viral hepatitis

Question 1

Hep A aetiology + spread

Answer 1

HAV RNA virus picornavirus

F-O or shellfish

Question 2

Hep A incubation

Answer 2

short incubation. acute, no chronic disease

Question 3

Hep A - clinical presentation

Answer 3

fever, malaise, anorexia, nausea, athralgia - then: jaundice, hepatosplenomegaly and adenopathy

Question 4

Hep A - diagnostic test

Answer 4

AST and ALT rise 22-40 days after exposure, returning to normal over 5-20 weeks

IgM rises from day 25 and means recent infection

IgG detectable

Question 5

Hep A treatment

Answer 5

supportive, monitor LF. Avoid alcohol. Rarely, interferon-a for fuliment hepatitis.

Question 6

Hep A prognosis

Answer 6

usually self-limiting (3-6 weeks).
F hep is rare.
Chronicity doesn’t occur

100% immunity after infection

Question 7

Hep B aeitiology

Answer 7

HBV, a DNA virus

spread: BBB

Question 8

Hep B serology

Answer 8

3 hep B antigens: envelope, core and surface (HBsAg, HBcAg, HBeAg

• HBsAg is present 1-6 months after exposure
• HBeAg 1.5-3 months after acute illness and implies high infectivity
• HBsAg persisting for >6 months defines carrier status + occurs in 5-10% of infections
• Antibodies to HBcAg imply past infection
• Antibodies to HBsAg alone imply vaccination

HBV PCR allows monitoring of response to therapy

Question 9

Hep B clinical presentation

Answer 9

Resemble hep A but arthralgia (pain in a joint) and urticaria (hives) are commoner

Question 10

Hep B treatment

Answer 10

Supportive, monitor LF
Avoid alcohol, immunize sexual contacts.
Anti-virals: e.g. tenofovir, entecavir
Aim: to clear HBsAg and prevent cirrhosis and HCC (risk is  if HBsAg and HBeAg +ve)

Question 11

Hep B chronicity

Answer 11

Majority of acute HBV infection → spontaneous resolution
5% → chronic (more common in immunocompromised) 2 options for treatment
1. PEG interferon alpha: immunomodulatory – stimulates immune response
- Not tolerated well: muscle ache, fever, lethargy
2. Nucleosite analogues: tenofevir, enteecavir: inhibit viral replication

Question 12

Hep C aetiology and spread

Answer 12

RNA flavivirus. Genotypes 1-6

Spread: blood bourne: transfusion (thousands of UK cases before 1990s, compensation available), IVDU, sexual, acupuncture,

Question 13

Hep C clinical presentation

Answer 13

Early infection is often mild/asymptomatic
~85% develop silent chronic infection
~25% get cirrhosis in 20yrs- of these ~4% get HCC. Chief reason for liver transplant in the West

RF for progression: male, older, higher viral load, use of alcohol, HIV, HBV

Question 14

Hep C diagnostic tests

Answer 14

LFT (AST:ALT

Question 15

Hep C natural history

Answer 15

30% spontaneous resolution. 70% →chronic hepatitis. (85% if have HIV).
Previous infection doesn’t = immunity

Question 16

Hep C SVR and treatment of chronic

SVR

Answer 16

SVR: sustained virological response varies between genotypes. SVR12/24 – undetected HVC RNA at 12 or 24 weeks after end of treatment.
Treatment: PEG-IFN + ribavirin + simeprivir
- PEG-IFN stimulates immune response
- Ribavirin is a HCV nucleoside inhibitor, stops viral RNA synthesis
- Simeprivir is a HCV protease inhibitor, preventing viral maturation through inhibiton of protein synthesis

Question 17

Hep D aetiology

Answer 17

Incomplete RNA virus (needs HBsAg for its assembely)
HBV vaccination prevents HDV
5% of HBV carriers have HDV co-infection

Spread: blood bourne, particularly IVDU

Question 18

Hep D treatment

Answer 18

Interferon-a has limited success (30%) → liver transplantation may be required

Question 19

Hep E cause and spread

Answer 19

Small RNA virus, similar to HAV
Genotype 3 in UK (eating sausages)

Spread: F-O transmission

Question 20

Hep E epidemiology

Answer 20

Associated with pigs

more common in older men

Question 21

Hep E natural history

Answer 21

(acute) self limiting usually

chronic in IS patients

Question 22

Hep E treatment

Answer 22

Self limiting usually

Vaccine in China, not in Europe