Patient with Jaundice: Viral Hepatitis Flashcards Preview

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Flashcards in Patient with Jaundice: Viral Hepatitis Deck (25):

What are the reasons for people becoming "yellow"

They are jaundiced.

  • Too much bilirubin
    • increased production of bilirubin (pre-hepatic)
    • decreased conjugation of bilirubin in the liver (hepatic)
    • decreased excretion of bilirubin from the liver (post-hepatic)


Why is he swollen and why is he bruising easily?

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Swollen; is odematous due to decreased albumin is low → low oncotic pressure in blood vessels → fluid leaking out

Bruising: Liver is the place where coagulation proteins are produced. 


Hepatitis is just inflammation of the liver, and can be caued by....

drugs (alcohol), viruses, bacteria (typhoid fever), autoimmune, ischaemic


Viral Hepatitis can be from....

  • Hepatitis viruses: the liver is the main site of replication
  • Others: Epstein-Barr, cytomegalovirus, HIV, Mumps, yellow fever


Describe the hepatitis viruses

The viruses themselves are unrelated.


called hepatitis viruses because they cause liver disease

HAV; RNA, high in undeveloped world

HBV: DNA virus common worldwide. Extremely infectious. can be spread through playground contact

HCV: RNA virus common in developed world. Less contagious

B and C are blood borne viruses: sex, sharing needles etc


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HDV requires??

HBV in order to infect.

Therefore it only ever adds infection to those already chronically infected with HBV. 


Stats of Asymptomatic infection, chronic infection, acute illness and if there's a vaccine (draw table) 

  • Babies transmitted vertically from HBV mum will 99% be asymptomatic
  • Immune system can become tolerant if infected young, and even when our IS matures, we still don't recognise the infection. Why individuals infected as a baby get chronic HBV later down the track
    • if infected later in life, even as toddler they have better outcome as IS has matured
  • Chronic HBV present for decades can cause cancer down the track. 
  • HCV: generally infection of adults, associated with needle sharing or sex. Can do,, but generally doesn't cause symptoms
    • ​can last in the body for decades
    • can cure HCV by 

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Describe Hepatitis B

  • Partially double stranded 
  • DNA virus
  • enveloped
  • hepatotropic DNA virus
  • hepadnaviridae
  • Surface protein: Hep B surface antigen. as the virus replicates in the liver there's a very large amount of surface antigen, most of which does not get used (seen as tubules), and spills out of liver into the bloodstream.
    • This is measured/used as a diagnostic tool to confirm current hepatitis B
    • Recombinant sureface antigen is what is used in the HBV vaccine
  • Drugs target the reverse transcriptase step of HBV, so these have similarities to the HIV treatment

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THe HBV X gene?

Has a role in hijacking the hepatocyte cells machinery to increase viral production. This is the oncogenic part of the virus and can lead to hepatocellular carcinoma

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HBV life cycle?

  1. HBV surface antigen binds to some sort of receptor on a liver cell
  2. Virus gets unpackaged and the DNA is transported into the nucleus
  3. Complementary circular DNA made → mRNA transcription 
    • small portions mimic mRNA exactly, go to ribosomes and initiate protein synthesis. Generally code for surface antigens
    • Long strands: hang out in cytoplasm, some get translated into protein and some don't. Only a few viral proteins made (creating a mismatch to the huge amounts of surface antigen produced)
    • Reverse transcription makes a DNA copy of the long viral strands


Hepatitis C

  • Positive sense RNA virus: THe RNA itself has the potential to infect
  • Spherical
  • enveloped
  • prior to 1988 was called "non-A non-B hepatitis"
  • not stored in the nucleus


Does HBV damage the liver cells it replicates in?

No which is fairly rare. The virus is replicating at a relatively modest rate. The person will be infected for months and months with a relatively long incubation period. The cell is damaged instead by the cytotoxic inflammatory T-cell response.

Because the HBV DNA is taken into DNA and transcribed, free floating DNA will be taken up and some put into chromosomes, so post-infection a small proportion is in the patients DNA. This can increase % of liver cancer and reactivation in the presence of immunosuppression. HAV and HCV DON'T get taken into genome.


HBV dispersion world wide?

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Done by measuring the HBV surface antigen is how this is measured.

HCV: in places with intravenous drug usage in places without a programm for this!

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Main risks for Hep viruses?

  • Main way to catch HAV is travel, reccomend a vaccine when tracelling
  • MSM are at risk with HAV and HBV
  • HBV main risk is vertical
  • HCV main risk in intrvenous drug use

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HAV diagnosis

Look for antibody against HAV.

IgM + yes disease is HAV

IgG + no yur disease is something else and you are immune to HAV, maybe vaccinated or caught when young


HAV RNA PCR is not usually required


HBV diagnosis

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three antigens

Surface antigen: to see if its current

- anti HBS: they are 'cured' or vaccinated

Early Ag: surrogate for replication, if found in blood you know there's lots of HBV DNA in the blood, and they are highly infectious

- anti- HBE: not really measured

Core Ag: never found in serum. Produced in cytoplasm and never in ribosomes. Therefore you will never get a blood test result for it but you can measure antibodies against. 

-anti HBC: 'cured' or acute infection; IgM

Quantify acute viral DNA in patient: acute infection will have huge amounts of DNA in blood




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Chronic HBV tests

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T cell response never really matures.

Core IgM wanes over time.

IgG is left= total anti-HBc

Core +, IgM - = IgG (chronic)

anti core, antibody -, IgM + = IgM

Surface antigen will persist


HCV diagnosis?

  1. Test for antibody against HCV (marks that they've had it at some point in their lives)
  2. then do a HCV RNA PCR : tells you if it's a current infection


Chronic Infection

  • Evidence of infection > 6 months: blood tests now and in 6 months
    • ie; HBSAg + for 6 months
    • ie; HCV RNA +
  • Most often diagnosed bc ALT is elevated
  • Immunotolerance


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Clearanceof Chronic HBV

  • HBEAg is often cleared in 20-30yr olds
    • Can result in a flare of active hepatitis
    • prognosis improves
  • HBSAg clearance is uncommon
    • ​<1% a year
  • Adult after 5 years
    • ​12-20% with chronc hep will develop cirrhosis (85% live at 5 yrs)
    • 20-25% with cirrhosis will decompensate (15-35% live at 5 yrs)
    • 6-15% with cirrhosis will develop hepatocellular carcinoma (few alive at 5yrs unless curable!!! cut it out or die)


Chronic HCV

  1. Acute infection (infected 100%)
  2. Chronic infection (6 months 80%)
  3. Cirrhosis (20 years 10%)
  4. Decompensated and hepatoceullar carcinoma (5years 2-3%)

Much better outcomes then HBV!!


Treatment of acute viral hepatitis?

  • not required: doesn't make a difference
  • supportive care
  • fulminant case - transplant, not very common


Treatment of chronic hepatitis?

To prevent cirrhosis and cancer

to reduce transmission

HBV: suppression. antiviral drugs, but this doesn't cure but hugely reduces risk

HCV: cure

Vaccination prevents HAV


Prevention of HBV

involves breaking the cycle of vertical transmission

  • Vaccinate 'at risk' to prevent the vert transmission.
    • screen pregnant women
    • if positive for HBSAg, ig high give mum during pregnancy
    • then give HBV Ig at birth
    • start HBV vaccination at birth (4 doses total, normal kids get 3)
    • test after last vaccine to check anti-HBS is >100IU/ml
  • Normally vaccinate infants at 6wks, 3mnths, 5 mnths

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