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FARMAKOTERAPI TERAPAN GANGGUAN HEPAR
Dra. Budi Suprapti, MSi
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Happy Karuningtyas, S.Farm
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Profil Tx Gangguan Hepar-praktekKasus1 Kasus 2 Kasus 3 Kasus 4
Sanmag syr Ampi inj RL inf NSUlseran Lasix inj KAEN inf PRCLesifit Aldacton PRC OMZHP pro Albumin Metoklopramid Metoklopramid
Neurodex Vit.K inj Comafusin infB Comp Magasida syr Laktulosa
Simetidin AntasidaLasix SucralfatSpironolakton AminolebanNeurodex Vit KSulfat ferrosus Sefotaksim
PropanololTrombo cell injDexamethasonSpironolakton
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GANGGUAN HEPAR- Anatomi – Fisiologi Liver- FS Normal Liver- Disfungsi liver- Katagori penyakit liver- Sirosis - Etiologi – patofisiologi - Manifestasi - Komplikasi
Terapi
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Dokumen medik kesehatan (DMK) - px
Nomor rekam medikData px : usia, jenis kelamin, BB/TBKeluhan px DiagnosaRiwayat penyakit dahuluRiwayat terapi dahuluCatatan perkembangan px (problem-kejadian-tindakan)Lembar instruksi dokterLembar catatan keperawatanLembar konsultasi, lembar discharge px
Profil terapi
Data laboratorikData klinik
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DOKUMEN MEDIK KESEHATAN (DMK) – PXData base pxIdentifikasi px
keluhandata lab/ klinikdiagnosa
patofisiologik-pxTerapi obatDRP-pencegahan, pengatasanPemantauan efek terapi obat--data lab
data klinikKonseling px 5
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KASUS
Ny R. 54 tahun, 65 kg, MRS dengan keluhan mual, muntah darah dan berak warna hitam. Pasien dengan keadaan perut membesar dan oedema. Pasien ini mempunyai riwayat sakit kuning saat kecil dan diabetes mellitus
Data klinik : TD 90/60, Suhu 37oC, Nadi 90 bpm Data lab :Bil. Total 3,22 (0,2-1mg/dl) SGOT 33 (0-34 mg/dl)Direk 1,00 (<0,3 mg/dl) SGPT 22 (0-35 mg/dl)Indirek 2,22 ( 0,75 mg/dl) Kreatinin 1,56 (0,5-1,5 mg/dl)
Albumin 1,8 (3,5-5 mg/dl) BUN 33 (6-19mg/dl)Leukosit 3000 (4000-10.000/mm3)Hemoglobin 4,7 (13-17 mg%)Trombosit 53.000 (150.000-400.000/mm3)Na/K 136 (135-145mmol/L) / 4 (3,5-5,5 mmol/L)GD 2 j pp 201 mg/dl
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GANGGUAN HEPARANATOMI – FISIOLOGI LIVER- Liver tda. 2 labus – Ka, Ki- Labus tda. lobulus- Lobulus – struktur hexagon -- tda. Sel-sel epitel ttt HEPATOSIT -Hepatosit – tersusun dalam palte hepatosit dalam supporting cell reticuloendothelial- Antar plate – ada vaskular ( kapiler ) – SINUSOID- Dalam sinusoid – sel kuffer ( fungsi fagositosis )- Liposit – metabolisme vit A.- Empedu – disekresi hepatosit – bile canaliculi – bile duct – gall bladder
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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
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Tipe disfungsi liver
• Disfungsi hepatosit-lobulus• Disfungsi sirkulasi (HT portal)
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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, kesetimbangan Na-air
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Katagori penyakit liver• Cholestasis (Familial, Obat, TPN, Sirosis
bilier)• Akut hepatitis (Virus A,B,C,D,E, obat, toksin)• Fulminant hepatitis (Virus, toksin, iskemi,
obat dll)• Kronik hepatitis (virus, autoimmun, obat dll.)• Sirosis (infeksi, obat, toksin, hemochroma
tosis, cystic fibrosis)
Jaundice . Hemolitik (hasil destruksi/metab. Heme). Hepatoselular (konjugasi abnormal). Obstruksi (defek ekskresi, cholestatis, obstruksi empedu)
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SIROSIS. Chirose-warna orange-kuning orange hati / liver
. Sirosis : distorsi irreversibel- architecture liver normal yang dikarakterisasi hepatic injury, fibrosis, regenerasi nodularpeningkatan jar. Ikat hepar- disorganisasi architecture – kerusakan vaskular
Etiologi : alkoholpenyakit liver kronikvirus dll
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Patogenesis fibrosis
. Respons immune
. Bagian dari proses wound healing
. Respons terhadap agen fibrinogenik
Patologi sirosis-karakterisasi. Distorsi architecture hepatik. Scaring- oleh karena peningkatan jaringan fibrous kolagen. Regenerasi nodul-2 yang dikelilingi scar tissue
micronodular < 3 mmmacronodular > 3 mm
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Manifestasi sirosis. Gejala – tanda : fatigue, nausea, vomiting, weight
loss, jaundice, hepatomegali
. Ekstra hepatik:. Palmar eritema . Spider angioma. Ginekomastia . Coagulopathy. Atropi testikular . Irregular menstruation. Pembesaran kelenjar parotid
. Manifestasi klinik. Hipertensi portal. Asites. Varises gastroesofageal. Splenomegali
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Komplikasi sirosis.OK. HT portal dengan shunting portal sistemik
. Varises esofageal
. Asites- SBP
. Splenomegali-trombositopenia
. Enchepalophaty
. Hiperestrogenemia
. Hiperglikemia
. Defisiensi asam empedu-malabsorpsi
. Sensitivitas obat. OK. Loss hepatosit
. Hipoglikemia, koagulopati (def. clotting factor sintesis), edema perifer
. Komplikasi lain :. Hepatorenal syndrome. Hepatocellular Ca
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Hipertensi portal. P. portal > 10 mm Hg
mempunyai arti klinik bila > 15 mmHg
. Terjadi obstruksi intrahepatik. Presinusoidal/ sinusoidal/ postsinusoidal
. Terjadi peningkatan resistensi vask. Intrahepatik
. Sirosis----pe↑ P dlm sinusoid -------- vena porta------ P ------- vascular beds
Splenomegalishunting portal ke sistemikmalabsorpsivarises esofageal
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ASITES. Akumulasi cairan dlm. Rongga peritonium Normal 400-900 ml/hari - kapiler, limfe, membran
peritoneal. P. sinusoid----- pe↑ aliran ke pembuluh limfatik
------overflow ke intercavity peritoneal --- -------asites
. Intestin ----- terjadi ↑P vena porta------rongga peritoneal
. Hipoalbuminemia
. Terjadi retensi Na (↓aliran darah ke ginjal )------stimulasi renin ------- aldosteron------- Na --------retensi air
!! Jumlah maksimum cairan diabsorpsikembali 800-1000 ml/hari
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Spontaneous bacterial peritonitis (SBP). Tjd. Spontan-peritonium tak ada proses
klirens. Ada perforasi- transudat + eksudat Bakteri patogen usus ----- rongga peritoneum. Cairan asites : vol. besar, protein +, tak ada
opsonisasi ---- media subur bakteri tumbuh(2/3 gram - , 1/3 gram +, anaerob jarang)
Peritonitis --- seeding bakteri dari cairan asites ----- dinding usus, saluran darah, limfa
Gejala : panasnyeri perutLeukositosis
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Hipoalbumin-edema perifer• Pe↓ sintesis albumin ----- pe ↓ P onkotik plasma
kesetimbangan hemodinamik tergangguasites, edema perifer.
Perdarahan varises esofageal
•Adanya sirkulasi kolateral (ok. Sirosis/ HT protal)varises esofageal
•Varises – mudah rupture --- massive bleedingUlser duodenal/gastrikKoagulopatiHematemesis-Melena
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Hepatic enchephalopaty (HE). Terjadi perubahan status mental ringanberat. Akibat dekompensasi lanjut Px liver
shunting portal -----sistemik----- CNS. Faktor presipitasi:
. Perdarahan GIT . Azotemia
. Infeksi . Deplesi vol-diuretik
. Obat sedatip . Hipo K
. Alkalosis metabolik. HE terjadi :
. Neurotoksin NH3– CNS
. Pe ↑ GABA pada Px liver
. Pe ↑ pembentukan false neurotransmitter dari AAA pada px liver
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Koagulopati. Fungsi sintesis faktor clotting. Pe ↓ absorpsi vit. K (bgt. Lemak/ bile salt)---- untuk
sintesis faktor II, VII, IX, X. Ketidakmampuan liver memetabolisme produk
degradasi fibrin--- koagulasi intravaskular
Splenomegali + hipersplenism
. Pembesaran spleen ok. ↑ P porta
. Trombositopeni + anemi ---- peningkatan elemen darah di spleen(Normal sel darah merah dibersihkan pada usia hidupnya 120 hari)
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LIVER FAILURE
Hypo- Portal Cholestasis NH4+ + HCO3-
Albuminemia Hypertension Fat Abs.
Ascites Exudative Varices Vitamin K enteropathy deficiency Urea
Hyperaldo Clotting factorsSteronism
Hypokalemia GI Bleeding Aromatic AA
Renal NH4+ Enteric AAProduction Break down
Hyper Ammonemia False Neuro transmiters
Alkalosis Hypervent. Encephalopathy
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PORTAL HYPERTENSION
Liver Damage
Hypoalbuminemia Ascites Malabsorption Vasodilation Portal Collateral Circulation
Splenomegaly
Aldosterone Blood presure
Clotting factors ECV CO
Thrombocytes Varices
Rupture
Bleeding Encephalopathy
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HEPATORENAL SYNDROME
ASITES
CO N SYMPATETIC
EDEMA VASOCONTRICTION
RENIN
ALDOSTERON
OLIGOURI RETENSI Na+ air
GFR
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TERAPI OBAT- SIROSISPENDEKATAN. Identifikasi-eliminasi penyebab sirosis. Profilaksis- Tx variceal bleeding. Asites – Tx farmakologi/ paracentesis. SBP. HE : diet
eliminasi CNS depressantme ↓ kadar ammonia darah
. Monitor hepatorenal syndrome
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HT portal-variceal bleeding1. Cegah perdarahan – profilaksis2. Tx acute variceal hemorrhage3. Cegah rebleeding-profilaksis sekunder
Ad 1. Cegah perdarahan-profilaksis. Me ↓ portal inflow + tekanan portal. Adrenergik blocker
propanolol 3 dd 10 mgnadolol 1 dd 20 mg
. Nitrat – Px kontraindikasi blocker
. Kombinasi blocker- nitrat bila respons blocker kurang
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Ad.2. Terapi acute variceal bleeding. Perdarahan- hematemesis melena.Tujuan Tx
. Resusitasi cairan cukup
. Koreksi koagulopati-trombositopenia
. Kendalikan bleeding
. Cegah rebleeding
. Preservasi fs liver. Hipotensi – c.kristaloid, plasma, hematokrit. Vit. K, fresh frozen plasma-------------- !! PT. Profilaksis koma- laktulosa, antibiotika. Vasopresin, terlipresin( ADH, vasoactive peptida) Octreotide, somastostatin ------ ES <<. Skleroterapi-injeksi endoskopi (EIS)
Etanolamin, tetradesil sulfat Na, Na Morrhuate,polidocanol
TIPS-Transjugular intrahepatic portosystemic shunt
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Ad.3 Cegah rebleeding-profilaksis sekunder. Blocker – long acting. EBL. EIS. Kombinasi blocker – nitrat
spironolakton
P portal < 12 mmHg
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ASITES. Diet garam 2 g/hari. Diuretik
Spironolakton 100 mg/hariFurosemid 40 mg/hari
?? Capaian?? Monitoring
. Asites >>-- paracentesis
SBP• AB broad spectrum• Ampisillin + aminoglikosida• Amoksisillin + klavulanat• Sefotaksim• OfloxacinAB diberikan sampai tanda-2 infeksi hilang
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Hepatic enchephalopaty (HE)
. Koreksi faktor presipitasi:deplesi vol. cairan – kristaloidhematemesis – blood producthipokalemi – koreksiinfeksi – antibiotikaSupplemen vitaminDiet rendah protein
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Hepatic enchephalopaty (HE)
. Terapi – patogenesisme ↓ ammonia darah
batasi protein intakelaktulosa – me ↓ pH usus
efek catharticreplacement bakteri prod.
ureaselaktobacillus acidopilusenterococcus faecum
neomisin, metronidazol. Hambat reseptor GABA-benzodiazepin :
Flumazenil. False neurotransmiter - BAA
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Hepatorenal syndrome
. Hilangkan-potensial nephrotoxic. NSAID. Aminoglikosida. Diuretik >>
. Pemberian cairan
. Dopamin
. Dopamin + norepinefrin