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Maddy - NMSP Exam II > Pharm - Movement Disorders > Flashcards

Pharm - Movement Disorders Flashcards

1
Q

MOA levodopa

A

agonist at dopamine receptors

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2
Q

benefits of coadministration of levodopa with carbidopa

A
  • doesn’t cross BBB
  • reduced metabolism
  • increased plasma levels
  • increased half life
  • increased levodopa available for entry into the brain
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3
Q

describe the wearing-off phenomenon

A

occurs with long-term treatment with levodopa

each dose of levodopa effectively improves mobility for a period of time but rigidity and akinesia returns rapidly at the end of the dosing interval

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4
Q

side effects levodopa

A

GI: anorexia, nausea, vomiting

CV: postural hypotnesion, HTN with large doses

Dyskinesia: choreoathetosis (movement of intermediate speed, between quick, flitting movements of chorea and the slower, writing movements of athetosis)

Behavioral: depression, anxiety, agitation, insomnia, somnolence, confusion, delusions, hallucinations, nightmares, euphoria

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5
Q

describe the on-off phenomenon

A

off-periods of marked akinesia alternate over the course of a few hours with on-periods of improved mobility but often marked dyskinesia

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6
Q

what can provide temporary benefit to patients with severe off-periods in off-on syndrome when taking levodopa

A

subcutaneous injections of apomorphine

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7
Q

drug interactions with levodopa

A

MAOIs

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8
Q

levodopa is contraindicated in what patients

A
  • psychotic pts
  • pts w/ angle-closure glaucoma
  • pts w/ history of melanoma or suspicious undiagnosed skin lesions
  • pts with active peptic ulcer
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9
Q

MOA and metabolism of bromocriptine

A

ergot alkaloid derivate that is a D2 agonist

28% bioavailability - peak plasma concentration at 13 hours

extensive first pass metabolism with CYP3A4

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10
Q

MOA and metabolism of pramipexole

A

affinity for D3 receptors

90% excreted unchanged in urine - peak plasma concentration at 2 hours

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11
Q

MOA and metabolism of ropinirole

A

affinity for D2 receptors

CYP450 metabolism - peak plasma concentration 1-2 hours

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12
Q

side effects for dopamine agonists

A

GI: anorexia, nausea, vomiting, constipation, dyspepsia, reflux

CV: postural hypotension, digital vasospasm, peripheral edema, cardiac arrhythmias

Dyskinesias: similar to levodopa

Mental Disturbances: confusion, hallucinations, delusions

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13
Q

dopamine agonists are contraindicated in those with _____

A
  • pts with psychotic illness
  • recent MI
  • active peptic ulceration
  • peripheral vascular dz
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14
Q

compare MAO-A and MOA-B

what is significant about MAO

A

A: preferentially metabolizes NE and 5-HT

B: preferentially metabolizes phenylethylamine and benzylamine

(dopamine and tryptamine are metabolized equally by MAO-A and MAO-B)

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15
Q

MOA and metabolism of selegiline

A

selectively irreversible MAO-B inhibitor

slows breakdown of dopamine and prolongs antiparkinsonian effects of levodopa

10% bioavailability

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16
Q

selegiline should not be taken in patients who are also taking _____

A

meperidine, TCAs, or SSRIs

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17
Q

what are the other two drugs that are MAO-B inhibitors like selegiline?

A

rasagiline and safinamide

18
Q

MOA tolcapone

A

catechol-O-methyltransferase (COMT) inhibitors

prolongs activity of levodopa by inhibiting its peripheral metabolism –> decreases clearance and increases bioavailability

19
Q

compare tolcapone and entacapone

A

both COMT inhibitors

tolcapone: central and peripheral acting
entacapone: peripher only

20
Q

side effects COMT inhibitors (tolcapone and entacapone)

A
  • orange discoloration to urine
  • diarrhea
  • abd pain
  • sleep disturbances
21
Q

MOA and administration of apomorphine

A

agonist at dopamine D2 receptors

injected subcutaneously

22
Q

adverse effects apomorphine

A
  • nausea
  • dyskinesias
  • drowsiness
  • sweating
  • hypotension
  • injection site bruising
23
Q

MOA amantadine

A

antiviral agent whose MOA in parkinsonism is unknown

24
Q

adverse effects amantadine

A
  • livedo reticlaris (purplish mottling of skin)
  • restlessness
  • depression, irritability
  • insomnia
  • agitation, excitement
  • hallucinations
25
Q

MOA benztropine

A

mAChR antagonist

26
Q

MOA biperiden

A

mAChR antagonist

27
Q

MOA orphenadrine

A

mAChR antagonist

28
Q

MOA procyclidine

A

mAChR antagonist

29
Q

MOA trihexyphenidyl

A

mAChR antagonist

30
Q

what drugs are used to treat tremor

A

beta blockers:

  • metoprolol
  • propranolol

antiepileptic:
- primidone

serotonin receptor agonist:
- topiramate

benzo:
- alprazolam

IM injection:
- botulinum toxin A

31
Q

what drugs are used to treat huntington’s

A

dopamine blockers:

  • reserpine
  • tetrabenazine
  • olanzapine
  • perphenazine
  • haloperidol
32
Q

what drugs are used to treat tics

A

neuroleptic antipsychotics:

  • tetrabenazine
  • haloperidol
  • pimozide

alpha-adrenergic agonists:

  • clonidine
  • guanfacine

IM injection:
- botulinum toxin A

33
Q

what drugs are used to treat RLS (restless leg syndrome)

A

dopamine agonists:
- levodopa

Benzos:

  • diazepam
  • clonazepam

Non-ergot dopamine agonists:

  • pramipexole
  • ropinirole

alpha 2 delta Ca2+ channel ligands

  • gabapentin
  • pregabalin
34
Q

what drugs are used to treat ALS

A

Riluzole

  • only drug to have any impact on survival with ALS
35
Q

MOA riluzole

A

inhibits glutamate release and blocks NMDA and kainite-type glutamate receptors and inhibits voltage-dependent NA+ channels

36
Q

what drugs are used to treat wilson dz

A
  • penicillamine
  • potassium disulfide
  • trientine
37
Q

MOA penicillamine

A

chelating agent that forms stable complex with copper and is readily excreted by the kidney

38
Q

adverse effects penicillamine

A
  • N/V
  • nephritic syndrome
  • myasthenia
  • optic neuropathy
39
Q

MOA potassium disulfide

A

reduces intestinal absorption of copper

40
Q

MOA trientine

A

increases fecal excretion of copper by decreasing GI absorption
- chelating agent

Maddy - NMSP Exam II (12 decks)

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