viral hepatitis Flashcards Preview

Liver + GI > viral hepatitis > Flashcards

Flashcards in viral hepatitis Deck (22)
Loading flashcards...

Hep A aetiology + spread

HAV RNA virus picornavirus

F-O or shellfish


Hep A incubation

short incubation. acute, no chronic disease


Hep A - clinical presentation

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


Hep A - diagnostic test

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


Hep A treatment

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


Hep A prognosis

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

100% immunity after infection


Hep B aeitiology

HBV, a DNA virus

spread: BBB


Hep B serology

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


Hep B clinical presentation

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


Hep B treatment

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)


Hep B chronicity

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


Hep C aetiology and spread

RNA flavivirus. Genotypes 1-6

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


Hep C clinical presentation

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


Hep C diagnostic tests



Hep C natural history

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


Hep C SVR and treatment of chronic


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


Hep D aetiology

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


Hep D treatment

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


Hep E cause and spread

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

Spread: F-O transmission


Hep E epidemiology

Associated with pigs
more common in older men


Hep E natural history

(acute) self limiting usually
chronic in IS patients


Hep E treatment

Self limiting usually
Vaccine in China, not in Europe