PENYAKIT HEPAR

KRONIK
(LOC
2)
dr. DANI ROSDIANA, SpPD
Bagian Ilmu Penyakit Dalam
FK Universitas Riau RSU Arifin Ahmad

 SIROSIS

HEPATIS
VARISES ESOFAGUS
LIVER FAILURE (GAGAL HATI)

Definition
Cirrosis

Hepatis (CH) secara anatomis

didefiniskan proses kronik diffuse dengan
fibrosis dan pembentukan nodul diikuti
dengan gangguan arsitektur hepar.
Fibrosis is not synonymous with cirrhosis
Nodule formation without fibrosis is not
cirrhosis

Production of cirrhosis

Tanpa memperhatikan etiologinya, gambaran

histopatologi liver nya sama

The response of the liver to necrosis :

collapse of hepatic nodule
formation of diffuse fibrous septa and nodular regeneration

Cirrhosis of the liver

Fibrogenesis
Conective

tissue matrix of normal liver :

- type 4 collagen
- laminin
- heparan sulphate
- protoglycan
- fibronectin

Cell injury

Proliferation of inflammatory blood

Kupffer cell and platelets

Ito cells
Release of cytokines and growth
Factors .

metalloproteinases
Activated Ito cells

Connective tissue component As a new

matrix

Sitokin-sitokin dilepaskan oleh sel-sel yang

mengalami inflamasi contoh :
Interleukine (Il) 1
Interleukine (Il) 6
TNF-
en
menghambat regenerasi hepar
menginduksi protein fase akut
menghambat sintesa albumin.
Interleukine (IL) 10

Growth factors
Initiated hepatic regeneration after insult
Hepatocyte growth factor (HGF)
produced by several types of cells
regulated by IL1, IL1, TGF, glucocorticoid
Epidermal growth factor (EGF)
Transforming growth factor (TGF) and

Regulate hepatic regeneration

ibrosis following hepato-cellular necrosis

Interface hepatitis zone 1
Confluent necrosis zone 3
Focal necrosis

portal-portal fibrou
bridges
central-central fib
bridges
focal fibrosis

ETIOLOGI
Viral infection (B or C)
Metabolic :

- NASH/ASH
- Iron overload
- Copper over load
- 1-Antitrypsin deficiency
- galactosemia
- Tyrosinaemia

Cholestasis
Hepatic venous outflow block
- CHF
- Budd-Chiari Syndrome

Autoimmune disease

Toxin and drug

Diagnosis sirosis hepatis

Dasar diagnosis :
Presentasi klinis
Pemeriksaan laboratorium
Pemeriksaan Imaging
Biopsy jika memungkinkan

Presentasi Clinic
A.

Anamnesis

Fatique and weight loss

anorexia

and flatulent dyspepsia

Abdominal
Jaundice,
Swelling

pain

dark urine

of leg and abdomen

Haemorrhage
Loss

of libido

Presentasi Clinic
B. Pemeriksaan Fisik
Hepatomegaly and or splenomegaly
Jaundice
Malnutrition
Pigmentation, vascular spider, palmar erythema
Purpura
White nail, clubbing finger
Ascites, abdominal wall vein
Parotid enlargement
Gynaecomastia, testicular atrophy
Dupuytrens contracture
Foetor hepaticum

Laboratory study
Hematology
biasanya anemia NN ringan
jika terjadi hipersplenisme: leukosit dan trombosit
turun
Prothrombin time : memanjang

Liver function test

Usually hyperbilirubinemia, conjungated or
mixed type
IgG increase but albumin decrease
AP usually increase slightly or normal
Transaminase and GGT usually mild increase.
SGOT-SGPT ratio usually > 1

Imaging study

Ultrasound (USG)
Untuk evaluasi ukuran, bentuk dan komposisi
Permukaan hepar
Ekogenitas
Nodul
Vena porta
Ascites
Duktus biliaris
Gallbladder
Spleen

Computed tomography (CT Scan)

and
Magnetic resonance tomography
(MRI)
Used

for special diagnostic

investigation :
Imaging of liver tumors more accurate.
Is it important when ablation, resection
or
chemoembolization were planned.

Child-Pugh classification
Parameter

number of point

1
2

Ascites
Moderate
Severe
Encephalopathy (grade)
34
Serum bilirubine
Child
3 class :
>3
A
<6
Serum
albumin
B
7-9
2.5-3.5
< 2.5
C
10-15
Prothrombine time (longer)

None
None
<2

12
2

> 3.5
<2

2-6

Complications of liver cirrhosis

Ascites

portal hypertension
porto-systemic encephalopathy
Hepato-renal syndrome
Hepato-pulmonal syndrome
Hypersplenism
Anemia
Esophageal varices
Hematemesis and melena