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25 Cards in this Set
- Front
- Back
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• Potassium Bromide
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Free bromide ions, thought to pass through ion channels along with Cl-
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• Phenobarbitol (Barbiturates)
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o MOA: limits repetitive firing of neurons, enhances GABA binding to the GABAa receptor
When GABA binds this receptor in the presence of Phenobarbital, Cl- chanel opens for longer periods of time (result is hyper polarization) |
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• Phenytoin (Hydantoins)
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o MOA: limits repetitive provoked action potentials, slows the rate of recovery of Na+ channels during inactivation (lengthens refractory period)
No enhanced GABA transmission, no GABA reuptake blockade |
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• Carbamazepine (iminostilbenes)
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o MOA: limits repetitive firing of action potentials evoked by depolarizing stimulus, slows voltage-gated Na+ channel recovery
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• Oxcarbazepine (iminostilbenes)
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o MOA: (similar to carbamazephine) limits repetitive firing of action potentials evoked by depolarizing stimulus, prolongs inactivation phase of Na+ channels
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• Ethosuximide (succinimides)
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o MOA: inhibits T currents in thalamic neurons, hypothesized action by antagoinism of voltage gated Ca++ ion channels (possible physical blocking of open Ca++ channels)
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• Valproic Acid
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o MOA: (similar to phenytoin and ethosuximide) inhibits cortex neuronal repetitive firings, prolongs recovery period of voltage gated Na+ channels
Also reduces T currents in thalamic neurons Hypothesized to increase GABA levels (increase GAD activity, and decreased GABA degradation via GABA Transaminase) |
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• Benzodiazepines
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o MOA: bind to specific subsets of GABAa receptors (a-1, a-1, or a-5 subunits only for seizure tx)
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• Gabapentin
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o MOA: DOES NOT mimic GABA, may promote non-vesicular release of GABA
Doesn’t affect activity of Ca++ channels |
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• Lamotrigine
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o MOA: blocks repetitive firing in cortical neurons, delaus Na+ channel recovery from inactivation state
Addn’l: inhibits synaptic glutamate release sometimes (via action on Na+ channels of glutamatergic neurons?) |
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• Levetiracetam
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o MOA: unknown—binds SVZA (effect unknown)
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• Tigabine
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o MOA: inhibits GAT-1 causing increased GABA levels in synaptic cleft
Lengthens duration of GABA induced inhibitory (Cl-) current |
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• Topiramate
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o MOA: hypothesized to antagonize AMPA receptors, reduces voltage-gated Na+ currents (possibly similar to phenytoin), activates a hyperpolarizing K+ channel
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• Zonisamide
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o MOA: inhibition of T currents (Ca++ currents), and repetitive neuronal firing by prolonging inactivation of voltage-gated Na+ channels
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• Vigabratrin
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o MOA: irreversible inhibitor of GABA-Transaminase, results in increased levels of GABA in synapse
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Which six drugs Prolongs (decreases rate of recovery) inactivation phase of Na+ therefore limits repetitive firing of action potentials?
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Phenytoin
Carbamazepine Lamotrigine Zonisamide Valproic acid Topiramate |
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Phenobarbital Effects on Cl- channels through GABA how?
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enhances GABA to GABAachannels stay open longer
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Valproic acid Effects on Cl- channels through GABA how?
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may increase GAD and decrease enzymes that degrade GABA
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Benzodiazepine Effects on Cl- channels through GABA how?
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binds specific subsets of GABAa and increases frequency of channel opening (positveallostericeffector)
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Tigabine Effects on Cl- channels through GABA how?
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inhibits GAT-1 (GABA reuptake transporter)
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Vigabatrin Effects on Cl- channels through GABA how?
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irreversible inhibitor of GABA-T increases opening of channels
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what are 5 drugs that have DDI with OCs
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Phenytoin
Phenobarbital Carbamazpine Tigabine Benzodiazepine |
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Ethosuximide has was effects on t currents?
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hypothesized to reduce by blocking Ca++ channels
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Valproic Acid has what effects on T currents
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reduces
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Zonisamide has what effects on T currents?
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inhibits
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