Viral Hepatitis Flashcards

1
Q

Where is HAV worst?

A

S America
Africa
Asia
Greenland

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2
Q

What type of Hepatitis is HAV?

A

Acute hepatitis IP 2-6 weeks
Often subclinical
Faecal-oral spread
Notifiable

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3
Q

How do the immunoglobulins change in HAV?

A

IgM rises first
IgG rises after
ALT spikes with IgM
HAV in stool just before and during infection

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4
Q

What is the molecular organisation of HBV?

A
  • The family Hepadnaviridae
  • Double-strained DNA with reverse transcriptase
  • Enveloped virions
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5
Q

Where are the clades endemic for HBV?

A

10 genotypes (A-J) with distinctive geographic distribution

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6
Q

How is HBV spread?

A
  • Sexual
  • Vertical
  • Blood products
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7
Q

What kind of infection is HBV?

A
  • ACUTE and CHRONIC
  • Chronic = 6 months or more
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8
Q

How does HBV antigens change over time?

A
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9
Q

What are the disease stages of HBV?

A
  • Immune tolerant
  • Immune reactive
  • Inactive HBV carrier state
  • HBeAg negative chronic HBV
  • HBsAg negative phase
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10
Q

When might HBV cause cirrhosis?

A

When baseline HBV DNA is >10^6

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11
Q

What is the treatment of chronic HBV?

A
  • Interferon alpha
  • Lamivudine
  • Adefovir
  • Tenofovir
  • Entecavir
  • Emtricitabine
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12
Q

Where is HCV highest?

A

Parts of SA, Africa, Asia

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13
Q

What is Hep C?

A
  • Flaviviridae
  • Mainly blood product spread
  • 60-80% chronicity
  • Natural history
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14
Q

What enzymes does HCV use?

A

NS3/4 serine protease, RNA helicase

NS5A

NS5B RNA dependent RNA polymerase

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15
Q

What type of infection is HCV?

A

Acute 20-40%

Chronic 60-80%

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16
Q

Antibodies/ ALT in HCV?

A

ALT spikes and then anti HCV

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17
Q

How do you treat acute HCV?

A

Peginterferon alfa

Protease inhibitors:

telaprevir

boceprevir

simeprevir

asunaprevir

paritaprevir (ABT-450/r)

grazoprevir (MK5172)

vaniprevir

faldaprevir

deleoprevir

ledipasvir

daclatasvir

ombitasvir (ABT- 267)

elbasvir (MK-8742)

sofosbuvir

dasabuvir (ABT-333)

beclabuvir (BMS- 791325)

ABT-072

deleobuvir

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18
Q

Where to the DAAV act?

A
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19
Q

Where is HDV high?

A

Some parts of SA and Africa

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20
Q

What is the serological course for HDV superinfection?

A
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21
Q
A
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22
Q

What is the serological course for HDV superinfection?

A
23
Q

Where is HEV worst?

A

Africa and Asia

24
Q

What is the most common acute hepatitis?

A

HEV

25
Q

What are the genotypes of HEV?

A

Genotype 1 and 2 – human, epidemic

Genotype 3 and 4 – swine and other

(humans accidental host = zoonosis)

Very little person to person spread

Case reports

Shellfish consumption, blood transfusion

Sausages, pig liver consumption

26
Q

How do you treat HEV?

A

supportive ? ribavirin

27
Q

What are the complications of HEV?

A

Incubation period 3-8 weeks

High mortality rate in pregnancy ( genotype 1)

RARE COMPLICATIONS

CNS disease – Bell’s palsy, Guillain Barre, other neuropathy

Chronic infection

28
Q

Is there a Vx for HEV?

A

VACCINE – EFFECTIVE - trials with recombinant HEVg1

In Nepalese military and Chinese (100 000)

29
Q

What is the serology of HEV?

A
30
Q
A
31
Q

What is the epidemiology of Hepatitis A?

A
  • Approx. 1.5 millions of cases worldwide annually
  • Developing countries with poor socio-economic conditions
  • 300-500 cases annually in the UK
  • Mostly among age 15-34 and non-travellers
  • Outbreaks among MSM (2016/17) & IVDU (2001 & 2017)
32
Q

What are the clinical manifestations of hepatitis A?

A
  • Wide disease spectrum from asymptomatic to fulminant hepatitis
  • Strong correlation with age: <10% symptomatic among children <6 years old versus 70% in adults
  • Typical symptoms: fever, malaise, anorexia/nausea, abdominal discomfort, diarrhoea, jaundice
  • Extra-hepatic diseases
  • Acute presentation; 99% resolution
  • NOT an aetiology for chronic hepatitis
33
Q

What is the diagnosis and treatment of HAV?

A

•Diagnostics based on HAV serology

ØAcute infection: IgM reactive; unlikely if bilirubin level < 30umol/L

ØPast infection: IgM non-reactive, IgG reactive

•Supportive treatment

34
Q

How do we alert public health for HAV?

A

•Notifiable disease in the UK – must alert HPT immediately upon diagnosis

  • Infectious period of index case: two weeks before onset of first symptoms and until one week after the onset of jaundice
  • Pre-exposure immunisation among population at risk
  • Post-exposure prophylaxis

ØWithin 14 days of exposure to index case: HAV vaccine +/- HNIG (for 60 years and above, chronic liver diseases inc CHB/CHC, immunocompromised contact)

ØOver 14 days: HAV vaccine +/- HNIG (for chronic liver diseases inc CHB/CHC, immunocompromised contact)

35
Q

What are the clinical manifestations of acute hepatitis?

A

•Age related presentation & prognosis in acute hepatitis B

ØNeonates & children: mostly asymptomatic or anicteric; 90% HBV-infected neonates develop CHB, and 30% among children age <5 years

ØAdult: 30-50% icteric hepatitis; 10% become CHB

  • 0.1-0.05% risk of fulminant hepatitis; related to co-infection with HCV/HDV
  • Maternal HBeAg/Ab status & HBV viral load

ØHBeAg as the most important risk predictor for vertical transmission

36
Q

What are the clinical manifestations of chronic hepatitis B?

A
  • Definition: persistence of HBsAg for 6 months or more after acute HBV infection
  • Complications

ØCirrhosis: 8-20% untreated CHB in 5 years;

ØHepatocellular carcinoma: the annual risk of 2-5% among CHB cirrhotic patients; affected by host (e.g. alcohol abuse) and viral factors (e.g. high HBV viral load & qHBsAg)

37
Q
A
38
Q

What is the epidemiology of hepatitis B?

A

Approximately 296 million people are living with CHB worldwide; CHB-related mortality at roughly 820,000 people per year

39
Q

How do you interpret HBV serology?

A
  • HBsAg: infection
  • HBsAb: immunity through either immunisation or past infection
  • HBcAb: exposure

ØIgM: acute infection

  • HbeAg: replication activity
  • HBeAB
40
Q
A
41
Q

What is the prevention/public health for HBV?

A
  • Acute hepatitis B: a notifiable disease
  • Pre-exposure prophylaxis

ØRoutine childhood immunisation in the UK since 2017

ØHigh risk population

•Post-exposure prophylaxis

ØNeonate born to mother living with hepatitis B

ØSexual partner: HBV vaccine +/- HBIG (within one week from the contact)

ØNeedle stick injury

42
Q

What is HDV?

A
  • Single-stranded, circular RNA genome
  • A defective virus that relies on HBV for propagation
  • Blood-borne transmission
  • Incubation period: 3-6 weeks
43
Q

What is the HBV/ HDV co-infection?

A

•HBV/HDV simultaneous co-infection

ØSimilar to classic acute hepatitis B; mostly self-limited

Ø<5% chronic infection

•HDV super-infection in CHB

Ø80% chronic infection

ØIncreased risk of cirrhosis and HCC than CHB alone

44
Q

What is the diagnosis/ treatment/ prevention of HDV?

A
  • Anti-HDV serology; other HDV investigations rarely used
  • PEG-interferon alpha licensed for HDV superinfection in CHB
  • Pre-exposure HBV immunisation
  • Acute HDV infection: notifiable disease
45
Q

What is Hep C?

A
  • The family Flaviviridae, genus Hepacivirus
  • Single-stranded, positive sense RNA genome
  • Blood borne transmission
  • Incubation period: 2-6 weeks
  • 58 million people living with chronic hepatitis C worldwide
  • 1.5 million new cases every year
46
Q

What is the clinical manifestations of Hep C?

A

•Acute infection

Ø30% spontaneous clearance

Ø70% become chronic hepatitis C (CHC)

  • Hepatic versus extra-hepatic manifestation
  • Cirrhosis (15-30% in 20 years) & HCC as complication of CHC
47
Q

What is the antibodies for HCV?

A
48
Q

What is the treatment of HCV?

A
  • Revolutionised the treatment for acute/chronic HCV infection
  • Any HCV cases should be considered
  • 8 or 12 weeks
  • Sustained virological response (SVR) at week 12
  • Pan-genotypic regimen
  • Single-tablet regimen
  • Drug-drug interaction
49
Q

What is the prevention/ public health of Hep C?

A
  • Acute hepatitis C: notifiable disease in the UK
  • Nil vaccine available
  • Nil post-prophylaxis available
  • Active HCV screening
  • Risk reduction (e.g. safe handling and disposal of sharps, protected sex)
50
Q

What is HEV?

A

•The family Hepeviridae, genus Orthohepevirus; species A strains (8 genotypoes) infect humans

ØG1 & G2: obligate human pathogens

ØG3 & G4: zoonotic; pigs & wild boar are natural hosts

  • Single-stranded, positive sense RNA genome
  • Quasi-enveloped HEV
  • Faeco-oral versus blood-borne transmission
  • Incubation period: 15-60 days
  • Approximately 20 million new HEV cases worldwide annually
  • 3.3m symptomatic hepatitis E
  • 44,000 mortality annually
  • UK is a HEV G3 endemic country
51
Q

What are the clinical manifestations of Hep E?

A
  • Mostly self-limited; advised against alcohol during the course
  • At risk population

ØPregnant women: G1; fulminant hepatic failure and obstetric complications (e.g. eclampsia and haemorrhage); 25% maternal mortality & high perinatal infant mortality

ØChronic liver disease patients

ØImmunocompromised patients: may develop chronic hepatitis E (G3 & G4)

•Hepatic versus extra-hepatic manifestations

52
Q

How do you diagnose HEV?

A
  • Immunocompetent: HEV serology
  • Immunocompromised: HEV PCR
53
Q

What is the treatment and prevention of HEV?

A
  • Only indicated in chronic hepatitis E as most acute HEV infection are self-limited
  • Acute HEV infection: a notifiable disease
  • HEV patient should avoid prepping food during the first 2 weeks
  • Immunocompromised and chronic liver disease patients should avoid consumption of undercooked meat (pork, wild boar and venison) and shellfish

ØHEV vaccination: only licensed in China