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Pharmacology > Anti-Epileptics > Flashcards

Anti-Epileptics Flashcards

1
Q

Screening test for Absence seizure drugs

A

Pentylenetetrazol

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2
Q

Screening test for GTCS and complex partial seizure drugs

A

Maximal Electroshock Test

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3
Q

MOA of drugs identified by Maximal Electroshock Test

A

prolonged inactivation of VG Na channels

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4
Q

Drugs that inhibit presynaptic glutamate VG Na channels

A

Lancosamide
Lamotrigine
Carbamezapine
Phenytoin

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5
Q

Drugs that inhibit presynaptic glutamate VG Ca channels

A

Ethosuximide
Lamotrigine
Pregabalin
Gabapentin

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6
Q

Drugs that inhibit presynaptic glutamate K channels

A

Retigabine

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7
Q

Drugs that inhibit glutamate SV2A (synaptic vesicle protein)

A

Levetiracetam

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8
Q

Drugs that inhibit presynaptic glutamate CRMP-2

A

Lacosamide

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9
Q

Drugs that inhibit postsynaptic glutamate AMPA receptors

A

Phenobarbital
Topiramate
Lamotrigine

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10
Q

Drugs that inhibit postsynaptic glutamate NMDA receptors

A

Felbamate

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11
Q

Drug that inhibits GAT-1

A

Tiagabine

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12
Q

Drug that inhibits GABA-T

A

Vigabatrin

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13
Q

Drugs that act on GABAa receptors

A

Benzo & Phenobarbital

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14
Q

MOA of tiagabine

A

Inhibits GABA reuptake by blocking GAT-1

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15
Q

MOA of vigabatrin

A

Prolongs GABA half life by blocking degradation via GABA-T

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16
Q

Hallmark of simple partial seizure

A

presevation of consciousness

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17
Q

Usual location of complex partial seizure

A

bilateral limbic system

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18
Q

Hallmark of complex partial seizure

A

automatism

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19
Q

Feature of secondarily generalized seizure

A

Amnestic

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20
Q

Length of tonic phase of GTCS

A

15-30sec

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21
Q

length of clonic phase of GTCS

A

60-120 sec

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22
Q

Seizure type with sudden onset and abrupt cessation

A

Petit mal (absence)

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23
Q

Duration of Absence seizures

A

10-45 sec

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24
Q

Age of onset of absence

A

childhood or adolesence

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25
Q

EEG findings of absence

A

2.5-3.5Hz spike and wave pattern

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26
Q

Presentation of atonic seizure

A

sudden loss of postural tone

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27
Q

Basis of epileptic treatment

A

empiric seizure classification

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28
Q

When is multipple drug therapy needed?

A

when two or more types of seizure occur in the same patient

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29
Q

How to discontinue anti-epileptics

A

reduce dose gradually

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30
Q

Most common cause of failure of therapy

A

faulty compliance

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31
Q

N substitution of heterocyclic ring

A

hydantoin

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32
Q

CN substitution of heterocyclic ring

A

Barbiturates

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33
Q

O substitution of heterocyclic ring

A

Oxazolidinedione

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34
Q

C substitution of heterocyclic ring

A

Succinamides

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35
Q

NH2 substitution of heterocyclic ring

A

Acetylureas

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36
Q

Conventional drugs used for all partial seizures and GTCS

A

Carbamenzapine, Phenytoin, Valproate

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37
Q

Conventional drugs for Absence

A

Ethosuxamide, Valproate

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38
Q

Conventional drug for myoclonic seizure

A

Valproate

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39
Q

Structure of phenytoin

A

diphenolhydantoin

2 phenols + hydantoin (N)

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40
Q

Substitution responsible for sedation

A

alkyl

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41
Q

Major MOA of phenytoin

A

block presynaptic VG Na channels in inactive state

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42
Q

reason for use dependent effect of phenytoin

A

preferential binding to and prolongation of inactivated state of VG Na channel

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43
Q

Presynaptic effects of phenytoin

A

decrease glutamate release

inscrease GABA release

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44
Q

Amount of absorption of phenytoin salt in GI tract

A

almost complete

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45
Q

Therapeutic levels of Phenytoin

A

10-20 mcg/mL

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46
Q

Oral therapy dose for adults (Phenytoin)

A

start at 300mg/day

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47
Q

Relationship between phenytoin dose and plasma concentrations

A

Non-linear (metabolism is saturable)

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48
Q

Why is Phenytoin not recommended to be given IM

A

drug precipitation in muscle occurs & unpredictable absorption

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49
Q

Drug interaction of Pheytoin

A

Enzyme INDUCER

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50
Q

Most common ADR of Phenytoin

A

diplopia and ataxia

gingival hyperplasia and hirsutism (less common)

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51
Q

ADRs of long term use of phenytoin

A

Coarsening of facial features, mild peripheral neuropahty, osteomalacia

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52
Q

Prodrug of Phenytoin

A

Fosphenytoin

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53
Q

Advantage of Fos phenytoin over phenytoin

A

more soluble

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54
Q

Fosphenytoin IV indication

A

convulsive status epilepticus

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55
Q

DOC for convulsive status epilepticus

A

Fosphenytoin IV

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56
Q

Sites of accumulation of Fosphenytoin

A

brain, liver, muscle, and fat

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57
Q

CSF concentration of Fosphenytoin

A

CSF concentration proportionate to free plasma level

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58
Q

After therapeutic level of drug is attained, how will small rises in drug level affect patient’s physiologic response?

A

toxicity symptoms due to saturation of metabolism

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59
Q

Toxicity of rapid IV push Fosphenytoin

A

cardiac arrhythmias

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60
Q

Moeity in carbamazepine structure

A

ureide

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61
Q

Indications of Carbamazepine

A

Trigeminal neuralgia

Neuropathic pain
Manic-depressive pX

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62
Q

Anti-epileptic drug used for trigeminal neuralgia

A

Carbamanzepine

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63
Q

AED drug similar to imipramine and other anti-depressants

A

Carbamazepine

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64
Q

MOA of carbamazepine

A

block presynaptic VG Na channels in inactive state

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65
Q

Is carbamazepine sedating?

A

No carbamazepine is not sedating

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66
Q

Drug interaction of Carbamanzepine

A

Enzyme INDUCER

can increase metabolism of Primidone, Phenytoin, Ethosuximide, Valproic Acid, Clonazepam

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67
Q

Active metabolite of carbamanzepine

A

Carbamazepine-10,11-epoxide

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68
Q

Therapeutic level where you may experience diplopia with carbamazepine

A

7mcg/mL

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69
Q

Drug interaction of Valproic Acid

A

Enzyme Inhibitor

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70
Q

Drug interaction of Phenobarbital

A

Enzyme INDUCER

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71
Q

Most common dose-related ADR of Carbamazepine

A

Diplopia and ataxia

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72
Q

Most common idosyncratic ADR of carbamazepine

A

erythematous skin rash

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73
Q

Most fatal idosyncratic ADRs of carbamazepine

A

blood dyscrasias, aplastic anemia, agranulocytosis within 4 months of treatment

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74
Q

Recommended action for carbamazepine toxicity

A

careful monitoring rather than discontinuation (unless persistent)

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75
Q

Benefit of Oxcarbazepine over carbamazepine

A

improved toxicity profile

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76
Q

Other dose-related ADRs of carbamazepine

A

mild GI upset
Hyponatremia
H2O intoxication

77
Q

Metabolite of Oxcarbazepine

A

Eslicarbazepine both R- and S+ form (excreted as gluconoride)

78
Q

Chirality of Eslicarbazepine

A

S+ enantiomer

79
Q

Toxicity profile of oxcarbazepine

A

less hypersensitivity

Hyponatremia is more common

80
Q

Indication for Eslicarbazepine Acetate (ESL)

A

adjunct or monotherapy for partial onset seizure

81
Q

drug that has autoinduction (enzyme inducer of itself)

A

carbamazepine

82
Q

ADR of eslicarbazepine acetate

A

headache, dizziness, nausea

Rare: hyponatremia, hypersensitivity, suicidal ideation (stronger in carbamazepine and oxcarbazepine)

83
Q

Drug with effect on oral contraceptives (and it’s effect)

A

Eslicarbazepine

decreases ethinylestradiol and levonorgestrel

84
Q

Metabolite of eslicarbazepine acetate (ESL)

A

Eslicarbazepine S+ only

85
Q

Metabolite of Fospheytoin

86
Q

Most potent between carbamazepine, oxcarbazepine, and eslicarbazepine?

A

carbamazepine (also most ADRs)

87
Q

Oldest non-sedative AED

88
Q

Oldest of the current AED

A

Phenobarbital

89
Q

Is phenobarbital sedating?

A

Yes phenobarbital is sedating

90
Q

When is phenobarbital a DOC

A

in infants only

91
Q

DOC for infants

A

phenobarbital

92
Q

MOA of phenobarbital (in relation to GABA)

A

Binds to GABAa Receptor allosterically to keep it open LONGER
(increase GABA effect)

93
Q

What type of channel is GABAa

A

Cl- channel

94
Q

pH reading of phenobarbital

A

weak acid (therefore increased absorption when plamsa is acidic and decreased absorption if plasma is basic)

95
Q

Mephobarbital structure

A

methylated phenobarbital

96
Q

metharbital structure

A

methylated barbital

97
Q

Primidone structure

A

2-desoxyphenobarbital

98
Q

Metabolites of Primidone

A

Phenobarbital

Phenyethanolamide (PEMA)

99
Q

MOA of Primidone

A

block presynaptic VG Na channels in inactive state

100
Q

Prodrug of phenobarbital and Phenylethanolamide

101
Q

Most effective plasma level of Primidone

A

8-12mcg/mL

102
Q

third line drug for partial seizures (refractory cases)

103
Q

Indication for felbamate

A

third line for partial seizures (refractory)

Lennox-Gastaut syndrome

104
Q

MOA of felbamate

A

use-dependent block of NMDA receptor (post synaptic Glutamate receptor)

Potentiates GABA a Receptor

105
Q

Lennox Gastaut Syndrome

A

epilepsy with different types of seizures (mostly tonic and atonic)
usually impaired cognitive function
EEG slowing and spike wave burst less than 2.5 Hz

106
Q

Therapeutic effects of Gabapentin and Pregabalin

A

anti-seizure and analgesic

107
Q

MOA of Gabapentin and Pregabalin

A

bind to VG Ca channels (presynaptic Glutamate)

= decrease in glutamate secretion

108
Q

True of False Gabapentin and Pregabalin can act directly on GABA receptors

A

False they do not act directly on GABA receptors even if they are GABA analogs
but they may act indirectly to increase GABA release

109
Q

ADR of Gabapentin and Pregabalin

A

Somnolence, dizziness, headache, ataxia, tremors

110
Q

Are Gabapentin and Pregabalin sedating?

A

Yes they are sedating

111
Q

Drug interaction of Gabapentin

A

NO enzyme induction (negligable drug interactions)

112
Q

Indications for Gabapentin

A 
Adjunct for partial and generalized T-C seizures
Monotherapy (but in high doses)
Neuropathic pain (POST HERPETIC NEURALGIA)
113
Q

AED for post-herpetic neuralgia

A

Gabapentin

114
Q

Indications for Pregabalin

A

Adjunct for partial and generalized T-C seizures
Neuropathic pain (POST HERPETIC NEURALGIA, DM NEUROPATHY, FIBROMYALGIA)
Generalized Anxiety disorder

115
Q

1st drug approved for Fibromyalgia

A

Pregabalin

116
Q

AED that can be used for generalized anxiety disorder

A

Pregabalin

117
Q

MOA of Lacosamide

A

enhances SLOW inactivation of presynaptic glutamate VG Na channels (other AEDs prolong FAST inactivation)
Binds to presynaptic glutamate CRMP-2

118
Q

Chirality of Lacosamide

A

R(+) enantiomer

119
Q

indication fro Lacosamide

A

adjunct for patial seizures (w/ or w/o secondary generalization)

120
Q

Age to prescribe Lacosamide

121
Q

ADRs of Lacosamide

A

Dizziness, headache, Nausea, Diplopia

122
Q

Drug interaction of Lacosamide

A

NO induction/inhibition of enzymes (negligable drug interaction)

123
Q

MOA of Lamotrigine

A

Blockage of presynaptic glutamate VG Na channels

Inhibit presynaptic glutamate Ca channels

124
Q

Indication of Lamotrigine

A

Monotherapy: Partial seizures, Absence, myoclonic seizures, Lennox-Gastaut

Bipolar Disorder

125
Q

AED used for Bipolar disorder

A

Lamotrigine

126
Q

ADRs of Lamotrigine

A

Somnolence, dizziness, headache, Nausea, Diplopia

127
Q

Is lamotrigine sedating?

A

Yes it is sedating

128
Q

MOA of Levetiracem

A

binds selectively to the synaptic vesicular protein SV2A`

129
Q

Drug interaction of Levitiracem

A

NO induction/inhibition of enzymes (negligable drug interaction)

130
Q

Indication of Levetiracem

A

Adult: Partial seizure
Children: Primary GTCS and Juvenile Myoclonic seizure

131
Q

ADRs of Levetiracem

A

Somnolence, Dizziness, Ataxia, ASTHENIA

132
Q

Is levetiracem sedating

133
Q

MOA of Retigabine or Ezogabine

A

K channel facilitator via KCNQ gene

134
Q

Retigabine Indication

A

Partial seizure in adults

135
Q

ADRs of Retigabine

A

Somnolence, dizziness, confusion, blurred vision, DYSARTHRIA

136
Q

MOA of Tiagabine

A

inhibit GABA reuptake via GAT-1 inhibition

137
Q

Tiagabine indication

A

Primary GTCS

138
Q

ADRs of Tiagabine

A

Nervousness, dizziness, difficulty concentrating, DEPRESSION, tremor

139
Q

MOA of topimarate

A

blockade of VG Na channels

Blocks postsynaptic glutamate AMPA receptors

140
Q

Topimarate indication

A

Monotherapy: partial and genralized T-C seizure, Lennox Gastaut Seizure

141
Q

ADRs of Topimarate

A

Somnolence, dizziness cognitive slowing, nervousnessm fatigue, paresthesias

142
Q

MOA of Vigabatrin

A

Irreversibly inhibits GABA-T = inhibited degradation of GABA

143
Q

Effect of Vigabatrin of GABAa Receptors

A

Desensitization due to increased GABA levels and prolonged activation

144
Q

Indication of Vigabatrin

A

Partial seizures and infantile spasms

145
Q

Which is the active enantiomer of vigabatrin

146
Q

ADRs of Vigabatrin

A

WEIGHT GAIN, drowsiness, dizziness, peripheral visual field defects

147
Q

Structural substitution of ethosuxamide

A

Succinamide (C)

148
Q

Indication of ethosuxamide

A

pure petit mal drug

149
Q

Most commonly used petit mal drug

A

Ethosuxamide

150
Q

Compare Phensuxamide and Metgsuxamide with ethosuxamide

A

Phensuxamide: less effective
Methsuxamide: more toxic

151
Q

MOA of ethosixamide

A

Effect on presynaptic glutamate Ca channels

Reduce low threshold T-Type Ca current in thalamic neurons

152
Q

3 drugs for Absence seizure

A

Ethosuxamide & Valproate > Lamotrigine

153
Q

Structure of Valproic Acid and Sodium Valproate

A

Fatty carboxylic Acid

154
Q

Active form of Valproic Acid and Sodium Valproate

155
Q

at what pH is valproic acid fully ionized

A

body pH (therefore it turns into active form in the body – valproate)

156
Q

MOA of Valproate

A

Blocks Na currents
Block NMDA receptor mediated excitation

Inhibit GAT-1 (reuptake)
Facilitate glutamic acid decarboxylase (GABA synthesis)

157
Q

Indications of Valproate

A

BROADD
Preferred in absence over ethosux only if with concomitant GTCS
Myoclonic seizure (unique and very dramatic)

Bipolar Disorder
Migraine Prophylaxis

158
Q

AED effective for migrane prophylaxis

159
Q

Drug interaction of Valproate with phenytoin

A

Valproate + Phenytoin = displace phenytoin from plasma proteins

160
Q

ADRs of Valproate

A 
GIT disturbance (common dose-related)
Fine tremors (high levels)
WEIGHT GAIN, hair loss (uncommon)
Hepatotoxicity (Idiosyncratic)
TERATOGENIC (Spina bifida, CVS, orofacial, digital deformities)
161
Q

Trimethadione structural substitution

A

oxazolidinedione

162
Q

Indication of thrimethadione

A

PREVIOUS DOC for absence (replaced by ethosuxamide)

163
Q

active metabolite of themethadione

A

dimethadione

164
Q

MOA of trimethadione

A

raises threshold for seizure discharge after repetitive thalamic stimulation (Ca current)

165
Q

How do you supress absence seizures?

A

inhibiting pacemaker action of thalamic neurons (Ca current)

166
Q

ADRs of Trimethadione

A

Sedation

CI w/ pregnancy

167
Q

Indication of Diazepam

A

DOC for status epilepticus (IV)

168
Q

Limit of Diazepam use for seizure control

A

tolerance develops to oral meds (not useful for long term) and sedation

169
Q

Indication of Lorazepam

A

Status epilepticus IV

170
Q

Lorazepam benefits over Diazepam

A

more effective and longer acting then diazepam

Easier to administer in IV (water based)

171
Q

Indication for Clonazepam

A

Absence
Myoclonic seizure
Infantile spasms

(long acting and very potent)

172
Q

Indication for Nitrazepam

A

Myoclonic seizure

Infantile spasm

173
Q

Indication for clorazepate dipotassium

A

Adjunct for complex partial seizure in adults

174
Q

Less sedating benzodiazepam

175
Q

Active metabolite of clobazam

A

norclobazam

176
Q

MOA of Acetazolamide

A

carbonic acid anhydrase inhibitor

Depolarizing effect of bicarbonate ions in neurons via GABA R ion channes may be diminished

177
Q

Limiting factor to Acetazolamide use

178
Q

Indication for Acetazolamide use

A

women with seizure exacerbation during menstruation

179
Q

DOC for inflantile spasms

A

Vigabatrin

180
Q

Drugs that work on infantile spasms

A

IM corticotropin or oral prednisone
Benzos (clonazepam or nitrazepam)
Vigabatrin (DOC)

181
Q

Most common status epilepticus

A

GT-T status epilepticus

182
Q

Definitive therapy for statue epilepticus

A

phenytoin

Phenobarbital (if refractory to phenytoin)

183
Q

teratogenic effect of Phenytoin

A

fetal hydantoin syndrome

cleft lip/palate, congenital heart disease, slowed growth, mental deficiency

184
Q

Teratogenic effects of Valproate

A

Spina Bifida

185
Q

Drugs that are most difficult to discontinue

A

barbiturates and benzodiazepams (weeks-months)

186
Q

When do you try to discontinue drugs?

A

when patient has been seizure free for 3-4 years

187
Q

Most dangerous effect of AED

A

respiratory depression (potentiated by alcohol)

188
Q

Treatment for overdose

A

supportive
do not use stimulants
ALKALINIZE URINE

189
Q

3 drugs that can be used for all types of seizures

A

valproate, topiramate, lamotrigine

Pharmacology (2 decks)

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