Patient with jaundice: Viral hepatitis Flashcards
Hepatitis scenario
Why jaundice?
Why swollen?
Why bruise easily?
1) ^ bilirubin, haemolysis, decreased conjugation in liver, decreased excretion from liver
2) less albumin/protein made in liver, oncotic pressure in vasculature low so fluid leaks out
3) clotting proteins less
Types of viruses that cause hepatitis
Intra hepatic: liver main site of replication
others: EBV, CMV, HIV, mumps, yellow fever
Hepatitis A B and C features
type, route, acute/chronic?, asymptomatic?, vaccine
D?
HAV: RNA, faecal oral, acute hepatitis, higher in children, lowers, yes
HBV: DNA, blood borne, acute, chronic, cirrhosis, cancer, more likely to be asymptomatic, yes,
HCV: RNA, blood borne, acute, chronic, cirrhosis, cancer, curative treatment
D: only with hep B
HAV, HBV, HCV
HAV: Asymptomatic illness: <5yrs ___ 5-10yrs ____, adults ___. Not chronic
HBV: Very likely to be _____. Chronic illness <1 yr ___, 1-5 yr ____, adult __
HCV: asymp in >80% of adults. Chronic in 5-85% of adults
HAV: Asymptomatic illness: <5yrs 90%, 5-10yrs 60%, adults 30%. Not chronic
HBV: Very likely to be asymptomatic. Chronic illness <1 yr 90%, 1-5 yr 10-25%, adult <5%
HCV: asymp in >80% of adults. Chronic in 5-85% of adults
Hep B viral features and diagnosis
- partially ____ stranded ___ virus. _____ DNA VIRus
- Diagnosis through measuring hepatitis B surface antigen in the blood. Vaccine is based on this
- Some of DNA has _______ _____, so some drugs to treat same as HIV
- _ gene involved in hijacking hepatocyte division, so _____ eventually
- partially double stranded DNA virus. HEPAtotrophic DNA VIRus
- Diagnosis through measuring hepatitis B surface antigen in the blood. Vaccine is based on this
- Some of DNA has reverse trascriptase, so some drugs to treat same as HIV
- X gene involved in hijacking hepatocyte division, so carcinoma eventually
HBV life cycle
- Binds to receptor (unsure what)
- DNA ____ and moved into nucleus, and ____ DNA made.
- ____ transcribed into ___ and ___ portions.
- ___ portions go to ____ and make viral proteins, ____ ____ and core antigen. So much made of S.A that it spills out
- ___ strand floats in cytoplasm, and some proteins translated ____.
- Infected for up to __ months, no damage to liver cell until immune system and cytotoxic T cells start
- Can incorporate ___ into our ___, slight increased risk of ____ or reactivation in ____
- Binds to receptor (unsure what)
- DNA unpackaged and moved into nucleus, and complementary DNA made.
- mRNA transcribed into large and small portions.
- Small portions go to ribosomes and make viral proteins, surface antigen and core antigen. So much made of S.A that it spills out
- Long strand floats in cytoplasm, and some proteins translated inefficiently.
- Infected for up to 3 months, no damage to liver cell until immune system and cytotoxic T cells start
- Can incorporate DNA into our genome, slight increased risk of carcinoma or reactivation in immunosuppression
Main risk factors and incubations for HAV, HBV and HCV
HAV: 4 weeks, travel is highest risk
HBV: 3-4 months, transfusion, MSM, vertical (pregnancy)
HCV: 6-7 weeks, and IVDU
Diagnosis of HAV
HAv RNA PCR, usually not needed due to HAV antibody! IgG+, disease something else, happen to be immune, used to be infected. IgM+, current
HBV diagnosis Antigens -1st, \_\_\_\_\_ if +ve, \_\_\_ \_\_\_\_ -\_\_\_\_\_: surrogate for \_\_\_\_/infectivity. High means lots around. Eag + \_\_\_\_ \_\_\_\_ -Core Ag/CAg: never found in serum A -anti-\_\_\_, only found in \_\_\_\_ or \_\_\_\_ people -anti \_\_\_: not usually measured -anti \_\_\_\_: \_\_\_ or \_\_\_ infection- Ig_
Antigens
-1st, HBsag, surface ag, if +ve, current infection
-HBeag, Early/E ag: surrogate for replication/infectivity. High means lots around. Eag + highly infectious
-Core Ag/CAg HBCag: never found in serum
A
-anti-HBS, only found in cured or vaccinated people
-anti HBE: not usually measured
-anti HBC: cured or acute infection- IgM
Acute and chronic HBV graphically
Acute: Post infection, ____ rises, with and overlap of_____. Peak illness at peak ____. ______ after resolution
Chronic: __ ____ ____ rises and falls, total _____ ___ ___ and ____ ____ plateau at high. SO if ____ _____ maybe chronic infection
Acute: Post infection, HBsag rises, with and overlap of IgM anti HBc. Peak illness at peak HBsag. anti HBs after resolution
Chronic: IgM anti HBc rises and falls, total anti Hbc IgG and HBsag plateau at high. SO if anti HBc IgM-, maybe chronic infection
HCV diagnosis
Antibody for HCV+ then PCRHCV RNA + genotype
Chronic hepatitis diagnosis
HBsag 6+ months
most often diagnosed because ALT is elevated
examples
1) HBSag +, anti-HBS -, anti- HBC+, anti HBC IgM-, HBeag +
2HBSag +, anti-HBS -, anti- HBC+, anti HBC IgM-, HBeag -
1) potentially chronic, unsure as not over 6 months
2) chronic carrier
Chronic HBV
____ cleared in 20-30 year olds. Can result in flareof active hepatitis
_____ clearance uncommon
Adult after 5 years:-
-__-__% with chronic hepatitis will develop ____, 85% alive after 5 years
-__-__% with ____ will decompensate, 15-35% alive at 5 years
-6-15% with cirrhosis will develop _____ _____, seldom alive at 5 years
HBEAg cleared in 20-30 year olds. Can result in flareof active hepatitis
HBSAg clearance uncommon
Adult after 5 years:-
-12-20% with chronic hepatitis will develop cirrhosis, 85% alive after 5 years
-20-25% with cirrhosis will decompensate, 15-35% alive at 5 years
-6-15% with cirrhosis will develop hepatocellular carcinoma, seldom alive at 5 years
Chronic HCV
after 20 years of chornic HCV, 10% cirrhosis and of that 2-3% decompensate or get HCC
