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47 Cards in this Set

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What is the 3 step pathyphysiology of a seizure?
1. Neurons can elaborate reponses leading to paroxymal bursts.
2. Abnormal neurons recuit normal ones to propagate the discharge of a seizure
3. Falure of normal inhibitory or enhancment of normal exicitatory activity.
When treating pts with epilepsy, should they be started off on a single or multiple agents?
Start on single agents with bolus for emergenices and start combinatino therapy if they fail 2 trials of single agents.
What rx are used for pratial seizures?
Carbamazepine
phenytoin
valproic acid
oxcarbazepine
lamotrigine
topiramate
Gabapentin
What rx are used for general tonic-clonic sieizures?
Phenytoin
carbamazepine/oxcarbazepine
valproic acid
topiramate
What rx are used for absence seizures?
Ethosuzimide
valproic acid
lamotrigine
What rx are used for myoclonic seizures?
Valproic acid
What rx are used for mixed seizures?
Lamotrigne and valpoic acid
What is the MOA of all antiseizures?
Elevate seixure threshold
Limit spread of abnormally discharged NTs
Stabilize cell membranes
Sucess depends on seizure type and pharacokinetic monitoring
Hydantoins= Phenytoin (Dilanton) and fosphenytoin (cerebyx)
MOA:
used for?
MOA:Limits spread of abnormally discharged NTs and stabilize cell membrane
Block Voltage dependent Na channels.
For partial and T/c seizures
A/e of hydantoins:
Secation, cognitive impairment, nystagums, ataxia
Peripherial neuropathy, gigivital hyperplasia, hirsutism, rash, bone loss
What is the dosing situation like with hydantoins?
One can give QD with ER capsules or suspension or multiple doses with chewables or parentral formulas. There is also IV available.
Barbituates: Phenobarbital (Luminal)
MOA:
For what kind of seizures?
MOA: Increases seizure threshold nad decreases excitatory NT activity (GABA binding)
Tonic clonic and partial seizures.
A/e:
Metabolized by liver so watch other meds.
Sedation,
depression
Hepatotoxicity
rash
hypotension and resp depression
hyperactivity in children
Barbituates: Primidone
(Mysoline)
MOA:
Same MOA as phenobarbital: increases seizure threashold nad decreases excitatory NT activity
Same a/e as phenobarbital
Carbamzepine (carbatrol, tegretol)
MOA:
MOA: Limits spread of abnormal NT discharge
Bloks V.G. Na channels
Liver metabolism: autoinducer, so increase dose
A/e:
n/v/d
Drowsiness, dizziness, blurred vision, *hematologic effects*
Rash, Hyponatremia and fluid retension
Valproic acid (depacon, depakote)
MOA:
Membrane stabilizer
Increases gaba levels
Blocks VG Na channels
Liver metabolism inhibitor
A/e:
GI
CNS: Drowsiness, ataxia, tremor
Increased liver fxn tests, hematologic
pancreatitis
wt gain
increase amonnia levels
Different forms of valproic acid available:
Sprincles, liquid, capsules, XR
injection
Succinamides: Ethosuximide (Zarontin)
MOA:
For:
MOA: Affects Na/K ATPase and calcium channels
Decreases Gamma-jydroxbutyrate
For ABSENCE SEIZURES ONLY
A/e of succinamides:
GI
CNS: drowsiness, parkinsonian movements...often goes away as therapy progresses
Benzodiazepines (Klonapin, Valium, Ativan)
MOA:
Enhances GABA activity
A/E:
Metabolism
Sedation, tolerance
Liver metabolism, no active metabolites
NEW AGENTS: Felbamate
MOA:
Limits spread of abnormal NT discharge and increases seizure threshold
A/e
CNS: Insomnia, dizziness, headache
GI: n.v.anorexia
Aoastic anemia
hepatic failure so monitor levels weekly and biweekly CBCs
Gabapentin (Neurontin)
MOA:
Eliminated:
Limits spread and uptake of excitatory NTs, increases GABA
*Renally eliminated*
Used for peripheral neuropathy
A/e:
CNS: Sedation, atxia, dizziness
Lamotrigine
MOA:
MOA:limits spread adn release of excitatory NTs by blocking Na chanels
A/e:
Rash! Titrate dose to avoid rash. (Steven-johnson syndrome)
Displopia, somnolence
Topiramate (Topamax)
MOA:
MOA:Potentiates GABA
Antagonizes glutamate
Blocks Na channels
Modulates Ca channels
A/E:
Parasthesias,
wt loss
GI
kidney stones
Tigabine (Gabitril)
MOA:
A/e
MOA: Inhibits GABA uptake
a/e: dizziness, sedation, HA depression GI
Oxcarbazepine (Trileptal)
MOA:
Similar to carbamazapine, limits spread of abnormally discharged NT through VG Na channels
*Does not induce own metabolism*
a/e:
CNS: nervousness, HA, dizziness
GI: Nausea
*HYPONATREMIA*
Rash
Levetiracetam (Keppra)
MOA:
A/e:
Unknown MOA
NO KNOWN RX INTERACTIONS
CNS: fatigue, altered behavior, anziety
infection
Zonisamide (Zonegran)
MOA:
Precautions:
Inhibits Na and Ca channels
CONTRAINDICATED IN PTS WITH ALLERGY TO SULFONAMIDES
A/e:
CNS: Somnolence, dizzziness, confusion
GI: Nausea, anorexia
Henatologic
Kidney stones
Pregabalin: Lyrica
MOA:
A.e:
Inhibits NT release
*Controlled substance*
CNS: Blurred vision, dizziness
GI: xerostomia
Vigabatrin (Sabril)
MOA:
A/e:
Increases GABA
Fatigue, headache, dizziness, drowsiness
agitation
what 2 drubs will interact to produce neurotoxic symptoms?
carbamazepine and lamotrigine
Phenytoin with what will incresae plasma levels of phenytoin:
Topiramate and Oxcarbazepine
Lamotrigine and what increase lamot. concentrations:
Valproic acid
Phenytoin and what decreases phenytoin plasma concentrations:
Valproic acid
Carbamazepine and what increase levels of carbamazepine?
valproic acid
Valproic acid and what increase its cocentration?
Felbamate
Which drug causes fetal hydantoin syndrome and neotatal hemmorhage?
What other rx should be avoided in pregnancy?
Phenytoin
Carbamazepine
valproic acid
phenobarbital
Which rx should be used in pregnancy?
Older agents are cat D, new ones are cat C, replete folic acid and Vit K