Interpretation of Clinical Laboratory Tests.pdf

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1. Interpretation of Clinical
Laboratory Tests

2. •Generally,laboratorytestsshouldbeorderedonlyiftheresultsof
thetestwillaffectdecisionsaboutthecareofthepatient.
•Theserum,urine,andotherbodilyfluidscanbeanalyzedroutinely.
•Avarietyoffactorscaninterferewiththeaccuracyoflaboratory
tests.
•Patient-relatedfactors(e.g.,age,gender,weight,height,timesince
lastmeal)canaffecttherangeofnormalvaluesforagiventest.
•Laboratory-basedissuescanalsoinfluencetheaccuracyof
laboratoryvalues.Forexample,aspecimencanbespoiledbecause
ofimproperhandlingorprocessing(e.g.,hyperkalemiadueto
hydrolysisofabloodspecimen);becauseitwastakenatawrong
time(e.g.,fastingbloodglucoseleveltakenshortlyafterameal);
becausecollectionwasincomplete(e.g.,24-hoururinecollection
thatdoesnotspanafull24-hourperiod);

3. UnitsofMeasure:
•TheInternationalSystemofUnits(SI)reports
clinicallaboratoryvaluesusingthemetric
system.Forexample,thebasicunitofmass
fortheSIsystem,themoleisnotinfluenced
bytheaddedweightofsaltorester
formulations.
•Themole,therefore,istechnicallyand
pharmacologicallymoremeaningfulthanthe
grambecauseeachphysiologicalreaction
occursonamolecularlevel.

4. ElectrolytesandBloodChemistries
Sodium:Normal:135–145mEq/Lormmol/L.
Sodiumisthepredominantcationofextracellularfluid(ECF).Onlya
smallamountofsodium(~5mEq/L)isinintracellularfluid(ICF).
Alongwithchloride,potassium,andwater,sodiumisimportantin
establishingserumosmolarityandosmoticpressurerelationships
betweenICFandECF.
Dietaryintakeofsodiumisbalancedbyrenalexcretionofsodium,
whichisregulatedbyaldosterone(enhancessodiumreabsorption),
natriuretichormone(increasesexcretionofsodium),and
antidiuretichormone(enhancesreabsorptionoffreewater).
Anincreaseintheserumsodiumconcentrationcouldsuggesteither
impairedsodiumexcretionorvolumecontraction.Conversely,a
decreaseintheserumsodiumconcentrationtoless-than-normal
valuescouldreflecthypervolemia,abnormalsodiumlosses,or
sodiumstarvation.

5. •Althoughhealthyindividualsareableto
maintainsodiumhomeostasiswithout
difficulty,patientswithkidneyfailure,heart
failure,orpulmonarydiseaseoftenencounter
sodiumandwaterimbalance.
•Inadults,changesinserumsodium
concentrationsmostoftenrepresentwater
imbalancesratherthansodiumimbalances.
•Hence,serumsodiumconcentrationsare
morereflectiveofapatient'sfluidstatus
ratherthansodiumbalance.

6. Potassium
Normal: 3.5–5.0 mEq/L or mmol/L:
potassiumisthemajorintracellularcationinthebody.Thepotassiumionin
theECFisfilteredfreelyattheglomerulusofthekidney,reabsorbedin
theproximaltubule,andsecretedintothedistalsegmentsofthe
nephron.
Becausethemajorityofpotassiumissequesteredwithincells,aserum
potassiumconcentrationisnotagoodmeasureoftotalbodypotassium.
Fortunately,theclinicalmanifestationsofpotassiumdeficiency(e.g.,fatigue,
drowsiness,dizziness,confusion,electrocardiographicchanges,muscle
weakness,musclepain)correlatewellwithserumconcentrations.
Theserumpotassiumconcentrationisbufferedandcanbewithinnormal
limitsdespiteabnormalitiesintotalbodypotassium.

7. •Prolongedintravenoustherapywithpotassium-freesolutionsina
patientunabletoobtainpotassiuminfoods(e.g.,nothingbymouth
[NPO]patient)canresultinhypokalemia.
•Hypokalemiacanalsobeinducedbyosmoticdiuresis(e.g.,
mannitol,glucosuria),thiazideorloopdiuretics,excessive
mineralocorticoidactivity,orprotractedvomiting.
•Thelossoflargeamountsofcolonicfluidthroughseverediarrhea
cancausepotassiumdepletionbecausefluidinthecolonishighin
potassiumcontent(i.e.,30–40mEq/L).
•Insulinandstimulationofβ
2-adrenergicreceptorscanalsoinduce
hypokalemiabecausebothincreasethemovementofpotassium
intocellsfromtheextracellularfluid.

8. •Hyperkalemiamostcommonlyresultsfrom
decreasedrenalexcretionofpotassium,
excessiveexogenouspotassiumadministration
(especiallywhencombinedwithapotassium-
sparingdiuretic),orexcessivecellular
breakdown(e.g.,hemolysis,burns,crush
injuries,surgery,infections).
•Metabolicacidosisalsocaninduce
hyperkalemiaashydrogenionsmoveintocells
inexchangeforpotassiumandsodium.

9. Blood Urea Nitrogen
Normal: 8–18 mg/dLor 2.8–6.4 mmol/L:
Ureanitrogenisanendproductofproteinmetabolism.
Itisproducedsolelybytheliver,istransportedinthe
blood,andisexcretedbythekidneys.
Theserumconcentrationofureanitrogen(i.e.,BUN)is
reflectiveofrenalfunctionbecausetheureanitrogen
inbloodisfilteredcompletelyattheglomerulusofthe
kidney,andthenreabsorbedandtubularlysecreted
withinnephrons.
Acuteorchronicrenalfailureisthemostcommoncause
ofanelevatedBUN.

10. Creatinine
Normal: 0.6–1.2 mg/dLor 50–110 µmol/L:
Creatinineisderivedfromcreatineand
phosphocreatine,majorconstituentsofmuscle.
Itsrateofformationforagivenindividualis
remarkablyconstantandisdeterminedprimarily
byanindividual'smusclemassorleanbody
weight.
Therefore,theSCrconcentrationisslightlyhigherin
muscularsubjects,butunliketheBUN,itisless
directlyaffectedbyexogenousfactorsorliver
impairment.

11. •AdoublingoftheSCrlevelroughly
correspondstoa50%reductionintheGFR.
•Thisgeneralruleofthumbonlyholdstruefor
steady-statecreatininelevels.

12. CreatinineClearance
Normal: 75–125 mL/minute or 1.25–2.08 mL/second:
Becausecreatinineisclearedalmostexclusively
throughtheglomerulusinthekidney,CrClcanbeused
asaclinicallyusefulmeasureofapatient'sGFR.
CrClservesasavaluableclinicalparameterbecause
manyrenallyeliminateddrugsaredoseadjustedbased
onthepatient'srenalfunction.
TodetermineactualCrCl,thepatient'surineis
collectedovera24-hourperiod,andtheconcentration
ofurinecreatinine(mg/dL),totalvolumeofurine
collectedoverthe24-hourperiod(mL/minute),and
SCr(mg/dL)aredetermined.

13. The Cockcroft-Gaultformula
the Jelliffemethod

14. GlycosylatedHemoglobin:
GlucosemoleculesirreversiblybindtoHgbwhich
resultsinglycosylatedHgb(A1c).
TheconcentrationofHgbA1c,therefore,reflectsa
patient'saveragebloodglucoseconcentrationoverthe
lifespanofcirculatingRBCs.
Incontrast,fastingglucoseserumconcentrationscan
fluctuateacutelybasedoneithermealsorinsulinuse.
Asaresult,measurementofHgbA1cconcentrations
providesamuchbettertoolforevaluatingchronic
diabetestherapy.

15. Calcium
Normal: 8.8 to 10.2 mg/dLor 2.20 to 2.55 mmol/L:
•Thetotalcalciumcontentresidesprimarilyinthebone,
withonlyabout1%freelyexchangeablewiththatin
theECF.
•Thisreservoirofcalciuminbonesmaintainsthe
concentrationofcalciumintheplasmaconstant
despitepronouncedchangesintheexternalbalanceof
calcium.
•Ifthehomeostaticfactors(i.e.,parathyroidhormone,
vitaminD,calcitonin)thatregulatethecalciumcontent
ofbodyfluidareintact,apatientcanlose25%to30%
oftotalbodycalciumwithoutachangeinthe
concentrationofcalciumionintheplasma.

16. •Areducedcalciumconcentrationusuallyimpliesadeficiencyin
eithertheproductionortheresponsetoparathyroidhormoneor
vitaminD.
•Theabnormalityintheparathyroidhormonesystemmightresult
fromhypomagnesemia, hypoparathyroidism, or
pseudohypoparathyroidism.
•TheabnormalityinthevitaminDsystemcanbecausedby
decreasednutritionalintake;decreasedabsorptionofvitaminD
secondarytogastrectomy,chronicpancreatitis,orsmallbowel
disease;decreasedproductionof25-hydroxycholecalciferoldueto
liverdisease;increasedmetabolismof25-hydroxycholecalciferol
becauseofenzyme-stimulatingdrugs(e.g.,phenobarbital,
phenytoin,rifampin);ordecreasedproductionof1,25-
dihydroxycholecalciferolduetochronicrenaldisease.

17. •Elevatedcalciumconcentrationsare
commonlyassociatedwithmalignancyor
metastaticdiseases.
•Othercausesofhypercalcemiainclude
hyperparathyroidism,Pagetdisease,milk-
alkalisyndrome,granulomatousdisorders,
thiazidediuretics,andvitaminDintoxication.

18. Uric Acid
Normal: 2.0 to 7.0 mg/dLor 0.12 to 0.42
mmol/L:
•Uricacidisanendproductofpurine
metabolism.Itservesnobiologicalfunction,is
notmetabolized,andmustbeexcreted
renally.
•Goutisusuallyassociatedwithincreased
serumconcentrationsofuricacidanddeposits
ofmonosodiumurate.

19. •Increasedserumuricacidconcentrationscan
resultfromeitheradecreaseinurate
excretion(e.g.,renaldysfunction)orexcessive
urateproduction(e.g.,increasedpurine
metabolismresultingfromcytotoxictherapy
ofneoplasticormyeloproliferativedisorders).
•Lowserumuricacidconcentrationsare
inconsequentialandareusuallyreflectiveof
drugsthathavehypouricemicactivity(e.g.,
highdosagesofsalicylates).

20. Proteins:
Prealbumin:
Prealbuminisaneffectiveandusefulmarkerof
immediatenutritionalstatus.
Hepaticdiseaseandmalnutritionareassociated
withdecreasesinbothalbuminand
prealbumin.Hodgkindisease,pregnancy,
chronicrenaldisease,andcorticosteroiduse
can increaseprealbuminserum
concentrations.

21. Albumin:
•hypoalbuminemicstatesarecommonlyassociatedwith
edemaandtransudationofECF.
•Alackofessentialaminoacidsfrommalnutritionor
malabsorption,orimpairedalbuminsynthesisbythe
liver,canresultindecreasedserumalbumin
concentrations.
•Mostformsofhepaticinsufficiencyareassociatedwith
decreasedsynthesisofalbumin.
•Albumincanbelostdirectlyfromthebloodbecauseof
hemorrhage,burns,orexudates,oritmaybelost
directlyintotheurinebecauseofnephrosis.

22. Enzymes
CreatineKinase:
Normal:0to150units/Lor0to2.5µkat/L
•TheCKenzyme,formerlyknownascreatine
phosphokinase,catalyzesthetransferofhigh-
energyphosphategroupsintissuesthatconsume
largeamountsofenergy(e.g.,skeletalmuscle,
myocardium,brain).
•TheserumconcentrationofCKcanbeincreased
bystrenuousexercise,intramuscularinjectionsof
drugsthatareirritatingtotissue(e.g.,diazepam,
phenytoin),acutepsychoticepisodes,crush
injuries,ormyocardialdamage.

23. Troponin
Normal:0to0.03ng/mLor0to0.03mcg/L
•Troponinsareproteinsthatmediatethe
calcium-mediatedinteractionofactinand
myosinwithinmuscles.
•Therearetwocardiac-specifictroponins,
cardiactroponinI(cTnI)andcardiactroponinT
(cTnT).WhereascTnTispresentincardiacand
skeletalmusclecells,cTnIispresentonlyin
cardiacmuscle.

24. Brain NatriureticPeptide
Normal: 0 to 100 pg/mLor 0 to 100 ng/L
•Brainnatriureticpeptide(BNP)isreleased
fromtheheartwhenincreaseddemandsare
placedonthemyocardialtissue.
•ElevationsinBNPareindicativeofpatients
withcongestiveheartfailure(CHF).

25. Liver Function Tests:
AspartateAminotransferase
Normal: 0 to 35 units/L or 0 to 0.58 µkat/L
TheASTenzyme,formerlycalled“serumglutamicoxaloacetic
transaminase,”isabundantinheartandlivertissueand
moderatelypresentinskeletalmuscle,thekidney,andthe
pancreas.
Incasesofacutecellularinjurytotheheartorliver,the
enzymeisreleasedintothebloodfromthedamagedcells.
Inclinicalpractice,ASTdeterminationshavebeenusedto
evaluatemyocardialinjuryandtodiagnoseandassessthe
prognosisofliverdiseaseresultingfromhepatocellular
injury.

26. AlanineAminotransferase
Normal:0to35units/Lor0to0.58µkat/L
•TheALTenzyme,formerlycalled“serumglutamicpyruvic
transaminase,”isfoundinessentiallythesametissuesthat
havehighconcentrationsofAST.
•ElevationsinserumALTaremorespecificforliver-related
injuriesordiseases.
•EvaluatingtheratioofALTtoASTcanbepotentiallyuseful,
particularlyinthediagnosisofviralhepatitis.
•TheALT/ASTratiofrequentlyexceeds1.0withalcoholic
cirrhosis,chronicliverdisease,orhepaticcancer.However,
ratios<1.0tendtobeobservedwithviralhepatitisoracute
hepatitis,whichcanbeusefulwhendiagnosingliver
disease.