Acute hepatitis Flashcards

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1
Q

Causes of acute hepatitis

A
  • Alcoholic hepatitis
  • Viral hepatitis (Hepatitis A-E, CMV, EBV)
  • Drug-induced hepatitis
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2
Q

Definition of alcoholic hepatitis

A

Inflammation of the liver due to significant alcohol consumption. This represents an early stage in alcoholic liver disease, commonly associated with fatty deposition in the liver (steatosis).

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3
Q

Clinical features of alcoholic hepatitis

A
  • Patients usually present feeling generally unwell, occasionally with a fever and jaundice
  • They may also have hepatomegaly due to steatosis
  • Hepatic encephalopathy may also be present
  • A high MCV and GGT often reflects excess alcohol intake
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4
Q

Management of alcoholic hepatitis

A
  • Alcohol cessation in the first instance with withdrawal prevention
  • Vitamin B1 replacement - Pabrinex IV then oral thiamine to prevent progression to Wernike encephalopathy
  • Nutritional supplementation
  • Assess severity using Maddrey score (discriminate factor) and offer corticosteroid to patients with DF >32
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5
Q

Effects of alcohol excess on various body systems

A

Liver

  • Alcoholic hepatitis
  • Alcoholic liver disease
  • Cirrhosis

GI

  • Oesophagitis
  • Gastritis
  • Pancreatitis
  • Cancer

CVS

  • Cardiomyopathy
  • Arrhythmias

CNS

  • Brain damage
  • Wernike encephalopathy
  • Korsakoff syndrome
  • Alcohol related seizures
  • Peripheral neuropathy

Haem

  • Megaloblastic anaemia
  • Folate deficiency
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6
Q

Alcohol withdrawal

What is it?

How long does it take for symptoms to appear?

What are the symptoms?

A

Alcohol withdrawal is a syndrome that occurs following an abrupt cessation of alcohol intake.

Withdrawal symptoms usually appear 4-12 hours post-consumption.

Coarse tremors, tachycardia, hypotension, confusion, occasional hallucinations and seizures.

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7
Q

Treatment of alcohol withdrawal

A

Benzodiazepines, dose and frequency are guided by the CIWA protocol

Patients should also be given IV thiamine replacement to prevent progression to Wernicke encephalopathy.

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8
Q

What is Wernicke encephalopathy?

What are the symptoms of Wernicke encephalopathy?

A

Wernicke encephalopathy refers to a neuropsychiatric emergency resulting from long-standing thiamine (B1) deficiency.

Usually presents with the triad of confusion, ataxia and ophthalmoplegia (nystagmus, lateral rectum palsy).

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9
Q

Treatment of Wernicke’s encephalopathy

A

IV thiamine replacement is effective if treated early, with improvement seen in 24-48 hours.

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10
Q

What is Korsakoff psychosis?

What are the symptoms?

How is it treated?

A

Korsakoff psychosis should be considered a continuum of Wernike encephalopathy at the later stages if not treated adequately.

The condition is characterised by anterograde and retrograde amnesia as well as confabulation.

Treated with IV thiamine should be given however, in most cases, the memory impairment is irreversible.

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11
Q

Which virus is the most common cause of viral hepatitis?

A

Hepatitis B (HBV)

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12
Q

What would positive HBsAg (hepatitis B surface antigen) serology indicate?

A

Active infection

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13
Q

What would positive HBeAg (hepatitis B e antigen) serology indicate?

A

E antigen is released during viral replication

Positive serology indicates acute phase of infection where virus is replicating quickly

The level correlates with infectivity

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14
Q

What would positive HBsAb (hepatitis B surface antibody) serology indicate?

A

Infection (active or past) or vaccination

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15
Q

What would positive HBeAb (hepatitis B e antibody) with negative HBsAg serology indicate?

A

The patient has been though a phase where the virus was replicating actively.

Patient is less infectious as there has been a good immune response.

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16
Q

What does positive serology for HBcAb (hepatitis B core antibody) IgM indicate?

A

Active infection

17
Q

What does positive HBcAb and negative HBsAg indicate?

A

Past infection

18
Q

How would you test for hepatitis B?

A

Screen:

  • HBcAb to test for previous infection
  • HBsAg to test for active infection

If positive:

  • HBeAg - how infective? How much viral replication?
  • HBV DNA - viral load
19
Q

Describe hepatitis D

How is it spread?

Consequence of hep D infection?

Treatment?

A

Hepatitis D is an incomplete RNA virus that is dependent on concurrent HBV infection for replication.

It has a blood-bourne mode of transmission.

Co-infection exacerbates the severity of acute hepatitis as well as increasing the risk of cirrhotic progression.

There is no treatment for hepatitis D so effective management of HBV is important.

20
Q

Hepatitis A

  1. How is it spread?
  2. How does it present?
  3. Complication?
  4. Management?
  5. Vaccine available?
A
  1. It is transmitted via the faecal-oral route usually by contaminated water or food.
  2. It presents with nausea, vomiting, anorexia and jaundice.
  3. It can cause cholestasis (slowing of bile flow through the biliary system) with dark urine and pale stools and moderate hepatomegaly.
  4. It resolves without treatment in around 1-3 months.
  5. Vaccination is available to reduce the chance of developing the infection.
21
Q

Hepatitis B

  1. Virus type?
  2. Spread?
  3. Presentation?
  4. Management?
  5. Complications?
A
  1. DNA virus
  2. Blood bourne, vertical, sexual
  3. Flu-like illness, general malaise, jaundice (30-50%)
  4. Acute - supportive (Most people fully recover from the infection within 2 months, however 10% go on to become chronic hepatitis B carriers). Chronic infection - PEG interferon +- antivirals (tenofovir/entecavir)
  5. Cirrhosis, hepatocellular carcinoma
22
Q

Hepatitis C virus

  1. Virus type?
  2. Spread
  3. Presentation?
  4. Investigations?
  5. Course?
  6. Managment?
  7. Complications?
  8. Vaccine?
A
  1. RNA virus
  2. Blood bourne, sexual
  3. May be asymptomatic, malaise, jaundice
  4. Investigations:
    • Hepatitis C antibody is the screening test
    • Hepatitis C RNA testing is used to confirm the diagnosis of hepatitis C, calculate viral load and assess for the individual genotype
  5. 1 in 4 fights off the virus and makes a full recovery

3 in 4 it becomes chronic

  1. Acute - supportive, Chronic - PEG interferon +- ribavirin +- antivirals
  2. Cirrhosis, hepatocellular carcinoma
  3. No vaccine
23
Q

Hepatitis E

  1. Virus type?
  2. Spread?
  3. Presentation?
  4. Management?
A
  1. RNA virus
  2. Faecal oral
  3. Usually asymptomatic
  4. Self limiting, no treatment required