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Clinical 2 (Part B) > 12 - Parkinson's > Flashcards

12 - Parkinson's Flashcards

1
Q

Second most common neurodegenerative disorder (after ______ disease)

A

Alzheimer’s

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2
Q

Prevalance of PD increases with ___ and higher among ____

A

age, males

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3
Q

True ethology of PD unknown but what are some factors?

A

Age
Genetics
Environment
Gender (males > females)

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4
Q

Briefly describe what’s going on/what causes parkinson’s disease

A

Overall, they have less dopamine present

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5
Q

What are the 4 cardinal motor features of PD?

A

1) Bradykinesia
2) Tremor at rest
3) Rigidity
4) Postural instability (instability of balance)

*PD is a slow, progressive, degenerative CNS disorder

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6
Q

Describe the diagnosis of PD

A

Bradykinesia PLUS either tremor at rest or rigidity

*postural instability of balance comes later

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7
Q

Describe the tremor at rest

A
  • 70% of patients
  • rhythmic, asymmetric -hands (pill rolling), feet, lip, jaw (not usually head or neck)
  • may disappear with voluntary movement and sleep
  • occurs in a body part that is relaxed and completely supported against gravity (ex. resting on a table or arm of chair)
  • suppressed with voluntary movement
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8
Q

How do we induce resting tremor ?

A

ask patient to count down from 10 out loud (the tremor worsens with mental stress)

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9
Q

Describe the rigidity

A
  • 90% of patients
  • Lead pipe, cogwheel (‘catches’)
  • neck, trunk, limbs
  • resistance to passive movement of the limbs/joints
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10
Q

Describe bradykinesia

A
  • 70% of patients
  • slowness of all movements including walking
  • difficulty initiating movement

*weakness, tremor, rigidity may contribute to but do not fully explain bradykinesia

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11
Q

Describe postural instability of balance

A
  • often later presentation
  • shuffling gait (becomes difficult to pick up feet)
  • narrow base, festination
  • freezing and falls
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12
Q

Is there muscle weakness in PD?

A

No; differentiates b/w motor cortex disorders

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13
Q

What are some other clinical features of PD?

A
  • depression
  • dementia
  • sleep disturbances
  • difficulty smelling
  • micrographia
  • dysphonia
  • dysphagia
  • hypomimia (lack of expression)
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14
Q

Describe the 4 dopaminergic pathways in the brain

A

1) Mesolimbic
- High DA = positive symptoms of schizophrenia

2) Mesocortical
- Low DA = negative symptoms of schizophrenia

3) Tuberinfudibular
- Low DA = hyperprolactinemia

4) Substantia nigra
- Extrapyramidal system (EPS)
- Low DA = Parkinson’s
- High DA = Dyskinesia

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15
Q

Describe how the substantial nivea is affected in parkinsons

A
  • Substantia nigra (SN) is normally black
  • SN controls movements and connects to the motor cortex
  • In parkinson’s, the SN cells (black cells) start to die off
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16
Q

The _____ of neurotransmitters (ACh and DA) is what allows us to have smooth movements.

A

balance

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17
Q

______ = “no go” or inhibitory neurotransmitter

A

acetylcholine

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18
Q

______ = “go” or excitatory neurotransmitter

A

dopamine

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19
Q

How are ACh and DA affected in Parkinsonism?

A

When dopamine is blocked:
ACh > DA

Thus, movement becomes jerky and stiff because there is a relative excess of “no go” neurotransmitter

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20
Q

What drugs block all 4 dopaminergic pathways in the brain?

A

Typical antipsychotics block all 4 pathways

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21
Q

What drugs block dopamine in the mesolithic pathway (less frequent EPS) ?

A

Atypical antipsychotics

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22
Q

____ agents also affect dopaminergic pathways

A

GI agents (prochlorperazine, promethazine, metoclopramide)

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23
Q

What is EPS (extrapyramidal symptoms) ?

A

abnormal body movements due to a blockade of dopamine in the brain

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24
Q

What are the 4 main types of EPS (extrapyramidal symptoms) ?

A
  • Dystonia
  • Akathisia
  • Pseudo-parkinsonism
  • Tardive dyskinesia
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25
Q

EPS (extrapyramidal symptoms):

Describe Dystonia

A
  • Sustained contraction
  • Acute onset = hours to days
  • Tardive onset = months to years
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26
Q

EPS (extrapyramidal symptoms):

Describe Akathisia

A
  • Restlessness
  • Acute onset = hours to days
  • Tardive onset = months to years
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27
Q

EPS (extrapyramidal symptoms):

Describe Pseudo-parkinsonism

A
  • Bradykinesia
  • Cogwheel-like tone/rigidity
  • Tremor
  • Onset < 30 days
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28
Q

EPS (extrapyramidal symptoms):

Describe Tardive Dyskinesia

A
  • Irregular/twisting movement
  • Ex. cheek puffing, facial grimacing, lip smacking
  • Onset: months to years (often irreversible)
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29
Q

______ is the worst for causing tar dive dyskinesia

A

haloperidol

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30
Q

What drugs can induce parkinson-like motor symptoms?

A
  • Antipsychotics (FGA > SGA)
  • Antiemetics (metoclopramide, prochlorperazine)
  • Older antihypertensives such as methyldopa
  • SSRI (serotonin may inhibit dopamine activity)
  • Valproic acid (GABA - bradykinesia, tremors)
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31
Q

What drugs can cause a resting tremor?

A
  • Lithium, VPA, SSRIs, TCAs
  • Amiodarone
  • Amphotericin B, co-trimoxazole
  • Cocaine, EtOH, MDMA
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32
Q

What are some risk factors for drug-induced parkinsonism ?

A
  • older age
  • female
  • high doses of offending drug
  • history of movement disorder
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33
Q

Drug-induced parkinsonism:

______ presentation

A

symmetric

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34
Q

Drug-induced parkinsonism:

Onset ______ ______ of starting drug

A

within weeks

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35
Q

Drug-induced parkinsonism:

May take ___ months for symptoms to resolve after discontinuation

A

2-6

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36
Q

Describe Drug-Induced NMS (neuroleptic malignant syndrome)

A
  • Life-threatening
  • Thought to be a result of a sudden decrease in dopaminergic transmission
  • Initiation or dose increase of antipsychotics (aka neuroleptics) = dopamine blocker&raquo_space;> decrease in DA transmission = NMS
  • Or sudden withdrawal or significant dose decrease of dopamine enhancers has resulted in NMS
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37
Q

What are the symptoms of Drug-Induced NMS (neuroleptic malignant syndrome)

A
  • FARM: Fever, Autonomic instability (unstable HR, BP, sweating, drooling) , Rigidity, Mental status changes
  • Delirium, severe immobility, mutism, tremor
  • Leukocytosis, rhabdomyolysis, high SCr
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38
Q

When do symptoms of parkinson’s appear?

A

When 60-80% of neurons (in substantia nigra) have been lost

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39
Q

In Substantia nigra:

_____ dopamine = parkinson’s

A

low

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40
Q

In Substantia nigra:

_____ dopamine = dyskinesia

A

high

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41
Q

In parkinson’s, we want to ______ dopamine

A

increase

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42
Q

There are two ways (MOA) to treat parkinson’s

What are they?

A

1) Enhance/increase dopamine
- Dopamine precursor = L-dopa converts to dopamine
- Dopamine agonist = activate dopamine receptors
- NMDA receptor antagonist = increases dopamine release
- COMT or MAO-B inhibitor = decrease dopamine metabolism

2) Block acetylcholine
- Anticholinergics: Block ACh (“no go” neurotransmitter) in the striatum

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43
Q

What are goals of therapy?

A

To improve motor and non-motor symptoms to maintain the best possible quality of life:

1) Preserve the ability to perform activities of daily living
2) Minimize adverse effects and treatment complications
3) Improve non-motor features such as cognitive impairment, depression, fatigue, sleep disorders

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44
Q

Early mild symptoms causing no disability (clumsiness of hands, fatigue, sensory discomfort):

Do these symptoms warrant therapy ?

A

Nope

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45
Q

When is therapy warranted?

A

When disability interferes with patient’s social, emotional or work life, therapy is warranted

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46
Q

How long is therapy?

A

Usually lifelong

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47
Q

What is the general aim of the pharmacotherapy ?

A

General aim is to increase dopamine or the relative impact of dopamine present

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48
Q

Describe the 6 areas of pharmacotherapy

A

1) Anticholinergic (block acetylcholine, relative increase in DA)
2) Amantadine (NMDA Antagonist, increases DA release)
3) MAO-B inhibitor (reduce DA breakdown)
4) COMT inhibitor (reduce levodopa breakdown)
5) Dopamine Agonist (directly stimulates DA receptors)
6) Levodopa (converted to DA by dopa decarboxylase)

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49
Q

____ is a precursor to dopamine

A

Levodopa

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50
Q

Why can’t dopamine be given directly?

A

Because it can’t cross the BBB (and that’s where it needs to be)

*Levodopa can cross the BBB and then be converted into dopamine in the BBB

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51
Q

Levodopa is always given with _______

A

A COMT or DDCI

COMT: Entacapone, tolcapone

DDCI: Carbidopa, benserazide

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52
Q

Give examples of anticholinergics

A
  • Trihexyphenidyl

- Benztropine

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53
Q

How to anticholinergics work?

A

Block acetylcholine in the striatum (in the CNS); increases relative effect of DA present

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54
Q

Describe the role of anticholinergics

A

Alone or Combination:

  • Recommend in patients with bothersome tremor < 60 yo
  • Modest antiparkinson effect - not as effective for more disabling features of PD
  • Side effects limit use (younger may tolerate)
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55
Q

What are some anticholinergic side effects?

A

urinary retention, dry eyes, dry skin, constipation, blurred vision, confusion, constipation, dry mouth, cognitive impairment, sedation, headache, increased HR, overheating

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56
Q

_____ patients may tolerate anticholinergics better

A

Younger (< 60 years)

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57
Q

Do we need to taper anticholinergics (Trihexyphenidyl and Benztropine) ?

A

Need to taper over 1 week when stopping to prevent Parkinson’s exacerbation (even if no perceived benefit was realized).

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58
Q

What is the mechanism of Amantadine ?

A

-Inhibits NMDA receptors and increases dopamine release from presynaptic terminals

59
Q

What is the role of Amantadine ?

A
  • Modest antiparkinson effect
  • Used early to help with tremor
  • Used later to reduce L-dopa dyskinesia
  • Better tolerated in young patients
60
Q

Side effects of Amantadine ?

A
  • CNS (confusion, insomnia, nervousness, hallucinations, dizziness, esp. elderly)
  • Anticholinergic (dry mouth)
  • GI upset
  • Hypotension
  • Abrupt withdrawal -> worsen PD/cause NMS
  • Tachyphylaxis
  • Livedo reticularis
61
Q

When should you take Amantadine ?

A

Take at AM/lunch to decrease insomnia

62
Q

What is Livedo reticularis ?

A
  • Cosmetic, not life threatening
  • Not dose-dependent
  • Reversible diffuse purplish-red mottling of the skin
  • Affects the upper or lower extremities +/- lower extremity edema
63
Q

What do COMT’s do ?

A

Prevent levodopa breakdown in periphery

Ex. Entacapone, tolcapone

64
Q

What do DDCI’s do ?

A

Prevents breakdown of dopamine

Ex. Carbidopa

65
Q

What do MAO-B inhibitors do?

A

Prevents dopamine breakdown

66
Q

What is the actual MOA of MAO-B inhibitors ?

A

Selective and irreversible MAO-B inhibitors in the brain.

Interferes with dopamine breakdown (in the CNS).

67
Q

Describe the role of MOA-B inhibitors ?

A
  • Mild to moderate symptomatic benefit
  • Early parkinson’s disease monotherapy
  • Add-on to Levodopa (1 hour extended “on time”)
  • Neuroprotective ?
68
Q

What are examples of MAO-B inhibitors ?

A
  • Selegiline

- Rasagiline

69
Q

MAO-B inhibitors:

When should you take Selegiline?

A

am/lunch to decrease insomnia

70
Q

MAO-B inhibitors:

Is tyramine intake a concern with Selegiline?

A

Should not be a concern at typical doses

71
Q

MAO-B inhibitors:

What should you avoid when taking Rasagiline?

A

High fat meals decrease levels

72
Q

MAO-B inhibitors:

Is tyramine intake a concern with Rasagiline?

A

Theoretical tyramine hypertensive crisis (but no diet restrictions)

73
Q

MAO-B inhibitors:

SE of Selegiline ?

A

insomnia, jitteriness, hallucinations, confusion, orthostatic hypotension, increased peak effects of L-dopa

74
Q

MAO-B inhibitors:

What is Selegiline metabolized to?

A

L-methamphetamine and L-amphetamine

75
Q

MAO-B inhibitors:

SE of Rasagiline ?

A

Minimal GI (ex. nausea - take with food), neuropsychiatric

76
Q

MAO-B inhibitors:

What do they interact with?

A

Drug interaction with serotonergic agents (ex. meperidine contraindicated, some antidepressants used with caution)

77
Q

Describe COMT inhibitors

Ex. entacapone, tolcapone

A
  • Reversible peripheral COMT inhibitor
  • Reduces GI metabolism of levodopa (prolongs half life and increases bioavailability)
  • Mild improvement in ADL and QOL scores in stable levodopa responders
  • *Typically used later as an add-on
78
Q

COMT inhibitors have no effect without ______.

A

Levodopa

-May provide up to 1-2 hour of extended “on” time for patients with “wearing off” for levodopa

79
Q

COMT Inhibitors:

Common side effects

A
  • N/V, ab pain
  • Brown orange urine/sweat discolouration (may stain clothes)
  • Increased sweating (initially)
  • Dopamine SE of L-dopa enhanced
80
Q

COMT Inhibitors:

Serious side effects

A
  • Delayed onset diarrhea (weeks-months later)
  • Dyskinesia, NMS
  • Hypotension
  • Hallucinations
81
Q

Dopamine agonist:

MOA

A

Directly stimulates dopamine receptors (i.e. mimics real dopamine)

82
Q

Dopamine agonist:

Describe the two types

A

Ergot-derived agonist:
-Bromocriptine

Non-ergot agonist:

  • Pramipexole
  • Ropinirole
  • Rotigotine
83
Q

Dopamine agonist:

Why is an ergot-derived agonist (ex. Bromocriptine) not 1st line?

A

cardiac valve disease

84
Q

Dopamine agonist:

What is the role of a non-ergot agonist ?

A
  • Alone in mild PD

- Adjunct to levodopa in patients with motor fluctuations

85
Q

What is more potent:

Dopamine agonist or Levodopa

A

Levodopa

86
Q

Compare dopamine agonists to Levodopa

A

Dopamine agonists:

  • Less potent than levodopa
  • Less motor complications but more side effects (ex. CNS, edema) than levodopa
87
Q

When would dopamine agonists be preferred over levodopa ?

A

in younger patients to delay levodopa dyskinesias

88
Q

Dopamine agonists may reduce the frequency of ___ periods and may allow levodopa dose reductions

A

“off”

89
Q

Dopamine agonists must be ______ slowly and up to therapeutic dose. (Otherwise - SE without much clinical benefit)

A

titrated

90
Q

Examples of dopamine agonists

A
  • Pramipexole
  • Ropinirole
  • Ritigotine ?
91
Q

Describe Ritigotine

A
  • Patch (good for people with difficulty swallowing or compliance issues)
  • *Not covered
92
Q

What are common side effects of dopamine agonists ?

A

nausea, cognitive impairment, hallucination, light-headed, lower extremity edema, postural hypotension, sedation, vivid dreaming

93
Q

What are serious side effects of dopamine agonists ?

A

impulsivity (pathologic gambling, hyper sexuality, shopping), psychosis, sleep attacks

Ergot derivatives: erythromelalgia/cardiac valve fibrosis

94
Q

Dopamine agonists can increase the frequency and severity of ??

A

levodopa-induced dyskinesias

95
Q

Dopamine agonist:

What can abrupt withdrawl/significant dose reduction do?

A

risk of NMS and not resolved with other PD drugs (need to resume DA)

96
Q

What is the most effective therapy for PD ?

A

Levodopa

97
Q

Why is Levodopa the most effective therapy for PD ?

A
  • Virtually all patients respond
  • Improves disability, prolongs capacity to maintain employment and ADL
  • Reduced mortality rate
98
Q

Levodopa:

Superior motor benefit but also associated with _____

A

dyskinesias

99
Q

If someone has early PD, should we automatically start with Levodopa ?

A

No way, consider amantadine or dopamine agonist first to “preserve” levodopa usefulness

100
Q

When is Levodopa very valuable?

A

In elderly patients

101
Q

DDCI

A

dopamine decarboxylase inhibitors (ex. carbidopa or benserazide)

102
Q

Levodopa is combined with ______

A

DDCI’s

103
Q

What do DDCI’s do ?

A
  • Allows increased L-dopa to cross BBB
  • Prevents conversion to dopamine in periphery
  • Minimize acute peripheral side effects (nausea, decreased BP)
104
Q

What does dopamine cause in the periphery and in the CNS?

A

Periphery: GI side effects (n/v) and can decrease BP

CNS: Movement (side effects can be h/a, vivid dreams, insomnia)

105
Q

What dose of carbidopa is required for it to sufficiently inhibit peripheral decarboxylase?

A

75mg/day

106
Q

Is it better to take LevoCarb with or without food ?

A
  • Better absorption if taken before meals

- But if significant nausea occurs, you can take with meals

107
Q

What types of food decrease Levocarb absorption?

A

protein rich foods

108
Q

Why should Levocarb CR (controlled release) not be used as initial therapy?

A
  • Less well absorbed
  • Less noticeable response since reaches CNS more slowly

*Makes evaluating and monitoring initial disease response more difficult

109
Q

What is Levocarb CR ineffective for?

A

Generally ineffective for “wearing off” effect in most:

  • Middle of night/very early AM symptoms
  • Likely adds about 90 mins to the duration of effect
110
Q

How do we switch from Levocarb regular release to Levocarb controlled release?

A
  • Only 70% bioavailable
  • Increase Levodopa dose by 20-30% when switching to CR for equivalent dose

Regular release Levodopa = 400 mg/day

CR release Levodopa = 480-520 mg/day

**Delayed onset may require supplemental regular release for optimal control in the mornings

111
Q

Compare peak times for regular release vs. controlled release Levocarb

A 
Regular = 0.5 hr
CR = 2 hr
112
Q

Describe Duodopa Gel

A
  • Levodopa/Carbidopa in a 100 mL cassette

- Intraduodenal infusion

113
Q

When is Duodopa Gel indicated ?

A
  • Severe, debilitating motor fluctuations and hyperdyskinesia
  • Despite optimized treatment with available meds
  • Long-term use of PEG-J tube

*Indicated and supervised only by neurologists/specialized providers in the management of Parkinson’s disease

$5000/month

114
Q

List the 2 most common side effects of Levodopa and how they can be managed

A

Nausea:

  • ensure 75-200mg carbidopa is being used
  • take with food
  • consider domperidone 5-10 mg PO TID before/with L-dopa/meals (max 30 mg/day -> arrhythmia)

Hypotension:

  • may need to lower dose of anti-HTN’s
  • ensure adequate water/salt intake
  • consider midodrine 7.5-15mg/day, domperidone, fludrocortisone
115
Q

List other SE of Levodopa

A

Other: hallucination, nightmares increased libido, motor fluctuations

116
Q

When does “wearing off”/”on-off” occur after starting Levodopa?

A

5-6 months (often 1-5 years) after starting levodopa

117
Q

Why does “wearing off”/”on-off” occur?

A
  • Progressive loss of neuronal dopamine storage and short levodopa t1/2
  • Waning effect of levodopa within 4 hours of last dose
118
Q

How can we manage “wearing off”/”on-off” of Levodopa ?

A
  • Smaller and more frequent levodopa dosing (take next dose 30-60 minutes earlier)
  • Consider adding a dopamine agonist
  • Consider adding a COMT inhibitor (Entacapone)
  • Consider adding a MAO-B inhibitor (Rasagiline)
  • Switch to CR Levodopa ?
  • Reduce protein in diet
119
Q

What are we watching for with Levodopa ?

A

watch for dyskinesia

120
Q

Describe what “delayed-on” and “no-on” is and what it can be due to.

A
  • A delayed or absent onset of drug effect, respectively

- Delayed gastric emptying or decreased absorption in the duodenum

121
Q

How can we manage “delayed-on” and “no-on” response if it is due to delayed gastric emptying?

A

Management of delayed gastric emptying:

-Chew/crush tablet and drink a full glass of water

122
Q

What can you give for a non-responsive/emergency of “delayed-on” and “no-on” ?

A

subcutaneous apomorphine

*recommended to take with domperidone (due to increased n/v)

123
Q

What is “freezing” ?

A

Sudden or episodic inhibition of lower-leg motor function:

  • Feet suddenly feel stuck to the floor
  • Anxiety/perceived obstacles encountered
  • Fall risk
124
Q

Management of “freezing” ?

A
  • physical therapy, assistance walking devices, sensory cues

* changes to antiparkinson drug regimen may not be helpful

125
Q

What causes the peak-dose “on” dyskinesias? Describe them.

A

-Too much dopamine

  • Involuntary repetitive, rapid/jerky movements
  • Usually neck, truck and lower/upper extremities
126
Q

How do we manage peak-dose “on” dyskinesias?

A
  • Add amantadine (antidyskinesia effect)
  • Decrease levodopa and add dopamine agonist
  • Decrease or stop COMT inhibitor/MAOB inhibitor

*watch for worsening of parkinson’s symptoms

127
Q

Describe “off-period” dystonia and when does it usually occur?

A

Sustained muscle contractions:
-Distal lower extremity (ex. clenching of toes, turning of foot)

-Usually occurs in early morning hours (waning drug levels)

128
Q

When does “off-period” dystonia improve?

A

with the first levodopa dose of the day

129
Q

Management of “off-period” dystonia

A
  • Chew regular release Levocarb tabs and take with carbonated drink to increase absorption
  • Controlled-release Levocarb (esp at bedtime)
  • Other: baclofen; focal injections of botox (for persistent focal dystonia)
130
Q

Parkinson disease therapy:
-Increase doses _____ until desired effect is seen, the max dose is achieved, or adverse effects become intolerable

*start low, go slow

A

weekly

131
Q

Parkinson disease therapy:

If partial response is seen, what do we do?

A

continue this drug and add the next drug in the sequence

132
Q

When adding adjuvant therapy to levocarb, we have to ____ the dose of levodopa?

A

reduce

133
Q

Is there a role for drug holidays in PD ?

A

no role for drug holidays as any benefit is usually short lived and comes with risks such as immobility, aspiration/pneumonia, severe depression

134
Q

Why should PD therapy not be d/c abruptly ?

A

parkinsonian crisis, NMS

135
Q

Initial pharmacologic management:

If they have functional impairment and they are over 60 years old or have severe impairment, what is first line?

A

Levodopa

136
Q

Initial pharmacologic management:

If they have functional impairment and they are under 60 with tremor ?

A

Anitcholinergic
or
Amantadine

137
Q

Initial pharmacologic management:

If they have functional impairment and they are under 60 ?

A
  • dopamine agonists
  • MAO-B inhibitor
  • levodopa
138
Q

If they have predominant end of dose “wearing off” with MILD/NO dyskinesia, how do we manage this ?

A
  • Increase levodopa
  • add entacapone
  • add dopamine agonist
  • add MAO-B inhibitor
  • change to slow release levodopa
139
Q

If they have predominant end of dose “wearing off” with MODERATE dyskinesia, how do we manage this ?

A
  • increase smaller dose levodopa frequency
  • add amantadine
  • decrease levodopa and add dopamine agonist
140
Q

If they have predominant dyskinesia with mild/no wearing off, what do we manage this?

A
  • decrease levodopa
  • add amantadine
  • discontinue anticholinergic
  • discontinue MAO-B or COMT inhibitor
141
Q

When will the pharmacologic response to levodopa deteriorate ?

A

within 6 months to 1 year

142
Q

When should a pharmacist monitor ?

A
  • weekly during titration period

- every 3 months once patient has been stabilized

143
Q

What are the main side effects that a pharmacist should be monitoring ?

A
  • monitor confusion, agitation, hallucinations, delusion, sleep disturbances, depression, increased appetite
  • dyskinesias
  • orthostatic hypotension
  • n/v
144
Q

List some non-pharms for parkinsons’

A
  • Patient/family education and support
  • Physical therapy to improve gait
  • Speech therapy to improve volume
  • Occupational therapy (for mobility, safety, driving skills, maintain social/family/work roles)
  • Nutrition counselling
  • Sleep hygiene

Clinical 2 (Part B) (30 decks)

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