FARMAKOTERAPI

SIROSIS-HEPATIK
(PBL-Kuliah Supplemen 2013)

Budi Suprapti
GANGGUAN HEPAR
- Anatomi – Fisiologi Liver
- FS Normal Liver
- Disfungsi liver
- Katagori penyakit liver
Sirosis
- Etiologi – patofisiologi
- Manifestasi
- Komplikasi Terapi

Monitoring
SIRKULASI DARAH
- 25 % CO : 1.5 L darah/menit
- Arteri hepatika
- Vena porta

Arteri Hepatika Vena porta

Sinusoid Liver

Vena sentral

Vena hepatik

Vena Cava Inferior

Atrium Ka-Jantung
FUNGSI LIVER - NORMAL
- Energi- interkonversi substrat
Metabolisme KH, prot., lipid
- Sintesis-sekresi prot.plasma, clotting factor
- Solubilisasi, transpor, storage :
. Sirkulasi empedu
. Lipoprotein-transpor lipid
. Vitamin, glycogen
- Protektif + klirens
. Fagositosis
. Metabolisme ammonia
. Sintesis glutathion
. Metabolisme obat, hormon
Manifestasi disfungsi liver
. Metab. Karbohidrat : hipo/hiperglikemia
. Metab. Lipid : akumulasi fat, xanthomas
. Metab./ sintesis Protein
hipoalbumin
hepatic enchephalopathy
(HE)
. Hilang Fs. Solubilisasi, storage
malabsorpsi vit K, jaundice/icterus
. Hilang fungsi protective + klirens
bakteri, endotoxin, ammonia,
hormon, kstb Na-air
 SIROSIS
. Chirose-warna orange-kuning orange hati / liver

. Sirosis : distorsi irreversibel- architecture liver normal

yang dikarakterisasi hepatic injury, fibrosis,
regenerasi nodular
peningkatan jar. Ikat hepar- disorganisasi
architecture – kerusakan vaskular

Etiologi : alkohol
virus
obat, toksin
faktor metabolik, dll
Tipe disfungsi liver
. Disfungsi hepatosit-lobulus
. Disfungsi sirkulasi (HT portal)
Manifestasi sirosis
Gejala – tanda :
• Asimptomatik
• Hepato-splenomegali
• Palmar eritema, pruritus, jaundice, spider angioma,
hiperpigmentasi
• Ginekomastia
• Asites, edema, efusi pleura, kesulitan bernafas
• Malaise, anoreksia, BB turun

Uji Lab.
• Hipoalbumin
• Peningkatan PT
• Trombositopenia
• Peningkatan alkalifosfatase
• Peningkatan AST, ALT, GGT
Clincal syndromes associated with viral hepatitis (Ganong)
Hepatitis Vruses
- HAV
- HBV
- HCV
- Delta
- HEV

Infection

Subclinical Acute Cholestatic

Hepatitis Hepatitis Hepatitis

Chronic
Chronic Fulminant Active
Persistent Hepatitis Hepatitis
Hepatitis ( massive ( continuing
( Carrier state ) necrosis ) Necrosis )

Cirrhosis Hepato
Cellular
carcinoma
Recovery
( with normal
Appearing,
Death
Regenerated liver )
Features of Clinically important hepatitis viruses (Dipiro)

Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E

Virus HAV HBV HCV HDV HEV
Genome ssRNA dsDNA ssRNA ssRNA ssRNA
Incubation 14-45 40-180 35-84 40-180 14-60
( days )
Transmission Fecal-oral Parenteral Parenteral Parenteral Fecal-oral
Sexual Sexual Sexual(?)
Perinatal Perinatal Perinatal
Mucous Mucous
membrane membrane
Serologic markers
Antigens HAVAg HBsAg HCVAAg HDVAg N/A
HBcAg
HBeAg
Abtibodies Anti-HAV Anti-HBs Anti-HCV Anti-HDV N/A
Anti-HBc
Anti—HBe
Viral markers HAVRNA HBV DNA HCVRNA HDVRNA N/A
DNA polymerase
Chronicitry (%) No 2-7 70-80 2-70 No
Hepatocellular Ca No Yes Yes Yes No
 HBsAg Anti-Hbs Anti-HBc HBeAg Anti-Hbe Interpretation

+ - IgM + - Acute HBV infection, high infectivity

+ - IgG + - Chronic HBV infection, high infectivity

+ - IgG - + Late acute or chronic HBV infection, low

infectivity
+ + + +/- +/- 1. HBsAg of one subtype and heterotypic anti-
HBs (common)
2. Process of seroconversion from HBsAg to anti-
HBs ( rare )
- - IgM +/- +/- 1. Acute HBV infection
2. Anti- HBc window
- - IgG - +/- 1. Low-level HBsAg carrier
2. Remote past infection
- + IgG - +/- Recovery from HBV infection

- + - - - 1. Immunization with HBsAg ( after vaccination )

2. remote past infection (?)
3. False- positive.

Commonly encountered serologic patterms in hepatitis B infection (Ganong)

SIKLUS REPLIKASI VIRUS HEPATITIS B
RESPONS IMMUN SELULAR TERHADAP VIRUS HEPATITIS B
 LIVER FAILURE

Hypo- Portal Cholestasis NH4+ + HCO3-

Albuminemia Hypertension
Fat Abs.

Ascites Exudative Varices Vitamin K

enteropathy deficiency Urea

Hyperaldo Clotting factors

Steronism

Hypokalemia GI Bleeding
Aromatic AA

Renal NH4+ Enteric AA

Production Break down

Hyper Ammonemia False Neuro

transmiters

Data Lab ?? Alkalosis Hypervent. Encephalopathy

Terapi ??
 PORTAL HYPERTENSION

Liver Damage

Hypoalbuminemia Ascites Malabsorption Vasodilation Portal

Collateral
Circulation

Splenomegaly

Aldosterone Blood presure

Clotting factors ECV CO

Thrombocytes Varices

Rupture

Bleeding Encephalopathy
 HEPATORENAL SYNDROME

ASITES

CO N SYMPATETIC

EDEMA
VASOCONTRICTION

GFR RENIN

ALDOSTERON

OLIGOURI RETENSI
Na+ air
SKENARIO, DATA PELENGKAP -- PEMBELAJARAN

Data pasien: Ny MN, 52 th, 55 kg, 155 cm, PNS

Keluhan: Lemah, mual, tidak nafsu makan 7 hari
sebelum MRS, perut agak membesar, gelisah,
beberapa kali berontak
Riwyt Px: Hepatitis B (2003), SH (2010)
Rwyt Ob : -
Data klinik : TD, Nadi, RR, T.ax, GCS, Nyri perut
Data lab : CBC, Bil total, direk, indirek, SGOT/PT,
Albumin, Elektrolit (Na, K, Cl), GDA, BUN, SCr, LED
Dx : Sirosis Hepatik-Asites, HE Terapi

Pasien : Kondisi ?
Penanganan prioritas?
Tujuan terapi ??
Obat terpilih ??
Regimen Obat??
Parameter keberhasilan Tx??
Drug related problems ??
SKENARIO
DATA TERAPI MRS : Indikasi?
Infus D5:Comafusin 1 : 1
Laktulosa po 3 dd C II Kapan harus masuk ??
Ciprofloksacin IV 2 x 200 mg
Antasida 3 x C I Kapan harus berhenti ??
Spironolakton 2 x 100mg
Sistenol 3 x 1 tab prn Monitoring ??
Infus albumin (H2)
Omeprazol IV 1 x 40 mg
Mthioson PO 3 x2 tab
DRP??  Pencegahan/solusi??
SKENARIO
H3 MRS - HEMATEMESIS MELENA
Data Klinik:
TD Kondisi kritis ?
Suhu
Nadi, RR, GCS, Nyeri perut Kapan harus masuk ?
TERAPI: Kapan harus berhenti ?
Inf.NS : D5 1 : 1
Sukralfat Monitoring ?
Laktulosa
Ciprofloxazin DRP?  Pencegahan/solusi?
Sistenol
Neomisin syr Tindakan lain?
Inj. Traneksamat
Vit K
PRC
Metoklopramid
Omeprazol
Terapi lain?
Methioson
TERIMA KASIH