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LAYANAN KEFARMASIAN PADA PENYAKIT HATI

LAYANAN KEFARMASIAN

PADA

PENYAKIT HATI

PENYAKIT HATI •   •   •   ACUTE LIVER DISEASE: Hepatitis, Toksisitas obat atau
PENYAKIT HATI
•  
ACUTE LIVER DISEASE: Hepatitis, Toksisitas obat atau alkohol
CHRONIC LIVER DISEASE
END STAGE LIVER DISEASE

ANATOMI

ANATOMI

HEPATOMEGALI

HEPATOMEGALI

PROBLEM MEDIK UMUM

lSeringkali asimtomatik meskipun tes lab tak normal lKomplikasi:

§Ascites, Spontaneous Bacterial Peritonitis (SBP) §Oedema §Hipertensi Portal §Hepatic Encephalopathy §Gangguan Koagulasi §Hepatorenal syndrome

COMMON DRP

Pemilihan obat yang kurang tepat Tak ada penyesuaian dosis ADR : HE, peningkatan Transaminase DILD (Drug Induced Liver Disease)

ASSESSMENT OF LIVER FUNCTION

lTdk ada tes yg dpt mengkuantifikasi fs hati lMarker Nekrosis Hepatoseluler :

§SGOT(AST) §SGPT(ALT) §ALP §GGT §Bilirubin lMarker Kapasitas Sintetis Hepar:

§Albumin, §Prothrombin Time

ACUTE LIVER DISEASE

Manifestasi: Hepatitis, Drug intoxication, alcohol toxication

Sign: Transaminase minimal 2x nilai normal, dpt disertai pe GGT, ALP

Symptom: mual, muntah, nyeri perut kuadran kanan bawah, jaundice

Dapat menyebabkan Acute or Chronic Hepatic Failure

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

lCharacteristics:

§Short course ( < 8 weeks) §Rare portal hypertension §Hepatic encephalopathy §Cerebral oedema §Reversible (regeneration)

TREATMENT

l

Goal: correcting metabolic abnormalities, preventing coma

l

Treatment include:

o

Coagulation defects with Vit K, Fresh Frozen Plasma, Trombocyte Concentrate

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 lLong course (months-years) lPortal hypertension lHepatic encephalopathy lRare cerebral oedema lIrreversible (scar formation) lForms:

§CIRRHOSIS HEPATIC §PRIMARY BILLIARY CIRRHOSIS

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
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
Moderate
Prothrombin Time
1-4
4-6
>6

CIRRHOSIS HEPATIC

v Progressive loss of basic hepatocyte function

v Loss of enzymes →↓ drugs & toxin handling

v Findings: jaundice, gynecomastia, spider navy, splenomegaly, erytema palmaris.

v Manifestasi: Hepatic encephalopathy, coagulopathy, Portal hypertension, Ascites, SBP, oesophageal/gastric varices, hepatorenal syndrome.

CIRRHOSIS HEPATIC

CIRRHOSIS HEPATIC

CH TREATMENT

lAscites management

lKoreksi nutritional deficiency (hati-hati dg iron replacement).

lTreatment of coagulopathy (Vit K / transfusi)

lImunitas ↓→ terapi infeksi agresif, profilaksis

lTerapi portal hypertension (bila+) dg propanolol

lVariceal Bleeding: Octreotide, somatostatin, TIPS, sclerotherapy

CH TREATMENT

Small

moderate amount of ascites

spironolactone 25 furosemide 20

100mg

80mg p.o.

resistant

spironolactone 25 furosemide 20 100mg 80mg p.o. resistant Massive ascitis Admission Sodium restriction 5

Massive ascitis

Admission

Sodium restriction 5

spironolactone/furosemide

7.5mg

7g/day

Sodium restriction 5 spironolactone/furosemide 7.5mg 7g/day tolvaptan 3.75 pottasium canrenoate 200 600mg furosemide 20

tolvaptan 3.75Sodium restriction 5 spironolactone/furosemide 7.5mg 7g/day pottasium canrenoate 200 600mg furosemide 20 100mg i.v.

5 spironolactone/furosemide 7.5mg 7g/day tolvaptan 3.75 pottasium canrenoate 200 600mg furosemide 20 100mg i.v.

pottasium canrenoate 200

600mg

7.5mg 7g/day tolvaptan 3.75 pottasium canrenoate 200 600mg furosemide 20 100mg i.v. beginning with 20mg, be

furosemide 20

100mg i.v.

beginning with 20mg, be increased, if necessary

albumin infusion

with 20mg, be increased, if necessary albumin infusion diuretic-resistant or diuretic-intractable ascites

diuretic-resistant or diuretic-intractable ascites

infusion diuretic-resistant or diuretic-intractable ascites Therapeutic paracenteses (+albumin infusion) cell-free and

Therapeutic paracenteses (+albumin infusion)

cell-free and concentrated ascites reinfusion therapy (CART)

cell-free and concentrated ascites reinfusion therapy (CART) resistant < 70 years of age Child-Pugh score 11
cell-free and concentrated ascites reinfusion therapy (CART) resistant < 70 years of age Child-Pugh score 11

resistant

< 70 years of age Child-Pugh scoreand concentrated ascites reinfusion therapy (CART) resistant 11 transjugular intrahepatic portosystemic stent-shunt

(CART) resistant < 70 years of age Child-Pugh score 11 transjugular intrahepatic portosystemic stent-shunt
(CART) resistant < 70 years of age Child-Pugh score 11 transjugular intrahepatic portosystemic stent-shunt
(CART) resistant < 70 years of age Child-Pugh score 11 transjugular intrahepatic portosystemic stent-shunt
(CART) resistant < 70 years of age Child-Pugh score 11 transjugular intrahepatic portosystemic stent-shunt

11

transjugular intrahepatic portosystemic stent-shunt (TIPS)

peritoneovenous shunt (PVS)

impossible

impossible

Serum T. Bil 10mg/dL, respiratory failure, DIC, SBP, gastrointestinal bleeding, peritoneal adhesion, untreated risky varices

Serum T. Bil 10mg/dL , respiratory failure, DIC, SBP, gastrointestinal bleeding, peritoneal adhesion, untreated risky

, respiratory

failure, DIC, SBP, gastrointestinal bleeding, peritoneal adhesion,

untreated risky varices

bleeding, peritoneal adhesion, untreated risky varices Liver transplantation Spontaneous bacterial Peritonitis

Liver transplantation

Spontaneous bacterial

Peritonitis (SBP)

transplantation Spontaneous bacterial Peritonitis (SBP) Third generation cephalosporins i.v. Serum Cr 1.0mg/dL BUN

Third generation cephalosporins i.v.

Peritonitis (SBP) Third generation cephalosporins i.v. Serum Cr 1.0mg/dL BUN 30mg/dL or T. Bil 4.0mg/dL +

Serum Cr 1.0mg/dL

BUN 30mg/dL or T. Bil 4.0mg/dL

Third generation cephalosporins i.v. Serum Cr 1.0mg/dL BUN 30mg/dL or T. Bil 4.0mg/dL + Albmin infusion
Third generation cephalosporins i.v. Serum Cr 1.0mg/dL BUN 30mg/dL or T. Bil 4.0mg/dL + Albmin infusion

+ Albmin infusion (1.5g/kg b.w.)

2

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

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 L-Isoleucine, L-Leucine, dan L-Valine) 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

lPredisposing factors: Hx of SBP, GI bleeding, UTI, bladder/intravasc. cath.,repeated paracentesis

lFindings: Abdo pain, fever, elevated WBC, renal failure, precipitation of HE

lTreatment: Cefotaxime 3x1-2 g for 5-10 days or Ceftriaxone 1x1g for 5-10 days, albumin 1g/kg on day 0 and day 3

lProphylaxis for reinfection: Cipro 1x750mg/week

HEPATORENAL SYNDROME

lRenal failure associated with liver disease lDefined by oligouria in euvolemia or hypervolemia lNo structural damages in the kidneys lManagement:

lrenal dose dopamine has not been proven to be beneficial lRRT lLiver 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, H 2 -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

lAcute Hepatic Injury

§Hepatocellular injury:Halothane, INH, Pamol, PZA

§Cholestatic injury:Steroid anabolik, OC, erythromycin, CPZ

§Mixed injury: Sulfonamida, rifampin, PAS

lChronic 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 2

Ny. SM, 58 th , 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?

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?