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What xis xStarling's xLaw xof xCapillary xforces? x
How xdoes xthis xexplain xwhy xa xnutritionally xdeficient xchild xwould xhave xedema? x- xANS-
Starling's xLaw xdescribes xhow xfluids xmove xacross xthe xcapillary xmembrane. xThere xare
xtwo xmajor xopposing xforces xthat xact xto xbalance xeach xother, xhydrostatic xpressure
x(pushing xwater xout xof xthe xcapillaries) xand xosmotic xpressure x(including xoncontic
xpressure, xwhich xpushes xfluid xinto xthe xcapillaries). x
Both xelectrolytes xand xproteins x(oncontic xpressure) xin xthe xblood xaffect xosmotic
xpressure, xhigh xelectrolyte xand xprotein xconcentrations xin xthe xblood xwould xcause
xwater xto xleave xthe xcells xand xinterstitial xspace xand xenter xthe xblood xstream xto xdilute
xthe xhigh xconcentrations. x
,On, xthe xother xhand, xlow xelectrolyte xand xprotein xconcentrations x(as xseen xin xa
xnutritionally xdeficient xchild) xwould xcause xwater xto xleave xthe xcapillaries xand xenter
xthe xcells xand xinterstitial xfluid xwhich xcan xlead xto xedema.
How xdoes xthe xRAAS x(Renin-Angiotensin-Aldosterone xSystem) xresult xin xincreased
xblood xvolume xand xincreased xblood xpressure? x- xANS-A xdrop xin xblood xpressure xis
xsensed xby xthe xkidneys xby xlow xperfusion, xwhich xin xturn xbegins xto xsecrete xrenin. x
Renin xthen xtriggers xthe xliver xto xproduce xangiotensinogen, xwhich xis xconverted xto
xAngiotensin xI xin xthe xlungs xand xthen xangiotensin xII xby xthe xenzyme x
Angiotensin-converting xenzyme x(ACE). xAngiotensin xII xstimulates xperipheral xarterial
xvasoconstriction xwhich xraises xBP. x
Angiotensin xII xis xalso xstimulating xthe xadrenal xgland xto xrelease xaldosterone, xwhich
xacts xto xincrease xsodium xand xwater xreabsorption xincreasing xblood xvolume, xwhile xalso
xincreased xpotassium xsecretion xin xurine.
,How xcan xhyperkalemia xlead xto xcardiac xarrest? x- xANS-Normal xlevels xof xpotassium xare
xbetween x3.5 xand x5.2 xmEq/dL. xHyperkalemia xrefers xto xpotassium xlevels xhigher xthat
x5.2 xmEq/dL. x
A xmajor xfunction xof xpotassium xis xto xconduct xnerve ximpulses xin xmuscles. xToo xlow
xand xmuscle xweakness xoccurs xand xtoo xmuch xcan xcause xmuscle xspasms. x
This xis xespecially xdangerous xin xthe xheart xmuscle xand xan xirregular xheartbeat xcan
xcause xa xheart xattack
The xbody xuses xthe xProtein xBuffering xSystem, xPhosphate xBuffering xSystem, xand
xCarbonic xAcid-Bicarbonate xSystem xto xregulate xand xmaintain xhomeostatic xpH, xwhat xis
xthe xconsequence xof xa xpH ximbalance x- xANS-Proteins xcontain xmany xacidic xand xbasic
xgroup xthat xcan xbe xaffected xby xpH xchanges. xAny xincrease xor xdecrease xin xblood xpH
xcan xalter xthe xstructure xof xthe xprotein x(denature), xthereby xaffecting xits xfunction xas
xwell
Describe xthe xlaboratory xfindings xassociated xwith xmetabolic xacidosis, xmetabolic
xalkalosis, xrespiratory xacidosis xand xrespiratory xalkalosis. x(ie xrelative xpH xand xCO2
, xlevels). x- xANS-Normal xABGs x(Arterial xBlood xGases) xBlood xpH: x7.35-7.45 xPCO2: x35-45
xmm xHg xPO2: x90-100 xmm xHg xHCO3-: x22-26 xmEq/L xSaO2: x95-100% x
Respiratory xacidosis xand xalkalosis xare xmarked xby xchanges xin xPCO2. xHigher x= xacidosis
xand xlower x= xalkalosis x
Metabolic xacidosis xand xalkalosis xare xcaused xby xsomething xother xthan xabnormal xCO2
xlevels. xThis xcould xinclude xtoxicity, xdiabetes, xrenal xfailure xor xexcessive xGI xlosses. x
Here xare xthe xrules xto xfollow xto xdetermine xif xis xrespiratory xor xmetabolic xin xnature. x-
If xpH xand xPCO2 xare xmoving xin xopposite xdirections, xthen xit xis xthe xpCO2 xlevels xthat
xare xcausing xthe ximbalance xand xit xis xrespiratory xin xnature. x
-If xPCO2 xis xnormal xor xis xmoving xin xthe xsame xdirection xas xthe xpH, xthen xthe
ximbalance xis xmetabolic xin xnature.
The xanion xgap xis xthe xdifference xbetween xmeasured xcations x(Na+ xand xK+) xand
xmeasured xanions x(Cl- xand xHCO3-), xthis xcalculation xcan xbe xuseful xin xdetermining xthe
xcause xof xmetabolic xacidosis. x