生理學(xué)-復(fù)件尿生成-自編newest

Formationand

ExcretionofUrine

HANXiaohua

Room423,BoyaBuildingOverallfunctionofthekidneys

Excretion：waste/foreignproductsRegulation：

-volumeandosmoticpressureoftheextracellularfluid.-acid-basebalanceofthebody.Secretion：

-renin,EPO,1,25-(OH)2vitaminD3

尿毒癥

-面色泛黃食欲不佳困倦乏力浮腫高血壓史鐵生第一屆：2006-3-9，慢性腎病的早期檢測和預(yù)防第二屆：2007.3.8，了解您的腎臟第三屆：2008.3.13，神奇的腎臟第四屆：2009.3.12，穩(wěn)定血壓，保持腎臟健康第五屆：2010.3.11,保護(hù)您的腎臟，控制糖尿病第六屆：2011.3.10，保護(hù)腎臟，挽救心臟第七屆：2012.3.8，捐獻(xiàn)腎臟，延續(xù)生命世界腎臟日（WorldKidneyDay）:

每年3月份第2個星期四ContentsFunctionalanatomyandbloodflowofkidneyGlomerularfiltrationSolutetransportintherenaltubuleandcollectingductUrinaryconcentrationanddilutionRegulationofurinaryformationClearanceSection1

FunctionalAnatomyandBloodFlowoftheKidneys80-120萬/kidney腎小體腎小管腎小球(毛細(xì)血管球)腎小囊(內(nèi)層、囊腔、外層)近端小管髓袢細(xì)段遠(yuǎn)端小管近曲小管髓袢降支粗段髓袢降支細(xì)段髓袢升支細(xì)段髓袢升支粗段遠(yuǎn)曲小管腎單位（一）NephronNephron（腎單位）

Corticalnephronandjuxtamedullarynephron

功能參與尿的生成參與尿液的濃縮和稀釋

(二）Juxtaglomerularapparatus(JGA,球旁器）

髓袢升支粗段靠近毛細(xì)血管網(wǎng)的部分致密斑球外系膜細(xì)胞球旁細(xì)胞（1）球旁細(xì)胞

(juxtaglomerularcell)

-入球小動脈特殊分化的平滑肌細(xì)胞

-分泌renin（2）致密斑（maculadensa)

-遠(yuǎn)曲小管起始部一小塊柱狀上皮細(xì)胞，呈斑狀隆起

-感受小管液中NaCl含量變化（3）球外系膜細(xì)胞

(extraglomerularmesangialcell)-吞噬和收縮功能腎A葉間A弓形A小葉間A入球小A毛細(xì)血管球

腎V葉間V弓形V小葉間V管周毛細(xì)血管網(wǎng)出球小A

(直小血管）

二RenalbloodflowCharacteristicofrenalbloodflow（1）Kidneysreceive20%ofcardiacoutput-94%inthecortex-5%intheoutermedulla-1%intheinnermedulla（2）Regulationofrenalbloodflow

ekidneysreceive1/4ofthecardiacoutput(1)Autoregulationofrenalbloodflow80180Myogenictheory(肌源學(xué)說）

arterialpressure

VesselwalltensionStretch-activatedcationchannelsVascularsmoothmusclecontractionopenVoltage-dependentcalciumchannelsleadingtoinfluxofCa2+-RBF,GFRNaClinmaculadensaafferentarteriolarresistanceTubulo-glomerularfeedbackmechanismAdenosineorATP?(2)Nervousandhumoral

regulationofrenalbloodflowSympatheticnerve

Humoralfactors

(-)RBF

(+)RBFEpinerphrinePGE2NorepinephrinePGI2angiotensinII心房鈉尿肽

ADHdopamineTXA2NOendothelinkinins(激肽）

Section2

FunctionofGlomerularFiltration

componentbloodplasmaInitialurinewater

protein

glucose

urea

uricacid

creatinine

chloride

sodium

potassium

90～93

7～9

0.1

0.03

0.002

0.001

0.37

0.32

0.02

93

(trace)

0.1

0.03

0.002

0.001

0.37

0.32

0.02

Initialurineisanultrafiltrate.Glomerularfiltrationrate(GFR,腎小球濾過率)

thevolumeofultrafiltrate

formedbybothkidneysperminute.GFR=125ml/min

RatioofGFRtorenalplasmaflow(%)FF:125ml/min660ml/min

Filtrationfraction(FF,濾過分?jǐn)?shù))19%ofRPFisfilteredintobowman’sspace.=19%*100%

Glomerularfiltrationmembrane

anditspermeability

-腎小球毛細(xì)血管內(nèi)皮細(xì)胞-基膜（basementmembrane)-腎小囊上皮細(xì)胞(podocytes)

窗孔網(wǎng)孔外層板致密板內(nèi)層板

網(wǎng)孔（4-8nm）（基膜膠原及糖蛋構(gòu)成微纖維網(wǎng)）

Fenestration

(窗孔，50-100nm）裂隙膜nephrin分子間孔道

濾過屏障:

Mechanicalbarrier

r<2.0nm,permeabler=2.0-4.2nm,thelargerthelessr>4.2nm,notpermeable

Electricalbarrier

positivecharged,easilypermeablenegativecharged,hardlypermeableGFR=KfXPUFFiltrationcoefficientEffectivefiltrationpressure（EFP）FactorsaffectingGFREFP=(腎小球毛細(xì)血管血壓+囊內(nèi)膠體滲透壓）

-（血漿膠體滲透壓+腎小囊內(nèi)壓）囊內(nèi)膠滲壓

入球端有效濾過壓=55–(30+15)=10mmHg

濾過平衡有效濾過壓=0

有效濾過壓=毛細(xì)血管壓-(血漿膠體滲透壓+腎小囊內(nèi)壓)1.Glomerulareffectivefiltrationpressure(1)Glomerularcapillarypressure-80-180mmHg:GFRnochange-40-50mmHg：GFRdecreasetozero(2)Capsularpressure（3）PlasmacolloidosmoticpressureFactorsaffectingGFR

2.Glomerularfiltrationmembrane-Permeability/Area3.Renalplasmaflow：

影響濾過平衡位置急性腎小球腎炎臨床：

-血尿、蛋白尿、少尿、水腫、高血壓Section3

SoluteTransportintherenaltubuleandcollectingductReabsorptionsubstancesaretransferredfromthetubularfluidtotheblood.

Secretionsubstancespassacrossthetubuleepitheliumtothetubularfluid.

一、SolutetransportReabsorption

-Water:99%-NaCl:most-Glucose:all-HCO3-:most-Urea:partial-Creatinine:noSecretion-H+-K+-NH3-Creatinine

Passivetransport-simplediffusion-facilitateddiffusion-solventdrag(溶劑拖曳)

Activetransport

-primaryactivetransport-secondaryactivetransport

EndocytosisMechanismforsolutetransportParacellularrouteBasolateralmembraneTightjunctionIntercellularspaceApicalcellmembraneTranscellularrouteSolutetransportindifferenttubules

ReabsorptionofNaClandwaterReabsorptionofglucose/aminoacidsHCO3-reabsorptionandH+secretionCa2+reabsorptionUreareabsorptionandsecretionSecretionofNH370%Na+K+Cl-H2OCa2+reabsorbed85%HCO3-reabsorbed100%Glucose,aminoacid:reabsorbedH+secreted（一）ReabsorptionofNaCl

andwater

Proximaltubule

(近端小管）

-70%ofNaClandwater2/3:近端小管前半段吸收

1/3:近端小管后半段吸收

H2OH2OEarlyproximaltubulesH2O重吸收大于Cl的重吸收，小管內(nèi)Cl濃度增高AnionHAnionHAnionlateproximaltubule:跨細(xì)胞和旁細(xì)胞途徑（一）ReabsorptionofNaCl

andwater

Proximaltubule

（近端小管）

-70%ofNaClandwater

Loopofhenle(髓袢）

-20%NaCl-15%H2O

速尿髓袢升支粗段：頂端膜對K通透性高，基底側(cè)膜對Cl通透性高，

K通過頂端膜K通道返回小管腔，造成小管內(nèi)電位比組織間隙高+6mVReabsorptionofNaClandwater

Proximaltubule

（近端小管）

-60-70%ofNaClandwaterLoopofhenle(髓袢）

-20%NaCl+15%H2ODistalconvolutedtubuleandcollectingduct

-12%NaCl-water:regulatedbyADH-Na+/K+:regulatedbyaldosterone(醛固酮)

遠(yuǎn)曲小管前段重吸收NaCl機(jī)制Thiadiazide噻嗪類

遠(yuǎn)曲小管后段重吸收NaCl機(jī)制Solutetransportindifferenttubules

ReabsorptionofNaClandwaterReabsorptionofglucoseHCO3-reabsorptionandH+secretionCa2+reabsorptionUreareabsorptionandsecretionSecretionofNH370%Na+K+Cl-H2OCa2+reabsorbed85%HCO3-reabsorbed100%Glucose,aminoacid:reabsorbedH+secretedGSGSGlucoseisonlyabsorbedbyproximaltubule.Glucosereabsorptioniscoupledtosodiumbysecondaryactivetransport.

(二）Reabsorptionofglucose

GLUT2Renalplasmaglucosethreshold(腎糖閾）

Theplasmaglucoseconcentration(180mg/dl)atwhichglucosebeginstoappearintheurine(尿中剛剛出現(xiàn)葡萄糖時的血糖濃度)

filteredreabsorbedexcretedPlasmaconcentrationGlucose300mg/dl

180mg/dl375mg/minTmTm(葡萄糖極限吸收量）

（三）HCO3-absorptionand

H+secretion{—{{Na+H++HCO3-Na+HCO3-H+H2CO3CO2+H2OH2CO3

H2O+CO2Na+HCO3-CarbonicanhydraseCarbonicanhydraseluminacellIntercellularspace（1）近端小管及髓袢：{—{Na+H++HCO3-Na+H2CO3CO2+H2OCarbonicanhydrasecellglutamineNH3H2PO4-HPO42-H+H+NH3NH4+NaCl+NH4Cl（2）遠(yuǎn)端小管及集合管

（四）K+reabsorption/secretion

K+absorption

-65-70%近端小管重吸收（溶劑拖曳）

-25%-30%髓袢重吸收K+secretion

-遠(yuǎn)端小管及集合管（尿K+主要來源）

-受到醛固酮調(diào)節(jié)

glutamineNH3H2PO4-HPO42-H+H+NH3NH4+NaCl+NH4ClNa+

吸收促進(jìn)K+分泌{—{Na+H++HCO3-Na+H2CO3CO2+H2OCarbonicanhydrasecellglutamineNH3H+NH3NH4+NaCl+NH4Cl（五）NH3Secretion（六）SecretionoforganicionsPAH:對氨基馬尿酸；αKG：α

酮戊二酸（谷氨酸代謝）（七）ReabsorptionofothersUrea

Reabsorption：近端小管、髓質(zhì)集合管（溶劑拖曳）Secretion：髓袢細(xì)端（易化擴(kuò)散）

Ca2+:solventdrag（PTH調(diào)節(jié)）

Aminoacid:sameasglucose

Protein:endocytosisatproximaltubulesSection4

UrinarydilutionUrinaryconcentration

尿滲透壓：50-1200mOsm/L

Plasma:300mOsm/L滲透壓計Urinarydilution/concentrationRole:maintainthebalanceofbodyfluidPolyuria:>2.5L/day

oliguria:<400ml/day

anuria:<100ml/day

比重計一、Urinarydilution

Location

distaltubuleandcollectingduct

Mechanism

髓袢升支粗段吸收

NaCl但對水不通透，

-水過剩抑制ADH分泌中樞性尿崩癥：ADH完全缺乏

Osmoticgradientinrenalmedulla

（必要條件）

ADH(+)二、UrinaryconcentrationOsmoticGradientintheRenalMedullaNa+H2OM1:對水不通透，對溶質(zhì)通透M2:對水通透，對溶質(zhì)不通透低滲溶液高滲溶液逆流倍增（countercurrentmultiplication）Establishmentofosmolalitygradientinthemedulla

Outermedulla(外髓部）

髓袢升支粗段主動重吸收NaCl，對水不通透。Innermedulla（內(nèi)髓部）

-內(nèi)髓部集合管擴(kuò)散出來的urea-髓袢升支細(xì)段擴(kuò)散出來的NaClH2O

ReabsorptionofNaClatthickascendinglimbofHenle’sloop

arethedrivingforceforestablishmentofosmolalitygradientinrenalmedulla

Urea

playsaspecialroleintheconcentratingmechanism

Roleofvasarecta(直小血管）inkeepinghighermedullaryosmoticpressure:

-帶走髓質(zhì)中多余水分和溶質(zhì)，維持腎髓質(zhì)的滲透梯度。

OsmoticgradientinrenalmedullaUrinaryconcentration&dilution

ADHPermeabilityofH2OIndistaltubuleandcollectingductThickascendinglimbUreaNaClVasarecta

Section5

RegulationofUrinaryFormationGlomerularfiltrationTubulereabsorptionTubulesecretionIntrarenalautoregulationNervousandhumoralregulationSoluteconcentrationintherenaltubuleGlomerulotubularbanlanceRenalsympatheticnerveADHRenin-angiotensin-

aldosteronesystemANP

1.Soluteconcentrationintherenaltubule

腎小管溶質(zhì)濃度小管液滲透壓水重吸收NaCl重吸收尿量/NaCl

Osmoticdiuresis（滲透性利尿）

-mannitol-diabetesmellitus（一）Intrarenalautoregulation

Changesoftheperitubularcapillarypressureandplasmacolloidosmoticpressure2.Glomerulotubularbalance-近端小管對水和Na+的重吸收率始終占GFR的65-70%tubule

QuantityofthefilteredglucoseandaminoacidWhenGFRincreases,theglucoseandaminoacidfilteredincreaseproportionally.Sodiumreabsorptioniscoupledwiththereabsorptionofglucoseandaminoacid.

Therefore,whenGFRincreases,thereabsorptionofsodiumandwaterincrease.（二）Renalsympatheticnerveα-Receptorβ-Receptorafferent&efferentarteriolescontractionDecreaseofGFRIncreaseofNaClandwaterreabsorptioninproximaltubuleandloopofHenle.GranularcellsreninagiotensinⅡaldosterone保Na+排K+UrineDirectaction（三）HumoralRegulation

Argininevasopressin(AVP)or

Antidiuretichormone(ADH)Renin-angiotensin-aldosteronesystemAtrianatriureticpeptide(ANP)Synthesis/SecretionSynthesizedinSupraopticnucleus(SON)andparaventicularnucleus

(PVN)inhypothalamus.Transportedbyhypothalamic-hypophysialtracttotheposteriorpituitary(neurohypophysis),whereitisreleasedintothebloodstream.

（1）ADH

IncreaseNaClreabsorptioninthickascendinglimbofHenle’sloopandpermeabilityofureaincollectingductofinnermedulla.Increasepermeabilityofwaterindistaltubuleandcollectingduct(main)ADHFunctionBindingofADHtoV2receptoractivatesGs-AC-cAMP-PKAsystem,thenvesiclescontainingwaterchannelprotein(AQP2)fusewithmembrane.-ADHenhancethetranscriptionofAQP2gene.-WhenADHisabsent,endocytosis(internalization)ofAQP2occurs.TheNobelPrizeinChemistry2003NobelLaureatesPeterAgre(1949.1.30--)ProfessorofbiologicalchemistryJohnsHopkinsUniversitySchoolofMedicine,Baltimore,USA“forthediscoveryofwaterchannels”Thehuntforthewaterchannels

Xenopusoocytes(非洲爪蟾卵母細(xì)胞)microinjectedwithCHIP28

mRNAswelledrapidlywhenplacedinahypo-osmoticmedium.CHIP28:channel-likeintegralmembraneprotein,28kDaCHIP28

=

AQP1-Theconstrictionregion(0.28nm)inhibitsthepassageofmoleculeslargerthanwater.-Becauseofthepositivechargeatthecenterofthechannel,positivelychargedionsaredeflected.Choroidplexus/脈絡(luò)叢；Cornea/角膜Lacrimalglands/淚腺;Testis/睪丸-AQP1(blue)：proximaltubuleanddescendingthinlimb.

AQP2(green)：apicalpartofcollectingductprincipalcells

AQP3(red)

AQP4(purple)basolateralofcollectingductprincipalcells.-AQP7(orange):apicalpartofstraightproximaltubules.PlasmaosmoticpressureosmoreceptorcellslocatedintheanteriorhypothalamusshrinkADH(1)PlasmaosmoticpressureFactorsaffectingADHrelease

crystalosmoticpressureplasmaADH

<=275-290mOsm/Lzero289-307mOsm/LADH+thirst

ForstimulatingADHrelease-IncreasedcrystalosmoticpressureformedbyNaClismosteffective-ureaareineffectiveWaterdiuresis(水利尿）b(2)Bloodvolume/BloodpressureBloodvolumeStretchreceptors（左心房、心包內(nèi)肺V)VagusnerveADHBloodpressureBaroreceptor(主動脈弓，頸動脈竇）ReninAngiotensinⅡFactorsaffectingADHrelease+ADHrelease:pain,nausea,nicotine,morphine

-ADHrelease:alcohol,ANP(3)OtherfactorsforADHreleaseFactorsaffectingADHreleaseReninSecretedbygranularcellsofjuxtaglomerularapparatusangiotensinogenangiotensinⅠangiotensinⅡaldosteronereninACESecretionFunctionACE:angiotensin-convertingenzymeBloodpressureofafferentarteriolesActivationofsympatheticnerve-

+?2-receptoringranularcellGFRNaClamountinthemaculadensaRegulationofreninreleaseAngiotensinⅡFacilitatesynthesisandsecretionofaldosterone(腎上腺皮質(zhì)球狀帶）StimulatereabsorptionofNaClintheproximaltubuleIncreasereleaseofADHInducethirst.ApotentvasoconstrictorUrine球狀帶：醛固酮束狀帶：糖皮質(zhì)激素網(wǎng)狀帶：雄激素球狀帶束狀帶網(wǎng)狀帶Aldosterone（醛固酮）SecretionZonaglomerulosaoftheadrenalcortexFunctionStimulatethereabsorptionofNa+andthesecretionofK+inthedistaltubuleandcollectingductIncreasesNa+channelinluminalmembraneInduceenzymesforATP

synthesisinmitochondriaStimulatesNa+pumpinbasolateralmembraneIncreasesK+secretion

(胞內(nèi)高K+

和小管腔內(nèi)負(fù)電位）

IncreaseCl-reabsorptionAldosteroneinducedproteinsECFLumenRegulationofaldosterone

AgⅡ

[K+](0.5-1.0mmol/L)

高血壓診斷：-收縮壓》140mmHg；-收縮壓》90mmHg

高血壓分類-原發(fā)性高血壓-繼發(fā)性高血壓

-腎性高血壓

-內(nèi)分泌疾病

-主動脈狹窄

腎實質(zhì)病變或腎動脈狹窄Cushing’sSyndrome治療高血壓常用藥物1）利尿劑：雙氫克尿塞2）β受體阻滯劑：雙氫克尿塞3）鈣通道阻滯劑

(Calciumchannelblocker）

-氨氯地平（絡(luò)活喜）；硝苯地平緩釋片

4）血管緊張素轉(zhuǎn)換酶抵制劑(ACEI)-卡托普利（開搏通）；苯那普利（洛汀新）5）血管緊張素Ⅱ受體阻滯劑(ARB）

-氯沙坦（科素亞）和纈沙坦6）α受體阻滯劑：哌唑嗪

InhibitreabsorptionofNaClincollectingductInhibitreninsecretionInhibitaldosteronesecretionInhibitADHsecretionAtrialnatriureticpeptide(ANP，心房鈉尿肽)Release：心房受牽拉（血容量增加）HyperaldosteronismorConn’ssyndorme

(原發(fā)性醛固酮增多癥)，病因：腎上腺皮質(zhì)（球狀帶）腫瘤或增生癥狀：

-高血壓

-低血鉀及低鉀癥候群（肌肉無力，腎濃縮功能下降，ECG缺鉀及心率失常）

-代謝性堿中毒Simonisa54-year-oldprofessorwhomaintainsahealthylifestyle.Recently,heexperiencedgeneralizedmuscleweaknessandheadaches.Heattributedtheheadachetothestressofpreparinghisgrant.Simonwenttothehospitalanddidseveralexaminations.Hisbloodpressurewassignificantlyelevatedat180/110mmHg.HisLaboratorytestswerelistedintable1.Arterialblood

pH:7.5/PCO248mmHg（normal：40）VenousbloodNa+142mEq/L(normal:140)K+2.0mEq/L(normal:4.5)HCO3-36mEq/L(normal:24)Cl-98mEq/L(normal:105)creatinine1.1mg/dl(normal:1.2)UrineNa+excretion200mEq/24h(normal)K+excretion1350mEq24h(elevated)24hcatecholaminenormalThephysiciansuspectedSimon’shypertensionwascausedbyanabnormalityintherenin-angiotension–aldosteronesystem.Heorderedadditionaltests:

plasmareninactivity:dereasedserumaldosterone:increasedserumcortisol:normalAcomputedtomographicscanconfirmedthepresenceofasingleadenoma(腺瘤）ontheleftadrenalgland.ThetestconfirmedthediagnosisthatProfSimonhadhyperaldosteronismWhatfactorsmayelevateSimon’sbloodpressure?

Whatspecificetiologyisruledoutbythenormalvaluefor24-hoururinarycatecholamineexcretion?Pa=cardiacoutput*TPR搏出量(心肌收縮力,

前/后負(fù)荷）+心率交感N縮血管物質(zhì)Pheochromocytoma(腎上腺嗜鉻細(xì)胞瘤瘤）wasruledoutBynormal24-hoururinarycatecholamineexcretion2.ThephysiciansuspectedSimonhadprimary

hyperaldosteronism.Howdoesanincreased

aldosteronelevelcauseincreasedbloodpressure?IncreasedaldosteroneincreasedNa+reabsorptionandK+secretioninthelatedistaltubuleandcollectingducts.SincetheamountofNa+intheECFdeterminestheECFvolume,increasedbloodvolumeproducesanincreaseinvenousreturn,thenthroughtheFrank-Starlingmechanism,increasecardiacoutput.3.ExplainwhySimon’surinaryNa+

excretionwasnormal.

Thisiscalledescapefromaldosterone(醛固酮逃逸）1）ECFvolumeexpansioninhibitsrenalsympatheticnerveactivity,whichinhibitsNa+reabsorptionintheproximaltubule.2)ECFvolumeexpansioncausesdilutionoftheperitubularcapillaryproteinconcentration,leadingtothedecreaseinNa+reabsorptioninproximaltubules3)ECFvolumeexpansionstimulatethesecretionofartrialnatriureticpeptide(ANP)4.Whatexplanationcanyougivefor

ProfessorSimons’hypokalemia?AldosteronestimulatesK+secretionbytheprinciplecellsoflatedistaltubulesandcollectingducts.5.ExplainProfessor’smuscleweaknessbased

onhisseverehypokalemia

WhentheextracellularK+concentrationislowerthannormal,therestingmembranepotentialoftheskeletalmusclecellsemorenegative.DecreasedplasmaCa2+-細(xì)胞外液量或BP升高抑制近端小管對Na+及水的重新收，從而減少Ca2+吸收（80%Ca2+溶劑拖曳方式吸收）-代謝性堿中毒減少Ca2+重吸收。6.Whatacid-baseabnormalitydidprofessorSimonhave?

Whatistheappropriatecompensationforthisdisorder?TheincreasedarterialpH7.5andHCO3-areconsistentwithmetabolicalkalisis.InadditiontoincreaseNa+reabsorptionandK+secretion,aldosteronestimulateH+secretionbytheintercalatedcellsofthelatedistaltubuleandcollectingduct.ThisH+secretionislinkedtoreabsorptiontoHCO3-,producingthemetabolicalkalosis.

Section６

Clearance(清除率）

兩腎在單位時間（每分鐘）內(nèi)能將多少毫升血漿中的某一物質(zhì)完全清除出去。這個完全清除了該物質(zhì)的血漿毫升數(shù)稱為該物質(zhì)的清除率(ml/min)

Thevolumeofplasmaclearedofaspecificsubstanceperminute一、Definitionofclearance

腎臟清除某物質(zhì)的量，相當(dāng)于多少毫升血漿所含該物質(zhì)的量

PC=UV(mg/min)

C=UV/P(ml/min)C=renalclearance(ml/min)P=plasmaconcentration(mg/dl)ofthesubstanceU=urineconcentration(mg/dl)ofthesubstanceV=flowrateofurineformation(ml/min)二、Calculationofclearance

某甲每分鐘尿量(V)1ml/min尿中某物質(zhì)的濃度（U）100mg/100ml血漿中該物質(zhì)的濃度（P）1mg/100ml

該物質(zhì)的血漿清除率

C=U×V／P＝100ml/min葡萄糖清除率：0ml/min尿素清除率：70ml/min

(三）Significanceofdetectingclearance

MeasuringGFRMeasuringrenalbloodflowDeducingthefunctionoftherenaltubule

Inulinisfiltered,butnotreabsorbedorsecretedbyrenaltubules

U×V=GFR×P C=GFR=U×V/P

=C=125ml/min125mg/100ml×1ml/min1mg/100ml1.MeasuringGFR

-ClearanceofInulin(菊粉清除率）

-Clearanceofendogenouscreatinine

（內(nèi)生肌酐清除率）U×V=C×PC=660ml/min（C：腎血漿流量）

RPF=C/55%=1200ml/min（血漿占全血55%）2.Detectingrenalbloodflow(RBF)

血漿中某一物質(zhì)在腎循環(huán)一周后完全被清除

Diodrast(碘銳特）orPAH（對氨基馬尿酸）

3.Deducingthefunctionofrenaltubule

C>GFR:secretion(肌酐C=175ml/min)

C<GFR:reabsorption

(ureaC=70ml/min)Section7

Micturition(尿的排放）Micturitionistheprocessbywhichtheurinarybladderemptieswhenitesfilledandisaspinalreflexcontrolledbythehighercenters150-250mL:尿意350-400mL：>700mL:痛覺及失控volumePressureInternalsphincterExternalsphincter

Detrusor（逼尿肌）

PelvicN（盆N，副交感）

HypogastricN

（腹下N，交感）PudendalN（陰部N)Micturitionreflex

膀胱內(nèi)尿量（400-500ml）

膀胱牽張感受器（+）盆神經(jīng)腦干、大腦皮層排尿反射高級中樞骶髓排尿反射初級中樞盆神經(jīng)膀胱逼尿?。虻纼?nèi)括約?。虻栏惺芷鳎ǎ╆幉可窠?jīng)尿道外括約肌開放

排尿陰部神經(jīng)Centraldiabetesinsipidus

(中樞性尿崩癥）Lisaisapostgraduatestudentwhoworkedpart-timeinapediatrician’soffice.RecentlyLisa’slifeseemedtorevolvearoundbeingclosetoabathroomandadrinkingfountain.Shewasurinatingeveryhour(polyuria)anddrinkingmorethan5Lofwaterdaily(polydipsia).Lisa’semployerwasconcernedandwonderedifshehadapsychiatricdisorderinvolvingcompulsivewaterdrinking(primarypolydipsia)ordiabetesinsipidusLisamadeanappointmentwithherphysician.Herphysicianfoundthephysicalexaminationwerenormal.Herbloodpressurewas105/70mmHg,herheartratewas85beats/min.

Lisa’sLaboratorytestvalues:

plasmaUrine

Na+:147mEqu/L(normal:140)Osmolarity:301mOsm/L(normal:290)70mOsm/LGlucose90mg/dl(70-100mg/dl)negativeLisa’sphysicianperformeda2-hourwaterdeprivation

test.Attheendofthetest,Lisa’surineosmolarityremainedat70mOsm/L.LisawastheninjectedsubcultaneoulywithdDAVP(ananalogueofargininevasopression).Afterinjection,Lisa’surineosmolarityincreasedto500mOsm/L.Becauseshehadnohistoryofheadinjuryandsubsequentmagneticresonanceimagingscansruledoutabraintumor,Lisa’sphysicianconcludedthatLisahaddevelopedaformofcentraldiabetesinsipidusLisastartedtreatmentwithdDAVPnasalspray.Shedescribedthesprayasamazing.AslongasLisausedthenasalspray,herurineoutputisnormal,andsheisnolongerconstantlythirsty.Whatisthenormalvalueforurineosmolarity?Describethemechanism

thatregulatetheurineosmolarityUrineosmolarity:50-1200mOsm/L>300mOsm/L:hyperosmoticurine<300mOsm/L:hyposmoticurineOsmoticgradientinrenalmedullaUrinaryconcentration&dilution

ADHPermeabilityofH2OIndistaltubuleandcollectingductThickaccendinglimbUreaNaClVasarectaTheinitialtestonLisa’bloodandurine

suggestedthatthecauseofthepolyuriawas

not