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Sirosis

Hepatic

Afifah Machlaurin, M.Sc., Apt


Anatomi Liver
Anatomi dan Fisiologi Liver
Apa
Fungsi
Liver
??
 www.medcinen
et.com
Apa itu Sirosis????
Cirrhosis is defined as a
diffuse process
characterized by fibrosis
and a conversion of the
normal hepatic architecture
into structurally abnormal
nodules. The end result is
destruction of hepatocytes
and their replacement by
fibrous tissue
Sirosis didefinisikan sebagai proses difus
ditandai dengan fibrosis dan konversi dari
arsitektur hati normal menjadi nodul
struktural abnormal. Hasil akhirnya
adalah penghancuran hepatosit dan
penggantian mereka oleh jaringan fibrosa

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Progression liver disease
www.healthfavo.com
Penyebab Sirosis
•Parasetamol
•amiodarone ETIOLOGY
•isoniazid (INH)
•methotrexate
•Methyldopa
•oxyphenisatin
•perhexiline
maleat
•vitamin A

•Virus Hepatitis B
•Virus Hepatitis C

11
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

The Child-Pugh classification system uses a


combination of physical and laboratory
findings to assess and define the severity of
cirrhosis
elevasi waktu protrombin
trombositopenia
encephalopathy,
dan asites

Anak-Pugh sistem klasifikasi


menggunakan kombinasi temuan fisik dan
laboratorium untuk menilai dan
menentukan keparahan sirosis
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Child-Pugh score
score 1 2 3
Albumin >3.5 3.5-2.8 <2.8
Bilrubin <2 2-3 >3
Ascites Absent Mild- Severe/
Moderate Refractory
HE Absent Mild (I-II) Severe (III-IV)
PT <4 sec. 4-6 sec. >6 sec.
prolongation (<1.7) (1.7-2.3) (>2.3)

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

 These agents reduce portal pressure by reducing portal


venous inflow via two mechanisms:
◦ decrease in cardiac output ((β1-adrenergic blockade)
◦ decrease in splanchnic blood flow (β2-adrenergic blockade).
 prevent bleeding  should be continued for life
 Target : to achieve a resting heart rate of 55 beats per
minute or a reduction of 25 percent from the base-line rate.
 Dose  propranolol 10 mg three times daily, or nadolol
20 mg once daily

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 β-Blocker non selektif, ex. Propanolol, nadolol

 Agen ini mengurangi tekanan portal dengan mengurangi aliran


vena porta melalui dua mekanisme:
 penurunan curah jantung ((β1-adrenergik blokade)
 penurunan aliran darah splanknik (β2-adrenergik blokade).
 mencegah perdarahan  harus dilanjutkan untuk hidup
 Target: untuk mencapai tingkat jantung istirahat dari 55 denyut per
menit atau pengurangan dari 25 persen dari tingkat dasar-line.
 Dosis  propranolol 10 mg tiga kali sehari, atau nadolol 20 mg
sekali sehari

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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

Transjugular Intrahepatic Portal-


systemic Shunt

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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

VARICES no β-Blocker non selective (prevention),


HEMORRHAGE Repeat Endoscopy

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

Tanda & gejala lain yg menyertai


Udem, rasa tidak enak di perut,
kaki bengkak, susah bernafas,
anoreksia, malaise, BB turun

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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

Pe↓ Tek Pe↑Tek Retensi Na


onkotik Plasma Hidrostatik kapiler dan Air

TRANSUDAT+EKSUDAT CAIRAN

Akumulasi cairan dlm rongga peritoneal

ASCITES + EDEMA PERIFER


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ALBUMIN

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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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