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PPNP 3 > Parkinson's Disease CA > Flashcards

Parkinson's Disease CA Flashcards

1
Q

What is Parkinson’s Disease?

A

A progressive neurodegenerative disorder that primarily affects movement, but also has non-motor symptoms

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2
Q

Which area of the brain is affected in Parkinson’s Disease?

A

pars compacta of the substantia nigra, which is part of the basal ganglia

where there is a loss of dopamine-producing neurons

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3
Q

What is dopamine?

A

a neurotransmitter that is essential for smooth and coordinated muscle movements

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4
Q

Pathophysiology of Parkinson’s Disease

A
  1. Degeneration of dopaminergic (dopamine-producing) neurons
    - Cause decrease in dopamine, impaired communication between substantia nigra and the striatum, abnormal activity in the motor circuits of the brain
  2. Overactivity of acetylcholine
    - Due to reduction in dopamine, which creates an imbalance between dopamine and acetylcholine
    - Causing tremors and rigidity
  3. Lewy bodies which disrupts function of neurons
    - Lewy bodies: abnormal protein aggregates, made up of a protein called alpha-synuclein that clumps together inside neurons
    - Disrupts function of neurons, induces apoptosis
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5
Q

Cardinal signs of Parkinson’s Disease

A
  1. Bradykinesia
  2. Rigidity
  3. Tremor at rest
  4. Postural instability (but occurs at a later stage)

Note: diagnosis requires 2 of 3

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6
Q

Clinical features of Parkinson’s Disease

A
  1. Tremor
    - present at rest
    - decreased by action
    - common in arms (pill-rolling movements)
    - can affect head, jaw and legs
    - can be unilateral or bilateral
  2. Rigidity
    - Increase in muscle tone
    - “Lead Pipe” rigidity: increased resistance in ROM in all limbs
    - “Cog-wheel” rigidity: rigidity combined with resting tremor (limbs move with small, jerky movement)
  3. Bradykinesia
    - Less movement (hypokinesia or akinesia)
    - Delay in initiation of movement (freezing)
    - Slow movements
    E.g. loss of facial expression (mask face), blinking, arm swinging
  4. Postural and gait abnormality
    - flexed posture (legs, arms, trunk and neck)
    - slow, short shuffling gait, “festinant gait”
  5. Others
    - mask face
    - slow monotonous voice
    - micrographia
    - drooling
    - excessive sweating
    -urinary urgency and incontinence
    - mental depression
    - dementia very rare
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7
Q

What is the onset of Parkinson’s Disease like?

A

Insidious, then unilateral, then bilateral

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8
Q

Risk factors for Parkinson’s Disease

A
  1. Old age
  2. Highly likely: Monozygotic co-twin (identical) with early-onset PD
  3. Probable: Positive family history
  4. Possible: Herbicides, pesticides, heavy metals, proximity to industry, rural residence, well water, repeated head trauma
  5. Possible protective effect: smoking, caffeine
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9
Q

Non-motor features of Parkinson’s Disease

A
  • loss of sense of smell
  • aches and pains
  • cognitive impairment: executive functions, memory
  • mood disorders, depression, anxiety, panic attacks, hallucinations, sleep disorders
  • dribbling of saliva (sialorrhoea)
  • autonomic symptoms
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10
Q

How is dopamine synthesised and broken down in the body?

A

Synthesis:
1. L-typrosine converted to L-dopa, catalysed by enzyme tyrosine hydroxylase

  1. L-dopa converted to dopamine, catalysed by enzyme DOPA decarboxylase

Breakdown:
1. Dopamine converted to homovanillic acid, catalysed by COMT & MAO)

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11
Q

What are the 4 main classes of drugs used to treat Parkinson’s Disease? (A Major Dose of Laughter)

A
  1. Anticholinergic agents
    e.g. artane,
  2. MAO-B inhibitors
    e.g. selegiline,
  3. Dopamine agonists
    e.g. bromocriptine,
  4. Levodopa
    e.g. madopar
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12
Q

What is Levodopa and how is it usually administered?

A
  • the precursor to dopamine
  • usually administered together with peripheral decarboxylase inhibitors (e.g. Carbidopa, or Levodopa+Carbidopa: Sinemet)
  • Most efficacious drug for symptomatic mgmt of both early & late PD
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13
Q

Why does Levodopa have to be prepared together with carbidopa?

A

To address dopamine production in the periphery, reduces adverse side effects

Carbidopa is a dopa decarboxylase inhibitor that does not cross the blood-brain barrier

Hence it blocks the enzyme in the periphery (outside the brain) but not in the brain.

This prevents the premature conversion of levodopa to dopamine in peripheral tissues, thereby reducing peripheral dopamine levels and the associated side effects

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14
Q

Nursing care for Parkinson’s Disease

A
  1. Emotional well-being
  2. Medication compliance
  3. PT (exercise regime, mobility, balance, freezing)
  4. OT (ADL and home safety)
  5. ST (safe feeding)
  6. Patient education
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15
Q

Why is dopamine not given directly?

A

Levodopa can cross the blood-brain barrier into the brain unlike dopamine, converted into dopamine once entered the brain

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16
Q

Side effects of the use of levodopa

A

ST:
- N&V
- Postural hypotension

LT:
- Motor fluctuations
- Tardive Dyskinesia (10%/year, if you take levodopa for 10 years… definitely will have dyskinesia AND it’s irreversible)—–involuntary repetitive body movements, which may include grimacing, sticking out the tongue or smacking the lips.

Dose of levodopa should be kept to MINIMUM to achieve good motor function

17
Q

What are COMT inhibitors and how are they used to treat Parkinson’s Disease?

A

e.g. Entacapone and Tolcapone

Are only effective when used as an adjunct to levodopa

MOA:
- Inhibit dopamine breakdown
- Blocks enzyme that converts levodopa into inactive form
- More levodopa avail to enter brain

18
Q

Side effects of the use of COMT inhibitors

A
  • Increase in abnormal movements (dyskinesias)
  • Liver dysfunction (tolcapone)
  • Nausea, diarrhoea
  • Urinary discolouration
  • Visual hallucinations
  • Daytime drowsiness, sleep disturbances
19
Q

What are MAO-B inhibitors and how are they used to treat Parkinson’s Disease?

A

e.g. Selegiline

Efficacious as a symptomatic MONOtherapy & may be used in early stages of PD (START WITH SELEGILINE)

MOA: Inhibit dopamine breakdown, may delay nigral brain cell degeneration (neuroprotective function

20
Q

Side effects of the use of MAO-B Inhibitors

A
  • Mild nausea
  • Dry mouth
  • Lightheadedness
  • Constipation
  • Confusion (can occur in elderly people with PD)
  • Hallucinations (can occur in elderly people with PD)
21
Q

What are anticholinergics and how are they used to treat Parkinson’s Disease?

A

e.g. Trihexyphenidyl (Artane)

Effective in controlling tremors

Peripherally acting agents may be useful in treatment of sialorrhoea (excessive prod of saliva)

May be used as symptomatic MONOtherapy or as adjunct to levodopa to treat tremors and stiffness in PD

MOA: Inhibitors at cholinergic receptors

22
Q

Side effects of the use of anticholinergics

A

(esp in elderly)

  • Dry mouth
  • Sedation
  • Constipation
  • Urinary retention
  • Delirium & confusion
  • Hallucinations
23
Q

What are dopamine agonists and how are they used to treat Parkinson’s Disease?

A

E.g. Bromocriptine (Parlodel)

Are efficacious as symptomatic monotherapy, may be used as adjunct to levodopa in treatment of PD

In younger PD pts, start with dopamine agonists then levodopa

MOA: Activate dopamine receptors, act directly on dopamine receptors of brain → reduce symptoms of PD

Note: Antiparkinsonian effects not superior to levodopa

Often used before levodopa to prevent/delay onset of motor complications (dyskinesia)

24
Q

Side effects of the use of dopamine agonists

A

Similar to levodopa
- ‘Ergot’ derivative - fibrosis
- Pedal edema
- Somnolence (increased sleepiness) with ropinirole, pramipexole
- Arrhythmia
- Pergolide: restrictive valvular heart disease

*rather mild compared to levodopa

25
Q

How is early symptomatic Parkinson’s Disease without complications managed?

A
  • May not even need oral meds if coping well
  • Recommend PT and exercise regime (stretching, maintain balance and posture)
  • Healthy and balanced diet
  • Knowledge on disease
  • Social support
26
Q

What are some factors that determine the choice of medication?

A
  1. Age (Younger pts to start from dopamine agonists)
  2. Stage of disease
  3. Level of activity
  4. Associated psychological factors
  5. Associated medical conditions
  6. Patient factors

PPNP 3 (19 decks)

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