Hepatic
07/24/2021 7
Progression liver disease
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Penyebab Sirosis
•Parasetamol
•amiodarone ETIOLOGY
•isoniazid (INH)
•methotrexate
•Methyldopa
•oxyphenisatin
•perhexiline
maleat
•vitamin A
•Virus Hepatitis B
•Virus Hepatitis C
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Penyebab Sirosis yang diturunkan :
Iron buildup in the body (hemochromatosis)
Cystic fibrosis
Copper accumulated in the liver (Wilson's
disease)
Poorly formed bile ducts (biliary atresia)
Inherited disorders of sugar metabolism
(galactosemia or glycogen storage disease)
Genetic digestive disorder (Alagille syndrome)
Liver disease caused by your body's immune
system (autoimmune hepatitis)
Iron penumpukan dalam tubuh (hemochromatosis)
cystic fibrosis
Tembaga terakumulasi dalam hati (penyakit Wilson)
Buruk terbentuk saluran empedu (bilier atresia)
Kelainan bawaan metabolisme gula (galaktosemia atau
penyimpanan glikogen penyakit)
Gangguan pencernaan genetik (Alagille syndrome)
Penyakit hati yang disebabkan oleh sistem kekebalan
tubuh Anda (hepatitis autoimun)
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Penyebab Lain Sirosis :
Chronic alcohol abuse
Hepatitis C
Hepatitis B
Fat accumulating in the liver (nonalcoholic fatty liver
disease)
Destruction of the bile ducts (primary biliary cirrhosis)
Hardening and scarring of the bile ducts (primary
sclerosing cholangitis)
Infection by a parasite common in developing
countries (schistosomiasis)
cryptogenic cirrhosis
Penyalahgunaan alkohol kronis
hepatitis C
hepatitis B
Lemak terakumulasi dalam hati (penyakit hati berlemak
nonalkohol)
Penghancuran saluran empedu (primary biliary cirrhosis)
Pengerasan dan jaringan parut pada saluran empedu (primary
sclerosing cholangitis)
Infeksi oleh parasit yang umum di negara berkembang
(schistosomiasis)
sirosis kriptogenik
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Tanda dan Gejala
Spider Angiomas
Gynae
c omast
ia
th e ma
Caput Medusa
a l ma r E ry
P
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Jaundice
Presentasi Klinik
Asymptomatic
Hepatomegaly, splenomegaly
Pruritus, jaundice, palmar erythema, spider
angiomata, hyperpigmentation
Gynecomastia, reduced libido
Ascites, edema, pleural effusion, and
respiratory difficulties
Malaise, anorexia, and weight loss
Encephalopathy
asimtomatik
Hepatomegali, splenomegali
Pruritus, ikterus, eritema palmaris, spider
angiomata, hiperpigmentasi
Ginekomastia, penurunan libido
Asites, edema, efusi pleura, dan kesulitan
pernafasan
Malaise, anoreksia, dan penurunan berat
badan
encephalopathy 07/24/2021 20
Presentasi Tes Laboratorium
Hypoalbuminemia
Elevated prothrombin time
Thrombocytopenia chronic liver disease
Elevated alkaline phosphatase sensitive marker for
cholestatic liver disease
Elevated aspartate transaminase (AST), alanine
transaminase (ALT) hepatocellular injury
and γ-glutamyl transpeptidase (GGT) obstructive
disorders that disrupt the flow of bile
Serum bilirubin common in end-stage liver
disease
hypoalbuminemia
Waktu protrombin tinggi
Trombositopenia penyakit hati kronis
Peningkatan alkali fosfatase penanda sensitif untuk
penyakit hati kolestatik
Aspartate transaminase Peningkatan (AST), alanin
transaminase (ALT) cedera hepatoseluler
dan γ-glutamil transpeptidase (GGT) gangguan
obstruktif yang mengganggu aliran empedu
Bilirubin serum umum pada penyakit hati stadium
akhir
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the highest predictive value
elevation of prothrombin time
Thrombocytopenia
encephalopathy,
and ascites
Interpretation:
Class A: 5-6 Class B: 7-9 Class C: 10-15
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Terapi non farmakologi...
VARISES
ESOFAGEAL
HT
HEPATIC
ENCHEPALOPATY PORTA ASITES
-SBP
L
SPLENOMEGALI/
HIPERSPLENISME
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HT PORTAL ???
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Management of HT Portal
β-Blocker non selektif, ex. Propanolol, nadolol
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β-Blocker non selektif, ex. Propanolol, nadolol
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Isosorbide mononitrate
Child A or B, isosorbide mononitrate (20 mg twice daily) plus
nadolol resulted in a reduction in the incidence of variceal bleeding
that was more than 50 percent greater than the reduction achieved
with nadolol monotherapy
isosorbid mononitrat
Anak A atau B, isosorbid mononitrat (20 mg dua kali sehari) ditambah
nadolol mengakibatkan penurunan kejadian perdarahan varises
yang lebih dari 50 persen lebih besar dibandingkan pengurangan
dicapai dengan nadolol monoterapi
TIPS
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1st Complication
Esophageal
Varices
Normal
Variceal Bleeding
Varises
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AASLD PRACTICE GUIDELINES
Prevention and Management of Gastroesophageal
Varices and Variceal Hemorrhage in Cirrhosis
No specific therapy
No VARICES
Repeat Endoscopy in 2-3 years
β-Blocker
Large VARICES no
EVL (Endoscopic Variceal Ligation)
HEMORRHAGE
Resusitasi cairan,transfusi darah
Ab profilaksis (max 7 days)
VARICEAL
Somatostatin, vassopresin
HEMORRHAGE
Sclerotherapy
TIPS
Recurrent
HEMORRHAGE β-Blocker + EVL
TIPS
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2nd Complication
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GUIDELINE THERAPY
Based on AASLD (American Association for the
Study of Liver Disease)
Goal therapy
◦ Pencegahan komplikasi serius (ex: SBP)
◦ Mengatasi ketidaknyamanan & peningkatan kualitas
hidup
Terapi non farmakologi
◦ Penghentian alkohol
◦ Pembatasan garam 2g/hari (tdk boleh < 120mEq/L)
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SIROSIS
↑Aldosteron
Pe↓ Albumin Plasma ↑Tek. Portal dan ADH
TRANSUDAT+EKSUDAT CAIRAN
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REKOMENDASI TERAPI
Diuretik
◦ Spioronolacton 100mg & furosemid 40mg 1.dd.1
◦ Target: penurunan BB max 0,5 kg/hari pd pasien
tanpa edema dan max 1kg/hari dg edema
◦ Peningkatan dosis dpt dilakukan max 400mg
spironolacton & 160mg furosemid
◦ Monitor: elektrolit (Na, K)
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SBP
Patogenesis
◦ Overproduksi bakteri, gangguan imun dan peningkatan
permeabilitas usus .
◦ Translokasi bakteri (migrasi transmural bakteri dari usus)
dan adanya endotoksin dalam cairan ascites)
Bakteri gram (-) Enterobacteriaceae
(ex: E. coli, K. pneumoniae, S. pneumoniae)
Diagnosa
◦ PMN ≥ 250 sel/mm3
◦ kultur (+)
◦ tanda-tanda infeksi
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Therapy
Antibiotika spektrum luas
◦ Cefotaxim 2g iv , 3 times daily (1st choice)
◦ Fluoroquinolon iv (norfloxacin 400mg once
daily or ciprofloxacin 750mg weekly) /
Amoxicilin-as.klavulanat iv
◦ Ciprofloxacin (500 mg twice daily for 7 days)
atau trimethoprim-sulfamethoxazole p.o
1.dd.1 u/ profilaksis
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3rd Complication
HEPATIC ENCEPHALOPATHY
•All neurological and psychological
symptoms in patients with liver
disease
•Characterized by various neurologic
symptoms
—Cognitive impairment
—Neuromuscular disturbance
—Altered consciousness
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Semua gejala neurologis dan psikologis
pada pasien dengan penyakit hati
Ditandai dengan berbagai gejala
neurologis
gangguan kognitif
gangguan neuromuskular
gangguan kesadaran
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The symptoms of HE are thought to result from an
accumulation of gutderived nitrogenous substances in
the systemic circulation as a consequence of shunting
through portosystemic collaterals bypassing the liver.
These substances then enter the CNS and result in
alterations of neurotransmitters that affect consciousness
and behavior.
Altered ammonia, glutamate, benzodiazepine receptor
agonists, and manganese are associated with HE.
However, serum ammonia levels are poorlycorrelated
with mental status in HE.
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Gejala HE diperkirakan akibat dari akumulasi
senyawa nitrogen gutderived dalam sirkulasi
sistemik sebagai akibat dari shunting melalui
agunan portosistemik melewati hati.
Zat-zat ini kemudian masukkan SSP dan
mengakibatkan perubahan neurotransmitter
yang mempengaruhi kesadaran dan perilaku.
Amonia diubah, glutamat, agonis reseptor
benzodiazepine, dan mangan yang terkait
dengan HE. Namun, kadar amonia serum yang
poorlycorrelated dengan status mental di HE.
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Metabolisme Amonia
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Batasi intake protein
Hilangkan bakteri penghasil urease
(lactobacillus acidophylus,
enterococcus faecum) : NEOMISIN,
METRONIDAZOL)
LAKTULOSA (me↓ pH + efek
Hambat reseptor
katartik)
GABA-BDZ :
FLUMAZENIL
HE
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Terapi… 49
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