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MJ- Pharm Exam 3 > Anti-Seizure Drugs- GK > Flashcards

Anti-Seizure Drugs- GK Flashcards

1
Q

What is the difference between epilepsy & seizures? Describe the differences.

A

difference = duration of symptoms

Epilepsy: chronic, recurrent

Seizures: Finite, resolves

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2
Q

A transient disturbance of cerebral function due to an abnormal paroxysmal neuronal discharge in the brain.

What is this?

A

Seizure

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3
Q

Which drugs lower seizure threshold?

A
  • theophylline
  • alcohol
  • high dose phenothiazines (anti-psychotics)
  • antidepressants (esp bupropion)
  • street drugs
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4
Q

What is the goal of treatment with anti-seizure medication?

A
  • eliminate symptoms (seizures) with minimal side effects
  • complete seizure freedom
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5
Q

______-_____% of pts may not be free from seizures and seizure control must be balanced with ___goals

A

20-35

QOL

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6
Q

When do we initiate therapy?

A
  • no risk factors, normal MRI, normal EEG
  • if risk factors present
  • pts who have had 2 or more unprovoked seizures
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7
Q

Probability of a second seizure is less than 10% in the first year and approximately 21% by the end of 2 years

This is true for what type of pts?

A

pts with no risk factors, normal MRI, normal EEG

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8
Q

It is critical to establish an accurate diagnosis of the _________ and ________

A

seizure type

epilepsy classification

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9
Q

It is estimated that up to ____% of patients with epilepsy are nonadherent to medication.

A

60

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10
Q

T/F: Monotherapy is preferred for pts with seizures.

A

TRUE

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11
Q

When should you consider stopping pt on meds?

A

Factors favoring successful withdrawal of ADS:

  • seizure free period of 2-4 years
  • complete seizure control within 1 year of onset
  • onset of seizures between 2-35y/o

AND

normal neurologic examination and EEG

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12
Q

What are the 3 mechanisms of action of ASD?

A
  1. Modifies ionic conductance (Na+, Ca++, K+)
  2. dimunition of glutamatergic transmission ( dec excitatory)
  3. Enhancement of GABAergic transmission (inc inhibitory)
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13
Q

Glutamate is a ______ transmission

A

excitatory

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14
Q

GABA is a ______ transmission

A

inhibitory

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15
Q

The ultimate effect is to inhibit the local generation of seizure discharges by what 2 mechanisms?

A
  1. Reduce ability of neurons to fire action potentials at high rate
  2. reduce neuronal synchronization
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16
Q

Which drugs diminish glutamate release at the presynaptic cleft?

A
  • Phenytoin
  • fosphenytoin
  • carbamazepine
  • oxcarbazepine
  • eslicabazepine acetate
  • lamotrigine
  • lacosamide
  • ethosuximide
  • retigabine
  • levetiracetam
  • brivaracetam
  • gabapentin
  • gabapentin enacarbil
  • pregabalin
  • perampanel
  • valproate
  • felbamate
  • adrenocorticotropin

POSSIBLY

  • topiramate
  • zonisamide
  • rufinamide
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17
Q

Which drugs act on the voltage gated Na+ channels at the presynaptic cleft?

A
  • phenytoin
  • carbamazepine
  • lamotrigine
  • lacosamide

POSSIBLY

  • topiramate
  • zonisamide
  • rufinamide
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18
Q

Which drug acts on the voltage gated Ca++ channels (T-type) at the presynaptic cleft?

A

ethosuximide

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19
Q

Which drug acts on the voltage gated K+ channels at the presynaptic cleft?

A

Retigabine (ezogabine)

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20
Q

Which drug inhibits the release of glutamate by binding to SV2A?

A

Levetiracetam

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21
Q

Which drugs inhibit the release of glutamate by binding to the a2S subunit of P/Q type Ca++ channel?

A

gabapentin, pregabalin

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22
Q

Which drug targets the post-synaptic ionotropic glutamate receptor AMPA?

A

PerAMPAnel

Perampanel

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23
Q

What drugs with a mixed/unknown MOA target the post-synaptic receptors?

A
  • Valproate
  • felbamate
  • topiramate
  • zonisamide
  • rufinamide
  • adrenocorticotropin
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24
Q

Which drugs enhance GABA inhibition?

A
  • Phenobarbital
  • primidone
  • benzodiazapines (diazepam, lorazepam, clonazepam)
  • tiagabine
  • vigabatrine

POSSIBLY

  • topiramate
  • felbamate
  • ezogabine
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25
Q

Which drugs enhance GABA by working on the GABAa receptor?

A
  • phenobarbital
  • primidone
  • benzodiazipines

POSSIBLY

  • topiramate
  • felbamate
  • ezogabine
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26
Q

Which drug enhances GABA by working on (blocking) the GAT-1 GABA transporter?

A

Tiagabine

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27
Q

Which drug enhances GABA by working on (blocking) GABA transaminase?

A

Vigabatrin

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28
Q

When GABA interacts at two sites between alpha and beta subunits, what channel does it trigger?

A

Triggers chloride channel opening

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29
Q

Between what sites do benzos bind at?

A

between alpha and gamma subunits

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30
Q

When benzos bind at a single site between alpha and gamma subunits, this facilitates the opening of the _____________.

Which benzos specifically?

A

chloride ion channel

Diazepam, Lorazepam

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31
Q

__________ is a benzo antagonist

A

flumazenil

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32
Q

Binding sites of benzos are distinct from those of the ________

A

barbituates

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33
Q

What 3 drugs can treat a newly diagnosed generalized absence?

A
  • ethosuximide
  • lamotrigine
  • valproic acid
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34
Q

What drugs can be used as alternatives for refractive absence?

A
  • clonazepam
  • topiramate
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35
Q

T/F: gabapentin is ineffective for new diagnosed generalized absence

A

TRUE

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36
Q

Ethosuximide MOA

A

blocks voltage gated Ca++ channels (T-type)

decreases glutamate

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37
Q

Clinical Application of Ethosuximide

A

Generalized absence

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38
Q

P-kinetics and interactions of Ethosuximide

A

long half-life

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39
Q

ADE of Ethosuximide

A

Headache

Blood dyscrasias

GI distress

HA

Ataxia

Drowsiness

Rash

Chronic: behavior changes

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40
Q

Lamotrigine MOA

A

Blocks voltage gated Na+ channels

decreases glutamate

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41
Q

Lamotrigine Clinical applications

A

generalized absence

generalized tonic-clonic

focal aware/impare

focal or generalized myoclonic

42
Q

Lamotrigine has many ______

A

drug interactions

43
Q

Lamotrigine ADEs

A

**Box warning: serious skin rash- start low & go slow

**Diplopia

HA

dizziness

hemophagocytic lymphohistiocytosis (HLH)

44
Q

Valproate/ Valproic Acid MOA

A

mixed/unknown

increased GABA

or

enhances GABA action

or

mimics at post synaptic receptors

45
Q

Valproate/Valproic Acid Clinical Applications

A

generalized tonic-clonic

generalized absence

focal aware/impaired

focal/generalized myoclonic

46
Q

Valproate/Valproic Acid ADEs

A

hepatotoxicity, teratogenic, pancreatitis, alopecia

47
Q

Clonazepam MOA

A

enhance GABA-A receptor responses

48
Q

Clonazepam clinical applications

A

generalized absence

focal/generalized myoclonic

infantile spasms

49
Q

Clonazepam P-kinetics/ interactions

A

>80% availability

50
Q

Clonazepam ADEs

51
Q

Topiramate MOA

A

mixed/unknown

AMPA receptor inhibitor

possibly blocks VG-Na+

enhances GABA activity

52
Q

Topiramate Clinical Applications

A

generalized absence

generalized tonic-clonic

focal aware/impaired

migraine

53
Q

Topiramate P-kinetics/interactions

A

both hepatic and renal clearance

54
Q

Topiramate ADEs

A

Cognitive slowing

confusion

sleepiness, GI sx, metabolic acidosis, pregnancy cat D

55
Q

Which 4 drugs do you want to avoid in tx of absence seizures?

A

carbamezapine

vigabatrin

gabapentin

tiagabine

56
Q

What 2 meds are ineffective in tx of absence seizures?

A

Phenytoin

Phenobarbital

57
Q

What are the 4 FDA approved meds to treat tonic-clonic seizures?

A

Lamotrigine

Levatriacetam

Perampanel

Topiramate

“The FDA Lama Levetated Per Toby’s request”

58
Q

What happens during the tonic phase of the generalized tonic-clonic seizure?

A
  • epileptic cry
  • cyanosis
  • incontinence
  • generalized stiffening of body and lumbs, back arched
59
Q

What happens during the Clonic phase of the generalized tonic-clonic seizure?

A
  • salivary frothing
  • cyanosis
  • eyes blinking
  • clonic jerks of limbs, body and head
60
Q

What takes place during the post-ictal confusional fatigue phase?

A

limbs and body limp

61
Q
  • LOC/fainting 30 sec- 5 min
  • general muscle contraction and rigidity 15-20 sec
  • violent rhythmic muscle contraction and relaxation
  • biting the cheek/tongue, clenched teeth/jaw
  • incontinence
  • stopped breathingor difficulty breathing during seizure
  • cyanosis

What kind of seizure does this describe?

A

Generalized tonic-clonic seizure

62
Q

What was given historically to pts who experienced generalized c-t seizures?

A

Phenytoin

carbamezapine

phenobarbital

valproid acid

63
Q

Levetiracetam MOA

A

Blocks synaptic release machinery (SV2A)

decreases glutamate

64
Q

Levetiracetam Clinical app

A

generalized t-c

focal aware/impaired

65
Q

Levetiracetam has minimal drug interactions

T/F?

66
Q

Levetiracetam ADEs

A

Behavioral problems

HA

sedation

seizures-focal onset

weakness

67
Q

Carbamezapine MOA

A

Blocks V-G Na+ channels

decreases glutamate

68
Q

Carbamezapine Clinical applications

A

generalized tonic-clonic

focal aware/imparied

69
Q

Carbamezapine P-kin and interactions

A

many drug interactions

induces own metabolism

70
Q

Carbamezapine ADEs

A

_***Box warning:_ serious derm rxns & HLA-B* 1502 allele (TEN; SJS) in Asians

Aplastic anemia & agranulocytosis

Ataxia

Diplopia

Hyponatremia

Metabolic Bone Disease (MBD) (Vit D and Ca++)

71
Q

What is an alt to carbamezapine that you can use for focal onset seizures?

What is diff about this drug?

A

Oxcarbazepine

shorter 1/2 life

active metabolite

longer duration

fewer interactions reported

72
Q

Lacosamide MOA

A

Blocks voltage gated Na+ channels

dec glutamate

73
Q

Lacosamide Clinicall applications

A

Generalized t-c seizures

focal aware/impaired

74
Q

Lacosamide ADE

A

small increase in PR interval

dizziness

headache

nausea

75
Q

Phenytoin MOA

A

blocks voltage gated Na channels

dec glutamate

76
Q

Phenytoin Clinical app

A

Gen t-c

focal aware/impaired

77
Q

Phenytoin p-kin and interactions

A

_***Box warning: CV risk w/rapid infusion_

variable absorption, dose-dependent elimination, protein binding, many drug int.

78
Q

Phenytoin ADE

A

ataxia

nystagmus

gingival hyperplasia

hirsutism

neuropathy

folate deficiency

MBD

79
Q

Phenobarbital MOA

A

Enhances GABAa receptor responses

80
Q

Phenobarbital Clinical app

A

gen t-c

focal aware/impaired

81
Q

Phenobarbital p-kin and interactions

A

long 1/2 life

inducer of P450

many interactions

82
Q

Phenobarbital ADEs

A

sedation

intellectual blunting

MBD

behavior changes

ataxia

83
Q

Gabapentin MOA

A

blocks synaptic release machinery A2S

dec glutamate

84
Q

Gabapentin Clinical applications

A

gen t-c

focal aware/impaired

85
Q

Gabapentin p-kin and interactions

A

variable bioavailability

renal elimination

86
Q

Gabapentin ADEs

A

ataxia

somnolence

weight gain

dizziness

87
Q

What are the 6 FDA approved drugs for Focal onset (partial) seizures?

A

Carbamazepine

Lacosamide

Phenobarbital

Phenytoin

Topiramate

Valproic Acid

“Carbs lack phenophen topval”

88
Q

What 3 drugs can be used in focal onset (partial) seizures as refractory monotherapy or adjunct?

A

Pregabalin

Vigabatrin

Perampanel

89
Q

Pregabalin MOA

A

Blocks synaptic release machinery A2S

decreases glutamate

90
Q

Pregabalin Clinical app

A

focal aware/impaired

91
Q

Pregabalin P-kin and interactions

A

renal elimination

92
Q

Pregabalin ADEs

A

ataxia

somnolence

weight gain

dizziness

93
Q

Vigabatrin MOA

A

GABA transaminase enhancing GABA activation

94
Q

Vigabatrin clinical app

A

focal aware/impaired

95
Q

Vigabatrin p-kin and interactions

A

renal elimination

96
Q

Vigabatrin ADEs

A

_**Box warning: permanent vision loss_

drowsiness, dizziness, psychosis, ocular effects

97
Q

MOA: blocks postsynaptic ionotropic glutamate receptors AMPA, dec glutamate

Clinical app: focal aware/impaired

P-kin: multiple metabolites with long 1/2 lifes

Interactions: substantial, with increased clearance caused by CYP3A

What drug?

A

Perampanel

98
Q

What drugs would you use for myoclonic seizures?

A

FDA approved:

levatriacetam

Alt:

Clonazepam

Topiramate

Valproic Acid

Zonisamide

99
Q

Drugs with minimal or rare interactions

A

Gabapentin

Levetiracetam

Pregabalin

Vigabatrin

MJ- Pharm Exam 3 (17 decks)

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