Liver Cirrhosis
Irreversible replacement of normal liver architecture by fibrous septa and regenerative nodules causes both failing synthetic function and obstructed blood flow, so every complication is one of these two mechanisms playing out.
Definition
Cirrhosis is the end stage of chronic liver injury, in which diffuse fibrosis and regenerative nodules replace normal architecture, impairing liver function and obstructing portal blood flow. It is compensated when asymptomatic and decompensated once complications appear.
First principles
Cirrhosis is a single architectural change with two independent downstream consequences
Whatever the cause (alcohol, viral hepatitis, non-alcoholic fatty liver disease, autoimmune or metabolic disease), chronic liver injury drives repeated cycles of hepatocyte death, stellate cell activation and collagen deposition, which progressively replace the normal lobular architecture with fibrous septa surrounding regenerative nodules of hepatocytes. This distorted architecture has two separate consequences that explain essentially the entire clinical picture: (1) the mass of functioning hepatocytes able to carry out synthetic and metabolic work falls, and (2) the fibrous scarring and nodules physically distort the hepatic sinusoids, obstructing blood flow through the liver and raising portal venous pressure. Every complication of cirrhosis is downstream of one or both of these two mechanisms.
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