Hepatic encephalopathy is the performance of end-stage liver cancer,Liver cancer is the leading cause of death lead (about 35%). Hepatic encephalopathy often serious cancer of the liver parenchyma damage or liver parenchyma with cirrhosis caused by the extensive damage. Upper gastrointestinal bleeding, infection, hypokalemia, surgical strikes, drainage and improper application of massive ascites and diuretics drugs detrimental to the liver is hepatic encephalopathy Common incentives. The current incentives only for its prevention and treatment, there is a lack of effective therapy. Because of illness later, the few successful treatment.
The pathogenesis of hepatic encephalopathy mechanism is not clear, some may be related to the following factors:
(1) Ammonia poisoning theory Under normal circumstances, the formation and removal of ammonia maintained a dynamic balance, so that blood ammonia levels remain normal. Serious damage to liver function, blood ammonia levels can be increased. Elevated blood ammonia levels can be increased or ammonia production (and) less than ammonia removal (ornithine circulatory disturbance) due.
(B) False doctrine neurotransmitter Catecholamines such as norepinephrine and dopamine in the nervous system neurotransmitter normal, usually catecholamines in the blood through the blood-brain barrier, so we must rely on brain catecholamine synthesis of nerve tissue itself . With a benzene ring protein diet such as the amino acid phenylalanine and tyrosine, in their intestinal bacteria from the slope can be formed role tyramine and phenylethylamine, such biogenic amines after being absorbed by the intestinal portal people liver.
(C) plasma amino acid imbalance theory Under normal circumstances, plasma levels of amino acids to maintain a more appropriate ratio. AAA (aromatic amino acid) have entered cells to generate more false neurotransmitter, and inhibit the normal neurotransmitter synthesis, which eventually led to the occurrence of hepatic encephalopathy. Plasma amino acid imbalance in neurotransmitters theory is false doctrine supplementary and development.
The pathogenesis of hepatic encephalopathy mechanism is not clear, some may be related to the following factors:
(1) Ammonia poisoning theory Under normal circumstances, the formation and removal of ammonia maintained a dynamic balance, so that blood ammonia levels remain normal. Serious damage to liver function, blood ammonia levels can be increased. Elevated blood ammonia levels can be increased or ammonia production (and) less than ammonia removal (ornithine circulatory disturbance) due.
(B) False doctrine neurotransmitter Catecholamines such as norepinephrine and dopamine in the nervous system neurotransmitter normal, usually catecholamines in the blood through the blood-brain barrier, so we must rely on brain catecholamine synthesis of nerve tissue itself . With a benzene ring protein diet such as the amino acid phenylalanine and tyrosine, in their intestinal bacteria from the slope can be formed role tyramine and phenylethylamine, such biogenic amines after being absorbed by the intestinal portal people liver.
(C) plasma amino acid imbalance theory Under normal circumstances, plasma levels of amino acids to maintain a more appropriate ratio. AAA (aromatic amino acid) have entered cells to generate more false neurotransmitter, and inhibit the normal neurotransmitter synthesis, which eventually led to the occurrence of hepatic encephalopathy. Plasma amino acid imbalance in neurotransmitters theory is false doctrine supplementary and development.
