T41b Antiepileptics Flashcards
Carbamazepine
antiepileptic. Class I Na+ influx voltage channel blocker in the refractory state after depolorization. decrease axonalconduction. preventing the propagation of seizure
DOA: variable absorption, nonlinear kinetics => zero kinetic elimination at high dose (constant rate despite concentration) therefor toxic doses reached faster. low therapeutic window.
Tx. Seizures (not generalized absecence seizures), TRIGEMINAL neuralgia PAIN, manic phase of bipolar disorder (mood stablizer)
ADV. inducer P450 and its own metabolism (CI porphyrias). CNS depression, gingival hyperplasia (sepsiemi or endocarditis), hirsutism, osteomalacia (decrease absorption and activation (hydroxylation due to phenytoin metabolism) vit D followed by hypo/hypercalcemia and secondary hyperparathyroidism with phosphate discasias), megaloblastic anemia (decrease absorption of folate due to conjugases being inhibited), aplastic anemia (immune response sue to high binding to plasma proteins - do WBC counts), teratogenic (cleft lip/palate and spinabifida). Rashes and steven Johnson syndrome. HyperADH by pituitary causing hypoNa+ and edema (CNS).
Ethosuximide
antiepilectic. Blocks thalamic T-type Ca+ channels
TX. seizures of absence
Gabapentin
antiepileptic. increase GABA release presynaptic. Inhibit glutamate Ca+ presynaptic channels inhbiting release.
DOA: 5-8 hrs. 100% bioavail. no metabolism, renal elimination (in pain, start at epi dose and, when see effect, increase)
TX. partial and generalized tonic-clonic seizures, some neuropathic PAIN, mood staibilizer bipolar disorder in** **pregnancy
ADV. _sedation/_somnolence, dizziness, ataxia, tremor, GI, imbalance in blood glucose., aplastic anemia, liver failure (both rare)
Lamotrigine
antiepileptic. Blocks Na+ channels and glutamate receptors antagonist
Tx. seizures (often as adjunct therapy), analgesic in neuropathic PAIN (decrese neural excitability)
ADV. hepatotoxic, steven-Johnson syndrome (HSR dermatitis)
Phenytoin
antiepileptic. Class I Na+ influx voltage channel blocker in the refractory state after depolorization. decrease axonalconduction. preventing the propagation of seizure
DOA: variable absorption, nonlinear kinetics => zero kinetic elimination at high dose (constant rate despite concentration) therefor toxic doses reached faster. low therapeutic window.
Tx. Seizures (not generalized absecence seizures), analgesic in neuropathic PAIN (decrese neural excitability)
ADV. inducer P450 (CI porphyrias). CNS depression, gingival hyperplasia (sepsiemi or endocarditis), hirsutism, osteomalacia (decrease absorption and activation (hydroxylation due to phenytoin metabolism) vit D followed by hypo/hypercalcemia and secondary hyperparathyroidism with phosphate discasias), megaloblastic anemia (decrease absorption of folate due to conjugases being inhibited), aplastic anemia (immune response sue to high binding to plasma proteins - do WBC counts), teratogenic (cleft lip/palate)
Pregabalin
antiepileptic. increase GABA release presynaptic. Inhibit glutamate Ca+ presynaptic channels inhbiting release.
Tiagabine
antiepileptic. inhibit GABA reuptake presynaptic.
Topiramate
antiepileptic. block glutamate AMPA receptors. Increase GABA release.
Valproic acid
antiepileptic. Class I Na+ influx voltage channel blocker in the refractory state after depolorization. decrease axonalconduction. preventing the propagation of seizure as well as inhibition of GABA transminase (GABA degradation) and block thalamic T-type Ca+ channels.
Tx. Seizures (all types), manic phase of rapid cycling bipolar (mood stabilizer), Migraines.
ADV_._ inhibits P450. Hepatotoxic metabolites, thrombocytopenia, pancreatitis, alopecia (causes frizzy-kinky), teratogen (spina bifida)
Vigabatrin
antiepileptic. inhibit GABA degradation at synapse.
Zonisamide
antiepileptic. adjunct
