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Neuro II Final DF > Kruse: DSA: Drugs for movement disorders > Flashcards

Kruse: DSA: Drugs for movement disorders Flashcards

1
Q

MAO-A preferentially metabolizes

A

norepinephrine and serotonin

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2
Q

MAO-B preferentially metabolizes

A

phenylethylamine and benzylamine

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3
Q

drugs equally metabolized by MAO-A and B

A

dopamine and tryptamine

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4
Q

selegiline

A

irreversible MAO-B inhibtior (inhibtis MAO-A at high doses)

-slows breakdown of dopamine to prolong effects of levodopa

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5
Q

selegiline is contraindicated in pts taking

A

TCAs, SSRIs, or meperidine

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6
Q

rsaagiline

A

irreversible inhibitor of MAO-B, more potent than selegiline

-treatment for early symptomatic PD

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7
Q

what most not be given with levodopa

A

nonselective MAO inhibtor bc of hypertensive crisis with accumulation of norepinephrine

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8
Q

COMT and levodopa

A

metaboloizes it to 3-O-methyldopa, which competes with levodopa for transport across the intestinal mucosa and BBB

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9
Q

COMT inhibitors _____ and _____ prolon activity of levodopa by inhibting peripheral metabolism

A

tolcapone (central and peripheral effects) and entacapone (peripheral effects only)

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10
Q

side effefcts of tolcapone

A

may cause increase in liver enzyme levels

  • rarely associated death from acute hepatic failure
  • side effects usually due to levodopa but include orange urine, diarrhea, ab pain, sleep disturbance
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11
Q

apomorphine use

A

dopamine agonist that acts at D2 receptors in caudate-putamen

-temporary relief of off-periods of akinesia in pts on dopaminergic therapy (benefit is 10 mintues)

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12
Q

apomorphine side effes

A

nausea (pretreat with antiemetic trimethobenzamide)

dyskinesias, drowsiness, sweating, hypotension, and injection site bruising

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13
Q

amantadine

A

antivairal agent whose MOA in parkinsomism is unknown

  • half-life 2-4 hours, peak at 1-4 hrs
  • may potentiate dopaminergic fnct by infulencing syn, release or reuptake of dopamine
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14
Q

amantadine adverse effects

A

restlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, confusion

may cause livedo reticularis (purple discolor of skin on legs)

-use with caution in pts with history of seizures or heart failure

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15
Q

mAChR antagonist may improve what but not what

A

tremor and rigidity but little effect on bradykinesia

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16
Q

anticholinergic agents used in PD

A

benztropine, biperiden, orphenadrine, procyclindine, trihexyphenidyl

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17
Q

AE of anticholinergic agents for PD

A

peripheral anticholinergic effects

sedation, mental confusion, constipation, urinaryu retention, blurred vision

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18
Q

B1 receptors have been impicated in some tremors and these respond well to

A

metoprolol and propranolol

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19
Q

symptomatic tremor can be controlled by antiepileptic drug ___ in smaler doses than those used to treat seizurews

A

primidone

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20
Q

topirimate

A

serotonin receptor agonist, effective in treatment of temor

21
Q

alprazolam

A

(benzo) along with IM injections of botulinum toxin A have been effective in some pts with tremor

22
Q

what drugs often alleviate chorea

A

drugs that impair dopaminergic NT like reserpine and tetrabenzine

-block vesicular monoamine transporter and deplete cerebral dopamine stores

23
Q

what enzymes are decreased in huntingtons

A

GABA glutamic acid decarboxylase (syn GABA) and choline acetyltransferase reduced in basal ganglia

-

24
Q

treatment for tics (most predictive and effective)

A

neuroleptic antipsychotics like pimozide

-bad side effects so not always first choice

25
Q

better choice for treatment of tics with less side effects

A

clonidine and guanfacine

26
Q

restless leg syndrome

A

respond to dopmaine agonist: levodopa, diazepam, conazepam, or opiates

-first line treatment is dopamine agonist PRAMIPEXOLE and ROPINIROLE

27
Q

ALS treament

A

riluzole only drug to have impact on survival in ALS (few months)

  • MOA: inhibtis glutamate release and blocks postsynaptic NMDA and kainite type glutamate receptors
  • inhibtis voltage dep sodium channels,
  • major AE are nausea and weakness
28
Q

Wilson disease

A

recessively inherited disorder of copper metabolism characteriszed by

  • biochem reduction in ceruloplasmin
  • increased copper in brain and viscera
  • signs of hepatic and neuro dysfunction
29
Q

treatment of wilson diseae

A

agents that reduce serum copper levels and low copper diet

  • penicillamine: chelating agent that forms stable complex with copper and readily excreted by kidney
  • potassium disulfide: reduces intestinal absorption of copper
  • trientine, zinc acetate, and zinc sulfate
30
Q

tremor

A

involuntary trembling or quivering

31
Q

postural tremor

A

tremor of a part during movement (outstretched upper limb when lifting a cup)

32
Q

essential tremor

A

termor of a part during movement

33
Q

levodopa MOA

A

agonist at dopamine receptor mainly D2

  • rapid absorbtion from SI, peak concentration at 1-2 hours
  • halflife is 1-3 hrs
  • 1-3% of levodopa actually enters brain unaltered bc rest is metabolzied by decarboxylation to dopamine
  • administer with DOPA decarboxylase inhibtor that does not corss BBB (carbidopa)
34
Q

best clinical result of levodopa

A

during first few years of treament

-wearing off phenomenon can occur during long term treatment

35
Q

AE levodopa: GI

A

in absence peripheral decarboxylase inhibitor causes anorexia, nausea and vomiting in 80% of pts, only 20% if given with carbidopa

36
Q

AE levodopa: cardiovascular

A

postural hypotension

hypertension with large doses or levodopa in combo with nonselective MAO inhibtior

37
Q

AE levodopa dyskinesias

A

occur in 80% of pts

choreoathetosis

38
Q

AE levodopa: behavior effectws

A

depression, anxiety, agitiation, insomnia

-atypical antipsychotic agents help counteract

39
Q

AE levodopa fluctuations in response on off pehnomenon

A

off periods: marked akinesia alternate over course of few hours with on periods of improved mobility

-subcut injection of apomorphine may provide temp benefit to those pts with severe off-periods

40
Q

contraindications of levodopa

A

pscyhotic pts, pts with angle closure glaucoma, pts with history of melanoma, caution with pts with active peptic ulcer

41
Q

bromocriptine

A

D2 agonist
28% bioavail, peak 1-3 hrs, 1/2 life = 15 hours

-extensive first pass metabolism

42
Q

dopamine receptor agonist

A

bromocriptine
pramipexole
ropinirole

43
Q

pramipexole

A

affinty for D3 receptors
-treat RLS
peak 2 hours, half life 8 hours
-90% excreted unchanged in urine

44
Q

ropiniirole

A

D2 recetpors agonist preference
approved for RLS
-metabolized by CYP1A2, if given with other agents metabolized by this enzyme, may reduce clearnce

-peak 1-2 hours, half life 6 hours

45
Q

AE dopamine agonist: GI

A

anorexia, nausea, vomitin

constipation, dyspepsia, refulx esophagitis

46
Q

AE dopamine agonist: cardriovascular

A

postural hypotension
bromocriptine may cause digital vasospasm
-if have peripheral edema and cardiac arrhythmias then discontinue therapy

47
Q

AE dopamine agonist: mental distubrnaces

A

confusion, hallucinations, delusions,

48
Q

contraindications to using dopamine receptor agonist

A

pts with history of psychotic illness, recent myocardial infarction, or with active peptic ulceration

Neuro II Final DF (4 decks)

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