Etiology

• Acute hepatic disease Liver: acute disease.
• Chronic hepatic disease Liver: chronic disease.

Pathophysiology

• Loss of hepatic function   →  
  • Impaired fat digestion and metabolism and increased mobilization from peripheral stores   →   hyperlipidemia.
  • Impaired carbohydrate metabolism   →   hypoglycemia or hyperglycemia.
  • Impaired protein synthesis   →   catabolism of body protein   →   increased ammonia levels and cachexia.
  • Loss of detoxifying capacity and development of arteriovenous shunts   →   hepatic encephalopathy.
  • Altered metabolism of hormones   →   disrupted circulating hormonal levels, eg insulin, glucagon, growth hormone, insulin-like growth factors, corticosteroids, catecholamines   →   polydipsia/polyuria (due to increased corticosteroids in liver failure), fluid retention.
  • Decreased synthesis of clotting proteins (plus vitamin K deficiency due to anorexia and fat maldigestion due to lack of bile acids)   →   coagulation disorders.
  • Loss of detoxifying capacity and development of arteriovenous shunts   →   hepatic encephalopathy.
• Acute fulminating liver failure   →   release of tissue thromboplastins and other stimulators of coagulation   →   DIC.
• Portal hypertension +/- concurrent hypoalbuminemia   →   ascites.
• Jaundice develops as result of failure of the hepatocytes to remove unconjugated bilirubin from circulation.
• In the normal animal this unconjugated bilirubin is conjugated with glucoronic acid which is excreted in the bile.
• Accumulation of bilirubin in the tissue results in yellow discoloration.

Timecourse

• Depends on underlying hepatic disease.