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151 Cards in this Set

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  • Back
what are the first generation epilepsy drugs?
carbamazepine, phenytoin, phenobarbital, valproic acid, clonazepam, ethosuximide
what drug is only effective against absence seizures?
ethosuximide
what are the second generation epilepsy drugs?
oxcarbazepine, gabapentin, pregabalin, ezogabine, lamotrigine, levetiracetam, topiramate, felbamate
what are the narrow spectrum epilepsy drugs?
carbamazepine, phenytoin, phenobarbital, ethosuximide which are 1st gen, and oxcarbazepine, gabapentin, pregabalin, ezogabine which are 2nd gen
what are the broad spectrum epilepsy drugs?
valproic acid and clonazepam which are 1st gen, and lamotrigine, levetiracetam, topiramate, felbamate, zonisamide which are 2nd gen
what NT alterations are responsible for seizures?
GABA and glutamate, GABA antagonists or glutamate agonists are convulsant
what type of drugs are anticonvulsant?
drugs that enhance GABA or inhibiti glutamate
what is the kindling model?
low intensity electrical stimulation repeatedly leads to seizure activity
what is the cause of generalized epilepsy?
strong genetic component, ion channel mutations
what channel is involved in absence seizures?
voltage gated T type Ca2+ channel, cortex activated by these channels, thalamocortical circuit is dysfunctional
what are some of the genetic mutations in ion channel receptors in epilepsy?
voltage gated Na channel subunit mutations(promotes depol and neuronal excitability), voltage gated K channel(prolong depol and increases neuronal hyperexcitability
what other ion channel undergoes a mutation that leads to epilepsy?
GABA A
what causes partial seizures?
focal lesions such as head trauma, stroke, tumors
what is the most prevalent partial seizure?
complex partial seizure arising from mesial temporal lobe, sensitive to damage
what is the most common lesion associated with mesial temporal lobe seizure?
hippocampal sclerosis
what occurs in the dentate gyrus?
high levels of neurogenesis for memory, damage can lead to altered firing
what are the three major categories for pharmacotherapy?
1)limit repetitive firing by promoting inactivated state of voltage gated Na channels 2)enhance GABA mediated synaptic inhibition(inhib Cl- ion channel)3)inhibition of voltage activated Ca2+ channels associated with T type Ca2+ currents
what type of drugs work on simple partial, complex partial and partial with secondary generalized tonic clonic seizures?
carbamazepine ,phenytoin, valproic acid, lamotrigine, topiramate, zonisamide
what is the function of benzodiazepines and barbiturates?
enhance GABA A receptors, enhances Cl- flow, hyperpolarizes the membrane
what type of seizures do benzodiazepines and barbiturates work on?
partial and tonic clonic seizures
at high doses what can benzodiazepines and barbiturates be used for?
status epilepticus
what inhibits GABA transport site preventing reuptake back into presynaptic cell?
Tiagabine
what are some characteristics of absence seizures?
presence of thalamic and neocortical discharge of 3/sec generalized spike and wave discharges
what was the first drug to show anti seizure activity without sedative effects?
phenytoin
what is phenytoin effective against?
partial seizures, at higher doses against tonic clonic seizures but NOT absence
what is the action of phenytoin at therapeutic doses?
slows recovery of Na 2+ channels from inactivation
what is the action of phenytoin at higher doses?
non selective effects including enhancing GABA
is phenytoin extensively or weakly bound?
extensively bound
what drug competes with phenytoin for protein binding?
valproate
what drug's metabolism does phenytoin inhibit?
warfarin, increase bleeding disorders
is phenytoin an enzyme inducer or inhibitor
inducer, can enhance metabolism of oral contraceptives
what are the A/E of phenytoin?
cosmetic:facial hair, skin problems, rash(sometimes Stevens Johnson), GINGIVAL HYPERPLASIA(>20%, treat with folic acid), osteoporosis(give vit D), megaloblastic anemia(give folate), mental dullness
what is the MOA of phenobarbital?
increase GABA A receptor mediated current, increases durationg of bursts, at higher doses can limit sustained repetitive firing(help status epilepticus)
what is phenobarbital effective for?
generalized tonic clonic and partial seizures, NOT effective in absence seizures
is phenobarbital an inducer or inhibitor?
inducer, faster metabolism of oral contraceptives
what are the A/Es of phenobarbital?
sedation early on, nystagmus and ataxia in excessive doses, cognitive dulling, agitation and confusion in the elderly, significant birth defects in pregnancy, hypoprothrombinemia with hemorrhage in newborns(prophylaxis in mother with vit K), osteoporosis (give vit D), megaloblastic anemia, mental dullness, behavioural toxicity in children
what is the MOA of carbamazepine?
limits firing of AP evoked by sustained depol, works by altering the rate of recovery of voltage gated Na channels from inactivation
what is carbamazepine the primary drug for?
partial(simple and complex) and generalized tonic clonic seizures
what should be monitored while on carbamazepine?
renal and hepatic fxn
what is another use for carbamazepine?
bipolar disorder including refractory patients
is carbamazepine an inducer or inhibitor?
inducer, increases metabolism of oral contraceptives
what are the A/E of carbamazepine?
drowsiness, vertigo, ataxia, blurred vision(should increase dose slowly), acute toxicity(coma, convulsions, resp depression), vomiting, aplastic anemia, agranulocytosis, hypersensitivity rxns
what is the advantage of oxcarbazepine?
prodrug that results in less potent enzyme inducer, does not interfere with warfarin, it does reduce steroid oral contraceptives
what is oxcarbazepine approved for?
monotherapy or adjunct therapy for partial seizures
what is the MOA of ethosuximide?
inhibit clonic seizures, reduces the low threshold of Ca2 currents, T type currents in thalamic neurons, does NOT inhibit sustained repetitive firing or enhance GABA responses
what is ethosuximide effective for?
absence seizures but NOT tonic clonic seizures
what are the A/E of ethosuximide?
parkinson like symptoms, photophobia, restleness, inability to concentrate and other CNS effects, uticaria, serious skin reactions, leukopenia, thrombocytopenia, aplastic anemia
what is the MOA of valproic acid?
inhibits sustained repetitive firing by depol, prolongs recovery of voltage activated Na channels from inactivation, increase GABA CNS levels, reduces T type Ca2 currents
what type of seizures is valproic acid effective for?
partial, myoclonic, tonic clonic and absence
what are the A/E of valproic acid?
anorexia, nausea, vomiting, sedation, ataxia, tremor, chronic effects in some patients(weight gain, alopecia, rash), can elevate hepatic transaminases
what are some drug interactions of valproic acid?
inhibits various liver enzymes, highly bound to albumin so can displace phenytoin, rare adverse interaction between valproate and clonazepam(ABSENCE STATUS EPILEPTICUS)
what population should valproic acid be avoided?
pregnant women, can effect cognitive development, should be AVOIDED in women during child bearing years, associated with polycystic ovary system
what is the MOA of clonazepam?
a benzodiazepine, increase frequency of GABA A activated Cl channels
what is clonazepam approved for?
absence seizures and myoclonic seizures
what are the A/E of clonazepam?
drowsiness, lethargy, cognitive effects
what is the MOA of gabapentin and pregabalin?
act at Ca2 channel subunit alpha2 delta1, may lead to increase GABA transport
what type of seizures are gabapentin and pregabalin effective for?
partial and some generalized seizures
what other conditions are gabapentin and pregabalin effective for?
migraine, chronic neuropathic pain, bipolar disorder
what are the A/Es of gabapentin and pregabalin?
somnolence, dizziness, ataxia, fatigue
what is the MOA of ezogabine?
targets neuron specific voltage gated K channels to dampen neuronal hyperexcitability
what is ezogabine effective for?
drug resistant partial seizures
what is the MOA of lamotrigine?
blocks sustained repetitive firing and delays recovery from inactivation of Na channels, may also inhibit glutamate release
what is lamotrigine metabolized by?
glucuronidation
what drugs interfere with lamotrigine metabolism?
valproate inhibits glucuronidation and phenytoin, carbamapezine, phenobarbital reduce the plasma concentration
what seizures is lamotrigine effective for?
partial and secondary generalized tonic clonic seizures, generalized tonic clonic seizures and in absence seizures
what is Lennox Gastaut syndrome?
multiple seizure types, mental retardation, refractoriness to anti seizure medication
what is the MOA of Levetriacetam?
unknown, binds to synaptic vesicle protein, SV2A
what seizures is levetriacetam effective for?
partial, generalized tonic clonic and myoclonic
what are the A/E of levetriacetam?
well tolerated, some somnolence, asthenia, dizziness, low incidence of thinking/memory problems, may cause mood changes
what are the drug interactions of levetriacetam?
none
what is the MOA of topiramate?
reduces voltage gated Na currents, activates hyperpolarizing K currents, enhances GABA currents, limits activation of AMPA receptors(glutamate receptors), also inhibits carbonic anhydrase, increases acidity which might suppress seizures
what is a PK issue with topiramate?
reduces oral contraceptive plasma levels
what conditions is topiramate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut, migraine prevention
what is the MOA of topiramate?
reduces voltage gated Na currents, activates hyperpolarizing K currents, enhances GABA currents, limits activation of AMPA receptors(glutamate receptors), also inhibits carbonic anhydrase, increases acidity which might suppress seizures
what are some A/E of topiramate?
somnolence, fatigue, weight loss, nervousness, precipitate renal caliculi, risk of glaucoma, cognitive impairment in 1/3 of the patients
what is a PK issue with topiramate?
reduces oral contraceptive plasma levels
what conditions is topiramate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut, migraine prevention
what is the MOA of felbamate?
inhibits NMDA responses and potentiates GABA evoked responses
what is the MOA of topiramate?
reduces voltage gated Na currents, activates hyperpolarizing K currents, enhances GABA currents, limits activation of AMPA receptors(glutamate receptors), also inhibits carbonic anhydrase, increases acidity which might suppress seizures
what is the MOA of topiramate?
reduces voltage gated Na currents, activates hyperpolarizing K currents, enhances GABA currents, limits activation of AMPA receptors(glutamate receptors), also inhibits carbonic anhydrase, increases acidity which might suppress seizures
what are some A/E of topiramate?
somnolence, fatigue, weight loss, nervousness, precipitate renal caliculi, risk of glaucoma, cognitive impairment in 1/3 of the patients
what conditions is felbamate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut syndrome
what is a PK issue with topiramate?
reduces oral contraceptive plasma levels
what is a PK issue with topiramate?
reduces oral contraceptive plasma levels
what is the MOA of topiramate?
reduces voltage gated Na currents, activates hyperpolarizing K currents, enhances GABA currents, limits activation of AMPA receptors(glutamate receptors), also inhibits carbonic anhydrase, increases acidity which might suppress seizures
what conditions is topiramate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut, migraine prevention
what conditions is topiramate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut, migraine prevention
what is the MOA of felbamate?
inhibits NMDA responses and potentiates GABA evoked responses
what are the A/Es of felbamate?
when given in combo with other large doses of other anticonvulsants, rash and potentially lethal toxicities
what is the MOA of zonisamide?
inhibits T type Ca2 currents, prolongs the inactivated state of voltage gated Na channels and inhibits brain carbonic anhydrase
what are some A/E of topiramate?
somnolence, fatigue, weight loss, nervousness, precipitate renal caliculi, risk of glaucoma, cognitive impairment in 1/3 of the patients
what conditions is felbamate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut syndrome
what are some A/E of topiramate?
somnolence, fatigue, weight loss, nervousness, precipitate renal caliculi, risk of glaucoma, cognitive impairment in 1/3 of the patients
what is a PK issue with topiramate?
reduces oral contraceptive plasma levels
what are the A/Es of felbamate?
when given in combo with other large doses of other anticonvulsants, rash and potentially lethal toxicities
what is the MOA of felbamate?
inhibits NMDA responses and potentiates GABA evoked responses
what is the MOA of felbamate?
inhibits NMDA responses and potentiates GABA evoked responses
what conditions is zonisamide useful for?
partial and generalized tonic clonic seizures, absence seizures, NOT myoclonic seizures
what conditions is topiramate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut, migraine prevention
what is the MOA of zonisamide?
inhibits T type Ca2 currents, prolongs the inactivated state of voltage gated Na channels and inhibits brain carbonic anhydrase
what conditions is felbamate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut syndrome
what conditions is felbamate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut syndrome
what are some A/E of topiramate?
somnolence, fatigue, weight loss, nervousness, precipitate renal caliculi, risk of glaucoma, cognitive impairment in 1/3 of the patients
what are the A/E of zonisamide?
somnolence, anorexia, dizziness, in children-hyperthermia and oligohydrosis , with other antiepileptic drugs-steven johnson, agranulocytosis, aplastic anemia
what are the A/Es of felbamate?
when given in combo with other large doses of other anticonvulsants, rash and potentially lethal toxicities
what conditions is zonisamide useful for?
partial and generalized tonic clonic seizures, absence seizures, NOT myoclonic seizures
what is the MOA of topiramate?
reduces voltage gated Na currents, activates hyperpolarizing K currents, enhances GABA currents, limits activation of AMPA receptors(glutamate receptors), also inhibits carbonic anhydrase, increases acidity which might suppress seizures
what is the MOA of felbamate?
inhibits NMDA responses and potentiates GABA evoked responses
what are the A/Es of felbamate?
when given in combo with other large doses of other anticonvulsants, rash and potentially lethal toxicities
what is the MOA of zonisamide?
inhibits T type Ca2 currents, prolongs the inactivated state of voltage gated Na channels and inhibits brain carbonic anhydrase
what is the MOA of zonisamide?
inhibits T type Ca2 currents, prolongs the inactivated state of voltage gated Na channels and inhibits brain carbonic anhydrase
what are the A/E of zonisamide?
somnolence, anorexia, dizziness, in children-hyperthermia and oligohydrosis , with other antiepileptic drugs-steven johnson, agranulocytosis, aplastic anemia
what is a PK issue with topiramate?
reduces oral contraceptive plasma levels
what conditions is felbamate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut syndrome
what conditions is topiramate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut, migraine prevention
what conditions is zonisamide useful for?
partial and generalized tonic clonic seizures, absence seizures, NOT myoclonic seizures
what conditions is zonisamide useful for?
partial and generalized tonic clonic seizures, absence seizures, NOT myoclonic seizures
what are the A/Es of felbamate?
when given in combo with other large doses of other anticonvulsants, rash and potentially lethal toxicities
what are some A/E of topiramate?
somnolence, fatigue, weight loss, nervousness, precipitate renal caliculi, risk of glaucoma, cognitive impairment in 1/3 of the patients
what are the A/E of zonisamide?
somnolence, anorexia, dizziness, in children-hyperthermia and oligohydrosis , with other antiepileptic drugs-steven johnson, agranulocytosis, aplastic anemia
what is the MOA of zonisamide?
inhibits T type Ca2 currents, prolongs the inactivated state of voltage gated Na channels and inhibits brain carbonic anhydrase
what are the A/E of zonisamide?
somnolence, anorexia, dizziness, in children-hyperthermia and oligohydrosis , with other antiepileptic drugs-steven johnson, agranulocytosis, aplastic anemia
what conditions is zonisamide useful for?
partial and generalized tonic clonic seizures, absence seizures, NOT myoclonic seizures
what is the MOA of topiramate?
reduces voltage gated Na currents, activates hyperpolarizing K currents, enhances GABA currents, limits activation of AMPA receptors(glutamate receptors), also inhibits carbonic anhydrase, increases acidity which might suppress seizures
what is the MOA of felbamate?
inhibits NMDA responses and potentiates GABA evoked responses
what are the A/E of zonisamide?
somnolence, anorexia, dizziness, in children-hyperthermia and oligohydrosis , with other antiepileptic drugs-steven johnson, agranulocytosis, aplastic anemia
what is a PK issue with topiramate?
reduces oral contraceptive plasma levels
what conditions is felbamate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut syndrome
what conditions is topiramate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut, migraine prevention
what are some A/E of topiramate?
somnolence, fatigue, weight loss, nervousness, precipitate renal caliculi, risk of glaucoma, cognitive impairment in 1/3 of the patients
what is the MOA of felbamate?
inhibits NMDA responses and potentiates GABA evoked responses
what are the A/Es of felbamate?
when given in combo with other large doses of other anticonvulsants, rash and potentially lethal toxicities
what is the MOA of zonisamide?
inhibits T type Ca2 currents, prolongs the inactivated state of voltage gated Na channels and inhibits brain carbonic anhydrase
what conditions is felbamate useful for?
partial and generalized seizures, refractory patients, Lennox Gastaut syndrome
what are the A/Es of felbamate?
when given in combo with other large doses of other anticonvulsants, rash and potentially lethal toxicities
what conditions is zonisamide useful for?
partial and generalized tonic clonic seizures, absence seizures, NOT myoclonic seizures
what is the MOA of zonisamide?
inhibits T type Ca2 currents, prolongs the inactivated state of voltage gated Na channels and inhibits brain carbonic anhydrase
what are the A/E of zonisamide?
somnolence, anorexia, dizziness, in children-hyperthermia and oligohydrosis , with other antiepileptic drugs-steven johnson, agranulocytosis, aplastic anemia
what conditions is zonisamide useful for?
partial and generalized tonic clonic seizures, absence seizures, NOT myoclonic seizures
what are the A/E of zonisamide?
somnolence, anorexia, dizziness, in children-hyperthermia and oligohydrosis , with other antiepileptic drugs-steven johnson, agranulocytosis, aplastic anemia
when do you start treating seizures?
after two unprovoked seizures, after the first if warranted by EEG discharges, abnormal neuro exam or other structural abnormality responsible for the seizure
what are the first line drugs for partial seizures?
carbamazepine, gabapentin, lamotrigine, levetiracetam, oxcarbazepine, phenobarbital, phenytoin, topiramate, valproate
what are the first line drugs for generalized seizures?
lamotrigine, levetiracetam, topiramate, valproate
what drugs are useful for absence seizures?
ethosuximide, valproate, lamotrigine
what drugs are useful for myoclonic convulsions?
valproic acid and levetiracetam
what is status epilepticus?
prolonged seizure, any type, greater than 30 min, give IV lorazepam, diazepam followed by phenytoin, phenobarbital, attend to HTN, hypoventilation
how should dosing of these drugs be handled?
gradual dose titration, improves CNS tolerability and reduces risk of idiosyncratic adverse effects, dose with least amount of sedation as possible
when can AEDs be discontinued?
can be considered after 2-4 years of seizure freedom, predictors of recurrence are adolescent onset, focal seizures, underlying neuro disorder, abnormal EEG at time of withdrawal, good outcome for idiopathic epilepsy syndrome of childhood
what is the long term prognosis?
excellent for most children with seizures, particularly if cryptogenic(unknown origin), long term mortality increased in childhood onset epilepsy
what are epileptics more likely to experience?
assault
how does alcohol affect epileptics?
the state of alcohol withdrawal aggravates the seizure, start sometime between 6-72 hrs after having 3 or more alcoholic drinks