Parkinsons disease Flashcards

(53 cards)

1
Q

What is Parkinsons disease?

A

Neurodegenerative disease resulting from loss of dopaminergic neurones in the substantia nigra

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2
Q

When does Parkinson’s become clinically apparent?

A

Not until >,50% of dopaminergic cell activity has been lost

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3
Q

What is Parkinsonism?

A

Umbrella term for the clinical syndrome involving bradykinesia plus at least 1 of tremor, rigidity, +/or postural instability.

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4
Q

Excluding PD, list 5 causes of Parkinsonism

A

Drug-induced parkinsonism
Cerebrovascular disease
Lewy body dementia
Multiple system atrophy
Progressive supranuclear palsy.

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5
Q

Name 2 drugs that can cause Parkinsonism

A

Antipsychotics
Metoclopramide

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6
Q

What triad of symptoms characterises Parkinson’s?

A

Resting tremor
Bradykinesia
Rigidity

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7
Q

What are the aetiological causes of Parkinson’s?

A

Idiopathic (most common)
Genetic (minority)

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8
Q

Describe epidemiology of Parkinsons

A

Mean age ~65y
M > F

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9
Q

Describe 3 features of bradykinesia in Parkinsons disease

A

Short, shuffling steps + reduced arm swing
Difficulty + slowness initiating movement
Poverty of movement (hypokinesia)

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10
Q

Describe the tremor in PD

A

Most marked at rest, 3-5 Hz
Worse when stressed or tired
Improves with voluntary movement/ action/ mental concentration
“Pill rolling”: thumb + index finger
Usually asymmetrical

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11
Q

Describe the rigidity in Parkinson’s disease

A

Lead-pipe: constant resistance felt when limb is passively flexed in the presence of hypertonia without tremor
OR
Cogwheel: regular intermittent relaxation of tension felt when limb is passively flexed in the presence of tremor + hypertonia.

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12
Q

List 6 autonomic/ non-motor symptoms seen in Parkinsons

A

Postural hypotension + falls
Constipation
Urinary frequency/ urgency
Dribbling of saliva
Sexual dysfunction
Anosmia

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13
Q

How can you screen for postural instability?

A

Pull test
Tendency to fall backwards after a sharp pull from the examiner.

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14
Q

Give 2 ways in which energy/ sleep if affected in Parkinson’s

A

REM sleep behaviour disorder
Fatigue

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15
Q

List 5 signs of Parkinsons

A
Mask like facies/ Hypomimia
Flexed posture
Quiet voice
Smaller hand writing (micrographia)
Drooling of saliva
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16
Q

Describe the gait in PD

A
Stooped  
Shuffling  
Small-stepped gait 
Reduced arm swing  
Difficulty initiating walking
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17
Q

What 2 features describe the onset of PD?

A

INSIDIOUS
Unilateral

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18
Q

What is meant by the terms “on” and “off” in relation to a PD patient?

A

ON: moving well, may have dyskinesias
OFF: stiff + bradykinetic

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19
Q

What psychological pathologies may arise with PD?

A

Depression
Dementia
Psychosis

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20
Q

How does drug-induced Parkinsonism differ?

A

Motor Sx are usually rapid onset + bilateral
Rigidity + rest tremor uncommon

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21
Q

Describe diagnosis of PD

A

Refer urgently to a specialist
Clinical dx
Response to dopaminergic therapy is supportive

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22
Q

What neuroimaging investigation can be used to differentiate PD from essential tremor?

A

DaTSCAN: single photon emission computed tomography (SPECT) using
123 I‑FP‑CIT

23
Q

List 5 drug classes for managing PD

A

Levodopa + dopa-decarboxylase inhibitor
Dopamine agonists
MAO-B inhibitors
COMT inhibitors
Anticholinergics

24
Q

What is the first line treatment if the motor symptoms are affecting the patient’s quality of life in PD?

A

Levodopa + carbidopa

25
What is the first line treatment if the motor symptoms are NOT affecting the patient's quality of life in PD?
Dopamine agonist (non-ergot derived) or Levodopa or Monoamine oxidase B (MAO‑B) inhibitor
26
Why must a dopamine decarboxylase inhibitor be given with Levodopa?
Prevents peripheral metabolism of levodopa to dopamine outside of the brain + hence reduces side effects
27
Give 3 advantages of Levodopa treatment
Most effective Tx for motor Sx More improvement in ADLs Fewer adverse effects e.g. excessive sleepiness, hallucinations, + impulse control disorders
28
Give a disadvantage of Levodopa treatment
More motor complications e.g. dyskinesia
29
List 5 common adverse effects of Levodopa
Dry mouth Anorexia Palpitations Postural hypotension Psychosis
30
Which adverse effects are due to the difficulty in achieving a steady dose of levodopa?
End-of-dose wearing off: Sx worsen towards end of dosage interval= decline of motor activity On-off phenomena: large variation in motor performance (normal function during on vs weakness + reduced mobility during off) Dyskinesias at peak dose: dystonia, chorea + athetosis
31
If a patient acutely cannot take levodopa orally, what must be given? Why?
Dopamine agonist patch as rescue medication To prevent acute dystonia
32
Name 2 monoamine oxidase B inhibitors
Selegiline Rasagiline
33
Give 2 advantages of MAO B inhbitors
Less motor complications Less adverse effects e.g. excessive sleepiness, hallucinations, + impulse control disorders
34
Give a disadvantage of MAO B inhibitors
Less improvement in motor Sx + daily functioning
35
What is the MOA of MAO-B inhibitors?
Inhibit breakdown of dopamine secreted by the dopaminergic neurons
36
Name 2 dopamine agonists (non-ergot)
Ropinirole Pramipexole
37
Give an advantage of dopamine agonists (non ergot)
Less motor complications
38
Give 2 disadvantages of dopamine agonists (non ergot)
Less improvement in motor Sx + daily functioning More adverse effects e.g. excessive sleepiness, hallucinations, + impulse control disorders
39
Why are ergot dopamine agonists no longer used first line? Name 2
Risk of pulmonary, retroperitoneal + cardiac fibrosis with long-term use and need for additional monitoring. Cabergoline, Bromocriptine
40
If ergot derived dopamine receptor agonists are used in PD, what must be performed?
Echocardiogram, ESR, creatinine + CXR obtained prior to Tx Patients should be closely monitored
41
Which drugs can be used as adjuncts to levodopa if a patient continues to have symptoms or has developed dyskinesia?
Dopamine agonist MAO‑B inhibitor Catechol‑O‑methyl transferase (COMT) inhibitor Amantadine
42
Name 2 COMT inhibitors
Entacapone Opicapone
43
What is the mechanism of action of COMT inhibitors?
prevent peripheral degradation of levodopa, allowing a higher concentration to cross the BBB hence used as adjunct
44
What are the benefits of adjunctive COMT in PD?
More improvement in motor Sx + daily functioning Lower risk of hallucinations than other drug classes.
45
What are the disadvantages of adjunctive COMT in PD?
More adverse effects such as excessive sleepiness + impulse control disorders
46
What is the probable mechanism of action of amantidine?
Increases dopamine release Inhibits uptake at dopaminergic synapses
47
List 6 side effects of Amantadine
Confusion Constipation Dizziness Dry mouth Slurred speech Livedo reticularis
48
What complications can arise due to missing/ not absorbing Parkinson's medication?
Acute akinesia Neuroleptic Malignant Syndrome
49
Give 3 factors increasing risk for impulse control disorders
Dopamine agonist therapy Hx of previous impulsive behaviours Hx of alcohol consumption and/or smoking
50
What drug can be used to manage drooling in Parkinson's?
Glycopyrronium bromide
51
Describe management of excessive daytime sleepiness in PD
No driving Medication adjustment Modafinil if alternative strategies fail.
52
Describe management of orthostatic hypotension in PD
Medication review If Sx persist: Midodrine (acts on peripheral alpha-adrenergic receptors to increase arterial resistance)
53
What class of drugs can be used to treat drug-induced parkinsonism? What do they do? Give 2 examples
Anti-muscarinics, block cholinergic receptors Help reduce tremor + rigidity Procyclidine Benzotropine