What is the biochemical mechanism of hepatic encephalopathy?

The biochemical mechanisms of hepatic encephalopathy can be categorized into ammonia toxicity, pseudo-neurotransmitter, tryptophan and manganese ion theory.
1. Ammonia poisoning: digestive tract is the main site of ammonia production, when cirrhosis and other diseases occur, the metabolism of NH3 by liver is weakened, and the body circulation transports NH3 to the brain, thus causing hepatic encephalopathy.
2. Pseudo-neurotransmitters: the liver’s clearance of intestinal tyramine and phenylethylamine is impaired, and these two substances enter the brain, and because they are similar to normal neurotransmitters, they are unable to make the brain function normally, thus impeding cerebral nerve conduction.
3. Tryptophan: In liver disease, the ability to synthesize clear protein is weakened, resulting in an increase of tryptophan in the blood, which is metabolized to 5-hydroxyindoleacetic acid after entering the brain, thus leading to hepatic encephalopathy.
4. Manganese ion: In liver disease, the manganese secreted by the liver cannot be excreted normally and enters the brain through blood circulation, thus leading to hepatic encephalopathy.
There are many mechanisms leading to hepatic encephalopathy, and thus there are many choices of treatment. When hepatic encephalopathy occurs, one should consult the doctor in time in order to improve the quality of life.