Infection of liver caused by hepatotropic viruses is known as viral hepatitis.
There are five main types of hepatotropic viruses –
– Hep-A →RNA virus – feco-oral route
– Hep-B →DNA virus – parentrally transmitted
– Hep-C →RNA virus – post transfusion
– Hep-D →RNA virus –super infection with hepatitis B
– Hep-E →RNA virus –water-born contaminated (as after flooding)
(1.) Acute Hepatitis –
The most common consequence of all hepatotropic viruses is acute inflammatory involvement of entire liver. In general type A,B,C,D,E show similar pathologic findings.
Grossly– The liver is slightly enlarged, soft & greenish.
1) Hepatocellular injury – There is variation in the degree of liver cell injury.
-Mildly injured hepatocytus appear swollen with granular cytoplasm which end to condense around the nucleus (ballooning degeneration)
– The nucleus become small & pyknotic & is eventually extruded from the cell, leaving behind necrotic mass called ‘councilman body’ by the process of apoptosis.
– Another type the hepatocellular necrosis is dropout necrosis in which isolated or small clusters of hepatocytes undergo lysis.
-Bridging necrosis is more severe form of hepatocellular injury in acute viral hepatitis & may progress to chronic hepatitis.
2) Inflammatory infiltrate – Infiltration by mononuclear inflammatory cells, usually in portal tract.
3) Kupffer Cell – Hyperplasia of kupffer cells contain phagocytosed cellular debris.
4) Cholestasis – Biliary stasis is not severe in viral hepatitis & may present as intracytoplasmic bile pigment granules.
5) Regeneration – Surviving adjacent hepatocytes undergo regeneration & hyperplasia.
(2.) Chronic Hepatitis –
It is defined as continuing or relapsing hepatic disease for more than 6 months with symptoms along with inflammation and necrosis. Pathologic features are common to both HBV, HCV infection.
- Piecemeal necrosis– It is defined as periportal destruction of hepatocytes at the limiting plate (piecemeal-piece by piece) expanded portal tracts are associated with proliferating bile ductules as a response to liver cell injury.
- Portal tract lesions-Inflammatory cell infiltration by lymphocyte, plasma cell and macrophages. Proliferated bile ductules is expanded portal tracts.
- Intralobular lesions-there are focal area of necrosis and inflammation with in the hepatic parenchyma, kupffer cell hyperplasia. More severe form of injury shows bridging necrosis (bands of necrosed hepatocytes that are bridge portal tract to central vein)
- Bridging fibrosis– there is a periportal fibrosis at the sites of interface hepatitis giving the portal tract stellate shaped appearance. End stage of chronic hepatitis is characterized by dense collagenous septa destroying lobular architecture & forming nodules.