<unk>  occurs due to long term liver injury which causes an imbalance between matrix production and degradation. The pathological hallmark of<unk>  is the development of scar tissue which leads to replacement of normal liver parenchyma, leading to blockade of portal blood flow and disturbance of normal liver function. When fibrosis of the liver reaches an advanced stage where distortion of the hepatic vasculature also occurs, it is termed as<unk>  of the liver. The pathogenesis of<unk>  involves inflammation, hepatic stellate cell activation, angiogenesis, and fibrogenesis. Kupffer cells are hepatic macrophages responsible for hepatic stellate cell activation during injury. Hepatic stellate cells (HSC) which are located in the subendothelial space of Disse, become activated in areas of liver injury and secrete transforming growth factor-beta 1 (TGF-β1), which leads to a fibrotic response and proliferation of connective tissue.<unk>  may also lead to hepatic microvascular changes including the formation of intra-hepatic shunts (due to angiogenesis and loss of parenchymal cells) and endothelial dysfunction. Fibrosis eventually leads to formation of septae that grossly distort the liver architecture which includes both the liver parenchyma and the vasculature, accompanied by regenerative nodule formation.
Cirrhosis pathophysiology
Non-alcoholic fatty liver disease pathophysiology
Alcoholic hepatitis pathophysiology
Drug induced liver injury pathophysiology
Hepatocellular carcinoma pathophysiology
Hepatocellular carcinoma risk factors
Hepatocellular carcinoma causes
Peliosis hepatis pathophysiology