Wm WGU D236 PATHOPHYSIOLOGY
m m
WGU D236 PATHOPHYSIOLOGY EXAM LATEST 2024
m m m m m m
QUESTIONS AND ANSWERS GRADED A+ m m m m
1. What is Starling's Law of Capillary forces? How does t
m m m m m m m m m
hismexplainmwhymamnutritionallymdeficientmchildmwouldmhaveme
dema?
Starling’sm Lawm describesm howm fluidsm movem acrossm them capillarym membrane.
Theremaremtwommajormopposingmforcesmthatmactmtombalancemeachmother,mhydrost
aticmpressurem(pushingmwatermoutmofmthemcapillaries)mandmosmoticmpressurem(in
cludingmonconticmpressure,mwhichmpushesmfluidmintomthemcapillaries).mBothmelec
trolytesmandmproteinsm(onconticmpressure)minmthembloodmaffectmosmoticmpressur
e,mhighmelectrolytemandmproteinmconcentrationsminmthembloodmwouldmcausemwate
rmtomleavemthemcellsmandminterstitialmspacemandmentermthembloodmstreammtomdilute
mthemhighmconcentrations.mOn,mthemothermhand,mlowmelectrolytemandmproteinm con
centrationsm(asmseenminmamnutritionallymdeficientmchild)mwouldmcausemwatermtoml
eavemthemcapillariesmandmentermthemcellsmandminterstitialmfluidmwhichmcanmleadmt
omedema.
2. How does the RAAS (Renin-Angiotensin-
m m m m
AldosteronemSystem)mresultminmincreasedmbloodmvolu
m
memandmincreasedmbloodmpressure?
Amdropminmbloodmpressuremismsensedmbymthemkidneysmbymlowmperfusion,m
whichminmturnmbeginsmtomsecretemrenin.mReninmthenmtriggersmthemlivermtomproduc
emangiotensinogen,mwhichmismconvertedmtomAngiotensinmIminmthemlungsmandmthe
nmangiotensinmIImbymthemenzymemAngiotensin-convertingmenzymem(ACE).
AngiotensinmIImstimulatesmperipheralmarterialmvasoconstrictionmwhichmraisesmB
P.mAngiotensinm IImism alsomstimulatingm themadrenalm glandmtomreleasem aldosteron
e,
,Wm WGU D236 PATHOPHYSIOLOGY
m m
whichmactsmtomincreasemsodiummandmwatermreabsorptionmincreasingmblo
odmvolume,mwhilemalsomincreasedmpotassiummsecretionminmurine.
3. How can hyperkalemia lead to cardiac arrest?
m m m m m m
Normalmlevelsmofmpotassiummarembetweenm3.5mandm5.2mmEq/dL.mHyperkale
miamrefersmtompotassiummlevelsmhighermthatm5.2mmEq/dL.mAmmajormfunctionmofmpo
tassiummismtomconductmnervemimpulsesminmmuscles.mToomlowmandmmusclemweaknes
smoccursmandmtoommuchmcanmcausemmusclemspasms.mThismismespeciallym dangerous
m inm them heartm musclem andm anm irregularm heartbeatm canm cause m
amheartmattack.
4. The body uses the Protein Buffering System, Phospha
m m m m m m m
temBufferingmSystem,mandmCarbonicmAcid-
mBicarbonatemSystemmtomregulatemandmmaintainmhomeosta
ticmpH,mwhatmismthemconsequencemofmampHmimbalance?
Proteinsmcontainmmanymacidicmandmbasicmgroupmthatmcanmbemaffectedmb
ympHmchanges.mAnymincreasemormdecreaseminmbloodmpHmcanmaltermthemstructur
emofmthemproteinm(denature),mtherebymaffectingmitsmfunctionmasmwell.
5. Describemthemlaboratorymfindingsmassociatedmwit
hmmetabolic
Wantmtomearnm$103mpermmonth?
,Wm WGU D236 PATHOPHYSIOLOGY
m m
acidosis, metabolic alkalosis, respiratory acidosis
andmrespiratorymalkalosis.m(iemrelativempHmandmC
O2mlevels).
, Wm WGU D236 PATHOPHYSIOLOGY
m m
NormalmABGsm(ArterialmBloodmGases)mBloodmpH:m7.35-
7.45mPCO2:m35-45mmmmHgmPO2:m90-100mmmmHgmHCO3-:m22-
26mmEq/LmSaO2:m95-100%
RespiratorymacidosismandmalkalosismaremmarkedmbymchangesminmPCO2.mHigher
=m acidosism andmlowerm =m alkalosism Metabolicmacidosism andmalkalosism aremcau
sedmbymsomethingmothermthanmabnormalmCO2mlevels.mThismcouldmincludemtox
icity,mdiabetes,mrenalmfailuremormexcessivemGImlosses.mHeremaremthemrulesmtomf
ollowmtomdeterminemifmismrespiratorymormmetabolicminmnature.m-
IfmpHmandmPCO2maremmovingminmoppositemdirections,mthenmitmismthempCO2mlev
elsmthatmaremcausingmthemimbalancemandmitmismrespiratoryminmnature.m-
IfmPCO2mismnormalmormismmovingmtinmthemsamemdirectionmasmthempH,mthenmthemi
mbalancemismmetabolicminmnature.
6. Themanionmgapmismthemdifferencembetweenmmeasuredmcationsm
(Na+mandmK+)mandmmeasuredmanionsm(Cl-mandmHCO3-
),mthismcalculationmcanmbemusefulminmdeterminingmthemcausemofm
metabolicmacidosis.mWhymwouldmanmincreasedmanionmgapmbemob
servedminmdiabeticmketoacidosismormlacticmacidosis?
Themanionmgapmismthemcalculationmofmunmeasuredmanionsminmthembloo
d.mLacticmacidmandmketonesmbothmleadmtomthemproductionmofmunmeasuredman
ions,mwhichmremovemHCO3-
m(ammeasuredmanion)mduemtombufferingmofmthemexcessmH+mandmthereforemlea
dsmtomanmincreaseminmthemAG.
7. Whymismitmimportantmtommaintainmamhomeostaticmbalan
cemofmglucoseminmthembloodm(iemdescribemthempathogenesism
ofmdiabetes)?
Insulinmismthemhormonemresponsiblemforminitiatingmthemuptakemofmgluco
sembymthemcells.mCellsmusemglucosemtomproducemenergym(ATP).mInmamnormalmin
dividual,mwhenmbloodmglucosemincreases,mthempancreasmismsignaledmtomprodu
cedminminsulin,mwhichmbindsmtominsulinmreceptorsmonmamcellsmsurfacemandminiti
atesmthemuptakemofmglucose.mGlucosemismamverymreactivemmoleculemandmifmleftmi
nmthemblood,mitmcanmstartmtombindmtomothermproteinsmandmlipids,mwhichmcanmleadm
tomlossmofmfunction.mAGEsmaremadvancedmglycationmendmproductsmthatmaremamr
esultmofmglucosemreactingmwithmthemendothelialmlining,mwhichmcanmleadmtomda
mageminmthemheartmandmkidneys.
8. Compare and contrast Type I and Type II Diabetes
m m m m m m m m
TypemImdiabetesmismcausedmbymlackmofminsulin.mWithmoutminsulinmsig
naling,mglucosemwillmnotmbemtakenmintomthemcellmandmleadsmtomhighmbloodmg
lucosem(hyperglycemia).mTypemImismusuallymtreatedmwithminsulinminjections
.mTypemIImdiabetesmismcausedmbymamdesensitizationmtominsulinmsignaling.mTh
eminsulinmreceptorsmaremnomlongermrespondingmtominsulin,mwhichmalsomleads
mtomhyperglycemia.m TypemIImismusuallymtreatedm withmdrugsmtomincreasemthem
sensitizationmtominsulinm(metformin),mdietarymandmlife-
stylemchangesmorminsulinminjections.
9. DescribemsomemreasonsmformampatientmneedingmdialysismAEIOU-
macidosis.m Electrolytes,m Intoxication/Ingestion,m overload,m uremia.m Patien
tsmwithmkidneymormheartmfailure.mAmbuildmupmofmphosphates,mureamandmma
gnesiummaremremoved
frommthembloodmusingmamsemi-
permeablemmembranemandmdialysate.mAEIOU:mA—macidosis;mE
m m
WGU D236 PATHOPHYSIOLOGY EXAM LATEST 2024
m m m m m m
QUESTIONS AND ANSWERS GRADED A+ m m m m
1. What is Starling's Law of Capillary forces? How does t
m m m m m m m m m
hismexplainmwhymamnutritionallymdeficientmchildmwouldmhaveme
dema?
Starling’sm Lawm describesm howm fluidsm movem acrossm them capillarym membrane.
Theremaremtwommajormopposingmforcesmthatmactmtombalancemeachmother,mhydrost
aticmpressurem(pushingmwatermoutmofmthemcapillaries)mandmosmoticmpressurem(in
cludingmonconticmpressure,mwhichmpushesmfluidmintomthemcapillaries).mBothmelec
trolytesmandmproteinsm(onconticmpressure)minmthembloodmaffectmosmoticmpressur
e,mhighmelectrolytemandmproteinmconcentrationsminmthembloodmwouldmcausemwate
rmtomleavemthemcellsmandminterstitialmspacemandmentermthembloodmstreammtomdilute
mthemhighmconcentrations.mOn,mthemothermhand,mlowmelectrolytemandmproteinm con
centrationsm(asmseenminmamnutritionallymdeficientmchild)mwouldmcausemwatermtoml
eavemthemcapillariesmandmentermthemcellsmandminterstitialmfluidmwhichmcanmleadmt
omedema.
2. How does the RAAS (Renin-Angiotensin-
m m m m
AldosteronemSystem)mresultminmincreasedmbloodmvolu
m
memandmincreasedmbloodmpressure?
Amdropminmbloodmpressuremismsensedmbymthemkidneysmbymlowmperfusion,m
whichminmturnmbeginsmtomsecretemrenin.mReninmthenmtriggersmthemlivermtomproduc
emangiotensinogen,mwhichmismconvertedmtomAngiotensinmIminmthemlungsmandmthe
nmangiotensinmIImbymthemenzymemAngiotensin-convertingmenzymem(ACE).
AngiotensinmIImstimulatesmperipheralmarterialmvasoconstrictionmwhichmraisesmB
P.mAngiotensinm IImism alsomstimulatingm themadrenalm glandmtomreleasem aldosteron
e,
,Wm WGU D236 PATHOPHYSIOLOGY
m m
whichmactsmtomincreasemsodiummandmwatermreabsorptionmincreasingmblo
odmvolume,mwhilemalsomincreasedmpotassiummsecretionminmurine.
3. How can hyperkalemia lead to cardiac arrest?
m m m m m m
Normalmlevelsmofmpotassiummarembetweenm3.5mandm5.2mmEq/dL.mHyperkale
miamrefersmtompotassiummlevelsmhighermthatm5.2mmEq/dL.mAmmajormfunctionmofmpo
tassiummismtomconductmnervemimpulsesminmmuscles.mToomlowmandmmusclemweaknes
smoccursmandmtoommuchmcanmcausemmusclemspasms.mThismismespeciallym dangerous
m inm them heartm musclem andm anm irregularm heartbeatm canm cause m
amheartmattack.
4. The body uses the Protein Buffering System, Phospha
m m m m m m m
temBufferingmSystem,mandmCarbonicmAcid-
mBicarbonatemSystemmtomregulatemandmmaintainmhomeosta
ticmpH,mwhatmismthemconsequencemofmampHmimbalance?
Proteinsmcontainmmanymacidicmandmbasicmgroupmthatmcanmbemaffectedmb
ympHmchanges.mAnymincreasemormdecreaseminmbloodmpHmcanmaltermthemstructur
emofmthemproteinm(denature),mtherebymaffectingmitsmfunctionmasmwell.
5. Describemthemlaboratorymfindingsmassociatedmwit
hmmetabolic
Wantmtomearnm$103mpermmonth?
,Wm WGU D236 PATHOPHYSIOLOGY
m m
acidosis, metabolic alkalosis, respiratory acidosis
andmrespiratorymalkalosis.m(iemrelativempHmandmC
O2mlevels).
, Wm WGU D236 PATHOPHYSIOLOGY
m m
NormalmABGsm(ArterialmBloodmGases)mBloodmpH:m7.35-
7.45mPCO2:m35-45mmmmHgmPO2:m90-100mmmmHgmHCO3-:m22-
26mmEq/LmSaO2:m95-100%
RespiratorymacidosismandmalkalosismaremmarkedmbymchangesminmPCO2.mHigher
=m acidosism andmlowerm =m alkalosism Metabolicmacidosism andmalkalosism aremcau
sedmbymsomethingmothermthanmabnormalmCO2mlevels.mThismcouldmincludemtox
icity,mdiabetes,mrenalmfailuremormexcessivemGImlosses.mHeremaremthemrulesmtomf
ollowmtomdeterminemifmismrespiratorymormmetabolicminmnature.m-
IfmpHmandmPCO2maremmovingminmoppositemdirections,mthenmitmismthempCO2mlev
elsmthatmaremcausingmthemimbalancemandmitmismrespiratoryminmnature.m-
IfmPCO2mismnormalmormismmovingmtinmthemsamemdirectionmasmthempH,mthenmthemi
mbalancemismmetabolicminmnature.
6. Themanionmgapmismthemdifferencembetweenmmeasuredmcationsm
(Na+mandmK+)mandmmeasuredmanionsm(Cl-mandmHCO3-
),mthismcalculationmcanmbemusefulminmdeterminingmthemcausemofm
metabolicmacidosis.mWhymwouldmanmincreasedmanionmgapmbemob
servedminmdiabeticmketoacidosismormlacticmacidosis?
Themanionmgapmismthemcalculationmofmunmeasuredmanionsminmthembloo
d.mLacticmacidmandmketonesmbothmleadmtomthemproductionmofmunmeasuredman
ions,mwhichmremovemHCO3-
m(ammeasuredmanion)mduemtombufferingmofmthemexcessmH+mandmthereforemlea
dsmtomanmincreaseminmthemAG.
7. Whymismitmimportantmtommaintainmamhomeostaticmbalan
cemofmglucoseminmthembloodm(iemdescribemthempathogenesism
ofmdiabetes)?
Insulinmismthemhormonemresponsiblemforminitiatingmthemuptakemofmgluco
sembymthemcells.mCellsmusemglucosemtomproducemenergym(ATP).mInmamnormalmin
dividual,mwhenmbloodmglucosemincreases,mthempancreasmismsignaledmtomprodu
cedminminsulin,mwhichmbindsmtominsulinmreceptorsmonmamcellsmsurfacemandminiti
atesmthemuptakemofmglucose.mGlucosemismamverymreactivemmoleculemandmifmleftmi
nmthemblood,mitmcanmstartmtombindmtomothermproteinsmandmlipids,mwhichmcanmleadm
tomlossmofmfunction.mAGEsmaremadvancedmglycationmendmproductsmthatmaremamr
esultmofmglucosemreactingmwithmthemendothelialmlining,mwhichmcanmleadmtomda
mageminmthemheartmandmkidneys.
8. Compare and contrast Type I and Type II Diabetes
m m m m m m m m
TypemImdiabetesmismcausedmbymlackmofminsulin.mWithmoutminsulinmsig
naling,mglucosemwillmnotmbemtakenmintomthemcellmandmleadsmtomhighmbloodmg
lucosem(hyperglycemia).mTypemImismusuallymtreatedmwithminsulinminjections
.mTypemIImdiabetesmismcausedmbymamdesensitizationmtominsulinmsignaling.mTh
eminsulinmreceptorsmaremnomlongermrespondingmtominsulin,mwhichmalsomleads
mtomhyperglycemia.m TypemIImismusuallymtreatedm withmdrugsmtomincreasemthem
sensitizationmtominsulinm(metformin),mdietarymandmlife-
stylemchangesmorminsulinminjections.
9. DescribemsomemreasonsmformampatientmneedingmdialysismAEIOU-
macidosis.m Electrolytes,m Intoxication/Ingestion,m overload,m uremia.m Patien
tsmwithmkidneymormheartmfailure.mAmbuildmupmofmphosphates,mureamandmma
gnesiummaremremoved
frommthembloodmusingmamsemi-
permeablemmembranemandmdialysate.mAEIOU:mA—macidosis;mE
