kuliahtumor hati

8/12/2019 kuliahTumor Hati

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ABSES HATI

Bentuk infeksi pada hati

Secara umum : Abses hati amubik

Abses hati pyogenik Causa: bakteri,parasit,jamur,maupun

nekrosis steril yg bersumber dari sistem g.i.

yg di tandai dgn adanya proses supurasidgn pembentukan pus yg t.d.: jaringan hati

nekrotik,sel inflamasi .


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Abses Hati Amuba

10 % PENDUDUK DUNIA,TERUTAMA NEGARA BERKEMBANGTERINFEKSI E.Histolytika

10 % MENIMBULKAN GEJALA

Insidens : Thailand 0,17 %Indonesia 5-15 % /tahun

LAKI LAKI > WANITA


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PATOGENESIS

Belum diketahui secara pasti

Diduga a.l. faktor virulensi parasit,nutrisi,imunodepresi pejamu,penurunan imunitas

seluler dan resistensi parasit

Mekanisme: strain e. histolytika ada yang

patogen dan non patogen


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E.histolytika nempel pada mukosa usus

perusakan sawar intestinal sel lysis

Penyebaran amuba dari usus kehatisebagian besar via vena porta


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GEJALA KLINIS

DEMAM

NYERI PERUT KANAN ATAS

HEPATOMEGALI

KADANG GEJALANYA TIDAK KHAS

ANOREKSIA

KADANG DEMAM


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PEMERIKSAAN LABORATORIUM

Umumnya leukositosis

Kelainan faal hati ringan sampai sedang

Serologi amuba , spesifik untuk daerah non

endemik


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PEMRIKSAAN PENUNJANG

ULTRASONOGRAFI

CT SCAN

THORAK FOTO


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DIAGNOSIS

DEMAM


HEPATOMEGALINYERI TEKAN

LEUKOSITOSIS

DIAFRAGMA LETAK TINGGI

SEROLOGI AMUBA MENDUKUNG

USG


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KRITERIA SHERLOCK

HEPATOMEGALI YANG NYERI TEKAN

LEUKOSITOSIS

PENINGGIAN DIFRAGMA KANAN DANPERGERAKAN YANG KURANG

ASPIRASI ADA PUS

USG ADA GAMBARAN RONGGA RESPON TERHADAP OBAT AMUBISID


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KOMPLIKASI

TERSERING RUPTUR

DAPAT TERJADI KE :

PLEURAPARU

PERIKARDIUM

USUS

INTRAPERITONEAL

KULIT


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PENGOBATAN

DERIVAT NITROIMIDAZOLE

DAPAT DIBERIKAN ORAL DAN INTRA

VENA DAPAT MEMBUNUH BTK TROPOZOIT

INTESTINAL,EKSTRA INTESTINAL,KISTA

DOSIS ANJURAN 4 x 500-750 mg 5sampai 10 hari

CHLOROQUIN


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TINDAKAN

BISA DILAKUKAN ASPIRASI CAIRAN

ABSES DENGAN GUIDED USG APABILA

ADA ANCAMAN RUPTUR DAN DIAMETER

> 7 CM

DI RSCM TINDAKAN INI MERUPAKAN

PROSEDUR BIASA

TINDAKAN BISA BERULANG-ULANG


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13

Kolesistitis/Gallstone

ALI IMRON YUSUF

DIVISI GASTRO-HEPATOLOGI BAG-

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


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KOLESISTITIS

Y I :Reaksi inflamasi akut dd

kandung empedu yg disertai

keluhan nyeri perut kanan atas,nyeri tekan dan panas badan.


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ETIOLOGI DAN PATOGENESIS

FAKTOR:STASIS CAIRAN EMPEDU ,INFEKSI

KUMAN DAN ISKEMIA DD KANDUNG EMPEDU.

PENYEBAB UTAMA : BATU KANDUNG EMPEDU

90 %.FAKTORLAIN:KEPEKATANCAIRANEMPEDU,KOLESTER

OL,LISOLESITIN,DAN P G YANG MERUSAK

DD K E.


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GEJALA KLINIS


NYERI TEKAN

PANAS

RASA SAKIT MENJALAR KEPUNDAK

ATAU SKAPULA KANAN

UMUMNYA W- GEMUK> 40 THN. MURPHY SIGN


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DIAGNOSIS

GEJALA KLINIS

ULTRASONOGRAFI

SKINTIGRAFI SAL-EMPEDU DGN RADIO

AKTIF,TP TEHNIK SUKAR.


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PENGOBATAN

ISTIRAHAT

OBAT PENGHILANG RASA SAKIT

ANTIBIOTIK

JIKA PERLU KOLESISTEKTOMI


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PROGNOSIS

85 % SEMBUH SPONTAN,TAPI

KANDUNG EMPEDU TEBAL,FIBROTIK

PENUH DGN BATU TDK BERFUNGSI.

KADANG MENJADI GANGREN,

EMPYEMA DAN PERFORASI,FISTEL,

ABSES HATI ATAU PERITONITIS.


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GALL STONE

SERING DITEMUKANDI NEGARA DIBARAT

SUKU INDIAN TINGGI : 40-70 %

DI BARAT JARANG MENGALAMI KOLIK

DI INDIAN 50% KOLIK DAN KOMPLIKASI:KOLESISTITIS,KOLANGITIS DAN PANKREATITIS


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PATOGENESIS BATU EMPEDU

DIPERLUKAN 3 FAKTOR UTAMA :

1.SUPERSATURASI KOLESTEROL

2.HIPOMOTILITAS KANDUNG

EMPEDU

3.NUKLEASI CEPAT


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JENIS BATU EMPEDU

BATU KOLESTEROL

BATU Ca BILIRUBINAT( PIG-COKLAT)

BATU PIGMEN HITAM


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GEJALA KLINIK

1 A SIMPTOMATIK

2 SIMPTOMATIK

3 DGN KOMPLIKASI Y I :KOLESISTITIS AKUT,IKTERUS,

KOLANGITIS DAN PANKREATITIS.


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MANIFESTASI KLINIK

1 KOLIK BILIER, INI O.K.SPASME TONIK AKIBATOBSTRK-TRANSIEN DUKTUS SISTIKUS OLEH BATU,BIASANYA TIMBUL MALAM HARI,NYE-

RI T.U. DIDAERAH EPIGASTRIUM.

2 KOLESISTITIS AKUT(90-95%)

3 KOLESISTITIS KRONIK4 KOLEDOKOLITIASIS DAN KOLANGITIS,INI O.K.

MIGRASI BATU KE DUK- KOLEDOKUS, GEJALA

UTAMA: NYERI 97%,IKTERIK-69%,TRIAS CHARCOT39%.


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DIAGNONIS

YANG PALING TEPAT DENGAN

E U SKEBERHASILAN: 97 % DIBANDING

USG BIASA.


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PE MERIKSAAN -RADIOLOGI

FOTO POLOS ABDOMEN

KOLESISTOGRAFI

PENATAHAN HATI DGN HIDA CT SCAN

PTC(PERKUTANIUS TRANS-KOLANG-

ERCP


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Table Risk Factors Associated with CholesterolGallstone Formation

Older Age

Female Gender

Obesity

Weight Loss

Total Parenteral

Nutrition

Pregnancy

Increased cholesterol secretion and decresedbile acid synthesis

Increased cholesterol secretion andincreased intestinal transit time

Cholesterol hypersecretion into bile andincreased cholesterol synthesis viaincreased HMG-CoA reductase activity

Cholesterol hypersecretion into bile, reducedbile acid synthesis and gallbladderhypomotility

Gallbladder hypomotility

Increased cholesterol secretion andgallbladder hypomotility

RISK FACTOR PROPOSED METABOLIC ABNORMALITY

T bl Ri k F A i d i h Ch l l


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Drugs

Clofibrate

Oral contra-ceptives

Estrogen treat-ment in women

Estrogen treat-ment in men

Progestogens

Ceftriaxone

Octreotide

Decreased bile acid concentration as a resultof suppression of 7 -hydroxylase activityand decreased ACAT activity

Increased cholesterol secretion

Cholesterol hypersecretion into bile andreduced bile acid synthesis

Cholesterol hypersecretion into bile

Diminished ACAT activity and increasedcholesterol secretion

Precipitation of an insoluble calcium-

ceftriaxone salt

Decreased gallbladder motility



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Genetic Predis-position

Native Americans

Scandinavians

Diseases of the Ter-minal IleumLipid Profile

Decreased HDLIncreased trigly-cerides

Apolipoprotein E-4

Increased cholesterol synthesis andreduced conversion of cholesterol into

bile saltsIncreased cholesterol secretion into bile

Hyposecretion of bile salts from diminishedbile acid pool

Increased activity of HMG-CoA reductaseIncreased activity of HMG-CoA reductase

Proposed pronucleator



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Table Common Clinical Manifestations of Gallstone Disease

SymptomsBILIARY COLIC

Severe, poorly localized epigastric or right upper quadrant visceral paingrowing in intensity over 15 min and remaining constant for 1-6 hr,often with nausea

Frequency of attacks varies from days to monthsGas, bloating, flatulence, and dyspepsia are not related to stones

ACUTE CHOLECYSTITIS

75% are preceded by attacks of biliary colic

Visceral epigastric pain gives way to moderately severe, localized pain inthe right upper quadrant, back, shoulder, or, rarely, chestNausea with some emesis is frequentPain lasting > 6 hr favors cholecystitis over colic

CHOLEDOCHOLITHIASIS

Often asymptomaticSymptoms (when present) are indistinguishable from biliary colic

Predisposes to cholangitis and acute pancreatitis

CHOLANGITIS

Charcots triad of pain, jaundice, and fever is present in 70%Pain may be mild and transient and is often accompanied by chillsMental confusion, lethargy, and delirium are suggestive of bacteremia


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Natural history

BILIARY COLIC

After initial attack, 30% have no further symptomsThe remainder develop symptoms at a rate of 6% per year and

severe complications at rate of 1% per year

ACUTE CHOLECYSTITIS

50% resolve spontaneously in 7-10 days without surgery

Left untreated, 10% are complicated by a localized perforation and1% by a free perforation and peritonitis

CHOLEDOCHOLITHIASIS

Natural history is not well defined, but complications are more

frequent and severe than for asymptomatic stones in thegallbladder

CHOLANGITIS

High mortality if unrecognized, with death from septicemiaEmergent decompression of the CBD (usually by ERCP) dramatically

improves survival.



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Physical findingsBILIARY COLIC

Mild-to-moderate gallbladder tendermess during an attack with mild

residual tenderness lasting daysOften a completely normal examination

ACUTE CHOLECYSTITIS

Febrile but usually < 102OF unless complicated by gangrene or perforationRight subcostal tenderness with inspiratory arrest (Murphy sign)Palpable gallbadder in 33%, especially in patients having their first attack

Mild jaundice in 20%, higher frequency in elderlyCHOLEDOCHOLITHIASIS

Often a completely normal examination if the obstruction is intermittentJaundice with pain suggests stones, whereas painless jaundice and a

palpable gallbladder favor malignancy

CHOLANGITISFever in 95%Right upper quadrant tenderness in 90%Jaundice in only 80%Peritoneal signs in only 15%Hypotension and mental confusion coexist in 15% and suggest gram-

negative sepsis


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DAFTAR PUSTAKA

BUKU AJAR IPD JILID 1 ED- IV

FUNDAMENTAL OF GASTROENTROLOGI, ALIHBAHASA DALDIONO DKK

KULIAH IPD Dr. YUKE, FK.UNPAD

GREENBERGER,JN,PAUMGARTNER,G;

DESEASE OF THE GALLBLADDER AND BILEDUCT in PRINCIPLES OF INTERNALMEDICINE,HORRISONS 15 th ED,VOL-2,ed-

BRAUNWALD ETALL,2001.THANKS FOR YOUR ATTENTION.

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