Antiseizure Quick Deck

Question 1

MOA: Stabilizes “inactivated” state of VG Na+ channels&raquo_space; decrease in repetitive firing

Answer 1

Carbamazepine

Question 2

Clinical Use: Partial/focal and secondarily generalized tonic-clonic seizures

Answer 2

Carbamazepine

Question 3

MOA: Blocks VG T-type dependent Ca2+ channel  disrupts pacemaker activity

Answer 3

Ethosuximide

Question 4

Clinical Use: Primary tx for absence seizures

Answer 4

Ethosuximide

Question 5

MOA: Prolongs Inactivation phase of VG Na+ channels  prevents rapid firing of AP (also see decreased GLUT)

Answer 5

Phenytoin

Question 6

Clinical Use: Partial/secondarily generalized tonic-clonic seizures

Answer 6

Phenytoin

Question 7

MOA: Increased inactivation of VG Na+ channels, blocks presynaptic VG Ca2+ channels (N, P/Q), enhances GABAA R currents, limits activation of AMPA-kainate subtypes of GLUT R

Answer 7

Topiramate

Question 8

Clinical Use: Focal and primarily generalized tonic-clonic seizures

Answer 8

Topiramate

Question 9

MOA: Decreases repetitive firing (multiple mechanisms)

Blocks VG Na+ & NMDA R, decreases GABA reuptake (GAT1), reduces flow of Ca2+ through T-type Ca2+ channels

Answer 9

Valproic Acid

Question 10

Clinical Use:Works for most!! Drug of choice for primarily generalized tonic-clonic seizures – complex partial/absence/myoclonic/atonic seizures, photosensitive epilepsy, juvenile myoclonic epilepsy

Answer 10

Valproic Acid

Question 11

Increases DURATION of GABAA R opening + depresses excitatory GLUT actions (binds to AMPA

Answer 11

Phenobarbital

Question 12

Increases FREQUENCY of GABAA R opening

Answer 12

Diazepam, Lorazepam

Question 13

Inhibits VG Ca2+ channels  decreases Ca2+ entry

Answer 13

Gabapentin