Hepatology Flashcards

1
Q

Acute hepatitis definition

A

Inflammation of the liver with little or no fibrosis and little or no nodular regeneration. There may be minor distortion of lobular architecture.

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2
Q

Cirrhosis definition

A

Extensive fibrosis of the liver with nodular regeneration (and hence distortion of architecture).

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3
Q

Acute hepatitis causes

A

Infection - most commonly acute infectious hepatitis A; but also hepatitis B, C, and E; infectious mononucleosis; cytomegalovirus; yellow fever; and amoebic hepatitis.

Chemical poisons and drugs - carbon tetrachloride; vinyl chloride; ethylene glycol; ethanol; methanol; halothane (repeated exposure); isoniazid and rifampicin; paracetamol; methotrexate; chlorpromazine.

Pregnancy (rare).

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4
Q

Outcomes of acute hepatitis

A

If the patient recovers, this is usually complete.

Rarely, progressive necrosis may affect almost the entire liver (fulminant hepatic failure or acute massive necrosis) progressing to hepatic coma and death.

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5
Q

Hepatitis A transmission

A

Faecal-oral, by food products such as shellfish.

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6
Q

Hepatitis A clinical presentation

A

After an incubation period of 2-6 weeks there is a gradual onset of influenza-like illness with fever, malaise, anorexia, nausea, vomiting and upper abdominal discomfort associated with tender enlargement of the liver and, less commonly, the spleen.

After 3-4 days the urine becomes characteristically dark and the stools pale - evidence of cholestasis.

Symptoms usually become less severe as jaundice appears, although pruritis may develop.

Jaundice and symptoms tend to improve after 1-2 weeks and recovery is usually complete, although mild symptoms continue for 3-4 months in a few patients.

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7
Q

Hepatitis A investigation

A

Antihepatitis A virus IgM in serum

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8
Q

Hepatitis A differentials

A
Obstructive jaundice
Drug jaundice
Glandular fever
Yellow fever (travellers)
Acute alcoholic hepatitis
Wilson’s disease
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9
Q

Hepatitis A management

A

Symptomatic treatment
Corticosteroids if jaundice is prolonged by intrahepatic cholestasis
Liver transplant if fulminant hepatic failure develops (rare)

Prophylaxis - active immunisation with inactivated virus is recommended for travellers in endemic areas

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10
Q

Hepatitis B transmission

A

Blood and serum, saliva, semen and vaginal secretions.

Most frequently transmitted by sexual activity, shared needles used by drug addicts, and from mother to child.

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11
Q

Hepatitis B clinical features

A

After a long incubation period of 6 weeks to 6 months, there is typically a gradual onset of lethargy, anorexia, abdominal discomfort, jaundice and hepatomegaly.

Occasionally immune-mediated extrahepatic manifestations occur with polyarthritis, skin rashes and glomerulonephritis.

Cholestatic hepatitis is rare.

Mutated viral strains may be associated with fulminant hepatic failure.

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12
Q

Hepatitis B investigations

A

Surface antigen (HepBsAg) appears in the blood about 6 weeks after acute infection and has usually gone by 3 months. The development of antibodies to HepBsAg usually follows acute infection and indicates immunity; in about 5% of cases antibodies do not appear and HepBsAg persists in the blood (carrier state).

Core antigen (HepBcAg) is usually found only in the liver.

Internal component (HepBeAg) appears in the blood about 6 weeks after acute infection and denotes high infectivity.

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13
Q

Hepatitis D

A

An incomplete RNA virus that depends on hepatitis B virus to replicate. It can cause an aggressive chronic hepatitis in HepBsAg-positive patients. Chronic infection is usually associated with progressive liver disease.

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