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Pharmacology Test #6 > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

1
Q

Seizure

A

single event of brain dysfunction with various forms, but commonly involving hypersynchrony of neuronal discharge in cortex

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2
Q

Epilepsy

A

disorder of chronic seizures; one of the oldest known brain disorders, associated with demonic possession in ancient times; prevalence is 1%

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3
Q

Partial seizure

A

involves one hemisphere

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4
Q

Simple seizure

A

sensory disturbances, 30-60 sec, retains consciousness

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5
Q

Complex seizure

A

lost consciousness, 1-2 min, aura, automatisms, amnesia after

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6
Q

Secondarily generalized seizure

A

turns into a generalize seizure, treated as such

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7
Q

Generalized seizure

A

involves both hemispheres, lost consciousness

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8
Q

Tonic/clonic (grand mal) seizure

A

stiffening (tonic) then jerking (clonic), 1-2 min

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9
Q

Absence

A

lapse in awareness, children, 100s per day

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10
Q

Myoclonic and Clonic seizures

A

brief contractions of body, local or generalized

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11
Q

Tonic seizures

A

stiffening only

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12
Q

Atonic seizures

A

loss of tone, falls

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13
Q

Status epilepticus

A

prolonged seizure (5 min), medical emergency

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14
Q

Seizure etiology

A
  1. stress
  2. head trauma
  3. infection
  4. fever
  5. tumors
  6. brain malformations
  7. genetic factors
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15
Q

What happens with neuronal firing in seizures

A

neurons fire in synchrony, producing large summations in current recorded from scalp electrodes

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16
Q

What happens with neuronal firing post-seizure

A

possibly less activity than pre-seizure, often termed post-ictal depression

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17
Q

Electrophysiological progression of a seizure

A
  1. Large excitatory synaptic current in seizure focus
  2. PDS induction and interictal spike/wave generation
  3. Secondary spikes/PDS coincide with seizure activity
  4. Postictal depression
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18
Q

What gives rise to the initial spike in the EEG?

A

thought to be from some form of enhanced excitatory synaptic current or diminished inhibitory current

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19
Q

Post-tetanic potentiation

A

cellular model where a tetanus (which would model a seizure) can induce a potentiated response from a synapse due to buildup of Ca2+ in the terminal during the tetanus; may be relevant to anticonvulsant drugs that manipulate Ca2+ channels

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20
Q

Long term potentiation

A

phenomenon where repeated stimulation strengthens synaptic connections, which could occur in seizures, perhaps explaining aspects of kindling and mirror foci; relevant to anti-glutamateric drugs that block NMDA and/or AMPA receptors

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21
Q

Paroxysmal depolarizing shift

A

describes cellular phenomenon that there are checks and balances in neurons that maintain proper balance of excitation/inhibition, but excessive excitation or reduced inhibition can result in excessive discharge characteristic of seizures

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22
Q

Epilepsy animal models

A
  1. Mirror foci
  2. Maximum electroshock
  3. Kindling
  4. Pentylenetetrazole
  5. Channelopathies
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23
Q

Mirror foci

A

a seizure focus is created on one side of the brain using various chemical or electrical methods, which is followed by spontaneous formation of another focus int he same brain area on the other hemisphere

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24
Q

Maximum electroshock

A

current applied to the brain is incrementally increased until a maximal seizure is elicited, providing a measure of seizure sensitivity; drugs are assayed for their ability to reduce the sensitivity to seizure formation, or to increase the current that is necessary to produce a seizure

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25
Q

Kindling

A

a brain area is repeatedly stimulated to produce a seizure focus, and drugs are assayed for their ability to suppress formation of this focus and/or to suppress seizure activity from this focus once formed

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26
Q

Pentylenetetrazole (PTZ)

A

a pro-convulsant drug that likely mediates its effects by blocking GABA-A receptors, thereby reducing inhibition and shifting the balance toward excitation of neurons; anticonvulsant drugs are sued to test suppression of PTZ-induced seizures

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27
Q

Channelopathies

A

genetic animal models that produce mutated ion channels to model mutations in human that are thought to produce seizure disorders

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28
Q

Drugs targeted to the VG Na+ channel

A
  1. Phenytoin
  2. Carbamazepine
  3. Lamotrigine
  4. Lacosamide
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29
Q

Drugs targeted to the VG Ca2+ channel

A
  1. Ethosuximide
  2. Lamotrigine
  3. Gabapentin
  4. Pregabalin
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30
Q

Drugs targeted to the K+ channels

A
  1. Retigabine
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31
Q

Drugs targeted to AMPA receptors

A
  1. Phenobarbital
  2. Topiramate
  3. Lamotrigine
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32
Q

Drugs targeted to NMDA receptors

A
  1. Felbamate
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33
Q

What do drugs targeted to the VG Na+ channel do?

A

drugs slow recovery from inactivation, preventing high frequency spiking

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34
Q

What do drugs targeted to the VG Ca2+ channel do?

A

drugs diminish excitability, especially at the synapse

35
Q

What do drugs targeted to the K+ channels do?

A

K+ channel openers; prolong refractory period and attenuate high frequency spiking

36
Q

What do drugs targeted to the AMPA receptors do?

A

block the receptors; blocking will diminish excitability

37
Q

What do drugs targeted to the NMDA receptors do?

A

block the receptors; block will diminish excitability, potentially inhibit LTP

38
Q

Why do anticonvulsants appear to selectively suppress firing in parts of the brain that exhibit rapid firing and depolarized membrane potentials?

A

because they interact with specific states of the voltage-gated sodium channels

39
Q

Describe the normal neuronal firing rate (frequency)

A

Lower frequency; drugs completely dissociate between spikes; activity is preserved

40
Q

Describe epileptic-style firing rates (frequency)

A

High frequency; drugs do not completely dissociate between spikes; block accumulates each spike; activity is suppressed

41
Q

Describe the normal neuronal membrane potential

A

Hyperpolarized Vm; drugs completely dissociates between spikes; activity is preserved

42
Q

Describe a depolarized neuron membrane potential

A

depolarized Vm prolongs drugs interaction with channel; high percentage of channels are always blocked; activity is suppressed

43
Q

What kind of block does lidocaine exhibit?

A

Frequency-dependent and voltage-dependent block

44
Q

What happens when you block GAT-1?

A

blocking transporter will permit GABA to build-up, decreasing excitability

45
Q

GAT-1 blocker

46
Q

What happens when you block GABA-T?

A

transaminase breaks down GABA, so block will increase levels

47
Q

GABA-T blocker

A

Vigabatrin

48
Q

How do benzodiazepines relate to seizures?

A

benzos act at allosteric site in GABAA receptor, augmenting Cl- current and decreasing excitability

49
Q

Standard seizure drugs

A
  1. Phenytoin
  2. Carbamazepine
  3. Ethosuximide
  4. Phenobarbital
  5. Benzodiazepines
  6. Valproate
50
Q

New seizure drugs

A
  1. Gabapentin
  2. Lamotrigine
  3. Tiagabine
  4. Topirimate
  5. Felbamate
  6. Levetiracetam
  7. Zonisamide
  8. Vigabatrin
51
Q

Phenytoin useful for

A

partial and generalized tonic/clonic seizures

52
Q

Phenytoin blocks

A

voltage-gated sodium channels, perhaps preferentially blocking repetitive spiking that occurs in seizures

53
Q

Carbamazine useful for

A

partial and generalized tonic/clonic seizures

54
Q

Carbamazine very similar to

A

similar in activity and clinical usefulness to phenytoin

55
Q

Ethosuximide blocks

A

specifically blocks T-type Ca2+ channels

56
Q

Ethosuximide useful for

A

only useful for absence seizures

57
Q

Benzodiazepines useful for which types of seizures

A

Status epilepticus and types of seizure clusters

58
Q

Two main benzodiazepines useful for seizures

A

Diazepam and Lorazepam

59
Q

MOA of phenobarbital

A

potentiates GABA at GABA-A receptors and at higher concentrations can directly activate the receptor

60
Q

Phenobarbital is useful for

A

partial and generalized tonic/clonic seizures, though rarely used due to sedation and safety concerns

61
Q

MOA of gabapentin

A

block of presynaptic voltage-gated Ca2+ channels, and enhancement of GABA levels

62
Q

Gabapentin is useful for

A

partial and generalized tonic/clonic seizures

63
Q

MOA of lamotrigine

A

block voltage-gated sodium channels as well as L-type Ca2+ channels, suppressing excitatory activity

64
Q

Lamotrigine is useful for

A

partial and myoclonic seizures and some usefulness in absence seizures

65
Q

MOA of tiagabine

A

blocks GAT-1, which will result in increased synaptic levels of GABA and therefore increased inhibition of postsynaptic cells

66
Q

Tiagabine used for

A

often used as adjunct or addition to those not responsive to monotherapy

67
Q

Adverse effects of tiagabine

A

can cause seizures in those taking it for other indications (non-epileptic patients), such as psychiatric disorders; somnolence, headache, depression

68
Q

MOA of topiramate

A

blocks VG Na+ channels, potentiates GABA, and antagonizes glutamate receptors; blocks repetitive firing, so likely an effect on VG sodium channels

69
Q

Use of topiramate

A

used in partial and generalized T/C seizures

70
Q

Drug of choice for unambiguous idiopathic generalized epilepsy

71
Q

MOA of valproate

A

blocks repetitive firing of neurons (VG Na+ channels), blocks NMDA current, enhances GABa levels

72
Q

Valproate used in

A

absence and generalized T/C seizures

73
Q

Adverse effects of valproate

A

teratogenic (spina bifida); should be avoided in patients with liver disease; GI (nausea/vomiting); weight gain

74
Q

Adverse effects of phenytoin

A

gingival hyperplasia, diplopia, ataxia, hirsuitism, teratogenic, low toxicity but many drug interactions

75
Q

Adverse effects of carbamazepine

A

nausea, ataxia, teratogenic

76
Q

Adverse effects of ethosuximide

A

GI, sleep disturbances, drowsiness, depression

77
Q

Adverse effects of benzodiazepines

A

sedation and tolerance

78
Q

Adverse effects of gabapentin

A

mild/moderate sedation, ataxia fatigue

79
Q

Adverse effects of lamotrigine

A

serious rash (with valproate), myoclonus

80
Q

Adverse effects of phenobarbitol

A

sedation, teratogenic

81
Q

Adverse effects of topiramate

A

sedation and somnolence

82
Q

Pharmacokinetic considerations with anticonvulsants

A
  1. Monitor plasma concentrations
  2. Be aware of dose-dependent elimination
  3. Induction and inhibition of hepatic enzymes
83
Q

Which anticonvulsants induce hepatic enzymes?

A

carbamazepine, phenytoin, phenobarbital

84
Q

Which anticonvulsants inhibit hepatic enzymes?

A

Valproate and topiramate

Pharmacology Test #6 (12 decks)

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