5 - Liver disease and Hep B Flashcards
Structure of the hepatitis B virus
Double stranded DNA virus
Epidemiology of hep B
most common cause of hepatitis
350million worldwide affected
HbeAg antigen
Secreted by infected cells (marker for active infection)
HBsAg antigen
First marker to appear and causes the production of anti-HBs
HbsAg 1-6months
Acute disease
HbeAg 1-3 months
Results from breakdown of infected liver cells
Marker for infectivity
Anti-HBc
Core antibody
implies previous or current infection
o IgM anti-HBc appears during acute or recent infection (6 months)
o IgG anti-HBc persists for life
Anti-Hbs (surface antibody) implies
Immunity
due to exposure or immunisation
negative in chronic disease as no immunity in this case
Transmission of hep b
Sexual intercourse
Blood
Bites from an infected person
Vertical - mother to infant
Clinical presentation of hep b
Acutely presents as flu-like Anorexia, loss of appetite Nausea RUQ pain Fever Malaise Jaundice
Signs of decompensated liver disease
Ascites
Encephalopathy
GI bleeding (varices)
Chronic hep B
> 6 months
if inactive - no significant harm
Carriers present with nausea, fatigue, RUQ pain
May progress to liver fibrosis, cirrhosis and HCC
Acute hep b symptoms
weight loss anorexia Nausea fatigue muscle or joint pain
Chronic hep b symptoms
Weight loss, anorexia, fatigue, bleeding easily, dark coloured urine, itchy skin, confusion, drowsiness, ascites, oedema, jaundice, spider naevi, hepatosplenomegaly.
Hep b specific investigations
HBsAg, HBeAg, anti-HBe, anti-HBs, anti-HB core
HBV genotype
HBV DNA quantification
Quantitative HCV RNA polymerase chain reaction (1 or 2 weeks post infection)
HCV antibody enzyme immunoassay (ELISA)