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Parkinsons Disease Pharm > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

Epidemiology for Parkinson’s

A

1 million ppl in the U.S
2:1 males
Usually occurs between 50 and 80 years of age (mean 55)

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2
Q

Etiology of Parkinson’s Disease

A

*most idiopathic
no clear triggers
some genetic aspect

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3
Q

Patho/Phys of Parkinson’s

A

progressive depletion of dopaminergic neurons in the substantia nigra (SN) of the basal ganglia

70-80% of dopamine lost by the time a patient presents with symptoms

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4
Q

What are Lewy Bodies

A

spherical, abnormal aggregates of protein) are found in the remaining DA cells in the SN

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5
Q

4 Clinical Characteristics Associated with Parkinson’s

A

Bradykinesia and akinesia: slowness of movement

Tremor: unilateral, at rest; described as “pill-rolling”

Rigidity: resistance to passive movement of the joints; “cog wheeling” or ratchet motion

Postural Instability

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6
Q

How do you diagnose Parkinson’s?

A

Bradykinesia and at least one of the following:
Limb muscle rigidity (often with cogwheel quality)
Resting tremor
Postural instability

If one of the above is present: possible diagnosis

If at least 2 are present: probable diagnosis

If at least 2 are present and positive response to antiparkinsonian pharmacotherapy: definitive diagnosis

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7
Q

Symptoms of idiopathic PD usually appear how? (2)

A

unilaterally and progress asymmetrically

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8
Q

3 Ddx for Parkinson’s?

A

Drug-Induced Parkinsonism antipsychotics

Parkinsonism-Plus Syndromes lots of different things that its degenerative neurologic d/o

Idiopathic Parkinsonism
Acute Dopaminergic Challenge
Carbidopa/levodopa or apomorphine used
Onset of motor effects observed within 30 minutes

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9
Q

5 Stages of Parkinson’s?

A

Stage 1: unilateral involvement only and no/minimal functional impairment

Stage 2: bilateral involvement but no impairment of balance

Stage 3: postural imbalance and some restricted activities; disability considered mild to moderate

Stage 4: patients severely disabled

Stage 5: patients confined to a wheelchair

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10
Q

What are 5 clinical predictors for progression of Parkinson’s?

A

Older age at onset

Rigidity or hypokinesia as presenting symptom

Male gender

Presence of comorbidities
Stroke
Auditory defects
Visual impairments

Decreased response to dopamine

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11
Q

What are 5 goals of pharmacotherapy for Parkinson’s?

A

Preserve motor function for as long as possible

Improvement of nonmotor features

Minimize adverse effects

Manage long-term complications of disease progression

Maintain best quality of life

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12
Q

6 medications used in Parkinson’s Disease?

A

MAO-B inhibitors

Amantadine

Anticholinergic symptom relief

Stimulation of endogenous D2 dopamine receptors (dopamine agonists, DAs)

(Carbidopa/levodopa)

(catechol-O-methyltransferase [COMT] inhibitor

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13
Q

Initiation of Pharmacotherapy depends on what? (2)

A

Begin treatment with MOA-B inhibitor or DA if patient is younger with functional impairment

Begin treatment with LD if patient is older, has cognitive impairment, or has moderate to severe functional impairment

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14
Q

MAO-B INHIBITORS – SELEGILINE (ELDEPRYL®) (5)

A

Irreversible MAO-B inhibitor
**not usually used due to Metabolized into a neurotoxic amphetamine derivative
Provides mild relief of symptoms vs. placebo
Allows for lower dose of LD when used in adjunct therapy
Can delay need for starting LD by 9 months

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15
Q

MAO-B INHIBITORS – RASAGILINE (AZILECT®) (4)

A

Second-generation irreversible selective inhibitor of MAO-B

Indicated as monotherapy in early PD (1 mg daily) or as adjunct to LD in advanced disease
Greater potency and may be neuroprotective (is not metabolized into potentially neurotoxic amphetamine-based metabolites)

Added to LD, improves motor fluctuations, reduces “off time”

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16
Q

MAO-B INHIBITORS – RASAGILINE (AZILECT®) Side effects(3)

A

headache, dizziness, nausea

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17
Q

AMANTADINE (SYMMETREL®) (5)

A

Antiviral agent with mild therapeutic effect in PD

MOA in PD unclear

Initiated in early stages when mild symptoms occur

Improvements in bradykinesia, rigidity, and tremor

Tachyphylaxis develops within 4-8 weeks***

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18
Q

Anticholinergic Agents (3)

A

When used, do not discontinue abruptly due to potential withdrawal reactions
Avoid in pts with cognitive deficits
used in early stages of parkinsons

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19
Q

DOPAMINE AGONISTS – DAS (3)

A

DAs can delay need for LD therapy for 4-5 years in 80% of patients

Patients less likely to develop dyskinesias and motor fluctuations when LD used as adjunct to DA therapy

**titrate by starting low and going slow!

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20
Q

DOPAMINE AGONISTS – DAS ERGOT DERIVATIVES (3)

A

Rarely used in PD

Bromocriptine (Parlodel®)
Moderate affinity for D2 and D3 dopamine receptors

Pergolide (Permax®)
Removed from the market March 2007; associated with cardiac valve fibrosis

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21
Q

DOPAMINE AGONISTS – DAS NON-ERGOT DERIVATIVES 4 medications used=

A

used regularly!
Pramipexole (Mirapex®)

Ropinirole (Requip®)

Rotigotine (Neupro®)

Apomorphine (Apokyn®)

22
Q

6 side effects for Non Ergot derivatives for dopamine agonists

A 
Nausea
Confusion
Orthostasis
Postural instability
Dizziness/light-headedness
Hallucinations
Rare:
Risk for daytime somnolence and “sleep attacks” 
Hypersexuality
Pathological behaviors
23
Q

DA – PRAMIPEXOLE (MIRAPEX®) (2)

A

Dosing adjustments are required for renally impaired patients
ER and IR used

24
Q

DA – ROPINIROLE (REQUIP®)

A

Titrate cautiously in patients with hepatic impairment
Monitor LFTs
IR and ER

25
Q

DOPAMINE AGONISTS – DASROTIGOTINE (NEUPRO®)

A

transdermal patch
Indicated for early-stage idiopathic PD and advanced stages
Side effects: application site reactions, nausea and vomiting, somnolence, dizziness, hallucinations, abnormal dreaming

26
Q

DOPAMINE AGONISTS – DAS APOMORPHINE (APOKYN®) (2)

A

FDA approved for intermittent treatment of hypomobility in patients with advanced stages of PD

Not recommended as 1st line therapy
Rescue of “delayed on”/ “no on” or “freezing episodes”

27
Q

DOPAMINE AGONISTS – DAS APOMORPHINE (APOKYN®)

Side effects and use for prophylaxis

A

Due to significant N/V, must use prophylaxis with an antiemetic
Start trimethobenzamide 3 days before apomorphine and continue for first 2 months of treatment (300 mg po TID)
Do not use with serotonin antagonists such as ondansetron – the combination may result in severe hypotension

Side effects: Nausea, vomiting, somnolence, dizziness, yawning

28
Q

DOPAMINE AGONISTS – DAS APOMORPHINE (APOKYN®) Disadvantages

A

Onset of therapeutic effect rapid

Peak plasma levels within 60 minutes

Administer a 2 mg test dose

Dosed 3-5 times/day, prn

Disadvantages
No oral dosing formulation (subcutaneous injection)
Patients may require someone else to inject once hypomobility had occurred

29
Q

LEVODOPA – LD

A

LD is an immediate precursor to dopamine
Improves motor symptoms from progressive loss of dopaminergic neuronal function

Cornerstone of treatment for PD
Nearly all patients will require supplementation with LD

In the periphery LD is rapidly metabolized to dopamine by L-amino acid decarboxylase
Dopamine cannot cross the BBB
LD alone causes significant nausea and vomiting at high doses required to achieve adequate concentrations within the substantia nigra

30
Q

Carbidopa/Levodopa side effects

A 
Nausea
Vomiting
Orthostasis
Confusion
Postural hypotension
Vivid dreams
Wearing-off fluctuations
Dyskinesias
31
Q

Carbidopa (CD) is what?

A

is a peripheral decarboxylase inhibitor
Used in combination with LD to increase LD’s bioavailability across the BBB
Carbidopa does not cross the BBB
80% less LD dose required to achieve same effect

32
Q

2 types of Carbidopa/Levodopa?

A

immediate release

controlled release

33
Q

Controlled release Carbidopa/ Levodopa should be taken with what?

A

Should be taken with food to slow movement through the GI tract

34
Q

Immediate release Carbidopa/ Levodopa should be avoided with what?

A

Avoid high-protein meals
Take 30 minutes before or 60 minutes after meals due to competition with other amino acids for gastrointestinal absorption

35
Q

What are 5 concerns with Carbidopa/ Levodopa?

A

End of dose wearing off

Peak-dose dyskinesia

“Delayed on” or “no on”

Freezing or start hesitation

Off period dystonias

36
Q

End of Dose Wearing Off is what?

A

Patients experience a wearing off effect and experience an increase in PD symptoms prior to the time of the next dose

37
Q

End of Dose Wearing off should be treated how?

A

Decrease dosing interval of LD (increase frequency)

Add MAO-B inhibitor, COMT inhibitor, or Dopamine agonist

38
Q

Peak Dose Dyskinesias is what?

A

May be thought of as excessive movement secondary to excessive striatal dopamine stimulation

39
Q

Peak Dose Dyskinesia should be treated how?

A

*Smaller and more frequent doses of CD/LD

Add amantadine

40
Q

“Delayed on” and “no on” is what?

A

May be due to delayed gastric emptying or decreased absorption in the duodenum.

41
Q

“Delayed on” and “no on” should be treated how?

A

Give on an empty stomach before meals
Use ODT formulation
Avoid CD/LD CR use
Add apomorphine

42
Q

Freezing, start hesitation is what?

A

Sudden, episodic inhibition of lower-extremity motor function

43
Q

Freezing, start hesitation should be treated how?

A

Increase CD/LD dose
Add Dopamine agonist or MAO-B inhibitor
Utilize physical therapy and assistive walking devices or sensory cues

44
Q

Off period Dystonia is what?

A

Sustained muscle contraction may occur; most common in distal lower extremity. Often occur in the early morning hours, prior to the first dose of L-dopa.

45
Q

Off period Dystonia should be treated how?

A

Add SR CD/LD
Add ropinirole CR at bedtime
Initiate Baclofen
Initiate Botulinum toxin

46
Q

Myoclonus is what?

A

Occurs during sleep; repetitive jerking of limbs may occur

47
Q

Myoclonus should be treated how?

A

Decrease nighttime LD dose

Initiate clonazepam

48
Q

COMT Inhibitors (3)

A

Has to be used in combo therapy
Can decrease “wearing-off”

Increases “on time” by 1-3 hours

49
Q

COMT INHIBITORS – ENTACAPONE (COMTAN®) (3)

A

No reports of hepatotoxicity
8 doses a day
Brownish-orange urinary discoloration may occur

50
Q

COMT INHIBITORS – TOLCAPONE (TASMAR®)

A

Longer t1/2 than entacapone
TID
Use limited due to potential for serious liver dysfunction (strict monitoring of LFTs)

Brownish-orange urinary discoloration may occur

51
Q

2 Other Therapies that are thought to be helpful?

A

Antioxidants
Vitamin E (alpha-tocopherol) 2,000 International units/day
Theorized to prevent neuronal damage
Doses >400 International units/day linked to ’d risk of cardiovascular adverse effects

Vitamin C (ascorbic acid)
Theorized to potentiate antioxidant activity of vitamin E

Parkinsons Disease Pharm (1 decks)

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