STUDI KASUS

FARMASI KLINIK
PADA
PENYAKIT HATI
 PERUBAHAN
FARMAKOKINETIK
 Perubahan hepatic blood flow (CH,hepatic
venous obstruction)clearance hepatik.
 Hepatocellular damage clearanceBA
 Cholestasisabsorbsi lipid soluble-drug ,
akumulasi obat yang billiary excreted
 Perubahan protein-binding free fraction
 Pergeseran cairan ke arah extra vaskuler
Vd
 Diarhea associated with hepatitis 
absorbsi
 PERUBAHAN
FARMAKODINAMIK

 Sensitivitas thd sedatif atau hipnotif

HE
 Hindari benzodiazepin, agen hipnotif,
opiat
 Hindari diuretik, obat yg sebabkan
gangguan keseimbangan elektrolit.
 Assessment of Liver Function
 Tdk ada tes yg dpt mengkuantifikasi fs hati
 Marker Nekrosis Hepatoseluler :
 SGOT(AST)
 SGPT(ALT)
 ALP
 GGT
 Bilirubin
 Marker Kapasitas Sintetis Hepar:
 Albumin,
 Prothrombin Time
 CLD SEVERITY
ASSESMENT
Child–Pugh Score, predictor severity of
CH,survival,risk variceal bleeding, dosage
adjustment

Score 1 2 3
Bilirubin(mg/dl) 1-2 2-3 >3
Albumin (mg/dl) >3,5 2.8-3.5 <2.8
Ascites None Mild Moderat
e
Prothrombin Time 1-4 4-6 >6
 ACUTE HEPATIC FAILURE

 May be fulminant (mortality rate 80%, Tierney) or

subfulminant
 Fulminant: HE dlm 8 mgg setelah hepatitis,
coagulopathy
 Subfulminant: HE > 8 mgg paska hepatitis
 Cause: Hepatitis B, Hepatitis C, drug-induced
(Paracetamol), idiosyncratic drug reaction, poisonous
mushrooms, malignancy (lymphomas), Wilson’s
disease, Reye’ syndrome, shock
 Presentation: jaundice minimal, SIRS, GI symptoms,
hemorrhagic phenomenon, lab test ( severe
hepatocellular damage)
 ACUTE HEPATIC FAILURE
 Characteristics:
 Short course ( < 8 weeks)
 Rare portal hypertension
 Hepatic encephalopathy
 Cerebral oedema
 Reversible (regeneration)
 TREATMENT

 Goal: correcting metabolic abnormalities, preventing coma

 Treatment include:
o Coagulation defects with Vit K, FFP, TC
o Imbalance acid-base, fluid and electrolyte
o Renal failure
o Hypoglycemia with Dextrose 40% or 10%
o Encephalopathy: avoid drugs that alter mental status, lactulose
is not effective in this setting
o Prophylactic antibiotics reduce the risk of infection
o Acetyl cystein for Pamol toxicity ( 140mg/kg followed by
70mg/kg every 4 hours for 17 doses)
o Avoidance to drug induced liver failure
o Liver Transplant
 CHRONIC LIVER DISEASE
Characteristics
 Long course (months-years)
 Portal hypertension
 Hepatic encephalopathy
 Rare cerebral oedema
 Irreversible (scar formation)
 Forms:
 CIRRHOSIS HEPATIC
 PRIMARY BILLIARY CIRRHOSIS
 CIRRHOSIS HEPATIC

 Progressive loss of basic hepatocyte

function
 Loss of enzymes drugs & toxin handling
 Findings: jaundice, gynecomastia, spider
navy, splenomegaly, erytema palmaris.
 Manifestasi: Hepatic encephalopathy,
coagulopathy, Portal hypertension, Ascites,
SBP, oesophageal/gastric varices,
hepatorenal syndrome.
 CH TREATMENT
 Ascites management
 Koreksi nutritional deficiency (hati-hati dg iron
replacement).
 Treatment of coagulopathy (Vit K / transfusi)
 Imunitas terapi infeksi agresif, profilaksis
 Terapi portal hypertension (bila+) dg propanolol
 Variceal Bleeding: Octreotide, somatostatin,
TIPS, sclerotherapy
 PRIMARY BILLIARY CIRRHOSIS
(PBC)
 Characteristic: autoimmune destruction of
intrahepatic bile ducts and cholestasis
 Insidious onset, progressive
 More women aged 40-60
 Complication: steatorrhea, xanthomas,
xanthelasma, osteoporosis, osteomalacia, portal
hypertension
 Presentation: jaundice, sign of portal
hypertension, pruritus, xanthomatous lesions.
 Lab: ALP↑, HDL chol ↑, Bil ↑
 TREATMENT
 Symptomatic, include
 Cholestyramin 3x4g in water or juice for the
pruritus or ondansetron
 Calcium supplementation
 Ursodeoxycholic acid 10-15mg/kg/d to slow the
progression, ↑ long term survival,  the risk of
oesophageal varices
 MTX 15mg/wk ↑liver histology
 Colchicine 2 x 0,6mg ↑ symptomp
 Corticosteroid, AZT of no benefit
 HEPATIC DISEASE
COMPLICATIONS
 ASCITES
 HEPATIC ENCEPHALOPATHY
 SBP
 HRS
 GERD
 PORTAL HYPERTENSION
 Ascites Management
 Ascites terbentuk o/k produksiatau absorpsi
dari cairan peritoneum. Hipertensi portal me
tekanan sinusoid berakibat produksi kelenjar
limfa 
 Komplikasi: SBP, GERD, LBP, HRS, mbilical
hernia.
 Management: bed rest, restriksi Na dan air,
stop alkohol, loop diuretik 1 x 40mg PO,
Spironolakton1x100mg
 Monitoring: BB 0,5kg/hari tanpa oedema,
1kg/hari bila ada oedema, elektrolit
 Konseling: Diuretik diminum pagi hari, hindari
NSAID
 HEPATIC ENCEPHALOPATHY
 DEF: Syndrome perubahan status mental
berhubungan dengan kegagalan hati dengan
karakteristik impaired cognitive skills,
worsened motor abilities, somnolence, coma
 Outcome: Pencegahan coma.
 Pencetus: konstipasi, infeksi, Bleeding GI,
hipokalemia, dehidrasi, benzodiazepin,
hipotensi
 Treatment:
o Intake BCAA  than AAA
HE (lanjutan)

 Treatment (lanjutan)
o Reduksi blood ammonia: laktulosa,
Neomycin 4 x 500 mg
o Benzodiazepin antagonis (Flumazenil)
0,2 –15 mg iv bila terapi konvensional
gagal.
 Monitoring:
o Kondisi pasien: status mental,
kesadaran
o Efek katartik: 3-4 kali
o Elektrolit.
 Spontaneous Bacterial
Peritonitis
 Common complications of ascites
 Causa: intestinal bacterial overgrowth, ↑
permeability of intestinal mucosa, ↓
neutrophil activity, ↓ phagocytic activity of
RES
 High mortality rate (40%, Quan), high
reinfection rate (70%)
 Spontaneous Bacterial
Peritonitis
 Predisposing factors: Hx of SBP, GI bleeding,
UTI, bladder/intravasc. cath.,repeated
paracentesis
 Findings: Abdo pain, fever, elevated WBC, renal
failure, precipitation of HE
 Treatment: Cefotaxime 3x1-2 g for 5-10 days or
Ceftriaxone 1x1g for 5-10 days, albumin 1g/kg
on day 0 and day 3
 Prophylaxis for reinfection: Cipro 1x750mg/week
 HEPATORENAL SYNDROME
 Renal failure associated with liver disease
 Defined by oligouria in euvolemia or
hypervolemia
 No structural damages in the kidneys
 Management:
 renal dose dopamine has not been proven to be
beneficial
 RRT
 Liver Transplant
 DRUG THERAPY MONITRING

 Kondisi klinik: Oedema, ascites, BB,

 Vital sign : BP, Nadi
 Kimia Klinik: elektrolit, albumin
 Implikasi Farmasi Klinik
 Assess kemungkinan Drug induced Hepatotoxicity
pada setiap Hepatitis
 Sering diiringi gangguan GIT, shg perlu antasid, H2-
Bloker
 Waspada thd obat highly-protein bound, monitor
efek samping
 Waspada intake Na terutama pd CH dg
ascites/oedema
 Awasi bila ada kelebihan cairan yg masuk
 Kurangi dosis, perpanjang interval untuk obat
highly metabolised in the liver khususnya pada CH
 Waspada thd obat yang dapat
memicu/memperburuk encephalopati
 Implikasi Farmasi Klinik
 Hindari obat yang dapat memperparah
Liver
 Stop Drug-induced hepatotoxicity
 Monitor efek samping obat lebih ketat,
karena peluang semakin besar.
 DRUG-INDUCED HEPATOXICITY
 Acute Hepatic Injury
 Hepatocellular injury:Halothane, INH, Pamol, PZA
 Cholestatic injury:Steroid anabolik, OC,
erythromycin, CPZ
 Mixed injury: Sulfonamida, rifampin, PAS
 Chronic Hepatic Injury
 Chronic Hepatitis: Metildopa, nitrofurantoin, Pamol,
Sulfonamida, INH
 Chronic cholestatic: Fenothiazin, amitryptiline
 Granulomatous hepatitis: Quinidin, Fenitoin,
diltiazem
 Cirrhosis: MTX
 Case 1
 Ny SH, 28 th, 53kg, 161cm
 Mengeluh panas selama > 2 minggu, batuk selama
> 1 bulan
 TTV: temp 37, 8°C, BP 110/80 mmHg, lemah
 Lab: Widal O 1/320; S 1/200, leuko (N), LED.
 Tx: Thiamphenicol selama 10 hari kemudian cravit
4 hari.
 Pada hari ke-14 ditemukan tanda KP dari hasil x-
ray paru, shg seketika tTx dirubah menjadi regimen
TB. Setelah satu minggu terlihat jaundice disertai
mual. Apa rencana farmasis terhadap kasus ini?
 Case 3
 Tn HM, 62 th, 58kg, 160cm
 MRS dengan gelisah, marah-marah,
tidak bisa diajak komunikasi. Mengaku
tidak pernah sakit berat/liver. Pada
pemeriksaan dijumpai jaundice,
erytema palmaris. Hasil lab
menunjukkan : Albumin 2,7 mg/dL; Na
126 meq/L, K 3,1 meq/L, SGOT 75
mg/dL; SGPT 56 mg/dL.Px didiagnosa
CH dg HE.
 Rekomendasi terapi apa yang dapat
diberikan thd kasus ini?
 Case 2
 Ny. SM, 58th, 55kg, 153cm
 MRS dg keluhan perut membesar disertai
mual, kembung, febris 38 °C, lemah,
anoreksia, insomnia. Px mengaku tidak
pernah sakit. Pada pemeriksaan fisik
dijumpai eritema palmaris, spider naevy dan
hsl lab menunjukkan hipoalbuminemia,
prolongasi PT 1,8 x normal, SGOT 53 mg/dL,
SGPT 49 mg/dL, leuko (N). Didukung hasil
USG, selanjutnya Px didiagnosa CH + susp
SBP. Bgmana rencana pelayanan farmasi?