K10 - Lab Digestif 2015

Laboratory
Assessment of
The Digestive
System Disorder
Kemas Yakub Rahadiyanto
Clinical Pathologist
2015
Disampaikan dalam kuliah IT tanggal 4 Maret 2015
Tujuan Instruksional
Mahasiswa mengetahui dan memahami
prinsip pemeriksaan laboratoris pada
kelainan sistem digestif dan hepatobilier
Mahasiswa mengetahui dan memahami
aspek pre analitik, analitik dan post
analitik pemeriksaan laboratoris
Mahasiswa mengetahui dan dapat
menginterpretasi hasil pemeriksaan
kelainan sistem digestif dan hepatobilier
dr. Kemas Yakub SpPK
Konsil Kedokteran Indonesia,SKDI 2012
Konsil Kedokteran Indonesia,SKDI 2012
Level of Competencies 4
Mouth
Liver
Candidiasis
Mouth ulcer
(apthous, herpes)
Stomach and
duodenum
Gastritis
Gastroenteritis
Fatty Liver
Hepatitis A
Uncomplicated
Hepatitis B
Amoebic Hepatitis
Abcess
Jejunum and Ileum

Enteritis
Level of Competencies 4
Pediatric
Gastro-esophageal refluks
Gastro-enteritis
Worms
Peritonitis Tuberculosis
Food Allergy
Level of Competencies 3B
Esophagus
Corrosive lesion of esophagus
Acute Abdomen
Ileus
Appendicular abcess
Stomach and duodenum

Gastro-duodenal ulcer
Gastro-intestinal bleeding
10
Level of Competencies 3A
Mouth
Colon
Glossitis
Esophagus
Reflux esophagitis
Acute Abdomen
Salphingitis
Acute appendicitis
Gall bladder, Bile

duct and Pancreas
Acute cholecystitis
Irritable Bowel
Sydrome
Necrotizing
enterocolitis
Diverticulosis /
diverticulitis
Colitis
Rectal anal prolaps
Proctitis
Haemorroids
11
Pediatric 3B
Gastro-enteritis with dehydration
Dehydration
Pediatric 3A
Malabsorbsion
Food Intolerance
Umbilical Hernia
Hepatitis
Cirrhosis of the liver
12
What kind of laboratory test

that related with the
digestive disorder?
13
Mouth
Thrush (Candidiasis, Moniliasis)
Biopsy, Site-specific (Skin), Specimen

Complete blood count, Blood
Gram stain (Vaginal scraping), Diagnostic
Oral cavity cytology, Specimen
Potassium hydroxide preparation, Specimen
Skin, Fungus, Culture (with Sensitivity)
Throat culture for Candida albicans, Culture
Vaginal culture
14
Mouth ulcer (apthous, herpes)

Complete blood count, Serum
Differential leukocyte count, Peripheral blood
Ferritin, Serum
Glucagon, Plasma
Iron, Serum
Potassium hydroxide preparation, Specimen
Sedimentation rate, Erythrocyte, Blood
T- and B-lymphocyte subset assay, Blood
Throat culture for Candida albicans, Culture
Tzanck smear, Specimen
Vitamin B12, Serum
15

Gastritis
Brushing cytology, Specimen, Diagnostic

Campylobacter-like organism test, Specimen
Folic acid, Serum
Gastrin, Serum
Gastroscopy, Diagnostic
Helicobacter pylori, Quick office serology,
Serum and titer, Blood
Histopathology, Specimen
16
Occult blood, Stool

Pepsinogen I and pepsinogen II, Blood
Urea breath test, Diagnostic
Vitamin B12, Serum
Gastroenteritis
Fecal leukocytes, Stool, Diagnostic
Meat fibers, Stool
Stool culture, Routine, Stool
17

Gastro-duodenal ulcer
ABO group and Rh type, Blood

Amylase, Serum
Brushing cytology, Specimen, Diagnostic
Endoscopic ultrasonography, Diagnostic
Gastrin, Serum
Gastroscopy, Diagnostic
Helicobacter pylori, Quick office serology,
Serum and titer, Blood
18
Lipase, Serum
Occult blood, Stool
Pepsinogen I and pepsinogen II, Blood
Washing cytology, Specimen
19
Gastro-intestinal bleeding
Blood urea nitrogen/creatinine ratio,
Blood
Esophagogastroduodenoscopy, Diagnostic
Occult blood, Stool
Type and crossmatch, Blood (Screen)
20
Esophagus
Reflux esophagitis
Corrosive lesion of esophagus
Gastro-esophageal refluks
Pediatric
Gastro-enteritis
Worms
21
Peritonitis Tuberculosis
Abdominal ultrasound,
Diagnostic
Amylase, Serum
Blood culture, Blood
Blood gases, Arterial, Blood
Body fluid (Ascitic fluid),
Amylase, Specimen
Anaerobic, Culture
Body fluid, Fungus, Culture
Mycobacteria, Culture
Body fluid (Ascitic fluid;
Urine), Routine, Culture
Body fluid analysis (Ascitic fluid),

Cell count, Specimen
Body fluid cytology (Ascitic
fluid), Specimen
Cerebrospinal fluid, Lactic acid,
Specimen
Chest radiography, Diagnostic
Computed tomography of the body
(Abdomen; with Contrast),
Diagnostic
C-reactive protein, Serum or
plasma
Electrolytes, Plasma or serum
Flat-plate radiograph of the
abdomen, Diagnostic
Genital, Candida albicans, Culture

Genital, Neisseria gonorrhoeae, Culture
Lactic acid, Blood
Lactate dehydrogenase, Blood
Liver battery, Serum
Magnetic resonance imaging, Diagnostic
Paracentesis, Diagnostic
Prothrombin time and international normalized ratio,
Blood
Sedimentation rate, Erythrocyte, Blood
23
Acute Abdomen
Salphingitis
Acute appendicitis
Appendicular abcess
Blood culture, Blood

Body fluid (Abscess), Anaerobic, Culture
Compression ultrasonography, Diagnostic
Computed tomography of the body (Abdomen),
Diagnostic
24
Differential leukocyte count, Peripheral blood

Histopathology (Postoperatively), Specimen
Infectious mononucleosis screening test, Blood
Occult blood, Stool
Pregnancy test, Routine, Serum, and Qualitative,
Urine
Urinalysis, Urine
Jejunum and Ileum

Enteritis
25
Colon
Irritable Bowel Sydrome

Necrotizing enterocolitis
Diverticulosis / diverticulitis
Colitis
Rectal anal prolaps
Proctitis
Haemorroids
Proctoscopy, Diagnostic
26
Gall bladder, Bile duct and

Pancreas
Acute cholecystitis
Alanine aminotransferase,
Serum
Alkaline phosphatase, Serum
Amylase, Serum
Aspartate aminotransferase,
Serum
Bilirubin, Serum
Computed tomography of
the body (Abdomen),
Diagnostic
Differential leukocyte count,
Peripheral blood
Gallbladder and biliary system

ultrasonography, Diagnostic
Hepatobiliary scan, Diagnostic
Gammaglutamyltranspeptidase, Blood
Glucose, Serum (Random)

Ornithine
carbamoyltransferase, Blood
Endoscopic retrograde
cholangiopancreatography,
Diagnostic
27
Liver
Fatty Liver
Alanine aminotransferase,
Serum
Antimitochondrial antibody,
Serum
Antinuclear antibody, Serum
Bilirubin, Total, Serum
Ceruloplasmin, Serum
Gammaglutamyltranspeptidase, Blood
Hepatitis serologies, Serum
Leucine aminopeptidase, Blood

Liver biopsy, Diagnostic
Liver scan, Diagnostic
Liver ultrasonography,
Diagnostic
5-Nucleotidase, Blood
Ornithine
carbamoyltransferase, Blood
Prothrombin time and
international normalized ratio,
Plasma
Striational antibody, Specimen
28
Hepatitis A
Acetaminophen, Serum
Alanine aminotransferase, Serum
Albumin, Serum
Albumin/globulin ratio, Serum
Alkaline phosphatase, Isoenzymes, Serum
Alpha-antitrypsin, Serum
Alpha-fetoprotein, Serum
Antimitochondrial antibody, Blood
29
Antismooth muscle antibody, Serum

Aspartate aminotransferase, Serum
Bilirubin, Direct, Serum
Bilirubin, Indirect, Serum
Bilirubin, Urine
C1q immune complex detection, Serum
C3 complement, Serum
C4 complement, Serum
Chemistry profile, Blood
Cytomegalovirus antibody, Serum
30
Epstein-Barr virus, Serology, Blood

Gamma-glutamyltranspeptidase, Blood
Hepatitis A antibody, IgM and IgG, Blood
Hepatitis B core antibody, Blood
Hepatitis B e antibody, Serum
Hepatitis B e antigen, Blood
Hepatitis B surface antibody, Blood
Hepatitis B surface antigen, Blood
Hepatitis C antibody, Serum
Hepatitis C genotype, Serum
31
Hepatitis delta antibody, Serum

Hepatitis serologies
Lactate dehydrogenase, Isoenzymes, Blood
Liver biopsy, Diagnostic
Liver scan, Diagnostic
Liver ultrasonography, Diagnostic
Lupus test, Blood
Methotrexate, Serum
32
5-Nucleotidase, Blood
Ornithine carbamoyltransferase, Blood
Protein electrophoresis, Serum
Prothrombin time and international normalized
ratio, Plasma
Salicylate, Blood
Toxoplasmosis serology, Serum
Urobilinogen, Urine
33
Uncomplicated Hepatitis B
Amoebic Hepatitis Abcess
34
LABORATORY
TEST OF
GASTROINTESTINAL
DISEASES
Kemas Yakub R, dr. SpPK
35
Stool Analysis
GI bleeding,
GI obstruction,
Obstructive jaundice,
Parasitic disease,
Dysentery,
Ulcerative colitis, and
Increased fat excretion.
36
An adult excretes 100 to 200 g of

fecal matter a day, of which as much
as 75% may be water. The feces are
what remain of the 8 to 10 L of
digested fluid-like material that enters
the intestinal tract each day, and oral
food and fluids, saliva, gastric
secretions, pancreatic juice, and bile
add to the formation of feces.
37
Feces are composed of the

following materials:
Waste residue of indigestible material (eg, cellulose)
from food eaten during the previous 4 days
Bile (pigments and salts): stool color is normally due
to bile pigments that have been altered by bacterial
action.
Intestinal secretions
Water and electrolytes
Epithelial cells that have been shed
Large numbers of bacteria
Inorganic material (10%-20%), chiefly calcium and
phosphates
Undigested or unabsorbed food (normally present in
very small quantities)
38
39
LABORATORY TEST OF
HEPATOBILIARY DISEASES AND
DISEASES OF THE PANCREAS
40
41
Anatomi &
Fisiologi Hati
Visceral organ
Berat 1.3 kg (adult).
Terletak pada sisi kanan bawah diaphragm.
Terlindung dibawah awcus costae dan pada
orang sehat normal tidak teraba ( palpated).
42
43
43
Perdarahan :
A. hepatica
300 ml/
V. porta
1050 ml/
Lobulus = unit
fungsional
50.000
100.000
lobulus/hepar
44
45
45
Principal Function of the Liver

Formation & secretion bile
Nutrient & vitamin metabolism
Glucose & other sugars
Amino acids
Lipid
Fat-soluble vitamins
Water-soluble vitamins
Inactivation various substances
Toxins
Steroids
Other hormones
Synthesis of plasma proteins
Acute phase proteins
Albumin
Clotting factors
Steroid-binding & other hormone-binding
proteins
Immunity
Kupffer cells
46
46
Menggolongkan tes fungsi

hati
Sirkulasi darah media kontras
Sistem biliar bilirubin & metabolit
Sel-sel hati zat disintesis
Tidak dapat memastikan causa

Derajat kerusakan
47
47
Tujuan pemeriksaan Faal

Hati
1. Untuk diagnosis: ada/tidaknya
penyakit hati & jenis penyakit hati
2. Skrining: dilakukan bila diduga ada
penyakit hati laten
3. Follow up penyakit hati
4. Prognosis: pada umumnya makin berat
kelainan faal hati makin besar
kerusakan prognosis makin buruk
48
5. Diagnosis Banding:
Hepatomegali
Ascites
Perdarahan Saluran Cerna
Ikterus
a) Ikterus Hemolitik (Prehepatik)
b) Ikterus Parenkimatik (Hepatik)
c) Ikterus Obstruksi (Post Hepatik)
49
Pemeriksaan Fungsi Hati
Total bilirubin, direct bilirubin

Alkaline phosphatase,
GGT,
Total protein,
A/G ratio, albumin,
AST & ALT
LDH,
viral hepatitis panel,
PT
50
Bilirubin
Produk akhir katabolisme heme
berasal dari : Hb, myoglobin dan
enzim pernafasan
Sebanyak 20 % bilirubin, bukan dari
heme eritrosit tua dari sel-sel
immatur di lien dan sumsum tulang
komponen ini akan meningkat pada
keadaan hemolitik
51
51
Metabolisme Bilirubin
Globin
RBC
Hemosiderin
Hb
Heme
Bilirubin
(plasma)
Urobilinogen
Ren :
Urobilin
Se
ba
gia
nk
ec
il
Bakteri usus
Feses :
Stercobilin
Empedu
- terikat Alb
-Tak larut dlm air
-Indirek / Bil. I
Hepar
Usus
-Bi bebas
-Pelepasan ikatan
albumin
-Dikonjugasi o asam
Glukoronidase
Bil. Diglukoronidase
(Bil. Direk / Bil. II)
52
METABOLISME BILIRUBIN
Katabolisme
Hb
JARINGAN
Sumber lain
Bilirubin
Terikat albumin
Unconjugated
PLASMA
Ginjal
Mikrosom
hepar
Bilirubin
diglukoronida
urobilinogen
sterkobilin
VF
usus
Unconj bilirubin
Bakteri usus
53
53
Menentukan Jenis Ikterus Penting untuk

Menentukan Terapi
Bilirubin total
dewasa
75% direk
25% indirek
Bilirubin total orang dewasa 0,1 1 mg%

Bilirubin direct 0,1 0,2 mg%
Bilirubin indirect 0,1 0,8 mg%
Bilirubin total anak-anak 0,9 2,0 mg%
54
Procedure
Obtain a 5-mL nonhemolyzed sample from
a fasting patient. Observe standard
precautions. Serum is used.
Protect the sample from ultraviolet light
(sunlight).
Avoid air bubbles and unnecessary shaking
of the sample during blood collection.
If the specimen cannot be examined
immediately, store it away from light and in
a refrigerator.
55
Bilirubin dalam
urine
Normal tidak ditemukan bilirubin
dalam urine
Adanya bilirubin dalam urine sering
mendahului gejala kuning
Penderita sering menjelaskan
urinenya berwarna kuning gelap 2
3 hari sebelum timbul kuning pada
sklera dan kulit
56
Urobilinogen dalam
urine
Tes urobilinogen merupakan LFT yang
paling lemah nilai diagnostiknya
karena hasilnya selalu meningkat
mulai dari kerusakan hati yang paling
ringan sampai kelainan yang paling
berat
Tes ini tidak dapat mengevaluasi
kelainan hati karena banyak penyakit
lain yang menyebabkan urobilinogen
urine meningkat
57
Urobilinogen urine meningkat pada:
Portal cirhosis
Penghancuran SDM yang meningkat
Hepatitis akut
Myocard infark
Pulmonary infark
58
Urobilinogen urine negatif

menunjukkan:
Obstruksi total dari saluran empedu
Anemia
Pemberian obat-obatan seperti Broad
Spectrum Antibiotic yang menekan
perobahan bilirubin menjadi
urobilinogen oleh bakteri usus
59
Typical acute Hepatitis

A. Tingkat prodromal
Pada tingkat ini ikterus belum tampak
SGOT & SGPT meningkat secara progresif
mulai dari 7 14 hari sebelum ikterus
Alkaline fosfatase normal atau sedikit
Ikterus indeks normal
Bilirubin sedikit terutama bil.
Diglukoronida
Urobilinogen urine kemudian
Bilirubin urine kadang-kadang (+) positif
60
B. Tingkat ikterik
Ditandai dengan timbulnya ikterus &
bilirubinuria jelas terlihat secara
makroskopis
Kadar bilirubin total terutama bil.
Diglukoronida.
Bila terlihat sklera ikterus bil. Total > 3
mg
Urobilinogen urine & feses
Alkaline fosfatase , SGOT & SGPT
Kolesterol total (N) tetapi kolest. Ester
Protein total & ratio A/G berubah
Elektroforese : ditemukan globulin
61
C. Tingkat Konvalesen
Penderita mulai berangsur sehat 2
6 minggu
Pemeriksaan lab. berangsur normal
(kembali normal 3 4 bulan)
62
Alcoholic Liver Disease

Pemakai alkohol jangka waktu lama
menyebabkan gangguan pada
metabolisme sel hati normal, yang
ditandai dengan peningkatan sintesa
fatty acid. Akibatnya menyebabkan
pembekakan sel lemak hati disebut
fatty liver
63
Pada keadaan lebih lanjut penyakit

ini dapat menyebabkan necrosis
pada sel-sel hati yang sering disertai
dengan stasis bilirubin dan jaundice
alcoholic hepatitis
Pada keadaan kronik dari alcoholic
liver disease ini sering menyebabkan
portal cirrhosis
64
Gambaran laboratorium
SGOT & SGPT necrosis sel-sel hati
Ratio SGOT & SGPT > 2 terjadi pada 70%
alcoholic liver disease
GGT enzim ini merupakan indikator
yang sensitif pada pemakai alkohol
kronis
ALP karena cholestasis tapi tidak
mempunyai korelasi dengan alcoholic
hepatitis
Bilirubin serum karena cholestasis
65
Serum immunoglobulin
PT karena sintesis protrombine, F
VII, IX & X
Dijumpai anemia macrocytic karena
defisiensi folic acid, anemia paling
sering terjadi pada alcoholic liver
disease
Terdapat leucocytosis radang pada
hati
66
Hepatitis Kronis
Disebut hepatitis kronis apabila
ditemukan gejala klinik lebih dari 6
bulan setelah fase akut hepatitis.
Hepatitis A tidak menyebabkan
hepatitis kronis
5 10% disebabkan oleh hepatitis B
20 40% disebabkan oleh keadaan
lain
67
Gambaran laboratorium
Hepatitis kronis
aktif
Peningkatan SGOT &
SGPT 9 10 x dari
normal
Peningkatan
globulin terutama IgG
Peningkatan serum
bilirubin (> 4 mg/dl)
Peningkatan ALP
Penurunan serum
albumin
Hepatitis kronis
persisten
Peningkatan SGOT
& SGPT < 5 x N
Peningkatan serum
bilirubin < 4 mg/dl
Peningkatan
globulin
Peningkatan ALP
68
Cirrhosis Hepatis
Yaitu kerusakan hati bentuk lanjut
yang ditandai oleh kerusakan
progresif parenkhim hati &
penambahan jaringan parut.
Portal cirrhosis (Laennec)
berhubungan dengan malnutrisi &
alkoholism
Bilier cirrhosis & post necrotic cirrhosis
merupakan lanjutan hepatitis
69
Pada keadaan inaktif, walaupun

tingkat cirrhosis sudah lanjut
pemeriksaan lab. seperti :
Bilirubin serum
ALP
Enzym
Test faal metabolisme
Masih
Normal
Akan tetapi test BSP menunjukkan retensi yang meningkat

70
Jika cirrhosis dalam keadaan aktif maka

hasil pemeriksaan lab = hepatitis ikterus
Dalam susunan protein didapat
perubahan-perubahan yang mempunyai
nilai diagnostik & prognostik
Protein serum terutama albumin, kadar
albumin ini dapat dipakai untuk follow up
Fraksi globulin
71
Tes respon protrombin terhadap vit. K

dapat dipakai untuk prognosis jika
tak ada respon prognosis jelek
Pada cirrhosis dapat dijumpai anemia
yang disebabkan oleh:
Perdarahan G.I akut / kronis
Defisiensi folic acid
Dapat dijumpai hematemesis & melena

bila ada komplikasi hipertensi portal
72
Bila ada ascites, bisa dijumpai

gangguan keseimbangan air &
elektrolit, dan juga hypoalbuminemia
Pada coma hepaticum amonia darah
sedangkan kadar ureum karena
kemampuan hati untuk mengubah
amonia menjadi ureum terganggu
73
Hepatic Failure
Kerusakan pada sel hati dapat
disebabkan oleh bermacam zat toxic
antara lain: alkohol, virus, obat-obatan.
Kerusakan sel hati ini dapat dalam
berbagai tingkatan. Pada umumnya
kerusakan:
50% disebabkan oleh virus hepatitis
25% disebabkan oleh obat-obatan
25% disebabkan oleh yang lain-lain
74
Kerusakan lebih pada hati dapat

menyebabkan gagal hati dimana terjadi
necrosis sel hati
Dapat terjadi oligouri sebagai
komplikasi dari penyakit hati
hepatorenal syndrome
Gambaran laboratorium:
Ditandai dengan bilirubin > 40 mg
sekresi bilirubin
75
albumin disebabkan sintesis protein

Kolesterol penurunan sintesis
kolesterol di hati
SGOT & SGPT lebih cepat
Glukose karena penyimpanan
glikogen di hati
PT karena penurunan sintesis
protrombin, F VIII, IX & X di hati
76
Fibrinogen karena sisntesis di hati

Amonium karena sintesis urea
Leukositosis menunjukkan massive
necrosis sel hati
77
Klasifikasi
Jaundice/ikterus
1. Prehepatik
- bilirubin total serum meningkat (bilirubin
unconjugated/indirek)
- Transaminase : N
- Alkali fosfatase : N
- Protein
:N
Penyebab: hemolisis / kelainan
metabolisme bilirubin
78
78
Klasifikasi
Jaundice/ikterus
2 Hepatik
- jaundice/ikterus: cepat
- Transaminase meningkat
- Albumin: menurun
Penyebab : penyakit hepar
79
79
Klasifikasi
Jaundice/ikterus
3 Post hepatik
- kegagalan cairan empedu mencapai
duodenum
- Bilirubin conjugated meningkat
- Alkali fosfatase meningkat
- Kolesterol total meningkat
- Steatorrhoe
- Malabsorpsi Vit A,D,E,K
80
80
Pemeriksaan Laboratorium
untuk
penyakit hati (hepatobilier)
Bilirubin total0,3-1 mg/dl

Bilirubin direk
< 0,25 md/dl
Alkali fosfatase (300C) 73-207 U/L
Aspartate transaminase laki-laki
sp 25 U/L
(AST/SGOT)
wanita sp 21 U/L
Alanin transaminase
laki-laki
sp 29 U/L
(ALT/SGPT)
wanita
sp 22 U/L
Gamma Glutamyl
laki-laki
8-38 U/L
Transpeptidase
wanita5-25 U/L
(GT)
81
81
Pemeriksaan Laboratorium
untuk
penyakit hati (hepatobilier)
Albumin
g/dL
globulin
Protrombin time (PTT)
3,5-5
0,5-1,5 g/dL
10-14
82
82
ENZIM-ENZIM OBSTRUKTIF
83
83
ALKALI FOSFATASE
Terdapat pada semua jaringan
Tu pada epitel usus, tubulus ginjal,
tulang (osteoblas), hati, plasenta
Yang berada dlm serum tu berasal
dari hati/traktus biliaris dan 50%
berasal dari tulang
84
84
ALKALI FOSFATASE
Meningkat tajam pada keadaan:
- obstruksi ekstrahepatik (10-12XN)
- Kanker tulang ( 10-25XN)
- Osteitis deformans (Peny Paget)
85
85
ALKALI FOSFATASE
Sedikit meningkat pada :
- Obstruksi intrahepatik
- hiperparatiroidisme
- penyembuhan sesudah fraktur
86
86
GT( Glutamyl
Transverase)
Berasal dari sistem hepatobilier
Meningkat pada semua jenis penyakit hati
Peningkatan 5-30 X N pada obstruksi
intra /post hepatik
Lebih sensitif daripada alkali fosfatase
untuk mendeteksi obstructive jaundice
kolangitis, kolesistitis, karena meningkat
lebih dini dan menetap lebih lama
87
87
GT ( Glutamyl
Transverase)
Bila kadarnya meningkat 2-5x N
hepatitis, fatty liver
Pada penyakit skeletal dan tulang
nilainya normal sehingga
pemeriksaan ini dapat dipakai untuk
memastikan apakah peningkatan
alkalifosfatase berasal dari
penyakit tulang atau hati
88
88
89
89
Pemeriksaan lain:
5 nucleotidase
Leusine aminopeptidase
90
90
SGOT DAN SGPT

Terdapat dalam sitoplasma dan
mitokondria sel hati
Pada kerusakan hati ringan, SGOT
yang masuk dalam plasma, adalah
SGOT yang berasal dari sitoplasma
91
91
SGOT DAN SGPT

Pada kerusakan hati berat : SGOT
dan SGPT berasal dari sitoplasma dan
mitokondria
Pada hepatitis virus : SGOT & SGPT
lebih dahulu meningkat sebelum
munculnya tanda-tanda klinis dan
gejala ikterus
Sangat meningkat pada hari ke 7-12
kembali normal setelah 3-5 minggu
92
92
SGOT DAN SGPT

SGPT > SGOT penyakit hepar
SGPT < SGOT SGOT>SGPT
penyakit miokard
93
93
UREUM
Hasil akhir katabolisme
protein/asam amino yang terbanyak
Disintesis dari amonia di dalam hati
Ekskresi tu melalui ginjal: urin,
sedikit melalui keringat
Ureum mengalami degradasi oleh
bakteri usus
94
94
Ureum
Ureum difiltrasi secara pasif di glomeruli
ginjal
(40-80%)
Urea N (kandungan nitrogen dalam ureum)
dalam whole blood < plasma atau serum
Kadar ureum dalam plasma dipengaruhi :
- intake protein dalam makanan
- kapasitas ekskresi oleh ginjal
95
95
UREUM dan UREA N

Kadar normal dalam plasma
Urea N : 7-18 mg/dL
Ureum : 15-35 mg/dL
Kadar normal dalam urine
Urea N : 12-20 mg/dL
Ureum : 25-43 mg/dL
96
96
AZOTEMIA
Peningkatan kadar ureum dan
kreatinin yang bermakna
Azotemia prerenal :
karena perfusi ginjal tidak cukup
filtrasi glomerulus menurun
Etiologi: :
dehidrasi, shock, penurunan volume
darah, bendungan jantung, katabolisme
protein yang meningkat
97
97
AZOTEMIA
Azotemia renal disebabkan:
- Glomerulonefritis
- Nefritis kronis
- Nefrosklerosis
- Tubular nekrosis
Azotemia Post renal:
- karena obstruksi saluran kemih sehingga
ureum diabsorpsi ke dalam sirkulasi
98
98
PENURUNAN KADAR
UREA-N SERUM
Nutrisi yang miskin
Intake cairan yang berlebihan
Pemberian cairan intra vena yang
berlebihan
Kehamilan
99
99
HEPATITIS
Peradangan hati
Peningkatan marker hepatitis
Akut & Kronis
100
Hepatitis A
Fase akut
Fase penyembuhan
40-90 hari
28-45 hari
Imunitas
(Thn)
Anti HAV (IgG +IgM)
IKTERUS
Anti HAV IgM

HAV
101
101
Hepatitis B
Inkubasi
4-12 mg
Fase akut
2-12 mg
Post infeksi
6bln-thn
Post fase akut

2-16 mg
Anti HBcAg
Anti HBe
Anti HBs
HBsAg
Anti HBcIgM
HBeAg
102
102
Hepatitis C
103
Hepatitis C
104
105
106
Tumor Marker of GID

FOB
CEA
Ca 19-9
107
108
Tumor markers
Tumor markers are usually proteins
which are produced from cancer cells or
as response to cancer
Cancer specific
Tissue specific
109
Tumor markers
Cancer specific of certain cancerous
tissue BUT large overlap (low specificity)
Tissue specific i.e PSA, AFP, B-HCG,

thyroglobulin
110
In oncology tumor markers are used:
Screening i.e PSA

Monitoring i.e AFP
Diagnosis (when biopsy is not feasible)
Determine prognosis
111
Tumor markers: CEA

Complex glycoprotein that is associated with
the plasma membrane of tumor cells, from
which may be released in the blood
Elevated specially in Colon cancer, But Also in
Pancreatic, Gastric, Lung, breast and Ovarian
cancer
ALSO in cirrhosis, inflammatory bowel
disease, chronic lung disease, pancreatits, 19%
of smokers, 3% of healthy population
112
Tumor markers: CEA

NOT satisfactory for screening for a
healthy population
Monitor of recurrence
Monitor of treatment
113
Tumor markers: CA 19-9

21-42% elevated in gastric ca
20-40% elevated in colonic ca
71-93% elevated in pancreatic
Useful for differentiated benign from
malignant disease
114
Tumor markers: AFP

Normal serum fetal protein synthesized
by the liver, yolk sac, gastrointestinal
tract
Heptocellular cancer:
diagnosis (>500)
screening of high risk population
115
Tumor markers: AFP

Testicular germ cell tumor (embrional or
endodermal):
diagnosis
monitor of recurrence & response
prognostic marker (>100.000 high risk)
Less frequent elevated: pancreatic ca
Gastric ca
Colonic ca
Bronchogenic ca
116
ASCO SPECIAL ARTICLE
2000 Update of Recommendations for the Use of Tumor Markers

in Breast and Colorectal Cancer:
Clinical Practice Guidelines of the American Society of Clinical Oncology
American Society of Clinical Oncology Tumor Markers Expert Panel
117
CEA as a Marker for Colorectal Cancer
1997 Recommendation : CEA is not recommended to be used as a screening test

for colorectal cancer.
2000 Recommendation : No change.
1997 Recommendation : CEA may be ordered preoperatively in patients with colorectal
carcinoma if it would assist in staging and surgical treatment planning.
Although elevated preoperative CEA (> 5 ng/mL) may correlate
with poorer prognosis, data are insufficient to support the use of CEA
to determine whether to treat a patient with adjuvant therapy.
118
1997 Recommendation : If resection of liver metastases would be clinically indicated,

it is recommended that postoperative serum CEA testing may be performed every
2 to 3 months in patients with stage II or III disease for 2 or more years after diagnosis.
An elevated CEA, if confirmed by retesting,
warrants further evaluation for metastatic disease but does not justify the institution
of adjuvant therapy or systemic therapy for presumed metastatic disease.
119
1997 Recommendation : Present data are insufficient to recommend routine

use of the serum CEA alone for monitoring response to treatment.
If no other simple test is available to indicate a response,CEA should be measured
at the start of treatment for metastatic diseaseand every 2 to 3 months during
active treatment.
Two values above baseline are adequate to document progressive disease
even in the absence of corroborating radiographs.
CEA is regarded as the marker of choice for monitoring colorectal cancer.
120
CA 19-9 As a Marker for Pancreatic Cancer

2006 recommendation for use of CA 19-9 as a screening test.
CA 19-9 is not recommended for use as a screening test for pancreatic cancer.
2006 recommendation for use of CA 19-9 to determine operability.
The use of CA 19-9 testing aloneis not recommended
for use in determining operability
or the results of operability in pancreatic cancer.
2006 recommendation for use of CA 19-9 to provide evidence of recurrence.
CA 19-9 determinations by themselves
cannot provide definitive evidence of disease recurrence without seeking
confirmation with imaging studies for clinical findings and/or biopsy.
121
CA 19-9 As a Marker for Pancreatic Cancer
2006 recommendation for use of CA 19-9 for monitoring response to therapy.

Present data are insufficient to recommend the routine use of serum CA 19-9
rules alone for monitoring response to treatment.
However, CA 19-9 can be measured at the start of treatment for locally advanced
metastatic disease and every 1 to 3 months during active treatment.
If there is an elevation in serial CA 19-9 determinations, this may be an indication
of progressive disease, and confirmation with other studies should be sought.
122
Fischbach, Frances Talaska

Title: Manual of Laboratory &
Diagnostic Tests, 7th Edition
Copyright 2004 Lippincott
Williams & Wilkins
123
124
Reference
Rohen JW, Chihiro Y, Elke LD; Color Atlas of Anatomy, 4th ed

Fischbach, FT; Manual of Laboratory & Diagnostic Tests, 7th
Ed, 2004, Lippincott Williams & Wilkins, 346 8, 386 - 95
Alterations in Hepatobiliary Function, Essential of
Pathophysiology
125
PUISI GELAP
Jantera sirna purnama
Gadis layu pada nisan terluka
Lahan kering pertiwi gulita
Harapan menyuram di dinding temaram
Tikam mentari pada jiwa yang kelam
Jasad hitam serigala tersungkur
Ngan-angan, mpi-mimpi, dewa langit terkubur
Kausalitas dalam galau tak tuntas
Nomor-nomor pada buku tanpa kertas
Damprat memuncrat pada batu
Itu sunyi tak juga membeku
Iwan Sulistiawan; Miskin tapi Sombong,
2009
126
PUISI GELAP
JAntera sirna purnama
GAdis layu pada nisan terluka
LAHan kering pertiwi gulita
HArapan menyuram di dinding temaram
TIkam mentari pada jiwa yang kelam
JAsad hitam serigala tersungkur
NGAN-angan, mpi-mimpi, dewa langit terkubur
KAUsalitas dalam galau tak tuntas
NOmor-nomor pada buku tanpa kertas
DAmprat memuncrat pada batu
Itu sunyi tak juga membeku
Iwan Sulistiawan; Miskin tapi Sombong,
2009
127
128
129

K10 - Lab Digestif 2015

Diunggah oleh

Informasi Dokumen

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

K10 - Lab Digestif 2015

Diunggah oleh

Hak Cipta:

Format Tersedia

Laboratory

Konsil Kedokteran Indonesia,SKDI 2012

Konsil Kedokteran Indonesia,SKDI 2012

Jejunum and Ileum

dr. Kemas Yakub SpPK

dr. Kemas Yakub SpPK

Stomach and duodenum

Gall bladder, Bile

dr. Kemas Yakub SpPK

dr. Kemas Yakub SpPK

What kind of laboratory test

dr. Kemas Yakub SpPK

Biopsy, Site-specific (Skin), Specimen

Mouth ulcer (apthous, herpes)

Stomach and duodenum

Brushing cytology, Specimen, Diagnostic

dr. Kemas Yakub SpPK

Occult blood, Stool

Stomach and duodenum

ABO group and Rh type, Blood

dr. Kemas Yakub SpPK

dr. Kemas Yakub SpPK

Body fluid analysis (Ascitic fluid),

Genital, Candida albicans, Culture

dr. Kemas Yakub SpPK

Blood culture, Blood

Differential leukocyte count, Peripheral blood

Jejunum and Ileum

Irritable Bowel Sydrome

Gall bladder, Bile duct and

Gallbladder and biliary system

Glucose, Serum (Random)

dr. Kemas Yakub SpPK

Hepatitis serologies, Serum

Leucine aminopeptidase, Blood

Liver battery, Serum

dr. Kemas Yakub SpPK

Antismooth muscle antibody, Serum

Epstein-Barr virus, Serology, Blood

Hepatitis delta antibody, Serum

dr. Kemas Yakub SpPK

dr. Kemas Yakub SpPK

Kemas Yakub R, dr. SpPK

An adult excretes 100 to 200 g of

Feces are composed of the

Kemas Yakub R, dr. SpPK

Kemas Yakub R, dr. SpPK

Kemas Yakub R, dr. SpPK

dr. Kemas Yakub SpPK

dr. Kemas Yakub SpPK

Principal Function of the Liver

Menggolongkan tes fungsi

Tidak dapat memastikan causa

Tujuan pemeriksaan Faal

Pemeriksaan Fungsi Hati

Total bilirubin, direct bilirubin

dr. Kemas Yakub SpPK

Menentukan Jenis Ikterus Penting untuk

Bilirubin total orang dewasa 0,1 1 mg%

Urobilinogen urine meningkat pada:

Urobilinogen urine negatif

Typical acute Hepatitis

Alcoholic Liver Disease

Pada keadaan lebih lanjut penyakit