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NMSP Week 1 > Pharmacology of Epilepsy (Segars) > Flashcards

Pharmacology of Epilepsy (Segars) Flashcards

1
Q

Membrane depolarization leads to?

A

1) Enhanced excitatory (glutamate) actions

2) Reduced inhibitor (GABA) function

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2
Q

Where do the anti-epileptic drugs (AED) that block the voltage-gated Na channels bind?

A

Interior side of voltage Na channel pore

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3
Q

When can AEDs access the pore in voltage-gated Na channels?

When can they not?

A

1) Activation gate is open

2) Activation gate is closed

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4
Q

What are examples of an AED Na channel blocker?

A

1) Lamotrigine
2) Carbamazepine (also other -azepine drugs)
3) Phenytoin
4) Topiramate
5) Valproic acid
6) Lacosamide (also other -amide drugs)

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5
Q

The probability of a Na channel blockade is proportional to?

A

Frequency of voltage Na channel opening and the dose

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6
Q

Lamotrigine, Carbamazepine, Phenytoin, Topiramate, Valproic acid, and Lacosamide have what effect on the state of Na ion channels?

Lacosamide can also have what effect on the state of voltage Na channels?

A

1) Prolong fast inactivation state of voltage Na channel

2) Enhance slow inactivation of the channel

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7
Q

What is the overall goal of blocking voltage gated Na channels?

A

Suppress excitatory (glutamate) actions

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8
Q

What are the AMPA receptor antagonists?

A

1) Topiramate (also a Na channel blocker)

2) Perampanel (has AMPA is name)

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9
Q

What is the overall goal of blocking AMPA receptors?

A

Suppress glutamate

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10
Q

What is the NMDA receptor antagonist?

A

Felbamate

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11
Q

What is the overall goal of blocking NMDA receptors?

A

Suppress glutamate

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12
Q

What channels mediate 3-Hz spike and wave activity in the thalamus?

This is a hallmark of what type of seizure?

A

1) T-type Ca2+ channels

2) Absence (petit mal) seizures

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13
Q

Antagonists of T-type Ca2+ channels target?

A

Cortex-thalamus oscillation

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14
Q

What drug is only used for absence seizures?

A

Ethosuximide

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15
Q

What are the antagonists of T-type Ca2+ channels?

A

1) Ethosuximide

2) Zonisamide (also a Na channel blocker)

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16
Q

What is the overall goal of blocking T-type Ca2+ channels?

A

Suppress glutamate

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17
Q

What drugs inhibit Synaptic Vesicle 2A (SV2A) protein?

A

1) Levetiracetam

2) Brivaracetam

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18
Q

What is the overall goal of blocking Synaptic Vesicle 2A (SV2A) protein?

A

Suppress glutamate

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19
Q

What drugs block the α2δ subunit of T-type Ca2+ channels?

A

1) Gabapentin

2) Pregabalin

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20
Q

What is the overall goal of blocking the α2δ subunit of T-type Ca2+ channels?

A

Suppress glutamate

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21
Q

What drug opens KCNQ K+ channels (pre-/post-synaptic)?

A

Ezogabine

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22
Q

What is the overall goal of opening the KCNQ K+ channels?

A

Suppress glutamate

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23
Q

What is the MOA of Topiramate and Perampanel?

A

AMPA receptor blockers

24
Q

What is the MOA of Ethosuximide and Zonisamide?

A

Ca2+ T-type Channel Blockers

25
Q

What is the MOA of Gabapentin and Pregabalin?

A

α2δ subunit Ca2+ Channel Blocker

26
Q

What is the MOA of Carbamazepine, Oxcarbazepine, Eslicarbazepine, Lamotrigine, Phenytoin, Rufinamide, Topiramate, Valproic acid, Lacosamide, and Zonisamide?

A

Na+ Channel Blockers

27
Q

What is the MOA of Felbamate?

A

NMDA Receptor Blockers

28
Q

What is the MOA of Levetiracetam and Brivaracetam?

A

Synaptic Vesicle 2A Protein Blockers

29
Q

What is the MOA of Ezogabine?

A

K+ Channel Openers

30
Q

When GABA(A) receptor is unoccupied what happens to the Cl- channel?

When it is occupied?

A

1) Closed

2) Opened

31
Q

What drug blocks the reuptake of GABA by blocking GAT-1 (GABA transproter-1)?

A

Tiagabine

32
Q

What drugs block the metabolism of GABA by blocking GABA-T (GABA Transaminase)?

A

1) Vigabatrin (Has GABA-T in name)

2) Valproic acid (also a Na channel blocker)

33
Q

What drugs increase GABA levels by stimulating GAD (glutamic acid decarboxylase)?

A

1) Valproic acid
2) Gabapentin (also blocks the α2δ subunit of T-type Ca2+ channels)
3) Pregabalin (also blocks the α2δ subunit of T-type Ca2+ channels)

34
Q

Tiagabine, Vigabatrin, Valproic acid, Gabapentin, and Pregabalin all act on what side of GABA-ergic Transmission?

A

Pre-Synaptic

35
Q

What is the MOA of Vigabatrin and Valproic acid?

A

GABA promoting agents by GABA-T inhibition

36
Q

What is the MOA of Tiagabine?

A

GABA promoting agent by GAT-1 inhibition

37
Q

What is the MOA of Valproic acid, Gabapentin, and Pregabalin?

A

GABA promoting agents by GAD stimulation

38
Q

Barbiturates, Benzodiazepines, and Topiramate all act on what side of GABA-ergic Transmission?

A

Post-Synaptic

39
Q

What happens when benzodiazepines bind to a distinct allosteric site?

A

Potentiate GABA binding causing Cl- channels to open with greater frequency

40
Q

What happens when barbiturates bind to a distinct allosteric site?

A

Increases the duration of Cl- channel opening

41
Q

Between barbiturates and benzodiazepines, which are GABA independent?

This has what effect at high doses?

A

1) Barbiturates

2) Barbiturates are more lethal

42
Q

What is a GABA agonist?

A

Topiramate

43
Q

What are the GABA promoting agents that work on the post-synaptic side?

A

1) Barbiturates (Phenobarbital, Primidone)
2) Benzodiazepines (Clonazepam, Clobazam, Lorazepam, Diazepam)
3) Topiramate

44
Q

What are the multiple MOA of topiramate?

A

1) Na+ channel blocker
2) AMPA receptor blocker
3) GABA agonist

45
Q

What are the multiple MOA of Valproic acid?

A

1) Na+ channel blocker
2) GABA promoting agent by GAD stimulation
3) GABA promoting agent by GABA-T inhibition

46
Q

What are the broad warning/risk of all AEDs?

A

1) Abrupt withdrawal of AED may cause status epilepticus

2) Suicidal behavior

47
Q

Why does phenytoin have many drug-drug interactions?

A

It is an inducer of CYP-450 enzymes

48
Q

What is an unique toxicity that can be caused by phenytoin?

A

Gingival hyperplasia

49
Q

Chronic administration of carbamazepine, phenytoin, phenobarbital and valproic acid can cause?

Why?

A

1) Osteoporosis

2) They induce CYP450-dependent vitamin D catabolism

50
Q

What are unique toxicities that can be caused by Carbamazepine?

A

1) Leukopenia
2) Neutropenia
3) Thrombocytopenia

51
Q

Oxcarbazepine which is an analogue of carbamazepine has fewer CNS/Hematological symptoms due to?

A

Formation of an alternative active metabolite

52
Q

What is an unique toxicity that can be caused by vigabatrin?

A

Permanent vision loss

53
Q

What interaction do the AED inducers have with contraceptives?

A

Increase clearance of oral hormonal contraceptives which increases risk of unplanned pregnancy

54
Q

What interaction do the AED inducers have with anticoagulants?

A

Increase clearance of warfarin which increases risk for thrombosis

55
Q

What interaction do the AED inducers have with antivirals?

A

Increase clearance of HIV medications which increases the risk for HIV replication

56
Q

How do Valproic acid and Lamotrigine increase the accumulation of other drugs?

How do Phenytoin, Carbamazepine & Phenobarbital cause reduction of parent drug?

A

1) Inhibit UGT

2) Induce UGT

57
Q

In the treatment of convulsive status epilepticus in adults what is given in the first IV?

What is given in the second IV?

A

1) Lorazepam

2) Levetiracetam

NMSP Week 1 (13 decks)

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