pharm of anticonvulsants Flashcards
(28 cards)
Fosphenytoin MOA
block voltage gated Na+ channels -> inhibit rapid repetitive AP’s
also secondarily decrease glutamate release and increase GABA release
Fosphenytoin ADME, therapeutics
prodrug (phenytoin); no active metabolites
highly bound to plasma proteins
IV and IM or oral with phenytoin
generalized tonic-clonic and partial seizures
Fosphenytoin AE’s and drug interaction
cardiovascular risk associated with rapid infusion
nystagmus, diplopia, gingival hyperplasia, ataxia, hirsutism
interactions with carbamazepine and topiramate
Ethosuximide MOA
blocks thalamic T-type Ca++ channels
Ethosuximide ADME, therapetuics
oral
half life ~40 hours
absence seizure
Ethosuximide AE’s and drug interactions
GI distress, lethargy, HA, uticaria valproic acid (decrease in metabolism, increase in steady-state concentration)
Levetiracetam MOA
binds synaptic vesicular protein (SV2A) to modulate glutamate and GABA release
Levetiracetam ADME, therapeutics
oral or IV
adjunctive
primary partial seizures in adults and children > 4yo
myoclonic seizures of juvenile myoclonic epilepsy
primary generalized epilepsy children > 6 yo
Barbiturates MOA
phenobarbital
facilitates GABA A activation -> increased DURATION of Cl- channel opening -> reduced excitation
Barbiturates ADME, therapeutics
IM or IV; half life ~4-5 days
partial seizures, tonic-clonic seizures, every seizure type for attacks that are hard to control
Barbiturates AE and drug interactions
respiratory and cardiac depression, tolerance and dependence, sedation, cognitive dysfunction
interactions: other sedative-hypnotics (alcohol), CNS depressants, increase CYP-450 enzymes
contraindication: porphyria (improperly made heme)
Stevens-Johnson syndrome
ethosuximide, phenytoin, carbamazepine
starts off flu-like and progresses to red / purple rash -> epidermal necrosis and sloughing
special toxicology of antiseizure drugs
stevens-johnson syndrome
teratogenicity
anticonvulsant hypersensitivity syndrome
antiseizure teratogenicity
fetal hydantoin syndrome: phenytoin, carbamazepine, phenobarbitol increased chances of malformation spina bifida: valproic acid
anticonvulsant hypersensitivity syndrome
fever, rash, organ (liver, kidney, blood) toxicity
higher risk with phenobarbitol, phenytoin, carbamazepine
flumazenil MOA
antagnoist to benzodiazepines
flumazenil therapeutics
used to reverse benzodiazepine induced CNS depressant effects (overdose, recovery from anesthetic and diagnostic procedures)
flumazenil AE’s
agitation, confusion, dizziness
benzodiazepines MOA
lorazepam, diazepam, midazolam
GABA a receptor agonist -> reduce FREQUENCY of Cl- channel opening
Benzodiazepines ADME
oral and parenteral
hepatic metabolism
Diazepam - active phase I metabolite -> longer half life (49 hr)
Lorazepam - no active metabolite, short half life
Benzodiazepines therapeutics
status epilepticus
benzodiazepines AE’s and drug interactions
sedation, tolerance and dependence, anterograde amnesia (surgery)
also used for date rape
interacts: other sedative hypnotics (alcohol), CNS depressants
Carbamazepine MOA
inactivation of voltage-gated Na+ channels, decreased synaptic transmission
Carbamazepine ADME, therapeutics
oral
induce microsomal enzymes which can alter clearance of other drugs
metabolite itself has anticonvulsive activity
partial seizures, tonic clonic seizures, trigeminal neuralgia, bipolar disorder (TCA)
