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Pharmacology > Chapter 13: Antiseizure Drugs > Flashcards

Chapter 13: Antiseizure Drugs Flashcards

1
Q

seizures are caused by ___ in the brain, so the treatment for them is to ___

A

irregular electrical activity, reduce electrical activity

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2
Q

___ is the primary excitatory NT in the CNS

A

glutamate

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3
Q

___ is the primary inhibitory NT in the CNS

A

GABA

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4
Q

if we consider neuronal circuits to exist in a balance of excitation and inhibition, a disturbance in this balance can lead to excessive activity which can lead to ___

A

seizures

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5
Q

the irregular AP of seizures disrupts CNS signalling and can lead to ___, ___, ___ or ___

A

unconsciousness, convulsions, confusion or altered awareness

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6
Q

blocking Na and Ca ion channels on the PRESYNAPTIC neuron has what effect on activity?

A

prevents glutamate release and lowers activity

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7
Q

blocking Na and Ca channels on the POSTSYNAPTIC neuron has what effect on activut?

A

reduces excitability of the postsynaptic neuron and lowers activity

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8
Q

what is the effect of increasing K channel efflux on activity?

A

more K out gives hyper polarization which reduces excitability

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9
Q

what is the effect of targeting synaptic fusion proteins (SV2A) on activity?

A

reduces fusion of NT vesicles with presynaptic membrane, inhibiting release and lowering activity

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10
Q

besides lowering excitability signals, we can also enhance ____ signals to reduces seizures

A

inhibitory

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11
Q

we can increase the inhibitory output of postsynaptic neuron by doing what 3 things concerning GABA?

A
  1. activate GABA A receptor
  2. preventing GABA reuptake
  3. preventing GABA metabolism
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12
Q

what needs to be inhibited to reduce GABA re-uptake at from the synapse?

A

GAT-1 transporter

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13
Q

what needs to be inhibited to reduce GABA metabolsim>

A

GABA transaminase

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14
Q

___ and ___ are examples of voltage gated Na channel blockers

A

carbamazepine, phenytoin

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15
Q

Na channels blockers bind to the ___ configuration and prevent the channel from ___

A

inactive; retiring to its resting state

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16
Q

what types of neurons are most susceptible to Na channel blockers?

A

those which are more active and spend more time at depolarized membrane potentials (those that cause seizures)

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17
Q

blocking Na channels uses 2 types of blocks, what are they and how do they work?

A
  1. use-dependent block: most active get blocked

2. voltage-dependent block: most depolarized get blocked

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18
Q

what is important about Na channel blockers having more selectivity for overactive neurons?

A

preserves normal neuronal function of other neurons and maintains na channel functions in other parts of the body, such as the heart

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19
Q

carbamazepine and phenytoin are ___ inducers

A

CYP

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20
Q

phenytoin is highly ____

A

protein bound

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21
Q

most drugs follow first order kinetics, where a ____ of drug is removed per unit time

A

constant fraction

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22
Q

in zero order kinetics, a constant ___ of drug is removed per unit time

A

quantity

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23
Q

when phenytoin levels in the blood rise too high, the ____ is reached and the kinetics switch from 1st to ___ order

A

max capacity of liver to metabolize the drug; 0

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24
Q

what is a consequence of phenytoin stitching over to 0th order at high doses?

A

even small increases in dose may cause large changes in serum drug concentrations and can lead to ADR very quickly

25
Q

the most common ADR observed with Na channel blockers result from reduced ____

A

neuronal transmission

26
Q

with high doses or Na channel blockers, ___ can occur due to reduced neuronal transmission in the CNS

A

sedation

27
Q

what are some ADR of Na channel blockers?

A
  1. visual disturbances (eye movement and double vision)
  2. dizziness
  3. ataxia
  4. sedation
  5. rare hypersensitivity reactions
28
Q

there is a relatively rare but important hypersensitivity reaction to phenytoin and other structurally similar drugs (carbemazepine), what is it called and what does it look like?

A

DRESS; drug rash with eosinophilla and systemic symptoms

29
Q

aside from DRESS; what are some other hypersensitivity reactions that can be seen w/ Na channel blockers?

A

rash, fever, agranulocytosis

30
Q

gabapentin was originally developed as a _____mimetic, however, it does not bind to the receptor or any other inhibitory receptor in the CNS at any relevant dose; however it is able to reduce ___

A

GABA; seizures

31
Q

gabapentin works by modulating the presence of ___ channels on membrane surface

A

Ca

32
Q

when gabapentin binds to the ___subunit of the Ca channel, what happens to the channel;?

A

alpha 2 delta; remains internalized, not trafficking back to the membrane like it normally would

33
Q

how does gabapentin preventing Ca channel trafficking to the membrane affect seizures?

A

less Ca channels means less Ca into neuron, leading to less NT release and reduced excitability

34
Q

gabapentin relies on a ___ for GI absorption

A

transporter

35
Q

how can the amount of gabapentin become saturated?

A

if the transporter becomes saturated

36
Q

gabapentin can be used to treat seizures, but is not the most effective; it is used mostly in the management of ___ where Ca channels appear upregulated

A

neuropathic pain

37
Q

ADR of gabapentin include :

A

drowsiness, dizziness, ataxia, tremor, headache

38
Q

retigabine is a ____ of K channels

A

positive allosteric modulator

39
Q

what is the effect of retigabine on seizures?

A

increase the efflux of K, causing hyper polarization, reducing excitability

40
Q

what are the ADR of retigabine?

A

drowsiness, dizziness, blurred vision, confusion

41
Q

what is the MOA of Levetiracetam for management of seizures?

A

bind to SVA 2 to prevent fusion of NT (glutamate) vesicles to presynaptic membrane, preventing their release and reducing activity

42
Q

does levetiracetam have hepatic metabolism? what is the effect of this?

A

no; results in few drug-drug interactions

43
Q

the majority of Levetiracetam is excreted in what form by what route?

A

unchanged; urine

44
Q

what are the ADR of Levetiracetam?

A

sedation, ataxia, dizziness

45
Q

barbiturates are more commonly used as ___ rather than sedatives

A

anti-seizure

46
Q

it is though that barbiturates may have additional mechanisms to managing seizures (besides Cl reducing activity), what are they?

A

may involve ca channels and/or AMPA receptors to further educe activity

47
Q

what is the MOA of Tiagabine?

A

inhibits the GAT-1 transporter, allowing GABA to remain in the synapse longer and prolongs the inhibitory effects of the GABA receptor

48
Q

Give 2 reasons drug-drug interactions may be high in Tiagabine

A
  1. highly protein bound

2. metabolized by CYP3A4, which metabolized most drug

49
Q

what are some ADR of Tiagabine?

A

dizziness, ataxia, drowsiness, tremor, confusion

50
Q

what is the MOA of Vigabatrin?

A

GABA transaminase inhibitor (blocks GABA metabolism)

51
Q

what allows Vigabatrin to have a long duration of action?

A

it binds reversibly to GABA-T

52
Q

Vigabatrin is structurally similar to ___

A

GABA

53
Q

what is a unique ADR of Viagabatrin? How serious is it?

A

may cause retinal dysfunction due to loss of GABA-T in retina. The vision loss is not substantial, but is irreversible

54
Q

t/f the effectiveness of anti-seizure drugs often outweighs the not knowing the MOA

A

t

55
Q

Valproate/ valproic acid is used in the treatment of ___ and __

A

seizures and mood disorders

56
Q

valproate has many drug interactions, including with __-and __

A

phenytoin and phenobarbital

57
Q

what are 2 common ADR of valproate?

A

significant weight gain and GI upset

58
Q

Topiramate likely acts on ___, ___ and ___ to reduce activity

A

Na channels, GABA receptors and glutamate receptors

59
Q

what are some ADRs of Topiramate?

A

impaired cognitive function, dizziness, weight loss

Pharmacology (49 decks)

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