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Books > Science & Mathematics > Physics > Applied physics & special topics > Biophysics
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Advances in Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy (Paperback, Softcover reprint of the original 1st ed. 1997)
Loot Price: R1,427
Discovery Miles 14 270
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Advances in Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy (Paperback, Softcover reprint of the original 1st ed. 1997)
Series: Advances in Experimental Medicine and Biology, 420
Expected to ship within 18 - 22 working days
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This volume contains the papers presented at the International
Symposium on "Cirrhosis, Hyperammonemia and Hepatic
Encephalopathy," held in Valencia, Spain, De- cember 2nd_4th, 1996.
Liver cirrhosis is one of the main causes of death in occidental
countries. There are other hepatic dysfunctions such as fulminant
hepatic failure, Reye's syndrome, or congenital deficiencies of
urea cycle enzymes which can also lead to hepatic encephalopathy,
coma and death. However, the molecular bases ofthe pathogenesis of
hepatic encephalopathy remain unclear. One ofthe consequences of
hepatic failure is the reduced ability to detoxify ammonia by
incorporating it into urea. This leads to increased blood ammonia
levels. Hyperam- monemia is considered one of the main factors
responsible for the mediation of hepatic encephalopathy and
classical clinical treatments are directed towards reducing blood
ammo- nia levels. Altered neurotransmission is an essential step in
the pathogenesis of hepatic encephalopathy. The first part of the
book is devoted to the discussion of the recent advances in the
understanding of the alterations of different neurotransmitter
systems in hepatic encephalopathy. The alterations of tryptophan
metabolism and neurotransmission in hepatic encephalopathy and the
implications for the clinical use of neuropsychoactive drugs are
reviewed. The alterations in glutamate transport and
neurotransmission in hepatic encephal- opathy due to acute liver
failure are also reviewed. The role of NMDA receptors in the
molecular mechanism of acute ammonia toxicity is discussed as well
as its modulation by metabotropic glutamate receptors and
muscarinic receptors.
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