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20 Cards in this Set
- Front
- Back
Na+ channel inhibitors for Epilepsy (4)
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Phenytion
Carbamazepine Iamotrigine Valproic Acid |
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GABA enhancers for Epilepsy (6)
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Phenobarbitol
Clonazepam Diazepam Lorazepam Tiagabine Vigabatrin |
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T-type Ca+ channel inhibitor for Epilepsy (absence)
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Ethosuximide
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Other drugs for Epilepsy (3)
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Topiramate
Levetiracetam Gabapentin |
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Cell physiological manifestations of SZ
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SZ activity is ass'd w/ high-frequency, rhythmic & coordinated firing of central neurons
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Strategy for pharmacological management of SZ
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1. High frequency APs (Na+ ch)
2. Enhancement of inhibitory GABA activity 3. Inhibition of T-type Ca+ ch (involved in mediating rhythmic electrical activity) |
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CP & management of Status epilepticus
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CP: >5 minutes of continued SZ activity or 2+ SZs w/out regaining consciousness; can be life-threatening
Management: 1. ABCs 2. Lorazepam 3. Phenytoin 4. If + signs of systemic distress, induce complete anesthesia. If - , Phenobarbital 5. More Phenobarbitol 6. Induce complete anesthesia |
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Acute triggers for status epilepticus
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electrolyte imbalances, renal failure, sepsis, CNS infection, head trauma, stroke, & drug OD. These are ass'd w/ higher mortality
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Chronic triggers for status epilepticus
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pre-existing epilepsy, SZs due to chronic use of EtOH, & CNS neoplasms. These are ass'd w/ a better prognosis
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Phenytoin, Carbamazepine, & Lamotrignine
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MoA: suppression of recovery from inactivation of voltage-gated Na+ channels
Ind: partial & general tonic clonic sz S/E: double vision, ataxia, rashes, & gingival hyperplasia (Phenytoin-saturation kinetics), alpastic anemia & granulocytosis (carbemazapine-must be monitored) Lamotrigine -for refractory partial sz |
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Phenobarbitol
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MoA: Increased duration of GABA(A) channel opening, thereby potentiating the GABA inhibitory activity
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Valproic acid
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MoA: Suppression of recovery from inactivation of voltage-gated Na+ channels, & at [higher] blocks ion conduction through the T-type Ca+ channels
Ind: absence sz (in a pt who also has other types of sz), & myoclonic sz Cont: Pregnancy-developmental abnormalities |
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Clonazepam, Diazepam, & Lorazepam
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MoA: Enhances ion conduction through the GABA(A) receptor channel by direct binding to the gamma subunit & increasing the frequency of channel opening, thus potentiating the GABA response
Ind: Diazepam & Lorazepam-for status epilepticus Pearl: development of tolerance |
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Tiagabine
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MoA: Blockade of GABA reuptake in neurons & glia
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Vigabatrin
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MoA: Enhances GABA activity by inhibition of the GABA degradative enzyme GABA transaminase
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Ethosuximide
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MoA: Blocks ion conduction through the T-type Ca+ channels
Ind: absence sz |
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Topiramate
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MoA: Na+ & Ca+ channel blockade, GABA potentiation, glutamate receptor antagonism
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Levetiracetam
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MoA: Unknown mech of action, but is known to bind to the presynaptic vesicle protein, SV2A (also binds Botox)
Ind: sz & pn |
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Gabapentin
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MoA: Enhances release of GABA at inhibitory synapses through as yet unknown mechanism. Reduces release of excitatory amino acids by binding to Ca+ channels
Ind: neuropathic pn |
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Lamotrigine
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Ind: for refractory partial sz
A/E: rashes, SJ syndrome |