Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

58 Cards in this Set

  • Front
  • Back
What are the only two inhibitory ACh NTs?
M2 & M4
What receptor does glutamate affect?
Which 5-HT receptor subtype in inhibitory?
What are the 7 sites of NT drug action?
AP in pre-synaptic fiber, synthesis, storage, metabolism, release, reuptake, degredation, NT receptor, and change in ion conduction @ receptor site.
What are the 4 prim mechanisms of seizure activity?
Excessive glutamate, activation of NMDA receptors, Ca2+ entry, & GABA inhibition
What are the three types of partial seizures?
Simple, complex, & secondarily generalized
What are the 5 types of general seizures?
Absence, myoclonic, tonic-clonic, atonic, and infantile spasms
What's the difference between general and partial seizures?
General affect both hemispheres; partial are localized
What are the sodium channel blockers?
Cabamazepine, oxazepine, phenytoin, fosphenytoin, zonisamide, and lamotragine
Which is the only AED with almost no hepatic metabolism?
What are the GABAergic AEDs?
Valproates, gabapentin, and tiagabine
Which AED blocks calcium channels?
Which AEDs block glutumate action?
Felbamate and topiramate
What's the MoA for Na+ channel blockers?
Less Na+ influx -> dlower depolarization -> slower firing rate -> longer inactivation state -> glutamate inhibition
Which 3 AEDs are available as IV?
Fosphenytoin, valproates, and levetiracetam
What is the metabolism of cabamazapine like?
Metabolized to active metabolites hepatically; autoinducer of CYP 3A4; active metabolite excreted renally
What happens to carbamazepine [] over time?
They decrease, so more is needed
What are the AEs of carbamazepine?
Sedation, low WBC count, rash, & rarely hepatotoxicity
Which AED is 1st line for children?
How is oxazapine different than carbamazepine?
Ox is a prodrug and is a less potent CYP 3A4 inducer
What is oxazapine metabolized to?
What are the PKs of phenytoin?
Hepatic metabolism through 3A4; 3A4 inducer; non-linear dosage response curve
Which is the only AED that is available IM?
What are the AEs of phenytoin?
sedation, rash, hypersensitivity (hepatic, fever, rash), cardio (hypotension, brady, QRS pronlongation)
Which AEs are seen more often in IV admin of phenytoin?
Cardio (hypotension, brady, QRS pronlongation), thrombophlebitis (tissue crystalization), and purple glove syndrome (extravasation of phenytoin)
What are the significant drug-drug ix w/ phenytoin?
3A4 substrates, protein binding competition (valproate displaces phenytoin), antacids (reduce bioavailability)
What is fosphenytoin and what is it soluble in?
prodrug of phenytoin w/ half-life conversion of 15 mins.; H2O soluble
What are the maximum rates of infusion for phenytoin and fosphenytoin and what is the proportion of these? What accounts for the difference?
50 mg/min (25 geriatric) for phen and 150 mg/min for fos; 3x; fos is water soluble
What two AEs are unique to zonisamide amongst AEDs?
agitation & sulfa allergy Cx
What are the AEs of of valproates?
N/V, more common hepatotoxicity, hyperammonemia (high [NH3])
PKs of gabapentin?
80-90 percent excreted unchanged renally
AEs of gabapentin
sedation, agitation, & N/V; not many D-D Ix
PKs of tiagabine?
Rapid and complete absorption through hepatic metabolism
AEs of tiagabine?
sedation and psych symptoms (hallucinations and paranoia)
Ethosuximide PKs and AEs?
Hepatic metabolism; GI upset, sedation, rash
PKs of felbamate & topiramate?
50 percent hepatic metabolism and 50 percent excreted unchanged in urine
Which has a greater risk for hepatotoxicity: felbamate or topiramate?
AEs of topiramate?
Dope amax (mem and conc) and aggressive behavior
Levetiracetam PKs:
Completely absorbed; 66 percent excreted unchanged by kidneys
AEs of levetiracetam?
sedation and headache
Which AEDs are >90% protein bound?
phenytoin, vaproates, & tigabine
Which BZD lacks active metabolites?
Which BZD has shortest half-life and longest?
Diaz and loraz
What is synonomous w/ schizo + symptoms? Relation to NT?
active and excess DA
What is synonomous w/ schizo - symptoms? Relation to NT?
passive & excess 5-HT
Difference between typicals and atypicals?
Atypicals exhibit greater 5-HT2 affinity and typicals exhibit greater D2 affinity
What effect does 5-HT2 blockade have?
Increased DA
Where do TCAs exert NE & 5-HT effects?
In synaptic cleft
PDs & PKs of TCAs?
Rapidly absorbed, large Vd (particularly cardiac & CNS tissue), extensively protein bound, prim hep metab
Anti-ACh, ortho hypot, hepatotox, lower seizure threshold, withdrawal syndrome
AEs of SSRIs?
Brady & EPS
irrevsible inhibition of of MAO -> increased NE, 5-HT, & DA within synapse
Hypertensive crisis, ortho hypoTN, hypokalemia, weight gain
D-D Ix?
Meperidine (CV instability, hyperpyrexia, coma)
Tyramine (food)
Mirtazapine MoA & PKs?
5-HT2 & 5-HT3 blockade; hepatic metab
Trazadone MoA & PKs
5HT2 blockade; hepat metab to active metabolites
Li MoA?
Reuptake inhibitor of 5HT and NE
Li PKs, Cx, & AE?
Rapid absorption and extensive clearing unchanged renally

Renal dys, dehydration, & Na+ depletion

Cognitive efects