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Neuro > Epilepsy Meds > Flashcards

Epilepsy Meds Flashcards

1
Q

What is the neuronal basis for epilepsy?

A

over-excitation

increased glutamate and aspartate

decreased inhibitory GABA

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2
Q

Generally, what do epilepsy drugs do?

A

suppress excitatory (glutamate)

enhance inhibitory (GABA)

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3
Q

The faster neurons fire in epilepsy, ___________

A

the faster meds can block the receptors to reduce activity

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4
Q

What drugs prolong fast inactivation of Na ion channels?

A

Stop/decrease APs by binding inside open gate:

Carbamazepine (azepines)
Lamotrigine
Phenytoin
Topiramate
Valproic acid
Lacosamide (amides)
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5
Q

What drug enhances slow inactivation of Na channels?

A

Lacosamide

–> doesn’t need activation gate of receptor open to work like other meds (can work with minimal open sodium channels)

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6
Q

What drugs block AMPA receptor on postsynaptic membrane so glutamate can’t activate it, thus decreasing APs/firing?

A

AMPA receptor antagonists:

topiramate
perampanel

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7
Q

What drug prolongs fast inactivation of Na channel (blocks it), blocks glutamate binding of AMPA receptor (antagonist), and increases frequency of GABA receptor transmission?

A

topiramate

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8
Q

What drug prevents binding of glutamate to NMDA receptor on postsynaptic membrane?

A

NMDA receptor antagonist:

Felbamate

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9
Q

T-type calcium channels are the hallmark of what seizure?

A

petit mal (absence)

inhibition of these channels decrease seizures

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10
Q

What drug inhibits T-type calcium channels and is only used for petit mal/absence seizures?

A

ethosuximide

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11
Q

What drug can block T-type calcium channel and sodium channels (prolong fast inactivation)?

A

Zonisamide

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12
Q

What drugs block synaptic vesicle SV2A (prevent glutamate from binding to presynaptic cleft, decreases release)?

A

levetiracetam

brivaracetam

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13
Q

What drugs block alpha 2 delta subunit of T-type calcium channels?

A

Gabapentin
Pregabalin

-both have GABA in name

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14
Q

What drug OPENS KCNQ potassium channels (pre and post) to hyperpolarize (stop AP) and stimulates GABA receptors in high doses?

A

Ezogabine

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15
Q

How does post-synaptic GABA transmission work?

A

when GABA receptor unoccupied–> inactive chloride channel

When GABA binds to its receptor–> chloride channel opens–> hyperpolarizes membrane to blunt AP

INHIBITORY

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16
Q

What is the significance of presynaptic GABA meds?

A

glutamate makes GABA, so meds increase conversion

meds that inhibit GABA metabolism (via GABA-T and SSD) or transport back to presynaptic neuron (via GAT-1) so there is more of it to inhibit neurons

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17
Q

What drug blocks GAT-1 (reuptake of GABA)?

A

tiagabine

18
Q

What drug blocks GABA-T (metabolizes GABA)?

A

Valproic acid

Vigabatrin

–>viGABATrin

19
Q

What drugs increase glutamic acid decarboxylase to produce more GABA?

A

valproic acid

gabapentin

pregabalin

20
Q

What drugs block the alpha-2-delta subunit of T-type calcium channels (decrease excitation) AND increase glutamic acid decarboxylase (produce more GABA)?

A

gabapentin

pregabalin

21
Q

What drug blocks SSD (stops metabolism of GABA)?

A

valproic acid

22
Q

What drugs enhance post-synaptic GABA transmission?

A

Barbiturates (phenobarbital/primidone)

Benzodiazapines (lorazepam, diazepam, clonazepam, clobazam)

Topiramate

23
Q

How do benzodiazepines work in seizures?

A

bind to distinct site–> potentiate GABA binding–> chloride channels open with greater frequency

need GABA present to work

24
Q

How to barbiturates work in seizures?

A

bind to distinct site on GABA and increase DURATION of chloride channel opening

don’t need GABA to work (high doses lethal c/t benzos)

25
Q

What 2 drugs are broad spectrum in treating seizures with 3 MOAs?

A

topiramate

valproic acid

26
Q

What drug treats rare, severe forms of epilepsy?

A

cannabidiol

only can be used in combo with other antiepileptic drugs

27
Q

What are the broad warnings for all antiepileptic meds?

A

abrupt withdrawal or stopping of meds increases risk of status epilepticus

suicidal ideation more likely

28
Q

Phenytoin

A

zero order, saturable

induces CYP450

gingival hyperplasia

hypocalcemia–> bone issues

29
Q

What drugs induce CYP450–> Vitamin D catabolism–> bone issues?

A

phenytoin

carbamazepine

phenobarbital

valproic acid

30
Q

Carbamazepine

A

auto-induction (loss of efficacy, recurrent seizures)

inducer CYP450

leukopenia/neutropenia/thrombocytopenia
–> bone marrow suppression

31
Q

What is an analogue of carbamazepine that is less-potent CYP450 inducer (less bone marrow suppression) and doesn’t have a toxic intermediate metabolite?

A

oxcarbazepine

32
Q

Phenobarbital

A

fatality risk (high doses d/t not dependent on GABA for rxn)

inducer CYP450

CNS depressant (how overdose with other depressants)

33
Q

Vigabatrin

A

permanent vision loss

can only prescribe with REMS program

34
Q

Antiepileptic drugs and oral contraceptives

A

oral contraceptives metabolized by CYP450

since antiepileptics (some) are inducers, more is cleared –> increased risk for failure and unplanned pregnancy

35
Q

Antiepileptic drugs and warfarin

A

increase clearance of warfarin (d/t induction of CYP450)–> less anticoag–> increase risk for clot

36
Q

Antiepileptic drugs and HIV meds

A

increase clearance of HIV meds via induction of CYP450–> increased risk for HIV replication

37
Q

What drugs inhibit conjugation of drugs by UGT–> accumulation of parent drug

A

valporic acid

lamotrigine

38
Q

What drugs induce conjugation of UGT–> reduce parent drug?

A

phenytoin

carbamazepine

phenobarbital

especially when given with valproic acid

39
Q

How do new drugs get around CYP450 system?

A

renal clearance

renal insufficiency requires dose adjustments (elderly especially)

40
Q

Treat status epilepticus

A

give benzodiazepine
–> lorazepam IV classic

fosphenytoin IV
OR
levetiracetam

Neuro (18 decks)

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