anti-epileptics Flashcards by Deana Cairo

mechanisms of anti-epileptics (5)

inactivate Na channels

inactivate Ca channels

reduce synaptic vesicle fusion

modulate glutamate receptors

modulate gaba receptors

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pathophysiology of epilepsy

too much excitation or too little inhibition

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are there increased or decreased levels of glutamate during seizures

increased

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what is the ionotropic receptor type for GABA?

GABA_A

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what is the metabotropic receptor type for GABA

GABA_B

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targets of anti-epileptic drugs

glutamate- decrease activity at receptors

increase activity of GABA at receptors

Increase release of GABA

Inhibit breakdown of GABA

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first line for treating status epilepticus

benzodiazepines: diazepam (valium), lorazepam (ativan)

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first line of drug for absence seizures

ethosuximide

valproic acid

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mechanism of benzodiazepines

increase affinity of GABA for the GABA_Areceptor

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where are benzodiazepines metabolized

liver

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side effects of benzodiazepines

sedative

withdrawal symptoms due to tolerance

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mechanism of vigabatrin

inhibit GABA-T to reduce GABA breakdown

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indication for vigabatrin (sabril)

complex partial seizures that are refractory to several others AEDs

infantile spasms

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drug interaction of vigabatrin

reduces plasma concentration of primidone

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side effects of vigabatrin

concentric visual field deficit (can be irreversible)

drowsiness

dizzinesss

weight gain

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what is carbamazepine indicated for

focal seizures and GTCSs

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mechanism of carbamazepine

block tetanic firing

increases Na channel inactivation, reduces transmitter release

potentiates GABA response

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what is carbamazepine used for other than seizures

bipolar disorder

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carbamazepine toxicities

ataxia, diplopia, nystagmus, dizziness

tolerance to side effects

aplastic anemia

rash- Stevens Johnson Syndrome, Toxic Epidermal Necrolysis

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what drugs should never be used with carbamazepine

drugs that inhibit hepatic metabolism- increases toxicity

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mechanism of phenytoin (dilantin)

blocks tetanic firing

increases Na channel inactivation

releases neurotransmitter release

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indication for phenytoin

focal seizures and GTCSs

status epilepticus

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notable phamacokinetic aspect of phenytoin

oral absorption peak time variable from patient to patient, difficult to get dosing within therapeutic range

functions at 1st order kinetic at low doses and zero order kinetics at high doses

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side effects of phenytoin

cardiac arrhythmias

dizziness

nystagmus

headaches

rash

gingival hyperplasia and hirsutism

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mechanism of primidone (mysoline)

similiar to phenytoin- increase Na channel inactivation notable mention- phenobarbital is a metabolite (enhances GABA_A receptor activity) but this is not thought to be part of the mechanism of action

what disorder is treated with primidone

focal dyscognitive seizures (not used much now in favor of carbamazepine and phenytoin)

primidone pharmacokinetics

slow, complete absorption half life 8-12 hours induces hepatic enzymes

primidone toxicities

drowsiness nystagmus and ataxia only at excessive doses

in what diagnoses would you prescribe topiramate

partial seizures and GTCSs anti-migraine/migraine prophylaxis

mechanism of action of topiramate

increase Na channel inactivation inhibits kainate/AMPA receptors Enhances GABA

side effects of topiramate (topamax)

somnolence fatigue weight loss nervousness congnitive impairment

indication for use of lamotrigine (lamictal)

partial seizures GTCSs

mechanism of action of lamotrigine

increase Na channel inactivation inhibit release of amino acids by acting on voltage gated Ca channels (decrease Na and decrease Ca)

side effects of lamotrigine

rash- usually only in children

indication for zonisamide

broad spectrum absence, myoclonic, infantile spasms

mechanism of zonisamide

Na channel (decrease Na) acts on T-type voltage gated Ca channels (decrease Ca)

side effects of zonisamide

drowsiness, cognitive impairment, skin rashes no interaction with other AEDs

indication for gabapentin

adjunct therapy: focal seizures chronic pain management

mechanism of gabapentin

decreases Ca- binds to voltage gated Ca channels, decreases glutamate release (does not interact with GABA_Aas designed) (inhibits GABA-T but not at physiologic concentrations)

drug interaction of gabapentin

very few! cimetidine and aluminum/magnesium antacids

which drugs are the most effective anti-epileptics (think mechanism of action)

drugs that block transmitter release (drugs that affect Ca channels, Na channels, or vesicle fusion blocking)

indication for levetiracetam

partial seizures and GTCSs

mechanism of action of levetiracetam (keppra)

targets synaptic vesicle protein 2A (SV₂A) protein ligand inhibit calcium dependednt amino acid transmitters by interfering with vesicle fusion

side effects of levetriacetam

dizziness somnolence weakness dermatologic conditions behavioral changes in psych patients

drugs that enhance GABA transmission

vigabatrin benzodiazepines barbiturates

drugs that cause Na channel inactivation (6)

phenytoin carbamazepine lamotrigine primidone topiramate zonisamide

what type of drugs should you choose for absence seizures

ones that affect Ca channels they are associated with T-type Ca channels

Drugs that affect T-type Ca channels

valproate ethosuximide

indication for ethosuximide

absence seizures and myoclonic seizures

mechanism of ethosuximide

inhibits T-type Ca channel activity in thalamic neurons

pharmacokinetics of ethosuximide (zarontin)

not protein bound metabolized by microsomal enzymes

side effects of ethosuximide

gastric distress- pain, nausea, vomiting

indication of valproic acid (depakote)

absence, generalized, and complex partial seizures

mechanism of valproic acid

decrease Na and Ca increase GABA similar to phenytoin- blocks tetanic firing by increasing Na inactivation, reduce transmitter release reduce T-type Ca channel activity inhibits breakdown of GABA

pharmacokinetics of valproic acid

90% protein bound well absorbed half life 9-18 hours

side effects of valproic acid

nausea, vomiting, GI distress sedation hepatotoxicity

what should you give during pregnancy

lowest effective dose of a monotherapy drug withdrawal dangerous for fetus

what drugs should you consider in simple/complex PARTIAL seizures?

conventional: carbamazepine or phenytoin recently developed: gabapentin, topiramate, lamotrigine, levetiracetam

drugs to consider for generalized tonic-clonic

conventional agents: carbamzepine, phenytoin and valproic acid recently developed: gabapentin, topiramate, lamotrigine, lacosamide

what drugs to consider for absence seizures

conventional agents- ethosuximide and valproic acid recently developed- lamotrigine

what drugs to consider for myoclonic seizures

conventional: valproic acid or clonazepam recently developed: levetiracetam

what drugs to consider for status epilepticus

lorazepam, diazepam, fosphenytoin, phenytoin, or phenobarbital