kuliahTumor Hati.ppt

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7/23/2019 kuliahTumor Hati.ppt http://slidepdf.com/reader/full/kuliahtumor-hatippt 1/35 1 ABSES HATI ABSES HATI  ALI IMRON YUSUF,SpPD,KGEH,FINASIM  ALI IMRON YUSUF,SpPD,KGEH,FINASIM DIVISI GASTRO-HEPATOLOGI DIVISI GASTRO-HEPATOLOGI BAG-I.PENYAKIT DALAM F.K. UNILA/RSUD BAG-I.PENYAKIT DALAM F.K. UNILA/RSUD Dr.ABD MOELOEK BANDAR LAMPUNG Dr.ABD MOELOEK BANDAR LAMPUNG

Transcript of kuliahTumor Hati.ppt

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11

ABSES HATIABSES HATI

 ALI IMRON YUSUF,SpPD,KGEH,FINASIM ALI IMRON YUSUF,SpPD,KGEH,FINASIM

DIVISI GASTRO-HEPATOLOGIDIVISI GASTRO-HEPATOLOGI

BAG-I.PENYAKIT DALAM F.K. UNILA/RSUDBAG-I.PENYAKIT DALAM F.K. UNILA/RSUDDr.ABD MOELOEK BANDAR LAMPUNGDr.ABD MOELOEK BANDAR LAMPUNG

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 ABSES HATI ABSES HATI

Bent! "n#e!$" p%&% '%t"Bent! "n#e!$" p%&% '%t"

Se(%r% )) * A+$e$ '%t" %)+"!Se(%r% )) * A+$e$ '%t" %)+"!

 A+$e$ '%t" pen"! A+$e$ '%t" pen"!

%$%* +%!ter",p%r%$"t,0%)r,)%pn ne!r$"$%$%* +%!ter",p%r%$"t,0%)r,)%pn ne!r$"$

$ter" +er$)+er &%r" $"$te) %$tr-"nte$t"n%$ter" +er$)+er &%r" $"$te) %$tr-"nte$t"n%

&" t%n&%" &n %&%n% pr$e$ $pr%$" &n &" t%n&%" &n %&%n% pr$e$ $pr%$" &npe)+ent!%n p$ t.&.* 0%r"n%n '%t"pe)+ent!%n p$ t.&.* 0%r"n%n '%t"

ne!rt"!,$e "n#%)%$" .ne!rt"!,$e "n#%)%$" .

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 A+$e$ H%t" A)+% A+$e$ H%t" A)+%

Diperkirakan diderita10 %Diperkirakan diderita10 % PENDUDUK DUNIA,PENDUDUK DUNIA,

  TERUTAMA NEGARA BERKEMBANG TERINFEKSI E.Histolytika TERUTAMA NEGARA BERKEMBANG TERINFEKSI E.Histolytika

10 % MENIMBULKAN GEALA10 % MENIMBULKAN GEALA

I!si"#!s $ Taila!" 0,1& %I!si"#!s $ Taila!" 0,1& %  Indonesia 5-15 % /tahunIndonesia 5-15 % /tahun

LAKI LAKI ' (ANITALAKI LAKI ' (ANITA

 

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PAT)GENESISPAT)GENESIS

Be) &"!et%'" $e(%r% p%$t"Be) &"!et%'" $e(%r% p%$t"

D"&% %.. #%!tr 2"ren$" p%r%$"t,ntr"$",D"&% %.. #%!tr 2"ren$" p%r%$"t,ntr"$",")n&epre$" pe0%),penrn%n ")n"t%$")n&epre$" pe0%),penrn%n ")n"t%$

$eer &%n re$"$ten$" p%r%$"t$eer &%n re$"$ten$" p%r%$"t

Me!%n"$)e* $tr%"n e. '"$tt"!% %&% %nMe!%n"$)e* $tr%"n e. '"$tt"!% %&% %n

p%ten &%n nn p%tenp%ten &%n nn p%ten

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E.'"$tt"!% ne)pe p%&% )!$% $$E.'"$tt"!% ne)pe p%&% )!$% $$

per$%!%n $%3%r "nte$t"n% $e $"$.per$%!%n $%3%r "nte$t"n% $e $"$.

Pene+%r%n %)+% &%r" $$ !e'%t"Pene+%r%n %)+% &%r" $$ !e'%t"$e+%"%n +e$%r 2"% 2en% prt%$e+%"%n +e$%r 2"% 2en% prt%

 

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GE4ALA KLINISGE4ALA KLINIS

DEMAMDEMAM

NYERI PERUT KANAN ATASNYERI PERUT KANAN ATAS

HEPATOMEGALIHEPATOMEGALI

KADANG GE4ALANYA TIDAK KHASKADANG GE4ALANYA TIDAK KHAS

 ANOREKSIA ANOREKSIA

KADANG DEMAMKADANG DEMAM

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PEMERIKSAAN LABORATORIUMPEMERIKSAAN LABORATORIUM

U))n% e!$"t$"$U))n% e!$"t$"$

Ke%"n%n #%% '%t" r"n%n $%)p%" $e&%nKe%"n%n #%% '%t" r"n%n $%)p%" $e&%n

Ser" %)+% , $pe$"#"! nt! &%er%' nnSer" %)+% , $pe$"#"! nt! &%er%' nn

en&e)"!en&e)"!

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PEMRIKSAAN PENUN4ANGPEMRIKSAAN PENUN4ANG

ULTRASONOGRAFIULTRASONOGRAFI

T SANT SAN

THORAK FOTOTHORAK FOTO

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DIAGNOSISDIAGNOSIS

DEMAMDEMAM

NYERI PERUT KANAN ATASNYERI PERUT KANAN ATAS

HEPATOMEGALI 5NYERI TEKANHEPATOMEGALI 5NYERI TEKAN

LEUKOSITOSISLEUKOSITOSIS

DIAFRAGMA LETAK TINGGIDIAFRAGMA LETAK TINGGI

SEROLOGI AMUBA MENDUKUNGSEROLOGI AMUBA MENDUKUNG

USGUSG

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KRITERIA SHERLOKKRITERIA SHERLOK

HEPATOMEGALI YANG NYERI TEKANHEPATOMEGALI YANG NYERI TEKAN

LEUKOSITOSISLEUKOSITOSIS

PENINGGIAN DIFRAGMA KANAN DANPENINGGIAN DIFRAGMA KANAN DANPERGERAKAN YANG KURANGPERGERAKAN YANG KURANG

 ASPIRASI ADA PUS ASPIRASI ADA PUS

USG ADA GAMBARAN RONGGAUSG ADA GAMBARAN RONGGA RESPON TERHADAP OBAT AMUBISIDRESPON TERHADAP OBAT AMUBISID

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KOMPLIKASIKOMPLIKASI

TERSERING RUPTUR.TERSERING RUPTUR.

DAPAT TER4ADI KE *DAPAT TER4ADI KE *

PLEURAPLEURA  PARUPARU

  PERIKARDIUMPERIKARDIUM

  USUSUSUS

INTRAPERITONEALINTRAPERITONEAL

  KULITKULIT

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PENGOBATANPENGOBATAN

DERIVAT NITROIMIDA6OLEDERIVAT NITROIMIDA6OLE

DAPAT DIBERIKAN ORAL DAN INTRADAPAT DIBERIKAN ORAL DAN INTRA

VENAVENA DAPAT MEMBUNUH BTK TROPO6OITDAPAT MEMBUNUH BTK TROPO6OIT

INTESTINAL,EKSTRA INTESTINAL,KISTAINTESTINAL,EKSTRA INTESTINAL,KISTA

DOSIS AN4URAN 7 8 9::-;9: ) 9DOSIS AN4URAN 7 8 9::-;9: ) 9$%)p%" 1: '%r"$%)p%" 1: '%r"

HLORO<UINHLORO<UIN

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TINDAKANTINDAKAN

BISA DILAKUKAN ASPIRASI AIRANBISA DILAKUKAN ASPIRASI AIRAN

 ABSES DENGAN GUIDED USG APABILA ABSES DENGAN GUIDED USG APABILA

 ADA ANAMAN RUPTUR DAN DIAMETER ADA ANAMAN RUPTUR DAN DIAMETER

= ; M= ; M

DI RSM TINDAKAN INI MERUPAKANDI RSM TINDAKAN INI MERUPAKAN

PROSEDUR BIASAPROSEDUR BIASA

TINDAKAN BISA BERULANG-ULANGTINDAKAN BISA BERULANG-ULANG

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1717

Kolesistitis-GallstoneKolesistitis-Gallstone

 ALI IMRON YUSUF ALI IMRON YUSUF

DIVISI GASTRO-HEPATOLOGI BAG-DIVISI GASTRO-HEPATOLOGI BAG-

I.PENYAKIT DALAM F.K. UNILA/RSUDI.PENYAKIT DALAM F.K. UNILA/RSUDDr.ABD MOELOEK BANDAR LAMPUNGDr.ABD MOELOEK BANDAR LAMPUNG

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KOLESISTITISKOLESISTITIS

Y I *Re%!$" "n#%)%$" %!t &&Y I *Re%!$" "n#%)%$" %!t &&

!%n&n e)pe& &"$ert%"!%n&n e)pe& &"$ert%"

!e'%n ner" pert !%n%n %t%$,!e'%n ner" pert !%n%n %t%$,ner" te!%n &%n p%n%$ +%&%n.ner" te!%n &%n p%n%$ +%&%n.

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ETIOLOGI DAN PATOGENESISETIOLOGI DAN PATOGENESIS

FAKTOR*STASIS AIRAN EMPEDU ,INFEKSIFAKTOR*STASIS AIRAN EMPEDU ,INFEKSI

KUMAN DAN ISKEMIA DD KANDUNG EMPEDU.KUMAN DAN ISKEMIA DD KANDUNG EMPEDU.

 PENYEBAB UTAMA * BATU KANDUNGPENYEBAB UTAMA * BATU KANDUNG

EMPEDU SEKITAR >:?.EMPEDU SEKITAR >:?.

FAKTORLAIN*KEPEKATAN AIRAN EMPEDU,FAKTORLAIN*KEPEKATAN AIRAN EMPEDU,

KOLESTEROL,LISOLESITIN,DAN P G YANGKOLESTEROL,LISOLESITIN,DAN P G YANG

MERUSAK DINDING KANDUNG EMPEDU.MERUSAK DINDING KANDUNG EMPEDU.

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GE4ALA KLINISGE4ALA KLINIS

NYERI PERUT KANAN ATASNYERI PERUT KANAN ATAS

NYERI TEKANNYERI TEKAN

PANASPANAS RASA SAKIT MEN4ALAR KEPUNDAKRASA SAKIT MEN4ALAR KEPUNDAK

 ATAU SKAPULA KANAN ATAU SKAPULA KANAN

UMUMNYA @ANITA GEMUK= 7: THNUMUMNYA @ANITA GEMUK= 7: THN MURPHY SIGNMURPHY SIGN

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DIAGNOSISDIAGNOSIS

GE4ALA KLINISGE4ALA KLINIS

ULTRASONOGRAFIULTRASONOGRAFI

SKINTIGRAFI SAL-EMPEDU DGN RADIOSKINTIGRAFI SAL-EMPEDU DGN RADIO AKTIF,TAPI TEHNIK SUKAR. AKTIF,TAPI TEHNIK SUKAR.

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PENGOBATANPENGOBATAN

ISTIRAHATISTIRAHAT

OBAT PENGHILANG RASA SAKITOBAT PENGHILANG RASA SAKIT

 ANTIBIOTIK ANTIBIOTIK 4IKA PERLU KOLESISTEKTOMI4IKA PERLU KOLESISTEKTOMI

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PROGNOSISPROGNOSIS

9 ? SEMBUH SPONTAN,TAPI9 ? SEMBUH SPONTAN,TAPI

KANDUNG EMPEDU TEBAL,FIBROTIKKANDUNG EMPEDU TEBAL,FIBROTIK

PENUH DGN BATU TDK BERFUNGSI.PENUH DGN BATU TDK BERFUNGSI.

KADANG MEN4ADI GANGREN,KADANG MEN4ADI GANGREN,

EMPYEMA DAN PERFORASI,FISTEL,EMPYEMA DAN PERFORASI,FISTEL,

 ABSES HATI ATAU PERITONITIS. ABSES HATI ATAU PERITONITIS.

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GALL STONEGALL STONE

 SERING DITEMUKANDI NEGARA DIBARATSERING DITEMUKANDI NEGARA DIBARAT

SUKU INDIAN TINGGI * 7:-;: ?SUKU INDIAN TINGGI * 7:-;: ?

DI BARAT 4ARANG MENGALAMI KOLIKDI BARAT 4ARANG MENGALAMI KOLIK

DI INDIAN 9:? KOLIK DAN KOMPLIKASI*DI INDIAN 9:? KOLIK DAN KOMPLIKASI*

KOLESISTITIS,KOLANGITIS DAN PANKREATITISKOLESISTITIS,KOLANGITIS DAN PANKREATITIS

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PATOGENESIS BATU EMPEDUPATOGENESIS BATU EMPEDU

DIPERLUKAN FAKTOR UTAMA *DIPERLUKAN FAKTOR UTAMA *

1.SUPERSATURASI KOLESTEROL1.SUPERSATURASI KOLESTEROL

C.HIPOMOTILITAS KANDUNGC.HIPOMOTILITAS KANDUNG

EMPEDUEMPEDU

.NUKLEASI EPAT.NUKLEASI EPAT

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4ENIS BATU EMPEDU4ENIS BATU EMPEDU

BATU KOLESTEROLBATU KOLESTEROL

BATU % BILIRUBINAT PIG-OKLATBATU % BILIRUBINAT PIG-OKLAT

BATU PIGMEN HITAMBATU PIGMEN HITAM

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GE4ALA KLINIKGE4ALA KLINIK

1 A SIMPTOMATIK1 A SIMPTOMATIK

C SIMPTOMATIKC SIMPTOMATIK

DGN KOMPLIKASI Y I * DGN KOMPLIKASI Y I *KOLESISTITIS AKUT,IKTERUS,KOLESISTITIS AKUT,IKTERUS,

  KOLANGITIS DAN PANKREATITIS.KOLANGITIS DAN PANKREATITIS.

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MANIFESTASI KLINIKMANIFESTASI KLINIK

1 KOLIK BILIER, INI O.K.SPASME TONIK AKIBAT1 KOLIK BILIER, INI O.K.SPASME TONIK AKIBATOBSTRUKSI TRANSIEN DUKTUS SISTIKUS OLEHOBSTRUKSI TRANSIEN DUKTUS SISTIKUS OLEHBATU, BIASANYA TIMBUL MALAM HARI,NYERIBATU, BIASANYA TIMBUL MALAM HARI,NYERITERUTAMA DIDAERAH EPIGASTRIUM.TERUTAMA DIDAERAH EPIGASTRIUM.

C KOLESISTITIS AKUT>:->9?C KOLESISTITIS AKUT>:->9?

KOLESISTITIS KRONIKKOLESISTITIS KRONIK

7 KOLEDOKOLITIASIS DAN KOLANGITIS,INI O.K.7 KOLEDOKOLITIASIS DAN KOLANGITIS,INI O.K.MIGRASI BATU KE DUK- KOLEDOKUS, GE4ALAMIGRASI BATU KE DUK- KOLEDOKUS, GE4ALA

UTAMA* NYERI >;?,IKTERIK->?,TRIAS HAROTUTAMA* NYERI >;?,IKTERIK->?,TRIAS HAROT>?.>?.

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DIAGNONISDIAGNONIS

YANG PALING TEPAT DENGANYANG PALING TEPAT DENGAN

  E U SE U SKEBERHASILAN* >; ? DIBANDINGKEBERHASILAN* >; ? DIBANDING

USG BIASA.USG BIASA.

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PE MERIKSAAN -RADIOLOGIPE MERIKSAAN -RADIOLOGI

FOTO POLOS ABDOMENFOTO POLOS ABDOMEN

KOLESISTOGRAFIKOLESISTOGRAFI

PENATAHAN HATI DGN HIDAPENATAHAN HATI DGN HIDA T SANT SAN

PT PERKUTANIUS TRANSHEPATIPT PERKUTANIUS TRANSHEPATI

KOLANGIOGRAFI KOLANGIOGRAFI ERPERP

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Table Risk Factors Associated withTable Risk Factors Associated with

Cholesterol Gallstone FormationCholesterol Gallstone Formation

Older AgeOlder Age

Female GenderFemale Gender

ObesityObesity

Weight LossWeight Loss

Total ParenteralTotal Parenteral

!trition!trition

PregnancyPregnancy

"ncreased cholesterol secretion and"ncreased cholesterol secretion anddecresed bile acid synthesisdecresed bile acid synthesis

"ncreased cholesterol secretion and"ncreased cholesterol secretion andincreased intestinal transit timeincreased intestinal transit time

Cholesterol hy#ersecretion into bile andCholesterol hy#ersecretion into bile andincreased cholesterol synthesis $iaincreased cholesterol synthesis $iaincreased %&G-CoA red!ctase acti$ityincreased %&G-CoA red!ctase acti$ity

Cholesterol hy#ersecretion into bile'Cholesterol hy#ersecretion into bile'red!ced bile acid synthesis andred!ced bile acid synthesis andgallbladder hy#omotilitygallbladder hy#omotility

Gallbladder hy#omotilityGallbladder hy#omotility

"ncreased cholesterol secretion and"ncreased cholesterol secretion andgallbladder hy#omotilitygallbladder hy#omotility

 R"(K FACTOR PROPO()* &)TA+OL"C A+OR&AL"T, 

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Table Risk Factors Associated withTable Risk Factors Associated withCholesterol Gallstone FormationCholesterol Gallstone Formation

*r!gs*r!gs

ClobrateClobrate

Oral contra-Oral contra-ce#ti$esce#ti$es

)strogen)strogentreat-ment intreat-ment inwomenwomen

)strogen)strogen

treat-ment intreat-ment inmenmen

ProgestogensProgestogens

Ce.tria/oneCe.tria/one

*ecreased bile acid concentration as a*ecreased bile acid concentration as ares!lt o. s!##ression o. 0res!lt o. s!##ression o. 0-hydro/ylase acti$ity and decreased-hydro/ylase acti$ity and decreasedACAT acti$ityACAT acti$ity

"ncreased cholesterol secretion"ncreased cholesterol secretion

Cholesterol hy#ersecretion into bile andCholesterol hy#ersecretion into bile andred!ced bile acid synthesisred!ced bile acid synthesis

Cholesterol hy#ersecretion into bileCholesterol hy#ersecretion into bile

*iminished ACAT acti$ity and increased*iminished ACAT acti$ity and increasedcholesterol secretioncholesterol secretion

Preci#itation o. an insol!ble calci!m-Preci#itation o. an insol!ble calci!m-

ce.tria/one saltce.tria/one salt

*ecreased gallbladder motility*ecreased gallbladder motility

R"(K FACTOR PROPO()* &)TA+OL"C A+OR&AL"T, 

α 

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Table Risk Factors Associated withTable Risk Factors Associated with

Cholesterol Gallstone FormationCholesterol Gallstone Formation

Genetic Predis-Genetic Predis-#osition#osition

  ati$e Americansati$e Americans 

(candina$ians(candina$ians

*iseases o. the Ter-*iseases o. the Ter-minal "le!mminal "le!m

Li#id ProleLi#id Prole  *ecreased %*L*ecreased %*L

  "ncreased trigly-"ncreased trigly-  ceridescerides  A#oli#o#rotein )-1A#oli#o#rotein )-1

"ncreased cholesterol synthesis and"ncreased cholesterol synthesis andred!ced con$ersion o. cholesterolred!ced con$ersion o. cholesterol

into bile saltsinto bile salts"ncreased cholesterol secretion into"ncreased cholesterol secretion into

bilebile

%y#osecretion o. bile salts .rom%y#osecretion o. bile salts .romdiminished bile acid #ooldiminished bile acid #ool

"ncreased acti$ity o. %&G-CoA"ncreased acti$ity o. %&G-CoAred!ctasered!ctase

"ncreased acti$ity o. %&G-CoA"ncreased acti$ity o. %&G-CoAred!ctasered!ctase

Pro#osed #ron!cleatorPro#osed #ron!cleator

 R"(K FACTOR PROPO()* &)TA+OL"C A+OR&AL"

Table Common Clinical &ani.estations o. GallstoneTable Common Clinical &ani.estations o. Gallstone

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Table Common Clinical &ani.estations o. GallstoneTable Common Clinical &ani.estations o. Gallstone*isease*isease

(ym#toms+"L"AR, COL"C

(e$ere' #oorly locali2ed e#igastric or right !##er 3!adrant$isceral #ain growing in intensity o$er 45 min and remainingconstant .or 4-6 hr' o.ten with na!sea

Fre3!ency o. attacks $aries .rom days to monthsGas' bloating' 7at!lence' and dys#e#sia are not related to stones

AC8T) C%OL)C,(T"T"(

059 are #receded by attacks o. biliary colic

:isceral e#igastric #ain gi$es way to moderately se$ere' locali2ed#ain in the right !##er 3!adrant' back' sho!lder' or' rarely'chest

a!sea with some emesis is .re3!entPain lasting ; 6 hr .a$ors cholecystitis o$er colic

C%OL)*OC%OL"T%"A("(

O.ten asym#tomatic(ym#toms <when #resent= are indisting!ishable .rom biliary colicPredis#oses to cholangitis and ac!te #ancreatitis

C%OLAG"T"(

Charcot>s triad o. #ain' ?a!ndice' and .e$er is #resent in 0@9Pain may be mild and transient and is o.ten accom#anied by

chills

&ental con.!sion' lethargy' and deliri!m are s!ggesti$e o.bacteremia

Table Common Clinical &ani.estations o. GallstoneTable Common Clinical &ani.estations o. Gallstone

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Table Common Clinical &ani.estations o. GallstoneTable Common Clinical &ani.estations o. Gallstone*isease*isease

at!ral history

+"L"AR, COL"C

A.ter initial attack' @9 ha$e no .!rther sym#tomsThe remainder de$elo# sym#toms at a rate o. 69 #er year

and se$ere com#lications at rate o. 49 #er year

AC8T) C%OL)C,(T"T"(

5@9 resol$e s#ontaneo!sly in 0-4@ days witho!t s!rgery

Le.t !ntreated' 4@9 are com#licated by a locali2ed#er.oration and 49 by a .ree #er.oration and #eritonitis

C%OL)*OC%OL"T%"A("(

at!ral history is not well dened' b!t com#lications are

more .re3!ent and se$ere than .or asym#tomatic stonesin the gallbladder

C%OLAG"T"(

%igh mortality i. !nrecogni2ed' with death .rom se#ticemia)mergent decom#ression o. the C+* <!s!ally by )RCP=

dramatically im#ro$es s!r$i$alB

Table Common Clinical &ani.estations o. GallstoneTable Common Clinical &ani.estations o. Gallstone

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Table Common Clinical &ani.estations o. Gallstone*isease*isease

Physical ndings+"L"AR, COL"C

&ild-to-moderate gallbladder tendermess d!ring an attack with

mild resid!al tenderness lasting daysO.ten a com#letely normal e/amination

AC8T) C%OL)C,(T"T"(

Febrile b!t !s!ally 4@DOF !nless com#licated by gangrene or#er.oration

Right s!bcostal tenderness with ins#iratory arrest <&!r#hy sign=

Pal#able gallbadder in 9' es#ecially in #atients ha$ing their rstattack &ild ?a!ndice in D@9' higher .re3!ency in elderlyC%OL)*OC%OL"T%"A("(

O.ten a com#letely normal e/amination i. the obstr!ction isintermittent

 Ea!ndice with #ain s!ggests stones' whereas #ainless ?a!ndice anda #al#able gallbladder .a$or malignancy

C%OLAG"T"(Fe$er in 59Right !##er 3!adrant tenderness in @9

 Ea!ndice in only @9Peritoneal signs in only 459%y#otension and mental con.!sion coe/ist in 459 and s!ggest

gram-negati$e se#sis

Table Common Clinical &ani.estations o. GallstoneTable Common Clinical &ani.estations o. Gallstone

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Laboratory ndings+"L"AR, COL"C

8s!ally normal

"n #atients with ndings o. only !ncom#licated biliary colic' anele$ated bilir!bin' alkaline #hos#hatase' or amylase s!ggestscoe/isting C+* stones

AC8T) C%OL)C,(T"T"(

Le!kocytosis o. 4D'@@@ to 45'@@@ with bandemia iscommon+ilir!bin may be D-1 mgHdL and transaminase and alkaline

#hos#hatase may be ele$ated e$en in the absence o. C+* stoneorhe#atic in.ection

&ild amylase ele$ation is seen e$en in absence o. #ancreatitis". bilir!bin ;1 or amylase ; 4@@@' s!s#ect C+* stone

C%OL)*OC%OL"T%"A("(

)le$ated bilir!bin and alkaline #hos#hatase seen with C+*obstr!ction

+ilir!bin ;4@ mgHdL s!ggests malignant obstr!ction or coe/isting

hemolysisTransient Is#ikeJ in transaminases or amylase s!ggests #assage o.

a stone

C%OLAG"T"(

Le!kocytosis in @9'  b!t remainder may ha$e normal W+C co!ntwith bandemia as the only hematologis nding

+ilir!bin ;D mgHdL in @9' b!t when D mgHdL the diagnosis maybe missed

Alkaline #hos#hatase is !s!ally ele$ated+lood c!lt!res are !s!ally #ositi$e' es#ecially d!ring chills or .e$er

s#ike' and grows two organisms in hal. o. #atients

*isease*isease

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DAFTAR PUSTAKADAFTAR PUSTAKA

BUKU A4AR IPD 4ILID 1 ED- IVBUKU A4AR IPD 4ILID 1 ED- IV FUNDAMENTAL OF GASTROENTROLOGI, ALIHFUNDAMENTAL OF GASTROENTROLOGI, ALIH

BAHASA DALDIONO DKKBAHASA DALDIONO DKK

KULIAH IPD Dr. YUKE, FK.UNPADKULIAH IPD Dr. YUKE, FK.UNPAD GREENBERGER,4N,PAUMGARTNER,GGREENBERGER,4N,PAUMGARTNER,G

DESEASE OF THE GALLBLADDER AND BILEDESEASE OF THE GALLBLADDER AND BILEDUT "n PRINIPLES OF INTERNALDUT "n PRINIPLES OF INTERNAL

MEDIINE,HORRISONS 19 t' ED,VOL-C,e&-MEDIINE,HORRISONS 19 t' ED,VOL-C,e&-BRAUN@ALD ETALL,C::1.BRAUN@ALD ETALL,C::1.

  THANKS FOR YOUR ATTENTION.THANKS FOR YOUR ATTENTION.