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Flashcards in Anticonvulsants Deck (60)
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1

4 ways to treat seizures

1. Blockade of excitatory input
2. Strengthening of inhibitory input (GABA)
3. Block Na channels
4. Block thalamic Ca channels

2

Block hyper-excitability by:

Elevate threshold for stimuli
Limit propagations discharged

3

Blockage of Na channel activation does what

Reduces the ability of Na channels to recover from inactivation to inhibit constant firing and increases threshold potential

4

Blocking of Ca channel does waht

ABSENCE SEIZURES
Reduces firing of thalamic neurons which are involved in cortical discharge and NT release (**)

5

Activation of GABA(A) leads to

Increase inflow of Cl and inhibit post-synaptic cells

6

GABA transmission can be enhanced by

block of GAT1 transporter and increase concentration in cleft

7

Antagonists of NMDA and AMPA glutamate receptors do what

Anticonvulsant activity bc glutamate is an excitatory NT

8

PD Properties of Classical AEDs

Narrow therapeutics
CNS depression (valproic is the least sedatative)
Hypersensitivity and hematotoxicity rxns
Teratogenicity and can cause unplanned pregnancy
Long half life
Multiple times a day dosing
Increased risk of osteoporosis bc interfere with Vit D metabolism

9

Induction of P450

Phenobarbital
Phenytoin
Carbamazepine

10

Inhibition of P450

Valproic acid

11

Phenytoin

Dilantin

12

Phenytoin MOA

Slows the rate of recovery of Na channels from inactivation

13

Phenytoin treats

Partial and tonic-clonic seizures

14

Water soluble form of phenytoin

Fosphenytoin

15

Phenytoin Elimination

Halflife increases with dose increase but concentration disproportinately increases with dose increases

16

Phenytoin down sides

Metabolized by CYP so many drug interactions

17

Phenytoin AE

CNS depression
Gingival hyperplasia
Inhibits release of ADH and insulin so hyperglycemia and glycosuria

18

Carbamazepine

Tegretol

19

Carbamazepine MOA

Slows the rate of recovery of Na channels from inactivation

20

Carbamazepine treates

Partial and tonic clonic

21

Down sides to carbamazepine

Induces its own metbaolism
Decreased halflife after chronic therapy
Active metabolites
Induces 2C, 3A, UGT

22

Carbamazepine AE

Acute toxication (stuper, coma)
Long term: drowsiness, vertigo, ataxia
SJS and necrolysis

23

Ethosuximide

Zarontin

24

Ethosuximide MOA

Blocks T type Ca channels in thalamus

25

Ethosuximide treats

absence seizures

26

Ethosuximide Metabolism

Liver
Few drug drug interactions

27

Ethosuximide AE

GI and CNS

28

Valproic acid

Depakene

29

Valproic acid MOA

Na blocker
Ca blocker
Enhances GABA

30

Valproic acid treats

Partial
Generalized epilepsies
Absence and myoclonic seizures