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Neuro II - Exam 2 > Drugs for Movement Disorders (Waller) - SRS > Flashcards

Drugs for Movement Disorders (Waller) - SRS Flashcards

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1
Q

What are the 7 drug categories we cover in this DSA?

A
  1. Levodopa and combinations
  2. Dopamine agonists
  3. monoamine oxidase inhibitors
  4. catechol-o-methyltransferase
  5. amantadine
  6. antimuscarinic agents
  7. Miscellaneous
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2
Q

What are the four (all red) levodopa and combination drugs?

A
  1. Levodopa
  2. Carbidopa
  3. Carbidopa/levodopa (Sinemet, Sinemet CR)
  4. Carbidopa/levodopa/entacapone (Stalevo)
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3
Q

What are the dopamine agonists we learned?

3 red, five tots

A
  1. Bromocriptine
  2. Pramipexole (Mirapex)
  3. Ropinirole (Requip)
  4. Rotigotine
  5. Apomorphine (Apokyn)
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4
Q

What are the MAOIs? 1 red, 2 total

A
  1. Rasagiline (Azilect)
  2. Selegiline
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5
Q

What are the antimuscarinic agents we need to know for movement disorders?

1 red, 5 total

A
  1. Benztropine (Cogentin)
  2. Biperiden
  3. Orphenadrine
  4. Procyclidine
  5. Trihexyphenidyl
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6
Q

What are the 15 miscellaneous drugs we learned about in this DSA?

no reds

A
  1. Metoprolol, propranolol
  2. Primidone
  3. Topiramate (Topamax)
  4. Alprazolam (Xanax)
  5. Botulinum toxin A
  6. Reserpine, tetrabenazine
  7. Olanzapine (Zyprexa)
  8. Perphenazine
  9. Haloperidol (Haldol), pimozide
  10. Clonidine, guanfacine
  11. Diazepam, clonazepam
  12. Penicillamine
  13. Potassium disulfide
  14. Trientine
  15. Zinc acetate, zinc sulfate
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7
Q

What is the MOA of levodopa?

A

stimulates D2 receptors

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8
Q

How does levodopa reach its target?

A

It can cross the BBB, and is decarboxylated to dopamine in brain tissue

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9
Q

What is one way we can reduce peripheral metabolism of levodopa, increasing t1/2, decrease levodopa doses by up to 75% and increase CNS entry?

A

Combination with a dopa decarboxylase inhibitor (carbidopa)

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10
Q

Levodopa…

  1. Does not stop progression of Parkinson’s disease but may lower mortality with early initiation.
  2. Best results obtained in 1st few years of treatment.

What is the long term result of this therapy?

A

Begins to diminish after 3-4 years.

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11
Q

What percent of patients have the following responses to levodopa:

Respond well

respond less well

unable to tolerate/do not respond

?

A

1/3 for each

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12
Q

levodopa ADRs include GI stuff like anorexia, nausea and vomiting. How can the various ADRs of levodopa be managed?

A
  1. Take with carbidopa
  2. Minimized by taking in divided doses, with or immediately after meals, or increasing total daily dose slowly.
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13
Q

What are the cardiovascular ADRs associated with levodopa? 4

A
  1. Tachycardia
  2. ventricular extrasystoles
  3. afib
  4. HTN
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14
Q

What are some of the behavioral ADRs of levodopa? 10

A
  1. depression
  2. anxiety
  3. agitation
  4. insomnia
  5. somnolence
  6. confusion
  7. delusions
  8. hallucinations
  9. nightmares
  10. euphoria, reported more commonly with combination (presumably due to higher levels in the brain).
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15
Q

What is a movement disorder that can occur in levodopa patients (ADR)?

A

Dyskinesia - 80% of patients on L-dopa over 10 yrs. Most often present with choreoathetosis of face and distal extremities.

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16
Q

What are the DDI’s to be aware of regarding L-dopa?

A
  1. Pyridoxine (vitamin B6) – increases extracerebral metabolism; may prevent therapeutic effect unless peripheral decarboxylase inhibitor also given.
  2. MAOIs – hypertension; do not give if taking MAOIs or within two weeks of MAOI discontinuation
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17
Q

What are four contraindications to Levodopa?

Why are they CI?

A
  1. Angle closure glaucoma - causes mydriasis
  2. psychosis - may worsen mental disease
  3. active peptic ulcer disease - GI bleeds
  4. malignant melanoma - levodopa is a melanin precursor
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18
Q

MOA for dopamine agonists?

A

MOA: act directly on postsynaptic dopamine receptors;

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19
Q

What are DA agonists important first line therapy for?

A

Parkinsons

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20
Q

What is one ADR of levodopa that is less common with DA’s?

A

Lower incidence of dyskinesias

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21
Q

Generally speaking, if a patient does not respond to Levodopa, will they have a response to DAs?

A

Nope

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22
Q

Certain dyskinesia fluctuations in clinical response to levodopa occur with increased frequency as treatment continues. What is meant by the following…

  • wearing-off
  • on-off phenomenon
A
  • wearing-off: rigidity and akinesia return at the end of the dosing interval (end-of-dose akinesia)
  • on-off phenomenon: unrelated to timing with Off-periods of marked akinesia alternate over the course of few hours with on-periods of improved mobility but often marked dyskinesia
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23
Q

Bromocriptine is derived from what?

(softball for ol’michael)

Study These Flashcards
A

Ergot Alkaloid

24
Q

MOA bromocriptine?

25
Pramipexole?
D3 agonist
26
MOA ropinirole?
D2 agonist
27
How is rotigotine applied? When is it useful in parkinsons?
Skin patch Useful in early parkinsons
28
In addition to anorexia, nausea and vomiting, what are some other GI ADRs that occur d/t DAs?
1. Constipation 2. dyspepsia 3. reflux esophagitis
29
What are the two cardiovascular ADRs of DA's? Which is dose-related? Which is usually at initiation of therapy? Which is caused by the ergot derivatives?
1. postural hypotension (particularly at initiation). 2. Ergot derivatives: painless digital vasospasm (dose-related complication of long-term therapy).
30
Mental disturbances are seen in DA therapy and include what?
1. confusion 2. hallucinations 3. delusions 4. disorders of impulse control
31
In what 4 situations are DAs CI?
1. history of psychotic illness 2. recent myocardial infarct 3. active peptic ulcer disease. 4. Best avoided in peripheral vascular disease (ergot-derived).
32
What are the two types of monoamine oxidase? What do each metabolize?
1. Monoamine oxidase A metabolizes norepinephrine, serotonin, and dopamine. 2. Monoamine oxidase B metabolizes dopamine selectively.
33
What is the MOA of selegiline at normal doses? High doses?
1. selective, irreversible inhibitor of MAO B at normal doses 2. Decreases breakdown of dopamine. 3. + MAOI A at higher doses
34
Selegiline Enhances and prolongs antiparkinsonism effect of levodopa (thereby allowing levodopa dose to be reduced) and may reduce what two phenomenon?
mild on-off or wearing-off phenomenon
35
MOA of Rasagiline?
1. **MOA:** irreversible inhibitor of MAO-B; more potent than selegiline.
36
What is Rasagiline used for?
1. **Therapeutic Use:** used as a neuroprotective agent and for early symptomatic treatment of Parkinson’s.
37
What DDI must you avoid when administering MAOI drugs?
combined administration of levodopa and a nonselective MAO inhibitor must be avoided because it may lead to a hypertensive crisis (due to peripheral accumulation of norepinephrine).
38
MOA of tolcapone and entacapone?
MOA: Inhibition of catechol-O-methyltransferase
39
In what patients may COMT inhibitors be useful?
Those who have developed response fluctuations
40
ADRs of COMTi?
1. **ADRs:** relate to increased levodopa exposure; but also may cause diarrhea, abdominal pain, orthostatic hypotension, sleep disturbances, and orange discoloration of urine.
41
MOA of apomorphine?
1. **MOA:** potent, non-ergot dopamine agonist; interacts with postsynaptic D2 receptors in caudate nucleus and putamen.
42
Therapeutic use for apomorphine?
1. temporary relief (“rescue”) of off-periods of akinesia in patients on optimized dopaminergic therapy.
43
apomorphine ADRs include nausea, dyskkinesias, drowsiness, sweating, hypotension and injection site bruising. What antiemetic is particularly good at curtailing the nausea?
trimethibenzamide
44
Amantadine is an antiviral agent with relatively weak antiparkinsonism properties. What is its MOA?
1. **MOA:** unclear, but may potentiate dopaminergic function by influencing the synthesis, release, or reuptake of dopamine.
45
Therapeutic use for amantadine?
1. may favorably impact bradykinesia, rigidity, and tremor. 2. May also help in reducing iatrogenic dyskinesias in patients with advanced disease
46
Amantadine **ADRs include r**estlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, and confusion (all can be reversed by stopping drug) as well as headache, heart failure, postural hypotension, urinary retention, and GI disturbances. What is a vascular condition these can cause?
Livedo reticularis - see purplish mottled skin
47
In what patients must amantadine be used with caution in (CI-ish)?
1. **CIs:** use with caution in patients with history of seizures or heart failure.
48
MOA of benztropine mesylate, biperiden, orphenadrine, procyclidine, trihexyphenidyl?
All centrally acting mAChR antagonists
49
What benefits do the antimuscarinic drugs have on a parkinsons patient? What do they explicitly have little effect on?
1. **Therapeutic Use:** may improve tremor and rigidity of parkinsonism but little effect on bradykinesia.
50
What receptors have been implicated in essential tremor? So how would you tx?
**_β1-receptors_** 1. propranolol 2. metoprolol **_Could also use..._** 1. primidone 2. topiramate 3. Alprazolam 4. Botox IM
51
What drugs help to alleviate the chorea seen in huntington's disease?
1. Drugs that impair dopaminergic neurotransmission (see mechanisms below) often alleviate chorea 2. either by: 1. Depletion of central monamines 2. blockade of dopamine receptors
52
What are the drugs used in huntingtons disease to deplete central monoamines?
Reserpine and tetrabenazine
53
MOA for reserpine and tetrabenazine?
block the vesicular monoamine transporter and deplete cerebral dopamine stores; the effects of tetrabenazine resemble reserpine but with less peripheral activity and a shorter duration of action
54
How do olanzapine, phenothiazines such as perphenazine, and butyrophenones such as haloperidol help Huntington disease patients with their chorea?
Blockade of dopamine receptors
55
1. Wilson’s disease, recessively inherited disorder of copper metabolism, characterized: 1. Biochemically by: reduced serum copper and ceruloplasmin (major copper-carrying protein in the blood) concentrations. 2. Pathologically by: markedly increased concentration of copper in the brain and viscera. 3. Clinically by: signs of hepatic and neurologic dysfunction (e.g., tremor, choreiform movements, rigidity, hypokinesia, and dysarthria and dysphagia). 2. Treatment includes agents that reduce serum copper levels and a low-copper diet. What is the drug used to deal with this?
Penicillamine Potassium Disulfide
56
MOA of penicillamine?
1. **MOA:** chelating agent; forms a stable complex with copper; readily excreted by the kidney.
57
MOA of potassium disulfide in tx of wilson's disease?
Decreased intestinal absorption of copper. (can use in addition to penicillamine)

Neuro II - Exam 2 (2 decks)

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