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dr. LAURA E.D. DAIRI

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DEFINITION - EPIDEMIOLOGY 

• CIRRHOSIS is a slowly progressing disease

in which healthy liver tissue is replaced withscar tissue, eventually preventing the liverfrom functioning properly. The scar tissueblocs the !ow of blood through the liver

and slows the processing of nutrients,hormones, drugs, and naturally producedto"ins

• #$I%#&IO'O()

 – In the *nited States, alcoholic cirrhosis a+ected-/0. peoples

 – In the *nited States, alcoholic cirrhosis accountsfor appro"imately 12 of deaths due to

cirrhosis.

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CAUSES OF CIRRHOSIS

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ALCOHOLIC CIRRHOSIS

•  Alcohol is the most commonly used drug in the

United States, & more than twothirds o! adultsdrin" alcohol each year 

• E#cessi$e chronic alcohol use can cause

se$eral di!!erent ty%es o! chronic li$er disease

alcoholic !atty li$er, alcoholic he%atitis,&alcoholic cirrhosis.

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PATOGENESIS

• $engguna alohol terus menerusmenimbulan erusaan hepatosit, 3broblasttermasu ativasi sel stelate hepati yangtelah mengalami transformasi edalammyo3broblast dan emampuan ontratilmerupaan loasi erusaan dari olagen.

•  Terbentu septa dari 4aringan iat yangmenghubungan periportal dan perisentral5one 6 trigonum porta dan vena sentral /membungus sel hati yang telah mengalamiregenerasi nodule.

• 7erusaan hepatosit yang berlan4ut disertaipembentuan collagen hati mengecilberbentu noduler, mengeras danterbentulah sirosis hati.

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GAMBARAN KLINIK 

• 7lini asimtomati  0/12 insidensi6laparatomy8autopsi9 onset pelan:  0 thn,

minum banya alohol, anoresia ; malnutrisi  <<,  sletal muscle, weaness = fati>ue.• Hepatoseluler disfungsi ; hipertensi portal  

 4aundice, varises bleeding, asites, H# perburuansalah satu fator berobat!

• $%  hati normal, besar, mengecil, 4aundice,eritema, spider, parotid8 larimal gland, clubbing3nger, splenomegali, muscle wasting, asites, lai:6gineomasti9 8 testicular atro38 dire efe  berurang hormonal destrusi 6#strogen9

• ? / menstrual irregularities• / Cause of death @ variceal bleeding, infesi

renal.

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LABORATORIUM

• Anemia  bleeding, hipersplenism, supresi

<& oleh alohol• S(OT  B " *'D• AST8A'T E : " @ AST sinteti dihalangi oleh

etanol,  amonia   clearence ;

shunting  H#• Coagulopati / albumin,globulin6reticulo endothel sistem9

• (luosa intolerance/endogen insulinresisten / buan %& linis

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• Diagnosis, berdasaran gabungan dari :

 Anamnese F Riwayat aloholi,Infesivirus

 $%   tanda roni liver stigmata

 'aboratorium <iopsi menyingiran penyebab lain

 *S(

• Prognosis : ai! i"a s#o$ a"!o%o"

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TREATMENT OF ALCOHOLIC CIRRHOSIS

• ALCOHOL ABSTINENCE&&

• Goo' n(#ri#ion• Long #)r* *)'i+a" s($)rision

• S+r))ning or +o*$"i+a#ions

• In #%) as)n+) o in)+#ion :G"(+or#i+oi's +an ) (s)', (#r)s#ri+#)' #o $a#i)n#s .i#% DF /a"()012

• Ora" $n#o3i4"in) 566 $ro'(+#ion oTNF-78

• Pr))n# #%) (s) o a+)#a*ino$%)

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• PORTAL HYPERTENSION is

 – #levation of the hepatic venous pressure gradient6HG$(9 E mmHg

• D))"o$)' 4

 – intrahepatic resistance of the passage ofblood !ow through the liver due to cirrhosis andregenerative nodules

 – splachnic blood !ow secondary tovasodilation within the splanchinc vascular bed

• R)s$onsi") or :

 – /ari+)a" H)*orrag%)

 – As+i#)s

 – H4$)rs$")nis*

  9HYPERTENSION-

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• Appro"imately 08 patients with cirrhosis will develop#sophageal varices, con3rmed by Routine #ndoscopy

• Another 08 patients with esophageal varices will developBLEEDING

• /ARICEAL HEMORRHAGE

 – Li) #%r)a#ing $ro")* .i#% 2;-1;< *or#a"i#4 ra#) asso+ia#)'.i#% )a+% )$iso') o "))'ing

• Ris! Fa+#ors:

 – Severity of Cirrhosis 6through Child $ughs Classi3cation9

 –  The height of wedged/hepatic vein pressure

 –  The si5e of the vari"

 – 'ocation of the vari"

 – Certain endoscopic stigmata 6Red Jale signs,Hematocystuc spots, di+use erythema, bluish color,cherry red spots, with nipple spots9

 –  Tense Ascites

ESOPHAGEAL /ARICES

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 Teanan $ortal  6HG$( E 0 mmHg9

$embuaan pembuluhpenghubung yang

telah ada

$embentuan olateralportal/sistemi dan

varises esofagus

 Teanan portal dan aliran

olateral portal  arenaamaan, alohol,ati3tas 4asmani,  

teanan

%ilatasi varises dan penipisandinding pembuluh

%esaan dinding  K

Garises pecahCatatan FHG$( F Hepatic Venous PressureGradient G#(L F Venous Endothelial Growth

Factor  6teanan intravariseal @ teanan lumen esofagus9

K %esaan dinding M //////////////////////////////////////////////////////////////////

N diameter  Tebal dinding varises

Angiogenesis6G#(L dll9

PATHOPHYSIOLOGY OF /ARICEALHEMORRHAGE

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 HEMORRHAGE

• $RI&AR) $RO$H)'ANIS

 – Screening by endoscopy for all cirrhosis patients – $rophyla"is achieved by giving DODS#'#CTIG#

<#TA <'OC7#R or GARIC#A' <AD% 'I(ATIOD

 – If Gariceal <leed 6;9 TREAT THE ACUTEBLEED&&F

• Gasoconstricting Agents 6Somatostatin 8 Octreotide9

• <alon Tamponade 6Sengstaen/<laemore tube 8&inessota Tube9

• Gariceal <and 'igation

•  Trans4ugular Intrahepatic $ortosystemic Shunt 6TI$S9

• $R#G#DTIOD OL R#<'##%ID(

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'his algorithm descri(es

an a%%roach to

management o! %atients

who ha$e recurrent(leeding !rom eso%hageal

$arices.

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Thank You 

'aura %airi