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Hepatitis B
By Gracy.
Features and
Epidemiology
Causes acute and chronic hepatitis
Infection is preventable by vaccination (95%
efficiency).
One of the most commoncauses of liver
cirrhosis.
HepatitisB virus (HBV) is the most common
viral hepatitis worldwide.
Highest prevalence :- Asia, sub-Saharan
Africa, South America, and the Middle East
In the United States :- Approximately2 million
people have chronic HBV.
Very low prevalence in children < 12 years of
age.
Transmission
The only reservoir for HBV:
humans.
Unprotected sexual
intercourse: ⅔ of cases.
Parenteral: e.g., shared IV
drug needles.
Mother to child: most
common.
Pathphysiology
HBV infects liver
cells expressing
viral peptides on
the surface
1
Peptides activate
lymphocytes
(CD8+ cytotoxic T
cells)
2
WBCs mount a
cellular immune
response against
infected liver cells
3
Destruction of
hepatocytes
4
Liver
inflammation
5
Clinical
presentation –
Acute
infection.
 Incubation time: 1–6 months
 ⅔ of individuals with acute infection are
asymptomatic.
 ⅓ of individuals develop symptoms of
acute hepatitis:
• Nausea and vomiting
• Jaundice
• Fever
• Tiredness
• Dark urine
• Abdominal pain
• Myalgias and arthralgias
 Symptom duration: often only a few weeks
 Death is rare.
Clinical
presentation –
Chronic
infection.
 When infection is acquired at a younger age, the
rate of progression to chronic hepatitis B is higher.
 Can lead to acute-on-chronic exacerbation.
 Acute reactivation:
• Asymptomatic
• May mimic the course of acute infection
• May develop liver failure
• Cirrhosis
• Hepatocellular carcinoma (HCC)
 Extrahepatic manifestations:
• Vasculitis :- Panarteritis nodosa, Sicca
syndrome, Raynaud syndrome, Uveitis.
• Neuritis and polyneuropathy.
• Glomerulonephritis.
• Skin rashes.
Diagnosis
 Viral markers :-
• Hepatitis B surface antigen.
• Hepatitis B surface antibody.
• Hepatitis B core antigen.
• Hepatitis B core antibody.
• HBV DNA.
Management –
Acute.
 No specific therapy available
 Treatment is supportive.
 Hepatitis B immune globulin and hepatitis B vaccine are
recommended for nonimmune household members
and sexual contacts.
Management –
Chronic.
 1st-line treatment:
• Pegylated interferon alfa (PEG-IFN-α)
• Entecavir (ETV)
• Tenofovir disoproxil fumarate (TDF)
 Treatment goals:
• Reversal of liver disease.
• ↓ DNA levels of HBV.
• Seroconversion to anti-Hbe
 Liver transplantation: the only curative treatment option
in cases of end-stage liver disease
Prevention
SCREENING. VACCINATION. POST EXPOSURE
PROPHYLAXIS.
Summary –
Hep B
Transmission Parenteral , Sexual , Perinatal.
Clinical course Flu, Jaundice , Hepatomegaly.
Acute vs chronic Acute > Chronic.
Vaccine Yes.
Mortality rate Low.
Carrier state Yes.
Extra hepatic
manifestation
Aplastic anemia , Glomerulonephritis
, Polyarthritis nodusa.
Laboratory
parameters
HBV DNA , HBsAg + Anti
HBs/HBc/Hbe antibodies.
Complication Cirrhosis , HCC.
Genome dsDNA.
Thank you

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Hepatitis B, introduction, symptoms, diagnosis, treatment, case presentation.

  • 2. Features and Epidemiology Causes acute and chronic hepatitis Infection is preventable by vaccination (95% efficiency). One of the most commoncauses of liver cirrhosis. HepatitisB virus (HBV) is the most common viral hepatitis worldwide. Highest prevalence :- Asia, sub-Saharan Africa, South America, and the Middle East In the United States :- Approximately2 million people have chronic HBV. Very low prevalence in children < 12 years of age.
  • 3. Transmission The only reservoir for HBV: humans. Unprotected sexual intercourse: ⅔ of cases. Parenteral: e.g., shared IV drug needles. Mother to child: most common.
  • 4. Pathphysiology HBV infects liver cells expressing viral peptides on the surface 1 Peptides activate lymphocytes (CD8+ cytotoxic T cells) 2 WBCs mount a cellular immune response against infected liver cells 3 Destruction of hepatocytes 4 Liver inflammation 5
  • 5. Clinical presentation – Acute infection.  Incubation time: 1–6 months  ⅔ of individuals with acute infection are asymptomatic.  ⅓ of individuals develop symptoms of acute hepatitis: • Nausea and vomiting • Jaundice • Fever • Tiredness • Dark urine • Abdominal pain • Myalgias and arthralgias  Symptom duration: often only a few weeks  Death is rare.
  • 6. Clinical presentation – Chronic infection.  When infection is acquired at a younger age, the rate of progression to chronic hepatitis B is higher.  Can lead to acute-on-chronic exacerbation.  Acute reactivation: • Asymptomatic • May mimic the course of acute infection • May develop liver failure • Cirrhosis • Hepatocellular carcinoma (HCC)  Extrahepatic manifestations: • Vasculitis :- Panarteritis nodosa, Sicca syndrome, Raynaud syndrome, Uveitis. • Neuritis and polyneuropathy. • Glomerulonephritis. • Skin rashes.
  • 7. Diagnosis  Viral markers :- • Hepatitis B surface antigen. • Hepatitis B surface antibody. • Hepatitis B core antigen. • Hepatitis B core antibody. • HBV DNA.
  • 8. Management – Acute.  No specific therapy available  Treatment is supportive.  Hepatitis B immune globulin and hepatitis B vaccine are recommended for nonimmune household members and sexual contacts.
  • 9. Management – Chronic.  1st-line treatment: • Pegylated interferon alfa (PEG-IFN-α) • Entecavir (ETV) • Tenofovir disoproxil fumarate (TDF)  Treatment goals: • Reversal of liver disease. • ↓ DNA levels of HBV. • Seroconversion to anti-Hbe  Liver transplantation: the only curative treatment option in cases of end-stage liver disease
  • 11. Summary – Hep B Transmission Parenteral , Sexual , Perinatal. Clinical course Flu, Jaundice , Hepatomegaly. Acute vs chronic Acute > Chronic. Vaccine Yes. Mortality rate Low. Carrier state Yes. Extra hepatic manifestation Aplastic anemia , Glomerulonephritis , Polyarthritis nodusa. Laboratory parameters HBV DNA , HBsAg + Anti HBs/HBc/Hbe antibodies. Complication Cirrhosis , HCC. Genome dsDNA.