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PATHOLOGY > Viral hepatitis > Flashcards

Viral hepatitis Flashcards

1
Q

what is hepatitis

A

inflammation of the liver

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2
Q

causes of hepatitis

A

ischemic

autoimmune

toxic
* alcohol
* drugs

metabolic

infections :

virus
* primary hepatotropic
* secondary hepatotropic

bacteria
* sepsis
* leptospirosis
* syphilis

parasites
* amoeba
* fasciola
* opisthorchis
* toxoplasma

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3
Q

primary hepatotropic causes of viral hepatitis

A

Hep A B C D E

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4
Q

Secondary hepatotropic causes of hepatitis

A

EBV
cytomegalovirus (CMV)
HIV
adeboviru s
parvovirus B19
rubella
coxsackievirus B
enteroviruses
ebola/marburg/lassa
yellow fever virus

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5
Q

epidemiology of Hep A

A

disease of developing world

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6
Q

what type of virus is Hep A

A

single stranded RNA

family - picornaviridae

genus - hepatoviridae

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7
Q

transmission of HAV

A

faeco-oral

particles in faeces then person to person

contaminated food/drink

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8
Q

incubation period of HAV

A

2-6wks

usually 28-30 days (1mo)

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9
Q

sx of acute hepatitis

A

non specific sx:
* fever
* malaise
* fatigue
* loss of appetite
* abdo pain - RUQ from liver distension

sx due to high BR
* jaundice
* dark urine
* pale, grey, or white stool
* puritis

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10
Q

lab findings for HAV

A

acute infection = anti-HAV IgM
(can be -ve in 1st wk of sx)

HAV RNA PCR for confirmation of acute cases

immunity (prev infection/vaccine) - anti-HAV IgG (or total HAV Ab)

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11
Q

when should you test for HAV IgM

A

when ALT >500

Impossible to have acute hep A when ALT not 500
Wont get IgE if in phase where ALT has not risen yet - false -ve

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12
Q

when is HAV infectious

A

2wk before sx ->
1 wk after jaundice

stay off work 7days after sx onset

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13
Q

is HAV notifyable disease

A

Yes

suspected and confirmed should be reported to UKHSA

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14
Q

px of HAV

A

Chance of fulminent hep and dying increase with age

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15
Q

is there a HAV vaccine

A

Yes

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16
Q

when should you vaccinate for HAV

A

travel to endemic

chronic liver disease

chronic HBV HCV

haemophilia

IVDU

MSM

occupational risk - lab, residential fascilities, sewage work

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17
Q

epidemiology of HBV

A

250 million carriers of HBsAg

increasing prevalence in some european countries - migration from high endemic countries

reducing prevalence in endemic countries (eg Taiwan)
* improved socioeconomic status
* vaccination
* effective treatment

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18
Q

what type of virus is HBV

A

DNA

family - hepadnaviridae

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19
Q

transmission of HBV

A

sexual

parenteral

vertical

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20
Q

incubation period for HBV

A

2-6mo

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21
Q

features of acute HBV infection

A

less than 5yrs old:
* asx
* 90% get chronic

adults:
* 40% sx
* 10% get chronic (surface ag for 6mo - most asx)
* 0.5-1% get cirrhosis, end stage liver disease, extraheptaic menifestation, hepatocellular ca

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22
Q

what constitutes chronic HBV

A

+ve HBsAg >6mo

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23
Q

structure of Hep B virus

A
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24
Q

what does HBsAg say

A

If +ve = active hep B
ie current infection

If -ve = not active

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25
Q

what does HBeAg indicate

A

if +ve = viral load is v high
Impossible to have +ve E and low viral load

active virus replication

high infectivity

26
Q

what does presence of anti-HBc IgM show

A

against core Ag

acute infection
1st 3mo of disease

27
Q

what does presence of anti-HBc IgG indicate

A

shows exposure to virus - shows have been exposed at some point -

can be past or ongoing chronic infection

28
Q

what does anti-HBe indicate

A

immune control - shift to eAg negativity - inactive carrier state

29
Q

what does anti-HBS show

A

immunity - vaccine/past infection

surface Ag cleared

30
Q

describe the change in Ag and Ab in change from acute HBV to chronic

A

e Ag takes longer to clear and may never be cleared

s Ag stay +ve

never rise in HBs Ab

IgM anti-core will clear
total anti-core will stay +ve

31
Q

describe the ag and Ab changes when HBV goes to recovery

A

HBsAg goes to 0 - no longer infection

total anti-c ab and anti-s ab = +ve

32
Q
A
note core IgG +ve in acute because report for IgG includes IgM - ie it is total Ig against core
33
Q

complications of HBV and ix

A

cirrhosis
* clinical - Child-Pugh score
* radiological - course echotexture, nodularity, portal HTN - splenomegaly
* transient elastography (USS - shows how much fibrosis) - >12.5 kPa
* histopath - gold standard - rarely done

hepatocellular ca
* Alpha-fetoprotein

need 6monthly USS

34
Q

indications for HBV treatment

A

depends on:

  • viral load - HB DNA
  • ALT
  • severity of liver disease
35
Q

what is the treatment for HBV

A

pegylated IFN-a
* strategy - induce long term immune control: eAg, sAg loss - eliminate virus
* SC for 48wks
* low tolerability -> flu like sx
* lots of CIs

nucleos(t)ide analogues
* inhibit viral replication by inhibiting viral DNA polymerase
* entecavir, tenofovir, lamivudine, adefovir
* long term oral - until HBsAg loss

36
Q

prevention of HBV

A

vaccination
* routine at 2, 3 and 4 mo

screening in pregnancy
* HBsAg +ve, HBeAg -ve = vaccine at birth + routine schedule
* HBsAg +ve, eAg +ve = vaccine at birth and HBIG within 48hrs

blood screening - donors

37
Q

epidemiology of HCV

A

1% global prevalence in 2015

38
Q

what type of virus is HCV

A

ssRNA

6 genotypes - 1 and 3 are most common cause of infection

flaviviridae

39
Q

transmission of HCV

A

blood products

needles

sharing banknotes to insufflate recreational drugs

40
Q

incubation period for HCV

A

2wks - 6mo

41
Q

acute HCV infection

A

mostly asx

20-40% will clear the infection

40-60% become chronic

42
Q

chronic HCV infection

A

incidental finding after ix for high ALT

chronic liver disease/cirrhosis
hepatocellular ca

Co-infection with HIV or hep B increases risk of complications

USS and AFP monitored

43
Q

HCV serology

A

AntiHCV +ve 4 wks after infection

HCV RNA if suspect acute infection

44
Q

treatment for HCV

A

curable

direct acting antivirals - good results
* bocepravir
* daclatasvir
* sofobuvir

12wk course, daily PO

People have chaotic lifestyle - find it hard to take - don’t want to prescribe if people wont take because resistance

45
Q

follow up for HCV

A

-ve RNA = no hep C ->

cleared disease so don’t need follow up.

And clear fibroscan = no damage to liver = don’t need USS or cancer screening

46
Q

prevention for HCV

A

no vaccine

screen blood, organs and tissue products

needle exchange programs

47
Q

structure of Hep D and how it relates to virulence

A

By itself doesn’t replicate
Only function if co-infection or super-infection

Benign hep virus
Hep B turns it destructive

48
Q

course of Hep D infection

A

Co infection
* severe acute disease but low risk of chronic - because:
* Eliminate b and d virus

If chronic hep b and have d exposure
* Get chronic d
* High risk of severe liver disease

49
Q

serology for HBV HDV co-infection

A
50
Q

serology of chronic HBV and HDV

A
51
Q

prevention of HDV

A

prevent HBV - vaccine, PEP

educate patients with HBV - risk behaviours, parenteral and sexual

52
Q

what type of virus is HEV

A

RNA

hepeviridae

4 genotypes infect human:

  • GT 1 and 2 - natural host = human, faeco-oral
  • GT 3 and 4 - natural host = pig/boar, zoonotic transmission - undercooked meat, organ transplant, blood transfusion
53
Q

incubation period for HEV

A

2-8 wks

54
Q

infection with genotypes 1 adn 2 of HEV

A

3 million sx infections/yr

brief
self-limiting

young adults - travel

30% mortality in pregnant women

55
Q

infection with genotypes 3 and 4 of HEV

A

> 2 million infections/yr

endemic in europe - France and Italy

asx 95%

effects older males

56
Q

chronic HEV infection

A

only in immunocomp

asx/mild

mildly deranged LFTs

even in asx - can lead to cirrhosis and death/transplant in some

57
Q

serology of HEV

A

IgG and IgM - bad assays, don’t rely on them

HEV RNA only in specific reference labs - used for screening of donors for haematological malignancies

immunocomp HEV RNA

chronic infection = HEV +ve >3mo

58
Q

extrahepatic manifestations of HEV

A
59
Q

HBV extrahepatic manifestation

A

polyarteritis nodosa

60
Q

HCV extrahepatic manifestation

A

cryoglobulin anaemia

61
Q

treatment of HEV

A

supportive

acute, severe - consider ribavirin

chronic - 3 mo of treatment in immunocomp

  • vaccination - only lisenced in China
  • screen blood products
  • avoid undercooked meat - pork, wild boar, venison
62
Q

summary of viral hep

A

Non-envolved (a and e ) - foecal oral

Envoloped - allow them to have parental transmission
Disintegrate in env because lipid layer not reliable

PATHOLOGY (94 decks)

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