Pathophysiology

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The main effects of chronic liver damage are reduced numbers of hepa-tocytes and disruption of the normal sinusoidal architecture, which alters blood flow through the liver and increases pressure in the portal vein (portal hypertension). Haphazard regeneration of hepatocytes in nodules and formation of fibrous scar tissue by Ito (stellate) cells disrupt sinusoidal architecture (see Chapters 8 & 10). Altered blood flow further compromises liver function.

Reduced hepatic function results in the accumulation of bilirubin and other toxins, causing jaundice and itching (see Chapter 25).

As the liver is the main regulator of carbohydrate, lipid and protein metabolism, chronic liver disease results in widespread metabolic dysregulation, with steady weight loss and wasting (see Chapter 24).

The liver is the main source of circulating plasma proteins, including critical clotting factors, so that patients develop a tendency to bleeding (coagulopathy) and have reduced circulating albumin (see Chapter 24).

As a result of portal hypertension, portosystemic shunting of blood occurs where the portal and systemic venous systems meet, allowing toxin-laden blood from the intestine to bypass the liver. This contributes to chronic hepatic encephalopathy (also known as portosystemic encephalopathy), because toxic metabolites from the intestine, particularly bacterial amines, interfere with cerebral function. Shunting also promotes the development of varices, which can rupture and bleed cata-strophically (see Chapter 10).

In addition, portal hypertension and splenic vein congestion result in splenomegaly, which leads to pooling of platelets in the spleen and thrombocytopenia. Congestion of the mesenteric veins, combined with hypoalbuminaemia can lead to transudation of fluid into the peritoneal cavity, causing ascites.

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