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33 Cards in this Set
- Front
- Back
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fosphenytoin
- routes (2) |
phenytoin pro-drug
with better solubility - IV or IM routes |
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phenytoin moa (4)
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BLOCKS VG Na+ channels.
-blocks high frequency firing of neurons through action on the VG Na+ channels. → (prolong inactivation of Na+ channels) [-] synaptic release of glutamate. Enhances release of GABA Alters Na+, K+ and Ca2+ conductance |
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phenobarbital moa (4)
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Enhances phasic GABA-A receptor responses
Reduces excitatory synaptic responses Enhances inhibitory transmission May selectively suppress abnormal neurons |
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primidone moa (4)
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Mechanism of action of primidone like that of phenytoin.
However, one of the metabolites is phenobarbital. The other metabolie is PEAM and is very in active…, but doesn’t do much However, All three compounds are active |
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ethosuximide moa
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Reduces low threshold Ca2+ currents (T-type)
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phenytoin/fosphenytoin PK
- absorption? - protein binding? - metabolites? - elimination? - t(1/2)? |
absorption: formulation dependent
binding: highly bound; displaced by phenylbutazone and sulfonamides active metabolites: none; metabolized by 2C9/10, 2C19 elimination: dose-dependent t(12/2) = 12-36 hr |
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phenobarbital PK
- absorption? - protein binding? - metabolites? - time to peak concentration? - t(1/2)? |
absorption: nearly complete
binding: insignificant active metabolites: none peak conc: 1/2-4 hr t(1/2) = 75-125 hr |
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primidone PK
- absorption? - protein binding? - metabolites? - time to peak concentration? - t(1/2)? |
absorption: well absorbed orally
binding: little active metabolites: phenobarbital, PEMA (phenylethylmalonamide) peak conc: 2-6 hr t(1/2) = 10-25 hr |
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ethosucimide PK
- absorption? - protein binding? - metabolites? - time to peak concentration? - t(1/2)? |
absorption: well absorbed orally
binding: none metabolites: completely metabolized to inactive compounds peak conc: 3-7 hr t(1/2) = 3-7 hr |
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phenytoin/fosphenytoin applications (5)
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gen. tonic-clonic seiaures,
partial seizures, status epilepticus, neuralgia, arrhythmia induced by cardiac glycosides |
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phenobarbital applications (6)
+ 2 primary uses |
Generalized tonic-clonic seizures,
partial seizures, myoclonic seizures, generalized seizures, neonatal seizures, status epilepticus 1°: alternative drug for focus & tonic-clonic seizures |
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primidone applications (2)
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generalized tonic-clonic seizures,
partial seizures |
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ethosuximide applications (1)
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first line therapy for uncomplicated absence seizures
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phenytoin/fosphenytoin adverse effects (7)
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Diplopia,
ataxia, gingival hyperplasia, hirsutism, neuropathy agranulocytosis (rare), nystagmus, facial coarsening |
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phenobarbital adverse effects (4)
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sedation,
cognitive issues, ataxia, hyperactivity |
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primidone adverse efffects (4)
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sedation,
cognitive issues, ataxia, hyperactivity |
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ethosuximide adverse effects (5)
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Gastrointestinal irritation,
lethargy, headache, dizziness, hyperactivity |
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phenytoin interactions (5)
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protein binding displaced by phenybutazone and sulfonamides
metabolized by 2C9/10 & 2C19 levels are increased by cimetidine, disulfiram, felbamate, & isoniazid levels are decreased by CBZ & phenobarbital PHT increases metabolism of CBZ, lamotrigine, levodopa, quinidine, warfarin, & OC's |
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phenytoin contraindications (2)
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hydantoin hypersensitivity
(hydantoin is 3C, 2N ring with two ketones; a component of phenytoin) |
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phenobarbital interactions (3)
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induces numerous P450's
increases valproate, CBZ. felbamate, phenytoin, and lamotrigine metabolism PHB levels can be increased by valproate or phenytoin |
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phenobarbital contraindications (4)
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porphyria (heme production disorder),
severe liver dysfunction, respiratory disease may exacerbate absence seizure |
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primidone contraindications (4)
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porphyria (heme production disorder),
severe liver dysfunction, respiratory disease may exacerbate absence seizure |
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primidone interactions (3)
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induces numerous P450's
increases valproate, CBZ. felbamate, phenytoin, and lamotrigine metabolism PHB levels can be increased by valproate or phenytoin |
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ethosuximide interactions
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decreased clearance with valproate
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ethosuximide contraindications
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hypersensitivity to ethosuximide
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carbamazepine moa
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blocks high frequency firing of neurons though action on VG Na channels
decreases synaptic release of glutamate |
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carbamazepine PK
- absorption? - protein binding? - metabolites? - time to peak concentration? - t(1/2)? |
well absorbed orally
no significant protein binding metabolized to active epoxide hepatic elimination t(1/2) = 36 hr |
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carbamazipine clinical uses (4)
oxcarbazepine? |
generalized tonic-clonic seizures,
partial seizures, bipolar disorder, trigeminal neuralgia oxcarbazepin less potent and not used for bipolar disorder |
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carbamazipine adverse effects (9)
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toxicity:
nausea, diplopia, ataxia, hyponatremia & water intoxication, headache, aplastic anemia, agranulocytosis, leukopenia, rash |
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carbamazipine interactions (3)
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can increase metabolism of phenytoin, primidone, ethosuximide, valproate, & clonazepam
clearance can be inhibited by propoxyphene & valproate concentrations can be decreased by phenobarbital & phenytoin |
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carbamazepine contraindications
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concomitant use of MAOI's
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How is oxcarbazepine similar to and different from carbamazipine in moa and PK?
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moa - similar to CBZ
PK similar to CBZ except: - shorter t(1/2) - active metabolite has a longer duration |
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How is oxcarbazepine similar to and different from carbamazipine in adverse effects and interactions?
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ae: similar, but generally less severe than CBZ
interactions: similar, but less enzyme induction so fewer drug interactions than CBZ fewer hypersensitivity reactions than CBZ, but may cause hyponatremia more often than CBZ CI: still CI for use with MAOI's |
