Patient with Jaundice: Viral Hepatitis Flashcards Preview

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Flashcards in Patient with Jaundice: Viral Hepatitis Deck (25):
1

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)

2

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. 

3

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

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

4

Viral Hepatitis can be from....

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

5

Describe the hepatitis viruses

The viruses themselves are unrelated.

HAV, HBV and HCV

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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6

HDV requires??

HBV in order to infect.

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

7

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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8

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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9

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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10

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

11

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

12

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.

13

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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14

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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15

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

16

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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17

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

18

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

19

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

20

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21

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)

22

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!!

23

Treatment of acute viral hepatitis?

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

24

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

25

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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