Wgu d236 pathophysiology exam

Wm WGU D236 PATHOPHYSIOLOGY
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WGU D236 PATHOPHYSIOLOGY EXAM LATEST 2024
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QUESTIONS AND ANSWERS GRADED A+ m m m m




1. What is Starling's Law of Capillary forces? How does t
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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-
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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
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whichmactsmtomincreasemsodiummandmwatermreabsorptionmincreasingmblo
odmvolume,mwhilemalsomincreasedmpotassiummsecretionminmurine.


3. How can hyperkalemia lead to cardiac arrest?
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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
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temBufferingmSystem,mandmCarbonicmAcid-
mBicarbonatemSystemmtomregulatemandmmaintainmhomeosta

ticmpH,mwhatmismthemconsequencemofmampHmimbalance?
Proteinsmcontainmmanymacidicmandmbasicmgroupmthatmcanmbemaffectedmb
ympHmchanges.mAnymincreasemormdecreaseminmbloodmpHmcanmaltermthemstructur
emofmthemproteinm(denature),mtherebymaffectingmitsmfunctionmasmwell.
5. Describemthemlaboratorymfindingsmassociatedmwit
hmmetabolic
Wantmtomearnm$103mpermmonth?

,Wm WGU D236 PATHOPHYSIOLOGY
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acidosis, metabolic alkalosis, respiratory acidosis
andmrespiratorymalkalosis.m(iemrelativempHmandmC
O2mlevels).

, Wm WGU D236 PATHOPHYSIOLOGY
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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
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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