In case study 6 we learned about PLP enzymes. In this case study we are going to
ID: 524091 • Letter: I
Question
In case study 6 we learned about PLP enzymes. In this case study we are going to look at how the drug vigabatrin is used to treat epilepsy by inhibiting the PLP-dependent enzymes GABA transaminase. Your job for this case study is to investigate a mechanism in which vigabatrin uses to inhibit GABA transaminase. Please provide an arrow pushing mechanism for how this works and label the type of reaction that is happening in the key inhibitory step. Also please provide a description of what causes epilepsy and how this drug can be used to treat that. Submit as a PDF or image. Stepwise mechanism for the formation of the covalently bond vigabatrin is shown. Arrows are used to illustrate how this inhibition happens and the key step is labeled. Description of what causes epilepsy is provided as well as an explanation of how this drug treats that.Explanation / Answer
Epilepsy :
Common causes of seizures by age:
In Newborns:
In Infants and Children:
In Children and Adults:
In Seniors:
Vigabatrin: mechanism of action -
is an antiepileptic drug that inhibits the breakdown of -aminobutyric acid (GABA) by acting as a suicide inhibitor of the enzyme GABA transaminase (GABA-T).
It is also known as -vinyl-GABA, and is a structural analogue of GABA, but does not bind to GABA receptors.
Vigabatrin helps lower GHB levels through GABA transaminase inhibition.
However, this is in the brain only; it has no effect on peripheral GABA transaminase, so the GHB keeps building up and eventually reaches the brain.
the compound's mechanism of action is very well-characterized in animal models and cell cultures.
* -Aminobutyric acid (GABA)-ergic synapses comprise approximately 30% of all synapses within the central nervous system, and therein underlies the primary mode of synaptic inhibition.
* Vigabatrin was rationally designed to have a specific effect on brain chemistry by inhibiting the GABA-degrading enzyme, GABA transaminase, resulting in a widespread increase in GABA concentrations in the brain.
* The increase in GABA functions as a brake on the excitatory processes that can initiate seizure activity.
*Despite the short half-life of vigabatrin in the body (5-7 h) and its relatively low concentration in cerebrospinal fluid (10% of the concentration observed in plasma), it has the profound effect of increasing GABA concentration in the brain for more than a week after a single dose in humans.
* This effect persists steadily over years of vigabatrin administration and results in significant and persistent decreases in seizure activity.
*Vigabatrin can be effective with once-daily dosing.
Treatment :
Indicated for adjunctive therapy in adults with refractory complex partial seizures.
500 mg PO q12hr initially, THEN increase by 500-mg increments qWeek to target dose of 1.5 g q12hr
No additional benefit shown with 6 g daily compared with 3 g daily; higher incidence of adverse effects associated with 6 g daily
Administration:
Oral solution preparation: Dissolve powder content from each 500 mg packet in 10 mL cold or room temp water (final concentration 50 mg/mL); prepare immediately before use
May take with or without food.
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