Final answer:
Hepatic encephalopathy's MOA involves the accumulation of neurotoxins like ammonia leading to GABA system dysregulation and neural inhibition. Both GABA and glutamine are implicated, but GABA's role in inhibitory neurotrasmission highlights its significance. Acute liver failure, particularly hyperacute cases, typically has a higher mortality compared to chronic failure.
Step-by-step explanation:
The mechanism of action (MOA) of hepatic encephalopathy involves the accumulation of neurotoxins in the brain, such as ammonia, which is normally cleared by the liver. When the liver fails, substances like ammonia and glutamine can accumulate, leading to alterations in neurotransmitter systems. One important neurotransmitter affected is gamma-aminobutyric acid (GABA), which can cause neurological and psychiatric abnormalities when dysregulated due to liver failure. This dysregulation can lead to a heightened inhibitory tone in the brain, contributing to the neuropsychiatric symptoms of encephalopathy.
Regarding whether GABA or glutamine is more responsible for encephalopathy, both play roles, and the balance between excitatory and inhibitory neurotransmitters (such as glutamate and GABA) is disrupted. However, GABA is often emphasized in the context of hepatic encephalopathy due to its role in inhibitory neurotransmission and evidence that GABAergic system dysfunction can contribute to the condition's clinical manifestations.
As for the question concerning mortality in different types of liver failure, acute liver failure generally has a higher mortality rate compared to chronic liver failure. The term 'hyperacute liver failure' refers to a more accelerated progression of liver failure, which may present with a rapid onset of encephalopathy. The rate of progression in hyperacute cases imposes an even greater risk and often requires urgent medical interventions to manage life-threatening complications.