module 3 anticonvulsants Flashcards
ethosuximide MOA
Ca channel inhibitor
blocks T-type Ca channels
ethosuximide AE
blood dyscrasias systemic lupus serious skin reactions slep disturbance aggressive psychosis mania GI upset N/V/D anorexia fatigue dizzy
ethosuximide administration
long half life
gabapentin MOA
Ca channel inhibitor
structural analog of GABA
blocks HAV Ca channels -> enhanced GABA-mediated inhibition
gabapentin use
not very effective for seizures
peripheral neuropathy
gabapentin AE
neuropsychiatric events DRESS somnolence CNS depression dizzy peripheral edema
gabapentin administration
short half life
gabapentin precaution
100% renally excreted
pregabalin MOA
Ca channel inhibitor
structural analog of GABA, more potent
blocks HVA Ca channels -> inc. GABA-mediated inhibition
pregabalin use
not very effective for seizures
peripheral neuropathy
pregabalin AE
neuropsychiatric events DRESS somnolence CNS depression dizzy peripheral edema angioedema
ezogabine MOA
K channel inhibitor
inc. transmembrane K currents, stabilize resting membrane potential
exogabine AE
BB: retinal abnml, potential vision loss urinary retention neuropsychiatric events QT prolongation CNS depression
benzodiazepines, clobazam, barbituates MOA
enhance GABA-mediated inhibition
- anticonvulsant
benzodiazepines, clobazam, barbituates AE
CNS depression
dependence: schedule IV drug
clobazam: serious skin reactions
vigabatrin MOA
structural analog of GABA
irreversibly inhibits enzyme GABA transaminase -> inc. GABA levels
vigabatrin AE
BB: permanent vision loss CNs depression anemia wt gain edema
vigabatrin administration
not significantly metabolized
renally eliminated
tiagabine MOA
inhibit GABA reuptake
tiagabine AE
cognitive/neuropsychiatric events
tiagabine precaution
hepatically metabolized
felbamate MOA
glutamate receptor inhibitor
inhibits NMDA receptor: inc. GABA activity
limits Na channel firing
felbamate AE
BB: acute hepatic failure, aplastic anemia
felbamate interactions
induces: 3A4
inhibits: 2C19
felbamate monitoring
liver
CBC
rufinamide MOA
may inhibit glutamate receptors
prolong inactive state of Na channels
rufinamide AE
CNS reactions
QT shortening
permapanel MOA
glutamate receptor inhibitor
noncompetitive AMPA-type glutamate receptor antagonist
permapanel AE
BB: serious pscyhiatric and behavioral reactions somnolence fatigue gait disturbance falls
permapanel precautions
hepatically metabolized
CYP3A4
schedule III drug
valproic acid and derivative MOA
mixed-action anticonvulsant
slows rate of Na channel recovery form inactivated state
limit T-type Ca channels
inc. GABA concentrations
valproic acid and derivative AE
BB: - hepatotoxicity - pancreatitis - fetal risk hematopoietic disorders hyperammonemia DRESS CNS depression GI s/s alopecia tremor
valproic acid and derivative precautions
preg
hepatically metabolized
protein bound: 80-90%
valproic acid and derivative monitoring
drug level: 50-100
CBC
liver
levetiracetam MOA
unknown
- inhibits burst firing w/out affecting nml excitability
- binds to synaptic vesicle protein SV2a
- opposes activity of negative modulators of GABA and glycine-gated currents
- partially inhibits N-type Ca channels
levetiracetam AE
behavior changes psychotic s/s somnolence fatigue hematologic abnml CNS depression irritability aggression
levetiracetam administration
protein bound: <10%
not extensively metabolized
66% renally excreted
topiramate MOA
mixed-action anticonvulsant
- blocks Na channels
- inc. GABA activity
- inhibit glutamate receptors
- inhibit carbonic anhydrase
topiramate AE
acute myopia angle closure glaucoma cognitive and neuropsychiatric AE oligohidrosis hyperthermia metabolic acidosis kidney stones
zonisamide MOA
blocks NA and T-type Ca channels
inhibits carbonic anhydranase
zonisamide AE
fatal sulfonamide reactions serious skin reactions hematological AE congitive and neuropscyhiatric AE oligohidrosis hyperthermia metabolic acidosis kidney stones
zonisamide interactions
hepatically metabolized: 3A4
