viral hepatitis Flashcards

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1
Q

known hep viruses

A

A,B,C,D,E, G
only A-E known to cause clinical disease
only B, C, D cause chronic infections (>6 months)

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2
Q

which hep diseases cause chronic infection

A

B, C, D

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3
Q

which hep disease cause clinical disease

A

A-E

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4
Q

hepatitis E causes

A

can cause chronic infections in transplant recipients, or immunosuppressed

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5
Q

other viruses causes hepatitis disease

A

EBV, CMV, yellow fever virus

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6
Q

more common hep viruses in Australia

A

B and C

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7
Q

you can only have hep d if

A

you have chronic hep B

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8
Q

hepatitis A is found

A

found world wide

hyper endemic in developing countries

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9
Q

hap A spread by

A

faecal orla route

excretion for 1-2 weeks before illness to 1 week after ilness

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10
Q

risk groups for hep A

A

child day-care centres and pre schools
MSM
IVDU
residential facilities for the intellectually disabled
travellers to Asia, Africa, South Pacific, central and South America

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11
Q

serotypes of hep A

A

only one serotype
infection gives life long immunity
vaccine very effective and long lasting protection with 2 doses

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12
Q

diagnosis of hep A

A

detection of IgM for acute disease (lasts 6-9 months)
IgG for immunity after natural infection
PCR of blood and stool

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13
Q

hep E spread

A
  • under developed countries, spread by contaminated water

- developed countries, spread fro contaminated food (pork)

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14
Q

hep E illness

A

5% develop jaundice, especially older men in developed countries
extra hepatic manifestations (neurological)
mortality up to 20%

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15
Q

hep E vaccine

A

none

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16
Q

hep E diagnosis

A

serology or PCR

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17
Q

hep E chronic disease

A

occurs in immunosuppressed or organ tranplant recipients

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18
Q

Hep B found in

A

highest in underdeveloped people
maintained through vertical transmission
especially in Asia
majority now have universal childhood vaccination campaigns

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19
Q

hep B in western countries

A
  • sexual transmission

- Australian cases usually from countries where it is endemic

20
Q

hep B clinical presentation

A

15-25% will die from cirrhosis for hepatocellular cancer if not given appropriate treatment
children show no symptoms and will be lifelong carriers

21
Q

outcomes of hep B transmission

A
  • no or moderate fibrosis with minimal risk of complications - can still develop hepatocellular carcinoma
  • develop cirrhosis - more common if high HBV viral load, HBeAg +ve, raised ALT, older, other liver toxins eg. alcohol
  • develop hepatocellular carcinoma, more common is cirrhotic, family history, ethnicity, male
22
Q

immune tolerance stage

A

high levels of viral load but immune system not reposting
HBeAg positive which is a reflection of high viral load
liver function tests normal

23
Q

immune clearance stage

A

abnormal LFTs
viral load reduces
at risk of progression to cirrhosis and hepatocellular carcinoma - should be referred for treatment

24
Q

immune control stage

A

normal LFTs
low viral load
HBeAg neg, HBeAb pos
may maintain this stage for the rest of life
low risk for chronic liver disease due to low viral load

25
Q

immune escape stage

A

virus changes such that it can escape immune control
high viral load, abnormal LFTs
at risk of progression to cirrhosis and hepatocellular carcinoma
e antibody positive but still high viral load

26
Q

antivirals for hep B

A

DNA virus goes to the nucleus and reproduces itself and produces an RNA copy
can do reverse transcriptase
takes RNA and turns it back to DNA to be packaged and excreted
antivirals act on reverse transcriptase - can’t produce genome so the virus can’t replicate

27
Q

antivirals examples

A

entecavir and tenofavir

28
Q

indications for antivirals in Hep B

A
  • immune clearance and immune escape phases - immune active
  • cirrhotics
  • pregnancy
  • immunosuppression
29
Q

HBV and pregnancy

A

HBeAg positive mothers - transmission 90% without prophylaxis
HBIG + vaccine at birth reduces risk of vertical transmission 90%
tenofovir in third trimester to reduce viral load

30
Q

cirrhosis

A

HCC in HBV can occur without cirrhosis but Is more likely in cirrhosis

31
Q

cirrhosis screening

A

ultrasound of the liver every 6 months for all hep B cases that are cirrhotic to intervene early If there is cancer

32
Q

staging

A

cirrhosis and fibrosis staging

checking renal function and coagulopathy

33
Q

HBV vaccine

A

universal for infants since 2000
subunit vaccine
immunity indicated if level HBsAb level >10

34
Q

hep D

A

deltavirus, defectieve satellite RNA virus

uses HBsAg coat (doesn’t have its own coat - borrows from hep B which is why Hep B coinfected needed)

35
Q

hep D causes

A

acute or persistent infection in HBsAg infected

36
Q

hep D diagnosis

A

screen with anti-HDV serology and confirm active infection with HDV viral load

37
Q

hep D vaccine

A

no vaccine

interferon therapy for 1-2 year with low response rate

38
Q

hepatitis C

A
lipid coated RNA virus 
no reverse transcriptase 
unstable genome 
- immune escape for chronic infection 
- antiviral resistance mutations
39
Q

hep C found

A

around the world
foci in underdeveloped countries
steady increase in australia with intravenous drug users

40
Q

transmission risks of hep C

A

parenteral (blood exposure)
- developed countries - IVDU, tattoos, transfusion
- developing countries - medical practises and traditional practises
vertical
sexual - low risk but increased with genital ulceration, higher risk with anal intercourse

41
Q

sexual transmission of hep C

A

low risk but increases with genital ulceration of anal intercourse

42
Q

serology for hep C

A

HCV total antibody
HCV antigen - not used in aus
no rapid point of care tests

43
Q

molecular diagnosis of hep C

A

qualitative PCR
viral load, genotyping
directly acting antiviral resistance mutation testing for those who have failed direct acting antivirals

44
Q

DAA

A

direct acting antivirals
current ones used in australia are pan-genotypic
epclusa, maviret, vosevi (escape treatment)

45
Q

HCV treatment

A
treatments have drug interactions 
some can't be used in renal impairment 
can cause reactivation in HBV/HCV confection 
can't be used in pregnancy 
treatment success in 90-95%