Hepatitis A&E Flashcards
What is the definition of hepatitis A or E?
Hepatitis caused by infection with the RNA viruses, hepatitis A (HAV) or hepatitis E virus (HEV), that follow an acute course without progression to chronic carriage.
Describe the pathogenesis of Hepatitis A
HAV is most commonly spread via the faecal-oral route. May occur sporadically or in epidemics. There have been reports of parenteral transmission in injecting drug users and haemophiliacs.
Both viruses replicate in hepatocytes and are secreted into bile.
Liver inflammation and hepatocyte necrosis is caused by the immune response, with targeting of infected cells by CD8 + T cells and natural killer cells.
Histology shows inflammatory cell infiltration (neutrophils, macrophages, eosinophils and lymphocytes) of the portal tracts, zone 3 necrosis and bile duct proliferation.
The virus may be shed in large numbers in faeces for up to a month.
Describe the HAV and HEV viruses.
HAV is a picornavirus and HEV is a calicivirus. Both are small non-enveloped single-stranded linear RNA viruses of around 7500 nucleotides, with transmission by the faecal–oral route.
Describe the epidemiology of HAV
HAV is endemic in the developing world, infection often occurs sub- clinically.
In the developed world, better sanitation means that seroprevalence is lower.
age of exposure ⬆️ and hence is more likely to be symptomatic.
Annual UK incidence is 5000 cases (seroprevalence around 5%).
What would a patient with HAV complain of in their history?
•Incubation period
•Prodromal phase
•Hepatitis
Incubation period for HAV or HEV is 3–6 weeks.
Prodromal period:
Malaise, anorexia (distaste for cigarettes in smokers), fever, nausea and
vomiting.
Hepatitis:
Prodrome followed by dark urine, pale stools and jaundice lasting around 3 weeks.
Occasionally, itching and jaundice last several weeks in HAV infection (owing to cholestatic hepatitis).
What would be found on examination of a patient with HAV?
Pyrexia, jaundice, tender hepatomegaly, spleen may be palpable (20%).
Absence of stigmata of chronic liver disease, although a few spider naevi may appear, transiently.
What investigations would you perform on a patient with suspected HAV?
Blood:
LFT (⬆️⬆️ AST and ALT, ⬆️ bilirubin, ⬆️ AlkPhos),
⬆️ ESR.
In severe cases, ⬇️ albumin and ⬆️ platelets.
Viral serology:
•Hepatitis A:
—Anti-HAV IgM (during acute illness, disappearing after 3–5 months),
—anti-HAV IgG (recovery phase and lifelong persistence).
•Hepatitis B and C viral serology is also necessary to rule out these infections.
Urinalysis:
Positive for bilirubin,
⬆️ urobilinogen.
How would you manage a patient with HAV?
No specific management.
Bed rest and symptomatic treatment (e.g. antipyretics, antiemetics).
Colestyramine for severe pruritus.
Prevention and control:
•Public health:
—Safe water, sanitation, food hygiene standards.
—Both are notifiable diseases.
—Personal hygiene and sensible dietary precautions when travelling.
•Immunization (HAV only):
—Passive immunization with IM human immunoglobulin is only effective for a short period.
—Active immunization with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas,
—high-risk individuals (e.g. residents of institutions).
What complications are associated with HAV and HEV?
Fulminant hepatic failure develops in 0.1% cases of HAV, 1–2% of HEV but up to 20% in pregnant women.
Cholestatic hepatitis with prolonged jaundice and pruritus may develop after HAV infection.
Post-hepatitis syndrome:
Continued malaise for weeks to months.
What is the prognosis for a patient with HAV?
Recovery is usual within 3–6 weeks.
Occasionally, a relapse during recovery.
There are no chronic sequelae.
There is no chronic carrier state.
Fulminant hepatic failure carries an 80% mortality.
