Seizure pharm Flashcards
General strategies of seizure meds
- decrease excessive rates of neuronal dishcarge w/in a focus
- prevent propagation of siezure activity from focus to other brain regions
Basic mechanism of action for antiseizure drugs
Affect abnormal membrane fnx; changes in voltage-regulated ion channels leading to excess depolarization,
correct decreased inhibition (increase GABA fnx),
reduce excitation (block glutamate)
alters ion conductance, use dependent on Na chans, ≠generation of repetive AP by keeping inactivation gate closed = increased refractory period
Phenytoin
MOA of Phenytoin and PharmK
alters ion conductance, use dependent on Na chans, ≠generation of repetive AP by keeping inactivation gate closed = increased refractory period
*depend on formulation, HIGH protein bound, use 10-20 mg
what would you prescribe to someone with General Tonic-Clonic or Partial seizures that affecgts Na channels to keep them inactive
Phenytoin: for tonic-clonic or partial seizures
Why do we measure blood levels of pt on Phenytoin
bc it’s dose dependent drug: there is NON-linear releationhip btwn daily dose of drug and steady-state plasma conc btwn individuals; daily dose varies person to person
What side effects, specifically CNS are seen with PHenytoin use?
CNS is dose/depend= nausea, anorexia, apathy, sedation, nystagmus.
NOn-dose dependent= gingiva hyperplasia, hirsuitism, teratogenic, rash
MOA of Carbamazepine
Sim MAO phenytoin; blocks Na chans at therapeutic conc, no GABA interaction. Unpredictable absorption w/ hepatic enZ induction
best med for PARTIAL seizures, NOT absence (contraindicated)
Carbamazepine
Causes dose releated toxicity; diplopia, ataxia, GI, drowsiness, rare blood dyscarsias (no dose related)
Carbamazapine
What drug is teratogenic that can cause spina bifida?
Cabamazepine
Impaired consciousness w/ staring spells, w/ or w/out eye blinks
Absence seizure
seizure recurring so close together baseline consciousness is not regained btwn episodes
status epilepticus
First line for absence seizures
Ethosuximide
reduces low-threshold (T-type) Ca++ current in thalamic nucleus
Ethosuximide for absence seizures
PharmK in Ethosuximide
well absorbed after oral, not protein bound, dist to entire body, met by liver w/ long ½ life
Side effects and toxicity seen with Ehtosuximide use
Sides/toxicity: gastric distress and lethargy and fatigue
MOA of Valproic Acid
Blocks repetitive firing, reduce T type Ca++ currents, increase GABA conc
PharmK: plasma bound, distributes extracell, ≠metobolism phenobarbital/phenytoin, carbamazepine
Valproic Acid
When can we use Valproic acid as seizure tx
absence seizure w/ or w/out tonic-clonic, general tonic-clonic, partial, myoclonic
Side effects of valproic acid
GI, wt gain, hair loss, Hepatotoxic, teratogenic (spina bifida)
MOA of Felbamate
At clycine modulatory site on NMDA receptor; potentiates GABA,