Download hepatitis - WordPress.com

DR. WAQAR
MBBS, MRCP
ASST. PROFESSOR
HEPATITIS
It means inflammation of the liver. There is
hepatocyte necrosis & inflammatory cell
infiltration in the liver.
There are many causes of hepatitis :
1) Viruses: Most common cause
2) Drugs ( panadol, some TB drugs)
3) Ischemia of liver( ischemic hepatitis)
4) Autoimmune
5) Alcohol
5) Poisons (carbon tetrachloride)
VIRAL HEPATITIS
A, B, C, D, E
( more common)
* Epstein Barr virus(EBV)
* Cytomegalovirus(CMV)
* Other rare viruses
( less common)
Viral hepatitis is of concern because of burden
of illness, potential for outbreaks & death.
Chronic HepB & C have a huge economic burden
also. Many cases are preventable.
Hepatitis can be acute or chronic.
1) Acute: Duration of the disease is less than 6
months.
2) Chronic: Duration is more than 6 months
(clinical S/S or abnormal blood tests)
*Hep A causeS only acute hepatitis
*Hep B,C,D &E can cause both, acute & chronic.
Chronic hepatitis B & C is the principal cause of
chronic liver disease, cirrhosis & hepatic cancer
HEPATITIS A
1) It is an RNA virus. Most common cause of
acute viral hepatitis.
2) More common in Asia, Africa, Mid.East, South
America.
3) Only acute hepatitis. No carrier state or
chronic hepatitis.Usually,does not happen twice.
Mode of transmission:
* Fecal-oral route( contamination of food &
water due to poor hygiene by food handlers)
* Saliva
Hep A contd.
Incubation Period: avg. is 28 days( time from
getting the virus till the onset of S/S)
Period of greatest infectivity:
• From 2 wks before onset of symptoms till
1-2 wks after onset of symptoms.
In this period of infectivity, the virus is shed in
the stools of the patient in high amounts.
Hep A contd.
Clinical Features:
Prodromal Phase ( first 1 -2 wks)
* Anorexia,nausea, malaise, bad taste, fever
*Jaundice is absent initially
Icteric Phase (next 3-6 wks)
* Above symptoms may improve
* Jaundice, pain in right upper quandrant, dark
urine, pale stools, tender hepatomegaly
Hep A contd.
Severity of disease: Usually mild to moderate S/S
but can be asymptomatic ( specially in children &
young ppl) or very severe disease called Fulminant
hepatic failure (F.H.F.) which is fatal.
INVESTIGATIONS
1) L.F.T.s: * High bilirubin
* AST & ALT are high ( 10 to 100 times)
* Alk. Phosphatase slightly high
2) Urine : Contains bilirubin & urobilinogen
3) Hep A antibody: Anti HAV ab.
* During acute infection: IgM type ( Diagnostic)
* After recovery: IgG type ab. appears in blood
TREATMENT
There is no special drug treatment. Disease is
self limited and recovers in 3-6 wks.
1)
2)
3)
4)
5)
Good nutrition( whatever can be tolerated)
Vitamin supplements
Avoid alcohol, panadol and some other drugs
Symptomatic treatment for complaints
FHF needs liver transplant.
PREVENTION
General Measures
Immunization
* Good hygiene
* Hep.A vaccine
* Drink bottled water
* HepA immunoin high risk areas
-globulins
* Avoid risky foods
1) Vaccine ( active immunization): Given to
* Travellers to high risk areas( Asia etc)
* Patients wth. chronic liver disease
* People working with sewage (toilet drains)
2) HepA Ig. ( passive immunization)
* Immunoglobulins are given to close contacts
of Hep A patients ( to prevent infection)
HEPATITIS B
Epidemiology:
* World wide problem( specially Africa, MidEast, S.America)
* 1/3rd of the world population has serological
evidence of past or present infection.
* About 1 million deaths occur per year due to
Hep B related liver disease & carcinoma
Structure of Hep B virus
1) Outer covering has
surface antigen( s ag.)
2) Inner center has:
* “e” ag.(antigen)
* HepB DNA
* “c” ag.
(so, 3 ag. plus DNA)
It is a DNA virus ( hep A &
hep C are RNA viruses)
SEROLOGIC MARKERS
1) After infection wth HepB, “s” antigen, “e” ag.
& HepB DNA appear in the blood.
2) “c” antigen never appears in the blood.
Antibodies which appear in the blood:
* Anti HB s ( against “s” ag.)
* Anti HB“e”( against“e” ag.)
* AntiHB “c” ( against “c” ag.)
Note that “c” antigen does not appear in blood
but c antibody appears.
Routes of Transmission
VERTICAL
(mother to fetus)
* Most common route
worldwide.
PARENTERAL
* Transmission by
body fluids (blood,
semen etc)
Modes of parenteral transfer
1) i.v. drug use : Coz drug abusers share needles
2) Transfusion of infected blood & blood
products: V. rare in developed countries coz of
blood screening.
3) Contaminated syringes
4) Needle stick injuries ( doctors &nurses at high risk)
5) Sexual transmission 6) Direct contact with blood of
HepB patient ( even minor abrasions are risky)
SPECTRUM OF HEP.B INFECTION
Hep. B can cause any of the following:
1) Acute hepatitis ( may lead to fulminant
hepatic failure in some cases)
2) Chronic hepatitis: Infection persists for more
than 6 months. May lead to cirrhosis &
hepatocellular cancer.
3) Carrier state: Virus is present in the body for
more than 6 months but no active hepatitis &
normal LFTs.
ACUTE HEP. B
1) Incubation Period: Very variable. Avg. 6 wks
2) S/S : * Jaundice + all others like Hep A
* May be asymptomatic
* 1% cases develop fulminant hep.failure
1) Extrahepatic features:
* Skin rash * Polyarthritis of small joints
* Glomerulonephritis (Membranous type)
4) Blood Tests:
a) LFTs: bili., AST & ALT (same like hepA)
b) Hep B serology ( antigens & antibodies)
contd.
SEROLOGY IN ACUTE HEP B
1) Antigens which appear
* “s”ag.
* “e”ag.
* HepB DNA levels( not
measured in acute hep.)
(all these disappear after
infection is finished)
2) Antibodies which
appear:
• AntiHBs (means
recovery)
* Anti HBe
* AntiHBc
Treatment of Acute Hep B
• Symptomatic
• No specific treatment
( Thank God this slide is small ! )
Chronic Hep B
1) Def.: Persistence of abnormal serology for more
than 6 months with or wthout S/S.
2) More chance of chronic infection in newborns
( by vertical transmission), children,& ppl. with
poor immunity).
3) Serology: * “s” ag. + * “e” ag. + * DNA +
4) S/S may be mild or absent. Often found on
routine tests.( LFTs & liver biopsy are abnormal)
5) Patient is highly infectious coz “e”ag. is present
6) If only “s” ag. is present & no “e”ag., it is chronic
carrier state & patient is less infectious. (LFTs &
liver biopsy are normal)
SO, REMEMBER
* IF “e” antigen is present in Hep B patient, he is
highly infectious.
• IF only “s” ag. is present , he is less infectious.
SO:
• Chr. Hep B: “s” ag. +, “e” ag. + , Abnormal LFTs
• Chr.carrier state: Only “s” ag. +. No “e” ag &
LFTS are normal.
TREATMENT OF CHR.HEP B
1) Drugs used:
* Nucleoside analogues: eg Entecavir
oral
* Nucleotide analogues: eg. Tenofovir
drugs
* Interferon ( Injections)
2) Treatment is 6 months to 1 yr.
3) Treatment is not given to chronic carriers(only
“s” ag. positive with normal LFTs)
PREVENTION OF HEP B.
1) Avoid risk factors ( iv drugs, needle sharing,
sexual contact wth. unknown or HepB positive
person, avoid direct contact wth blood, no
sharing of razors etc.
2) Vaccine: Given routinely to everyone.
* 3 doses: 0, I month,6 mnth(from the 1st dose)
3) Immune globulins: Given to a person if he has
not received vaccine before, & now has a high risk
exposure eg. needle stick injury from Hep.B patient,
sexual exposure or newborns of ‘s’ ag. + mothers
OUTCOME
Untreated Hep B can lead to cirrhosis &
hepatocellular cancer
REMEMBER
* Vaccine produces protective antibody over
after time (wks to months) but lasts long.
* Immunoglobulins provide immediate
protection that lasts for a short time.
HEP C
1) Epidemiology: Occurs worldwide but very
common in Africa & Egypt.
2) Mode of Spread: (Parenteral)
* i.v. drug use ( West) * Blood transfusion
(developing countries) * Contaminated needles
& instruments (surg., dental) * Sexual
transmission is very less(<1%) *Perinatal : <1%
* Contact with infected blood( razors, cuts)
3) There are 6 subtypes of HepC ( 1 to6)
* Type 1 : More severe disease
* Type 2 &3: Less severe disease & good
response to treatment.
WHAT HAPPENS AFTER INFECTION
1) Only 10-20% patients are able to clear the virus
from their body. They may get mild S/S after
infection.
1) Most patients develop chronic hepatitis
1)
2)
3)
4)
CHRONIC HEP C
Usually asymptomatic & detected by chance on
routine blood tests(slightly high AST & ALT). LFTS
often fluctuate.
Often presents after many yrs., as cirrhosis
Mild jaundice, fatigue may occur
Extrahepatic features: GN, arthritis,
cryoglobulins in the blood
DIAGNOSIS (HEP C)
1) HepC antibody ( Anti HCV ab.):
* It is the initial test done
* Becomes positive about 2 months after infection
* Antibody is not protective(opposite of Hep B)
* False +ve & -ve may occur.
2) HepC RNA levels (by PCR):
* This is actual virus level in the blood
* Appears in blood in 1-2 wks of infection
3) Liver Biopsy: Not done for diagnosis, but only
done before treatment to see fibrosis
TREATMENT
1) Offered to most patients
2) Response to treatment depends on genotype
& some other factors( type2 & 3 has very
good response & can be cured).
3) Till recently, only the following combination
was used: * Oral Ribavirin + * Interferon inj
4) Latest treatments are all oral & free of
interferons. They are given for 3 months.
( Sofosbuvir, Simeprevir etc)
( CAN YOU REMEMBER THESE NAMES? )
OTHER THINGS IN MANAGEMENT
1) Patient counselling:
* Don’t donate blood or tissue
* No iv drugs, no needle/razor sharing
* Explain that there is a risk of sexual transmiss-ion although small.
* Avoid alcohol ( can worsen the disease)
2) Check for Hep B, Hep A and vaccinate if –ve.
3) Check for HIV
VACCINE
No vaccine or immunoglobulins are available as
yet.
OUTCOME
Without treatment, Hep C can lead to cirrhosis
and hepatocellular carcinoma ( liver cancer).
HEP D
1) Hep D virus is unable to cause infection on its
own.It requires the presence of HepB virus to
replicate.
2) Infection can occur alongwith HepB ( coinfection) or occurs in a person who has
HepB from before.
3) Risk factors, mode of spread & S/S are like
Hep B.
4) Treatment of chronic Hep D: INTERFERON
HEP E
1)
2)
3)
4)
Mode of transmission is like HepA (fecal-oral)
Infection is self limited.
Occurs in developing countries
Mortality is high if it occurs in pregnancy.