Liver Fibrosis

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Fibrosis is one way in which the liver responds to injury. It commonly occurs in association with chronic hepatic injury, and represents a repair stage in response to diseases that lead to necrosis and inflammation. The process is complex and involves increased deposition of extracellular matrix in the liver, following injury-induced activation of stellate cells.

The distribution pattern of fibrosis is a reflection of the pathogenesis of the condition, and can indicate the type of underlying pathology.

Patterns of Fibrosis

Centrilobular (periacinar) Fibrosis

This involves fibrosis around the hepatic venule (centrilobular vein). It is associated with chronic toxic injury since hepatocytes in this region are involved in drug metabolism. It is also associated with chronic passive congestion due to long-term right sided congestive heart failure.

Periportal (biliary) Fibrosis

This involves fibrosis that is mostly confined to the portal region, and is associated with chronic inflammatory conditions that lead to inflammation in the portal triads.

Post-Necrotic Scarring

This occurs following massive hepatic necrosis where large areas of parenchyma are lost and replaced by fibrosis.

Bridging (diffuse) Fibrosis

This is the sequel to chronic parenchymal injury, such as prolonged inflammation or numerous episodes of zonal necrosis. Fibrosis occurs throughout lobules and leads to bridging between portal areas, or between portal regions and central veins, causing pseudolobulation.

Although all types of fibrosis can lead to hepatic dysfunction if severe enough, bridging fibrosis is more likely to impair hepatic function than any of the other types.

Hepatic fibrosis is now known to be potentially reversible, provided the source of injury is removed. If the insult persists, however, fibrosis can be self-perpetuating, resulting in a small scarred liver with functional failure.

Also see: Cirrhosis

Liver Fibrosis Learning Resources
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Maxie, M.G. (2007) Pathology of Domestic Animals Volume 2 (Fifth Edition), Elsevier Saunders.

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