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Systems Screening II > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is the etiology of PD?

A

true etiology is unknown; but thought to be caused by:

  1. Genetic - early onset
  2. Environmental factors - exposure to pesticides (MPTP) and heavy metals (iron, manganese), rural living and drinking well water
  3. Substantia nigra has a region that naturally has high levels of oxidative stress because free radicals are generated from dopamine metabolism by monoamine oxidase
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2
Q

What are the two hallmarks pathologic features of PD?

A
  1. Severe loss of dopaminergic neurons in the substantia nigra that project to the nigrostriatal pathway
  2. Presence of Lewy Bodies (neuronal cytoplasmic filamentous aggregates composed of the presynaptic protein α-synuclein)
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3
Q

When dopamine is depleted, what neurotransmitter takes over?

A

ACh

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4
Q

What is the goal for pharmacologic tx of PD?

A

Goal - To provide maximum relief of symptoms and maintain independence of movement
- Neuroprotection – no drugs unequivocally proven to be neuroprotective

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5
Q

What are the 3 types of treatment for PD?

A
  1. Symptomatic (all PD drugs here)
  2. Neuroprotective - nothing on the market
  3. Restorative - nothing on the market
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6
Q

What are the major medications available for the treatment of PD motor symptoms

A
  1. Levodopa – dopamine precursor
  2. Dopamine agonists - Stimulate dopamine receptors
  3. Monoamine oxidase (MAO) B inhibitors – inhibit dopamine breakdown
  4. Catechol-O-methyl transferase (COMT) inhibitors
  5. Anticholinergic agents
  6. Amantadine
    - start low, go slow with all of these drugs
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7
Q

Most effective treatment for PD symptoms; Drug of first choice for bradykinesia; MOA – immediate precursor to dopamine that is able to cross the blood brain barrier (BBB) and be metabolized to dopamine

A

Levodopa (L-Dopa)
- Administered in combination with a peripheral decarboxylase inhibitor = Carbidopa - stops the L-Dopa from being broken down into dopamine in the periphery (dopamine can’t cross the blood brain barrier)

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8
Q

MOA- Inhibits peripheral conversion of L-dopa to dopamine; Reduces peripheral side effects of dopamine (N/V and orthostatic hypotension) and results in higher CNS concentrations of dopamine; Doesn’t cross BBB; Can decrease L-DOPA dose by about 75%

A

Carbidopa

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9
Q

Why should people taking carbidopa-levodopa before a meal?

A

competes with amino acid transporters for absorption

- generally taken 3x per day, before meals

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10
Q

ADRs of this drug:
Early - Nausea/vomiting, Sedation, Postural hypotension, Discoloration urine/sweat, Vivid dreams
Late - Dyskinesia, Impulse control disorder, Sleep attacks, Confusion, Hallucination, Nightmares, Motor complications

A

L-Dopa

- increased amount of time spent on this drug = increase side effects, with lower effectiveness

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11
Q

What are the motor complications of L-Dopa?

A
  1. End of dose “ wearing off” - neuronal storage capacity is lost over time
  2. Delayed “on” and/or no “on” response (Lack of motor symptom effect or delay to effect; May be an extension of the wearing off phenomenon)
  3. Freezing
  4. Dyskinesias
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12
Q

How would you manage freezing with L-Dopa?

A
  • Least amenable to medication alterations/ interventions
    1. Increase carbidopa/levodopa dose
    2. Add dopamine agonist or MAO-B inhibitor
    3. Physiotherapy along with assistive walking devices
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13
Q

How would you manage “wearing off” with L-Dopa?

A
  1. Increasing dosing frequency and/or dose
  2. Initiating CR formulation
  3. Addition of other PD medication – Dopamine agonist, MOA-B inhibitor, COMT inhibitor
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14
Q

How would you manage dyskinesia with L-dopa?

A
  • this is due to the actual drug, not the disease
    1. Smaller doses carbidopa/levodopa
    2. Add amantadine
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15
Q

How would you manage delayed “on” and/ or no “on” response with L-dopa?

A
  1. Take on empty stomach
  2. ODT – bypass first pass metabolism
  3. AVOID CR (if they’re not responding to IR, they won’t respond to CR)
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16
Q

MOA: stimulate postsynaptic dopamine receptors in the corpus striatum directly; Efficacy is thought to be largely through stimulation of D2 receptors

A

Dopamine agonists

17
Q

What are the types of dopamine agonists?

A
  1. Non-ergot Dopamine Agonists:
    - Pramipexole (Mirapex) - tablet
    - Ropinirole (Requip) - tablet – smoking decreases Ropinirole levels in body
    - Apomorphine (Apokyn) –rescue therapy, subcutaneous injection (highest ADR or nausea/ vomiting)
    - Rotigotine (Neupro) - patch
  2. Ergot Dopamine Agonists
    - Bromocriptine (Parlodel) - tablet/ capsule = Least effective and carries risk for fatal pulmonary fibrosis, Rarely used
    - don’t abruptly stop (withdrawal)
18
Q

ADRs of this drug:
Nausea, Hallucinations/ delusions, Lower extremity edema, Sedation, Sleep attacks, Impulse control disorders or compulsive behaviors, Confusion, Lightheadedness, Postural hypotension, Vivid dreaming

A

Dopamine agonist

    • = more seen in this drug than L-Dopa
  • elderly more susceptible to this
19
Q

How do you decide to give a pt dopamine agonists vs L-dopa

A
  • Younger aged pos (60-65 yrs) start dopamine agonist first; reserving L-dopa for later in illness
  • older pts more likely to experience psychosis
20
Q

MOA: Irreversibly inhibit MAO-B [over MAO-A] which prolongs dopaminergic activity in the brain by blocking dopamine metabolism; Will provide modest symptomatic benefit as monotherapy;

A

MAO-B Inhibitors

21
Q

MAO-B inhibitor; Metabolic pathways of selegiline leads to L-amphetamine and L-methamphetamine
can cause insomnia and jitterines; Lipophilic and enters the BBB rapidly; BID

A

Selegiline

22
Q

MOA: reduces the peripheral (entacapone) and central (talcapone) methylation of levodopa; Increases the plasma half life of levodopa (50-100%); Produces more stable plasma levodopa concentrations; Prolongs the therapeutic effect of each dose of levodopa ; Increase “on” time and reduce “off” time by about 1-3 hours

A

COMT inhibitors

  • Helps reduce breakdown of L-Dopa
  • helps controls “on” time better than CR
23
Q

COMT inhibitor:
Very short half life needs to administered with each levodopa dose; Considered one of the 1st line choices for managing motor fluctuations with levodopa

A

Entacapone

24
Q

COMT inhibitor:
Inhibits both central and peripheral COMT; Strict liver enzyme monitoring in the first 6 months of therapy ; Informed content signature required ; Dosed TID

A

Tolcapone

- associated with fatal liver toxicity

25
Q

ADRs of this drug:
Dopaminergic effects; Brownish-orange urinary discoloration; Hallucinations; Confusion; Nausea; Orthostatic hypotension; 5-18% of patients develop diarrhea weeks to months after starting the drug (Do not respond well to antidiarrheal agents well); Reports of fatal liver toxicity (tolcapone only)

A

COMT inhibitors

26
Q

Typically for young people with early PD and severe tremor only; Can be used as monotherapy ; Lack significant bradykinesia or gait disturbance; Also useful in patients with more advanced disease who have persistent tremor despite levodopa or dopamine agonists

A

Anticholinergics

27
Q

What are the anticholinergic medications?

A
  1. Benztropine (Cogentin) – tablets, IV solution

2. Trihexyphenidyl (Artane) – Tablet, oral solution

28
Q

ADRs for this drug:

Memory impairment, Confusion, Hallucinations, Sedation, Dry mouth, Blurred vision, Constipation, Urinary retention

A

Anticholinergic

- slow everything down

29
Q

An antiviral agent that has mild antiparkinsonian activity; Provides modest symptomatic benefit for tremor, rigidity and bradykinesias; MOA is uncertain, but dopaminergic and nondopaminergic mechanisms (inhibition of glutamatergic NMDA receptors) are implicated

A

Amantadine

  • ADRs = Confusion, hallucinations and nightmares
  • About 50% of patients will benefit from monotherapy with amantadine, if stated early in the disease when mild symptomatic
  • problem with drug is that it can stop working within 4-8 wks
30
Q

Most Effective Surgical Technique; Useful for tremor, dyskinesia, gait disorder, and start hesitation; A battery-powered neurostimulator is implanted subcutaneously below the clavicle and provides constant electrical stimulation, via electrode wires to the targeted brain structure.; Require routine adjustments of the electrical stimulation parameters

A

Deep brain stimulation

31
Q

second-most-common etiology of parkinsonism in the elderly after Parkinson’s disease (PD)

A

Drug-induced Parkinsonism

  • bilateral Parkinsonism, without resting tremor
  • 6.8% pts misdiagnosed with PD
32
Q

When should we have PT with patients with PD?

A
  • coordinate PT with peak effects of drugs

- during “drug holidays” - symptoms increase, so PT is important to help maintain motor functions

33
Q

How would you manage delayed “on” and/or no “on” response with L-Dopa?

A
  • Lack of motor symptom effect or delay to effect ; May be an extension of the wearing off phenomenon
    1. Take on empty stomach
    2. ODT – bypass first pass metabolism
    3. AVOID CR (if they’re not responding to IR, they won’t respond to CR)
34
Q

Drug’s disadvantages: Less effective in reducing motor symptoms compared to L-Dopa; Has a significantly reduced risk of development of motor complications compared to L-Dopa; Can be used an monotherapy (except bromocriptine); Useful as adjuncts to L-dopa therapy in patients who are no longer achieving adequate response

A

Dopamine agonists

35
Q

Drug’s advantages:
Does not require intact dopaminergic neurons; Agonists do not compete with amino acids for transport into the CNS; Agonists have longer half-lives, allowing less frequent dosing; Agonists do not undergo oxidative metabolism and do not form free radicals that lead to oxidative stress

A

Dopamine agonists

36
Q

What are the two types of MAO-B inhibitors?

A
  1. Selegiline

2. Rasagiline

37
Q

Appears to improve outcomes in early and advanced PD (less functional decline and reduces off-time in patients with motor fluctuations); Considered one of the 1st line choices for managing motor fluctuations with levodopa; Similar to selegiline, but without amphetamine metabolites and has greater potency in MAO-B inhibition

A

Rasagiline
Formulation: tablet
Administration: QD

38
Q

ADRs of these types of drugs: Nausea, Headache, Orthostatic hypotension, Hallucinations, Tyramine reactions are rare “cheese effect” (Causes BP to spike due to eating cheese )

A

MAO-B inhibitors

** = main ADR

Systems Screening II (27 decks)

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