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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
Kindling
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
26
Pentylenetetrazole (PTZ)
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
27
Channelopathies
genetic animal models that produce mutated ion channels to model mutations in human that are thought to produce seizure disorders
28
Drugs targeted to the VG Na+ channel
1. Phenytoin 2. Carbamazepine 3. Lamotrigine 4. Lacosamide
29
Drugs targeted to the VG Ca2+ channel
1. Ethosuximide 2. Lamotrigine 3. Gabapentin 4. Pregabalin
30
Drugs targeted to the K+ channels
1. Retigabine
31
Drugs targeted to AMPA receptors
1. Phenobarbital 2. Topiramate 3. Lamotrigine
32
Drugs targeted to NMDA receptors
1. Felbamate
33
What do drugs targeted to the VG Na+ channel do?
drugs slow recovery from inactivation, preventing high frequency spiking
34
What do drugs targeted to the VG Ca2+ channel do?
drugs diminish excitability, especially at the synapse
35
What do drugs targeted to the K+ channels do?
K+ channel openers; prolong refractory period and attenuate high frequency spiking
36
What do drugs targeted to the AMPA receptors do?
block the receptors; blocking will diminish excitability
37
What do drugs targeted to the NMDA receptors do?
block the receptors; block will diminish excitability, potentially inhibit LTP
38
Why do anticonvulsants appear to selectively suppress firing in parts of the brain that exhibit rapid firing and depolarized membrane potentials?
because they interact with specific states of the voltage-gated sodium channels
39
Describe the normal neuronal firing rate (frequency)
Lower frequency; drugs completely dissociate between spikes; activity is preserved
40
Describe epileptic-style firing rates (frequency)
High frequency; drugs do not completely dissociate between spikes; block accumulates each spike; activity is suppressed
41
Describe the normal neuronal membrane potential
Hyperpolarized Vm; drugs completely dissociates between spikes; activity is preserved
42
Describe a depolarized neuron membrane potential
depolarized Vm prolongs drugs interaction with channel; high percentage of channels are always blocked; activity is suppressed
43
What kind of block does lidocaine exhibit?
Frequency-dependent and voltage-dependent block
44
What happens when you block GAT-1?
blocking transporter will permit GABA to build-up, decreasing excitability
45
GAT-1 blocker
Tiagabine
46
What happens when you block GABA-T?
transaminase breaks down GABA, so block will increase levels
47
GABA-T blocker
Vigabatrin
48
How do benzodiazepines relate to seizures?
benzos act at allosteric site in GABAA receptor, augmenting Cl- current and decreasing excitability
49
Standard seizure drugs
1. Phenytoin 2. Carbamazepine 3. Ethosuximide 4. Phenobarbital 5. Benzodiazepines 6. Valproate
50
New seizure drugs
1. Gabapentin 2. Lamotrigine 3. Tiagabine 4. Topirimate 5. Felbamate 6. Levetiracetam 7. Zonisamide 8. Vigabatrin
51
Phenytoin useful for
partial and generalized tonic/clonic seizures
52
Phenytoin blocks
voltage-gated sodium channels, perhaps preferentially blocking repetitive spiking that occurs in seizures
53
Carbamazine useful for
partial and generalized tonic/clonic seizures
54
Carbamazine very similar to
similar in activity and clinical usefulness to phenytoin
55
Ethosuximide blocks
specifically blocks T-type Ca2+ channels
56
Ethosuximide useful for
only useful for absence seizures
57
Benzodiazepines useful for which types of seizures
Status epilepticus and types of seizure clusters
58
Two main benzodiazepines useful for seizures
Diazepam and Lorazepam
59
MOA of phenobarbital
potentiates GABA at GABA-A receptors and at higher concentrations can directly activate the receptor
60
Phenobarbital is useful for
partial and generalized tonic/clonic seizures, though rarely used due to sedation and safety concerns
61
MOA of gabapentin
block of presynaptic voltage-gated Ca2+ channels, and enhancement of GABA levels
62
Gabapentin is useful for
partial and generalized tonic/clonic seizures
63
MOA of lamotrigine
block voltage-gated sodium channels as well as L-type Ca2+ channels, suppressing excitatory activity
64
Lamotrigine is useful for
partial and myoclonic seizures and some usefulness in absence seizures
65
MOA of tiagabine
blocks GAT-1, which will result in increased synaptic levels of GABA and therefore increased inhibition of postsynaptic cells
66
Tiagabine used for
often used as adjunct or addition to those not responsive to monotherapy
67
Adverse effects of tiagabine
can cause seizures in those taking it for other indications (non-epileptic patients), such as psychiatric disorders; somnolence, headache, depression
68
MOA of topiramate
blocks VG Na+ channels, potentiates GABA, and antagonizes glutamate receptors; blocks repetitive firing, so likely an effect on VG sodium channels
69
Use of topiramate
used in partial and generalized T/C seizures
70
Drug of choice for unambiguous idiopathic generalized epilepsy
Valproate
71
MOA of valproate
blocks repetitive firing of neurons (VG Na+ channels), blocks NMDA current, enhances GABa levels
72
Valproate used in
absence and generalized T/C seizures
73
Adverse effects of valproate
teratogenic (spina bifida); should be avoided in patients with liver disease; GI (nausea/vomiting); weight gain
74
Adverse effects of phenytoin
gingival hyperplasia, diplopia, ataxia, hirsuitism, teratogenic, low toxicity but many drug interactions
75
Adverse effects of carbamazepine
nausea, ataxia, teratogenic
76
Adverse effects of ethosuximide
GI, sleep disturbances, drowsiness, depression
77
Adverse effects of benzodiazepines
sedation and tolerance
78
Adverse effects of gabapentin
mild/moderate sedation, ataxia fatigue
79
Adverse effects of lamotrigine
serious rash (with valproate), myoclonus
80
Adverse effects of phenobarbitol
sedation, teratogenic
81
Adverse effects of topiramate
sedation and somnolence
82
Pharmacokinetic considerations with anticonvulsants
1. Monitor plasma concentrations 2. Be aware of dose-dependent elimination 3. Induction and inhibition of hepatic enzymes
83
Which anticonvulsants induce hepatic enzymes?
carbamazepine, phenytoin, phenobarbital
84
Which anticonvulsants inhibit hepatic enzymes?
Valproate and topiramate

Pharmacology Test #6 (12 decks)

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