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Sistim Hepatobilier
BLOK TRAKTUS DIGESTIVUS
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Hati tdd : 4 lobus :- Kanan
- Kiri- Kuadratus ( sentral anterior & inferior )- Kaudatus (sentral & posterior )
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Unit Histologik = Lobulus Sel hati bentuk poligonal Inti vesikuler
ukleoli !enon"ol Sitoplas!a bergranul# tersusunseperti barisan ( $ord ) se$araradier dari vena sentralis%
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FUNGSI HATI
I% ungsi Sintetik : smbr plasma globulin ;α 1- antitrypsin, prot koagulasi
II% ungsi 'kskresi : bilirubin,kolstrol, urobilinogn
III% ungsi etabolik
- !tabolism Lmakas"lmak triglisri#a,kolstrol,$os$olipi#- !tabolism %arbo&i#rat
&ati smbr glukosa plasmanormal ' #r absorbsi makanan #i usus, puasa ' glikognolisis
( glukonognsis
gu#ang glikogn ; #$isinsi glukosa, as"lmak )# ba#an kton- !tabolism *rotin
pusat utama katabolism protin #an sintsis ura
- +toksi$ikasipran pnting #alam #toksi$ikasi komponn nitrogn #ari usus,
obatan kimia.i
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!/T0+/ */!/I%SAAN HATI
% *alpasi : pe!besaran# per!ukaan+% US,% .I4% /rteriografi
0% 12-S$an3% I5*SI H/2I
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2I0*SI HATI
Indikasi :Hepato!egali# 6aundi$e# Hepatitis#Sirosis#/bnor!alitas
72 8ang !enetap#assa tu!or9abses# keterlibatan hati pada sarkoidosis# bruselosis# tuberkulosis# S7'#/!iloidosis# He!okro!atosis# U5
Kontraindikasi :*erdarahan diathesis# asites !asif#
Ko!plikasi:*erdarahan : ke!atian ( "arang )'!pedu*eritonitis
Sakit s9d Sho$k
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KELAINAN HEPATOSIT- Kerusakan ok toksik / imunologik menyebabkan hepatosit membengkak
/ oedem : Balooning Degeneration
> Sitoplasma bergumpal dan terlihat jernih> Terkadang : material empedu masuk ke dlm hepatosit : difus,
seperti berbusa ( Foamy egeneration !
> "uga bisa terdapat : besi, #opper, bahan-bahan empedu
> $enumpukan droplet pd hepatosit dikenal : ST%&T'SS
- )ekrosis *oagulati+a
> epatosit bengkak dan ruptur : egenerasi idrofik / )ekrosis
itik
> )ekrosis hepatosit sekeliling +ena sentral : Sentrolobuler )ek.> Fo#al )ekrosis : )ek terbatas pd beberapa sel pd lobulus hati
> l nek hepatosit men#apai antara parenkhim periportal dan
saluran0 portal : $ie#emeal )e#rosis
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> "ejas / infeksi berat menyerang lobulus hati : portal ke portal,
portal ke sentral, sentral ke sentral : ridging )e#rosis
> )ekrosis seluruh obulus : Submassi+e )erkrosis
> )ekrosis seluruh hati : 1assi+e )e#rosis
- Fibrosis Hati
> menumpuknya #olagen pd hepatosit : sekeliling sal portal, +ena
portal atau langsung pd sinusoid> ama kelamaan : serabut fibrous mengelilingi seluruh hati
: ridging Fibrosis
> Fibrosis berlanjut 2 "ejas parenkhim hati : hati menjadi ter-bagi0
menjadi nodul-nodul berupa regenerasi hepatosit yang dikelilingi
jaringan parut : SIROSIS HEPATIS
- %nd stage of li+er disease
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egenerasi : eg% 7e!ak eg% Hidrofik eg% eather8
eg% Hialin eg% *eni!bunan ,likogen
ekrosis
- ek% okal - ek% *ie$e!eal- ek% ;onal - ek% Sub !asif
- ek% 6e!batan 9 !asif
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I % T / U S ( 6aundi$e )
+ ? !g9 @!l seru!
ilirubin : hsl penguraian he!oglobin di .'S Klasifikasi :
> tgtng tipe aku!ulasi bilirubin ( dire$t9indire$t)
> sesuai pen8ebab : he!olitik# hepatoselular# obstruk-
tif
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3 $as tr)a#inya Iktrus
1. ase pe!bentukan bilirubin berlebihanSel darah !erah pe$ah : he! pig!enbiliverdin bilirubin unkon"ungasi
+% ase 2ransportasi
ilirubin unkon"ungasi tdk larut dl! airerada dl! darah terikat dengan albu!inSbgn ke$il : terikat alfa globulin
diserap kedl! parenkhi! hati%
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2idak larut dl! air# toksik#
te!bus Ablood-rain barrierBkelainan pada otak : krniktrus
3. ase !etabolis!e unkon"ugasi dl! hatiKon"ungasi dgn + !olekul as% ,lukoronideisekresi sbgi : bilirubin diglukoronidase kesal% '!pedu bilirubin kon"ugasi :
di deteksi dl! urin
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4. ase 'kskresi
il% Kon"ugasi dala! kantong e!pedudiekskresi ke duodenu!%
ilirubin diubah !en"adi urobilinogenoleh bakteri di usus
elalui sisti! sirkulasi enterohepatik ke!bali pada hati
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GAGAL HATI
Terjadi hanya bila peny hati merusak > 34 5 organ hati , ok -
kemampuan #adangan fungsi hati yg hebat
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Gagal Hati Akut
- Keban8akan ok : neksrosis sel hati 8g !asif okhepatitis viral# kera$unan obat9bhn ki!ia# fatt8
$hange-Sindro!a .e8e : ,H/ C 'n$epalopath8
-*erle!akan hati akut pd keha!ilan : tri!ester terakhir
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Gagal Hati %ronis sering ok sirosis hati # diikuti nekrosis sel hati progresif#
fibrosis# regenerasi noduler
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*en8akit ? pen8akit pada Hati
Hpatitis 4iral akutHpatitis kronik ' akti$ #an prsistn
Hpatitis non 4iral ' %olangitis #anabss
• Hpatitis in#uksi obat 5 ba&an toksi•
*nyakit Hati in#uksi alko&ol• Sirosis Hpatik• Noplasma
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Hpatitis 6irus A '
Hp In$ksiosa 5 /pi# Virus A menular : makanan / minuman
Klinis dan patologis : sulit bedakan dgn HV B
Nekrosis – degenerasi – regenerasi : bersama
!eranan !atologi Klinik ""
!rognosis Baik.
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Hepatitis Virus B : Hepatitis Serum
*nularan ' parntral, #ir7t 7onta7t, s8ual 7onta7t, ibu-)anin, non pi#mik, &omo s8 ' riskan*rogrsi$ ' karir asimptomatik 9 H%* 9 atau H%A6aksinasi anti H26 ' 7ga& sirosis atau H::
Hepatitis Virus Non A Non B
*enularan : parenteral ( transfusi darah )Inkubasi : @ !ingguanfestasi Klinik : = Hep Dirus / dan
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H/*ATITIS %0NI%
*eradangan parenki! hati tanpa pen8e!buhan ? 3 bulan klinis C bioki!ia
/ll ages# all seE ukan pen8akit : ku!pulan sindro! ok berbagai agen ( obat- obatan# virus# dll ) F3G Hpatitis %ronik *rsistn
Hpatitis %ronik Akti$
Klinis sulit dibedakan : histopatologi : tidak !e!uaskanata klinis C ioki!ia C Histopatologi : penting untuk
!ana"e!en
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Hpatitis %ronik *rsistn
2idak berbaha8a : re!isi spontan bbrp bulan *arenkhi! hati batas nor!al *ortal 2riad !elebar C infiltrasi sel radang li!fosit# sel histiosit
*ie$e!eal e$rosis (-) Klinis : ringan atau asi!pto!atis# ikterus# hepato!egali
ringan# peninggian transa!inase# Hs/g (C) +@-3@
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Hpatitis %ronik Akti$
ukan pen8akit : sindro! ok berbagai pen8ebab : virus# obat# autoi!un%
• Hs/, : @-3• 5bat : oksifenisati# alfa !etildopa# isoniaJid• *en8%
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Sirosis Hepatis
*roses ter!inal pen8% Hati kronis :
• ibrosis difus• .egenerasi nodul• *erub% /rsitektur vaskularisasi parenkhi!
ibrosis !en8eluruh# difusibrosis tipis s9d tebal# progresif# irrevers%2i!bulkan hipertensi portal C gagal hati
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EFEK
KLINIS
SIROSIS
HATI
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NEOPLASMA HATI
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> Hepatosit : /deno!a# Hepato!a
> 'pitel uktus '!pedu : Kolangio!a# *apilo!a# Kistadeno!a# Kolangiokarsino!a
> 1a!puran : Hepato!a & Kolangiokarsino!a
> *e!buluh darah : He!angio!a# 7i!fangio!a# /ngiosarko!a
> esenkhi! : ibro!a# 7ipo!a# 7eio!io!a
esotelio!a
> eoplas!a $a!puran : Hepatoblasto!a# 2erato!a#esenkio!a
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*ri!ar8 enignadeno!a# angio!a# lipo!a# et$
alignant
hepato$ellular $ar$ino!a#$holangiosar$o!a# angiosar$o!a#hepatoblasto!a
Se$ondar8 (!etastastati$) ost$o!!on
NEOPLASMA
HATI
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H/*AT0!A ( Karsino!a Hepatoseluler )
• 2u!or ganas dari hepatosit
• 7aki-laki :
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Neoplasma Hati :
"inak : - *a+ernous emangioma
- $eliosis epatis
- S#lerosing ile u#t &denoma
- i+er *ell &denoma
- Fo#al )odular yperplasia
1aligna : - epato#ellular *ar#inoma
- *holangiosar#oma
- 1alignant 6as#ular )eoplasm
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Karsinoma epar :
gbrn nodul soliter yg
bsr, sbgn besar tidak
berkapsul
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Hepato Celller Car!inoma
Normal
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Metastati! A"eno!ar!inoma Hepar
Normal
+i
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+iagnos% 2u!or !arker
/lpha-fetoprotein (/*) (>0@@ng9!l) Sensitivit8 = 3@ /* also elevates in ger! $ell tu!ors and !etastati$ $an$er in
the liver 'levated /* = high risk for H11
+% I!aging Ultrasound 12 s$an
.I
7Depen" on man# $a!tors%
• Prpose "iagnose or s!reening&
• E'pertise o$ "o!tor
• (alit# o$ "i$$erent s!anner at a parti!lar $a!ilit#
• E!onomi! !onsi"eration
• Ot)er !on"ition t)at nee" to be !onsi"ere" *s!) as
!lastrop)obia or +i"ne# impairment,
• et!
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8. iopsy or Fine )eedle &spiration (F)&!
. efiniti+e diagnosis
. *ompli#ation
leeding (less in F)&!
Seeding (rare in F)&!
. isad+antages
iffi#ult to distinguish 9ell-differentiated ** fromnormal li+er, adenoma, or pre#an#er
e;uired highly skilled pathologist as often only a
#luster of #ells is a+ailable for e+aluation in F)&
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%AN+UNG
SALUAN /!*/+U
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F0 proble! klinik sisti! bilier :• Kolelitiasis•
Kolesistitis• eoplas!a
H 7' 7 H
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1H57' C 7I2H5 C I/SIS
Common condition in which
gallstones form within biliarysystem
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%ollitiasis < 2atu /mp#u =
• un$ul !endadak• 8eri epigastriu!• e!a! 9 !enggigil
Si!pto! Kolesistitis
Sering bersa!aan
Sulit bedakan : Kolelitiasis ?
Kolesistitis
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'pide!iologi 9 'tiologi
• US/ : @-+@ populasi = batu e!pedu• > 4@ thn# Lanita !ultipara >># ge!uk• /ne!ia he!olitik : predisposisi• 5bat !ngdng estrogen : resiko +M
kontrasepsi : obesitas• *atogenesis > :
2ahapan :° Saturasi $airan e!pedu° *e!bentukan inti
° *erke!bangan batu e!pedu
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Cholesterol related vs
bilirubin related
AGE SEX RACIAL
>>> L! >>"#E$ A#ERICA$ %$A&I'E(#EXICA$(CA)CASIA$
E&C***
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• *btkn atu '!pedu : tgtng kelarutan kolesteroldl! $airan e!pedu%
• a8a larut kolesterol : tgtng ratio as% '!pedu C
fosfolipid C Kolesterol• Saturasi kolesterol : >>> bila ratio as%e!pedu dgn
kolesterol NNN• or!al : kolesterol tdk larut dl! air l! $airan e!pedu : kolesterol dilapisi Jat
hidrofilik = gara! e!pedu C lesitin
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Kandung empedu
terisi dengan b?bagai
jenis batu, dindingmenipis ok fibrosis
$btkn batu empedu :
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$btkn batu empedu :
• Sekresi kolesterol >>>>
• Sekresi as. %mpedu / lesitin @@@@
• Sekresi as%e!pedu >>> : postur ge!uk# pe -n8erapan kolesterol tinggi
•
efisiensi gara! e!pedu 9 lesitin NNN : ggnsirkulasi enterohepatik : sintesa NNN
• atu pig!en e!pedu : viskositas bilirubin un
kon"ungasi
/ne!ia he!olitik : sekresi bilirubin unkon%>>pengentalan bilirubin
*ATH0G/N/SIS
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*ATH0G/N/SIS
cholesterol
bile salt
bilirubin
+ILE
,* +ile constituent
-* +iliary stasis
.* Inflammation /Infection
0* bstruction
Precipitation
Lamination
Hardening
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*atologi
• Sbgn bsr batu e!pedu : kandung e!pedu
• 2iga "enis : atu kolesterol ( G@ )
atu *ig!en - Kalsiu!atu 6enis 1a!puran
• atu Kolesterol : FG kolesterol C kalsiu!
karbonat C kalsiu! fosfat C bilirubinatatu : O -0 $!# oval# kuning pu$at# trans
lusen# pe!otongan : susunan radial# sentru! (C)
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• atu *iP!en : kalsiu! bilirubinat# hita!#Q "et-bla$kR# O - $!# !ultiple#
pe!otongan : ho!ogen# konfigurasi lapi-san (-)• iEed-stone : "!lh ban8ak# Qfa$etedR# konfi
gurasi $in$in konsentris
ukosa kandung e!pedu : pd te!patbatu : lipofag ( kolesterolosis ) = ber$akkuning-keputihan# ltr blkng $airan e!pedu :StraLberr8 Kandung '!pedu
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,e"ala :
• ≥ 0@ asi!pto!atik ( silent gall bladder )• Sering !endadak : n8eri epigastriu!# de!a!#• Sering bersa!aan : kolesistitis
• Ikterus obstruktif : pen8u!batan duktuskoledokus
• ispepsi kandung e!pedu : ditusuk 9 ter -bakar di epigastriu!
• atu Kandung e!pedu : ti!bulkan karsino!a
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:H/!I:AL
:0!*0SITI0N
*ATH0G/N/SIS !0*H0L0G?
iEed stones (0-F@)
*redo!inant :1holesterol
Heterogenous !iEture
($holesterol C bile
pig!ents C $al$iu! salts)
ile $onstituents
C
ile stasis
C
Infe$tion
ultiple
Hard
a$etted !ulberr8
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:ompli7ations o$ gallbla##r stons
A7ut 7&ol7ystitis
prsistnt ston impa7tion in t& 7ysti7 #u7t 7auss t&gallbla##r to b7om #istn## an# progrssi4ly in$lam# 8prin7 pain o$ biliary 7oli7, prsists an# .orsns o4rgro.t& o$ 7oloni@ing ba7tria, a77umulation o$ pus in t&
gallbla##r
b7om n7roti7 - pr$oration an# pri7&ol7ysti7 abs7ss
:&roni7 gallstons may 7aus progrssi4 $ibrosis o$ t& gallbla##r .all an# loss
o$ gallbla##r $un7tion, trm# 7&roni7 7&ol7ystitis .it& in$iltration by lymp&o7yts, plasma 7lls, an# ma7rop&ags 7al7i$i7ation may o77ur in t& .all
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+IAGN0SIS
R$&GE$ 1X2ray3!E4I$I&E
!IAG$SIS5
S'.U I7I.UI & /7K/7I' *H5S*H/2/S'US,
/,'2I1 .'S5/1' 1H57/,I5,./
'.1*755 2'S2
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T/AT!/NT
SUGI:AL
:&ol7yst7tomy
N0N SUGI:AL
5ral dissolutiontherap8
1onta$t dissolutiontherap8
.e$ur T
efinite treat!ent
- or $hroni$ loL-
grade
% l i titi
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%olsistitis
= radang kandung e!pedu : akut# kronik# eksaserbasi akut
Sering indikasi bedah abdo!enG@-F@ : bersa!aan dgn kolelitiasis
*en8ebab : l! "elas
- Iritasi ke!is : viskositas kolesterol dl! $airane!pedu- Infeksi bakteri : '%1oli# entero$o$$i- atu ( inisiator )- Infeksi siste!ik
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%olsistitis Akut :
.ingan :- distensi kandung e!pedu- kongesti pblh drh erat : - besar# regang# ede!atous
- hipere!i C ditutupi eksudat fib- rinosupuratif
- ber$ak hita! krn gangrenosa
%olsistitis %ronis :• e!besar !engkerut : retraksi "ar% ikat
• *er!ukaan luar : halus# fibrosis• inding !enebal : putih keabuan• Htpl : tanda radang kronis
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,e"ala :
• Sakit abdo!en atas : sa!pai ke bahu :kolik• e!a!# !ual# dan !untah• 7eukositosis•
apat ti!bul : Kolangitis# /bses Hati• erlan"ut : ruptur gangren : peritonitis
A>@A