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NMSK Exam 2: Neuro > 5. Drugs for Movement Disorders > Flashcards

5. Drugs for Movement Disorders Flashcards

1
Q

GO TO DRUGS

A
  1. Levodopa
  2. Carbidopa
  3. Levodopa + carbidopa
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2
Q

Dopamine R AGO

A
  1. Apomorphine
  2. Bromocriptine
  3. Pramipexole
  4. Ropinirole
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3
Q

MAO-I

A
  1. Rasagiline
  2. Selegiline
  3. Safinamide
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4
Q

Catechol-O-methyltransferase inhibitors

A

COMT breaks down Levodopa => 3-O methyldopa, which competes for Levodopa for transport ancross the intestinal mucosa and BBB. COMT-I prevent metabolism of Levodopa=> prolong activity of Levodopa => ⬆︎ bioavailability and ⬇︎ clearance.

  1. Entacapone
  2. Tolcapone
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5
Q

Anticholinergic drugs (5)

A

Central-acting mAChR ANT => improve tremor and rigidity in those with PD, but l_ittle effect on Bradykinesia._

  • 1. Benztropine
  • 2. Biperiden
  • 3. Orphenadrine
  • 4. Procyclidine
  • 5. Trihexyphenidyl
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6
Q

Miscellaneous Drugs for Movement Disorders

A
  1. Riluzole
  2. Reserpine
  3. Tetrabenazine
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7
Q

Pathological Hallmark of Parkinsons Disease

A
  1. Loss of pigmented, dopaminergic neurons in the substantia nigra
  2. Lewy bodies (intracellular inclusions)
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8
Q

How does our brain regulate movement?

A
  1. CTX sends messages to the Basal Ganglia, specifically the key processing center, the striatum (caudate + putamen).
  2. Striatum then sends [stimulatory/inhibitory messages] to CTX.
  3. However, dopaminergic neurons in the SNPc (Substantia Nigra Pars Compacta) release DA and inhibit GABAergic output in the striatum via the nigrostriatal pathway.
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9
Q

Under normal conditions, dopaminergic neurons in the substantia nigra inhibit the GABAergic output from the _________

A

Striatum

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10
Q

_______ neurons excite GABAergic neurons of the striatum.

A

Cholinergic

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11
Q

What is the problem in Parkinsons?

A

KO if DA neurons in the SNPc ➜ GABAeric neurons not inhibited ➜

↑ inhibition to the CTX ➜ movement disorders

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12
Q

Based on the pathology, how do we treat those with PD?

A
  1. DA AGO
  2. Anticholinergic agents
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13
Q

Levodopa (L-Dopa)

  1. What is Levodopa?
  2. MOA?
  3. Use?
  4. Absorption?
A
  1. Immediate metabolic precursor to DA that crosses the BBB (DA does NOT cross BBB)
  2. Dopamine AGO
  3. PD, does not stop progression but ⬇︎ mortality.
  4. Taken orally and peaks in plasma after 1-2 hours. Only 1-3% enters the brain unaltered. Thus, it is taken with Carbidopa (DOPA decarboxylase inhibitor), which does not cross the BBB and ⬇︎ peripheral metabolism ➜ ⬆︎plasma levels, 1/2 life, and Levodopa that reaches the brain and ⬇︎ the daily requirement for Levodopa.
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14
Q

In order to ⬇︎ peripheral metabolism of Levodopa and ⬆︎ the amount that reaches the brain, what is taken with it?

A

Levodopa + Carbidopa

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15
Q

What kind of drug is Carbidopa?

A

DOPA decarboxylase inhibitor

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16
Q

How does Levodopa + Carbidopa alter the symptoms, compared to Levodopa alone?

A
  • Significantly ⬇︎ the adverse peripheral effects of: nausea, vomiting, and postural hypotension!
  • But may ⬆︎ the adverse behavioral effects
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17
Q

Levodopa SE?

A
  1. GI symptoms:
    1. Levodopa alone (80% of pts): anorexia, N/V
    2. Levodopa + Carbidopa: ⬇︎ SE
  2. CV effects
    1. Postural hypotension at first, but ⬇︎ with use.
    2. If take large amounts with MOA-I or sympathomimetics: Hypertension
  3. Dyskinesias
    1. ​Choreoathetosis (80% of pts): movement of intermediate speed of face and distal extrememties
  4. Behavioral effects
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18
Q

When does using Levodopa produce the BEST results and why?

A
  • First few years of using
  • Long-term usage => “wearing-off phenomenon”: every does only proves sx for 1-2 hours, but rigidity and akinesia rapidly return. Increasing the dose and frequency is not the best idea bc ⬆︎ dyskinesias
19
Q

What is the “on-off phenomenon” associated with Levodopa?

A
  • Off-periods (not taking drug) = marked akinesia alternate over the course of a few hours
  • On-periods = improved mobility but often marked dyskinesia
20
Q

What drug and via what route, may provide temporary benefit to those patients with severe off-periods while taking Levodopa?

A

SQ injection of Apomorphine: ⬇︎ akinesia

21
Q

Levodopa CI

A
  1. MAO-I (or within 2 weeks of DQ): HTN crisis
  2. Psychotic patients
  3. Close-angle glaucoma
  4. Melanoma and undiagnosed skin lesions
  5. Active peptic ulcer => GI bleeding
22
Q

Why are Dopamine-R AGO preferred over Levodopa?

Except in who?

A
  • ⬇︎ response flucations and ⬇︎ dyskinesias that occur with long-term usage of Levodopa
  • Dont respond well to Levodopa = dont respond well to DA-R AGO.
23
Q

How are DA-R AGO given?

A
  • Alone
  • + levodopa + carbidopa
  • In patients taking Levodopa and who have end-of-dose akinesia or on-off phenonemon.
24
Q

Which DA-Receptor AGO is an D2-R AGO and ergot alkaloid derivative?

  • Name its other uses
  • Metabolism
  • Peak concentration and 1/2 life
A
  • Bromocriptine
  • Treats = endocrine disorders (hyperprolactinemia, prolactin-secreting adenoma, acromegaly)
  • Metabolized by: CYP3A4
  • Peak concentration: 1-3 hours
  • 1/2 life = 15 hours
25
Q

Ropinirole

  1. MOA
  2. Name other uses
  3. Metabolism
A
  1. D2-R AGO
  2. RLS
  3. CYP450 (CYP1A2)
26
Q

Which DA-Receptor AGO has preferential affinity for D3 receptors?

  • Name other uses
  • How is it excreted?
A

Pramipexole

    • Treats: Restless Leg Syndrome (RLS)
    • 90% excreted by kidney; so adjust dose if kidney problems.
27
Q

DA-R AGO

Side Effects

A
  1. GI:
    1. anorexia, N/V (decrease if taken with meals), constipations, dyspepis
  2. CV:
    1. Postural HTN at first.
    2. Digital vasospam with long term use
    3. If develops peripheral edema/cardiac arrhythmias = DQ
  3. Dyskinesias: reverse by ⬇︎ total dose
  4. Mental disturbances: confusion, hallucination, psych reactions that are MORE severe than Levodopa
28
Q

DA-R AGO

Contraindications

A
  1. Psychotic patients
  2. Active peptic ulcer
  3. Recent MI
  4. Periperal vascular disease (vasoconstricting effects)
29
Q

What is the difference between MAO-A and MAO-B?

Similarities?

A
  • MAO-A: breaks down NE and 5HT
  • MAO-B: breaks down phenylethylamine and benzylamine
  • Both equally break down Dopamine and Tryptamine.
30
Q

Selegiline

  • Type of drug
  • MOA
  • Uses
A
  • Selective MOA-B inhibitor, but non-selective at high doses.
  • MAO-B-I; slows down the breakdown of DA
  • Uses
      1. Prolongs antiparkinsonian effects of levodopa
      1. Reduce on-off/wearing-off phenomenom
      1. Adjunct to ppl not responding well to Levodopa
31
Q

Selegiline

  • CI
A
  • CI in ppl taking
    • 1. Meperidine
    • 2. TCAs
    • 3. SSRIs
  • bc increase risk of serotonin syndrome
32
Q

What drugs act similar to Selegiline?

A
  1. Rasagiline
  2. Safinamide
33
Q

What drug should not be taken with nonselective MAO-I?

A

Levodopa + non-selective MAO-I = NO

=> HTN crisis

34
Q

COMT-I

  1. Use
  2. How are the two COMT-I different?
  3. SE?
A
  1. Pts taking Levodopa who have developed response fluctuations
  2. Tolcapone => central and peripheral acting; Entacapone => peripheral acting only.
  3. SE are mostly due to Levodopa, but can cause
    1. Yellow pee
    2. Diarrhea/ Abdominal pain
    3. Sleep problems
35
Q

Apomorphine

  1. MOA
  2. Use
  3. AE
A
  1. MOA: D2-R AGO
  2. Use: SQ injection for quick, temporary relief of off-periods of akinesia in patients that take DA ➜ works in 10 minutes
  3. AE= Nausea, dyskinesias, drowsiness, hypotension
36
Q

What can be used to prevent nasuea that Apomorphine causes?

A

Trimethobenzamide

37
Q

AE of Anticholinergic Drugs (mAChR ANT) used to treat PD (tremor and rigity)

A
  1. Sedation
  2. Confusion
  3. Constipation/urinary retention
  4. Blurred vision
38
Q

What drugs are good for tremors?

A

B1-R blockers

  1. Metaprolol
  2. Propanolol

Antiepileptic drugs

  1. Primidone

Other

  1. Topirimate = 5HT AGO
  2. Alprazolam = benzo
  3. Botulinum toxin A (IM injections)
39
Q

What drugs are good to alleviate chorea seen in Huntingtons Disease?

A

Drugs that impair dopaminergic neurotransmission

  1. Reserpine
  2. Tetrabenazine
40
Q

What drug/class is the most predictive and effective pharmacologic approach for treating Tics?

Adverse effects?

A
    • Neuroleptic antipsychotics: pimozide
    • Cause extrapyramidal syndromes, WG, sedation, irritability, and various phobias
41
Q

Which drugs are effective in the treatment of Tics and have less adverse effects?

A

- α-adrenergic agents: clonidine and guanfacine

  • Injection of botulinum toxin A at tic site is beneficial in some cases
42
Q

Symptoms are Restless Leg Syndrome may resolve with correction of which co-existing deficiency?

A

Iron-deficiency anemia

43
Q

Which drug is the only drug to have any impact on survival in ALS and may prolong survival by a few months?

- MOA and AE?

A

Riluzole

  1. Inhibits glutamate release and blocks postsynaptic NMDA- and kainite-type glutamate receptors
  2. Inhibits VGNa+ channels
    • Adverse effects: nausea and weakness
44
Q

Which drugs may be used in the treatment of Wilson disease?

How does each drug work?

A
  • Penicillamine,
  • Potassium Disulfide,
  • Trientine, Zinc acetate, Zink sulfate
  1. Penicillamine: chelating agent, forms stable complex w/ copper and is readily excreted by kidney
  2. Potassium disulfide: reduces intestinal absorption of copper
  3. Trientine (chelating agent); zinc acetate and zinc sulfate (increase fecal excretion of copper by decreasing GI absorption)

NMSK Exam 2: Neuro (15 decks)

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