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NEUROANATOMY > Pharmacotherapy for Movement Disorders > Flashcards

Pharmacotherapy for Movement Disorders Flashcards

1
Q

under normal conditions the SNc favors the which pathway?

A

direct pathway

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2
Q

in PD the activity of which pathway predominates?

A

indirect pathway

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3
Q

___________ receptor activation appears to be most important in gating the balance of the direct and indirect pathways

A

D2

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4
Q

what are the 5 main strategies for PD pharmacotherapy?

A
  1. replace DA
  2. Stimulate DA receptors
  3. Enhance DA release
  4. Inhibit DA metabolism
  5. Alter DA/ACh
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5
Q

which drug is the single most effective treatment for PD?

A

L-DOPA

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6
Q

Which drug can completely ameliorate all the symptoms of PD, particularly during initial treatment?

A

L-DOPA

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7
Q

what is the MOA of L-DOPA?

A

replenishes DA Stores in the remaining DA terminals in the striatum

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8
Q

L-DOPA is converted in the periphery and brain to dopamine by what enzyme?

A

L-aromatic aminoacid decarboxylase (L-AAD)

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9
Q

99% of systemically administered L-DOPA is converted to dopamine in the periphery, and is principally excreted in the urine as what two substances?

A

HVA & DOPAC

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10
Q

L-DOPA has to be co-administered w/ what drug?

A

carbidopa

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11
Q

what is the MOA of cabidopa?

A

inhibits L-aromatic amino acid decarboxylase (L-AAD)
-prevents metabolism of L-DOPA to dopamine in the periphery (you want L-DOPA to remain unchanged so it can cross the BBB)

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12
Q

what are the two main benefits of using carbidopa with L-DOPA?

A

reduces the amount of L-DOPA needed by up to 75% & reduces side effects due to reduced level of peripheral DA

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13
Q

the GI and CV adverse effects of L-DOPA are due to what?

A

due to the response to L-DOPA monotherapy

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14
Q

what are the GI adverse effects of L-DOPA monotherapy?

A

anorexia, N/V, tend to decrease w/ repeated use

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15
Q

what are the CV adverse effects of L-DOPA monotherapy?

A

arrhythmias, tachycardia, ventricular extrasystoles, Afib, incidence tends to be low except in those predisposed, also orthostatic hypotension

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16
Q

the behavioral and dyskinesias are adverse effects of L-DOPA therapy with what other drug?

A

carbidopa

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17
Q

what are the behavioral adverse effects of L-DOPA combo therapy w/ carbidopa?

A

depression, anxiety, delusion, agitation, insomnia, hallucinations, nightmares, euphoria. (antipsychotics are used to alleviate this problem)

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18
Q

what are the dyskinesias associated with L-DOPA combo therapy with carbidopa?

A

chorea, myoclonus, tics, tremor

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19
Q

the adverse effects for which drug have fluctuations in response like a “on-off phenomenon”?

A

L-DOPA

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20
Q

what is the main drug interaction with L-DOPA, that causes an increase in L-DOPA metabolism?

A

vitamin B6 (pyridoxine)

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21
Q

why is it not ok to give L-DOPA to pts on MAO-A inhibitors?

A

hypertensive crisis

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22
Q

what are some of the contrindications for L-DOPA therapy?

A

psychotic pts, glaucoma (angle-closure), cardiac disease, peptic ulcer, melanoma

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23
Q

Therapy with L-DOPA is often effective for how many years?

A

3-5 yrs (often delayed until symptoms of PD yield functional impairment)

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24
Q

What is the rationale behind dopamine agonist therapy?

A

to activate D2 receptors to reduce the activation of the indirect pathway?

25
Q

what are the advantages to dopamine agonist therapy?

A
  • doesn’t have to be converted to active compound
  • no toxic metabolites
  • doesn’t compete w/ other substances for GI absorption or crossing BBB
  • may be more selective (reducing adverse effects)
26
Q

what kind of drugs are considered the preferred therapeutic strategy for early PD?

A

dopamine agonists

27
Q

which kind of drugs may be used in combo w/ L-DOPA in advanced PD to reduce the “on-off” phenomenon?

A

dopamine agonists

28
Q

name the drug: D2 agonist/D1 partial agonist

A

bromocriptine

29
Q

name the drug: D1/D2 agonist

A

apomorphine

30
Q

name the drug: D2 selective, may also act as a free radical scavenger

A

pramipexole

31
Q

name the drug: D2 selective, metabolized by CYP1A2

A

Ropinirole

32
Q

which drug is an antiviral agent that was found to alleviate parkinsonian symptoms?

A

Amantadine

33
Q

how long do the effects of amantadine last?

A

effects are modest and short-lived

34
Q

how is amantadine excreted?

35
Q

what are the adverse effects of amantadine?

A 
restlessness
depression
agitation
irritability
insomnia
excitement
hallucinations
confusion
overdose may produce psychosis
other adverse effects similar to L-DOPA and dopamine agonists
36
Q

which drug is contraindicated in pts w/ history of seizures or heart failure?

A

amantadine

37
Q

which drug is a selective MAO-B inhibitor that retards the breakdown of dopamine?

A

Selegiline

38
Q

metabolites of selegiline include what two drugs that increase dopamine release?

A

amphetamine & methamphetamine

39
Q

what is the indication for selegiline?

A

used primarily in pts whose responsiveness to L-DOPA has declined (little effect when administered alone)

40
Q

what are some of the drug interactions of selegiline?

A

don’t take w/ meperidine, TCAs, or SSRIs

41
Q

what are the adverse effects of selegiline?

A

May potentiate the adverse effect of L-DOPA

42
Q

name the drug: a new more potent inhibitor of MAO-B approved for combo therapy w/ levodopa in late-stage or alone in early PD?

A

rasagiline

43
Q

name the two drugs that are selective inhibitors of COMT?

A

entacapone, tolcapone

44
Q

what is the MOA of entacapone and tolcapone?

A

prolongs the action of L-DOPA, reduces the production of 3OMD which may compete w/ L-DOPA for transport carriers in GI and BBB
-increases the bioavailability of L-DOPA

45
Q

What is the indication for enacapone, tolcapone?

A

helpful in reducing fluctuation responses to L-DOPA

46
Q

name the inhibitors of DA metabolism that are both rapidly absorbed, highly bound to protein, half-life about 2 hrs?

A

entacapone, tolcapone

47
Q

which COMT inhibitor has both central and peripheral effects?

48
Q

which COMT inhibitor has only peripheral effects?

A

entacapone

49
Q

which COMT inhibitor is preferred b/c the other one may result in increased liver enzymes and hepatic failure (requires pt consent)

A

entacapone is preferred

tolcapone (causes increased liver enzymes and hepatic failure, requires pt consent)

50
Q

what are the muscarinic antagonists used to block cholinergic activation in the striatum (3)

A

benztropine
diphenhydramine
trihexyphenidyl

51
Q

what are the adverse effects of the muscarinic antagonists used to treat PD?

A

drowsiness, mental slowness, inattention, confusion, delusions, hallucinations, and mood changes

52
Q

using muscarinic antagonists to treat PD are contraindicated in pts with what conditions?

A

prostatic hyperplasia
OBD
glaucoma
(avoid concomitant use of drugs with antimuscarinic effects-like TCAs or antihistamines)

53
Q

what is the trinucleotide repeat found in huntington’s?

A

CAG (glutamine, polyglutamine expansion)

54
Q

the huntingtin gene is located on what chromosome?

55
Q

Huntington’s disease has a loss of cholinergic neurons in the striatum but a greater and earlier loss is observed in WHICH NEURONS that project to the external globus pallidus (indirect pathway) thus decreasing the output (STN) of the indirect pathway?

A

loss is observed in the striatal medium spiny GABAergic neurons which project to GPe

56
Q

what are the 2 main drugs used to treat HD associated depression?

A

Fluoxetine

carbamazepine

57
Q

what are the central dopamine depleting agents drugs used to treat HD associated chorea?

A

reserpine and tetrabenazine

58
Q

what are teh dopamine antagonists that are used to treat HD associated chorea?

A

chlorpromazine and haloperidol

59
Q

what is the proposed MOA of the drugs used to treat HD associated chorea?

A

thought to be able to block D2 receptors

NEUROANATOMY (11 decks)

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