WGU PATHOPHYSIOLOGY D236 ACTUAL EXAM ALL QUESTIONS AND WELL ELABORATED ANSWERS TOP RATED VERSION FOR ALREADY A+ GRADED HIGHLY RECOMMENDED |NEW AND REVISED

WGU PATHOPHYSIOLOGY D236
ACTUAL EXAM ALL QUESTIONS AND
WELL ELABORATED ANSWERS TOP
RATED VERSION FOR ALREADY A+
GRADED HIGHLY RECOMMENDED
|NEW AND REVISED
WhatmismStarling'smLawmofmCapillarymforces?m



Howmdoesmthismexplainmwhymamnutritionallymdeficientmchildmwouldmhavemedema?m-
mCORRECTmANSWERmStarling'smLawmdescribesmhowmfluidsmmovemacrossmthemcapillarymmembrane.


mTheremaremtwommajormopposingmforcesmthatmactmtombalancemeachmother,mhydrostaticmpressurem(p


ushingmwatermoutmofmthemcapillaries)mandmosmoticmpressurem(includingmonconticmpressure,mwhich
mpushesmfluidmintomthemcapillaries).m




Bothmelectrolytesmandmproteinsm(onconticmpressure)minmthembloodmaffectmosmoticmpressure,mhighm
electrolytemandmproteinmconcentrationsminmthembloodmwouldmcausemwatermtomleavemthemcellsmand
minterstitialmspacemandmentermthembloodmstreammtomdilutemthemhighmconcentrations.m




On,mthemothermhand,mlowmelectrolytemandmproteinmconcentrationsm(asmseenminmamnutritionallymdef
icientmchild)mwouldmcausemwatermtomleavemthemcapillariesmandmentermthemcellsmandminterstitialmflui
dmwhichmcanmleadmtomedema.



HowmdoesmthemRAASm(Renin-Angiotensin-
AldosteronemSystem)mresultminmincreasedmbloodmvolumemandmincreasedmbloodmpressure?m-
mCORRECTmANSWERmAmdropminmbloodmpressuremismsensedmbymthemkidneysmtriggersmprodcutionmof


mrenin




Reninmtriggersmthemlivermtomproducemangiotensinogen,mandmconvertsmitmintomAngiotensinmImandma
ngiotensinmIImbymthemenzymem

,Angiotensin-
convertingmenzymem(ACE).mAngiotensinmIImstimulatesmperipheralmarterialmvasoconstrictionmwhichm
raisesmBP.m



AngiotensinmIImstimulatemthemadrenalmglandmtomreleasemaldosterone,mwhichmactsmtomincreasemsodi
ummandmwatermabsorptionmincreasingmbloodmvolume,mwhilemalsomincreasedmpotassiummsecretionm
inmurine.



Howmcanmhyperkalemiamleadmtomcardiacmarrest?m-
mCORRECTmANSWERmNormalmlevelsmofmpotassiummarembetweenm3.5mandm5.2mmEq/dL.mHyperkale


miamrefersmtompotassiummlevelsmhighermthatm5.2mmEq/dL.m



Ammajormfunctionmofmpotassiummismtomconductmnervemimpulsesminmmuscles.mToomlowmcausesmmus
clemweaknessmtoommuchmcanmcausemmusclemspasms.m



Thismismespeciallymdangerousminmthemheartmmusclemandmanmirregularmheartbeatmcanmcausemamhear
tmattack



ThembodymusesmthemProteinmBufferingmSystem,mPhosphatemBufferingmSystem,mandmCarbonicmAcid-
BicarbonatemSystemmtomregulatemandmmaintainmhomeostaticmpH,mwhatmismthemconsequencemofmam
pHmimbalancem-
mCORRECTmANSWERmAnymincreasemormdecreaseminmbloodmpHmcanmaltermthemstructuremofmthemprot


einm(denature),mtherebymaffectingmitsmfunctionmasmwell



Describemthemlaboratorymfindingsmassociatedmwithmmetabolicmacidosis,mmetabolicmalkalosis,mrespi
ratorymacidosismandmrespiratorymalkalosis.m(iemrelativempHmandmCO2mlevels).m-
mCORRECTmANSWERmNormalmABGsm(ArterialmBloodmGases)mBloodmpH:m7.35-7.45mPCO2:m35-


45mmmmHgmPO2:m90-100mmmmHgmHCO3-:m22-26mmEq/LmSaO2:m95-100%m

,Metabolicmacidosismphmlessmthanm7.35mandmlowmHC03.mMetabolicmalkolosismphmgreatermthanm7.35
mandmsomismhco3mbothmofmthesemcanmbemcausedmmymdka.mifmthemphmandmpco2mlevelsmaremgoingminmt


hemsamemdirectionmitmismmetabolicmifmtheymaremgoingminmamdifferentmdirectionmitmismrespiratory

Respiratorymalkolosismphmgreatermthanm7.35andmpco2mismdecreased.mrepsiratorymacidosismismphmles
smthanm7.35mandmpco2mgreatermthan



Themanionmgapmismthemdifferencembetweenmmeasuredmcationsm(Na+mandmK+)mandmmeasuredmanio
nsm(Cl-mandmHCO3-
),mthismcalculationmcanmbemusefulminmdeterminingmthemcausemofmmetabolicmacidosis.m



Whymwouldmanmincreasedmanionmgapmbemobservedminmdiabeticmketoacidosismormlacticmacidosis?m-
mCORRECTmANSWERmThemanionmgapmismthemcalculationmofmunmeasuredmanionsminmthemblood.m




Lacticmacidmandmketonesmleadmtomthemproductionmofmunmeasuredmanions,mthereforemleadsmtomanmi
ncreaseminmthemAG.



Whymismitmimportantmtommaintainmamhomeostaticmbalancemofmglucoseminmthembloodm(iemdescribemt
hempathogenesismofmdiabetes)?m-
mCORRECTmANSWERmInsulinmismthemhormonemresponsiblemforminitiatingmthemuptakemofmglucosemby


mthemcells.mCellsmusemglucosemtomproducemenergym(ATP).m




Inmamnormalmindividual,mwhenmbloodmglucosemincreases,mthempancreasmismsignaledmtomproducedmi
nminsulin,mwhichmbindsmtominsulinmreceptorsmonmamcellsmsurfacemandminitiatesmthemuptakemofmgluco
se.m



Glucosemifmleftminmthemblood,mcanmtombindmtomproteinsmandmlipids,mwhichmcanmleadmtomlossmofmfunc
tion.mleadingmtomdamageminmthemheartmandmkidneys.



ComparemandmcontrastmTypemImandmTypemIImDiabetesm-
mCORRECTmANSWERmTypemImdiabetesmismcausedmbymlackmofminsulin.mWithmoutminsulinmsignaling,mgl

, ucosemwillmnotmbemtakenmintomthemcellmandmleadsmtomhighmbloodmglucosem(hyperglycemia).mTypemIm
ismusuallymtreatedmwithminsulinminjections.m



TypemIImdiabetesmismcausedmbymamdesensitizationmtominsulinmsignaling.mTheminsulinmreceptorsmarem
nomlongermrespondingmtominsulin,mwhichmalsomleadsmtomhyperglycemia.m



TypemIImismusuallymtreatedmwithmdrugsmtomincreasemthemsensitizationmtominsulinm(metformin),mdieta
rymandmlife-stylemchangesmorminsulinminjections.



Describemsomemreasonsmformampatientmneedingmdialysism-mCORRECTmANSWERmAEIOU-
acidosis.mElectrolytes,mIntoxication/Ingestion,moverload,muremia.mPatientsmwithmkidneymormheartmf
ailure.m



Ambuildmupmofmphosphates,mureamandmmagnesiummaremremovedmfrommthembloodmusingmamsemi-
permeablemmembranemandmdialysate.m



AEIOU:m

A—acidosis;m

E—electrolytesmprincipallymhyperkalemia;m

I—ingestionsmormoverdosemofmmedications/drugs;m

O—overloadmofmfluidmcausingmheartmfailure;m

U—uremiamleadingmtomencephalitis/pericarditis



Comparemandmcontrastmhemodialysismandmperitonealmdialysis.m



Whatmaremsomemreasonsmformampatientmchoosingmonemovermthemother?m-
mCORRECTmANSWERmHemodialysismusesmammachinemtompumpmbloodmfrommthembodyminmonemtube


mwhilemdialysatem(mademofmwater,melectrolytesmandmsalts)mismpumpedminmthemseparatemtubeminmth