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IPAP 21-2 Soph Semester > Parkinson’s Drugs For Block III > Flashcards

Parkinson’s Drugs For Block III Flashcards

(58 cards)

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1
Q

What is the pathophys of Parkinson’s

A

caused by an imbalance between dopamine (DA) and acetylcholine (ACh) neurons on innervation of gamma-aminobutyric acid (GABA) receptors

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2
Q

What are the S/s of PArkinsons

A

Tremor, Rigidity, Dyskenesia, Akenesia, Bradykinesia, Postural/ Gait Disturbance

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3
Q

Clinical presentation Parkinson’s?

A

Flat affect, reduced blinking, flat face, Depression, Dementia, Psychosis

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4
Q

Which drugs can induce Parkinson’s like S/s

A

Antipsychotics (i.e. phenothiazines) and Antiemetics

Prochloroperazine (Compazine) (Antiemetic)

Chlorpromazine (Thorazine) (antiemetic)

Trifluoperazine (Stelazine) (1* typical)

Thioridazine (Mellaril) (1* typical)

Haloperidol (Haldol) (1* typical)

Metoclopramide (Reglan) (GI Benzamide)

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5
Q

Which Dopamine agent is best at Tx improving motor disability

A

Levodopa

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6
Q

Which Dopamine Agent is best at Lessing Motor complications

A

Dopamine agonists

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7
Q

What are the 1st line monotherapy Tx for Parkinson’s

A

Dopamine agonists

Bromocriptine (Parlodel)

  • Semisynthetic ergot derivate
  • Rarely used

Rotigotine (Neupro)

  • Non-Ergot
  • Transdermal system
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8
Q

What are the ADE of Dopamine Agonists Bromocriptine and Rotigotine

A

Pleuropulmonary and/or cardiac fibrosis is a concern
-Chest x-ray with abnormal pulmonary exam

Postural hypotension, dizziness

Hallucinations, mental confusion

GI disturbances

Digital vasospasm and leg cramps

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9
Q

What Parkinson’s Drugs are used for RLS

A

Pramipexole (Mirapex)
Ropinirole (Requip)

(NONERGOT)

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10
Q

What is the clinical use of Pramipexole

A

Effective as monotherapy for mild parkinsonism and in patients with advanced disease

Allows the dose of levodopa to be reduced and smoothing out response fluctuations in advance disease.

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11
Q

What is the clincal use of Ropinirole

A

Affective as monotherapy in patients with mild disease

Allows the dose of levodopa to be reduced and smoothing out response fluctuations in advance disease

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12
Q

Parkinson’s pts with advanced disease should get:

With mild disease should get?

A

Advanced: Pramipexole
Mild: Ropinirole

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13
Q

What is the clinical use of Apomorphine

A

acute, intermittent treatment of “off” episodes associated with advanced Parkinson disease;

recurring hypomotility, “off” episodes

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14
Q

What is the MOA of Apopmorphine

A

Dopamine receptor agonist (Short-acting)

Stimulates post-synaptic D2-type receptors

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15
Q

How must apomorphine be titrated

A

Must be titrated in a setting where BP can be monitored

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16
Q

What should be done if a pt misses a Apomprphine does x 1 wk

A

If patient does not dose for more than 1 week, reinitiate at 0.2ml dose and increase

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17
Q

What are the ADE of apomorphine

A

Severe N/V

Ortho hypotension
Hallucinations
Dyskinesia
Somnolence

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18
Q

What is the prophylaxis Tx for N/V with apomorphine

A

prophylaxis with trimethobenzamide (anti-emetic) 3 days prior to initiating apomorphine and continued for the first month of therapy, if not indefinitely

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19
Q

What are the contraindications of Apomorphine

A

5-hydroxytryptamine-3 antagonists (5-HT3) antagonists (ondansetron, granesitron, dolasetron, palonosetron) causes severe hypotension and loss of consciousness

IV use (thrombus formation)

Sulfite sensitivity (preservative)

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20
Q

How must apomorphine be admin

A

Sub Q!

IV use= thrombus formation

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21
Q

What drugs should apomorphine be avoided in

A

5-hydroxytryptamine-3 antagonists (5-HT3) antagonists (ondansetron, granesitron, dolasetron, palonosetron)

causes severe hypotension and loss of consciousness

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22
Q

What is the MOA of carbidopa

A

Aromatic L-Amino Acid decarboxylase (AAAD) inhibitor that does not cross the BBB

Prevents some peripheral conversion and metabolism of levodopa to dopamine in the peripheral tissues thereby allowing increased availability of levodopa to cross into the CNS

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23
Q

What is the MOA of Levodopa

A

Precursor to dopamine that has the ability to cross the BBB
and replenish depleted dopamine in the brain

Converted into dopamine in the periphery

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24
Q

How long does levodopa have effect till it begins to decline

Study These Flashcards
A

“Honeymoon”: patients normally respond favorably to levodopa for 3-5 years then the effects start to decline

25
What are the ADE of Carbidopa and Levodopa
Acute Effects (excessive dopamine): nausea, vomiting, postural hypotension, confusion, agitation, hallucinations, cardiac arrhythmias Dyskinesias (excessive dopamine): Drug induced abnormal involuntary movements, including dystonia Treatment: decrease levodopa dose or add an anticholinergic or amantadine as an anti-dyskinetic drug
26
What is the Tx for dyskinesia induced by levodopa
Treatment: decrease levodopa dose or add an anticholinergic or amantadine as an anti-dyskinetic drug
27
What is the role of amantadine
Anti-dyskinesia medication
28
How do we treat the “wearing off” period of Levodopa
“Wearing Off” phenomenon: end of dose deterioration, symptoms return before the next dose Treatment: add dopamine agonist, adding a MAO-B inhibitor, a COMT inhibitor or increasing the frequency dose of levodopa (shorten the dosing interval)
29
How do we treat the “on- OFF” phenomenon of Levodopa
unpredictable return of symptoms without respect to the dosing interval Severity changes ranging from akinesia (off periods) to mobility with dyskinesias (on periods) Treatment: add dopamine agonist, adding a MAO-B inhibitor, a COMT inhibitor or redistributing dietary protein (high-protein diet reduces levodopa absorption; must keep steady intake)
30
What effect does a high protein diet have on Levodopa
Reduces absorption
31
What pts should not receive L-dopa
Contraindications: - psychotic illness - narrow-angle glaucoma - use of non-selective MAOI’s Precautions: Peptic Ulcer Disease (PUD) Malignant Melanomas: levodopa is a precursor of skin melanin and conceivably may activate malignant melanoma
32
What is the association of L-Dopa and skin cancer
levodopa is a precursor of skin melanin and conceivably may activate malignant melanoma
33
What is the clinical use of MAO-B inhibitors
Symptomatic control of (mild to moderate) Parkinson Disease Adjunct therapy for patients with Parkinson’s Disease and motor fluctuations
34
Pts on Selegiline and Rasagiline should avoid what medications
Patients on MAO-B Inhibitors should avoid medications that increase the risk of Serotonin Syndrome
35
What is the MOA of selegiline
Irreversibly inhibits the metabolism of dopamine by MAO-B that results in increased dopamine levels in the brain
36
Does Selegiline effect MAO-A ?
Does not inhibit MAO-A (degrades: norepinephrine and serotonin) much lower risk for hypertensive crisis Loses selectivity at doses > 10mg/day
37
When should the last dose of selegiline be taken to avoid insomina
Last dose should be early afternoon to prevent insomnia
38
What is the clinical use for Selegiline
Used in conjunction with levodopa Mild Disease: may be used alone to try and delay the need for levodopa in early Parkinson’s disease (effects have not been robust)
39
What drug can be used as monotherapy in order to delay the use of L-dopa
Selegiline
40
What is Selegiline metabolized to
Amphetamine, can cause insomnia
41
What is the MOA of Rasagiline
MOA-B non selective inhibitor
42
Which is more potent, Selegiline or Rasagiline
Rasagiline 5x more potent
43
Because Selegiline and Rasagiline are MAO-b inhibitors what foods should be avoided
avoid tyramine containing foods | ex; aged cheeses, air-dried or cured meats, tap/draft beers, etc
44
What is the MOA of a COMT inhibitor
prevents the breakdown of dopamine, more levodopa available to cross blood-brain barrier
45
What is the clincal indications for COMT-I
Manage motor fluctuations (“wearing-off” effect) Adjunct to levodopa/carbidopa in patients with response fluctuations or who have failed or can not use other therapies
46
What is the urine ADE of COMT-I
Entacapone causes orange discolored urine
47
Since COMT-I increase the concentration of dopamine, what are the ADE
Increase Dopamine: diarrhea, dyskinesias, nausea, anorexia and hallucinations
48
When should tolcapone (MAO-I) be used
After Entacapone has failed Hepatotoxic: get liver function tests (LFTs) at baseline and on a regular basis Written informed consent is advised by manufacturer for patients who have failed Entacapone
49
What is the major ADE of tolcapone
Liver toxicity
50
How should Entacapone be used (MAO-I)
Must use with carbidopa/levodopa Does not cross BBB
51
What is the combination of Carbidopa/l-dopa/Entacapone called
Stalevo
52
How are anticholinergics used in the Tx of Parkinson’s
Mechanism of Action: block the excitatory neurotransmitter acetylcholine to try and restore balance with dopamine Clinical Use: - Most effective on tremors and rigidity - DOC for drug-induced (anti-psychotics) parkinsonism - Does not relieve symptoms of tardive dyskinesia
53
Since Benzotropine and Trihexyphenidyl are anticholinergics, what are their ADE
dry mouth, blurred vision, dry eyes, constipation, urinary retention, confusion, and arrhythmias
54
What are the DOC for drug induced Parkinson’s
Benzotropine or Trihexyphenidyl
55
What is the clincal use of Amantadine
Posses symptomatic benefits and may reduce dyskinesias caused by levodopa or dopamine agonists Not as effective on bradykinesia, rigidity, tremor and dyskinesia as anticholinergics
56
What is the major ADE of Amantadine
Livedo reticularis (RASH)
57
How do you tx parkinson drug induced hallucination
``` Stop medications that may contribute to psychosis in the following order: -anticholinergics, -amantadine, -selegiline, -dopamine agonists, levodopa/carbidopa ``` Avoid typical antipsychotics, risperidone, and olanzapine; worsens Parkinson symptoms
58
How do you Tx the cognitive disorders of drug induced Parkinson’s
Discontinue/reduce Parkinson disease medications as tolerated If antipsychotics are needed treat with newer neuroleptics: Quetiapine (Seroquel) Clozapine (Clozaril): probably best but unacceptable side effects (agranulocytosis)

IPAP 21-2 Soph Semester (20 decks)

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