간경변 II형: 병태생리학

Cirrhosis develops through inflammation, immune system activation, and hepatocyte death. Inflammation recruits immune cells that release cytokines like tumor necrosis factor-alpha and interleukin-1, triggering transforming growth factor-beta production. These processes activate hepatic stellate cells, stimulate collagen production, and cause liver cell death, collectively driving progressive liver damage and fibrosis.

Hepatic stellate cells normally store vitamin A in a quiescent state. When activated by inflammatory signals, they transform into myofibroblasts and produce excess collagen and extracellular matrix proteins. Continuous activation leads to dense fibrous tissue accumulation that replaces normal liver tissue, distorting the liver's architecture and impairing its function.

As fibrosis progresses, dense fibrous bands accumulate within liver tissue, distorting normal architecture. Hepatocyte death triggers disorganized regeneration, creating regenerative nodules—clusters of liver cells surrounded by fibrous tissue. These nodules further distort vascular and biliary structures, increasing resistance to portal blood flow and leading to portal hypertension.

Fibrosis and regenerative nodules in the liver distort normal vascular architecture, increasing resistance to portal blood flow. This elevated pressure in the portal vein causes portal hypertension, which can trigger serious complications including ascites, splenomegaly, and bleeding from esophageal or gastric varices.

Chronic liver injury triggers inflammation that recruits immune cells and promotes oxidative stress and reactive oxygen species production. Inflammatory cytokines damage liver tissue, disrupt cellular balance, and initiate fibrogenesis. This sustained inflammation accelerates hepatocyte injury and perpetuates the cycle of liver damage and fibrotic remodeling.

Hepatocyte apoptosis and necrosis accelerate liver damage, prompting regeneration attempts. However, surrounding fibrosis disrupts this regenerative process, resulting in disorganized regeneration and regenerative nodules rather than normal tissue repair. This impaired regeneration perpetuates structural distortion and progressive functional decline in the liver.

Advanced cirrhosis reduces the liver's ability to detoxify substances, allowing toxins like ammonia to accumulate and cause hepatic encephalopathy. The liver's diminished metabolic capacity also leads to kidney dysfunction, hormonal problems, and potential multi-organ failure in severe cases of decompensated cirrhosis.