p p p
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WhatpispStarling'spLawpofpCapillarypforces?
Howpdoespthispexplainpwhypapnutritionallypdeficientpchildpwouldphavepedema?p-
✅✅Starling'spLawpdescribesphowpfluidspmovepacrosspthepcapillarypmembrane.pTherepareptwopmajorp
p
opposingpforcespthatpactptopbalancepeachpother,phydrostaticppressurep(pushingpwaterpoutpofpthepcapillar
ies)pandposmoticppressurep(includingponconticppressure,pwhichppushespfluidpintopthepcapillaries).
Bothpelectrolytespandpproteinsp(onconticppressure)pinpthepbloodpaffectposmoticppressure,phig
hpelectrolytepandpproteinpconcentrationspinpthepbloodpwouldpcausepwaterptopleavepthepcellspa
ndpinterstitialpspacepandpenterpthepbloodpstreamptopdilutepthephighpconcentrations.
On,pthepotherphand,plowpelectrolytepandpproteinpconcentrationsp(aspseenpinpapnutritionallypdeficientpchi
ld)pwouldpcausepwaterptopleavepthepcapillariespandpenterpthepcellspandpinterstitialpfluidpwhichpcanpleadpto
edema.
p
HowpdoespthepRAASp(Renin-Angiotensin-
AldosteronepSystem)presultpinpincreasedpbloodpvolumepandpincreasedpbloodppressure?p-
✅✅Apdroppinpbloodppressurepispsensedpbypthepkidneyspbyplowpperfusion,pwhichpinpturnpbeginsptopsecr
p
eteprenin.
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Reninpthenptriggerspthepliverptopproducepangiotensinogen,pwhichpispconvertedptopAngiotensinpIpinptheplun
gspandpthenpangiotensinpIIpbypthepenzyme
Angiotensin-
convertingpenzymep(ACE).pAngiotensinpIIpstimulatespperipheralparterialpvasoconstrictionpwhichpraisespBP.
AngiotensinpIIpispalsopstimulatingpthepadrenalpglandptopreleasepaldosterone,pwhichpactsptopincreasepsodiu
mpandpwaterpreabsorptionpincreasingpbloodpvolume,pwhilepalsopincreasedppotassiumpsecretionpinpurine.
Howpcanphyperkalemiapleadptopcardiacparrest?p-p✅✅Normalplevelspofppotassiumparepbetweenp3.5pand
5.2pmEq/dL.pHyperkalemiaprefersptoppotassiumplevelsphigherpthatp5.2pmEq/dL.
Apmajorpfunctionpofppotassiumpisptopconductpnervepimpulsespinpmuscles.pTooplowpandpmusclepweaknesspo
ccurspandptoopmuchpcanpcausepmusclepspasms.
Thispispespeciallypdangerouspinpthepheartpmusclepandpanpirregularpheartbeatpcanpcausepapheartpattack
,WGU D236 Pathophysiology Exam,
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ThepbodypusespthepProteinpBufferingpSystem,pPhosphatepBufferingpSystem,pandpCarbonicpAcid-
p BicarbonatepSystemptopregulatepandpmaintainphomeostaticppH,pwhatpispthepconsequencepofpappHpim
balancep-
✅✅ProteinspcontainpmanypacidicpandpbasicpgrouppthatpcanpbepaffectedpbyppHpchanges.pAnypincrea
p
seporpdecreasepinpbloodppHpcanpalterpthepstructurepofpthepproteinp(denature),ptherebypaffectingpitspfu
nctionpaspwell
Describeptheplaboratorypfindingspassociatedpwithpmetabolicpacidosis,pmetabolicpalkalosis,prespiratorypaci
dosispandprespiratorypalkalosis.p(ieprelativeppHpandpCO2plevels).p-
✅✅NormalpABGsp(ArterialpBloodpGases)pBloodppH:p7.35-7.45pPCO2:p35-45pmmpHgpPO2:p90-
p
100pmmpHgpHCO3-:p22-26pmEq/LpSaO2:p95-p100%
RespiratorypacidosispandpalkalosisparepmarkedpbypchangespinpPCO2.pHigherp=pacidosispandplowerp=palk
alosis
MetabolicpacidosispandpalkalosisparepcausedpbypsomethingpotherpthanpabnormalpCO2plevels.pThispcouldpin
cludeptoxicity,pdiabetes,prenalpfailureporpexcessivepGIplosses.
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Herepareptheprulesptopfollowptopdeterminepifpisprespiratoryporpmetabolicpinpnature.p-
IfppHpandpPCO2parepmovingpinpoppositepdirections,pthenpitpisptheppCO2plevelspthatparepcausingpthepimbala
ncepandpitpisprespiratorypinpnature.
-
IfpPCO2pispnormalporpispmovingpinpthepsamepdirectionpasptheppH,pthenpthepimbalancepispmetabolicpinpnatur
e.
Thepanionpgappispthepdifferencepbetweenpmeasuredpcationsp(Na+pandpK+)pandpmeasuredpanionsp(Cl-
andpHCO3-),pthispcalculationpcanpbepusefulpinpdeterminingpthepcausepofpmetabolicpacidosis.
p
Whypwouldpanpincreasedpanionpgappbepobservedpinpdiabeticpketoacidosisporplacticpacidosis?p-
✅✅Thepanionpgappispthepcalculationpofpunmeasuredpanionspinpthepblood.
p
Lacticpacidpandpketonespbothpleadptopthepproductionpofpunmeasuredpanions,pwhichpremovepHCO3-
(apmeasuredpanion)pdueptopbufferingpofpthepexcesspH+pandpthereforepleadsptopanpincreasepinpthepAG.
p