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Benign Liver Disease, Cirrhosis, and Portal Hypertension
Cirrhosis is the end-stage of chronic liver disease characterized by degeneration of the normal hepatic architecture and replacement with fibrosis. Clinically these patients present with loss of hepatocellular function, including coagulopathy, encephalopathy, and jaundice. The hepatocellular fibrosis causes increased resistance to transhepatic flow, leading to portal hypertension, ascites, varices, and a number of physiologic syndromes.
I
Pathophysiology
- 1.
Acute and chronic liver injury leads to generation of cytokines interleukin-1, interleukin-6, tumor necrosis factor (TNF)-α, transforming growth factor β-1, and epidermal growth factor.
- 2.
Progressive destruction of hepatocytes, bile ducts, and vascular endothelial cells results in cellular proliferation, regeneration, and fibrous scar formation.
- 3.
Activation of hepatic stellate cells (Ito cells) leads to proliferation, vitamin A depletion, fibrosis, contraction, and obliteration of the perisinusoidal space of Disse.
II
Morphology
Fibrous septa seen in cirrhosis due to the accumulation of extracellular matrix divides hepatic regenerative nodules.
- 1.
Micronodular—smaller than 3 mm, uniform nodules involving virtually every hepatic lobule indicative of early disease
- 2.
Macronodular—nodules of varying sizes greater than 3 mm with irregular hepatocytes
- 3.
Mixed—micronodular and macronodular present in equal proportions
III
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