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YR6: NEURO > Parkinsons disease > Flashcards

Parkinsons disease Flashcards

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
Q

What is the first line treatment if the motor symptoms are NOT affecting the patient’s quality of life in PD?

A

Dopamine agonist (non-ergot derived)
or
Levodopa
or
Monoamine oxidase B (MAO‑B) inhibitor

26
Q

Why must a dopamine decarboxylase inhibitor be given with Levodopa?

A

Prevents peripheral metabolism of levodopa to dopamine outside of the brain + hence reduces side effects

27
Q

Give 3 advantages of Levodopa treatment

A

Most effective Tx for motor Sx
More improvement in ADLs
Fewer adverse effects e.g. excessive sleepiness, hallucinations, + impulse control disorders

28
Q

Give a disadvantage of Levodopa treatment

A

More motor complications e.g. dyskinesia

29
Q

List 5 common adverse effects of Levodopa

A

Dry mouth
Anorexia
Palpitations
Postural hypotension
Psychosis

30
Q

Which adverse effects are due to the difficulty in achieving a steady dose of levodopa?

A

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
Q

If a patient acutely cannot take levodopa orally, what must be given? Why?

A

Dopamine agonist patch as rescue medication
To prevent acute dystonia

32
Q

Name 2 monoamine oxidase B inhibitors

A

Selegiline
Rasagiline

33
Q

Give 2 advantages of MAO B inhbitors

A

Less motor complications
Less adverse effects e.g. excessive sleepiness, hallucinations, + impulse control disorders

34
Q

Give a disadvantage of MAO B inhibitors

A

Less improvement in motor Sx + daily functioning

35
Q

What is the MOA of MAO-B inhibitors?

A

Inhibit breakdown of dopamine secreted by the dopaminergic neurons

36
Q

Name 2 dopamine agonists (non-ergot)

A

Ropinirole
Pramipexole

37
Q

Give an advantage of dopamine agonists (non ergot)

A

Less motor complications

38
Q

Give 2 disadvantages of dopamine agonists (non ergot)

A

Less improvement in motor Sx + daily functioning
More adverse effects e.g. excessive sleepiness, hallucinations, + impulse control disorders

39
Q

Why are ergot dopamine agonists no longer used first line? Name 2

A

Risk of pulmonary, retroperitoneal + cardiac fibrosis with long-term use and need for additional monitoring.
Cabergoline, Bromocriptine

40
Q

If ergot derived dopamine receptor agonists are used in PD, what must be performed?

A

Echocardiogram, ESR, creatinine + CXR obtained prior to Tx
Patients should be closely monitored

41
Q

Which drugs can be used as adjuncts to levodopa if a patient continues to have symptoms or has developed dyskinesia?

A

Dopamine agonist
MAO‑B inhibitor
Catechol‑O‑methyl transferase (COMT) inhibitor
Amantadine

42
Q

Name 2 COMT inhibitors

A

Entacapone
Opicapone

43
Q

What is the mechanism of action of COMT inhibitors?

A

prevent peripheral degradation of levodopa, allowing a higher concentration to cross the BBB
hence used as adjunct

44
Q

What are the benefits of adjunctive COMT in PD?

A

More improvement in motor Sx + daily functioning
Lower risk of hallucinations than other drug classes.

45
Q

What are the disadvantages of adjunctive COMT in PD?

A

More adverse effects such as excessive sleepiness + impulse control disorders

46
Q

What is the probable mechanism of action of amantidine?

A

Increases dopamine release
Inhibits uptake at dopaminergic synapses

47
Q

List 6 side effects of Amantadine

A

Confusion
Constipation
Dizziness
Dry mouth
Slurred speech
Livedo reticularis

48
Q

What complications can arise due to missing/ not absorbing Parkinson’s medication?

A

Acute akinesia
Neuroleptic Malignant Syndrome

49
Q

Give 3 factors increasing risk for impulse control disorders

A

Dopamine agonist therapy
Hx of previous impulsive behaviours
Hx of alcohol consumption and/or smoking

50
Q

What drug can be used to manage drooling in Parkinson’s?

A

Glycopyrronium bromide

51
Q

Describe management of excessive daytime sleepiness in PD

A

No driving
Medication adjustment
Modafinil if alternative strategies fail.

52
Q

Describe management of orthostatic hypotension in PD

A

Medication review
If Sx persist: Midodrine (acts on peripheral alpha-adrenergic receptors to increase arterial resistance)

53
Q

What class of drugs can be used to treat drug-induced parkinsonism? What do they do? Give 2 examples

A

Anti-muscarinics, block cholinergic receptors
Help reduce tremor + rigidity
Procyclidine
Benzotropine

YR6: NEURO (47 decks)

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