Epileptic Drugs

Question 1

Three basic MOAs of antiepilieptics

Answer 1

Promote inactivated states of Na+ channels, enhancement of GABA inhibition (pre or post synaptic), and inhibition of Ca+2 channels

Question 2

What MOA is exploited in absence seizures

Answer 2

Inhibition of Ca+2 channels

Question 3

Common ADE of antiepileptics

Answer 3

Suicidal ideation (1-24 wks after starting)

Question 4

What is the common practice in regards to an antiepileptic drug regimen?

Answer 4

Start one. Doesn’t work= try different. Doesn’t work= polypharmacy

Question 5

Route of admin

Answer 5

Oral

Question 6

Which ones have protein binding

Answer 6

Valproate and phenytoin

Question 7

Where are they metabolized?

Answer 7

Hepatic and urinary

Question 8

Long or short half lives with antiepileptics

Answer 8

Long

Question 9

Azns of what genotype should be weary of developing Stevens-Johnson

Answer 9

HLA-B1502

Question 10

The abrupt discontinuation of antiepileptics can cause what?

Answer 10

status epilepticus (increased freq of seizures)

Question 11

Which Na+ channel inhibitors show zero-order kinetics

Answer 11

Pheytoin and fosphenytoin

Question 12

T/F: Phenytoin induces CYPs

Answer 12

T

Question 13

ADE of phenytoin and fosphenytoin

Answer 13

Gingival hyperplasia, dermatologic effects, hirtuism, nystagmus, headache

Question 14

Which Na+ channel inhibitor has a BBW of agranulocytosis?

Answer 14

Carbamazepine

Question 15

Which Na+ channel blocker upregulates its own metabolism and thus must be dose regulated?

Answer 15

Carbamazepine

Question 16

Cat X Na+ channel blocker

Answer 16

Valproic acid

Question 17

ADEs of Valproate

Answer 17

Heme (thrombocytopenia and increased INR), CNS affects (somnolence), Nausea, hepatotox

Question 18

Na+ channel blockers that causes parasthesia and vision slowing

Answer 18

Topiramate

Question 19

2 weak carbonic anhydrase inhibitors

Answer 19

Topiramate and Zonisamide

Question 20

Special MOA of topiramate

Answer 20

Block Na channels and increase GABA and decrease glutamate

Question 21

Na+ blocker with ADE of dizziness, headache and diplopia

Answer 21

Lacosamide

Question 22

Special thoughts about lamotrigine (Na+ blocker)

Answer 22

BBW for serious rash and no effects on CYP

Question 23

Na+ blocker that may increase K efflux and block Ca channels as well

Answer 23

Oxycarbazepine

Question 24

Topiramate and Zonisamides affects on carbonic anhydrase can lead to what?

Answer 24

Renal stones and acidosis

Question 25

Na+ blocker that accumulates in RBCs and can cause anorexia

Answer 25

Zonisamide

Question 26

Gaba potentiator that has BBW for anemia and hepatic dx

Answer 26

Felbamate

Question 27

GABA potentiators used in epileptics

Answer 27

Clonazepam, phenobarbitol and felbamate

Question 28

Ca+ blockers used in epileptics

Answer 28

Gabapentin, pregabalin, and ethosuximide

Question 29

MOA of gabapentin and pregabalin specifically

Answer 29

Decrease alpha-1-delta-1 subunit on calcium channels

Question 30

Ca channel blocker with ADE affecting GI

Answer 30

ethosuximide

Question 31

Antiepileptic drug that has an MOA of URTI

Answer 31

levetiracetam

Question 32

Lamotrigine, carbamazepine, levetiracetam, oxcarbazepine are DOC for what type of seizures

Answer 32

Partial and secondary

Question 33

Valproate, lamotrigine, and levetiracetam are DOC for what type of seizures?

Answer 33

Tonic-clonic

Question 34

DOCs for absence seizures

Answer 34

Valproate and ethosuximide

Question 35

What do you immediately give in status epilepticus

Answer 35

IV lorazepam

Question 36

DOCs for myoclonic and atonic seizures

Answer 36

Valproate, lamotrigine, and levatiracetam

Question 37

SJS is not reported in what two drugs

Answer 37

Clonazepam and lacosamide

Question 38

Three drugs with blood tox

Answer 38

Lamotrigine, felbamate, valproate

Question 39

Five teratogens

Answer 39

Lamotrigine, carbamazepine, pheytoin, topiramate, phenobarbital, valproate