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Neuro boiz > PD > Flashcards

PD Flashcards

1
Q

What are the 3 cardinal sign of PD?

A

1) Tremor
2) Akinesia/ Bradykinesia
3) Rigidity

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2
Q

How is PD diagnosed?

A

Based on clinical signs, physical examination, history, where 2 out of 3 cardinal signs must be present

Lab test and imaging are used to rule out other causes, not used for diagnosis

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3
Q

For idiopathic PD, what are some of the features at initial presentation?

A

1) Asymmetric
2) Positive response to levodopa or apomorphine
3) Postural instability not present
4) Less rapid progression
5) Autonomic dysfunction not present

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4
Q

What are some of the activities of daily living (ADLs) affected by PD?

A

1) Mobility
2) Feeding self
3) Grooming, personal hygiene
4) Toileting
5) Showering/Bathing
6) Continence (Bowel and Urinary)

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5
Q

What are some of the risk associated with PD?

A

1) Choking
2) Pneumonia
3) Falls

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6
Q

What are some of the causes of PD?

A

1) Loss of dopaminergic neurons in substantia nigra
2) Age-related loss of neurons
3) Environmental toxins/ insults
4) Genetics

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7
Q

How do you “measure” severity of PD?

A

Via Hoehn and Yahr staging

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8
Q

Describe the stages of H&Y scale

A

1 - Symptoms on one side
2 - Bilateral symptoms, no balance impairment
3 - Impaired postural reflexes, physically independent
4 - Severe disability, but still able to stand and walk unassisted
5 - Wheelchair bound or bedridden

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9
Q

What does H&Y scale assess?

A

The severity of the motor symptoms. Higher stage = More motor impairment

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10
Q

If a patient is on PD treatment, what should be assessed?

A

The H&Y stage when a person is in the “on” treatment stage, and also in the “off” treatment stage

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11
Q

What are some of the non motor symptoms associated with PD?

A

1) Cognitive impairment - Dementia
2) Psychiatric symptoms - Psychosis
3) Autonomic dysfunction - Constipation, salivation, orthostatic hypotension, N/V
4) Fatigue

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12
Q

At clinical onset of PD, the patient has already lost ___ of functioning neuron?

A

80%

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13
Q

What are the features observed in early/ young onset PD?

A

1) Lesser cognitive decline
2) Earlier motor complication
3) Dystonia (common initial presentation)
4) Slower disease progression

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14
Q

Which drug class in preferred in early/young onset PD?

A

Dopamine agonist > Levodopa

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15
Q

What are the goals of PD treatment?

A

1) Manage symptoms
2) Maintain function and autonomy
3) NOT to replace dopamine or cure PD

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16
Q

True or false: No treatment of PD has even been shown to be neuroprotective

A

True

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17
Q

What are the non-pharmacological options for treatment of PD?

A

1) Physical therapy (Stretching, posture, walking)
2) Occupational Therapy (Mobility aids, home and workplace safety)
3) Surgery
4) Speech and swallowing

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18
Q

Which drugs increase central dopamine and dopamine transmission?

A

1) Levodopa + DCI
2) Dopamine agonist
3) MAO B inhibitors
4) COMT inhibitors

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19
Q

Which drugs correct imbalance in other pathways

A

1) Anticholinergics

2) NMDA antagonist

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20
Q

What are the examples of DOPA decarboxylase inhibitors?

A

1) Carbidopa

2) Benserazide

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21
Q

Dopamine in blood causes what peripheral SEs?

A

1) Postural hypotension

2) N/V

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22
Q

What does MAO-B do?

A

Metabolize dopamine in the CNS

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23
Q

What is Levodopa effective in treating?

A

Most effective drug in treatment of cardinal symptoms, especially bradykinesia and rigidity

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24
Q

What is Levodopa not effective in treating?

A

Less effective in treatment of speech, postural reflex and gait disturbances

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25
Q

What can’t dopamine be used in the treatment of PD?

A

Dopamine can’t pass the BBB

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26
Q

Peripheral conversion of Levodopa to dopamine is catalysed by?

A

1) COMT
2) Dopa carboxylase
3) MAO

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27
Q

Where is levodopa absorbed at?

A

Proximal part of small intestine

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28
Q

What factor affected the absorption of Levodopa?

A

Absorption is decreased with high fat or high protein meal. Take 2-4 hours apart.

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29
Q

Do we remove protein from a PD patient’s diet?

A

No, PD patients must still take a high protein diet as PD causes muscle atrophy.

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30
Q

Do DCI cross the BBB?

A

No

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31
Q

How much DCI is needed to saturate dopa carboxylase?

A

75-100 mg daily

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32
Q

What is the DCI: Levodopa ratio is Simenet and Madopar?

A

Simenet - 1:4 or 1:10

Madopar - 1: 4

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33
Q

What is the DCI present in Simenet and Madopar?

A

Simenet - Carbidopa

Madopar - Benserazide

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34
Q

What are the adverse effects of Levodopa?

A

1) N/V
2) Orthostatic hypotension
3) Drowsiness
4) Hallucination, psychosis
5) Dyskinesias (3-5 years onset after initiating tx)

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35
Q

What are some of the motor complications with Levodopa?

A

1) “On-off” phenomenon
2) ‘Wearing off’ effect
3) Dyskinesias

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36
Q

Describe the ‘Wearing off’ effect

A

Effects of Levodopa wanes before the end of the dosing interval.

Shortened ‘on’ time as duration of treatment progresses

Associated with disease progression

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37
Q

How do you manage the ‘wearing off’ effect?

A

1) Modify times of administration

2) Using modified-release preparation at appropriate times

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38
Q

What are some of the symptoms of Levodopa induced dyskinesia?

A

1) Dyskinesia are involuntary and uncontrollable
2) Twitching, jerking
3) Peak dose dyskinesia
4) Dystonia

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39
Q

How do you manage Levodopa induced dyskinesia?

A

Add amantadine, or replace specific dose with modified-release levodopa

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40
Q

What is the relation with PD progression and levodopa dose?

A

As PD progresses, response threshold increases while dyskinesia threshold decreases. Need more levodopa to bring serum concentration up to a range where it will elicit a response. However, higher dose = increase dyskinesia risk

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41
Q

What causes changes in levodopa response overtime?

A

Changes in pre and post synaptic receptors

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42
Q

How is sustained release levodopa different from immediate release levodopa?

A

1) Designed to release levodopa/ DCI over a longer period (4-6 hrs)
2) Lower bioavailability compared to IR

43
Q

How do you dose adjust SR levodopa and IR levodopa?

A

IR to SR: Generally increase dose needed by 25-50%

CR to IR: Generally decrease dose needed

44
Q

What symptom is SR levodopa useful for?

A

Stiffness in waking, take SR @ bedtime

45
Q

What are the administration instructions for Sinemet SR?

A

Do not crush

46
Q

What are the administration instructions for Madopar HBS?

A

Do not open capsule

47
Q

What are the DDI with Levodopa?

A

1) Pyridoxine (Vitamin B6)
2) Iron
3) Protein
4) Antidopaminergic drugs

48
Q

How does Pyridoxine cause DDI with Levodopa?

A

It is a cofactor for dopa carboxylase. Generally not a problem if levodopa is administered with DCI, but be aware of possible interaction with high dose Vit B6 such as Neurobion

49
Q

What are some of the antidopaminergic drugs that cause DDI with Levodopa?

A

1) Metoclopramide, prochlorperazine
2) 1st gen antipsychotics
3) Risperidone
4) Non-selective MAOIs

50
Q

What is the antiemetic of choice in PD? Why?

A

Domperidone. Cross BBB less than Metoclopramide and Prochlorperazine

51
Q

What are the two classes of dopamine agonist?

A

1) Ergot Derivatives

2) Non-ergot derivatives

52
Q

What are the dopamine agonist in ergot derivative class?

A

1) Bromocriptine
2) Cabergoline
3) Pergolide

53
Q

What are the dopamine agonist in non-ergot derivative class?

A

1) Ropinirole
2) Pramipexole
3) Rotigotine (Transdermal)
4) Apomorphine (Subcutaneous)

54
Q

Which dopamine agonist class is commonly used in SG?

A

Non-ergot

55
Q

MOA of dopamine agonist?

A

Act on D2 receptors in the basal ganglia and mimics the action of dopamine

56
Q

How is Ropinirole metabolized?

A

Mainly via the liver into inactive metabolites

57
Q

How is Pramipexole excreted?

A

Mainly unchanged in the urine

58
Q

What are some of the dopaminergic SE of dopamine agonist?

A

1) Peripheral SE (Less ortho hypotension in patients taking Ropinirole)
2) Leg odema
3) Hallucinations (Visual > Auditory)
4) Somnolence, day time sleepiness
5) Compulsive behaviours

59
Q

What are some of the non-dopaminergic SE of dopamine agonist?

A

1) Fibrosis (Lower risk with non-ergot agents)

2) Valvular heart disease (Higher incidence in ergot-derived agents)

60
Q

Are there any clinical differences in efficacy between Levodopa and Dopamine agonist?

A

No.

61
Q

Which group of patient is dopamine agonist more commonly used in?

A

Younger PD patients, to maximise treatment and delay onset of levodopa-induced motor complications

62
Q

What is dopamine agonist’s place in the management of PD?

A

1) Monotherapy in young-onset PD
2) Adjunct to levodopa in moderate/ severe PD
3) Management of motor complications caused by levodopa

63
Q

Is Pergolide registered in Singapore?

A

No

64
Q

What formulation is Pramipexole and ropinirole available in?

A

IR and SR forms

65
Q

What are the MAO-B inhibitors used in PD?

A

1) Selegiline
2) Rasagiline

Both are irreversible, has a short half-life but long duration of action

66
Q

Are MAO-B effective for monotherapy?

A

Yes, especially for early stages of PD

67
Q

How is Selegiline excreted?

A

Hepatically metabolised to amphetamines, which are stimulating (can lead to insomnia)

68
Q

Dose of Selegiline?

A

5mg OM to BD, if BD, 2nd dose in afternoon

69
Q

How is Rasagiline excreted?

A

Not metabolized to amphetamines

70
Q

Dose of Rasagiline?

A

0.5mg to 2mg OD

71
Q

DDIs with MAO-B inhibitors?

A

1) SSRI, TCAs, SNRIs (washout period recommended)
2) Pethidine, tramadol
3) Linezolid (5-HT uptake inhibiting effect)
4) Dextromethorphan
5) Dopamine
6) Sympathomimetics such as nasal decongestants
7) Another MAOI

72
Q

DFIs with MAO-B inhibitors?

A

Food containing Tyramine (Cheese, yeast products)

73
Q

What is MAO-B inhibitors’ place in the management of PD?

A

1) Monotherapy in early stage, adjunct in later stages
2) More commonly used in early stages of young onset PD
3) Improvement not as great as Levodopa and dopamine agonist

74
Q

What is COMT? Function?

A

Catechol-O-Methyl transferase. Major metaboliser of Levodopa in the presence of a DCI

75
Q

Which drugs are in COMT inhibitor class?

A

1) Entacapone (Only one available in SG)

2) Tolcapone

76
Q

How does COMT-I help in PD?

A

Decrease “off” time by inhibiting the metabolism of levodopa, lengthening levodopa duration of action

77
Q

Can COMT-I be used as monotherapy?

A

No, not effective without concurrent levodopa. MUST BE TAKEN WITH LEVODOPA

Enters CNS minimally as well

78
Q

SEs of Entacapone?

A

1) Diarrhoea
2) Urine discolouration (May be due to Entacapone or Levodopa)
3) May cause dyskinesia upon initation
4) May potentiate other dopaminergic effects

79
Q

What forms are entacapone available as?

A

1) Comtan: Entacapone alone

2) Stalevo: Levodopa + Carbidopa + Entacapone

80
Q

DDI of Entacapone?

A

1) Iron, calcium supplement (Chelated by iron/ calcium)
2) Avoid concurrent non-selective MAOI (but safe with MAOBi)
3) Any catecholamine drugs
4) Enhance anticoagulant effect of warfarin

81
Q

MOA of Entacapone?

A

Selective, reversible, COMT-I

82
Q

Main differences between Tolcapone and Entacapone?

A

1) Tolcapone more potent and longer duration of effect (Off target decreased by 2-3 hours vs 1-2 hours)

2) Entacapone: Monitoring of LFT not required.
Tolcapone: Monitor LFT every 2-4 weeks for 6 months

3) Tolcapone not registered in SG

83
Q

Why are anticholinergics used in PD?

A

To control tremors

84
Q

What are the SEs of Anticholinergics?

A

1) Dry mouth
2) Blurred vision
3) Urinary retention
4) Constipation

85
Q

What are the anticholinergics commonly used in PD?

A

1) Benztropine

2) Trihexyphenidyl (benzhexol)

86
Q

Increased glutamatergic activity is linked to?

A

Development of and maintenance of levodopa-induced dyskinesias

87
Q

Which NMDA antagonist is used in PD?

A

Amantadine.

Memantine has no good evidence for an effect on levodopa induced dyskinesia for it to be recommended for routine clinical use.

88
Q

What is the proposed MOA for Amantadine?

A

1) NMDA antagonist
2) Anticholinergic
3) Upregulates D2 receptors or increase sensitivity of D2 receptors

89
Q

How is Amantadine excreted?

A

Renally excreted

90
Q

SEs of Amantadine?

A

1) Nausea
2) Light-headedness
3) Insomnia
4) Hallucination
5) Confusion
6) Livedo reticularis

91
Q

How to do prevent insomnia as a result of Amantadine use?

A

Give 2nd dose in the afternoon, not at night

92
Q

Which drugs should be avoided when on Amantadine?

A

Memantine. Can causes excessive stimulation leading to psychosis like behaviour

93
Q

Place of Amantadine in management of PD?

A

1) Adjunctive

2) Manages levodopa-induced dyskinesia

94
Q

What are some examples of alternative/complementary medicines used in management of PD?

A

1) Co-enzyme Q10 (Safe but not effective)
2) Creatine (Safe but not effective)
3) Vit E
4) Glutathione
5) Riboflavin
6) Lipoic acid
7) Acetyl carnitine
8) Curcumin

95
Q

What are the two types of Parkinsonism?

A

1) Vascular parkinsonism

2) Drug-induced parkinsonism

96
Q

Describe the features of vascular parkinsonism

A

1) Usually bilateral
2) Usually no resting tremors
3) Usually stepwise in progression
4) Vascular risk factors are present (DM, HTN, HL)
5) Increasing age is a risk factor
6) Mostly not caused by infarct/lesion in the basal ganglia

97
Q

Is levodopa useful in managing symptoms of vascular parkinsonism?

A

No, since it is not caused by infarct/lesion in the basal ganglia

98
Q

Describe the features of drug-induced parkinsonism

A

1) Symptoms tend to occur bilaterally
2) Withdrawal of offending drug leads to improvement in symptoms in 8 weeks
3) More common in females

99
Q

What are the common offending agents of drug-induced parkinsonism?

A

1) Dopamine receptor blockers such as antipsychotics (FGA, and SGA at high doses)
2) Antiemetic and gastric motility agents

100
Q

What can causes Parkinson hyperpyrexia syndrome?

A

1) Changes in dopaminergic treatment
2) Provoked by trauma, surgery, pulmonary gastrointestinal and UTI
3) May have no apparent trigger

101
Q

What happens in severe cases of Parkinson hyperpyrexia syndrome?

A

Patient becomes progressively more immobile and rigid, symptoms deteriorate rapidly.

No responses to dopaminergic rescue medications

102
Q

What are the systemic complication of Parkinson hyperpyrexia syndrome?

A

1) Decreased consciousness leading to aspiration pneumonia
2) Rhabdomyolysis
3) Deep vein thrombosis, Pulmonary embolism, DIVC as a result of immobility leading to hypercoagulability

103
Q

What is the management of Parkinson hyperpyrexia syndrome

A

1) If cause is due to a decrease in dopaminergic meds, reinstate previous treatment and increase dose of levodopa gradually
2) If PO route cannot be used, use Rotigotine patch or amatadine injection
3) Use dantrolene or bromocriptine

104
Q

Why are people with PD admitted into acute care

A

Due to complications as a result of PD, such as pneumonia, falls or uncontrolled PD symptoms

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