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Hepatitis B - Coggle Diagram
Hepatitis B
Classification (1)
Local inflammation of the liver. Bloodborne virus transmitted via Birth from mother to child, sexual partner, sharing needles and potential workplace injury (needleprick).
Chronic infection occurs in 10% adults but >90% in infants. But Hep B virus is generally happy in the liver and doesn't have much viral effect - which can stay for 25 years before symptomatic. Only when immune system recognise abonormalities and attack liver infected cells symptoms occur.
HBcAg = Hep B core anti, indicator of active viral replication
HBsAg = Hep B surface antigen, indicator of infectious and is used to make the Hep B vaccine
HBeAg = Hep B e antigen, indicator of active and highly infectious with poor prognosis and increased risk of HCC
Active uptake into liver cells. cccDNA is formed by reverse transcriptase which is very stable and remains, but is inactive.
Acute HBV (2)
Initial 6 months post infection. >95% of adults will seroconvert and form antibodies (HBsAg is cleared and anti-HBsAb are produced. But only 10% of children will seroconvert but will generally remain asymptomatic.
Mechanism: Immune response attacks the infected liver cells causing cell damage. If immune system is well equipped, recognise and quickly clear the virus, there will be less damage.
The longer the battle, the more damage to the liver.
MHC class I: more specific response and less damage the liver
TNFa and Interferon gamma: less specific and more damage to the liver.
Anti-HBsAb = non-chronic
Anti-HBeAb = seroconversion target in chronic disease
Anti-HBc = reactivation prophylaxis risk?
Transmission, Screening and Vaccination (4)
Infection via blood, semen and vaginal fluid contact. Other external methods include injecing drugs, sharing needles, tattoos and piercings are highest prevalence.
Screening for Hep B is rarely done. Ethically not well accepted - "targeting" specific groups of people and those who undertake specific behaviours (prisoners, drug users etc).
Vaccine for Hep B is available. Targeted to high risk populations such ATSIs, injecting drug users, and healthcare workers in 1988
Universal HBV vaccine program for infants and children in 1996
80% will develop antibodies due to the vaccine (highly immunogenic uptake) and effective immunity for 95% of people. Covers for 5-10 years but starts to drop off.
Goals of treatment (5)
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Suppress viral load to prevent cccDNA formation and HCC potential.
OR
Sustain off-therapy Anti-HBe-Ab seroconversion
Who to treat?
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Depends on viral load, liver function, severity and presence of cirrhosis.
Treatment (6)
Oral NRTI
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Disadvantages: Indefinite duration (maybe lifetime of treatment), unknown long term safety, and risk of resistance
First Line: Tenoforvir, Entecavir - proven effective and potent. Entecavir has limited HIV activity.
Second line: Lamivudine - (resistance in 70% in 5 years), Telbivudine - ( new drug, cross resistance with lamivudine and not HIV approved)
Adefovir - (10-15% patients don't respond)
Emtricitabine - (unlicenced for HBV and potential falre ups if stopped. Resistance similar to lamivudine)
Peg-IFN
Advantages: Finite duration, no resistance, and higher rates of Anti-HBeAb and Anti-HBsAb seroconversion with 12 months of thearpy.
Disadvantages: Moderate antiviral effect (doesn't kill the virus, just promotes the immune system to kill it) - which can induce cirrhosis or worsen it, poor tolerability compared to NRTIs and subcut injections
Monitoring .
3rd month to assess response, then 6th month and checks on VL, ALT and seroconversion status
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