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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 still operates at sufficient efficiency to remove ammonia from the portal blood.
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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.
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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.
    
Blood ammonia concentration may also be eleavted in animals with:
 
Blood ammonia concentration may also be eleavted in animals with:
*Congenital abnormalities of enzymes of the urea cycle (such as argininosuccinate synthetase).
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*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.
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*Deficiencies of the substrates of the urea cycle, such as with experimental '''arginine deficiency''' in cats.
    
High blood ammonia concentrations are the most common cause of [[Hepatic Encephalopathy|'''hepatic encephalopathy''']] (HE).
 
High blood ammonia concentrations are the most common cause of [[Hepatic Encephalopathy|'''hepatic encephalopathy''']] (HE).
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