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54 CNS > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Cardinal symptoms of PD

A
  1. Tremor at rest
  2. Rigidity (muscular)
  3. Akinesia/bradykinesia - slowness and poverty of movement
  4. Postural instability
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2
Q

Diagnosis of PD

A

At least 2 out of 3 of TRA

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3
Q

Idiopathic PD features at initial presentation

A
  1. Asymmetric
  2. Positive response to levodopa or apomorphine
  3. Postural instability (& falls) NOT present
  4. Less rapid progression
  5. Autonomic dysfunction NOT present
  6. Neuroimaging (???????)
  7. Impaired olfaction (?)
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4
Q

What tools are used to measure disease progression?

A

Hoehn and Yahr Staging
Unified Parkinson’s disease Rating Scale (UPDRS)

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5
Q

Hoehn and Yahr Stage 1

A

Unilateral involvement

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6
Q

Hoehn and Yahr Stage 2

A

Bilateral symptoms; NO balance impairment

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7
Q

Hoehn and Yahr Stage 3

A

Impaired postural reflexes; physically independent

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8
Q

Hoehn and Yahr Stage 4

A

Severe disability, yet able to walk or stand unassisted

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9
Q

Hoehn and Yahr Stage 5

A

Wheelchair bound or bedridden

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10
Q

UPDRS (1)

A

Mentation, behaviour, mood

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11
Q

UPDRS (2)

A

Activities of daily living

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12
Q

UPDRS (3)

A

Motor examination

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13
Q

UPDRS (5)

A

Complications of Therapy

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14
Q

MDS-UPDRS (1)

A

Non-motor Experiences of Daily living

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15
Q

MDS-UPDRS (2)

A

Motor experiences of daily living

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16
Q

MDS-UPDRS (3)

A

Motor examination

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17
Q

MDS-UPDRS (4)

A

Motor complications

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18
Q

Non-motor symptoms

A
  1. Dementia
  2. Depression
  3. Psychosis
  4. Sleep disorder
  5. Constipation
  6. GI motility
  7. Orthostatic hypotension
  8. Sialorrhoea
  9. Fatigue
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19
Q

Early onset PD has ____ disease progression

A

Slower

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20
Q

Early onset PD has less ______

A

Cognitive decline

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21
Q

Early onset PD has earlier ________

A

Motor complications

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22
Q

What is the common initial presentation of early onset PD?

A

Dystonia (involuntary muscle contractions that cause slow repetitive movements or abnormal postures that can sometimes be painful)

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23
Q

Drug preference for early onset PD

A

Dopamine agonist > levodopa

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24
Q

Does dopamine pass through BBB?

A

NO

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25
Q

Does L-DOPA pass through BBB?

A

Yes

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26
Q

What is the precursor of L-DOPA?

A

L-tyrosine

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27
Q

How is L-DOPA formed?

A

Hydroxylation by tyrosine hydroxylase (from L-tyrosine)

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28
Q

What is the precursor of dopamine?

A

L-DOPA

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29
Q

How is dopamine formed?

A

Decarboxylation by AADC (from L-DOPA)

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30
Q

What is dopamine broken down into?

A
  1. DOPAC (by MAO)
  2. 3-O-M-DOPA (by COMT)
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31
Q

Short term side effects of Levodopa

A

N/V, postural hypotension

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32
Q

Which symptoms is Levodopa best for?

A

Rigidity
Bradykinesia

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33
Q

Bioavailability of Levodopa

A

~33%

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34
Q

Levodopa is transported by ______.

A

Active saturable carrier system

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35
Q

Levodopa’s absorption decreases with _____.

A

High fat & protein meal

36
Q

What can be combined with Levodopa to enhance therapeutic effects?

A

DOPA decarboxylase inhibitors (DCI)

37
Q

Levodopa:DCI

A

1:4 (sinement, madopar)
1:10 (sinemet)

38
Q

Dose required daily to saturate DOPA decarboxylase

A

75-100mg

39
Q

Motor complications of Levodopa

A
  1. On-off
  2. Wearing off (modify time of administration or switch to modified release at appropriate times)
  3. Dyskinesia (add Amantadine & switch to modified released Levodopa)
40
Q

What is useful for reducing stiffness on walking?

A

Sinemet SR
Madopar HBS

41
Q

Administration instruction for Sinemet SR

A

Do not crush

42
Q

Administration instruction for Madopar HBS

A

Do not open capsule

43
Q

Dose adjustment when switching from IR to CR Levodopa/DCI

A

Increase dose

44
Q

Dose adjustment when switching from CR to IR Levodopa/DCI

A

Decrease dose

45
Q

Levodopa DDI (1)

A

Pyridoxine
- Cofactor of DOPA decarboxylase, generally not a problem if administer with DCI

46
Q

Levodopa DDI (2)

A

Iron
Affect Levodopa absorption - space out administration

47
Q

Levodopa DDI (3)

A

Protein
Affect Levodopa absorption - space out administration

48
Q

Levodopa DDI (4)

A

Dopamine antagonists
- Metoclopramide, prochlorperazine (use domperidone for PD)
- SGA
- Risperidone

49
Q

MOA of dopamine agonist

A

Acts on D2 receptors
Mimic action of dopamine

50
Q

Examples of dopamine agonists

A

Pramipexole
Pergolide
Ropinirole

51
Q

Is Pramipexole ergot derived?

A

No

52
Q

Is Pergolide ergot derived?

A

Yes

53
Q

Is Ropinirole ergot derived?

A

No

54
Q

Dopamine agonists are preferred in ____ patients because_____.

A

Younger
Prevent or delay onset of motor complications

55
Q

Dopamine agonists have less ________ than levodopa.

A

Motor complications

56
Q

Common side effects of dopamine agonists

A

N/V, orthostatic hypotension, headache, dizziness and cardiac arrthymia

57
Q

Side effects of ergot-derived dopamine agonists

A

Peritoneal fibrosis
Cardiac valve regurgitation

58
Q

Side effects of no-ergot derived dopamine agonists

A

Sedation
Hallucinations
Somnolence
Daytime sleepiness

59
Q

Dopamine agonists have ____ half-life and duration of action than Levodopa.

A

Longer

60
Q

pK of Ropinirole

A

Mainly metabolised by liver (to inactive metabolites)

61
Q

pK of Pramipexole

A

Excreted largely unchanged in urine

62
Q

Pergolide is ____ registered in Singapore!

A

NOT

63
Q

Pramipexole & Ropinirole are available in ___ & ___ form.

A

IR
SR

64
Q

Neupro patches - active ingredient? available in SG?

A

Rotigotine
Exemption item

65
Q

MOA of MAO inhibitors

A

Inhibit breakdown of dopamine

66
Q

MAO-A

A

Peripheral, 5HT, NE

67
Q

MAO-B

A

Central, DA

68
Q

MAO inhibitors for PD

A

Selegiline
Rasagiline

69
Q

Selegiline & Rasagiline are selective for MAO-_?

A

MAO-B (but not totally selective)

70
Q

Selegiline is suitable for ___ stage of PD, and used as ____therapy.

A

Early
Monotherapy

71
Q

Dose of Selegiline in PD

A

5mg OM to BD (2nd dose in the afternoon)

72
Q

pK of Selegiline

A

Hepatically metabolised to amphetamines, which are stimulating

73
Q

MAO-Bi side effects

A

Heartburn, loss of appetite
Anxiety, palpitation, insomnia
Nightmares, visual hallucination

74
Q

DDIs of MAO-Bi

A

SSRIs, SNRIs, TCAs - washout recommended!

75
Q

Food interactions with MAO-Bi

A

Tyrosine! (metabolised by both MAO-A and MAO-B)

76
Q

MOA of COMT inhibitors

A

Inhibit dopamine breakdown
Major metaboliser of levodopa in the absence of DCI

77
Q

Benefits of COMT inhibitors

A

Increases duration of each dose of levodopa, beneficial in decreasing “wearing off” responses

78
Q

COMT inhibitors place in therapy

A

Used as adjunct to levodopa or levodopa/DCI

79
Q

COMT inhibitors used in PD

A

Entacapone
Tolcapone

80
Q

Important counselling point with Entacapone

A

Will cause diarrhoea, urine discolouration (orange)

81
Q

Entacapone is a _____, _____ inhibitor.

A

Selective, reversible

82
Q

Entacapone may cause ____ upon initiation, requiring ___________.

A

Dyskinesia
Decrease dose of levodopa

83
Q

MOA of NMDA antagonist

A

Binds directly to the glutamate site of the NMDA receptor to inhibit the action of glutamate

84
Q

MOA of Amantadine

A

a. Enhance release of stored dopamine
b. Inhibit presynaptic uptake of catecholamine
c. Dopamine receptor agonist
c. NMDA receptor antagonist

85
Q

NMDA antagonist place in therapy in PD

A

Adjunctive to levodopa

86
Q

Anticholinergic used in PD

A

Trihexyphenidyl

87
Q

Advantages of anticholinergics

A

May be effective in controlling tremor
Peripherally acting agents may be useful in treating sialorrhoea

54 CNS (13 decks)

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