钾代谢障碍 酸碱平衡紊乱.ppt_第1页
钾代谢障碍 酸碱平衡紊乱.ppt_第2页
钾代谢障碍 酸碱平衡紊乱.ppt_第3页
钾代谢障碍 酸碱平衡紊乱.ppt_第4页
钾代谢障碍 酸碱平衡紊乱.ppt_第5页
已阅读5页,还剩72页未读 继续免费阅读

下载本文档

版权说明:本文档由用户提供并上传,收益归属内容提供方,若内容存在侵权,请进行举报或认领

文档简介

DisordersofPotassiumMetabolism,Outline,NormalpotassiummetabolismandregulationHypokalemiaHyperlalemiaCasediscussion,1.thetotalpotassiumofbody:intracellular:98(140-160mmol/L)extracellular:2(3.5-4.5mmol/L),Normalpotassiummetabolism,2.potassiumpresentsinthefood,suchasmilk,peanutpotatoes,saltsubstitute.Potassiumexcretepathway:kidneythroughurine:90Stool(feces):10Sweatnormalserumpotassium:3.5-5.5mmol/Lbalancebetweenintra-andextracellularK+normal:15h,3.regulationofpotassiumhomeostasis,TranscellulartransferRenalregulation,(1)PotassiumtranscellulartransferPump-leakmechanismfactors:PotassiumconcentrationinECFAcid-basebalanceInsulinCatecholamineOsmolarityExerciseTotalbodypotassium,(2).RenalregulationforpotassiumexcretionGlomerularfiltrationReabsorptionbytheproximaltubuleandtheloopofHenleRegulationofpotassiumexcretioninthedistalandcollectingtubules,Sodium-potassiumATPasePermeabilityofluminalmembraneforpotassiumReabsorptionincollectingtubulesHydrogen-potassiumATPase-protonpump,Mechanismofpotassiumexcretionindistalandcollectingtubules:,Influencingfactorsofpotassiumexcretionindistalandcollectingtubules:PotassiumconcentrationinECFAldosteroneDistalflowrateAcid-basebalance(3)PotassiumexcretionincolonThesameastheexcretioninkidney,4.physiologicalfunctionofpotassium,maintaincellularmetabolismmaintaincellularrestingmembranepotentialregulatetheosmolarityandacid-basebalance,Disorderofpotassiummetabolism,Normalserumpotassium:3.5-5.5mmol/LHypokalemiaHyperkalemia,5.influencingfacterofpotassiumhomeostasisacidosisalkalosishypoxiaseruminsulinserumdamageofcellsK+ADSK+catabolismanabolismdistalflowratedistalflowrate,1.Definition:Hypokalemiaisdefinedasadecreaseinserumpotassiumlevellessthan3.5mmol/L.,.hypokalemia,2.causes,(1).intake(2).dischargedigestivetractkidneys:skin,GI:vomiting;diarrhea;GastrointestinalsuctionSkin:excessivesweatsfurosemidediureticlossesdiamoxdiureticphaseofARFrenal:primaryhyperaldosteronismlackofmagnesiumrenaltubularacidosisosmoticdiuresis,(3).AbnormalitydistributionofpotassiummoveintocellsacutealkalosisinsulinoverdoseBariumpoisoningBeta-receptorexcitomotoryhypokalemicperiodicparalysis,3.alterationsofmetabolismandfunction,NervecellsskeletalmusclesgastrointestinalsmoothmuscleMyocardialcells,Effectsonbody(1).nervesandmusclesacutehypokalemiaexcitability0mvserumK+-30mvAP-60mvTP(Et)-90mvRP(Em)hyperpolarization,(2).Heartarrhythmia0mvserumK+-30mv-60mv-90mvdepolarization,Excitability:K+ECFK+permeabilitydepolarizationrepolarizationexcitabilityECGTwaveConductivity:RP0phaseofAPconductivityconductiveblockunidirectionalblockECGP-R,Autorhythmicity:Contractility:acute;chroniceffectsonheartcardiacexcitabilitycardiacconductivitycardiacautomaticitycardiaccontractibility,(3).Renalpolyuria(sensitivityofADH)(4).GIsmoothmusclesHyperpolarization(5).acid-basebalancemetabolicalkalosisparadoxicalaciduria,4.principlesofpreventionandtreatment,1.treatmentofprimarydisease2.principlesofpotassiumcompensationoralapplicationisbetterGivepotassiumaccordingtotheurineconcentration40mmol/L,slowly10-20mmol/htoobserve:heartratecardiacrhythmconsciousnessacidbase,1.definition:hyperkalemiaisdefinedasserumpotassiumexceeding5.5mmol/L.,.hyperkalemia,2.causes,(1).increasedintakeofpotassium(2).Impairedrenalpotassiumexcretion:renaldysfunctionALDpotassium-sparingdiuretics,(3).abnormalpotassiumtranscellularditributionacuteacidosishypoxiaATPtissuedamagehyperkalemicperiodicparalysisDiabetesBeta-receptorinhibbitor,3.alterationsofmetabolismandfunction,(1).effectonneuromuscularexcitability:(2).effectsonheartcardiacexcitabilitycardiacconductivitycardiacautomaticitycardiaccontractibility(3).effectontheacid-basebalanceacidosisparadoxicalalkalineurine,skeletalmuscle8mmol/LRP(depolarization)excitabilitystabbing;tremor8mmol/LRPinactivationofNa+channeldepolarizationparalysis,heart(hyperkalemiaK+permeability)5.5-7mmol/LRPEexcitability7-9mmol/LRPE,Twave;QTshortcardiacarrest,PRQT,Autorhythmicity:K+outwardofphase4SpontaneousdepolarizationheartrateConductivity:RPNa+inwardofphase0conductivityconductiveblockunidirectionalblockContractility:inhibitionofCa2+inwardflowcontractilityacid-basebalanceacidosisparadoxicalalkalineurine,4.principlesofpreventionandtreatment,treatmentofprimarydiseasedecreaseuptakeofK+cutdowntotalamountofbodypotassiumdialysision-exchangeresininduceK+uptakebycells.applicationofcalciumandsodium,Summary,NormalpotassiummetabolismandregulationHypokalemiahyperkalemiadefinitioncausesalterationsofmetabolismandfunctionprinciplesofpreventionandtreatmentCasepresentation,ThepHoftheECFismaintainedwithinthenarrowrangeof7.357.457.8!,I.Acid-basehomeostasis1.Theacidsandbasesintheblood1)Acids,Respiratoryacid(Volatileacid)H2CO3CO2+H2OH2CO3H+HCO3-,MetabolicacidTheproductofmetabolismofaminoacid:phosphophoryn,nuclericacidphosphoricacidmethionine,cysteinesulfuricacidpurineuricacid(gout)Lacticacid(TheliverremovesandconvertstoG)Ketoacids(pyruvicacid,acetoaceticacid,hydroxybutyricacid),2)BaseThefruitsandvegetablesarerichinalkalisalt,e.g.sodiumcitrate,potassiumcitrate.,2.ControlofpH1)ThebuffersystemsBuffersarethefirstdefenseagainstpHdisorders,andactimmediately.AlkalisaltoftheacidBuffersystem:Weakacid,NaHCO3BicarbonatebufferpairH2CO3TobuffermetabolicacidandbaseinECFHbbufferpairsinRBCtobufferrespiratoryacid.HPO42-PhosphatebufferpairH2PO4-TobufferinICF,2)RespiratorycontributionTherespiratorysystemistheseconddefenseagainstpHdisorders,andneedsseveralminutes.H2CO3TherateanddepthH2CO3H+ButwhenPaCO280mmHg,therateanddepth.H2CO3TherateanddepthH2CO3H+,3)RenalcontributionThekidneyisthethirddefenseagainstacid-basedisorders.MetabolicacidExcretionofacidReabsorptionofbaseMetabolicacidExcretionofacidReabsorptionofbaseBaseExcretionofacidExcretionofbase,Thekidneyscancompensateforrespiratoryacidimbalancesbyexcretionofmetabolicacids.(Indirectly)H2CO3ExcretionofmetabolicacidH2CO3Excretionofmetabolicacid,Therenalcompensationrequiresseveraldaystobefullyeffective.,4)EffectsofK+andCl-onpHregulationAcidosiscancausehyperkalemia,andalkalosiscancausehypokalemia.H+K+HCO3-Cl-,3.ThedeterminationofpHpH=pKa+logHCO3-/H2CO3Iftheratiois20:1,thepHwillbe7.4,4.Themainindicatorsoflaboratoryaboutacid-basebalance1)pH:Thenormalrangeis7.357.45AnormalrangeofpHrepresentsNodisturbanceinacid-basebalanceAcid-baseimbalancewithcompletecompensationAmixedacidosisandalkalosiswhichhaveoppositeeffectonpHandoffseteachother.,3situations:,2)PaCO2:Normalrangeis3842mmHg(40mmHg).(3346mmHg)PaCO2isanindicatoroftheeffectivenessofrespiratoryexcretingofcarbonicacid.IfPaCO2,meanshypoventilationormetabolicalkalosisaftercompensationPaCO2,meanshyperventilationormetabolicacidosisaftercompensation,3)HCO3-:Thenormalrangeis2433mmol/L.Itisanindicatoroftherenalexcretionofmetabolicacid.HCO3-meansanexcessofmetabolicacids(metabolicacidosisorrespiratoryalkalosisaftercompensation).HCO3-meansadeficitofmetabolicacidsoranexcessofbase(metabolicalkalosisorrespiratoryacidosisaftercompensation).,StandardbicarbonateSB(2227mmol/L)ActualbicarbonateABABSB,hypoventilation;ABSB,hyperventilationBufferbaseBBBaseexcessBECO2combinepower(CO2CP),4)AG(aniongap):AGdescribesthedifferencebetweenunmeasuredanion(UA)andunmeasuredcation(UC).AG=Na+-(Cl-+HCO3-).Thenormalrangeis1014mmol/L(12mmol/L).,II.Acid-baseimbalances1.Metabolicacidosis1)Concept:Metabolicacidosisreferstoaprimarydeficitinbasebicarbonate,thepHfalls.,2)Causes:(1)IncreaseinmetabolicacidsExcessproductionofmetabolicacidsE.g.fastingandstarvation,diabeticketoacidosis,lacticacidosis(shock,hypoxia,heartfailure,anemia).DecreasedlossofmetabolicacidsE.g.renalfailure,renaltubularacidosis-IOverdoseofacidicmedicine(aspirin).AGisincreased.,(2)IncreaseinbicarbonatelossE.g.Severediarrhea,intestinalfistulasRenaltubularacidosis-II.OverdoseofNH4+,releasesHClAGisnormal.,3)Compensation:(1)Buffersystemandcell(2)SignsofcompensationKussmaulbreathingAcidurine,4)Manifestations(1)Heartfailure:Hyperkalemia_cardiacarrhythmiaImpairmyocardialcontraction(2)Decreasedresponseofcapillarytocatecholamines_Shock(3)DepressionofneuralfunctionLethargy,disorderofconsciousness,coma.(4)ChangesofosseoussystemRenalrickets肾性佝偻病,osteomalacia骨软化症,4)LaboratoryfindingspH,HCO3-,PaCO2ifthereiscompensationofrespiratorysystem.,Casestudy:Arterialblood:pH7.21PaCO226mmHgPaO2108mmHgHCO3-12mmol/LNa+135mmol/LK+2.0mmol/LCl-110mmol/LUrine:pH5.0,(1)A36-year-oldmanwashospitalizedwitha3-dayhistoryoffeverandwaterydiarrhea.Thebloodpressureis90/60mmHg,thepulseis112/minute,therespiratoryrateis24/minute,andthetemperatureis37.5C.Thelaboratoryresultswereobtained.,2.Respiratoryacidosis1)Concept:RespiratoryacidosisisdefinedasadecreaseofpHinducedbyprimaryincreaseinplasmaH2CO3.,2)CausesRespiratoryacidosiscanoccurasanacuteorachronicdisorder.(1)AcuterespiratoryacidosisE.g.acuterespiratoryinfections,chestinjuries,pulmonaryedema.(2)ChronicrespiratoryacidosisE.g.chronicobstructivelungdisease,chronicbronchitis.,3)Compensation:Buffersystemandcell4)Manifestations:Headache,cardiacarrhythmiasandneurologicabnormalities.Neurologicmanifestationsmaybemoreprominentinrespiratoryacidosisthaninmetabolicacidosis.“CO2narcosis”Themechanism:,(1)CO2crossestheblood-brainbarrierrelativelyeasily,andcandilatethebloodvesselsinthebrainandleadtobrainedema.(2)CO2canalsodecreasethepHofthecerebrospinalfluid,andmakedepressionofneuralfunction,likeweakness,confusion,paralysis,stuporandcoma.,5)LaboratoryfindingspH,PaCO2,HCO3-ifthereiscompensationofkidneys(chronic).,3.Metabolicalkalosis1)Concept:Metabolicalkalosisreferstoaprimaryincreaseinbasebicarbonate,thepHelevates.2)Causes:(1)DecreaseofacidE.g.vomiting(Ileus:intestinalobstruction).(2)IncreaseofbaseE.g.antacids,transfusionwithcitratedblood,hyperaldosteronism.Saline-responsivealkalosisandsaline-resistantalkalosis,3)Compensation4)ManifestationsAlkalosiscancauseincreasedexcitabilityofnervoussystem,likehyperactivereflexes,musclehypertonicity,tetanyetc.,5)LaboratoryfindingspH,HCO3-,PaCO2ifthereiscompensationofrespiratorysystem.,4.Respiratoryalkalosis1)Concept:RespiratoryalkalosisisdefinedasanincreaseofpHinducedbyprimarydecreaseinplasmaH2CO3.2)Causes:HyperventilationE.g.anxiety,hysteria,fever,earlysalicylate(aspirin)toxicity,misuseofmechanicalventilation.,3)Compensation4)ManifestationsTetany5)LaboratoryfindingspH,PaCO2,HCO3-(dependonthenormalrenalfunction).,5.Mixedacid-baseimbalancesConcept:Twoormoreprimaryacid-baseimbalancesexistatthesametime.,Bact

温馨提示

  • 1. 本站所有资源如无特殊说明,都需要本地电脑安装OFFICE2007和PDF阅读器。图纸软件为CAD,CAXA,PROE,UG,SolidWorks等.压缩文件请下载最新的WinRAR软件解压。
  • 2. 本站的文档不包含任何第三方提供的附件图纸等,如果需要附件,请联系上传者。文件的所有权益归上传用户所有。
  • 3. 本站RAR压缩包中若带图纸,网页内容里面会有图纸预览,若没有图纸预览就没有图纸。
  • 4. 未经权益所有人同意不得将文件中的内容挪作商业或盈利用途。
  • 5. 人人文库网仅提供信息存储空间,仅对用户上传内容的表现方式做保护处理,对用户上传分享的文档内容本身不做任何修改或编辑,并不能对任何下载内容负责。
  • 6. 下载文件中如有侵权或不适当内容,请与我们联系,我们立即纠正。
  • 7. 本站不保证下载资源的准确性、安全性和完整性, 同时也不承担用户因使用这些下载资源对自己和他人造成任何形式的伤害或损失。

评论

0/150

提交评论