Acute hepatitis can be caused by viruses, toxins, drugs, or autoimmune processes. The most common causes are viral hepatitis A, E, B, C, and D. Hepatitis A and E are usually self-limiting and do not result in chronic liver disease. Hepatitis B, C, and D can become chronic, increasing the risk of cirrhosis and liver cancer. Symptoms of acute hepatitis include fatigue, nausea, abdominal pain, and jaundice. Treatment focuses on relieving symptoms; vaccination helps prevent hepatitis A and B. Complications can include liver failure, chronic liver disease, or aplastic anemia.

2. ACUTE HEPATITIS
BY: ABDUR RAUF RAJPUT

3. HEPATITIS
 Acute parenchymal liver damage can be caused by many agents.
 Implies inflammation of liver characterized by presence of
inflammatory cells in the tissue of liver.
 The condition can be self limiting, healing on its own or can
progress to scaring of liver .
 Hepatitis is acute when it last less than 6 weeks and chronic
when it persist longer.
 A group of viruses known as hepatitis viruses causes most cases
of liver damage worldwide.
 Hepatitis can also be due to toxin (Alcohol) other infection or
from auto immune process
 It may run a subclinical course when the affected person may
not feel ill.
 The patient become unwell and symptomatic when disease
impair liver function.

4. CAUSES OF ACUTE HEPATITIS
• Viral hepatitis: Hepatitis A,E (more than 95% of viral
cause), B,C.
• Herpes simplex, CMV, EBV, yellow fever virus.
• Non viral infection: Toxoplasma, leptospira, Q fever.
• Alcohol
• Toxins: Amanita toxin in mushroom, carbon
tetrachloride
• Drugs: Paracetamol
• Autoimmune condition
• Metabolic Disease e.g. Wilson disease.

5. SYMPTOMS
• Clinically, the course of acute hepatitis varies widely from mild
symptoms requiring no treatment to fulminant hepatic failure .
 Acute viral hepatitis is more likely to be asymptomatic in younger
people. Symptomatic individuals may present after convalescent
stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.
 Initial features are of nonspecific flu-like symptoms, common to
almost all acute viral infections and may include malaise, muscle
and joint aches, fever, nausea or vomiting, diarrhea, and headache.
 More specific symptoms, which can be present in acute hepatitis
from any cause, are: profound loss of appetite, aversion to smoking
among smokers, dark urine, yellowing of the eyes and skin (i.e.,
jaundice) and abdominal discomfort.
 Physical findings are usually minimal, apart from jaundice (33%) an
tender hepatomegaly (10%). There can be occasional
lymphadenopathy (5%) or splenomegaly (5%).

6. HEPATITIS A VIRUS
• It`s a member of picorna virus family.
• Single stranded RNA virus.
• Incubation period 2-6 weeks.
• Mode of Transmission Feco-Oral Route.
• Epidemiology HAV is most common type of viral hepatitis
occurring world wide.
 Disease common in children in young adult
 It is common in day care Centre, prisons , travelers to
developing countries.
 No carrier state
 No chronic hepatitis
 No hepatocellular carcinoma

7. INVESTIGATION
 Liver biochemistry
 A raised serum AST and ALT which can some time be
very high
 In icteric stage the serum biluribin will be high
 Hematological test: leucopinia with relative
lymphocytosis
 ESR is raised.
 SEROLOGY :
 Active infection Anti HAV IgM
 RECOVERY Anti HAV IgG

8. COURSE & PROGNOSIS
• The prognosis is excellence with most patient making
a complete recovery.
• Mortality in young adult is 0.1% but it Increase with
age.
• Death is due to fulminant hepatic necrosis.
• HAV never progress to chronic liver disease.

9. TREATMENT
SYMPTOMATIC
• Prevention:
ACTIVE VACCINATION
PASSIVEIMMUNOGLOBULINS
Who should be vaccinated
Individual with chronic HBV & HCV.
Individual with close contact/
Individual specially who are male homosexual.
Peoples traveling to Endemic areas.
• Immunoglobulins can be effective in outbreak of
hepatitis in school & nursery.

10. HEPATITIS E VIRUS
 Hepatitis E
 Hepatitis E virus (HEV) is an RNA virus , which causes a
hepatitis clinically very similar to hepatitis A. It is enterally
transmitted, usually by contaminated water.
 Epidemics have been seen in many developing
countries. It has a mortality from fulminant hepatic failure
of 1-2% which rises to 20% in pregnant women.
 There is no carrier state and it does not progress to
chronic liver disease.
• An ELISA for IgG and IgM anti-HEV is available for
diagnosis.
• HEV RNA can be detected in the serum or stools by PCR
(polymerase chain reaction).
 Prevention and control depend on good sanitation and
hygiene.

11. HEPATITIS D VIRUS
 This is caused by the hepatitis D virus (HDV or delta virus).
 It is an incomplete RNA particle enclosed in a shell of HBsAg.
It is unable to replicate on its own but is activated by the
presence of HBV.
 It is particularly seen in intravenous drug abusers but can
affect all risk groups for HBV infection.
 Hepatitis D viral infection can occur either as a co-infection
with HBV or as a superinfect ion in an HBsAg-positive patient..
 Diagnosis is confirmed by finding serum IgM anti-delta. Super
infection results in an acute flare-up of previously quiescent
chronic HBV infection. A rise in serum AST or ALT may
indication of infection.
 Fulminant hepatitis can follow both types of infection but is
more common after co-infection.

12. HEPATITIS B VIRUS
 Double stranded DNA virus
 Incubation period 4-20 weeks
 Mode of Transmission
BLOOD
SEXUAL
BREAST FEEDING
PREGNANCY
HBV is one of the most comman cause of chronic liver
disease and hepatocellular carcinoma worldwide.

13. EPIDEMOLOGY:-
Approximately 1/3rd of population have serological
evidence of past or current infection with hepatitis B-
virus and approx: 350-400 millions are chronic HBsAg
carrier.
• The virus can be seen in semen and saliva.
• Vertical transmission during prenatal period is most
comman cause of infection worldwide and carries high
risk of ongoing chronic infection.

14. HEPATITIS B VIRUS GENOME

15. Significance of viral markers in
hepatitis B
Antigens
 HBsAg :Acute or chronic infection
 HBeAg :Acute hepatitis B Persistence implies: continued
infectious state ,increased severity of disease
 HBV DNA : Implies viral replication Found in serum and liver
Antibodies
 Anti-HBs :Immunity to HBV; previous exposure ;vaccination
 Anti-HBe :Seroconversion
 Anti-HBc :
 IgM Acute hepatitis B (high titre) .
 IgG Past exposure to hepatitis B .

17. CLINICAL COURSE

18. TREATMENT OF HBV
SYMPTOMATIC:
 PREVENTION:
 ACTIVE VACCINATION
 PASSIVEIMMUNOGLOBULINS
WHO SHOULD BE VACCINATED?
 Doctors & Nurses
 Pregnant mothers having hepatitis B infection
 Paramedic staff.

19. COMPLICATION ACUTE VIRAL
HEPATITIS
 Acute liver failure
 Cholestatic hepatitis
 Aplastic anemia
 Chronic liver disease e.g cirrhosis
 Relapsing hepatitis.