Miscellaneous Quiz / Seizure Drugs

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Can you name the Seizure Drugs?

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Drugs Use: First choice for most partial seizures & used commonly for generalized tonic-clonic seizures (either primary or secondary), used in combo for status epilepticus. Not for
Pregabalin class
Drug SE: Acute: stupor or coma, hyperirritability, convulsions, & resp depression. Chronic: drowsiness, vertigo, ataxia, diplopia, & blurred vision. Hematologic disorders (aplastic
Fosphenytoin class
Drug MOA: Inhibits GABA uptake (GAT-1 transporter isotype)
Drug P-kinetics: oral, good bioavailability
Drug P-kinetics: Oral absorption, completely absorbed (peaks after 3-7 hrs) partitions in H2O compartments. No PRO binding; [plasma] = [CSF]. Metabolized in liver by hydroxylation
Levetiracetam class
Drug use: Third line for refractory partial seizures, but does have effectiveness Lennox Gastaut syndrome
Drug Use: Third line for absence seizures behind succinimides
Drug P-kinetics: Mainly excreted in urine
Drug MOA: Inteferes w/ synaptic vesicle PRO (SV2A)
Drug P-kinetics: adjunct drug for complex partial seizures (drowsiness and lethargy common -- raise doses slowly).
Drugs P-kinetics cont: Metabolism: liver (CYP2C9/10 and CYP2C19) para-hydroxylation, then glucuronidation, metabolites are inactive, excreted in urine. DOSE DEPENDENT (saturable) a
Drug interactions: Valproic acid decreases ethosuximide clearance
Drug MOA: Similar to carbemazepine
Drug Use: adjunctive therapy for partial-onset seizures (w or w/o generalization)
Drug interactions: CYP inducers (e.g. phenobarbital and phenytoin) may increase metabolism; and enzyme inhibitors (erythromycin, isoniazid, cimetidine, fluoxetine) inhibit metaboli
Drug Use: adjunctive therapy for partial seizures
Drugs SE: Neurologic: Nystagmus (early); Ataxia and diplopia (adjust dose); incoordination; confusion; sedation (at high plasma levels); gingival hyperplasia and hirsutism (very co
Drug P-kinetics: Similar to phenytoin. Used in pts hypersensitive to phenytoin. Saturable metb
Clonazepam class
Drug P-kinetics: Good oral absorption, not PRO bound, liver metabolized
Drug P-kinetics: Administer slowly and inc. dose
Class Drug Interactions: PRO binding: displaced by other drugs (e.g. sulfonamides), leading to increased [free]; hypoalbuminemia-raising dose to maintain total drug concentration m
Drug P-kinetics: Good oral absorption, plasma protein bound (not displaced by other drugs), induces microsomal enzymes, active metabolites
Drug SE: Somnolence, asthenia & dizziness. Rare: anemia, leukopenia
Drug P-kinetics: Good oral absorption, taking w/ meals delays absorption & decreases toxicity. Fully ionized (anion is active) and PRO bound. Half-life 9-18 h; dose dependent clear
Drug Use: First line for generalized tonic-clonic seizures or monotherapy for partial seizures in adults, myclonic siezures, atypical absence, Lennox Gastaut. Alternative therapy f
Ethotoin class
Drug P-kinetics: IV for SE; can be more effective & durable than diazepam.
Drug P-kinetics: Activity is not correlated w/ plasma half life, eliminated via kidneys
Drugs MOA: Allosteric activator of GABA mediated Cl- conductance
Drug effects: inc. CO2, decreasing the depolarizing action of bicarbonate ions (moving through GABA receptor ion channels)
Drug interactions: Less hepatic enzyme induction than carbamazepine --> fewer drug interactions.
Drug P-kinetics: Glucuronide is the active metabolite (10-hydroxycarbamazepine)
Drug Use: Adjunctive for partial & genralized tonic-clonic seizures, certain myoclonias, febrile seizures & infantile spasms
Drug use: similar to phenobarbital
Drug Use: First line for generalized tonic-clonic siezures, atypical absence, myoclonic, atonic, effects against Lennox-Gastaut and West's syndrome. Used in the preventative mgmt o
Drug interactions: does not effect levels of other seizure drugs
Congeners of phenytoin
Drug SE: N/v & GI complaints (common & dose related - start drug gradually), abd pain, heartburn (gradual start, temporary reduction helps). common elevation in hepatic enzymes; he
Drug Use: Febrile seizures (Benzodiezepine first), second line for simple partial, grand mal & as adjunct for SE
Drug SE: Somnolence, dizziness, ataxia, HA, & tremor
Drug inteeractions: Displaces phenytoin from plasma proteins, inhibits metabolism of many drugs (phenobarbital [can cause stupor or coma], phenytoin & carbamazepine).
Drug SE: Gastric distress, transient lethargy, rare skin rash & more marrow suppression (periodic monitoring necessary)
Drug Use: limited use because of rapid tolerance: epileptic women during menses
Diazepam class
Tiagabine class
Felbamate class
Chlorazepate class
Drug effects: Raises threshold for firine of repetitive thalamic firing
Drug interactions: Valproate doubles half life, decreased by CYP inducing drugs & oral contraceptives
Drug MOA: NMDA receptor blockade
Gabapentin class
Drug P-kinetics: stops seizures, IV or rectally for SE. Chronic oral use ineffective b/c of tolerance.
Drug MOA: inhances inactivation of Na channels, blocks neurotrophic factor intracellular cascades (collapsin-response mediatior protein, CRMP-2)
Drug SE: skin rash, sedation, & behavioral changes
Drug interactions: Inc. plasma phenytoin & valproic acid but dec. carbamazepine levels
Drug SE: minor: nervousness, dizziness, tremor, difficulty concentrating & depression. Discontinue if psychosis confusion, or somnolence occurs. Rash common
Drug Use: Current 1st line drug for partial seizures (with others), except not used in SE. Established efficacy on mania, mood stabilization, bipolar disorder (lithium alternative)
Drugs that decrease seizure threshold
Drug Use: Similar to carbamazepine (less potent)
Drug MOA: Similar to phenytoin. Blocks Na+ channels, inhibits repetive firing in cells; decreases synaptic transmission. Also inhibition of catecholamine uptake. Effective against
Drug SE: Similar to carbamazepine (perhaps less tox). Fewer hypersensitivy reactions.
Drug Use: Similar to phenytoin
Drug SE: Less toxic and less side effects than phenytoin.
Drug MOA: Several, inc. GABA transmission, effects Na channel opening
Drugs effects: increase GABAergic transmission
Drug SE: Drowsiness, dizziness and wt. Gain, less common: psychosis & confusion & visual field defects, animal studies: intramyelinic edema
Drug Use: Similar to phenytoin but less efficacious
Drug P-kinetics: Oral, well absorbed, duration 8-12h, secreted by kidney. Effectiveness declines in 2-3 days.
Oxcarbazepine class
Drug SE: dizziness, HA, nausea, and diplopia
Drug Contraindications: Hepatic cirrhosis
Drug effects: Reduces low threshhold (T-type) Ca++ currents in thalamic neurons, responsible for generating rhythmic cortical discharge in absence attack. Reduces thalamic firing
Drug MOA: Inhibits gCa++, Na+/K+ atpase & inhibits GABA aminotransferase
Drug Use: mgmt of epilepsy pts w/ porphyria
Drug MOA: inhibition of Carbonic Anhydrase
Drug SE: Relatively safe but marked sedation
Drug P-kinetics: Not metabolized renal excretion, short half life
Drug interactions: No hepatic enzyme induction. Drug interactions are negligible
Ethosuximide class
Excitatory glutaminergic projection neurons that communicate in & out of cortex, layers III, IV, and V - synchronous firing is responsible for seizures
Drug P-kinetics: Metabolized to PEMA & phenobarbital (steady state after 20 days)
Drug MOA: Similar to phenytoin w/ active metabolite = phenobarbital & PEMA
Zonisamide class
Drug Use: First line for generalized tonic-clonic, partial, and absence seizure (Ethosuximide preferred b/c of drug's hepatotoxicity), atypical absence, myoclonic seizures
Drug MOA: Similar to phenytoin, also inhibition of Ca channels, & glutaminergic receptors
Mephobarbital class
Drug SE: Drowsiness, cognitive impairment
Mephenytoin class
Lamotrigine class
Drug Use: First line for absence (petit mal)--only use
Phenobarbital class
Inhibitory GABAergic interneurons that communicate between cortical neurons - can be overcome during seizure
Valproic acid class
Drug MOA: Probably effects Na channels, Kainate & AMPA receptor inhibition, potentiates GABA inhibitory effects
Drug effects: Na+ & Ca++ channel conductance
Drug Use: Adjunct therapy for partial seizures, also effective for neuropathic pain tx (indicated to tx postherpetic neualgia), also mgmt of migraine HA
Drug interactions: Birth control pills are less effective
Classes/Drugs effects: Decreased repetitive neuronal firing
Drug MOA: Similar to ethosuximide effects on gCa++
Drug SE: Significant toxicity. Neurologic: dizziness, HA, diplopia, nausea, somnolence ataxia. Sytemic: hypersensitivity, skin rash (1-2% life threatening in children--SJS)
Class MOA: State dependent Na+ channel blockade, prolongs inactivated state (and thus refractory period), Ca++ mediated neurotransmitter release.
Topiramate class
Drugs P-kinetics cont: Therapeutic plasma level 10 - 20 ug/mL. Toxic level > 20 ug/mL. Oral dosage: typical starting dose 300mg/d; frequently insufficient to reach therapeutic plas
Acetazolamide class
Lorazepam class
Drug SE: Significant toxicity issue, aplastic anemia & hepatitis (=3rd line)
Drugs P-kinetics: Oral. Absorbtion: intestines - complete, 3-12 h depending on formulation. Usually dissolved in propylene glycol which can be cardiotoxic; IM - unpredictable, prec
Drug MOA: Alters GABA metabolism, decrease Ca entry presynaptically?
Drug SE: Similar to phenobarbital
Drugs Use: Continuous seizure activity: gran-mal, status epilepticus. Febrile seizures. Or alternative therapies for absence and atypical absence, myoclonic and atonic seizues. Use
Drug SE: Mostly during first 4 wks (dose-related; give drug slowly) = somnolence, fatigue, dizziness, significant psychomotor & cognitive slowing, paresthesia, increased IOP, nervo
Drug P-kinetics: Rapidly absorbed, glucuronidated, 55% protein bound
Drug SE: Sedation, hemeralopia, mild metabolic acidosis, idiosyncratic derm reactions, reversible nephrotic syndrome
Trimethadione class
Drug interactions: Little effect to other antiseizure drugs
Drug Use: Partial seizures & West's syndrome, infantile spasm (w/ corticotropin)
Drug MOA: Blocks sustained repetitive firing - inhibits Na+ currents and increases GABA levels in the brain. Increase membrane K+ conductance (high levels)
Primidone class
Drug P-kinetics: long acting; one of the best for absence seizures, works for myoclonic seizures; prominent sedative effect; start with low doses -- raise over weeks)
Vigabatrin class
Phenytoin class
Drug SE: Idiosyncratic reactions (rash, agranulocytosis, hepatitis) more frequent.
Drug MOA: Inhibits GABA transaminase (results in more GABA release)
Drug P-kinetics: Similar to phenytoin. Saturable to nirvanol, the active metabolite
Drug SE: Hypokalemia, hyperchloremic metabolic acidosis, phosphatemia -> increased pH in urine may cause Ca-PO4 stones, hyperammonemia in cirrhotics
Carbamazepine class

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