Laboratory Analysis

of
Some Common
Liver & Biliary Tract
Diseases
LaboratoriumAnalisisBeberapaHatiCommon&PenyakitSaluranbilier
dr. Dumais A.A. Mandagie

1. PASSIVE CONGESTION OF THE LIVER :

Secondary to right heart failure :
Incresed pressure widening of
sinusoids destroy hepatocytes
Laboratory findings:
Mild Increase of AST / ALT, followed by
increase in Bilirubin and ALP.
PASIFKEMACETANDARIHATIYANG:
Sekunder
untukgagaljantungkanan:tekananpelebaranmengal
ami
peningkatandarisinusoidhepatositmenghancurkan
Laboratoriumtemuan:
RinganPeningkatanAST/ALT,diikutiolehkenaikanBiliru
bindanALP.

2. FATTY LIVER :
Usually without any or mild symptoms.
Sometimes + Inflammation (steatohepatitis)
severe chronic liver disease eg Cirrhosis
Etiology : Alcohol, DM, Obesity, etc
Morphologically : fatty infiltration in
hepatocytes.
Laboratory : usually mild. AST / ALT / ALP /
GGT increase slightly. Albumin / Bilirubin
normal.
Keadaan yangs sering terjadi, kebanyakan org
gemuk krena penumpukan lemak,,

 LEMAKHATI:
Biasanyatanpagejalaatauringan.
Kadangkadang+Peradangan(steatohepatitis)peny
akithatiyang parahkronismisalnyaSirosis
Etiologi:Alkohol,DM,Obesitas,dll
Morfologi:infiltrasilemakdalamhepatosit.
Laboratorium:biasanyaringan.AST/ALT/ALP/
GGTmeningkatsedikit.Albumin/Bilirubinnorm
al.
KeadaanyangsSeringterjadi,LemakGemukkr

3.CHOLESTASIS :
Disturbance of bile flow (Intra- and/or
extra-hepatic obstruction.
Hambatan pada alliran empedu dan
bilirubin
Laboratory findings:
Local intra-hepatic cholestasis :
Bilirubin N, ALP / GGT(gamma glutase
)increase
More longer and large cholestasis :
Bilirubin / ALP / GGT increase;
Cholesterol / PT increase;

 Cholestasis:
Gangguanaliranempedu(Intradan/atauobstruksiekstra-hati.
HambatanPADAalliranempedudanbiliru
bin
Laboratoriumtemuan:
Lokalintrahepaticcholestasis:BilirubinN,ALP/GGT
(gammaglutase)meningkatkan
Lebihpanjangdanbesarkolestasis:Bilirub
in/ALP/GGTmeningkat;Kolesterol/PT
meningkat;

4.ACUTE HEPATITIS :
Etiology :
Hepatitis Viruses (A, B, C, D, E)
Other Viruses (CMV, EBV, HerpesVaricella [kutil dan saraf], Arbovirus,
Echovirus, Adenovirus, etc)
Salmonella, Parasites
Toxic (Medicines, Alcohol, Toxins)
Autoantibodies, etc
7

 HEPATITISAKUT:
Etiologi:
Virushepatitis(A,B,C,D,E)
LainVirus(CMV,EBV,herpesVaricella[danSarafKutil],arbovirus,Echovirus
,adenovirus,dll)
Salmonella,Parasit
Beracun(Obat,Alkohol,Toksin)
Autoantibodies,dll

4.ACUTE HEPATITIS (VIRUS) :

Classical course of the disease :
Incubation period prodromal
symptoms clinical jaundice
convalescent phase.
Incubation period :
Differ among viruses (from few weeks
to months).

 HEPATITISAKUT(VIRUS):
Klasikperjalananpenyakit:
Masa
inkubasigejalaprodromalikterusklini
sfasesembuh.
Masa inkubasi:
Berbedaantaravirus(daribeberapa
mingguuntukbulan).

4.ACUTE HEPATITIS (VIRUS) :

Classical Jaundice X Variations :
Non-icteric, Cholestasis
Fulminant, Chronic Liver cirrhosis
and Hepatoma
Subclinical Recovered Immune or
healthy carrier (inactive state)

11

 HEPATITISAKUT(VIRUS):
KlasikPenyakit kuningXVariasi:
Non-icteric,cholestasis
Fulminan,kronisLiversirosis
danhepatoma
SubklinisSembuhkekebalanat
au"sehat"pembawa(keadaantidak
aktif)

4.ACUTE HEPATITIS (VIRUS) :

Laboratory Findings:
Classical type :
Transaminases (ALT > AST ) Increased;
start in prodromal phase & peak at
appearnce of jaundice
ALP and GGT increased
Bilirubinuria & acholic faeces before
jaundice appear then followed by
hyperbilirubinemia & bilirubinuria.
13

 HEPATITISAKUT(VIRUS):
LaboratoriumTemuan:
Klasiktype:
Transaminase(ALT>AST)Meningkatnya;mulai
padafaseprodromal&puncakpadaappearncep
enyakit kuning
ALPdanGGTmeningkat
Bilirubinuria&tinjaacholicsebelumpenyakit
kuningmunculkemudian
diikutidenganhiperbilirubinemia&bilirubinuria.

4.ACUTE HEPATITIS (VIRUS) :

Laboratory Findings:
Classical type :
ALT & AST increase, followed by
hyperbilirubinemia
Bilirubinuria (-) before blood bilirubin
return to N
Urinary urobilinogen vary : Increase
(end of prodromal), Decrease (peak of
jaundice), Increase (convalescence).
15

 HEPATITISAKUT(VIRUS):
LaboratoriumTemuan:
Klasiktype:
ALT&ASTmeningkat,diikutidenganhiperbili
rubinemia
Bilirubinuria(-)sebelumkembalibilirubindar
ahkeN
Urobilinogenurinbervariasi:Kenaikan(akhir
prodromal),Penurunan(puncakpenyakit
kuning),Kenaikan(pemulihan).

4.ACUTE HEPATITIS (VIRUS) :

Laboratory Findings:
Fulminant type :
ALT & AST very high increase (fast),
followed by fast decrease + worst
clinical picture + increased PT
Cholestatic type :
ALP, GGT and Bilirubin highly increase
Unicteric type : Bilirubin N
17

 HEPATITISAKUT(VIRUS):
LaboratoriumTemuan:
Fulminanketik:
ALT&ASTpeningkatanyang sangat
tinggi(cepat),diikutidenganpenurunangam
bar+terburukkliniscepat+PTmeningkat
Kolestasis,ketik:
ALP,GGTdanBilirubinyang
sangatmeningkatkan
Unictericketik:BilirubinN

5.CHRONIC HEPATITIS :
Process continues for > 6 months
(inflammation, laboratory abnormality,
HBsAg +, Anti-HCV +
Etiology :
Hepatitis Viruses, Metabolic, Several
kinds of drugs, auto-immunity

19

 HEPATITISKRONIS:
Prosesberlanjut>6bulan(radang,k
elainanlaboratorium,HBsAg+,AntiHCV+
Etiologi:
Virushepatitis,Metabolik,Beberapa
jenisobat,auto-imunitas

6.LIVER CIRRHOSIS :
Destruction of the liver architecture,
deposit of connective tissue with
nodule formation. Clinically : Latent &
Decompensated forms.
Latent form: Laboratory : ALT & AST
mildly increase (AST > ALT), GGT
increased, Urinary Urobilinogen
increased, 2 hour BA may increase,
most of LFT normal
Sirosis hati:
Pemusnahanarsitekturhati,penyimpananjaringanpe
nghubungdenganpembentukanbintil.Klinis:Laten&
dekompensasibentuk.
Bentuklaten:Laboratorium:ALT&ASTsedikitkenaika

21

6. LIVER CIRRHOSIS :
Decompensated form:
Laboratory :
Urine : Urobilinogen increase, Bilirubin +
Serum : Bilirubin increase, Albumin decrease,
Gamma-Globulin increase, polyclonal, betagamma-bridge); AP & GGT increased, AST & ALT
increased. Plasma PT increased without response
to Vit.K
Dekompensasibentuk:
Laboratorium:
Urine:Urobilinogenmeningkat,Bilirubin+
Serum:Bilirubinnaik,turunAlbumin,GammaGlobulinmeningkat,poliklonal,beta-gammajembatan);AP&GGTmeningkat,AST&ALTmeningkat.PlasmaPT
meningkattanparesponterhadapVit.K
22

7. HEPATOMA : (Hepatocellular Carcinoma)

Space occupaying lesion (SOL).
Etiologc factors : HBV, HCV, Hepatic Cirrhosis,
Aflatoxin
Laboratory : Cholestatic enzymes increased,
Hepatocellular enzymes increased, impaired
coagulation tests, Gamma-Globulin
increased, AFP highly increased, Ferritin and
Vit-B12 increased.
Hepatoma:(CarcinomaHepatocellular)
Spaceoccupayinglesi(SOL).
Etiologcfaktor:HBV,HCV,Sirosishati,Aflatoksin
Laboratorium:Cholestaticenzimmeningkat,Hepatocellularenz
immeningkat,teskoagulasiterganggu,GammaGlobulinmeningkat,AFPsangatmeningkat,FeritindanVit-

23

8.LIVER FAILURE :
Jaundice +/- ; Haemolysis
Blood Ammonia increased
Albumin decreased
Abnormal coagulation tests
HATIKEGAGALAN:
Penyakit kuning+/-;hemolisis
Amoniadarahmeningkat
Albuminmenurun
Teskoagulasiabnormal

24

9.IRON OVERLOAD STATES :

A. Genetic / Idiopathic
Haemochromatosis
Diagnosis : Fe Increased, Transferin
saturation increased, Serum Ferritin
increased. Biopsy : Fe increased.
B. Secondary / Acquired
Haemochromatosis
Found in : Thalassemia, Repeated
blood transfusion, High Dietary Iron,
Transferin deficiency.
25

 KELEBIHANBESI
Genetik/hemokromatosisidiopatik
Diagnosa:PeningkatanFe,kejenuhanTr
ansferinmeningkat,SerumFeritinmenin
gkat.
Biopsi:Femeningkat.
Sekunder/Acquiredhemokromatosis
Ditemukan
di:Thalasemia,transfusidarahberulang,Hi
ghDietBesi,Transferindefisiensi.

10. BILE / GALLBLADDER STONE :

Etiology : Bile composition, Stasis, Infection
Clinically : a variety of pictures
Laboratory findings :
according to its clinical form :
silent
acute / chronic cholecystitis
obstruction of main bile duct
Empedu/kantong empeduBATU:
Etiologi:Empedukomposisi,Stasis,Infeksi
Klinis:berbagaigambar
Laboratoriumtemuan:
sesuaidenganbentukklinis:
"diam"
akut/kroniskolesistitis
penyumbatansaluranempeduutama

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10. BILE / GALLBLADDER STONE :

Types :
Pigment stone (+ calcium, small,
hard, black / dark green)
Cholesterol stone (white or
yellowish)
Mixed stone
Empedu/kantong empeduBATU:
Jenis:
Pigmentbatu(+kalsium,kecil,keras,hita
m/hijautua)
Kolesterolbatu(putihataukekuning28