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ANS Pharmacology > Anti Seizure Pharm > Flashcards

Anti Seizure Pharm Flashcards

1
Q

What are the drugs of choice for myotonic/atonic/clonic seizures

A

Benzodiazepines (1), Clonazepam (2)

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2
Q

What are the drugs of choice for tonic/clonic seizures

A

Carbamazepine, phenytoin, phenobarbital

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3
Q

What are the drugs of choice for simple complex?

A

Lacosamide (1), Gabapentin, pregabalin, oxcarbazepine, Tiagabine, vigabatrin, ezogabin

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4
Q

What are the broad spectrum anti epileptic drugs?

A

Valproate (old version), Lamotrigine (impt new one), topirimate, levetiracetam, zonisamide

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5
Q

Which drugs limit excitation

A

Phenytoin, ethosuximide, carbamazepine, lamotrigine, fosphenytoin, levitiracetam, oxcarbazepine, zonisamide

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6
Q

What drugs enhance inhibition?

A

phenobarbital, diazepam, tiagabine, vigabatrin

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7
Q

What drugs limit excitation and enhance inhibition

A

valproate, topirimate

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8
Q

What are the two channels where AEDs antagonize excitation

A

Voltage gated Na channels, low threshold Ca channels

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9
Q

MOA for Phenytoin

A

Antagonize VGSC

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10
Q

MOA for carbamazepine

A

antagonize VGSC

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11
Q

MOA for lacosamide

A

Antagonize VGSC

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12
Q

MOA for lamotrigine

A

antagonize VGSC

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13
Q

MOA for oxcarbazepine

A

antagonize VGSC

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14
Q

MOA for zonisamide

A

antagonize VGSC

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15
Q

What are the two distinct mechanisms for VGSC modulation

A

Fast inactivation and slow inactivation (dimmers)

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16
Q

What drugs use the fast inactivation of Na channels

A

Traditional: phenytoin, carbamazepine

New AEDs: lamotrigine, oxcarbazepine

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17
Q

What drugs use the slow inactivation mechanism for inactivation of Na channels

A

New AEDs: lacosamide

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18
Q

What Fast acting VGSC antagonist binds more effectively and has less side effects on cognitive function

A

phenytoin

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19
Q

What fast acting VGSC antagonist binds less effectively, making it more effective in blocking high frequency firing

A

Carbamazepine

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20
Q

How is lamotrigines MOA different from phenytoin and carbamazepine?

A

Besides targeting VGSC, it also targets N and P type voltage gated Ca channels in cortical neurons and neocortical potassium currents

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21
Q

Lacosamide acts on which state of the sodium channel

A

Stabilizes the slow inactivated state

22
Q

What drug is the most effective at reducing the amplitudes and frequency of sustained repetitive firing spikes

A

lacosamide

23
Q

What is the hallmark of a abscence (petit mal) seizures

A

3Hz spike and wave activity in the thalamus - mediated by T type Ca channels

24
Q

Ethosuximide (condition tx, MOA, sedation?)

A

It is a narrow spectrum that is only used for abscence seizures. It only limits excitation (Ca channel). It is non-sedating

25
Q

What are the side effects of valproate

A

weight gain, tremor, hair loss, and lethargy. Assc with neural tube defects

26
Q

What is the MOA for zonisamide?

A

blocking voltage dependent sodium channels and blocking T type calcium channels

27
Q

MOA for tiagabine

A

inhibits GABA reuptake

28
Q

MOA for vigabatrin

A

inhibit GABA metabolism

29
Q

What drugs enhance post synaptic GABAergic neuronal transmission

A

phenobarbital, primidone (prodrug of phenobarbital), benzodiazapines

30
Q

What is the drug of choice for absence seizures

A

Ethosuximide

31
Q

MOA for benzodiazepines

A

Bind to distinct site –> allosteric change –> potentiate GABA binding –> chloride channels open. Does not work without GABA

32
Q

MOA for Phenobarbital

A

bind to distinct site–>allosteric change–>potentiate GABA binding–> open Cl channel. At high levels, it is GABA independent indicating that it is more lethal than BZD

33
Q

Adverse effects of phenobarbital

A

significant sedation, lethal respiratory depression, has abuse and addiction potential

34
Q

What are the causes of status epilepticus (continuous seizures)?

A

drug withdrawl (EtOH, BZD, opioids, AEDs), stimulant abuse (cocaine), poisons (strychnine), Brain tumor, high fever

35
Q

Tx for status epilepticus?

A

BZD- lorazepam (not distributed as quickly) or diazepam (absorbed, distributed, and redistributed quickly). If the seizure is not stopped –>Fosphenytoin

36
Q

drug of choice for myoclonic seizure

A

Clonazepam (a benzodiazepine)

37
Q

C/C the multiple MOA for Topirimate and valproic acid

A 
VGSC - both
LGSC - topirimate
T type Ca Channel - valproic acid
Increase GABA - both
Potentiates GABA R - topirimate
38
Q

Gabapentin MOA

A

binds to voltage dependent Ca channels

39
Q

MOA for leviteracetam

A

binds to synaptic vesicle protein SV2A - blunts glutamate release

40
Q

Type of clearance of Pregabalin

A

100% renal

41
Q

MOA for Ezogabine

A

Opens voltage gated K channels

42
Q

What are the pharmacokinetics/dynamics of phenytoin

A

0 order pharmacokinetics - doubling drug doesnt double serum level
inducer of CYP 450 enzymes

43
Q

What are the toxicities associated with phenytoin

A

Gingival hyperplasia, hirsutism, hypocalcemia, osteoporosis

44
Q

What are the complications assc with carbamazepine

A

inducer of CYP 450 enz ( it will induce its own metabolism)
aplastic anemia - leukopenia, neutropenia, thrombocytopenia
hypocalcemia & osteoporosis ( Vit D catabolizism –> inc PTH)

45
Q

What is the therapeutic window for AEDs

A

usually 2 fold

46
Q

What AEDs have mixed clearance

A

Topiramate, oxcarbazepine, levetiracetam, zonisamide

47
Q

How does oxcarbazepine differ from carbamazepine?

A

oxcarbazepine doesnt have an active metaolite

They both are assc with hyponatremia tho

48
Q

What drugs are 100% renally cleared

A

Gabapentin, pregabalin

49
Q

What is the serious side effect assc with lamotrigine?and mechanism?

A

stevens-johnson syndrome - assc with concurrent use with valproate. They inhibit conjugation of drugs by UGT enz

50
Q

What is the serious side effect of topiramate

A

nephrolithiasis

51
Q

What AEDs is assc with major congenital malformations

A

valproic acid

ANS Pharmacology (3 decks)

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