B59, Acute and chronic hepatitis

Question 1

What are all of the potential causes of acute hepatitis?

Answer 1

1. Viral
   
   • ​​Hepatitis viruses A-E
   • Yellow fever, flavivirus
   • EBV, can cause mild hepatitis during acute infectious mononucleosis
   • CMV can cause acute hepatitis in neonates and IC’d patients
   • HSV2 can cause hepatitis in IC’d
2. Alchol
3. Toxin
   
   • ​​Amanita toxin in mushrooms, Carbon tetrachloride
4. Drugs
   
   • ​​Acetominophen/paracetamol, amoxicillin, isoniazid, TB medications
5. Autoimmune conditions, SLE
6. Wilson’s disease

Question 3

What are the causes of chronic hepatitis?

Answer 3

Although the hepatitis viruses are responsible for most cases, there are many other causes:

i. Wilson disease ‐ Autosomal disorder characterized by copper deposition in tissues.
ii. α1‐antitrypsin deficiency ‐ A1AT is not secreted properly and instead accumulates in the liver (emphysema).
iii. Chronic alcoholism
iv. Drugs
v. Autoimmunity

Question 4

Characteristics of Autoimmune Hepatitis

Answer 4

Causes a chronic hepatitis that can be mild or severe. with an overall 5% progression to cirrhosis which is the main cause of mortality.

• Female predominance
• No serologic signs of infection
• Elevated serum IgG
• Infiltration of CD4+ T cells into the liver.
• Other autoimmune disorders are present in 60% of patients, SLE, thyroiditis, RA, sjogrens, ulcerative colitis.
• Exclusion of other possiblities

Autoantibodies:

• The main circulating autoantibodies, although not specific for the disease, are antinuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA) in type 1 disease and, in type 2 autoimmune hepatitis, anti-liver-kidney microsome-1 antibodies (ALKM-1) and anti-liver cytosol antibody-1 (ALC-1)

Question 5

How does autoimmune hepatits histology differ from viral chronic hepatitis?

Answer 5

In autoimmune hepatitis,

Scarring and fibrosis occurs rapidly after acute cell injury that causes confluent necrosis.

But even though fibrosis has occured, it usually remains asymptomatic and subclinical for many years.

By the time symptoms are observed, there is frequently a burned-out cirrhosis, with advanced scarring, and very little ongoing injury or inflammation, and abundant plasma cells.