Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
58 Cards in this Set
- Front
- Back
|
What are the only two inhibitory ACh NTs?
|
M2 & M4
|
|
|
What receptor does glutamate affect?
|
NMDA
|
|
|
Which 5-HT receptor subtype in inhibitory?
|
5-HT1
|
|
|
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?
|
Levetiracetam
|
|
|
What are the GABAergic AEDs?
|
Valproates, gabapentin, and tiagabine
|
|
|
Which AED blocks calcium channels?
|
Ethosuximide
|
|
|
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?
|
carbamazepine
|
|
|
How is oxazapine different than carbamazepine?
|
Ox is a prodrug and is a less potent CYP 3A4 inducer
|
|
|
What is oxazapine metabolized to?
|
carbamazepine
|
|
|
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?
|
Fosphenytoin
|
|
|
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?
|
Felbamate
|
|
|
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?
|
Loraz
|
|
|
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
|
|
|
TCA AEs?
|
Anti-ACh, ortho hypot, hepatotox, lower seizure threshold, withdrawal syndrome
|
|
|
AEs of SSRIs?
|
Brady & EPS
|
|
|
MAOI MoA?
|
irrevsible inhibition of of MAO -> increased NE, 5-HT, & DA within synapse
|
|
|
MAOI AEs?
|
Hypertensive crisis, ortho hypoTN, hypokalemia, weight gain
|
|
|
D-D Ix?
|
Meperidine (CV instability, hyperpyrexia, coma)
Sympathmimetics 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 |
