1. SEVERE, DIFFUSE, HEPATIC FIBROSIS
- a post-necrotic and post-inflammatory response.
- hepatocyte injury causes release of IGF-1, which acts as a mitogen for stellate cells.
- Kupffer (and other) cells make TGF-beta, prompting stellate cells to turn into myofibroblasts
- fibroblasts and myofibroblasts proliferate. Collagen (types I, III, XVIII) and fibronectin are produced.
- because the myofibroblasts produce collagen and ECM in the space of Disse, the normal fenestrations in hepatic endothelium become closed.
- closure of fenestrations causes blood to be shunted through the liver and into the hepatic vein, functionally bypassing hepatocytes.
- eventually fibrosis will connect portal and central areas.
2. NODULAR REGENERATION
- a post-necrotic response.
- 75% of liver can be removed before liver dysfunction occurs
- liver can regenerate up to 80% of its mass and will function if the connective tissue framework remains intact
3. BILE DUCT HYPERPLASIA
- may be associated with necrosis, inflammation, toxins, blockage of bile ducts
- proliferation of bile duct epithelium is concentrated in portal areas.
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