Miscellaneous Quiz / Seizure Drugs

Random Miscellaneous Quiz

Can you name the Seizure Drugs?

 Plays Quiz not verified by Sporcle

Forced Order
Also try: 2-Letter Blitz
Score 0/130 Timer 20:00
Drug Use: adjunctive therapy for partial seizures
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
Fosphenytoin class
Diazepam class
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
Drug SE: Similar to carbamazepine (perhaps less tox). Fewer hypersensitivy reactions.
Drugs effects: increase GABAergic transmission
Drug Contraindications: Hepatic cirrhosis
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)
Drug P-kinetics: oral, good bioavailability
Phenobarbital class
Vigabatrin class
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 interactions: Valproate doubles half life, decreased by CYP inducing drugs & oral contraceptives
Drug Use: mgmt of epilepsy pts w/ porphyria
Drug SE: Gastric distress, transient lethargy, rare skin rash & more marrow suppression (periodic monitoring necessary)
Clonazepam class
Carbamazepine class
Drug SE: Drowsiness, dizziness and wt. Gain, less common: psychosis & confusion & visual field defects, animal studies: intramyelinic edema
Drug SE: Idiosyncratic reactions (rash, agranulocytosis, hepatitis) more frequent.
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 MOA: Similar to phenytoin, also inhibition of Ca channels, & glutaminergic receptors
Chlorazepate class
Drug interactions: Less hepatic enzyme induction than carbamazepine --> fewer drug interactions.
Drug P-kinetics: adjunct drug for complex partial seizures (drowsiness and lethargy common -- raise doses slowly).
Classes/Drugs effects: Decreased repetitive neuronal firing
Drugs Use: Continuous seizure activity: gran-mal, status epilepticus. Febrile seizures. Or alternative therapies for absence and atypical absence, myoclonic and atonic seizues. Use
Drugs MOA: Allosteric activator of GABA mediated Cl- conductance
Mephenytoin class
Drug SE: Less toxic and less side effects than phenytoin.
Drug MOA: inhibition of Carbonic Anhydrase
Drug Use: Partial seizures & West's syndrome, infantile spasm (w/ corticotropin)
Class MOA: State dependent Na+ channel blockade, prolongs inactivated state (and thus refractory period), Ca++ mediated neurotransmitter release.
Drug SE: minor: nervousness, dizziness, tremor, difficulty concentrating & depression. Discontinue if psychosis confusion, or somnolence occurs. Rash common
Drug effects: inc. CO2, decreasing the depolarizing action of bicarbonate ions (moving through GABA receptor ion channels)
Drug SE: Hypokalemia, hyperchloremic metabolic acidosis, phosphatemia -> increased pH in urine may cause Ca-PO4 stones, hyperammonemia in cirrhotics
Drug P-kinetics: Similar to phenytoin. Used in pts hypersensitive to phenytoin. Saturable metb
Drug Use: Adjunct therapy for partial seizures, also effective for neuropathic pain tx (indicated to tx postherpetic neualgia), also mgmt of migraine HA
Primidone class
Drug P-kinetics: Not metabolized renal excretion, short half life
Drug use: Third line for refractory partial seizures, but does have effectiveness Lennox Gastaut syndrome
Inhibitory GABAergic interneurons that communicate between cortical neurons - can be overcome during seizure
Lorazepam class
Drug SE: Drowsiness, cognitive impairment
Drug SE: skin rash, sedation, & behavioral changes
Drug P-kinetics: Administer slowly and inc. dose
Drug interactions: Valproic acid decreases ethosuximide clearance
Zonisamide class
Drug SE: Similar to phenobarbital
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: Mainly excreted in urine
Oxcarbazepine class
Drug interactions: Little effect to other antiseizure drugs
Tiagabine class
Levetiracetam class
Drug Use: Similar to phenytoin
Drug Use: Adjunctive for partial & genralized tonic-clonic seizures, certain myoclonias, febrile seizures & infantile spasms
Drug effects: Na+ & Ca++ channel conductance
Drug Use: Third line for absence seizures behind succinimides
Drug SE: Sedation, hemeralopia, mild metabolic acidosis, idiosyncratic derm reactions, reversible nephrotic syndrome
Drug P-kinetics: Oral, well absorbed, duration 8-12h, secreted by kidney. Effectiveness declines in 2-3 days.
Gabapentin class
Drug Use: Febrile seizures (Benzodiezepine first), second line for simple partial, grand mal & as adjunct for SE
Phenytoin class
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
Drug Use: Similar to phenytoin but less efficacious
Drug P-kinetics: IV for SE; can be more effective & durable than diazepam.
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
Drug MOA: Several, inc. GABA transmission, effects Na channel opening
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 MOA: Similar to phenytoin. Blocks Na+ channels, inhibits repetive firing in cells; decreases synaptic transmission. Also inhibition of catecholamine uptake. Effective against
Drug Use: Similar to carbamazepine (less potent)
Drug P-kinetics: Glucuronide is the active metabolite (10-hydroxycarbamazepine)
Drug Use: First line for absence (petit mal)--only use
Drug SE: Significant toxicity issue, aplastic anemia & hepatitis (=3rd line)
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
Drug interactions: No hepatic enzyme induction. Drug interactions are negligible
Drug interactions: Inc. plasma phenytoin & valproic acid but dec. carbamazepine levels
Ethosuximide class
Drug P-kinetics: Good oral absorption, plasma protein bound (not displaced by other drugs), induces microsomal enzymes, active metabolites
Drug MOA: Similar to phenytoin w/ active metabolite = phenobarbital & PEMA
Drug MOA: NMDA receptor blockade
Drug MOA: Similar to carbemazepine
Valproic acid class
Mephobarbital class
Drug SE: Somnolence, dizziness, ataxia, HA, & tremor
Congeners of phenytoin
Drug SE: Somnolence, asthenia & dizziness. Rare: anemia, leukopenia
Drug SE: Significant toxicity. Neurologic: dizziness, HA, diplopia, nausea, somnolence ataxia. Sytemic: hypersensitivity, skin rash (1-2% life threatening in children--SJS)
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: dizziness, HA, nausea, and diplopia
Drug P-kinetics: Metabolized to PEMA & phenobarbital (steady state after 20 days)
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 interactions: Birth control pills are less effective
Drug Use: limited use because of rapid tolerance: epileptic women during menses
Drug P-kinetics: Rapidly absorbed, glucuronidated, 55% protein bound
Drug interactions: does not effect levels of other seizure drugs
Drug MOA: Inteferes w/ synaptic vesicle PRO (SV2A)
Lamotrigine class
Drug interactions: CYP inducers (e.g. phenobarbital and phenytoin) may increase metabolism; and enzyme inhibitors (erythromycin, isoniazid, cimetidine, fluoxetine) inhibit metaboli
Drug MOA: Similar to ethosuximide effects on gCa++
Drug MOA: Alters GABA metabolism, decrease Ca entry presynaptically?
Felbamate class
Drug SE: Mostly during first 4 wks (dose-related; give drug slowly) = somnolence, fatigue, dizziness, significant psychomotor & cognitive slowing, paresthesia, increased IOP, nervo
Drugs that decrease seizure threshold
Drug effects: Raises threshold for firine of repetitive thalamic firing
Drug MOA: Blocks sustained repetitive firing - inhibits Na+ currents and increases GABA levels in the brain. Increase membrane K+ conductance (high levels)
Pregabalin class
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 MOA: Inhibits gCa++, Na+/K+ atpase & inhibits GABA aminotransferase
Drug SE: Relatively safe but marked sedation
Drug MOA: Inhibits GABA uptake (GAT-1 transporter isotype)
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 Use: adjunctive therapy for partial-onset seizures (w or w/o generalization)
Trimethadione class
Topiramate class
Drug P-kinetics: Similar to phenytoin. Saturable to nirvanol, the active metabolite
Drug use: similar to phenobarbital
Ethotoin class
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
Excitatory glutaminergic projection neurons that communicate in & out of cortex, layers III, IV, and V - synchronous firing is responsible for seizures
Drug inteeractions: Displaces phenytoin from plasma proteins, inhibits metabolism of many drugs (phenobarbital [can cause stupor or coma], phenytoin & carbamazepine).
Drug MOA: Inhibits GABA transaminase (results in more GABA release)
Drug P-kinetics: Activity is not correlated w/ plasma half life, eliminated via kidneys
Drug P-kinetics: Good oral absorption, not PRO bound, liver metabolized
Acetazolamide class
Drug MOA: Probably effects Na channels, Kainate & AMPA receptor inhibition, potentiates GABA inhibitory effects
Drug SE: Acute: stupor or coma, hyperirritability, convulsions, & resp depression. Chronic: drowsiness, vertigo, ataxia, diplopia, & blurred vision. Hematologic disorders (aplastic
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)

You're not logged in!

Compare scores with friends on all Sporcle quizzes.
Join for Free
Log In

You Might Also Like...

Show Comments


Created Aug 21, 2011ReportFavoriteNominate

Top Quizzes Today

Score Distribution

Your Account Isn't Verified!

In order to create a playlist on Sporcle, you need to verify the email address you used during registration. Go to your Sporcle Settings to finish the process.

Report this User

Report this user for behavior that violates our Community Guidelines.