Hepititis B Flashcards
Describe the pathogenesis of HBV.
Transmission is by sexual contact, blood and vertical transmission.
Antibody and cell-mediated immune responses to viral replication lead to liver inflammation and hepatocyte necrosis.
Histology can be variable, from mild to severe inflammation and changes of cirrhosis.
Describe the Hepatitis B Virus
HBV is an enveloped, partially double-stranded DNA virus. It can occur in the body in three forms.
The Dane particle is the complete virus and consists of a 42nm particle with a 27nm diameter core. Core contains HBV DNA polymerase in an outer coat.
HBV core antigen is formed of core protein containing incompletely double stranded circular DNA and the DNA polymerase/reverse transcriptase.
Various viral proteins are produced, including core antigen (HBcAg), surface antigen (HBsAg) and e antigen (HBeAg).
HBeAg is a marker of ⬆️ infectivity.
List the risk factors associated with contracting HBV.
Hepatitis B infection is associated with: •IV drug abuse, •unscreened blood and blood products, •infants of HbeAg-positive mothers •sexual contact with HBV carriers.
Risk of persistant HBV infection varies with age, with younger individuals, especially babies, more likely to develop chronic carriage.
Genetic factors are associated with ⬆️ rates of viral clearance.
Describe the epidemiology of Hepatitis B
Common.
350 million worldwide infected with HBV;
1–2 million deaths annually.
Common in Southeast Asia, Africa and Mediterranean countries.
HBV is relatively uncommon in the UK.
What would a patient presenting with HBV complain of in their history?
Incubation period 3–6 months;
1- to 2-week prodrome
malaise, headache, anorexia, nausea, vomiting, diarrhoea and RUQ pain.
May experience serum-sickness-type illness (e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash).
Jaundice then develops with dark urine and pale stools.
Recovery is usual within 4–8 weeks.
One per cent may develop fulminant liver failure.
Chronic carriage may be diagnosed after routine LFT testing or if cirrhosis or decompensation develops.
What would you find on examination of a patient with HBV?
•Acute
•Chronic
Acute:
•Jaundice, pyrexia, tender hepatomegaly, splenomegaly and cervical lymphadenopathy in 10–20%.
•Occasionally, urticaria/maculopapular rash.
Chronic:
•May have no findings;
•signs of chronic liver disease or decompensation.
What investigations would you perform in a patient with suspected HBV?
Viral serology: •Acute HBV: —HbsAg positive, —IgM anti-HbcAg. •Chronic HBV: —HbsAg positive, —IgG anti-HBcAg, —HbeAg positive or negative (latter in precore mutant variant). •HBV cleared or immunity: —Anti-HBsAg positive, —IgG anti-HBcAg.
PCR:
•For detection of HBV DNA is the most sensitive measure of ongoing viral replication.
LFT: ⬆️⬆️ AST and ALT. ⬆️ Bilirubin. ⬆️ AlkPhos.
Clotting:
⬆️ PT in severe disease.
Liver biopsy:
Percutaneous, or transjugular if clotting is deranged or ascites is present.
How would you manage a patient with hepatitis B?
Prevention: Blood screening, Immunisation of susceptible individuals, instrument sterilization, safe sex practices.
Passive immunization:
Hepatitis B immunoglobulin (HBIG) following acute exposure and to neonates born to HbeAg-positive mothers (in addition to active immunization).
Active immunization:
Recombinant HbsAg vaccine for individuals at risk and neonates born to HBV-positive mothers.
—Immunization against HBV protects against HDV.
Acute HBV hepatitis:
•Symptomatic treatment with bed rest, antiemetics, antipyretics and cholestyramine for pruritus.
•Notification to the consultant in communicable disease control.
Chronic HBV:
•Indications for treatment with antivirals:
—HbeAg-positive or HbeAg-negative chronic hepatitis (depending on ALT and HBV DNA levels),
—compensated cirrhosis and HBV DNA >2,000 IU/mL,
—decompensated cirrhosis and detectable HBV DNA by PCR.
Patients may be treated with interferon alpha (standard or pegylated, which has ⬆️ half-life), or nucleos/tide analogues (adefovir, entecavir, telbivudine, tenofovir, lamivudine).
—The role of lamivudine as primary therapy has diminished due to high rates of drug resistance.
—Interferon alpha is a cytokine which augments natural antiviral mechanisms.
Side-effects include flu-like symptoms, fever, chills, myalgia, headaches, bone marrow suppression and depression, necessitating discontinuation in 5–10% of patients.
What possible complications are associated with Hepatitis B?
- Fulminant hepatic failure (1%),
- chronic HBV infection (around 10% adults, much higher in neonates),
- cirrhosis and hepatocellular carcinoma,
- extrahepatic immune complex disorders including glomerulonephritis,
- polyarteritis nodosa.
Superinfection with HDV may lead to acute liver failure or more rapidly progressive disease.
What is the prognosis for patients with HBV?
In adults, 10% infections become chronic, and of these, 20–30% will develop cirrhosis.
Factors predictive of a good response to interferon include high serum transaminases, low HBV DNA, active histological changes and the absence of complicating diseases.
Define hepatitis B.
Hepatitis caused by infection with hepatitis B virus (HBV), which may follow an acute or chronic (defined as viraemia and hepatic inflammation continuing >6 months) course.
