Regarding Hepatic encephalopathy false is
(C) Decreased GABA > The toxic substances that accumulate in the setting of liver failure and affect the brain are still not well understood. They have been thought to include ammonia (NH3) and mercaptans. Ammonia is normally converted to urea by the liver and, as with mercaptans, is produced by the bacterial breakdown of protein in the intestines.> Ammonia, at the modestly increased concentrations that commonly occur in precoma HE (0.15 mM-0.75 mM), has been shown to increase GABA-induced chloride current in cultured neurons, probably by modifying the affinity of the GABA(A) receptor for GABA.> An elevated serum ammonia level is characteristic but not essential, and correlates poorly with the level of encephalopathy. The cerebrospinal fluid is usually normal or may show increased protein with increased GABA levels.> The concentrations of short-chain fatty acids in peripheral venous blood were significantly elevated in patients with hepatic encephalopathy caused by cirrhosis> Ammonia is the substance most often incriminated in the pathogenesis of encephalopathy.> Many, but not all, patients with hepatic encephalopathy have elevated blood ammonia levels, and recovery from encephalopathy is often accompanied by declining blood ammonia levels.> Other compounds and metabolites that may contribute to the development of encephalopathy include mercaptans (derived from intestinal metabolism of methionine), short-chain fatty acids, and phenol.> False neurochemical transmitters (e.g., octopamine), resulting in part from alterations in plasma levels of aromatic and branched- chain amino acids, may also play a role.> An increase in the permeability of the blood-brain barrier to some of these substances may be an additional factor involved in the pathogenesis of hepatic encephalopathy.> Several observations suggest that excessive concentrations of y-aminobutyric acid (GABA), an inhibitory neurotransmitter, in the CNS are important in the reduced levels of consciousness seen in hepatic encephalopathy.> Increased CNS GABA may reflect failure of the liver to extract precursor amino acids efficiently or to remove GABA produced in the intestine.
Increased ammonia in blood
Increased mercaptans in blood
Decreased GABA
Increased short chain fatty acids.
Miscellaneous