Hepatic encephalopathy is a disease where cirrhosis and portosystemic shunts can lead to decreased NH3 ammonia metabolism leading to neuropsychiatric dysfunction. It can be triggered by increased ammonia production and absorption due to a GI bleed, constipation, or decreased ammonia excretion. The treatment is lactulose which increases ammonium ion NH4+ generation and rifaximin which decreases the number of ammonia-producing bacteria. Glutamate transporters do not have a known role in the pathophysiology of Reye syndrome, but they are implicated in the pathophysiology of hepatic encephalopathy, which occurs when ammonia joins with glutamate in the brain.
See this question on lactulose also in the block.
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