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35 Cards in this Set

  • Front
  • Back

carbamazepine

Na channel blocker


For treating seizures

phenytoin

Na channel blocker


For treating seizures

topiramate

Na channel blocker


For treating seizures

zonisamide

Na channel blocker


For treating seizures

lamotrigine

Na channel blocker


For treating seizures

valproate

Na and Ca channel blocker


For treating seizures

ethosuximide

Ca channel blocker


For treating seizures

benzos/barbs

GABAa recep agonist

tiagabine

prolongs presence of GABA in synapse

vigabatrin

inhibits degradation of GABA

L-dopa

drug that restores DA in brain

carbidopa

drug that inhibits L-dopa metabolism in periphery, increasing its CNS levels

pramipexole/ropinirole

DA agonists


for treatment of PD

benztropine/trihexyphenidyl

anti-ACh drugs


for treatment of PD



selegiline/rasagiline

selective MAO-B inhibitor (MAO-B degrades DA in striatum)


for treatment of PD

entacapone

COMT inhibitor (COMT degrades DA)


acts in periphery only


for treatment of PD

tolcapone

COMT inhibitor (COMT degrades DA)


acts centrally and peripherally


for treatment of PD

amantadine

NMDA inhibitor


treatment of L-dopa-induced dyskinesia

MPTP

drug byproduct that induces PD

donepezil

AChE inhibitor


when combined with memantine, shown to have greater benefit


for treatment of AD


tx often fails b/c of systemic side fx, untreatable tissue atrophy, and because AD is very complex

rivastigmine/galantamine

AChE inhibitor


for treatment of AD


tx often fails b/c of systemic side fx, untreatable tissue atrophy, and because AD is very complex

tacrine

AChE inhibitor


for treatment of AD


rarely used d/t adverse side fx


tx often fails b/c of systemic side fx, untreatable tissue atrophy, and because AD is very complex

memantine

noncompetitive NMDAR antags; acts on Mg to prevent excitotoxicity


when combined with donepezil, shown to have greater benefit

atypical antipsychs/mood stabilizers/antideps

used to treat behavioral symps of AD

riluzole

only approved tx for ALS


unknown MOA, but fx include glutamate inhibits, NMDA/kainate inhib, Na inhib

baclofen

GABAb agonist


for treating ALS spasticity (ALS causes loss of upper motor neurons, which means loss of GABA)

diazepam

GABAa agonist


for treating ALS spasticity (ALS causes loss of upper motor neurons, which means loss of GABA)

amitriptyline

TCA


anti-ACh drug to prevent excessive saliva production in ALS

acamprosate

helps prevent alcoholic relapse


MOA: modulates changes in glutamatergic & GABAergic activity associated w/ EtOH use


doesn't prevent withdrawal

naltrexone

opioid antagonist (opioids are involved in reinforcement pathways)


can block dependency fx of morphine when co-adm

disulfiram

ALDH inhibitor


increases acetaldehyde levels (can cause toxicity)


poor compliance and potential DDIs w/ EtOH-containing OTCs

clonidine

a2 agonist


effective at reducing CNS hyperactivity associated w/ acute opioid withdrawal

naloxone

drug for reversing opioid ODs

amphetamine

directly acting drug that has highest increase of DA release


MOA: causes dumping of DA in synapse through DAT uptake

cocaine

directly acting drug that has a high increase of DA release


MOA: inhibits DAT, which is responsible for uptake of DA in synapse