapidityofphase0depolarizationsmallerthannormalconductivity

Cardiacarrhythmiasduetoincreasedexcitability,shortenedERP,prolongedSNP,increasedautorhythmicityanddecreasedconductivity

Theconductingsystemofthehearta:effectiverefractoryperiod;b:relativerefractoryperiod

c:supranormalperiodRMPandAPofaVentricularMuscleCelloftheHeart

conductivityandcardiacarrhythmias——reentryofexcitationSchematicdiagramshowingreentryofexcitationinaPurkinje’sfiber-ventricularmusclecircuit(1)normal

(2)conductionsloweddown(3)monodirectionalblockstalk

stalkstalkventricularmuscleventricularmuscleventricularmusclestalkstalkbranchAbranchBventricularmuscle

conductionsloweddownmonodirectionalblock+(4)VentricularprematureexcitationresultedfromreentryofexcitationactionpotentialmonodirectionalblockreentryofexcitationECG4.Effectsoncontractility

increasedinacutehypokalemia,

decreasedinchronichypokalemiaEffectsontheKidneyfunctionalandmosphologicalchanges

EffectsonMetabolismcarbohydratemetabolism,proteinmetabolism,acid-basebalanceEffectsontheNervousSystemdocumentedsymptoms,contradictoryreports

PrinciplesofPreventionandTreatmentⅠ.MeasuresagainstthecausesⅡ.Replacementtherapywithpotassium1.Oralreplacement:40~120mmolofK/day2.IVinstillation:KCl≤40mmol/L,≤10mmolofK/h

Neverinject!Monitorserum[K+]andECGHyperkalemia

serum[K+]>5.5mmol/L,amedicalemergency

EtiologyandPathogenesisInadequateexcretionofKRenalfailure,hypoaldosteronism,KsparingdiureticsRedistributionofKinthebodytissueinjury,acidosis,insulindeficiency,familialhyperkalemicperiodicparalysisIncreasedintakeofK—rapidIVKadministration

EffectsontheBodyⅠ.EffectsonneuromuscularexcitabilityInmildtomoderatehyperkalemiatheratioof[K+]ito[K+]eRMPlessnegativethannormal,excitabilityabnormalsensibility(paresthesia),diarrheaSeverehyperkalemia,RMPdecreasedtolevelofTMP,depolarizationblockmuscleweakness,paralysis,dizziness,comaⅠ.EffectsonneuromuscularexcitabilityⅡ.Effectsontheheart1.EffectsonexcitabilityInmildtomoderatecases,excitability,phase0upstrokesmallerandslower;Phase2plateauprolonged,phase3repolarizationshortened

Inseverecases,noAPcanbeinducedcardiacarrestEffectsontheBodyEffectsontheBodyⅠ.EffectsonneuromuscularexcitabilityⅡ.Effectsontheheart1.Effectsonexcitabil