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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
what does HBeAg indicate
if **+ve = viral load is v high** Impossible to have +ve E and low viral load **active virus replication** **high infectivity**
26
what does presence of anti-HBc IgM show
*against core Ag* **acute infection** 1st 3mo of disease
27
what does presence of anti-HBc IgG indicate
shows exposure to virus - shows **have been exposed at some point** - can be **past or ongoing chronic** infection
28
what does anti-HBe indicate
immune control - shift to eAg negativity - inactive carrier state
29
what does anti-HBS show
**immunity** - vaccine/past infection surface Ag cleared
30
describe the change in Ag and Ab in change from acute HBV to chronic
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
describe the ag and Ab changes when HBV goes to recovery
**HBsAg goes to 0** - no longer infection **total anti-c ab and anti-s ab = +ve**
32
33
complications of HBV and ix
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
indications for HBV treatment
depends on: * viral load - **HB DNA** * ALT * severity of liver disease
35
what is the treatment for HBV
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
prevention of HBV
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
epidemiology of HCV
1% global prevalence in 2015
38
what type of virus is HCV
**ssRNA** 6 genotypes - 1 and 3 are most common cause of infection flaviviridae
39
transmission of HCV
blood products needles sharing banknotes to insufflate recreational drugs
40
incubation period for HCV
2wks - 6mo
41
acute HCV infection
mostly asx 20-40% will clear the infection 40-60% become chronic
42
chronic HCV infection
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
HCV serology
AntiHCV +ve **4 wks** after infection **HCV RNA if suspect acute infection**
44
treatment for HCV
**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
follow up for HCV
-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
prevention for HCV
no vaccine screen blood, organs and tissue products needle exchange programs
47
structure of Hep D and how it relates to virulence
By itself doesn’t replicate Only function if co-infection or super-infection Benign hep virus Hep B turns it destructive
48
course of Hep D infection
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
serology for HBV HDV co-infection
50
serology of chronic HBV and HDV
51
prevention of HDV
prevent HBV - vaccine, PEP educate patients with HBV - risk behaviours, parenteral and sexual
52
what type of virus is HEV
**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
incubation period for HEV
2-8 wks
54
infection with genotypes 1 adn 2 of HEV
3 million sx infections/yr brief self-limiting young adults - travel **30% mortality in pregnant women**
55
infection with genotypes 3 and 4 of HEV
>2 million infections/yr endemic in europe - France and Italy **asx 95%** **effects older males**
56
chronic HEV infection
only in **immunocomp** asx/mild mildly deranged LFTs even in asx - can lead to cirrhosis and death/transplant in some
57
serology of HEV
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
extrahepatic manifestations of HEV
59
HBV extrahepatic manifestation
polyarteritis nodosa
60
HCV extrahepatic manifestation
cryoglobulin anaemia
61
treatment of HEV
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
summary of viral hep
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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