anti-epileptics Flashcards Preview

Pharmacology - Exam 2 > anti-epileptics > Flashcards

Flashcards in anti-epileptics Deck (62)
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1

mechanisms of anti-epileptics (5)

inactivate Na channels

inactivate Ca channels

reduce synaptic vesicle fusion

modulate glutamate receptors

modulate gaba receptors

2

pathophysiology of epilepsy

too much excitation or too little inhibition

3

are there increased or decreased levels of glutamate during seizures

increased

4

what is the ionotropic receptor type for GABA?

GABAA

5

what is the metabotropic receptor type for GABA

GABAB

6

targets of anti-epileptic drugs

glutamate- decrease activity at receptors

increase activity of GABA at receptors

Increase release of GABA

Inhibit breakdown of GABA

7

first line for treating status epilepticus

benzodiazepines: diazepam (valium), lorazepam (ativan)

8

first line of drug for absence seizures

ethosuximide

valproic acid

9

mechanism of benzodiazepines

increase affinity of GABA for the GABAreceptor

10

where are benzodiazepines metabolized

liver

11

side effects of benzodiazepines

sedative

withdrawal symptoms due to tolerance

 

12

mechanism of vigabatrin

inhibit GABA-T to reduce GABA breakdown

13

indication for vigabatrin (sabril)

complex partial seizures that are refractory to several others AEDs

infantile spasms

14

drug interaction of vigabatrin

reduces plasma concentration of primidone

15

side effects of vigabatrin

concentric visual field deficit (can be irreversible)

drowsiness

dizzinesss

weight gain

16

what is carbamazepine indicated for

focal seizures and GTCSs

17

mechanism of carbamazepine

block tetanic firing

increases Na channel inactivation, reduces transmitter release

potentiates GABA response

18

what is carbamazepine used for other than seizures

bipolar disorder 

19

carbamazepine toxicities

ataxia, diplopia, nystagmus, dizziness

tolerance to side effects

aplastic anemia

rash- Stevens Johnson Syndrome, Toxic Epidermal Necrolysis

20

what drugs should never be used with carbamazepine

drugs that inhibit hepatic metabolism- increases toxicity

21

mechanism of phenytoin (dilantin)

blocks tetanic firing

increases Na channel inactivation

releases neurotransmitter release

22

indication for phenytoin

focal seizures and GTCSs

status epilepticus

23

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

24

side effects of phenytoin

cardiac arrhythmias

dizziness

nystagmus

headaches

rash

gingival hyperplasia and hirsutism

25

mechanism of primidone (mysoline)

similiar to phenytoin- increase Na channel inactivation

notable mention- phenobarbital is a metabolite (enhances GABAA receptor activity) but this is not thought to be part of the mechanism of action 

26

what disorder is treated with primidone

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

27

primidone pharmacokinetics

slow, complete absorption

half life 8-12 hours

induces hepatic enzymes

28

primidone toxicities

drowsiness

nystagmus and ataxia only at excessive doses

29

in what diagnoses would you prescribe topiramate

partial seizures and GTCSs

anti-migraine/migraine prophylaxis

30

mechanism of action of topiramate

increase Na channel inactivation

inhibits kainate/AMPA receptors

Enhances GABA