pharm of anticonvulsants Flashcards

1
Q

Fosphenytoin MOA

A

block voltage gated Na+ channels -> inhibit rapid repetitive AP’s
also secondarily decrease glutamate release and increase GABA release

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2
Q

Fosphenytoin ADME, therapeutics

A

prodrug (phenytoin); no active metabolites
highly bound to plasma proteins
IV and IM or oral with phenytoin
generalized tonic-clonic and partial seizures

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3
Q

Fosphenytoin AE’s and drug interaction

A

cardiovascular risk associated with rapid infusion
nystagmus, diplopia, gingival hyperplasia, ataxia, hirsutism
interactions with carbamazepine and topiramate

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4
Q

Ethosuximide MOA

A

blocks thalamic T-type Ca++ channels

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5
Q

Ethosuximide ADME, therapetuics

A

oral
half life ~40 hours
absence seizure

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6
Q

Ethosuximide AE’s and drug interactions

A
GI distress, lethargy, HA, uticaria
valproic acid (decrease in metabolism, increase in steady-state concentration)
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7
Q

Levetiracetam MOA

A

binds synaptic vesicular protein (SV2A) to modulate glutamate and GABA release

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8
Q

Levetiracetam ADME, therapeutics

A

oral or IV
adjunctive
primary partial seizures in adults and children > 4yo
myoclonic seizures of juvenile myoclonic epilepsy
primary generalized epilepsy children > 6 yo

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9
Q

Barbiturates MOA

A

phenobarbital

facilitates GABA A activation -> increased DURATION of Cl- channel opening -> reduced excitation

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10
Q

Barbiturates ADME, therapeutics

A

IM or IV; half life ~4-5 days

partial seizures, tonic-clonic seizures, every seizure type for attacks that are hard to control

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11
Q

Barbiturates AE and drug interactions

A

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)

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12
Q

Stevens-Johnson syndrome

A

ethosuximide, phenytoin, carbamazepine

starts off flu-like and progresses to red / purple rash -> epidermal necrosis and sloughing

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13
Q

special toxicology of antiseizure drugs

A

stevens-johnson syndrome
teratogenicity
anticonvulsant hypersensitivity syndrome

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14
Q

antiseizure teratogenicity

A
fetal hydantoin syndrome:
phenytoin, carbamazepine, phenobarbitol
increased chances of malformation
spina bifida:
valproic acid
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15
Q

anticonvulsant hypersensitivity syndrome

A

fever, rash, organ (liver, kidney, blood) toxicity

higher risk with phenobarbitol, phenytoin, carbamazepine

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16
Q

flumazenil MOA

A

antagnoist to benzodiazepines

17
Q

flumazenil therapeutics

A

used to reverse benzodiazepine induced CNS depressant effects (overdose, recovery from anesthetic and diagnostic procedures)

18
Q

flumazenil AE’s

A

agitation, confusion, dizziness

19
Q

benzodiazepines MOA

A

lorazepam, diazepam, midazolam

GABA a receptor agonist -> reduce FREQUENCY of Cl- channel opening

20
Q

Benzodiazepines ADME

A

oral and parenteral
hepatic metabolism
Diazepam - active phase I metabolite -> longer half life (49 hr)
Lorazepam - no active metabolite, short half life

21
Q

Benzodiazepines therapeutics

A

status epilepticus

22
Q

benzodiazepines AE’s and drug interactions

A

sedation, tolerance and dependence, anterograde amnesia (surgery)
also used for date rape
interacts: other sedative hypnotics (alcohol), CNS depressants

23
Q

Carbamazepine MOA

A

inactivation of voltage-gated Na+ channels, decreased synaptic transmission

24
Q

Carbamazepine ADME, therapeutics

A

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)

25
Q

carbamazepine AE’s, interactions

A

diplopia, ataxia, idiosyncratic blood dyscrasia, aplastic anemia and agranulocytosis (leukopenia)
interacts: related to liver enzyme inducing properties, other anticonvulsants

26
Q

Valproic acid and divalproex MOA

A

inactivate Na+ channel, inhibit T-type Ca++ channel, increase GABA in brain at high concentrations by inhibiting GABA transaminase

27
Q

Valproic acid and divalproex ADME, therapeutics

A

oral, good bioavailability

absence seizures, generalized tonic-clonic seizures, control tonic-clonic seizures

28
Q

Valproic acid and divalproex AE’s, interactions

A

nausea, vomiting, GI complaints, potenial lethal idosyncratic hepatotoxicity
interacts: inhibits metabolism of several drugs (phenytoin, carbamazepine, phenobarbital)
displaces phenytoin from plasma proteins (causes phenytoin to be present longer)
contraindication: pregnancy