Acute and chronic viral hepatitis. Etiology & pathogenesis. Basic morphologic classification. Microscopic and gross pathomorphology.
Hepatitis is the general term given to a specific histopathological pattern of hepatocyte injury with inflammation (and scarring in chronic cases). First we shall give the pathomorphological description that defines hepatitis, and then move on to the various etiologies and breakdowns.
Gross morphology
- In mild acute states may only appear slightly mottled, in severe states may shrink to 500g, become limp and red covered with a wrinkled baggy capsule.
- In chronic hepatitis there may be evidence of scarring or widespread nodularity surrounding the scaring
- The entire liver may be involved or only patches
Microscopic morphology
- Mononuclear infiltrates predominate in all phases of most hepatic disease due to the fact they invoke T-cell mediated immunity. As such the distinction between acute and chronic (usually acute = neutrophils, chronic = monocytes) is based on pattern of injury, with acute hepatitis often showing less inflammation and more hepatocyte death
- Injury and inflammation can vary based on etiology. Hepatocyte injury has two forms:
- Ballooning degeneration (swelling) which eventually leads to cell rupture with cells appearing to have dropped out, leaving a collagen reticular framework behind
- Apoptosis where cells shrink and become intensely eosinophilic. When in the parenchyma this is known as lobular hepatitis
- In severe cases we can see central portal bridging necrosis followed by even worse parenchymal collapse
- In chronic cases we also expect to see a degree of patchy cellular regeneration. As well as portal inflammation with mononuclear portal infiltrates.
- In most severe chronic cases scarring and nodule formation leads to the development of cirrhosis with increased risk of malignancy
Now we shall consider some of the causes, firstly Viral hepatitis
- Hepatitis A
- ssRNA, fecal-oral contamination, 2-6 week incubation, never chronic, not unusual in poor countries (endemic), virus not toxic to hepatocytes
- Hepatitis B
- dsDNA, parenteral, sexual and perinatal transmission, 4-26 week incubation, 10% chronic
- Can cause acute hepatitis with recovery, non progressive chronic hepatitis, progressive chronic hepatitis or can be benign. Has vaccine
- Microscopically, has all of the above mentioned features of hepatitis, as well as showing the diagnostic ground glass cell (large, pale, granular cytoplasm due to HBsAg accumulating in the endoplasmic reticulum).
- Hepatitis C
- ssRNA, parenteral, intranasal cocaine RF, 2-26 weeks, 80% chronic,
- Can cause acute or chronic hepatitis, but in acute stage is asymptomatic often
- We see typical microscopic features listed above, as well as fatty change, lymphoid infiltrates in portal tracts and bile duct injury
- Hepatitis D