Changes

==Description==

==Description==

'''Hepatic encephalopathy''' is characterised by a complex of neurological abnormalities that may occur in the presence of advanced liver disease.  By far the most common cause in dog and cat is [[Portosystemic Shunt]] (PSS), although a marked reduction in functional mass of hepatic tissue can also lead to hepatic encephalopathy.  In rare cases, when severe acquired shunt due to hepatobiliary disease and congenital PSS have been ruled out, congenital urea enzyme cycle deficiencies and organic acidaemias, where there is lack of ability to degrade ammonia to urea, can be considered.

'''Hepatic encephalopathy''' is characterised by a complex of neurological abnormalities that may occur in the presence of advanced liver disease.  By far the most common cause in dog and cat is [[Portosystemic Shunt]] (PSS), although a marked reduction in functional mass of hepatic tissue can also lead to hepatic encephalopathy.  In rare cases, when severe acquired shunt due to hepatobiliary disease and congenital PSS have been ruled out, congenital urea enzyme cycle deficiencies and organic acidaemias, where there is lack of ability to degrade ammonia to urea, can be considered.

This is a reversible abnormality of the cerebral metabolism.  Its pathogenesis is not yet fully understood.  Increased concentration of ammonia level is the most common cause of this disease manifestation, due to its toxicity effect on brain cells.  Due to the lack of urea cycle in the brain, ammonia in cerebrospinal fluid (CSF) is detoxified into glutamine.  Level of glutamine can be shown to correlate with clinical signs.  Aromatic amino acids, especially tryptophan and its metabolites, share an antiport transporter with ammonia in CSF.  Consequently, dogs with congenital PSS are reported to have increased aromatic amino acid concentrations in CSF.  Increased ammonia concentrations also have a number of other effects on the central nervous system, including a reduction in serotonin activity, an increased in NMDA (N-methyl-D-aspartic acid) and peripheral-type benzodiazepine receptors.

This is a reversible abnormality of the cerebral metabolism.  Its pathogenesis is not yet fully understood.  Increased concentration of ammonia level is the most common cause of this disease manifestation, due to its toxicity effect on brain cells.  Due to the lack of urea cycle in the brain, ammonia in cerebrospinal fluid (CSF) is detoxified into glutamine.  Level of glutamine can be shown to correlate with clinical signs.  Aromatic amino acids, especially tryptophan and its metabolites, share an antiport transporter with ammonia in CSF.  Consequently, dogs with congenital PSS are reported to have increased aromatic amino acid concentrations in CSF.  Increased ammonia concentrations also have a number of other effects on the central nervous system, including a reduction in serotonin activity, an increased in NMDA (N-methyl-D-aspartic acid) and peripheral-type benzodiazepine receptors.

The sources responsible for an increase in ammonia levels include:

The sources responsible for an increase in ammonia levels include: