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20 Cards in this Set

  • Front
  • Back
Na+ channel inhibitors for Epilepsy (4)
Phenytion
Carbamazepine
Iamotrigine
Valproic Acid
GABA enhancers for Epilepsy (6)
Phenobarbitol
Clonazepam
Diazepam
Lorazepam
Tiagabine
Vigabatrin
T-type Ca+ channel inhibitor for Epilepsy (absence)
Ethosuximide
Other drugs for Epilepsy (3)
Topiramate
Levetiracetam
Gabapentin
Cell physiological manifestations of SZ
SZ activity is ass'd w/ high-frequency, rhythmic & coordinated firing of central neurons
Strategy for pharmacological management of SZ
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)
CP & management of Status epilepticus
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
Acute triggers for status epilepticus
electrolyte imbalances, renal failure, sepsis, CNS infection, head trauma, stroke, & drug OD. These are ass'd w/ higher mortality
Chronic triggers for status epilepticus
pre-existing epilepsy, SZs due to chronic use of EtOH, & CNS neoplasms. These are ass'd w/ a better prognosis
Phenytoin, Carbamazepine, & Lamotrignine
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
Phenobarbitol
MoA: Increased duration of GABA(A) channel opening, thereby potentiating the GABA inhibitory activity
Valproic acid
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
Clonazepam, Diazepam, & Lorazepam
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
Tiagabine
MoA: Blockade of GABA reuptake in neurons & glia
Vigabatrin
MoA: Enhances GABA activity by inhibition of the GABA degradative enzyme GABA transaminase
Ethosuximide
MoA: Blocks ion conduction through the T-type Ca+ channels
Ind: absence sz
Topiramate
MoA: Na+ & Ca+ channel blockade, GABA potentiation, glutamate receptor antagonism
Levetiracetam
MoA: Unknown mech of action, but is known to bind to the presynaptic vesicle protein, SV2A (also binds Botox)
Ind: sz & pn
Gabapentin
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
Lamotrigine
Ind: for refractory partial sz
A/E: rashes, SJ syndrome