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LaboratoryAssessment ofThe Digestive

System Disorder

Kemas Ya’kub RahadiyantoClinical Pathologist

2015

Disampaikan dalam kuliah I tanggal ! "a#et 2015

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u$uan Inst#uksional

• "ahasis%a mengetahui dan memahamip#insip peme#iksaan labo#ato#is padakelainan sistem digesti& dan hepatobilie#

• "ahasis%a mengetahui dan memahamiaspek p#e analitik' analitik dan postanalitik peme#iksaan labo#ato#is

• "ahasis%a mengetahui dan dapatmenginte#p#etasi hasil peme#iksaankelainan sistem digesti& dan hepatobilie#

d#( Kemas Yakub )pPK 2

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Konsil Kedokteran Indonesia,SKDI 2012

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Konsil Kedokteran Indonesia,SKDI 2012

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d#( Kemas Yakub )pPK *

Level of Competencies 4

• "outh – Candidiasis – "outh ulce#

+apthous' he#pes,• )tomach and

duodenum – -ast#itis – -ast#oente#itis

• .i/e# – atty .i/e# – epatitis

– 3ncomplicatedepatitis 4 – moebic epatitis

bcess

• e$unum and Ileum – 6nte#itis

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.e/el o& Competencies !

• Pediat#ic – -ast#o8esophageal #e9uks – -ast#o8ente#itis – :o#ms – Pe#itonitis ube#culosis – ood lle#gy

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.e/el o& Competencies ;4• 6sophagus

– Co##osi/e lesion o& esophagus

• cute bdomen – Ileus – ppendicula# abcess

• )tomach and duodenum – -ast#o8duodenal ulce# – -ast#o8intestinal bleeding

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.e/el o& Competencies ;• "outh

– -lossitis• 6sophagus

– Re9u< esophagitis• cute bdomen

– )alphingitis – cute appendicitis

• -all bladde#' 4ileduct and Panc#eas – cute cholecystitis

• Colon – I##itable 4o%el

)yd#ome – =ec#oti>ing

ente#ocolitis – Di/e#ticulosis ?

di/e#ticulitis – Colitis – Rectal anal p#olaps – P#octitis – aemo##oids

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• Pediatric 3B – -ast#o8ente#itis %ith dehyd#ation – Dehyd#ation

• Pediatric 3A – "alabso#bsion – ood Intole#ance – 3mbilical e#nia – epatitis – Ci##hosis o& the li/e#

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d#( Kemas Yakub )pPK 1;

:hat kind o& labo#ato#y test

that #elated %ith thedigesti/e diso#de#@

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E "outh ulce# +apthous' he#pes, – Complete blood count, "erum

– #i$erential leu%oc&te count, Peripheral blood

– 'erritin, "erum – !luca on, Plasma

– ron, "erum – Potassium hyd#oanck smea#' )pecimen – itamin 4 12 ' )e#um


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d#( Kemas Yakub )pPK 1F

)tomach and duodenum

• -ast#itis – 4#ushing cytology' )pecimen' Diagnostic – Campylobacter 8like o#ganism test' )pecimen – olic acid' )e#um – -ast#in' )e#um – !astroscop&, #ia nostic – Helicobacter pylori , uic% o-ce serolo &,

"erum and titer, Blood – .istopatholo &, "pecimen

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– /ccult blood, "tool – Pepsinogen I and pepsinogen II' 4lood – 0rea breath test, #ia nostic

– itamin 4 12 ' )e#um

• -ast#oente#itis – 'ecal leu%oc&tes, "tool, #ia nostic – Meat 1bers, "tool – "tool culture, 2outine, "tool

d#( Kemas Yakub )pPK 1G

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)tomach and duodenum

• -ast#o8duodenal ulce# – 4 g#oup and Rh type' 4lood – mylase' )e#um – 4#ushing cytology' )pecimen' Diagnostic – Complete blood count' 4lood – 6ndoscopic ult#asonog#aphy' Diagnostic – -ast#in' )e#um – !astroscop&, #ia nostic – Helicobacter pylori , uic% o-ce serolo &,

"erum and titer, Blood

d#( Kemas Yakub )pPK 1*

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– .istopatholo &, "pecimen – Lipase, "erum

– /ccult blood, "tool – Pepsinogen I and pepsinogen II' 4lood – :ashing cytology' )pecimen


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• -ast#o8intestinal bleeding – Blood urea nitro en creatinine ratio,

Blood

– Complete blood count, Blood – 6sophagogast#oduodenoscopy' Diagnostic – /ccult blood, "tool – T&pe and crossmatch, Blood ("creen)


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6sophagus• Re9u< esophagitis• Co##osi/e lesion o& esophagus• -ast#o8esophageal #e9uks


Pediat#icE -ast#o8ente#itisE :o#ms

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Peritonitis Tuberculosis

• bdominal ult#asound'Diagnostic• mylase' )e#um• 4lood cultu#e' 4lood• 4lood gases' #te#ial' 4lood• 4ody 9uid + scitic 9uid,'

mylase' )pecimen• 4ody 9uid + scitic 9uid,'

nae#obic' Cultu#e• 4ody 9uid' ungus' Cultu#e• 4ody 9uid + scitic 9uid,'

Mycobacteria ' Cultu#e• 4ody 9uid + scitic 9uidH

3#ine,' Routine' Cultu#e

• 4ody 9uid analysis + scitic 9uid,'Cell count' )pecimen• Bod& uid c&tolo & (Ascitic

uid), "pecimen• Ce#eb#ospinal 9uid' .actic acid'

)pecimen

• Chest #adiog#aphy' Diagnostic• Complete blood count, Blood• Computed tomog#aphy o& the body

+ bdomenH %ith Cont#ast,'Diagnostic

• C+reactive protein, "erum or

plasma• *lectrol&tes, Plasma or serum• lat8plate #adiog#aph o& the

abdomen' Diagnostic

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– -enital' Candida albicans ' Cultu#e – -enital' Neisseria gonorrhoeae ' Cultu#e – istopathology' )pecimen – .actic acid' 4lood – .actate dehyd#ogenase' 4lood – .i/e# batte#y' )e#um – "agnetic #esonance imaging' Diagnostic – Pa#acentesis' Diagnostic – P#oth#ombin time and inte#national no#mali>ed #atio'

4lood – )edimentation #ate' 6#yth#ocyte' 4lood

d#( Kemas Yakub )pPK 2;

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Acute Abdomen

• )alphingitis• cute appendicitis

• ppendicula# abcess – Blood culture, Blood – Bod& uid (Abscess), Anaerobic, Culture – Complete blood count, Blood

– Comp#ession ult#asonog#aphy' Diagnostic – Computed tomog#aphy o& the body + bdomen,'

Diagnostic

d#( Kemas Yakub )pPK 2!

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d#( Kemas Yakub )pPK 2F

ColonE I##itable 4o%el )yd#omeE =ec#oti>ing ente#ocolitisE Di/e#ticulosis ? di/e#ticulitisE ColitisE Rectal anal p#olapsE P#octitis

• aemo##oids – Complete blood count' 4lood – Proctoscop&, #ia nostic

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Liver

• lanine aminot#ans&e#ase')e#um

• lkaline phosphatase' )e#um• ntimitochond#ial antibody'

)e#um• ntinuclea# antibody' )e#um• 4ili#ubin' otal' )e#um• Ce#uloplasmin' )e#um• Complete blood count' 4lood• -amma8

glutamylt#anspeptidase' 4lood

• epatitis se#ologies' )e#um

• .eucine aminopeptidase' 4lood

• E .i/e# batte#y' )e#um• .i/e# biopsy' Diagnostic• .i/e# scan' Diagnostic• .i/e# ult#asonog#aphy'

Diagnostic• 5 8=ucleotidase' 4lood• #nithine

ca#bamoylt#ans&e#ase' 4lood• P#oth#ombin time andinte#national no#mali>ed #atio'

Plasma• )t#iational antibody' )pecimen

d#( Kemas Yakub )pPK 2*

Fatty Liver

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• epatitis – cetaminophen' )e#um – lanine aminot#ans&e#ase' )e#um – lbumin' )e#um – lbumin?globulin #atio' )e#um – lkaline phosphatase' Isoen>ymes' )e#um – lkaline phosphatase' )e#um – lpha8antit#ypsin' )e#um – lpha8&etop#otein' )e#um – ntimitochond#ial antibody' 4lood


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– ntiLsmooth muscle antibody' )e#um – spa#tate aminot#ans&e#ase' )e#um – E 4ili#ubin' Di#ect' )e#um

– 4ili#ubin' Indi#ect' )e#um – 4ili#ubin' 3#ine – C1M immune comple< detection' )e#um – C; complement' )e#um – C! complement' )e#um – Chemist#y p#oAle' 4lood – Cytomegalo/i#us antibody' )e#um

d#( Kemas Yakub )pPK ;0

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– 6pstein84a## /i#us' )e#ology' 4lood – -amma8glutamylt#anspeptidase' 4lood – epatitis antibody' Ig" and Ig-' 4lood

– epatitis 4 co#e antibody' 4lood – epatitis 4 e antibody' )e#um – epatitis 4 e antigen' 4lood – epatitis 4 su#&ace antibody' 4lood – epatitis 4 su#&ace antigen' 4lood – epatitis C antibody' )e#um – epatitis C genotype' )e#um

d#( Kemas Yakub )pPK ;1

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– epatitis delta antibody' )e#um – E epatitis se#ologies – istopathology' )pecimen

– .actate dehyd#ogenase' Isoen>ymes' 4lood – E .i/e# batte#y' )e#um – .i/e# biopsy' Diagnostic – .i/e# scan' Diagnostic – .i/e# ult#asonog#aphy' Diagnostic – .upus test' 4lood – "ethot#e

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– 5 8=ucleotidase' 4lood – #nithine ca#bamoylt#ans&e#ase' 4lood – P#otein elect#opho#esis' )e#um

– P#oth#ombin time and inte#national no#mali>ed#atio' Plasma – )alicylate' 4lood – o

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• 3ncomplicated epatitis 4• moebic epatitis bcess

d#( Kemas Yakub )pPK ;!

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Kemas Yakub R' d#( )pPK ;F

)tool nalysis• -I bleeding'• -I obst#uction'

• bst#ucti/e $aundice'• Pa#asitic disease'• Dysente#y'

• 3lce#ati/e colitis' and• Inc#eased &at e

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Kemas Yakub R' d#( )pPK ;G

• n adult e

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Kemas Yakub R' d#( )pPK ;*

eces a#e composed o& the&ollo%ing mate#ialsO

• :aste #esidue o& indigestible mate#ial +eg' cellulose,om &ood eaten du#ing the p#e/ious ! days

• 4ile +pigments and salts,O stool colo# is no#mally dueto bile pigments that ha/e been alte#ed by bacte#ialaction(

• Intestinal sec#etions• :ate# and elect#olytes• 6pithelial cells that ha/e been shed• .a#ge numbe#s o& bacte#ia

• Ino#ganic mate#ial +10N820N,' chie9y calcium andphosphates• 3ndigested o# unabso#bed &ood +no#mally p#esent in

/e#y small Muantities,

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Kemas Yakub R' d#( )pPK ;7

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Kemas Yakub R' d#( )pPK !0

. 4 R RY 6) 6P 4I.I RY DI)6 )6) =DDI)6 )6) 6 P =CR6 )

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Kemas Yakub R' d#( )pPK !1

i

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!2

natomi isiologi ati

• isce#al o#gan

• 4e#at 1(; kg +adult,(• e#letak pada sisi kanan ba%ah diaph#agm(• e#lindung diba%ah a%cus costae dan pada

o#ang sehat no#mal tidak te#aba + palpated,(

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!;dr. Kemas Yakub SpPK 43

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!!

• Pe#da#ahan O – ( hepatica

;00 ml?’

– ( po#ta 1050 ml?’• .obulus Q unit

&ungsional – 50(000 L

100(000lobulus?hepa#

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!5dr. Kemas Yakub SpPK 45

Principal Function of the Liver

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!F46

Principal Function of the Liver Formation & secretion bile

Nutrient & vitamin metabolism•Glucose & other sugars• Am !o ac ds•" p d•#at$soluble % tam !s• ater$soluble % tam !s

Inactivation various substances

• 'o( !s•Stero ds•)ther hormo!esSynthesis of plasma proteins• Acute phase prote !s• Album !•*lott !g +actors•Stero d$b !d !g & other hormo!e$b !d !gprote !s

Immunity •Kup++er cells

"enggolongkan tes &ungsi

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!Gdr. Kemas Yakub SpPK 4,

enggolongkan tes &ungsihati

• )i#kulasi da#ah media kont#as• )istem bilia# bili#ubin metabolit• )el8sel hati >at disintesis

• ' dak dapat memast ka! causa• -era at kerusaka!

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!*

Tu5uan pemeri%saan 'aal.ati

1( 3ntuk diagnosisO ada?tidaknyapenyakit hati $enis penyakit hati

2( )k#iningO dilakukan bila diduga adapenyakit hati laten

;( ollo% up penyakit hati!( P#ognosisO pada umumnya makin be#at

kelainan &aal hati makin besa#ke#usakan p#ognosis makin bu#uk

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!7

5( Diagnosis 4andingOE epatomegaliE scitesE Pe#da#ahan )alu#an Ce#naE Ikte#us

a, Ikte#us emolitik +P#ehepatik,b, Ikte#us Pa#enkimatik + epatik,

c, Ikte#us bst#uksi +Post epatik,

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50

Peme#iksaan ungsi ati• Total bilirubin, direct bilirubin• Al%aline phosphatase,• -- '• Total protein,• ?- #atio' albumin,• A"T 6 ALT•

.D '• /i#al hepatitis panel'• P

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51dr. Kemas Yakub SpPK 5/

Bilirubin

• P#oduk akhi# %atabolisme heme • be#asal da#i O b' myoglobin dan

en>im pe#na&asan• )ebanyak 20 N bili#ubin' bukan da#i

heme e#it#osit tua da#i sel+sel

immatur di lien dan sumsum tulang komponen ini akan meningkat padakeadaan hemoliti%

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52

!" 0bGlob !

0eme0emos der !

1 l rub !2plasma

$1 bebas

$ ter kat Alb$'ak larut dlm a r

$ !d rek 1 l.

0epar

$Pelepasa! kata!album !

$- ko! ugas o asamGlukoro! dase

1 l. - glukoro! dase21 l. - rek 1 l.

#$pedu

%sus

%ro&ilino'en

!akteri ususen (

%ro&ilin

Feses (

Sterco&ilin

S e b a g a ! k e c l

"etabolisme 4ili#ubin

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5;dr. Kemas Yakub SpPK 53

M*TAB/L "M* B L 20B 7

Kata&olis$e

)& !iliru&in*erikat al&u$in%ncon+u'atedPLAS A

Su$&er lain

-A I./A. /in+al

ikroso$hepar

F

usus

!akteri usus

!iliru&indi'lukoronida

%ncon+ &iliru&in

uro&ilino'en

sterko&ilin

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5!

1 l rub ! totalde asa

,57 d rek 857 !d rek

9e!e!tuka! :e! s kterus Pe!t !g u!tuk9e!e!tuka! 'erap

• 1 l rub ! total ora!g de asa ;

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55

P#ocedu#e• btain a 58m. nonhemoly>ed sample om

a &asting patient( bse#/e standa#dp#ecautions( )e#um is used(

• P#otect the sample om ult#a/iolet light+sunlight,(

• /oid ai# bubbles and unnecessa#y shakingo& the sample du#ing blood collection(

• I& the specimen cannot be e

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5F

4ili#ubin dalamu#ine

• =o#mal tidak ditemukan bili#ubindalam u#ine

• danya bili#ubin dalam u#ine se#ingmendahului ge$ala kuning

• Pende#ita se#ing men$elaskanu#inenya be#%a#na kuning gelap 2 L; ha#i sebelum timbul kuning padaskle#a dan kulit

3# bili d l

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5G

3#obilinogen dalamu#ine

• es u#obilinogen me#upakan . yangpaling lemah nilai diagnostiknyaka#ena hasilnya selalu meningkat

mulai da#i ke#usakan hati yang paling#ingan sampai kelainan yang palingbe#at

• es ini tidak dapat menge/aluasikelainan hati ka#ena banyak penyakitlain yang menyebabkan u#obilinogenu#ine meningkat

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3# bili #i i&

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57

3#obilinogen u#ine negati&menun$ukkanO

• bst#uksi total da#i salu#an empedu• nemia

• Pembe#ian obat8obatan sepe#ti 4#oad)pect#um ntibiotic yang menekanpe#obahan bili#ubin men$adi

u#obilinogen oleh bakte#i usus

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F0

ypical acute epatitis( ingkat p#od#omal

Pada tingkat ini ikte#us belum tampak)- )-P meningkat seca#a p#og#esi&

mulai da#i G L 1! ha#i sebelum ikte#uslkaline &os&atase no#mal atau sedikit ↑Ikte#us indeks no#mal4ili#ubin sedikit ↑ te#utama bil(Digluko#onida3#obilinogen u#ine ↑ kemudian ↓4ili#ubin u#ine kadang8kadang + , positi&

4( i k t ikt #ik

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F1

4( ingkat ikte#ikDitandai dengan timbulnya ikte#us bili#ubinu#ia $elas te#lihat seca#amak#oskopisKada# bili#ubin total ↑ te#utama bil(Digluko#onida(

4ila te#lihat skle#a ikte#us bil( otal S ;mg3#obilinogen u#ine &eses ↑

lkaline &os&atase↑' )- )-P ↑Koleste#ol total +=, tetapi kolest( 6ste# ↓P#otein total #atio ?- be#ubah6lekt#o&o#ese O ditemukan ↑ γ globulin

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F2

C( ingkat Kon/alesenPende#ita mulai be#angsu# sehat T 2 LF minggu

Peme#iksaan lab( be#angsu# no#mal+kembali no#mal ; L ! bulan,

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F;

lcoholic .i/e# Disease

Pemakai alkohol $angka %aktu lamamenyebabkan gangguan padametabolisme sel hati no#mal' yangditandai dengan peningkatan sintesa&atty acid( kibatnya menyebabkanpembekakan sel lemak hati disebut

&atty li/e#

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F!

• Pada keadaan lebih lan$ut penyakitini dapat menyebabkan nec#osispada sel8sel hati yang se#ing dise#taidengan stasis bili#ubin dan $aundice

alcoholic hepatitis• Pada keadaan k#onik da#i alcoholic

li/e# disease ini se#ing menyebabkanpo#tal ci##hosis

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F5

-amba#an labo#ato#ium• )- )-P ↑ nec#osis sel8sel hati• Ratio )- )-P S 2 te#$adi pada G0N

alcoholic li/e# disease

• -- ↑ en>im ini me#upakan indikato#yang sensiti& pada pemakai alkoholk#onis

• .P ↑ ka#ena cholestasis tapi tidakmempunyai ko#elasi dengan alcoholichepatitis

• 4ili#ubin se#um ↑ ka#ena cholestasis

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FF

• )e#um immunoglobulin ↑• P ↑ ka#ena ↓ sintesis p#ot#ombine'

II' IU U• Di$umpai anemia mac#ocytic ka#ena

deAsiensi &olic acid' anemia palingse#ing te#$adi pada alcoholic li/e#

disease• e#dapat leucocytosis #adang padahati

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FG

epatitis K#onis• Disebut hepatitis k#onis apabila

ditemukan ge$ala klinik lebih da#i Fbulan setelah &ase akut hepatitis(

• epatitis tidak menyebabkanhepatitis k#onis

• 5 L 10N disebabkan oleh hepatitis 4• 20 L !0N disebabkan oleh keadaan

lain

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F*

-amba#an labo#ato#ium• .epatitis %ronis

a%tif – Peningkatan )-

)-P 7 L 10 < da#i

no#mal – Peningkatan γ globulin te#utama Ig-

– Peningkatan se#umbili#ubin +S ! mg?dl,

– Peningkatan .P – Penu#unan se#um

albumin

• .epatitis %ronispersisten – Peningkatan )-

)-P V 5 < = – Peningkatan se#um

bili#ubin V ! mg?dl – Peningkatan γ

globulin

– Peningkatan .P

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F7

Ci##hosis epatis• Yaitu ke#usakan hati bentuk lan$ut

yang ditandai oleh ke#usakanp#og#esi& pa#enkhim hati penambahan $a#ingan pa#ut( – Po#tal ci##hosis +.aennec,

be#hubungan dengan malnut#isi

alkoholism – 4ilie# ci##hosis post nec#otic ci##hosis me#upakan lan$utan hepatitis

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G0

• Pada keadaan inakti&' %alaupuntingkat ci##hosis sudah lan$utpeme#iksaan lab( sepe#ti O – 4ili#ubin se#um – .P – 6n>ym – est &aal metabolisme

9as h?ormal

Aka! tetap test 1SP me!u! ukka! rete!s @a!g me! !gkat

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G;

• 4ila ada ascites' bisa di$umpaigangguan keseimbangan ai# elekt#olit' dan $uga hypoalbuminemia

• Pada coma hepaticum amonia da#ah↑ sedangkan kada# u#eum ↓ ka#enakemampuan hati untuk mengubahamonia men$adi u#eum te#ganggu

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G!

epatic ailu#e• Ke#usakan pada sel hati dapat

disebabkan oleh be#macam >at to

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G5

-amba#an labo#ato#iumO

Ditandai dengan ↑ bili#ubin S !0 mg ↓ sek#esi bili#ubin

• Ke#usakan lebih pada hati dapatmenyebabkan gagal hati dimana te#$adinec#osis sel hati

• Dapat te#$adi oligou#i sebagaikomplikasi da#i penyakit hati

hepato#enal synd#ome

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GF

• ↓ albumin disebabkan sintesis p#otein ↓• Koleste#ol ↓ penu#unan sintesis

koleste#ol di hati• )- )-P ↓ lebih cepat• -lukose ↓ ka#ena penyimpanan

glikogen di hati ↓• P ↑ ka#ena penu#unan sintesis

p#ot#ombin' III' IU U di hati

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8lasi1%asi

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G*dr. Kemas Yakub SpPK ,=

8lasi1%asi 9aundice i%terus

:; Prehepati% 8 bili#ubin total se#um meningkat +bili#ubin

uncon$ugated?indi#ek, 8 #ansaminase O = 8 lkali &os&atase O =

8 P#otein O = PenyebabO hemolisis %elainanmetabolisme bilirubin

8lasi1%asi

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G7dr. Kemas Yakub SpPK ,>


< .epati%

8 $aundice?ikte#usO cepat 8 #ansaminase meningkat 8 lbuminO menu#un

Pen&ebab = penyakit hepa#

8lasi1%asi

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*0dr. Kemas Yakub SpPK =;


3 Post hepati% 8 kegagalan cai#an empedu mencapai

duodenum 8 4ili#ubin con$ugated meningkat 8 lkali &os&atase meningkat 8 Koleste#ol total meningkat 8 )teato##hoe 8 "alabso#psi it 'D'6'K

Pemeri%saan Laboratorium

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*1dr. Kemas Yakub SpPK =/

untu%pen&a%it hati (hepatobilier)

• 4ili#ubin total0';81 mg?dl 4ili#ubin di#ek V 0'25 md?dl• lkali &os&atase +;00C, G;820G 3?.• spa#tate t#ansaminase laki8laki sp 25 3?. + ) ?)- , %anita sp 21 3?.• lanin t#ansaminase laki8laki sp 27 3?. + . ?)-P , %anita sp 22 3?.• -amma -lutamyl laki8laki *8;* 3?.

#anspeptidase %anita5825 3?. +γ - ,

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*2dr. Kemas Yakub SpPK =8

Pemeri%saan Laboratoriumuntu%

pen&a%it hati (hepatobilier)

• lbumin ;'585g?d.• γ globulin 0'581'5 g?d.• P#ot#ombin time +P , 10W81!W

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*;dr. Kemas Yakub SpPK =3

6=XI"86=XI" 4) R3K I

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*!dr. Kemas Yakub SpPK =4

AL8AL '/"'ATA"*• e#dapat pada semua $a#ingan

• u pada epitel usus' tubulus gin$al'

tulang +osteoblas,' hati' plasenta• Yang be#ada dlm se#um tu be#asal

da#i hati?t#aktus bilia#is dan 50Nbe#asal da#i tulang

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*5dr. Kemas Yakub SpPK =5

AL8AL '/"'ATA"*

• "eningkat ta$am pada keadaanO 8 obst#uksi ekst#ahepatik +10812U=, 8 Kanke# tulang + 10825U=,

8 steitis de&o#mans +Peny Paget,

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*Fdr. Kemas Yakub SpPK =6

AL8AL '/"'ATA"*

• "edi%it menin %at pada = 8 bst#uksi int#ahepatik 8 hipe#pa#ati#oidisme

8 penyembuhan sesudah aktu#

!T( !lutam&l

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*Gdr. Kemas Yakub SpPK =,

!T( !lutam&lTransverase)

• 4e#asal da#i sistem hepatobilier

• "eningkat pada semua $enis penyakit hati

• Peningkatan >+3? @ 7 pada obst#uksiint#a ?post hepatik

• Lebih sensitif daripada al%ali fosfatase

untuk mendeteksi obstructive jaundice kolangitis' kolesistitis' ka#ena meningkatlebih dini dan menetap lebih lama

!T ( !lutam&l

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**dr. Kemas Yakub SpPK ==

!T ( !lutam&lTransverase)

• 4ila kada#nya meningkat 7 hepatitis' &atty li/e#

• Pada penyakit skeletal dan tulangnilainya no#mal sehinggapeme#iksaan ini dapat dipakai untukmemasti%an apa%ah penin %atan

al%alifosfatase berasal daripen&a%it tulan atau hati

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*7dr. Kemas Yakub SpPK =>

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70dr. Kemas Yakub SpPK >;

Peme#iksaan lainO

• 5’ nucleotidase• .eusine aminopeptidase

"!/T #A7 "!PT

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71dr. Kemas Yakub SpPK >/

"!/T #A7 "!PT

• e#dapat dalam sitoplasma danmito%ondria sel hati

• Pada %erusa%an hati rin an ' )-yang masuk dalam plasma' adalah)- yang be#asal da#i sitoplasma

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"!/T #A7 "!PT

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7;dr. Kemas Yakub SpPK >3

"!/T #A7 "!PT

• )-P S )- pen&a%it hepar

• )-P V )- )- S)-P pen&a%it mio%ard

02*0M

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7!dr. Kemas Yakub SpPK >4

02 0M

• asil akhi# katabolismeprotein asam amino yang te#banyak

• Disintesis da#i amonia di dalam hati

• 6ksk#esi tu melalui in5al= urin 'sedikit melalui %erin at

• 3#eum mengalami deg#adasi olehba%teri usus

%reu$

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75dr. Kemas Yakub SpPK >5

%reu$

reum d + ltras secara pas + d 'lo$eruli'in+al034056

rea ? 2ka!du!ga! ! troge! dalam ureumdalam whole blood 7 plas$a atau seru$

Kadar ureu$ dala$ plas$a dipen'aruhi ( $ !take prote ! dalam maka!a! $ kapas tas ekskres oleh g ! al

02*0M d 02*A 7

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7Fdr. Kemas Yakub SpPK >6

02*0M dan 02*A 7

• 8adar normal dalam plasma 3#ea = O G81* mg?d. 3#eum O 158;5 mg?d.

• 8adar normal dalam urine 3#ea = O 12820 mg?d. 3#eum O 258!; mg?d.

A /T*M A

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7G

dr. Kemas Yakub SpPK >,

A /T*M A• Peningkatan kada# ureum dan

%reatinin yang be#makna• ADotemia prerenal = ka#ena pe#&usi gin$al tidak cukup

Alt#asi glome#ulus menu#un• *tiolo i= =

dehid#asi' shock' penu#unan /olumeda#ah' bendungan $antung' katabolismep#otein yang meningkat

A /T*M A

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7*

dr. Kemas Yakub SpPK >=

A /T*M A• ADotemia renal disebab%an=

8 -lome#uloneitis 8 =eitis k#onis 8 =eoskle#osis 8 ubula# nek#osis

• ADotemia Post renal= 8 ka#ena obst#uksi salu#an kemih sehingga

u#eum diabso#psi ke dalam si#kulasi

P*70207A7 8A#A2

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77

dr. Kemas Yakub SpPK >>

02*A+7 "*20M• =ut#isi yang miskin

• Intake cai#an yang be#lebihan

• Pembe#ian cai#an int#a /ena yangbe#lebihan

• Kehamilan

.*PAT T "

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100

• Pe#adangan hati – Peningkatan ma#ke# hepatitis• kut K#onis

epatitis A

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101

dr. Kemas Yakub SpPK /;/

.epatitis A

)A

IK*# %S

243 8 hari

Fase akut

Anti )A I'/ 9I' 6

Anti )A I'

Fase penye$&uhan03:0 hari

I$unitas*hn6

epatitis B

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102

dr. Kemas Yakub SpPK /;8

.epatitis B

)!eA'

)!sA'

Anti )!cA'

Anti )!cI'

Anti )!e Anti )!s

!kubas4$/8 mg

Fase akut2312 $'

Post fase akut231; $'

Post !+eks6bl!$th!

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epatitis C

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10!

epatitis C

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105

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10*

Tumor markersTumor markers

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107


• Tumor markers are usually proteinswhich are produced from cancer cells or

as response to cancer• Cancer specific

• Tissue specific

T kT k

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110


• Cancer specific of certain canceroustissue BUT large overlap (low specificity)

• Tissue specific i.e PS ! "P! B#$C%!

thyroglo&ulin

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111

'n oncology tumor markers are used

• Screening i.e PS

• onitoring i.e "P• *iagnosis (when &iopsy is not feasi&le)• *etermine prognosis

Tumor markers C+Tumor markers C+

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112

Tumor markers CTumor markers C

• Comple, glycoprotein that is associated withthe plasma mem&rane of tumor cells! fromwhich may &e released in the &lood

• +levated specially in Colon cancer! But lso inPancreatic! %astric! -ung! &reast and variancancer

• -S in cirrhosis! inflammatory &oweldisease! chronic lung disease! pancreatits! /01of smokers! 21 of healthy population


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11;


• 3 T satisfactory for screening for ahealthy population

• onitor of recurrence

• onitor of treatment

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Tumor markers "PTumor markers "P

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11F

Tumor markers PTumor markers P

• Testicular germ cell tumor (em&rional orendodermal)diagnosis

monitor of recurrence ; responseprognostic marker (9/66.666

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11G

AS"< SP#"IAL A *I"L#

2000 %pdate of eco$$endations for the %se of *u$or arkersin !reast and "olorectal "ancer("linical Practice /uidelines of the A$erican Society of "linical

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11*

/>>, Becomme!dat o! C *DA s !ot recomme!ded to be used as a scree! !g test +or colorectal ca!cer.

8;;; Becomme!dat o! C ?o cha!ge.

/>>, Becomme!dat o! C *DA ma@ be ordered preoperat %el@ ! pat e!ts th colorectalcarc !oma + t ould ass st ! stag !g a!d surg cal treatme!t pla!! !g. Although ele%ated preoperat %e *DA 2E 5 !g m" ma@ correlate

th poorer prog!os s< data are !su++ c e!t to support the use o+ *DA to determ !e hether to treat a pat e!t th ad u%a!t therap@.


"#A as a arker for "olorectal "ancer

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117

/>>, Becomme!dat o! C + resect o! o+ l %er metastases ould be cl ! call@ !d cated<t s recomme!ded that postoperat %e serum *DA test !g ma@ be per+ormed e%er@

8 to 3 mo!ths ! pat e!ts th stage or d sease +or 8 or more @ears a+ter d ag!os s.

A! ele%ated *DA< + co!+ rmed b@ retest !g< arra!ts +urther e%aluat o! +or metastat c d sease but does !ot ust +@ the !st tut o! o+ ad u%a!t therap@ or s@stem c therap@ +or presumed metastat c d sease.


"#A as a arker for "olorectal "ancer

"#A k f " l t l "

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120

/>>, Becomme!dat o! C Prese!t data are !su++ c e!t to recomme!d rout !e use o+ the serum *DA alo!e +or mo! tor !g respo!se to treatme!t.

+ !o other s mple test s a%a lable to !d cate a respo!se

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121

"A 1:3: As a arker for Pancreatic "ancer

2006 recommendation for use of CA 1 ! as a screenin" test# *A />$> s !ot recomme!ded +or use as a scree! !g test +or pa!creat c ca!cer.

2006 recommendation for use of CA 1 ! to determine operability#

'he use o+ *A />$> test !g alo!e s !ot recomme!ded +or use ! determ ! !g operab l t@

or the results o+ operab l t@ ! pa!creat c ca!cer.

2006 recommendation for use of CA 1 ! to provide evidence of recurrence# *A />$> determ !at o!s b@ themsel%es

ca!!ot pro% de de+ ! t %e e% de!ce o+ d sease recurre!ce thout seek !g co!+ rmat o! th mag !g stud es +or cl ! cal + !d !gs a!d or b ops@.

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122

2006 recommendation for use of CA 1 ! for monitorin" response to therapy# Prese!t data are !su++ c e!t to recomme!d the rout !e use o+ serum *A />$> rules alo!e +or mo! tor !g respo!se to treatme!t.

0o e%er< *A />$> ca! be measured at the start o+ treatme!t +or locall@ ad%a!cedmetastat c d sease a!d e%er@ / to 3 mo!ths dur !g act %e treatme!t.

+ there s a! ele%at o! ! ser al *A />$> determ !at o!s< th s ma@ be a! !d cat o! o+ progress %e d sease< a!d co!+ rmat o! th other stud es should be sought.

"A 1:3: As a arker for Pancreatic "ancer

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Kemas Yakub R' d#( )pPK 12;

• ischbach' #ances alaska• itleO "anual o& .abo#ato#y

Diagnostic ests' Gth 6dition• Copy#ight Z200! .ippincott

:illiams :ilkins

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d#( Kemas Yakub )pPK 12!

Re&e#ence

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125

Re&e#ence• Rohen :' Chihi#o Y' 6lke .DH Color Atlas of Anatomy ' ! th ed• ischbach' HManual of Laboratory & Diagnostic Tests ' Gth

6d' 200!' .ippincott :illiams :ilkins' ;!F L *' ;*F 8 75• lte#ations in epatobilia#y unction' 6ssential o&

Pathophysiology

P3I)I -6. P

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12F

I%an )ulistia%anH "iskin tapi )ombong'2007

ante#a si#na pu#nama-adis layu pada nisan te#luka.ahan ke#ing pe#ti%i gulita

a#apan menyu#am di dinding tema#am ikam menta#i pada $i%a yang kelam asad hitam se#igala te#sungku#=gan8angan' mpi8mimpi' de%a langit te#kubu#Kausalitas dalam galau tak tuntas

=omo#8nomo# pada buku tanpa ke#tasDamp#at memunc#at pada batuItu sunyi tak $uga membeku

P3I)I -6. P

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12G

I%an )ulistia%anH "iskin tapi )ombong'2007

9Ante#a si#na pu#nama!A dis layu pada nisan te#lukaLA. an ke#ing pe#ti%i gulita.A #apan menyu#am di dinding tema#amT kam menta#i pada $i%a yang kelam

9Asad hitam se#igala te#sungku#7!A7 8angan' mpi8mimpi' de%a langit te#kubu#8A0 salitas dalam galau tak tuntas

7/mo#8nomo# pada buku tanpa ke#tas

#A mp#at memunc#at pada batutu sunyi tak $uga membeku

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12*

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k10 - lab digestif 2015

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