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

Kruse: DSA: Drugs for movement disorders Flashcards

(48 cards)

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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

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A

serotonin receptor agonist, effective in treatment of temor

21
Q

alprazolam

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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

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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

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A

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

-

24
Q

treatment for tics (most predictive and effective)

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A

neuroleptic antipsychotics like pimozide

-bad side effects so not always first choice

25
better choice for treatment of tics with less side effects
clonidine and guanfacine
26
restless leg syndrome
respond to dopmaine agonist: levodopa, diazepam, conazepam, or opiates -first line treatment is dopamine agonist PRAMIPEXOLE and ROPINIROLE
27
ALS treament
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
Wilson disease
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
treatment of wilson diseae
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
tremor
involuntary trembling or quivering
31
postural tremor
tremor of a part during movement (outstretched upper limb when lifting a cup)
32
essential tremor
termor of a part during movement
33
levodopa MOA
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
best clinical result of levodopa
during first few years of treament | -wearing off phenomenon can occur during long term treatment
35
AE levodopa: GI
in absence peripheral decarboxylase inhibitor causes anorexia, nausea and vomiting in 80% of pts, only 20% if given with carbidopa
36
AE levodopa: cardiovascular
postural hypotension hypertension with large doses or levodopa in combo with nonselective MAO inhibtior
37
AE levodopa dyskinesias
occur in 80% of pts | choreoathetosis
38
AE levodopa: behavior effectws
depression, anxiety, agitiation, insomnia -atypical antipsychotic agents help counteract
39
AE levodopa fluctuations in response on off pehnomenon
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
contraindications of levodopa
pscyhotic pts, pts with angle closure glaucoma, pts with history of melanoma, caution with pts with active peptic ulcer
41
bromocriptine
D2 agonist 28% bioavail, peak 1-3 hrs, 1/2 life = 15 hours -extensive first pass metabolism
42
dopamine receptor agonist
bromocriptine pramipexole ropinirole
43
pramipexole
affinty for D3 receptors -treat RLS peak 2 hours, half life 8 hours -90% excreted unchanged in urine
44
ropiniirole
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
AE dopamine agonist: GI
anorexia, nausea, vomitin | constipation, dyspepsia, refulx esophagitis
46
AE dopamine agonist: cardriovascular
postural hypotension bromocriptine may cause digital vasospasm -if have peripheral edema and cardiac arrhythmias then discontinue therapy
47
AE dopamine agonist: mental distubrnaces
confusion, hallucinations, delusions,
48
contraindications to using dopamine receptor agonist
pts with history of psychotic illness, recent myocardial infarction, or with active peptic ulceration

Neuro II Final DF (4 decks)

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