WGU pathophysiology D236 Questions with Correct Answers 2025

WGU pathophysiology D236 Questions
with Correct Answers 2025
WhatAisAStarling'sALawAofACapillaryAforces?A

HowAdoesAthisAexplainAwhyAaAnutritionallyAdeficientAchildAwouldAhaveAedema?A-
ACORRECTAANSWERS-

Starling'sALawAdescribesAhowAfluidsAmoveAacrossAtheAcapillaryAmembrane.AThereAareAtwo
AmajorAopposingAforcesAthatAactAtoAbalanceAeachAother,AhydrostaticApressureA(pushingAwa

terAoutAofAtheAcapillaries)AandAosmoticApressureA(includingAonconticApressure,AwhichApush
esAfluidAintoAtheAcapillaries).A

BothAelectrolytesAandAproteinsA(onconticApressure)AinAtheAbloodAaffectAosmoticApressure,A
highAelectrolyteAandAproteinAconcentrationsAinAtheAbloodAwouldAcauseAwaterAtoAleaveAtheA
cellsAandAinterstitialAspaceAandAenterAtheAbloodAstreamAtoAdiluteAtheAhighAconcentrations.A

On,AtheAotherAhand,AlowAelectrolyteAandAproteinAconcentrationsA(asAseenAinAaAnutritionallyA
deficientAchild)AwouldAcauseAwaterAtoAleaveAtheAcapillariesAandAenterAtheAcellsAandAintersti
tialAfluidAwhichAcanAleadAtoAedema.
HowAdoesAtheARAASA(Renin-Angiotensin-
AldosteroneASystem)AresultAinAincreasedAbloodAvolumeAandAincreasedAbloodApressure?A-
ACORRECTAANSWERS-

AAdropAinAbloodApressureAisAsensedAbyAtheAkidneysAbyAlowAperfusion,AwhichAinAturnAbegins
AtoAsecreteArenin.A




ReninAthenAtriggersAtheAliverAtoAproduceAangiotensinogen,AwhichAisAconvertedAtoAAngioten
sinAIAinAtheAlungsAandAthenAangiotensinAIIAbyAtheAenzymeA

Angiotensin-
convertingAenzymeA(ACE).AAngiotensinAIIAstimulatesAperipheralAarterialAvasoconstrictionA
whichAraisesABP.A

AngiotensinAIIAisAalsoAstimulatingAtheAadrenalAglandAtoAreleaseAaldosterone,AwhichAactsAto
AincreaseAsodiumAandAwaterAreabsorptionAincreasingAbloodAvolume,AwhileAalsoAincreasedA

potassiumAsecretionAinAurine.
HowAcanAhyperkalemiaAleadAtoAcardiacAarrest?A-ACORRECTAANSWERS-
NormalAlevelsAofApotassiumAareAbetweenA3.5AandA5.2AmEq/dL.AHyperkalemiaArefersAtoApo
tassiumAlevelsAhigherAthatA5.2AmEq/dL.A

AAmajorAfunctionAofApotassiumAisAtoAconductAnerveAimpulsesAinAmuscles.ATooAlowAandAmu
scleAweaknessAoccursAandAtooAmuchAcanAcauseAmuscleAspasms.A

,ThisAisAespeciallyAdangerousAinAtheAheartAmuscleAandAanAirregularAheartbeatAcanAcauseAa
AheartAattack

TheAbodyAusesAtheAProteinABufferingASystem,APhosphateABufferingASystem,AandACarboni
cAAcid-
BicarbonateASystemAtoAregulateAandAmaintainAhomeostaticApH,AwhatAisAtheAconsequence
AofAaApHAimbalanceA-ACORRECTAANSWERS-

ProteinsAcontainAmanyAacidicAandAbasicAgroupAthatAcanAbeAaffectedAbyApHAchanges.AAnyAi
ncreaseAorAdecreaseAinAbloodApHAcanAalterAtheAstructureAofAtheAproteinA(denature),Athereb
yAaffectingAitsAfunctionAasAwell
DescribeAtheAlaboratoryAfindingsAassociatedAwithAmetabolicAacidosis,AmetabolicAalkalosis,
ArespiratoryAacidosisAandArespiratoryAalkalosis.A(ieArelativeApHAandACO2Alevels).A-

ACORRECTAANSWERS-NormalAABGsA(ArterialABloodAGases)ABloodApH:A7.35-

7.45APCO2:A35-45AmmAHgAPO2:A90-100AmmAHgAHCO3-:A22-26AmEq/LASaO2:A95-100%A

RespiratoryAacidosisAandAalkalosisAareAmarkedAbyAchangesAinAPCO2.AHigherA=AacidosisAa
ndAlowerA=AalkalosisA

MetabolicAacidosisAandAalkalosisAareAcausedAbyAsomethingAotherAthanAabnormalACO2Alev
els.AThisAcouldAincludeAtoxicity,Adiabetes,ArenalAfailureAorAexcessiveAGIAlosses.A

HereAareAtheArulesAtoAfollowAtoAdetermineAifAisArespiratoryAorAmetabolicAinAnature.A-
IfApHAandAPCO2AareAmovingAinAoppositeAdirections,AthenAitAisAtheApCO2AlevelsAthatAareAca
usingAtheAimbalanceAandAitAisArespiratoryAinAnature.A

-
IfAPCO2AisAnormalAorAisAmovingAinAtheAsameAdirectionAasAtheApH,AthenAtheAimbalanceAisAm
etabolicAinAnature.
TheAanionAgapAisAtheAdifferenceAbetweenAmeasuredAcationsA(Na+AandAK+)AandAmeasured
AanionsA(Cl-AandAHCO3-

),AthisAcalculationAcanAbeAusefulAinAdeterminingAtheAcauseAofAmetabolicAacidosis.A

WhyAwouldAanAincreasedAanionAgapAbeAobservedAinAdiabeticAketoacidosisAorAlacticAacidos
is?A-ACORRECTAANSWERS-
TheAanionAgapAisAtheAcalculationAofAunmeasuredAanionsAinAtheAblood.A

LacticAacidAandAketonesAbothAleadAtoAtheAproductionAofAunmeasuredAanions,AwhichAremov
eAHCO3-
A(aAmeasuredAanion)AdueAtoAbufferingAofAtheAexcessAH+AandAthereforeAleadsAtoAanAincreas

eAinAtheAAG.
WhyAisAitAimportantAtoAmaintainAaAhomeostaticAbalanceAofAglucoseAinAtheAbloodA(ieAdescrib
eAtheApathogenesisAofAdiabetes)?A-ACORRECTAANSWERS-
InsulinAisAtheAhormoneAresponsibleAforAinitiatingAtheAuptakeAofAglucoseAbyAtheAcells.ACellsA
useAglucoseAtoAproduceAenergyA(ATP).A

,InAaAnormalAindividual,AwhenAbloodAglucoseAincreases,AtheApancreasAisAsignaledAtoAprodu
cedAinAinsulin,AwhichAbindsAtoAinsulinAreceptorsAonAaAcellsAsurfaceAandAinitiatesAtheAuptake
AofAglucose.A




GlucoseAisAaAveryAreactiveAmoleculeAandAifAleftAinAtheAblood,AitAcanAstartAtoAbindAtoAotherApr
oteinsAandAlipids,AwhichAcanAleadAtoAlossAofAfunction.A

AGEsAareAadvancedAglycationAendAproductsAthatAareAaAresultAofAglucoseAreactingAwithAthe
AendothelialAlining,AwhichAcanAleadAtoAdamageAinAtheAheartAandAkidneys.

CompareAandAcontrastATypeAIAandATypeAIIADiabetesA-ACORRECTAANSWERS-
TypeAIAdiabetesAisAcausedAbyAlackAofAinsulin.AWithAoutAinsulinAsignaling,AglucoseAwillAnotAb
eAtakenAintoAtheAcellAandAleadsAtoAhighAbloodAglucoseA(hyperglycemia).ATypeAIAisAusuallyAtr
eatedAwithAinsulinAinjections.A

TypeAIIAdiabetesAisAcausedAbyAaAdesensitizationAtoAinsulinAsignaling.ATheAinsulinAreceptors
AareAnoAlongerArespondingAtoAinsulin,AwhichAalsoAleadsAtoAhyperglycemia.A




TypeAIIAisAusuallyAtreatedAwithAdrugsAtoAincreaseAtheAsensitizationAtoAinsulinA(metformin),A
dietaryAandAlife-styleAchangesAorAinsulinAinjections.
DescribeAsomeAreasonsAforAaApatientAneedingAdialysisA-ACORRECTAANSWERS-AEIOU-
acidosis.AElectrolytes,AIntoxication/Ingestion,Aoverload,Auremia.APatientsAwithAkidneyAorAh
eartAfailure.A

AAbuildAupAofAphosphates,AureaAandAmagnesiumAareAremovedAfromAtheAbloodAusingAaAse
mi-permeableAmembraneAandAdialysate.A

AEIOU:A
A—acidosis;A
E—electrolytesAprincipallyAhyperkalemia;A
I—ingestionsAorAoverdoseAofAmedications/drugs;A
O—overloadAofAfluidAcausingAheartAfailure;A
U—uremiaAleadingAtoAencephalitis/pericarditis
CompareAandAcontrastAhemodialysisAandAperitonealAdialysis.A

WhatAareAsomeAreasonsAforAaApatientAchoosingAoneAoverAtheAother?A-
ACORRECTAANSWERS-

HemodialysisAusesAaAmachineAtoApumpAbloodAfromAtheAbodyAinAoneAtubeAwhileAdialysateA(
madeAofAwater,AelectrolytesAandAsalts)AisApumpedAinAtheAseparateAtubeAinAtheAoppositeAdir
ection.AWasteAfromAtheAbloodAdiffusesAthroughAtheAsemipermeableAmembraneAseparating
AtheAbloodAfromAtheAdialysate.A




PeritonealADialysisAdoesAnotAuseAaAmachine,AbutAinsteadAinjectsAaAsolutionAofAwaterAandAg
lucoseAintoAtheAabdominalAcavity.ATheAperitoneumAactsAasAtheAmembraneAinsteadAofAdialy
sisAtubing.ATheAwasteAproductsAdiffuseAintoAtheAabdominalAcavityAandAtheAwasteAsolutionAi
sAthenAdrainedAfromAtheAbody.A

, PeritonealAdialysisAoffersAcontinuousAfiltrationAandAisAlessAdisruptionAtoAtheApatient'sAdailyA
routines.AHowever,AitAdoesArequireAsomeAtrainingAofAtheApatientAandAisAnotArecommendedA
forAindividualsAwhoAareAoverweightAorAhaveAsevereAkidneyAfailure.A

HemodialysisAprovidesAmedicalAcare,AbutA3AtimesAaAweekAforAseveralAhoursAsittingAatAaAho
spitalAorAclinic.AIndividualsAwithAacuteAkidneyAfailureAareArecommendedAtoAuseAhemodialys
is.
HowAdoesAhomeostasisAandAmaintainingAoptimalAphysiologicalAhealthAimpactAyourAwellbei
ng?A-ACORRECTAANSWERS-
HomeostasisAactsAtoAcreateAaAconstantAandAstableAenvironmentAinAtheAbodyAdespiteAinter
nalAandAexternalAchanges.AProteinsAandAotherAcellularAprocessesArequireAoptimalAconditio
nsAinAorderAtoAcarryAoutAtheirAfunctions.A

AlterationsAinApH,AsaltAconcentration,Atemperature,AglucoseAlevels,Aetc.AcanAhaveAnegativ
eAeffectsAonAhealth,AsoAitAisAvitalAforAmechanismsAthatAregulateAhomeostasisAtoAfunctionApr
operlyAforAmaintainingAgoodAhealth
DifferentiateAbetweenAInnateAImmunityAandAAdaptiveAImmunityA?A-
ACORRECTAANSWERS-

TheAinnateAimmuneAsystemAencompassesAphysicalAbarriersAandAchemicalAandAcellularAde
fenses.APhysicalAbarriersAprotectAtheAbodyAfromAinvasion.ATheseAincludeAthingsAlikeAtheAs
kinAandAeyelashes.AChemicalAbarriersAareAdefenseAmechanismsAthatAcanAdestroyAharmful
Aagent.AExamplesAincludeAtears,Amucous,AandAstomachAacid.A




CellularAdefensesAofAtheAinnateAimmuneAresponseAareAnon-
specific.ATheseAcellularAdefensesAidentifyApathogensAandAsubstancesAthatAareApotentiallyA
dangerousAandAtakesAstepsAtoAneutralizeAorAdestroyAthem.A

AdaptiveAimmunityAisAanAorganism'sAacquiredAimmunityAtoAaAspecificApathogen.AAsAsuch,Ai
t'sAalsoAreferredAtoAasAacquiredAimmunity.AAdaptiveAimmunityAisAnotAimmediate,AnorAdoesAi
tAalwaysAlastAthroughoutAanAorganism'sAentireAlifespan,AalthoughAitAcan.A

TheAadaptiveAimmuneAresponseAisAmarkedAbyAclonalAexpansionAofATAandABAlymphocytes,A
releasingAmanyAantibodyAcopiesAtoAneutralizeAorAdestroyAtheirAtargetAantigen
WhatAisAaAwayAthatAAdaptiveAImmunityAcanArecruitAinnateAimmunity?A-
ACORRECTAANSWERS-

TheAinnateAimmuneAresponseAtoAmicrobesAstimulatesAadaptiveAimmuneAresponsesAandAin
fluencesAtheAnatureAofAtheAadaptiveAresponses.A

Conversely,AadaptiveAimmuneAresponsesAoftenAworkAbyAenhancingAtheAprotectiveAmecha
nismsAofAinnateAimmunity,AmakingAthemAmoreAcapableAofAeffectivelyAcombatingApathogen
icAmicrobes
WhyAareAsomeAinfectionsAharderAonAchildrenAwhileAotherAinfectionsAareAharderAonAtheAeld
erly?A-ACORRECTAANSWERS-
ChildrenAhaveAnotAbeenAexposedAtoAmanyApathogensAyet,AsoAtheyAlackAmemoryAcellsAand
AhaveAnotAbuilt-upAimmunityAyet.A