Difference between revisions of "Ammonia"
| (One intermediate revision by one other user not shown) | |||
| Line 6: | Line 6: | ||
*Bacterial degradation of undigested amino acids and purines in the colon. | *Bacterial degradation of undigested amino acids and purines in the colon. | ||
| − | The urea which is produced from ammonia is excreted in urine. A failure to excrete nitrogenous waste results in [[azotaemia]] which may cause the clinical syndrome of [[Uraemia|uraemia]]. | + | The urea which is produced from ammonia is excreted in urine. A failure to excrete nitrogenous waste results in [[Kidney Renal Failure - Pathology|azotaemia]] which may cause the clinical syndrome of [[Uraemia|uraemia]]. |
==Clinical Significance== | ==Clinical Significance== | ||
| − | Even in the most severe forms of liver failure, the urea cycle usually | + | 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. |
| − | + | 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 | + | Blood ammonia concentration may also be eleavted 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. | ||
Revision as of 10:36, 3 November 2010
Description
Ammonia is a by-product of protein degradation which is transported in the portal vein and metabolised to urea in the liver via the urea cycle. Some ammonia is also used in the synthesis of glutamine. Ammonia is generated in healthy animals through the following physiological processes:
- Hepatic catabolism of body proteins and of proteins absorbed from the gut, including those obtained after gastro-intestinal haemorrhage.
- Metabolism of glutamine by enterocytes of the small intestine; enterocytes obtain 25% of their energy by this process.
- Bacterial and intestinal degradation of urea by urease in the colon.
- Bacterial degradation of undigested amino acids and purines in the colon.
The urea which is produced from ammonia is excreted in urine. A failure to excrete nitrogenous waste results in azotaemia which may cause the clinical syndrome of uraemia.
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.
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 porto-systemic shunts and 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:
- 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.
High blood ammonia concentrations are the most common cause of hepatic encephalopathy (HE).