Antiepileptic pharmacotherapy Flashcards
MOA of Na+ blocking antiepileptics
Binds to inactive form of Na+ channels, resulting in preferential inhibition of epileptic focus
MOA of Ca++ blocking antiepileptics
Thanlmic T-type Ca++ channels inhibit absence seizures
Presynaptic HVA Ca++ channels- suppresses Glu signalling
Ways of enhancing GABA signalling
Activate GABA-A receptors
inhibit GABA re-uptake GAT-1
Inhibit GABA degredation GABA-T
Ways of antagonizing glutamanergic transmission
antagonize receptors
block glu release SV2A
MOA of Ca++ blocking antiepileptics
Thanlmic T-type Ca++ channels inhibit absence seizures
Presynaptic HVA Ca++ channels- suppresses EAA release
Ways of antagonizing glutamanergic transmission
antagonize receptors
block glu release SV2A
Phenytoin MOA
blocks Na+ channels
Pharmacokinetics of phenytoin
oral, IV (fosphenytoin)
non-linear elimination- need to monitor in blood
plasma protein binding
hepatic CYP metabolism
Therapeutic use of phenytoin
focal and tonic-clonic seizures, SE
not effective against absence seizures
Drug interactions with phenytoin
OCPs, warfarin
Adverse effects of phenytoin
CNS- nystagmus, ataxia, and sedation Rash and SJS hirsutism blood dyscrasias teratogenic gingival hyperplasia
MOA of carbamazepine
Na+ channel blockade
carbamazepine pharmacokinetics
linear kinetics
autoinduction of CYP3A4
Therapeutic use of carbamazepine
generalized tonic-clonic seizures, simple and complex partial seizures
trigeminal neuralgia
bipolar disorder
Adverse effects of carbamazepine
CNS- drowsiness, ataxia, vertigo, diplopia, blurred vision; nausea
hyponatremia
Boxed warning- rash and SJS, asian variant more susceptible
teratogenic
Valproic acid MOA
blocks Na+ channels
Blocks T-type Ca++ channels
Stimulates GABA synthesis and inhibits degredation
Therapeutic use of valproic acid
broad spectrum anti-seizure
absence, focal and tonic-clonic seizures
bipolar disorder and migraine prophylaxis