Escolar Documentos
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Cultura Documentos
Introduction:
Inflammation of Liver
Viral, immune, drugs, toxins & other.
Acute, Chronic & Fulminant - types
Viral Hepatitis
Hepatitis A, B, C, D, E, & other
Specific
Fulminant hepatitis
Cirrhosis
Acute Hepatitis:
1. Incubation phase.
2. Symptomatic pre-icteric / prodromal phase.
3. Symptomatic icteric phase.
4. Convalescence.
Hepatitis-6
PRODROMAL :
3-4 HARI S/D 2-3 MGG,LELAH, ANOREKSIA,
MUAL, HIPERPIREKSIA RINGAN,NYERI PERUT
KANAN ATAS, SAKIT KEPALA, NYERI OTOT
IKTERIK :
1-4 MGG URIN GELAP, HEPATOMEGALI,
SPLENOMEGALI.
KONVASELEN :
MULAI MENGHILANGNYA IKTERUS,NAFSU
MAKAN BAIK.
Shashi-Aug-17
Hepatitis-7
Acute Chronic
1. Ballooning deg. Ground glass (B)
2. Cholestasis Apoptosis
3. Apoptosis Periportal Necrosis
4. Periportal Necrosis Macrophages
5. Macrophages Portal Lymphoid
6. Inflammation infiltrate
7. Portal inflammation Bridging fibrosis
Shashi-Aug-17
Hepatitis-8
HEPATITIS AKUT - A
Shashi-Aug-17
Hepatitis-9
PATOGENESE :
. HISTOLOGIS :
NEKROSIS SEL HATI
DIIKUTI INFILTRASI LIMFOSIT, MAKROFAG,
SEL PLASMA, EOSINOFIL DAN NEUTROFIL.
Shashi-Aug-17
Hepatitis-11
GEJALA KLINIS
-ASYMPTOMATIS
-SYMPTOMATIS JAUNDICE SELF LIMITED
SEMBUH DALAM 8 MINGGU
-CHOLESTASIS JAUNDICE DALAM 10 MINGGU
ATAU LEBIH
-RELAPSE
-FULMINANT HEPATITIS (JARANG HIDUP)
-PENINGGIAN TRANSAMINASE > 10-20 KALI
-GEJALA KLINIS KLASIK TDD :
PRODROMAL (FLU LIKE SYNDROME)
FASE IKTERIK
FASE PENYEMBUHAN
Shashi-Aug-17
Hepatitis-12
DIAGNOSTIK :
Gejala klinis, pemeriksaan fisik dan laboratorium.
Berdasarkan ditemuinya Ig M anti HAV
PENATALAKSANAAN :
- Tidak ada yang spesifik, bersifat :
- Suportif
- Simptomatis
Prognosis
- Prognosis baik, angka kematian akibat hepatitis
fulminan 0,1 - 0,2%.
- Dilaporkan terjadi 0,13 - 0,35% kasus hospitalisasi.
Shashi-Aug-17
Hepatitis-13
PENCEGAHAN :
POLA HIDUP YANG BAIK DAN BERSIH.
SECARA UMUM :
HIGIENE PERORANGAN, LINGKUNGAN
SANITASI YANG BAIK,PEMAKAIAN AIR BERSIH,
PEMBUANGAN EKSKRETA, PEMBUATAN
SUMUR YANG MEMENUHI STANDAR.
VAKSINASI
Shashi-Aug-17
Hepatitis-14
IMUNISASI PASIF :
Shashi-Aug-17
Hepatitis-15
IMUNISASI AKTIF :
Shashi-Aug-17
Hepatitis-16
Shashi-Aug-17
Hepatitis-17
Hepatitis B - Clinical
Features
Incubation period: Average 60-90 days
Range 45-180 days
Clinical illness (jaundice): <5 yrs, <10%
5 yrs, 30%-50%
Acute case-fatality rate: 0.5%-1%
Chronic infection: <5 yrs, 30%-90%
5 yrs, 2%-10%
Premature mortality from
chronic liver disease: 15%-25%
Shashi-Aug-17
Hepatitis-18
Shashi-Aug-17
Hepatitis-19
Shashi-Aug-17
Hepatitis-20
HBeAg anti-HBe
Total anti-HBc
Titer
0 4 8 12 16 20 24 28 32 36 52 100
Weeks after Exposure
Shashi-Aug-17
Hepatitis-21
Outcome of Hepatitis B Virus Infection
100 by Age at Infection 100
80 80
60 60
Chronic Infection
40 40
20 20
Symptomatic Infection
0 0
Birth 1-6 months 7-12 months 1-4 years Older Children
and Adults
Age at Infection
Shashi-Aug-17
Hepatitis-22
Hepatitis B Virus
Modes of Transmission
Sexual
Parenteral
Perinatal
Shashi-Aug-17
Hepatitis-23
Injecting
Drug Use
(15%)
Unknown (31%)
Other (1%)
* Includes sexual contact with acute cases, carriers, and multiple partners.
Source: CDC Sentinel Counties Study of Viral Hepatitis
Shashi-Aug-17
Hepatitis-24
Elimination of Hepatitis B Virus
Transmission United States
Strategy
Prevent perinatal HBV transmission
Routine vaccination of all infants
Vaccination of children in high-risk groups
Vaccination of adolescents
all unvaccinated children at age 11-12
high-risk adolescents at all ages
Vaccination of adults in high-risk groups
Shashi-Aug-17
Hepatitis-25
Low/Not
High Moderate Detectable
Shashi-Aug-17
Hepatitis-26
Fulminant Hepatitis:
Hepatic failure with in 2-3 weeks.
Reactivation of chronic or acute hepatitis
Massive necrosis, shrinkage, wrinkled
Collapsed reticulin network
Only portal tracts visible
Shashi-Aug-17
Hepatitis-27
GAMBARAN KLINIS
IKTERUS PROGRESIF
Shashi-Aug-17
Hepatitis-28
IMUNOPATOGENESE DARI FULMINAN HEPATITIS
Shashi-Aug-17
PATOGENESE
Hepatitis-29 FULMINAN HEPATITIS OLEH VIRUS
Shashi-Aug-17
Hepatitis-30
ETIOLOGI
VIRAL HEMORAGIC FEVER VIRUS
HEPATITIS VIRUS SITOMEGALOVIRUS
HEPATITIS A HERPES SIMPLEX VIRUS
HEPATITIS B EPSTEIN BARR VIRUS
HEPATITIS C PARAMIXOVIRUS
HEPATITS E ADENOVIRUS
HEPATITIS G
PREGNANCY RELATED
ACUTE FATTY LIVER OF PREGNANCY
HELLP SINDROME
Shashi-Aug-17
Hepatitis-31
IDIOSINKRINASI METABOLIC
HALOTHANE INBORN METABOLISM ERROR
ISONIAZID GALACTOSEMIA
RIFAMPISIN FRUCTOSE INTOLERANCE
VALPROIC ACID TYROSINEMIA
DISULFIRAM NEONATAL IRON STORAGE
NSAID DISEASE
NORTRIPTYLINE WILSON DISEASE
REYE SYNDROME ALFA 1 ANTITRIPSIN DEFF.
HERBAL MEDICINE
MISC
BUDD CHIARI SYNDROME
VENO OCCLUSIVE DISEASE
AUTOIMUNE HEPATITIS
ISCHEMIC SHOCK LIVER
PRIMARY GRAFT NON FUNCTIONIN LIVER
TRANSPLANTED PATIENT
HEAT STROKE
Shashi-Aug-17
ADULT ONSET STILLS DISEASE
Hepatitis-32
TATALAKSANA
N-ASETIL SISTEIN
PENDEKATAN
FARMAKOLOGI PROSTAGLANDIN
HAEMOPERFUSI ARANG
KOLOUMN HEPATOSIT
PENDEKATAN REGULASI SITOKIN
MOLEKULER
REGULASI KASKADE KOAGULASI
INHIBISI APOPTOSIS
HEPATOSIT GROWTH FACTOR
HEPATOSIT TRANSPLANT
TRANSPLANTASI
LIVER TRANSPLANT
Shashi-Aug-17
Hepatitis-33
Shashi-Aug-17
Hepatitis-34
Shashi-Aug-17
Hepatitis-35
Chronic Hepatitis C
Factors Promoting Progression
or Severity
Increased alcohol intake
Age > 40 years at time of infection
HIV co-infection
Other
Male gender
Chronic HBV co-infection
Shashi-Aug-17
Hepatitis-36
HCV RNA
Titer
ALT
Normal
0 1 2 3 4 5 6 1 2 3 4
Months Years
Time after exposure
Shashi-Aug-17
Hepatitis-37
120
100 Decline in injection
80 drug users
60
40 Decline in
transfusion recipients
20
0
1960 1965 1970 1975 1980 1985 1989 1992 1995 1998 2001
Year
Source: Hepatology 2000;31:777-82; Hepatology 1997;26:62S-65S;
CDC, unpublished data
Shashi-Aug-17
Hepatitis-38
Injectingdrug use
Transfusion, transplant from infected donor
Occupational exposure to blood
Mostly needle sticks
Iatrogenic (unsafe injections)
Birth to HCV-infected mother
Sex with infected partner
Multiple sex partners
Shashi-Aug-17
Hepatitis-39 HCV Prevention and Control
Shashi-Aug-17
Hepatitis-42 HCV Counseling
Shashi-Aug-17
Hepatitis-43 HCV Counseling
Mother-to-Infant Transmission of HCV
Shashi-Aug-17
Hepatitis-44 HCV Counseling
Shashi-Aug-17
Hepatitis-45
Diagnostik :
Ditemuinya anti HCV. (minggu 5-6 setelah terpapar)
Peninggian transaminase pada minggu ke-2 s/d 26,
puncaknya minggu ke-5 s/d 12.
Kadar ALT biasanya meninggi pada pasien lebih dari
15 kali dari batas atas normal.
RNA HCV (+) menetap pada yang terinfeksi.
Gejala :
Banyak kasus asimtomatik
Flu-like sindrome, anoreksia, BB menurun, nyeri
abdominal, mialgia, atralgia dan fatigue.
Simptom yang jarang : demam dan rash.
Jaundice < 1/3 pasien.
Shashi-Aug-17
Hepatitis-46
HEPATITIS AKUT - D
Terdeteksi bersamaan dengan virus Hepatitis B.
HDV (+) diseluruh dunia berhubungan dengan
prevalensi infeksi HBV (+).
Lebih dominan didaerah tropikal dan subtropikal.
Infeksi HDV di negara berkembang lebih besar dari
pada di negara maju (Barat).
Manifestasi klinis dari coinfeksi atau super infeksi
bervariasi dari asimptomatis sampai yang berat
80% kasus kronik hepatitis D menjadi sirosis dalam
5-10 tahun.
Gold standard diagnosis : HDV RNA (+) atau HDAg (+)
liver.
Shashi-Aug-17
Hepatitis-47
Transmisisi :
Melalui parenteral, seksual, transfusi, jarum suntik,
haemodialisis.
Infeksi HDV dapat berupa koinfeksi atau superinfeksi
dengan HBV.
Prevalensi Geografis :
+ 5% carier HbsAg terinfeksi dengan HDV
Diagnosa :
HDV (+) di serum dan liver, HDV RNA dan HDAg (+)
Diagnosa dini dengan IgM anti HD
Shashi-Aug-17
Hepatitis-48
Gambaran Klinis :
Biasanya berat dan ikterus
Amino transferase meningkat
Pencegahan :
Dengan cara vaksinasi HBV
Therapi :
Tidak banyak bermanfaat dengan pemberian
antivirus dan immunodulator
Shashi-Aug-17
Hepatitis-49
HEPATITIS AKUT E
Tidak berkapsul, sporadis , bersifat akut.
Terdistribusi di Asia, Timur Tengah, sebagian Afrika, dan
Meksiko.
Transmisi fecal oral route.
Paling sering pada dewasa muda.
Masa inkubasi 2 - 10 minggu.
Mortalitas : 25 %.
Bersifat asimptomatis dan anikterik
Diagnosa :
HEV (+) , anti HEV (+) dan HEV RNA (+)
Tidak ada yang spesifik untuk terapi hepatitis E
Shashi-Aug-17
Hepatitis-50
HEPATITIS AKUT G
Termasuk Flava virus.
Terdistribusi secara luas.
Ditularkan melalui parenteral, seksual
dan perinatal.
HGV RNA dideteksi dengan PCR.
HGV tidak mempengaruhi respon untuk
terapi antiviral.
Shashi-Aug-17