Chapt er 2

Bl ood Chemi st r y Test s ( Par t I )

Key Ter ms, Abbr evi at i ons, and Ac r ony ms

bi car bonat e, HC03 l ow- densi t y l i popr ot ei n, LDL

bi l i r ubi n l yt es
bl ood buf f er syst em magnesi um, Mg+
bl ood ur ea ni t r ogen, BUN noni nsul i n- dependent di abet es
cal ci um, Ca+ mel l i t us, NI DDM

Chem 12, Chem24 phosphor us, P; phosphat e, P04

chl or i de, Cl - post pr andi al bl ood sugar t est ,

chol est er ol PPBS, 2- hour PPBS

C- pept i de pot assi um, K+

cr eat i ni ne r adi oi mmunoassay

di r ect or conj ugat ed bi l i r ubi n SMAC 12

f ast i ng bl ood sugar t est , FBS sodi um, Na+

gl ucagon st andar d or al gl ucose t ol er ance

t est , SOGTT
gl ucose t ol er ance t est , GTT
t ot al bi l i r ubi n
hi gh- densi t y l i popr ot ei n, HDL
t r i gl ycer i de
i ndi r ect or unconj ugat ed bi l i r ubi n
ur i c aci d
i nsul i n
ver y- l ow- densi t y l i popr ot ei n,
i nsul i n- dependent di abet es
VLDL
mel l i t us, I DDM
l i popr ot ei n
30 Chapt er 2

Lear ni ng Obj ect i ves

Upon compl et i on of t hi s chapt er , t he l ear ner shoul d be abl e t o :

1 . I dent i f y and def i ne t he bl ood chemi st r y t est s pr esent ed i n t hi s

chapt er .
2. Or gani ze bl ood chemi st r y t est s accor di ng t o def i ned cat egor i es.
3 . Expl ai n t he ef f ect s of i ncr eased or decr eased s er umel ect r ol yt e l evel s .
4 . Compar e t he di agnost i c si gni f i cance of var i ous bl ood sugar and
r el at ed t est s .
5 . Compar e t hr ee t ypes of l i popr ot ei ns and t hei r i nf l uence on
at her oscl er ot i c di seases .
6 . Assess t he di agnost i c i mpor t ance of t he met abol i c end pr oduct t est s i n
r el at i on t o l i ver and ki dney f unct i on .

I nt r oduct i on
Bl ood chemi st r y t est s pr ovi de a means of measur i ng t he bl ood l evel s of
var i ous body chemi cal s . The pr esence, absence, i ncr ease, or decr ease i n t he
l evel s of t hese chemi cal s ar e usef ul di agnost i c t ool s. Few di seases exhi bi t an
abnor mal i t y i n a si ngl e chemi st r y t est . Sever al bl ood chemi st r y t est s mus t
be per f or med i n or der t o i dent i f y t he abnor mal pat t er ns est abl i shed f or a
par t i cul ar di sease . Moder n cl i ni cal l abor at or i es ar e equi pped t o conduct a
var i et y of t est s usi ng a si ngl e bl ood sampl e .
Al l member s of t he heal t h car e i ndust r y qui ckl y bec ome f ami l i ar wi t h
abbr evi at i ons such as SMAC 12, Chem12, Chem24, and so f or t h . Each of
t hese not at i ons r el at es t o an aut omat ed bl ood chemi st r y panel . SMAC 12
st ands f or Sequent i al Mul t i pl e Anal yzer by Techni con, whi c h i s an aut o-
mat ed met hod used t o anal yze t wel ve di f f er ent chemi cal component s of
t he bl ood . Chem 12 and Chem 24 al so r ef er t o aut omat ed bl ood t est i ng
met hods used t o anal yze t wel ve and t went y- f our di f f er ent chemi cal c om-
ponent s of t he bl ood, r espect i vel y .
Aut omat ed bl ood chemi st r y t est r esul t s ar e r epor t ed as chemi st r y pr o-
f i l es and cont ai n t est r esul t s as wel l as t he r ange of nor mal f or each t est . Fi g-
ur e 2- 1 i s a sampl e chemi st r y pr of i l e . The pr of i l e cont ai ns t he name of t he
t est , t he i ndi vi dual ' s t est r esul t s, and t he nor mal r ange . Abnor mal r esul t s
 Bl ood Chemi st r y Test s ( Par t I ) 31

MEMORI AL COMMUNI TY HOSPI TAL

Anyt own,Mi chi gan

CHEMI STRY PROFI LE

RUN ON 11/ 21/ -

WATSON, MARK MR# 00- 00- 00 COLLECTED: 0800

Nor mal Range

NA 136 mEq/ L ( 136- 145)

K 6 . 4 ( H) * mEq/ L ( 3 . 5- 5 . 5)

CL 103 mEq/ L ( 90- 110)

BUN 24 ( H) * mg/ dl ( 10- 20)

Cr eat i ni ne 1 . 6 ( H) * mg/ dl ( 0 . 7- 1 . 5)

Ur i c aci d 9. 5 ( H) * mg/ dl ( 2 . 1- 8 . 5)

Cal ci um 7. 5 mg/ dl ( 9 . 0- 10 . 5)

Phosphor us 5 . 0 ( H) * mg/ dl ( 2 . 7- 4 . 5)

Gl ucose 60 ( L) * mg/ dl ( 70- 115)

Tot al Bi l i 0 .1 mg/ dl ( 0 . 1- 1 . 0)

Chol t ot 150 mg/ dl ( 110- 200)

Tr i gl ycer i de 41 mg/ dl ( 40- 160)

* i ndi cat es abnor mal r esul t s : H = hi gh and L = l ow.

Fi gur e 2- 1 . Sampl e bl ood chemi st r y pr of i l e

ar e hi ghl i ght ed . Test r esul t s ar e ex pr es s ed as mi l l i equi val ent per l i t er

( MEQ/ L) and mi l l i gr amper deci l i t er ( MG/ DL) .
Many bl ood c hemi s t r y t est s c an be cat egor i zed under sever al br oad
headi ngs . Thi s chapt er cover s bl ood c hemi s t r y t est s t hat meas ur e el ec-
t r ol yt es, bl ood sugar s and gl ucose, l i pi ds and l i popr ot ei ns, and met abol i c
end pr oduct s . Chapt er 3 addr es s es enz y me, hor mone, and pr ot ei n t est s, as
wel l as sever al t hyr oi d f unct i on t est s .
32 Chapt er 2

El ect r ol yt e Test s
The t er m el ect r ol yt e r ef er s t o t he posi t i vel y ( +) or negat i vel y ( - ) char ged
par t i cl es cal l ed i ons . El ect r ol yt es ar e pr esent i n t he body' s ext r acel l ul ar
f l ui d, f l ui d out si de t he cel l s t hat i ncl udes bl ood ser umor pl asma, and i n t he
body' s i nt er st i t i al f l ui d, t he f l ui d i n t he space bet ween cel l s . El ect r ol yt es ar e
al so f ound i n t he i nt r acel l ul ar f l ui d, t he f l ui d wi t hi n t he cel l i t sel f .
I n bl ood chemi st r y st udi es, el ect r ol yt es gener al l y r ef er t o t he f our
pl asma i ons : sodi um, pot assi um, chl or i de, and bi car bonat e . These pl asma
i ons ar e al so r ef er r ed t o as l yt es and ar e t he ones most commonl y measur ed
when el ect r ol yt es ar e or der ed as a l abor at or y t est . Thr ee l ess commonl y
measur ed el ect r ol yt es i ncl ude cal ci um, magnesi um, and phosphat e.
Pl asma el ect r ol yt es ar e cat egor i zed as cat i ons, t he posi t i vel y char ged
i ons of sodi um, pot assi um, cal ci um, and magnesi um; and as ani ons, t he
negat i vel y char ged i ons of chl or i de, bi car bonat e, and phosphat e. Negat i ve
and posi t i ve i ons must be kept i n bal ance f or bl ood t o r emai n neut r al . Tabl e
2- 1 di spl ays t he names, chemi cal symbol s, and some maj or f unct i ons of t he
seven el ect r ol yt es di scussed i n t hi s chapt er .

Sodi um ( Na+)

Sodi umhas t he hi ghest ext r acel l ul ar concent r at i on of al l el ect r ol yt es mea-

sur ed i n t he pl asma and pl ays a pr i mar y r ol e i n cont r ol l i ng t he di st r i but i on
of body wat er bet ween ext r acel l ul ar and i nt r acel l ul ar f l ui d. Sodi um i s i n-
vol ved i n t he t r ansmi ssi on of ner ve i mpul ses and hel ps hear t muscl e r et ai n
i t s abi l i t y t o cont r act .
Because sodi um i s necessar y f or cr i t i cal bodi l y f unct i ons, t he body i s
abl e t o mai nt ai n an over al l base l evel of pl asma sodi um. I n heal t h t he l ev-
el s of sodi um ar e kept wi t hi n a ver y nar r ow r ange; i n di sease onl y sl i ght
changes i n over al l concent r at i on ar e not ed.

Nor mal Range

136- 145 mEq/ L

Var i at i ons f r om Nor mal . Hyper nat r emi a, an i ncr eased pl asma sodi um
l evel , i s r el at i vel y unc ommon . Hyper nat r emi a i s associ at ed wi t h dehydr a-
t i on and i nsuf f i ci ent wat er i nt ake, Conn' s syndr ome ( t he excessi ve secr e-
 Bl ood Chemi st r y Test s ( Par t I ) 33

Tabl e 2- 1. Names, Chemi cal Symbol s, and Funct i ons of El ect r ol yt es

El ect r ol yt e Sy mbol Funct i ons

Sodi um Na+ Di st r i but i on of wat er bet ween ext r acel l ul ar

and i nt r acel l ul ar f l ui d
Ner ve i mpul ses
Hear t muscl e cont r act i bi l i t y
Pot assi um K+ Ner ve conduct i on
Muscl e act i vi t y
Car di ac muscl e f unct i on
Cal ci um Ca+ Bones and t eet h
Muscul ar cont r act i on
Ner ve i mpul ses
Coagul at i on Fact or I V
Magnesi um Mg+ Muscul ar cont r act i on
Car bohydr at e met abol i sm
Coagul at i on pr ocess
Di s t Chl
r i
or i de buCI -t i on of wat er bet ween cel l s and
pl asma
Aci d/ base bal ance
Bi car bonat e HC03 Mai nt enance of nor mal pH
Tr anspor t at i on C0 2 f r omt i ssue t o l ungs
Phosphat e P0 4 Gener at i on of bony t i ssue
Phosphor us P Gl ucose and f at met abol i sm
Ener gy t r ansf er and st or age

t i on of al dost er one) , hyper adr enal i sm or Cushi ng' s di sease, di abet es i n-

si pi dus, and coma .
Hyponat r emi a, a decr eased sodi uml evel , usual l y r ef l ect s an excess of
body wat er . Condi t i ons t hat may cause an act ual r educt i on i n pl asma
sodi umi ncl ude sever e bur ns, sever e di ar r hea, sever e nephr i t i s, di abet es,
cyst i c f i br osi s, Addi son' s di sease ( par t i al or compl et e f ai l ur e of adr eno-
cor t i cal f unct i on) , mal absor pt i on syndr ome, and cer t ai n di ur et i c medi ca-
t i ons .
34 Chapt er 2

I nt er f er i ng Ci r cumst ances. Recent t r auma, sur ger y, or shock may cause i n-

cr eased s odi uml evel s . Or al cont r acept i ves, anabol i c st er oi ds, cor t i cost er oi ds,
and l axat i ves may be l i nked t o i ncr eased sodi um l evel s . Decr eased l evel s
may be caused by di ur et i cs, vasopr essi n, and sodi umi nt r avenous ( I V) f l ui ds .

Pot assi um( K+)

About 90%of pot assi umi s concent r at ed wi t hi n t he cel l s and t he r emai nder
i s cont ai ned i n bl ood and bone. Pl asma pot assi um i nf l uences ner ve con-
duct i on, muscl e act i vi t y, and, mos t i mpor t ant , car di ac f unct i on . Mi ni mal
changes i n pl asma pot assi uml evel s can hav e pr of ound and adver se af f ect s
on hear t muscl e . Si nce t he ki dneys do not r eabsor b or conser ve pot assi um,
adequat e di et ar y i nt ake i s necessar y t o pr event pot assi umdef i ci ency .

Nor mal Range

Adul t 3 . 5- 5 . 0 mEq/ L
Chi l dr en 3 . 4- 4 . 7 mEq/ L
I nf ant 4 . 1- 5 . 3 mEq/ L

Var i at i ons f r om Nor mal . An i ncr ease i n pl asma pot assi um l evel s, hyper -
kal emi a, i s usual l y at t r i but ed t o r enal f ai l ur e . Ot her c ommon causes of hy-
per kal emi a i ncl ude aci dosi s, Addi son' s di sease, i nt er nal hemor r hage, and
massi ve t i ssue or cel l ul ar damage . Si nce 90% of pot assi um i s cont ai ned
wi t hi n t he cel l s, cel l damage as i n cases of bur ns, chemot her apy, and di s-
semi nat ed i nt r avascul ar coagul at i on ( DI C) r esul t s i n t he r el ease of pot as-
s i umi nt o t he bl ood .
Hypokal emi a, a decr ease i n pl asma pot assi um, i s mos t of t en associ at ed
wi t h l oss of f l ui d f r om t he gast r oi nt est i nal t r act . Ther ef or e, any di sease
pr ocess t hat causes di ar r hea or sever e vomi t i ng has t he pot ent i al f or cr eat
i ng pot assi umdef i ci ency . Ot her di sor der s associ at ed wi t h hypokal emi a i n-
cl ude mal absor pt i on syndr omes, hyper al dost er oni sm ( i ncr eased secr et i on
of al dost er one) , Cushi ng' s syndr ome, and r enal t ubul ar aci dosi s .
Hypokal emi a can cause ser i ous car di ac pr obl ems such as pr emat ur e
vent r i cul ar cont r act i on, par oxysmal at r i al t achycar di a, vent r i cul ar t achy-
car di a, and vent r i cul ar f i br i l l at i on . Pl asma pot assi um l evel s of 2 . 5 mEq/ L
or l ess, or 6 . 5 mEq/ L or mor e can cause hear t pr obl ems t hat l ead t o deat h .
 Bl ood Chemi st r y Test s ( Par t I ) 35

I nt er f er i ng Ci r cumst ances . Veni punct ur e, i nt r avenous f l ui d admi ni st r a-

t i on, and cer t ai n medi cat i ons can al t er pl asma pot assi uml evel s . The com-
mon pr act i ce of openi ng and cl osi ng t he f i st wi t h a t our ni quet i n pl ace
pr i or t o veni punct ur e may i ncr ease pot assi um l evel s . I nt r avenous f l ui d
admi ni st r at i on wi t hout adequat e pot assi umsuppl ement s can l ead t o pot as-
s i umdepl et i on . Medi cat i ons t hat may cause an i ncr eased pot assi um l evel
i ncl ude hepar i n, hi st ami ne, manni t ol , and l i t hi um. Dr ugs t hat may cause a
decr eased l evel ar e i nsul i n, aspi r i n, ci spl at i n, and pot assi um wast i ng di -
ur et i cs .
Di et ar y habi t s do not usual l y i nt er f er e wi t h pl asma pot assi uml evel s . A
r el at i vel y wel l - bal anced di et wi l l pr ovi de an adequat e suppl y of pot as-
s i um. Howev er , excessi ve l i cor i ce i ngest i on can cause a decr ease i n pl asma
pot assi um l evel s .

Cal c i um ( Ca+)

Appr oxi mat el y 98% of al l cal ci um i s st or ed i n bones and t eet h. Cal ci um

t hat i s pr esent i n t he bl oodst r eamci r cul at es i n t he i oni zed, or f r ee st at e, and
i n a pr ot ei n- bound f or mwi t h al bumi n. I t i s t he i oni zed f or mof cal ci um t hat
i s used i n bodi l y pr ocesses such as muscul ar cont r act i on, car di ac f unct i on-
i ng, hor mone secr et i on, cel l di vi si on, and t he t r ansmi ssi on of ner ve i m-
pul ses . I oni zed cal ci um i s essent i al f or bl ood coagul at i on .

Nor mal Range

Tot al pl asma cal ci um 9 . 0- 10 . 5 mg/ dl

Fr ee cal ci um 3 . 9- 4 . 6 mg/ dl

Var i at i ons f r om Nor mal . Hyper cal cemi a, i ncr eased pl asma cal ci um, i s as-
soci at ed wi t h many di seases but i s mos t cl i ni cal l y si gni f i cant i n i t s associ -
at i on wi t h cancer . The most c ommon cause of i ncr eased cal ci um i n t he
bl ood i s met ast at i c bone di sease . Cancer s of t he l ung, br east , t hyr oi d, ki d-
ney, and t est es ar e l i kel y t o met ast asi ze t o bone . Hodgki n' s di sease, mul t i -
pl e myel oma, and l eukemi a may al so cause hyper cal cemi a . Ot her di sor der s
or condi t i ons associ at ed wi t h i ncr eased cal ci um l evel s ar e hyper par at hy-
r oi di sm, Paget ' s di sease of bone, pr ol onged i mmobi l i zat i on, and Addi son' s
di sease .
36 Chapt er 2

Si nce muc h of t he pl asma cal ci um i s bound t o al bumi n, decr eased

pl asma cal ci uml evel s, hypocal cemi a, can be r el at ed t o a l ower ed pl asma al -
bumi n l evel . Onc e t hi s possi bi l i t y has been el i mi nat ed, hypocal cemi a can be
i ndi cat i ve of hypopar at hyr oi di smand r enal f ai l ur e . Vi t ami n D def i ci enci es
and mal absor pt i on associ at ed wi t h spr ue, cel i ac di sease, and pancr eat i c
dysf unct i ons cont r i but e t o decr eased pl asma cal ci uml evel s . Si nce cal ci umi s
essent i al f or cl ot t i ng, any condi t i on t hat decr eases t he amount of i oni zed cal -
c i umcan subsequent l y l ead t o coagul at i on and hemost asi s pr obl ems .

I nt er f er i ng Ci r cumst ances . Cer t ai n di et ar y consi der at i ons can i nt er f er e

wi t h accur at e pl asma cal ci um t est r esul t s . Vi t ami n D i nt oxi cat i on or exces-
si ve mi l k i ngest i on, def i ned as t hr ee quar t s of mi l k per day, can cause an i n-
cr ease i n pl asma cal ci um.
Pr escr i pt i on and over - t he- count er dr ugs such as hepar i n, magnes i um
sal t s, or al cont r acept i ves, aspi r i n, and cor t i cost er oi ds and excessi ve use of
l axat i ves may cause a decr ease i n pl asma cal ci um. Dr ugs t hat i nf l uence an
i ncr ease of pl asma cal ci um i ncl ude l i t hi um, vi t ami n D, t hi azi de di ur et i cs,
t hyr oi d hor mone, and hydr al azi ne, an ant i hyper t ensi ve medi cat i on .

Magnes i um ( Mg+)

The bul k of magnes i um i s combi ned wi t h cal ci um and phosphor us i n t he

bones, wi t h ver y smal l amount s pr esent i n t he bl oodst r eam. Magnes i umi s
necessar y f or muscul ar cont r act i on, car bohydr at e met abol i sm, and pr ot ei n
synt hesi s . I t i s usual l y f i l t er ed by t he ki dney t hr ough t he gl omer ul us, and
r eabsor bed i nt o t he bl oodst r eam by t he r enal t ubul e . Magnes i um l evel s
can be used as an i ndi cat or of met abol i c act i vi t y and r enal f unct i on. Si nce
magnes i um i s pr esent i n a var i et y of f oods, a nor mal di et wi l l mai nt ai n t he
body' s magnes i um suppl y .

Nor mal Range

1 . 6- 3 . 0 mEq/ L

Var i at i ons f r om Nor mal . An i ncr ease i n pl asma magnes i um, hy per magne-
semi a, i s usual l y caused by r enal dysf unct i on or f ai l ur e. Ot her di seases or
syndr omes associ at ed wi t h i ncr eased magnes i um l evel s i ncl ude hypot hy-
 Bl ood Chemi st r y Test s ( Par t I ) 37

r oi di sm, Addi son' s di sease, and dehydr at i on . Excessi ve i ngest i on of mag-

nesi um vi a ant aci ds, such as mi l k of magnesi a, wi l l al so cause an i ncr ease
i n pl asma magnes i um.
Hy pomagnes emi a, decr eased pl asma magnesi um, i s usual l y due t o
s ome t ype of chr oni c di et ar y or i nt est i nal absor pt i on pr obl em. Di seases such
as ul cer at i ve col i t i s, chr oni c al cohol i sm, chr oni c pancr eat i t i s, and chr oni c di
ar r hea wi l l exhi bi t decr eased magnes i uml evel s . Ot her si t uat i ons t hat r esul t
i n hy pomagnes emi a i ncl ude t oxemi a of pr egnancy, hyper t hyr oi di sm, hy-
popar at hyr oi di sm, ci r r hosi s of t he l i ver , and excessi ve secr et i on of t he hor -
mone al dost er one .
Magnes i um def i ci enci es can be cor r ect ed by t he pr oper admi ni st r at i on
of magnes i umsul f at e . Ear l y s y mpt oms of magnes i umdef i ci t i ncl ude mus -
cl e cr amps, t r emor s, and i nsomni a . I t shoul d be not ed t hat decr eases i n ur i
nar y magnes i ummay be det ect ed bef or e decr eases i n pl asma magnes i um.
Low l evel s of cal ci um and pot assi ummay mas k t he pr esence of hy pomag-
nesemi a .

I nt er f er i ng Ci r cumst ances . A var i et y of medi cat i ons can i nt er f er e wi t h l ab-

or at or y meas ur ement of magnes i uml evel s . Pr ol onged t r eat ment i nvol vi ng
l i t hi um, magnes i um pr oduct s such as ant aci ds and l axat i ves, and sal i cyl at e
pr oduct s such as aspi r i n wi l l cause a f al se i ncr ease i n pl asma magnes i um
l evel s . Thi s i s par t i cul ar l y possi bl e i n t he f ace of r enal dysf unct i on. Ad-
mi ni st r at i on of cal ci um gl uconat e, whi c h i s used t o r epl eni sh t he body' s
cal ci um r eser ves, can al so i nt er f er e wi t h t est i ng met hods and cause a f al se
r esul t t hat i ndi cat es a decr eased magnes i uml evel .

Chl or i de ( CI -)

Chl or i de, an i mpor t ant negat i vel y char ged el ect r ol yt e, i s pr esent i n t he ex-
t r acel l ul ar spaces i n combi nat i on wi t h s odi umand hydr ogen . Chl or i de has
t wo mai n bodi l y f unct i ons : t o hel p cont r ol t he di st r i but i on of wat er be-
t ween t he cel l s and bl ood pl asma and t o hel p mai nt ai n t he aci d- base bal -
ance i n t he body .

Nor mal Range

90- 110 mEq/ L

38 Chapt er 2

Var i at i ons f r om Nor mal . Var i at i ons i n chl or i de l evel s mus t al ways be con-
si der ed i n r el at i on t o ot her el ect r ol yt es, par t i cul ar l y s odi um and bi car bon-
at e . An i ncr ease i n pl asma chl or i de wi l l cor r espond t o an i ncr ease i n s odi um
l evel s or a decr ease i n pl asma bi car bonat e l evel s . Measur i ng chl or i des can be
hel pf ul i n di agnosi ng aci d- base and wat er bal ance di sor der s .
I ncr eases i n pl asma chl or i de l evel s ar e seen i n dehydr at i on, ecl ampsi a,
Cushi ng' s syndr ome, and anemi a . Pl asma chl or i de i s decr eased wi t h se-
ver e vomi t i ng, di ar r hea, bur ns, and heat exhaust i on . Ot her di seases and
syndr omes t hat r esul t i n chl or i de def i ci t s i ncl ude ul cer at i ve col i t i s, Addi -
son' s di sease, and di abet i c aci dosi s .

I nt er f er i ng Ci r cumst ances . Dr ugs t hat may cause an i ncr ease i n chl or i de

l evel s ar e andr ogens, cor t i sone pr epar at i ons, est r ogens, and nonst er oi dal
ant i - i nf l ammat or y dr ugs . Decr eased chl or i de l evel s can be associ at ed wi t h
cor t i cost er oi ds, hydr ocor t i sone, and di ur et i cs cont ai ni ng t hi azi de or mer -
cur y .

Bi car bonat e ( HCO, )

Bi car bonat e pl ays an i mpor t ant r ol e i n t he bl ood buf f er syst em, whi c h
hel ps mai nt ai n t he nor mal bl ood pH of 7. 4 . Si mpl y put , t he bl ood buf f er sys-
t em i s act i vat ed by a bui l dup of posi t i vel y char ged hydr ogen i ons i n t he
body . W hen t hi s bui l dup occur s, bi car bonat e, a negat i vel y char ged i on,
combi nes wi t h t he hydr ogen t o pr oduce a weak aci d, or buf f er , cal l ed car -
boni c aci d . Af t er a ser i es of chemi cal r eact i ons, an equi l i br i umi s est abl i shed
and pH l evel s ar e hel d wi t hi n t he nor mal r ange . Var i at i ons i n bi car bonat e
concent r at i ons wi l l af f ect t he pH l evel s i n bl ood .
Bi car bonat e al so ser ves as a t r anspor t mec hani s mt o mov e car bon di ox-
i de ( CO2. ) f r om t he body t i ssues t o t he l ungs wher e i t i s exhal ed . Car bon
di oxi de i s a wast e pr oduct and mus t be r emov ed f r omt he bl oodst r eam.

Nor mal Range

22- 26 mEq/ L

Var i at i ons f r om Nor mal . Decr eased bi car bonat e concent r at i ons r esul t s i n
aci dosi s, a bl ood pH of 7 . 35 or l ess . Aci dosi s i s seen i n r enal f ai l ur e, a var i -
et y of r espi r at or y di seases i n whi ch t he l ungs r et ai n car bon di oxi de, and
poor l y cont r ol l ed di abet es mel l i t us .
 Bl ood Chemi st r y Test s ( Par t 1) 39

I ncr eased bi car bonat e concent r at i ons r esul t s i n al kal osi s, a bl ood pH
gr eat er t han 7. 45 . Al kal osi s i s associ at ed wi t h hyper vent i l at i on, excess i n-
t ake or r et ent i on of bi car bonat e, and l oss of gast r i c aci d due t o vomi t i ng or
pot assi umdepl et i on .

Phos phat e ( PO, ) ; Phos phor us ( P)

About 85% of t he body' s phosphor us i s f ound i n bones and t eet h and i s

combi ned wi t h cal ci um. The r est of phosphor us i s i n t he sof t t i ssues . Phos-
phor us i n t he bl ood exi st s as phosphat e, whi c h i s necessar y f or t he gener -
at i on of bony t i ssue ; t he met abol i sm of gl ucose, f at s, and pr ot ei ns ; and t he
st or age and t r ansf er of ener gy . The r ange of nor mal f or adul t phosphat e
l evel s i s si gni f i cant l y di f f er ent t han t he r ange of nor mal f or chi l dr en . The
di f f er ence i s par t i al l y at t r i but ed t o t he i ncr eased l evel of gr owt h hor mone
pr esent i n chi l dr en unt i l puber t y .
Due t o t he r el at i onshi p bet ween cal ci umand phosphor us, bl ood phos-
phat e concent r at i on i s cl osel y l i nked t o pl asma cal ci um. I ncr eased phos-
phor us l evel s ar e accompani ed by a decr ease i n cal ci um and, conver sel y,
decr eased phosphor us l evel s ar e accompani ed by an i ncr ease i n cal ci um.

Nor mal Range

Adul t s 2. 7- 4 . 5 mg/ dl
Chi l dr en 4 . 5- 5 . 5 mg/ dl

Var i at i ons f r om Nor mal . Hypopphosphat emi a, i ncr eased phosphor us

l evel , i s mos t c ommonl y associ at ed wi t h ki dney dysf unct i on as i n r enal i n-
suf f i ci ency, sever e nephr i t i s, and r enal f ai l ur e . Hypopar at hyr oi di sm, i n-
cr eased gr owt h hor mone, vi t ami n D excess, bone t umor s, and Addi son' s
di sease al so demonst r at e i ncr eased phosphat e concent r at i ons . I n mos t of
t hese si t uat i ons, a decr ease i n pl asma cal ci um i s al so pr esent and di agnos-
t i cal l y si gni f i cant .
Hypophosphat emi a, decr eased phosphor us l evel , i s associ at ed wi t h
hyper par at hyr oi di sm, r i cket s i n chi l dhood, ost eomal aci a i n adul t s, mal -
absor pt i on syndr omes, mal nut r i t i on, and an excessi ve amount of i nsul i n
i n t he body . Hy pophos phat emi a i s accompani ed by an i ncr ease i n pl asma
cal ci um.
40 Chapt er 2

I nt er f er i ng Ci r cumst ances . A f al se i ncr ease i n phosphat e f ol l ows t he use of

l axat i ves or enemas . Or al l axat i ves may i ncr ease phosphor us l evel s as muc h
as 5 mg/ dL wi t hi n a f ew hour s . Dest r uct i on of r ed bl ood cel l s wi l l al so
cause hyper phosphat emi a .

Bl ood Gl ucose and Rel at ed Bl ood Sugar Test s

Gl ucose, a si mpl e sugar , i s t he mai n bl ood car bohydr at e and a maj or sour ce
of ener gy f or al l cel l s . The f ast i ng bl ood sugar ( FBS) , post pr andi al bl ood
sugar ( PPBS) , and t he gl ucose t ol er ance t est ( GTT) , or st andar d or al gl ucose
t ol er ance t est ( SOGTT) , ar e t hr ee of t he most f r equent l y per f or med bl ood
sugar t est s and ar e used t o det er mi ne t he l evel of gl ucose i n t he bl ood . Var i -
at i ons i n bl ood gl ucose l evel s ar e br oadl y cat egor i zed as hyper gl ycemi a, or
i ncr eased bl ood sugar l evel s, and hypogl ycemi a, or decr eased bl ood sugar
l evel s .
Rel at ed bl ood sugar t est s measur e t he body' s abi l i t y t o pr oduce i nsul i n
and gl ucose . I nsul i n and gl ucose pr oduct i on can be moni t or ed by measur -
i ng bl ood l evel s of C- pept i de, t he r esi due of i nsul i n f or mat i on ; gl ucagon, a
hor mone t hat st i mul at es t he pr oduct i on of gl ucose ; and i nsul i n, t he hor -
mone r esponsi bl e f or gl ucose met abol i sm. Tabl e 2- 2 i dent i f i es each bl ood
gl ucose t est and r el at ed di agnost i c appl i cat i ons .

Tabl e 2- 2. Bl ood Gl ucose and Rel at ed Bl ood Sugar Test s

Test Di agnost i c Appl i cat i on

Fast i ng bl ood sugar ( FBS) Di abet es scr eeni ng

Post pr andi al bl ood sugar ( PPBS) Conf i r ms di abet es

Gl ucose t ol er ance t est ( GTT) Rul e out di abet es; conf i r m hypogl ycemi a

C- pept i de Secr et or y f unct i on of pancr eat i c bet a cel l s ;

i nappr opr i at e i nsul i n i nj ect i on

Gl ucagon Assess pancr eat i c condi t i ons and di sor der s

I nsul i n Di abet es ; secr et or y f unct i on of pancr eat i c

al pha cel l s
 Bl ood Chemi st r y Test s ( Par t I ) 41

Fast i ng Bl ood Sugar ( FBS)

The f ast i ng bl ood sugar t est measur es t he pl asma l evel of gl ucose . Resul t s
ar e r epor t ed as t he number of mi l l i gr ams per deci l i t er ( mg/ dl ) of bl ood .
The t est i s per f or med t o det ect any di sor der of gl ucose met abol i sm, pr i -
mar i l y di abet es, and i s al so used t o assess t he management of di abet es . As
t he name i mpl i es, t he cl i ent mus t r ef r ai n f r omeat i ng appr oxi mat el y f our t o
t wel ve hour s pr i or t o t he t est . I f t he cl i ent i s an i nsul i n- dependent di abet i c,
bot h f ood and i nsul i n can be wi t hhel d unt i l t he bl ood speci men i s dr awn .

Nor mal Range

Adul t s 70- 115 mg/ dl

Chi l dr en 60- 110 mg/ dl
Newbor ns 30- 80 mg/ dl

Var i at i ons f r om Nor mal . An i ncr ease i n bl ood gl ucose, hyper gl ycemi a,
usual l y i ndi cat es di abet es . Myocar di al i nf ar ct i on, meni ngi t i s, or encephal i -
t i s, al l of whi c h pr oduce acut e st r ess i n bodi l y pr ocesses, may al so cause an
el evat ed bl ood gl ucose l evel . Ot her condi t i ons associ at ed wi t h hyper -
gl ycemi a i ncl ude an i ncr eased secr et i on of gl ucocor t i coi ds f r omt he adr enal
gl ands as seen i n Cushi ng' s di sease, pi t ui t ar y and pancr eat i c adenomas,
pancr eat i t i s, hyper t hyr oi di sm, and chr oni c i l l ness or i nact i vi t y .
Hyper gl ycemi a i s somet i mes seen dur i ng pr egnancy and i s cal l ed
gest at i onal di abet es . The condi t i on i s usual l y di agnosed dur i ng t he l at t er
hal f of t he pr egnancy and i s caused by an i ncr eased secr et i on of t he pl a
cent al hor mone l act ogen . Lact ogen can i nhi bi t t he act i on of i nsul i n,
t her eby i ncr easi ng t he bl ood gl ucose l evel . Gest at i onal di abet es pr esent s a
r i sk t o t he f et us and mot her and mus t be cl osel y moni t or ed t hr oughout t he
pr egnancy .
Hypogl ycemi a, a decr ease i n bl ood gl ucose, i s of t en caused by an over -
dose of i nsul i n or ski ppi ng meal s . Ot her causes of hypogl ycemi a i ncl ude
pancr eat i c i sl et cel l mal i gnancy, sever e l i ver damage, hypot hyr oi di sm, cor -
t i sol def i ci ency, and pi t ui t ar y hor mone def i ci ency.

I nt er f er i ng Ci r cumst ances . Many dr ugs can i nt er f er e wi t h f ast i ng bl ood

sugar r esul t s . St er oi ds, par t i cul ar l y pr edni sone, and di ur et i cs can si gni f i -
cant l y al t er t est r esul t s . Anest hesi a, st r ess, and obesi t y may al so af f ect bl ood
gl ucose l evel s .
42 Chapt er 2

Post pr andi al Bl ood Sugar ( PPBS) ; Two- Hour Post pr andi al Bl ood Sugar
( 2- hour PPBS)

Whi l e many pr act i t i oner s use t he f ast i ng bl ood sugar t est r esul t s as a pr i -
mar y scr een f or di abet es mel l i t us, t he post pr andi al bl ood sugar t est ( PPBS)
i s of t en used t o conf i r m t he di agnosi s . Pr i or t o t he t est t he cl i ent f ast s
over ni ght and t hen consumes a meal t hat cont ai ns appr oxi mat el y 100 gr ams
of car bohydr at es, or dr i nks a speci al 100- gr am car bohydr at e dr i nk . Two
hour s af t er eat i ng, a venous bl ood sampl e i s dr awn and anal yzed . The pur -
pose of t he PPBS t est i s t o assess t he body' s r esponse t o t he i ngest i on of car -
bohydr at es i n a meal .
Li ke t he f ast i ng bl ood sugar t est , t he post pr andi al bl ood sugar t est mea-
sur es t he pl asma l evel of gl ucose . The val ue of t he post pr andi al t est i s i t s
abi l i t y t o i dent i f y di abet i c condi t i ons t hat may not be cl ear l y r eveal ed by
t he f ast i ng bl ood sugar t est .

Nor mal Range

Age 50 or l ess 70- 140 mg/ dl

Age 50- 60 70- 150 mg/ dl
Age 60+ 70- 160 mg/ dl

Var i at i ons f r om Nor mal . A t wo- hour post pr andi al gl ucose l evel gr eat er
t han 200 mg/ dl i s i ndi cat i ve of di abet es mel l i t us .

I nt er f er i ng Ci r cumst ances . Di seases and condi t i ons t hat af f ect t he r esul t s of

t he f ast i ng bl ood sugar t est wi l l al so af f ect t he post pr andi al bl ood sugar
t est . Smoki ng dur i ng t he t est per i od can cause an i ncr eased gl ucose l evel .

Gl ucose Tol er ance Test ( GTT) ; St andar d Or al Gl ucose Tol er ance Test
( SOGTT)

The gl ucose t ol er ance t est i s a t i med t est of t he gl ucose concent r at i on i n bot h

t he bl ood and ur i ne. Thi s t est i s used t o conf i r m or r ul e out di abet es and i s a
def i ni t i ve t est f or di agnosi ng hypogl ycemi a . Af t er f ast i ng over ni ght , t he
cl i ent i s gi ven a concent r at ed amount of gl ucose di ssol ved i n a f l avor ed,
wat er - based dr i nk . Bl ood and ur i ne sampl es ar e col l ect ed over a t hr ee- t o
f our - hour per i od .
 Bl ood Chemi st r y Test s ( Par t I ) 43

I n heal t h, t he i nsul i n r esponse i s i mmedi at e and i n suf f i ci ent quant i t y t o

t ol er at e t he gl ucose l oad and t o mov e t he gl ucose f r omt he bl ood t o t he cel l s
of t he body . Ther e wi l l be a mi ni mal and t empor ar y r i se i n pl asma gl ucose
l evel s wi t hi n t he f i r st hour , wi t h a r et ur n t o nor mal l evel s i n t he second
hour of t est i ng .

Nor mal Range

Fast i ng 70- 115 mg/ dl

30 mi n l ess t han 200 mg/ dl
1 hour l ess t han 200 mg/ dl
2 hour s l ess t han 140 mg/ dl
3 hour s 70- 115 mg/ dl
4 hour s 70- 115 mg/ dl

Var i at i ons f r om Nor mal . I ndi vi dual s who ar e di abet i c or hypogl ycemi c
wi l l not be abl e t o t ol er at e t he gl ucose l oad admi ni st er ed dur i ng t he gl u-
cose t ol er ance t est . Di abet i c cl i ent s wi l l exhi bi t i ncr eased gl ucose l evel s t hat
exceed 190 mg/ dl at one hour ; 165 mg/ dl at t wo hour s ; or 145 mg/ dl at
t hr ee hour s . Di f f er ent t ypes of di abet es can be i dent i f i ed by t he gl ucose el -
evat i on at speci f i c t i me i nt er val s .
Ty pe I I or noni nsul i n- dependent di abet es mel l i t us ( NI DDM) , whi ch i s
char act er i zed by a del ay i n t he secr et i on of i nsul i n or a decr eased number of
i nsul i n r ecept or si t es, di spl ays an el evat ed gl ucose l evel unt i l t he t wo- hour
poi nt . Ty pe I or i nsul i n- dependent di abet es mel l i t us ( I DDM) , whi ch may
be char act er i zed by a l ack of i nsul i n or t he absence of i t s secr et i on, di spl ays
an el evat ed gl ucose l evel t hr oughout t he t est per i od . Gest at i onal di abet es
al so di spl ays an el evat ed gl ucose l evel t hr oughout t he t est per i od .
The hypogl ycemi c i ndi vi dual wi l l al so have t r oubl e handl i ng t he gl u-
cose l oad admi ni st er ed dur i ng t he gl ucose t ol er ance t est . The gl ucose l oad
wi l l t r i gger hi gh i nsul i n l evel s, whi c h wi l l i n t ur n mobi l i ze t he gl ucose t o
l eave t he bl ood . Consequent l y t he bl ood gl ucose l evel wi l l dr op bel ow nor -
mal at t wo hour s, and r emai n l ow f or t he r emai nder of t he t est per i od . Fi g-
ur e 2- 2 i s a gr aphi c r epr esent at i on of pl asma gl ucose l evel s and t he possi bl e
di sor der s i dent i f i ed by t he gl ucose t ol er ance t est .

I nt er f er i ng Ci r cumst ances. Ci r cumst ances sur r oundi ng t he pat i ent ' s l i f est yl e
can i nt er f er e wi t h t est r esul t s. Smok i ng and exer ci se dur i ng t he t est per i od
44 zyxwvuts
zyxwvuts
Chapter 2

300 lp*

I
-
-
-
IDDM and Gestational Diabetes

zyxwvut
zyxwvu I - NIDDM
Normal Response
Hypoglycemia

zy
I
Fasting 1 2 3 4
Time (hours)
Glucose Tolerance Test (GTT) Graph
~ ~~ zyxwvutsrqpon
ngure 2-2. Blood glucose levels associated with disorders identified by the glucose toler-
ance test.

can stimulate glucose levels. Prolonged inactivity and weight reduction di-
eting prior to testing can produce inaccurate results.
Specific drugs and medications will interfere with glucose tolerance.
These include insulin, large doses of aspirin, oral contraceptives, estrogens,
anti-inflammatory drugs, nicotine, lithium,and thiazide diuretics.

C-Peptide

C-peptide is formed in the islets of Langerhans, specifically the beta cells,

of the pancreas during insulin production. Since insulin and C-peptide are
secreted into the bloodstream in near equal amounts, measuring C-peptide
levels provides a reliable indication of blood insulin levels. The C-peptide
test is also used to assess the secretory function of the beta cells, and to
identify individuals who may be injecting insulin for nontherapeutic rea-
sons. C-peptide levels are reported as nanogram per milliliter (ng/mL).
The C-peptide test is particularly helpful in measuring blood insulin
levels in diabetic patients who have developed insulin antibodies as a re-
sult of being treated with pork or bovine insulin. C-peptide is not affected
by the presence of insulin antibodies.

Normal Range
0.78-1.89 ng/rnL
 Bl ood Chemi st r y Test s ( Par t I ) 45

Var i at i ons f r omNor mal . I ncr eased C- pept i de l evel s ar e associ at ed wi t h i n-

sul i noma, a beni gn t umor of t he bet a cel l s of t he pancr eas t hat causes t he
excessi ve secr et i on of i nsul i n . Si nce mos t C- pept i de i s degr aded i n t he ki d-
ney, r enal f ai l ur e r esul t s i n el evat ed C- pept i de l evel s .
Decr eased C- pept i de l evel s ar e associ at ed wi t h a r adi cal pancr eat ec-
t omy and di abet es mel l i t us . Fi ct i t i ous hypogl ycemi a, hypogl ycemi a caused
by secr et i ve i nj ect i on of i nsul i n, can be i dent i f i ed vi a decr eased l evel s of C-
pept i de .

I nt er f er i ng Ci r cumst ances . Obesi t y and or al hypogl ycemi c medi cat i ons or

agent s may al t er C- pept i de t est r esul t s .

Gl uc agon

Gl ucagon, a hor mone secr et ed by pancr eat i c al pha cel l s, assi st s i n t he mai n-
t enance of bl ood gl ucose l evel s . When bl ood gl ucose l evel s decr ease,
gl ucagon st i mul at es t he conver si on of gl ycogen i nt o gl ucose, whi c h r esul t s
i n an i ncr ease i n bl ood gl ucose . Gl ycogen, t he st or ed f or m of gl ucose, i s
f ound pr i mar i l y i n t he l i ver . Measur i ng pl asma gl ucagon l evel s assi st s i n
di agnosi ng pancr eat i c condi t i ons and di sor der s . Gl ucagon l evel s ar e r e-
por t ed as pi cogr amper mi l l i l i t er ( pg/ mL) .

Nor mal Range

50- 200 pg/ mL

Var i at i ons f r om Nor mal . Gl ucagon l evel s i ncr ease i n t he pr esence of acut e
pancr eat i t i s, di abet es mel l i t us, sever e di abet i c ket oaci dosi s, and gl uca-
gonoma, a pancr eat i c al pha cel l t umor . Si nce gl ucagon may be met abol i zed
by t he ki dneys, chr oni c r enal f ai l ur e or ki dney t r anspl ant r ej ect i on has t he
pot ent i al t o cause i ncr eased gl ucagon l evel s . Decr eased gl ucagon l evel s ar e
associ at ed wi t h chr oni c pancr eat i t i s, l oss of pancr eat i c t i ssue, and i di opat hi c
gl ucagon def i ci ency .

I nt er f er i ng Ci r cumst ances . Li f est yl e ci r cumst ances t hat may al t er gl uca-

gon t est r esul t s i ncl ude pr ol onged f ast i ng or moder at e t o heavy exer ci se .
Ther apeut i c i nt er vent i ons t hat al t er gl ucagon t est r esul t s consi st of r a-
di oact i ve scans wi t hi n f or t y- ei ght hour s of t est i ng ; dr ugs such as i nsul i n
46 Chapt er 2

and gl ucocor t i coi ds t hat may i ncr ease gl ucagon l evel s ; and dr ugs such as
secr et i n and pr opr anol ol t hat may decr ease gl ucagon l evel s .

I nsul i n

I nsul i n, a hor mone secr et ed by pancr eat i c bet a cel l s, r egul at es met abol i sm
of car bohydr at es and i s r esponsi bl e f or mai nt ai ni ng a const ant bl ood gl u-
cose l evel . I nsul i n l ower s bl ood gl ucose l evel s by pr omot i ng t he t r anspor t
of gl ucose f r om t he bl oodst r eam i nt o t he cel l s . I nsul i n l evel s can be mea-
sur ed by r adi oi mmunoassay, a t echni que t hat uses r adi oact i ve subst ances
t o det er mi ne t he concent r at i on of speci f i c bl ood const i t uent s . I nsul i n l evel s
ar e r epor t ed as mi cr ouni t s per mi l l i l i t er ( gU/ mL) .

Nor mal Range

4- 20 gU/ mL

Var i at i ons f r om Nor mal . Di seases such as acr omegal y, Cushi ng' s syn-
dr ome, and i nsul i noma ( a beni gn t umor of t he i nsul i n secr et i ng cel l s of t he
pancr eas) ar e associ at ed wi t h an i ncr eased l evel of i nsul i n . Decr eased i n-
sul i n l evel s ar e seen pr i mar i l y i n di abet es .

I nt er f er i ng Ci r cumst ances . Food i nt ake and obesi t y may cause f al se i n-

cr eases i n i nsul i n l evel s . Recent admi ni st r at i on of r adi oi sot opes may af f ect
t est r esul t s, as wi l l use of or al cont r acept i ves . Ot her dr ugs t hat may cause
i ncr eased i nsul i n l evel s i ncl ude cor t i cost er oi ds and l evodopa .

Li pi d Pr of i l e
Li pi ds ar e f at subst ances t hat pr ovi de ener gy t o t he body ; ar e necessar y f or
t he pr oduct i on of st er oi d hor mones and bi l e aci ds; and have a r ol e i n cr eat -
i ng cel l membr anes . Two domi nant l i pi ds ar e chol est er ol and t r i gl ycer i de .
Chol est er ol and t r i gl ycer i des ar e t r anspor t ed i n t he bl oodst r eamby l i popr o-
t ei ns, whi ch ar e compl ex mol ecul es consi st i ng of pl asma pr ot ei ns and
l i pi ds. Li popr ot ei ns ar e cat egor i zed as hi gh- densi t y l i popr ot ei ns ( HDL) ,
chol est er ol - r i ch pl asma pr ot ei ns; ver y- l ow- densi t y l i popr ot ei ns ( VLDL) ,
 Bl ood Chemi s t r y Test s ( Par t I ) 47

t r i gl ycer i de- r i ch pl asma pr ot ei ns ; and l ow- densi t y l i popr ot ei ns ( LDL) , t he

chol est er ol - r i ch pr oduct of ver y- l ow- densi t y l i popr ot ei n br eak down .
A l i pi d pr of i l e i ncl udes measur i ng pl asma l evel s of chol est er ol , t r i gl yc-
er i des, HDLs , LDLs, and VLDLs . The pur pose of t he l i pi d pr of i l e i s t o de-
t ect di sor der s of l i pi d met abol i sm and t o assess t he r i sk of at her oscl er osi s,
ar t er i oscl er ot i c hear t di sease ( ASHD) , and per i pher al vascul ar di sease .
Tabl e 2- 3 i dent i f i es each l i pi d t est and r el at ed di agnost i c appl i cat i ons .

Tabl e 2- 3. Li pi d Pr of i l e Test s

Test Di agnos t i c Appl i c at i on

Chol est er ol At her oscl er osi s ; cor onar y ar t er y di sease

Hi gh- densi t y l i popr ot ei n ( HDL)
Ver y- l ow- densi t y l i popr ot ei n ( VLDL)
Low- densi t y l i popr ot ei n ( LDL)
Tr i gl ycer i de
" Pr ot ect i ve" f or at her oscl er osi s
Maj or sour ce of chol est er ol - r i ch l ow-
densi t y l i popr ot ei ns
Deposi t s chol est er ol i nt o t he per i pher al
t i ssue ; ASHD; at her oscl er osi s ;
per i pher al vascul ar di sease
Cor onar y and vascul ar di sease ; f at
met abol i sm

Chol est er ol

One of t he most t est ed l i pi ds i n t he body, chol est er ol i s somet i mes onl y as-
soci at ed wi t h ar t er i oscl er ot i c vascul ar di sease . Chol est er ol , however , i s an
i mpor t ant c omponent of t he body and i s necessar y f or t he pr oduct i on of
bi l e aci ds, st er oi ds, and cel l ul ar membr anes . I n addi t i on, chol est er ol pl ays
a r ol e i n mai nt ai ni ng t he ski n' s r esi st ance t o wat er - sol ubl e subst ances and
pr event s excess evapor at i on of wat er f r omt he body .
About 75%of chol est er ol i s t r anspor t ed i n t he bl oodst r eam vi a l ow-
densi t y l i popr ot ei ns, and t he r emai ni ng 25% i s bound t o hi gh- densi t y
l i popr ot ei ns . I n t he past , bl ood chol est er ol was r epor t ed onl y as t ot al
chol est er ol . Cur r ent l abor at or y pr act i ces i ncl ude t he meas ur ement of
hi gh- densi t y l i popr ot ei ns, l ow- densi t y l i popr ot ei ns, and ver y- l ow- densi t y
l i popr ot ei ns .
48 Chapt er 2

Nor mal Ranges . Nor mal r anges wi l l var y wi t h age, di et , and geogr aphi c
l ocat i on . Si nce t her e ar e many var i abl es t hat af f ect pl asma chol est er ol l ev-
el s, most r ef er ences gi ve a desi r abl e r ange based pr i mar i l y on age . Under
most ci r cumst ances, an upper l i mi t of 200 mg/ dl or l ess i s desi r abl e .

Adul t / el der l y l ess t han 200 mg/ dl

Chi l dr en 120- 200 mg/ dl
I nf ant 70- 175 mg/ dl
Newbor n 53- 135 mg/ dl

Var i at i ons f r om Nor mal . Hi gh l evel s of chol est er ol ar e associ at ed wi t h at h-

er oscl er osi s and an i ncr eased r i sk of cor onar y ar t er y di sease . Ot her di s-
eases l i nked t o el evat ed chol est er ol i ncl ude uncont r ol l ed di abet es, obesi t y,
and hypot hyr oi di sm. Type I I f ami l i al hyper chol est er ol emi a i s an i nher i t ed
di sor der char act er i zed by hi gh l evel s of pl asma chol est er ol and ear l y evi -
dence of at her oscl er osi s . Hyper l i pi demi a t ype I I A i s anot her name f or t ype
I I f ami l i al hyper chol est er ol emi a .
Decr eased l evel s of chol est er ol occur when chol est er ol i s not absor bed
f r omt he gast r oi nt est i nal t r act as i n mal absor pt i on syndr omes, l i ver di sease,
hyper t hyr oi di sm, anemi a, and sepsi s . Ot her condi t i ons associ at ed wi t h de
cr eased chol est er ol i ncl ude per ni ci ous anemi a, hemol yt i c j aundi ce, sever e
i nf ect i ons, and t er mi nal st ages of debi l i t at i ng di seases such as cancer .

I nt er f er i ng Ci r cumst ances. Pr egnancy and r emoval of t he ovar i es wi l l cause

el evat ed chol est er ol r esul t s . Dr ugs t hat cause an i ncr eased chol est er ol l evel
i ncl ude adr enocor t i cot r opi c hor mone, anabol i c st er oi ds, or al cont r acept i ves,
Di l ant i n, di ur et i cs, and vi t ami n D. Decr eased chol est er ol l evel s ar e associ -
at ed wi t h dr ugs l i ke al l opur i nol , andr ogens, er yt hr omyci n, Mevacor , ni aci n,
and ni t r at es .

Hi gh- Densi t y Li popr ot ei n ( HDL)

Hi gh- densi t y l i popr ot ei ns ( HDL) ar e pl asma pr ot ei ns t hat f unct i on as car -

r i er s of pl asma chol est er ol . Measur i ng t he chol est er ol cont ai ned i n t he HDL
mol ecul e i s pr edi ct i ve of t he i ndi vi dual ' s r i sk f or cor onar y ar t er y di sease . I t
i s bel i eved t hat t he HDL mol ecul e car r i es chol est er ol f r omt he per i pher al
t i ssues of t he body t o t he l i ver , wher e t he chol est er ol i s conver t ed i nt o bi l e
 Bl ood Chemi st r y Test s ( Par t I ) 49

aci ds and event ual l y excr et ed . Chol est er ol t hat i s par t of t he hi gh- densi t y
l i popr ot ei n mol ecul e wi l l not be deposi t ed i n bl ood vessel wal l s . Because of
t hi s, HDL i s somet i mes r ef er r ed t o as t he " good" chol est er ol and i s be-
l i eved t o have a pr ot ect i ve ef f ect on t he ci r cul at or y syst em.

Nor mal Range

Men >45 mg/ dl

Women >55 mg/ dl

Var i at i ons f r om Nor mal . Some var i at i ons i n hi gh- densi t y l i popr ot ei n l ev-
el s ar e based on gender and age . I ncr eases i n HDL l evel s ar e not of t en seen
as pr obl emat i c . Howev er , si nce t he l i ver i s r esponsi bl e f or t he met abol i sm
of HDL, a nont her apeut i c el evat i on of HDL l evel s can si gni f y l i ver di sease .
Mos t i ndi vi dual s ar e mor e concer ned about l ow HDL l evel s .
Decr eased avai l abi l i t y of hi gh- densi t y l i popr ot ei ns may l eave mor e
chol est er ol f r ee t o be deposi t ed i n t he per i pher al t i ssue of t he body . Low
l evel s of HDLs i ncr ease t he r i sk of ASHD.

I nt er f er i ng Ci r cumst ances . Li f est yl e f act or s t hat i nf l uence HDL l evel s i n-

cl ude s mok i ng and al cohol i ngest i on, whi ch decr eases HDLs . Exer ci se can
r ai se HDL l evel s . Dr ugs t hat may cause a l i popr ot ei n i ncr ease ar e aspi r i n,
or al cont r acept i ves, st er oi ds, and sul f onami des .

Ver y- Low- Densi t y Li popr ot ei n ( VLDL) ; Low- Densi t y Li popr ot ei n ( LDL)

Ver y- l ow- densi t y l i popr ot ei ns ( VLDLs) ar e pl asma pr ot ei ns c ompos ed pr i -

mar i l y of t r i gl ycer i des and smal l amount s of chol est er ol . The VLDLs t r ans-
por t t r i gl ycer i des f r omt he l i ver t o t he per i pher al t i ssue . The br eak down of
VLDLs i s a maj or sour ce of l ow- densi t y l i popr ot ei ns ( LDLs) , whi ch ar e
chol est er ol - r i ch pl asma pr ot ei ns . I ncr eased l evel s of ver y- l ow- densi t y
l i popr ot ei n i s accompani ed by i ncr eased l evel s of l ow- densi t y l i popr ot ei ns .
Ver y- l ow- densi t y l i popr ot ei ns ar e associ at ed wi t h at her oscl er osi s, but not
t o t he s ame degr ee as l ow- densi t y l i popr ot ei ns .
Low- densi t y l i popr ot ei n, a pr i mar y t r anspor t er of chol est er ol , del i ver s
and deposi t s t he chol est er ol i nt o t he per i pher al t i ssues . Because of t hi s
f unct i on, LDLs ar e somet i mes r ef er r ed t o as " bad" chol est er ol and ar e as-
soci at ed wi t h at her oscl er osi s, ASHD, and per i pher al vascul ar di sease .
50 Chapt er 2

The VLDL and LDL l evel s ar e mat hemat i cal cal cul at i ons t hat ut i l i ze t he
t ot al chol est er ol , t r i gl ycer i de, and HDL val ues . The VLDL i s usual l y ex-
pr essed as a per cent age of t he t ot al bl ood chol est er ol . The LDL i s det er
mi ned by subt r act i ng t he HDL mi nus one- f i f t h of t he t r i gl ycer i de l evel
f r om t he t ot al chol est er ol . The VLDL and LDL l evel s can be cal cul at ed
manual l y or as par t of an aut omat ed l i pi d pr of i l e t est .

Nor mal Range

Low- densi t y l i popr ot ei n 60- 180 mg/ dl

Ver y- l ow- densi t y l i popr ot ei n 25- 50%of t ot al chol est er ol l evel

Var i at i ons f r om Nor mal . El evat ed LDL l evel s i ncr ease t he i ndi vi dual ' s r i sk
f or ASHD and per i pher al vascul ar di sease . Ot her di seases associ at ed wi t h i n-
cr eased LDLs i ncl ude t ype I I A f ami l i al hyper l i pi demi a, mul t i pl e myel oma,
hypot hyr oi di sm, ki dney and l i ver syndr omes, and di abet es .
I ncr eased VLDL l evel s ar e pr i mar i l y caused by t ype I V hyper l i pi demi a,
a c ommon f or mof i ncr eased l i popr ot ei ns t hat i s somet i mes f ami l i al . Ty pe I V
hyper l i pi demi a i s al so cal l ed endogenous hyper t r i gl ycer i demi a . Ot her di s
eases associ at ed wi t h el evat ed VLDDs i ncl ude al cohol i sm, obesi t y, di abet es
mel l i t us, chr oni c r enal di sease, and pancr eat i t i s . A di et r i ch i n f at t y f oods and
ani mal f at s may al so el evat e LDL and VLDL l evel s. Mal nut r i t i on and mal -
absor pt i on syndr omes wi l l r esul t i n decr eased LDL and VLDL l evel s .

I nt er f er i ng Ci r cumst ances . Ver y- l ow- densi t y l i popr ot ei n and l ow- densi t y

l i popr ot ei n r esul t s can be al t er ed by bi nge eat i ng . Dr ugs t hat i ncr ease l i po-
pr ot ei n l evel s i ncl ude or al cont r acept i ves, est r ogen, pr ogest i n, and st er oi ds .

Tr i gl ycer i de

Tr i gl ycer i des, t he mai n f or mof st or ed f at i n humans, ar e an i mpor t ant sour ce

of ener gy . Tr i gl ycer i des exi st s i n t he bl oodst r eam and ar e t r anspor t ed
t hr oughout t he body by VLDLs and LDLs . Excess pl asma t r i gl ycer i des ar e
st or ed i n t he body' s adi pose t i ssue .
Meas ur ement of t r i gl ycer i de l evel s i s par t of t he l i pi d pr of i l e . The t r i gl yc-
er i de t est i s used t o eval uat e t he i ndi vi dual ' s r i sk of cor onar y and vascul ar
di sease, and t o i dent i f y at her oscl er osi s . The t est can al so pr ovi de i nf or mat i on
about t he body' s abi l i t y t o met abol i ze f at .
 Bl ood Chemi st r y Test s ( Par t I ) 51

Nor mal Range . Var i at i ons i n t r i gl ycer i de r anges ar e af f ect ed by gender ,

age, and di et .

Men 40- 190 mg/ dl

Women 35- 160 mg/ dl
Chi l dr en 30- 100 mg/ dl

Var i at i ons f r om Nor mal . El evat ed t r i gl ycer i de l evel s i ncr ease t he i ndi vi d-
ual ' s r i sk of at her oscl er osi s, ASHD, and per i pher al vascul ar di sease . Ot her
cl i ni cal condi t i ons associ at ed wi t h i ncr eased t r i gl ycer i des i ncl ude al l t ypes
of hyper l i pi demi a, poor l y cont r ol l ed di abet es, pancr eat i t i s, ki dney syn-
dr omes, and t oxemi a . I ndi vi dual s wi t h a hi st or y of myocar di al i nf ar ct i on
may s how i ncr eased t r i gl ycer i des f or up t o one year post i nf ar ct i on . Ahi gh-
car bohydr at e di et may cont r i but e t o hi gh t r i gl ycer i de l evel s .
Decr eased t r i gl ycer i de val ues ar e sel dom seen as a cl i ni cal pr obl em.
Genet i c def ect s and chr oni c pr obl ems of mal nut r i t i on and mal absor pt i on
s y ndr ome wi l l exhi bi t decr eased t r i gl ycer i de l evel s . Ot her di seases associ
at ed wi t h l ow t r i gl ycer i des ar e chr oni c obst r uct i ve pul monar y di sease,
br ai n i nf ar ct i on, and hyper t hyr oi di sm.

I nt er f er i ng Ci r cumst ances . A t empor ar y i ncr ease i n t r i gl ycer i des can be t r i g-

ger ed by al cohol consumpt i on and a pr et est meal hi gh i n f at s . Pr egnancy,
or al cont r acept i ves, and est r ogen ar e al so associ at ed wi t h el evat ed val ues .
Dr ugs t hat may decr ease t r i gl ycer i de l evel s i ncl ude ascor bi c aci d, t he ant i -
t umor enz y me aspar agi nase, and l i pi d- l ower i ng agent s such as cl of i br at e .

Met abol i c Test s

The met abol i c pr ocesses of t he body r esul t i n t he pr oduct i on and el i mi na-
t i on of a var i et y of wast e pr oduct s k nown as met abol i c end pr oduct s . Fr e-
quent l y per f or med met abol i c end pr oduct t est s i ncl ude bi l i r ubi n, a wast e
pr oduct of hemol ysi s ; bl ood ur ea ni t r ogen ( BUN) , a t est t hat measur es
pl asma ur ea, t he ni t r ogenous wast e pr oduct of pr ot ei n met abol i sm; cr eat i -
ni ne, t he wast e pr oduct f or med i n t he muscl es ; and ur i c aci d, a wast e pr od-
uct der i ved f r om t he br eak down of nucl ei c aci ds . Anal yzi ng pl asma
bi l i r ubi n and bl ood ur ea ni t r ogen l evel s pr ovi des t he cl i ni ci an wi t h val uabl e
i nf or mat i on about l i ver f unct i on . Bl ood ur ea ni t r ogen, cr eat i ni ne, and ur i c
52 Chapt er 2

aci d pl asma l evel s assi st i n di agnosi ng ki dney pr obl ems . Tabl e 2- 4 i dent i f i es
each met abol i c end pr oduct t est and r el at ed di agnost i c appl i cat i ons .

Tabl e 2- 4 . Met abol i c End Pr oduct s Test s

Test Di agnost i c Appl i cat i on

Bi l i r ubi n Dest r uct i on of RBCs ; l i ver dysf unct i on

Bl ood ur ea ni t r ogen ( BUN) Li ver and ki dney f unct i ons
Cr eat i ni ne Ki dney excr et or y f unct i on ; decr eased muscl e
mass
Ur i c aci d Di agnost i c f or gout

Bi l i r ubi n

Bi l i r ubi n i s a wast e pr oduct r esul t i ng f r omt he l ysi s of r ed bl ood cel l s and

t he r el ease of hemogl obi n. The heme ( i r on) por t i on of t he hemogl obi n mol -
ecul e i s conver t ed i nt o t he bi l e pi gment bi l i r ubi n . Bi l i r ubi n i s a yel l ow
pi gment . An abnor mal l y i ncr eased bl ood concent r at i on cr eat es a j aundi ced
di scol or at i on of t he ski n, whi t es of t he eyes, and muc ous membr anes .
Bi l i r ubi n i s el i mi nat ed f r om t he body t hr ough a compl ex pr ocess i n-
vol vi ng t he l i ver . Ther e ar e t wo mai n f or ms of bi l i r ubi n : i ndi r ect or uncon-
j ugat ed bi l i r ubi n, whi ch i s t r anspor t ed t o t he l i ver as a bi l i r ubi n- al bumi n
compl ex and conver t ed t o di r ect or conj ugat ed bi l i r ubi n t hat i s event ual l y
excr et ed i n f eces and ur i ne . Li ver mal f unct i on can i nhi bi t t hi s pr ocess . Con-
sequent l y bi l i r ubi n wi l l not be conver t ed t o excr et abl e pr oduct s and wi l l ac-
cumul at e i n t he bl ood .
Bi l i r ubi n t est i ng can i ncl ude measur i ng t he l evel s of i ndi r ect bi l i r ubi n,
di r ect bi l i r ubi n, and t ot al bi l i r ubi n, t he s umof di r ect and i ndi r ect bi l i r ubi n .

Nor mal Range

Tot al bi l i r ubi n 0 . 2- 1 . 0 mg/ dl

I ndi r ect bi l i r ubi n 0 . 1- 0 . 7 mg/ dl
Di r ect bi l i r ubi n 0 . 1- 0 . 3 mg/ dl
Newbor n t ot al bi l i r ubi n 1- 12 mg/ dl
 Bl ood Chemi st r y Test s ( Par t 1) 53

Var i at i ons f r om Nor mal . El evat ed i ndi r ect bi l i r ubi n i s usual l y associ at ed
wi t h i ncr eased dest r uct i on of r ed bl ood cel l s, dest r uct i on of hemogl obi n as
seen i n hemol yt i c anemi as, per ni ci ous anemi a, si ckl e cel l anemi a, t r ansf u-
si on r eact i ons, and hemol yt i c di sease of newbor ns .
Abnor mal l y el evat ed i ndi r ect bi l i r ubi n concent r at i ons may al so i ndi -
cat e l i ver dysf unct i on i n t hat t he l i ver i s unabl e t o conver t i ndi r ect bi l i r ubi n
t o di r ect bi l i r ubi n . Hepat i c di seases associ at ed wi t h el evat ed i ndi r ect bi l i r u-
bi n i ncl ude hepat i t i s, ci r r hosi s, and ext ensi ve l i ver t umor s .
An i ncr ease i n di r ect bi l i r ubi n l evel s usual l y i ndi cat es an i nabi l i t y t o ex-
cr et e bi l i r ubi n . Gal l st ones, t umor s, bi l e duct obst r uct i on, and cancer of t he
pancr eat i c head can cause i ncr eases i n di r ect bi l i r ubi n .

I nt er f er i ng Ci r cumst ances. I mpr oper handl i ng of t he bl ood sampl e can

al t er t est r esul t s . Exposur e of t he speci men t o sunl i ght or hi gh- i nt ensi t y ar -
t i f i ci al l i ght at r oom t emper at ur e wi l l decr ease bi l i r ubi n concent r at i on .
Shaki ng t he bl ood speci men and t he pr esence of ai r bubbl es may al so de-
cr ease bi l i r ubi n l evel s .
Dr ugs t hat cause i ncr eased bi l i r ubi n i ncl ude al l opur i nol , anabol i c
st er oi ds, ascor bi c aci d, di abi nese, codei ne, st er oi ds, di ur et i cs, and or al con-
t r acept i ves . Dr ugs associ at ed wi t h decr eased l evel s ar e bar bi t ur at es, caf -
f ei ne, peni ci l l i n, and hi gh doses of sal i cyl at es .

Bl ood Ur ea Ni t r ogen ( BUN)

The BUN t est measur es t he amount of ur ea ni t r ogen i n t he bl ood . Ur ea, t he

end pr oduct of pr ot ei n met abol i sm, cont ai ns ni t r ogen, i s f or med i n t he l i ver ,
car r i ed vi a t he bl ood t o t he ki dneys, f i l t er ed i n t he gl omer ul us, and subse-
quent l y excr et ed . Bl ood ur ea ni t r ogen i s di r ect l y r el at ed t o t he met abol i c
f unct i on of t he l i ver and t he excr et or y f unct i ons of t he ki dneys . Thi s t est i s
used as a gr oss i ndi cat or of gl omer ul ar abi l i t y t o f i l t er ur ea f r omt he bl ood .
Whi l e near l y al l ki dney di seases cause i nadequat e ur ea excr et i on and a
subsequent r i se i n BUN, ot her condi t i ons wi l l af f ect BUN l evel s as wel l .
Ki dney f unct i on i s mor e accur at el y assessed usi ng t he BUN i n conj unct i on
wi t h cr eat i ni ne t est r esul t s .

Nor mal Range

Adul t 10- 20 mg/ dl

Chi l d 5- 18 mg/ dl
54 Chapt er 2

Var i at i ons f r om Nor mal . Azot emi a, i ncr eased BUN l evel s, i s usual l y
caused by i nadequat e excr et i on due t o ki dney di seases such as gl omer u-
l onephr i t i s, pyel onephr i t i s, and acut e t ubul ar necr osi s . Ot her causes of
azot emi a ar e ur i nar y obst r uct i on, excessi ve amount s of pr ot ei n i nt ake and
met abol i sm, dehydr at i on, myocar di al i nf ar ct i on, and chr oni c gout . De-
cr eased BUN l evel s ar e seen i n l i ver f ai l ur e, over hydr at i on vi a excessi ve i n-
t r avenous f l ui ds, mal nut r i t i on, i mpai r ed absor pt i on, and pr egnancy .

I nt er f er i ng Ci r cumst ances . Di et ar y habi t s and age can af f ect BUN l evel s .

Low- pr ot ei n, hi gh- car bohydr at e di et s can decr ease bl ood ur ea ni t r ogen,
and a hi gh- pr ot ei n di et wi l l i ncr ease BUN. I nef f i ci ent concent r at i on of t he
ur i ne can cause i ncr eased BUN l evel s i n t he el der l y . Dr ugs t hat may cause
i ncr eased BUN l evel s ar e cephal ospor i ns, ci spl at i n, aspi r i n, t et r acycl i nes,
and t hi azi de di ur et i cs . St r ept omyci n may cause a decr eased BUN.

Cr eat i ni ne

Cr eat i ni ne i s a wast e pr oduct of cr eat i ne phosphat e, a subst ance used i n

skel et al muscl e cont r act i on. Pr oduct i on of bot h cr eat i ne phosphat e and cr e-
at i ni ne i s a f unct i on of muscl e mas s and i s not af f ect ed by di et , age, gender ,
or exer ci se . Si nce cr eat i ni ne i s excr et ed sol el y by t he ki dney, pl asma cr eat i -
ni ne l evel s pr ovi de di agnost i cal l y si gni f i cant i nf or mat i on about ki dney ex-
cr et or y f unct i on .
Al t hough t he pl asma cr eat i ni ne t est i s a mor e sensi t i ve i ndi cat or of ki d-
ney di sease t han t he BUN, bot h ar e used t o di agnose i mpai r ed ki dney f unc-
t i on . These t est s ar e i mpor t ant component s of r enal f unct i on st udi es .

Nor mal Range

Adul t 0 . 7- 1 . 5 mg/ dl
Chi l dr en 0 . 3- 0 . 7 mg/ dl

Var i at i ons f r om Nor mal . I ncr eased pl asma cr eat i ni ne l evel s ar e di r ect l y as-
soci at ed wi t h ki dney mal f unct i on . Howev er , about 50%of ki dney f unct i on
mus t be l ost bef or e cr eat i ni ne l evel s r i se . Renal condi t i ons l i ke gl omer u-
l onephr i t i s, pyel onephr i t i s, acut e t ubul ar necr osi s, and ur i nar y t r act ob-
st r uct i on wi l l cause i ncr eased cr eat i ni ne l evel s. Di seases t hat af f ect ki dney
f unct i on or t hat i ncr ease muscl e mas s ar e al so associ at ed wi t h el evat ed
 Bl ood Chemi st r y Test s ( Par t 1) 55

pl asma cr eat i ni ne. Exampl es of t hese di seases i ncl ude di abet es, condi t i ons
t hat i mpai r r enal bl ood f l ow, acr omegal y, and gi gant i sm.
Decr eased cr eat i ni ne l evel s ar e associ at ed wi t h decr eased muscl e mas s .
Muscl e depl et i on or wast i ng i s seen i n sever e debi l i t at i on, st ar vat i on, and
muscul ar dyst r ophy .

I nt er f er i ng Ci r cumst ances . Si nce cr eat i ni ne i s not af f ect ed by di et , exer ci se,

or hor mones, t he maj or i nt er f er i ng ci r cumst ances ar e dr ugs or medi cat i ons .
Cr eat i ni ne val ues may be i ncr eased by chemot her apeut i c agent s such as
ci spl at i n, and dr ugs t hat ar e t oxi c t o t he ki dneys such as cephal ospor i ns .

Ur i c Ac i d

Ur i c aci d i s a pr oduct t hat i s f or med by t he br eak down of nucl ei c aci ds .

Mos t ur i c aci d i s excr et ed by t he ki dneys and s ome i s excr et ed by t he gas-
t r oi nt est i nal t r act . The mai n pur pose of t he ur i c aci d t est i s t o di agnose gout ,
a condi t i on i n whi ch ur i c aci d set t l es i n t i ssues and j oi nt s, par t i cul ar l y j oi nt s
of t he bi g t oe . The ur i c aci d t est i s al so used t o moni t or t he t r eat ment of gout .

Nor mal Range

Men 2 . 1- 5 . 5 mg/ dl
Women 2 . 0- 6. 6 mg/ dl
Chi l dr en 2 . 5- 5 . 5 mg/ dl

Var i at i ons f r om Nor mal . Hyper ur i cemi a, i ncr eased ur i c aci d i n t he bl ood, i s
a r esul t of excessi ve pr oduct i on of ur i c aci d . Over pr oduct i on of ur i c aci d i s
caused by excessi ve cel l dest r uct i on and t he subsequent br eak down of nu-
cl ei c aci ds ; excessi ve cel l pr oduct i on and dest r uct i on as seen i n l eukemi a ;
and i nef f i ci ent excr et i on of ur i c aci d, as i n ki dney f ai l ur e . Condi t i ons asso-
ci at ed wi t h hyper ur i cemi a ar e l y mphomas , met ast at i c cancer , st ar vat i on,
mul t i pl e myel oma, l ead poi soni ng, and many ot her chr oni c and syst emi c
di seases .
Decr eased ur i c aci d l evel s ar e seen i n Wi l son' s di sease, a r ar e i nher i t ed
di sor der of copper met abol i sm. Fanconi ' s syndr ome, a gr oup of di sor der s
t hat i ncl ude r enal t ubul e dysf unct i on, t he pr esence of gl ucose and phos
phat e i n t he ur i ne, and bi car bonat e wast i ng, exhi bi t s decr eased ur i c aci d
l evel s i n t he bl ood .
56 Chapt er 2

I nt er f er i ng Ci r cumst ances . Al t hough st r ess may cause an i ncr ease i n ur i c

aci d l evel s, dr ugs such as ascor bi c aci d, l ow- dose aspi r i n, caf f ei ne, ci spl at i n,
di ur et i cs, and Al domet ar e mor e c ommonl y associ at ed wi t h hyper ur i cemi a .
Decr eased ur i c aci d l evel s may be caused by dr ugs such as hi gh- dose as-
pi r i n, I mur an, cor t i cost er oi ds, est r ogens, and war f ar i n .

Summar y
Bl ood chemi st r y t est s pr ovi de a means of measur i ng var i ous chemi cal
component s of t he bl ood . Var i at i ons i n pl asma l evel s of t hese chemi cal
c ompounds pr ovi de t he cl i ni ci an wi t h val uabl e di agnost i c i nf or ma-
t i on .
Bl ood chemi st r y t est s can be cat egor i zed under t he f ol l owi ng headi ngs :
el ect r ol yt es, bl ood sugar s and gl ucose, l i pi ds and l i popr ot ei ns, met a-
bol i c end pr oduct s, enzymes, hor mones, and pr ot ei n t est s .
Pl asma el ect r ol yt es i ncl ude sodi um, pot assi um, cal ci um, magnes i um,
chl or i de, bi car bonat e, and phosphat e.
The mos t c ommonl y meas ur ed el ect r ol yt es ar e s odi um pot assi um,
chl or i de, and bi car bonat e .
Var i at i ons i n one or mor e el ect r ol yt es can be caused by a wi de var i et y
of di seases f r om dehydr at i on t o met ast at i c bone di sease . Conver sel y,
var i at i ons i n one or mor e el ect r ol yt es may al so cause pr obl ems t hat i n-
cl ude decr eased cont r act i l i t y of hear t muscl e and wat er r et ent i on .
Bl ood gl ucose and r el at ed bl ood sugar t est s ar e used t o assess t he pr o-
duct i on and met abol i sm of gl ucose, t he mai nt enance of bl ood gl ucose
l evel s, and t he pr oduct i on of i nsul i n .
The f ast i ng bl ood sugar , post pr andi al bl ood sugar , and gl ucose t ol er -
ance t est measur e bl ood gl ucose l evel s .
C- pept i de, gl ucagon, and i nsul i n l evel t est s moni t or t he pr oduct i on of
i nsul i n and gl ucagon .
Di seases associ at ed wi t h var i at i ons i n bl ood gl ucose and i nsul i n r ange
f r om di abet es mel l i t us t o pancr eat i c cel l t umor s .
Al i pi d pr of i l e i ncl udes measur i ng pl asma l evel s of chol est er ol , t r i gl yc-
er i des, hi gh- densi t y l i popr ot ei ns, ver y- l ow- densi t y l i popr ot ei ns, and
l ow- densi t y l i popr ot ei ns .
 Bl ood Chemi st r y Test s ( Par t 1) 57

" Var i at i ons i n pl asma l i pi d l evel s ar e pr edi ct i ve of at her oscl er osi s, ar t e-

r i oscl er ot i c hear t di sease, cor onar y ar t er y di sease, and per i pher al vas-
cul ar di sease.
" Met abol i c end pr oduct t est s i ncl ude bi l i r ubi n, bl ood ur ea ni t r ogen, cr e-
at i ni ne, and ur i c aci d .
" Bi l i r ubi n and bl ood ur ea ni t r ogen ar e di agnost i cal l y si gni f i cant f or l i ver
di seases and di sor der s .
" Bl ood ur ea ni t r ogen, cr eat i ni ne, and ur i c aci d ar e per f or med i n or der t o
di agnose ki dney pr obl ems .

CHAPTER REVI EW

1 . I dent i f y t he f ol l owi ng bl ood chemi st r y t est s :

a . Measur es pl asma i ons of sodi um, pot assi um,

chl or i de, and bi car bonat e

b . Pr i mar y scr een f or di abet es mel l i t us

c. Def i ni t i ve t est f or hypogl ycemi a

d. Hi ghl y r el i abl e t est f or conf i r mi ng di abet es

mel l i t us di agnosi s

e . Measur es abi l i t y of l i ver t o conver t gl ycogen

t o gl ucose

f. Measur es bl ood i nsul i n l evel s i n t he f ace of

i nsul i n ant i bodi es

Mos t c ommonl y or der ed l i pi d t est

h. I dent i f i es f ami l i al t ype I V hyper l i pi demi a

i. I dent i f i es t ype I I A f ami l i al hyper l i pi demi azyxwvutsrqponmlkjihgfedcbaZYXWVUTSRQP

Pr ovi des i nf or mat i on about t he body' s

abi l i t y t o met abol i ze f at
58 Chapt er 2

k . I dent i f i es hemol ysi s, l i ver dysf unct i on, bi l e

duct obst r uct i on, and r el at ed di seases

1. Measur es met abol i c f unct i on of t he l i ver and

excr et or y f unct i on of t he ki dneys

m. Sensi t i ve i ndi cat or of r enal di sease

n . Di agnost i c f or gout

2 . Or gani ze t hese bl ood t est s accor di ng t o t he f ol l owi ng cat egor i es :

a. Bl ood gl ucose and r el at ed t est

b . El ect r ol yt e t est s

c. Li pi d pr of i l e

d . Met abol i c end pr oduct t est s

Bi car bonat e Gl ucagon Post pr andi al bl ood

sugar
Bi l i r ubi n Gl ucose t ol er ance t est
Pot assi um
Bl ood ur ea ni t r ogen Hi gh- densi t y
l i popr ot ei n Sodi um
Cal ci um
I nsul i n Tr i gl ycer i de
Chl or i de
Low- densi t y Ur i c Aci d
Chol est er ol
l i popr ot ei n
Ver y- l ow- densi t y
C- pept i de
Magnes i um l i popr ot ei n
Cr eat i ni ne
Phosphat e
Fast i ng bl ood sugar

3 . I dent i f y a di sease t hat i s r el at ed t o an i ncr ease and decr ease of each pl asma el ec-
t r ol yt e .

El ect r ol yt e I ncr ease Dec r eas e

a. Sodi um

b . Pot assi um
 Bl ood Chemi st r y Test s ( Par t 1) 59

c. Cal ci um

d. Magnes i um

e. Chl or i de

f. Bi car bonat e

g . Phosphat e

4 . Br i ef l y di scuss t he met abol i c end pr oduct t est s accor di ng t o t he f ol l owi ng ques-

t i ons:

a . Whi c h t est s ar e per f or med t o i dent i f y r enal pr obl ems? Why ?

b . What ar e s ome of t he r enal di sor der s i dent i f i ed by i ncr eased and decr eased
t est l evel s?

c. Whi c h t est s ar e used t o assess l i ver f unct i on? Why ?

d . What t ypes of l i ver dysf unct i on ar e i dent i f i ed by t hese t est s? What ar e s ome
of t he speci f i c l i ver di seases or di sor der s i dent i f i ed by i ncr eased and de-
cr eased t est l evel s?

Case St udi es

1 . El si e El l i ason, a 70- year - ol d woman, was admi t t ed t o t he emer gency r oomof t he

hospi t al wi t h sever e vomi t i ng and di ar r hea . She has been exper i enci ng t hese
s y mpt oms f or t he past sever al days . The ER physi ci an suspect s t hat she i s expe
r i enci ng hypokal emi a . What el ect r ol yt e t est woul d t he physi ci an or der t o conf i r m
hypokal emi a and what mi ght t he r esul t be? W hy i s t hi s par t i cul ar el ect r ol yt e i m-
por t ant t o nor mal body f unct i on? What i mpact di d Ms . El l i ason' s physi cal s y mp-
t oms have on t he el ect r ol yt e?

2. Dr . Ri ce, an i nt er ni st , or der ed an FBS on Al f r ed Hol ms, a 54- year - ol d mal e di a-

bet i c . Accor di ng t o t he pat i ent r ecor d, t he FBS was 250 mg/ dl . Does t hi s t est r esul t
60 Chapt er 2

i ndi cat e hypogl ycemi a or hyper gl ycemi a? What i s t he di f f er ence? Coul d t hi s be a

f or mof gest at i onal di abet es? Di scuss whet her Dr . Ri ce woul d or der a PPBS and a
GTT and what val ue t hey woul d ser ve.

3. Cr yst al Hampt on i s a 60- year - ol d f emal e wi t h a di agnosi s of t ype I V hyper l i pi -

demi a. I n r evi ewi ng her r ecor d, you di scover t hat t he physi ci an has or der ed a
l i pi d pr of i l e. What i s a l i pi d pr of i l e and what speci f i c subst ances does i t measur e?
Pr oj ect what t he r esul t s mi ght be i n Mr s . Hampt on' s case? One of t he f at s bei ng
measur ed i s cal l ed " good chol est er ol , " what i s t he medi cal t er m f or " good cho-
l est er ol " and what i s t he f unct i on of t hi s t ype of chol est er ol ? How woul d t he t est
r esul t s di f f er i f t hi s wer e a mal e pat i ent ?

Chal l enge Act i vi t y

Descr i be t he bl ood chemi st r y t est s, and t he r esul t s of t hose t est s, t hat

woul d be associ at ed wi t h each di agnost i c st at ement i n t he f ol l owi ng l i st .
I s t her e any one t est t hat speci f i cal l y i dent i f i es each di sease? Whi ch, i f
any, of t hese di seases have si mi l ar bl ood chemi st r y t est r esul t s?

Cushi ng' s di sease ( hyper adr enal i sm)

Hypogl ycemi a
Pancr eat i t i s