Changes

==Clinical Significance==

==Clinical Significance==

Even in the most severe forms of liver failure, the urea cycle usually still operates at sufficient efficiency to remove ammonia from the portal blood.

Even in the most severe forms of liver failure, the urea cycle usually continues to remove ammonia sufficiently from the portal blood to prevent clinical symptoms.

However, in animals where the portal blood is diverted directly into the systemic circulation, blood ammonia concentrations may rise because it is not removed by the liver.  This abnormal pattern of blood flow occurs with [[Portosystemic Shunt|'''porto-systemic shunts''']] and [[Hepatic Microvascular Dysplasia|'''microvascular dysplasia''']].  These animals also have a low blood urea concentration because ammonia is not converted to this product.

In animals where the portal blood is diverted directly into the systemic circulation, however, blood ammonia concentrations may rise because it is no longer being removed by the liver.  This abnormal pattern of blood flow occurs with [[Portosystemic Shunt|'''porto-systemic shunts''']] and [[Hepatic Microvascular Dysplasia|'''microvascular dysplasia''']].  Affected animals also have low blood urea concentrations because ammonia is not being converted to urea.

Blood ammonia concentration may also be eleavted in animals with:

Blood ammonia concentration may also be elevated in animals with:

*Congenital '''abnormalities of enzymes of the urea cycle''' (such as argininosuccinate synthetase).

*Congenital '''abnormalities of enzymes of the urea cycle''' (such as argininosuccinate synthetase).

*Deficiencies of the substrates of the urea cycle, such as with experimental '''arginine deficiency''' in cats.

*Deficiencies of the substrates of the urea cycle, such as with experimental '''arginine deficiency''' in cats.