The liver has a remarkable regenerative capacity -- remove half of the liver and the remaining half regrows to its original size in about a month! However if you destroy the extracellular matrix framework that gives the liver its architecture, the result is cirrhosis.

Cirrhosis is the final step in the dozens of diseases that destroy the matrix framework of the liver. These include several diseases that we have already studied in lab: hepatitis B & C and alcoholic liver (like in Lab 1). Because of the liver's regenerative capacity, longstanding chronic injury (and inflammation) is required to elicit fibrosis (and ultimately cirrhosis) in the kidney.

Compare the cirrhotic liver to the normal.

How would you describe the gross and histologic changes associated with cirrhosis?

Pay particular attention to whether the injury affects the portal tracts and/or the central veins.

What is the organ to the right of the cirrhotic liver in the first gross image? Does it appear normal?

Remember cardiac sclerosis from Lab 2? How is the fibrosis in cirrhosis different?

Cirrhosis represents the inability of the liver to repair itself after injury to it's matrix framework. Histologically you will see fibrosis bridging from portal tract to portal tract outlining nodules of regenerated parenchyma. Portal veins are relatively spared until the end of the disease. This is in contrast to cardiac sclerosis which causes the preferential fibrosis around the central vein.

Cirrhosis increases the resistance to portal blood flow causing portal hypertension. Portal hypertension causes backup into the attached splenic vein, which causes splenic congestion (splenomegaly). The effects of portal hypertension are extensive and will be discussed next year.