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Parkinson's > Anti-Parkinson's medication management > Flashcards

Anti-Parkinson's medication management Flashcards

1
Q

What should be offered first line for patient’s in which motor symptoms are affecting their quality of life?

A

Levodopa

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2
Q

What should be offered first line for patient’s who have motor symptoms but are not affecting their quality of life?

A

Consider a choice between:
Dopamine agonists
Levodopa
Monoamine oxidase B inhibitors

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3
Q

When is add on therapy required?

A

When dyskinesia and motor fluctuations develop, which may occur in the ‘wearing off period’

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4
Q

What is the appropriate add on therapy?

A

Firstly ensure that the first line therapy is optimised, and then consider a choice between:
Dopamine agonists
Monoamine oxidase B inhibitors
Catechol-O-methyl transferase inhibitors as an adjunct to Levodopa
If Levodopa is not currently being taken, you would consider initiating it here

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5
Q

When should the drug amantadine be considered?

A

When dyskinesia (involuntary uncontrolled movements) is an adequately managed by existing therapy, use of amantadine should be considered.

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6
Q

What effects does Levodopa have on motor functions?

A

Initial use of Levodopa contributes to 80% experiencing an improvement in motor function particularly rigidity and bradykinesia, with 20% restored to nearly normal motor function.
However the effectiveness of the medication declines due the natural progression of the disease and perhaps receptor down-regulation but shows an overall increase life expectancy.

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7
Q

When should patients start Levodopa?

A

It really depends patient to patient, Levodopa can be assumed to only work for a number of years so patients choice when to start the medication is dependent upon their situation at the time - are they still working? And how significantly symptoms are affecting their quality of life at that time?

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8
Q

What are some of the adverse effects associated Levodopa?

A

Dyskinesia
Fluctuations in clinical state (known as the off period)
Acute side effects including:
- Nausea and anorexia
- Hypotension
- Sleep disturbances
- Psychological side effects including in 20% of patients confusion, nightmares but also can produce schizophrenia side effects

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9
Q

When does dyskinesia associated with L-dopa use occur?

A

Usually begins about 2 years after beginning Levodopa therapy and incidence gradually increases with prolonged use and peak therapeutic use (50% of patients by Year 5).
This involves involuntary movement of the face, arms and trunk

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10
Q

When do fluctuations in the clinical state occur associated with L-dopa use?

A

This is associated with the ‘on-off’ phenomena of L-dopa use. This is not seen in untreated Parkinson’s disease.
An ‘on’ period means that the plasma concentration of L-dopa and hence dopamine are sufficient in controlling Parkinson’s symptoms.
An ‘off’ period therefore occurs when the plasma concentration drops often at night or in the morning and the patient experiences Parkinson’s symptoms.

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11
Q

Which medication can help to reduce fluctuations in the clinical state?

A

COMT inhibitors such as Entacapone or by using sustained release preparations over night to ensure a more stable plasma concentration of L-dopa.

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12
Q

What are the two combination therapies available for Parkinson’s?

A

Carbidopa and Levodopa = Co-Careldopa (Sinemet)
Benserazide and Levodopa = Co-Beneldopa (Madopar)

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13
Q

What is the purpose of the combination therapies?

A

Carbidopa and Benserazide are DOPA decarboxylase inhibitors, preventing the peripheral metabolism of Levodopa into dopamine leading to unwanted side effects and ensuring a sufficient concentration is able to cross the BBB for CNS metabolism to dopamine, to act at dopaminergic receptors in the substantia nigra.

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14
Q

What is the dosing regimen for Levodopa?

A

Up to a maximum 800mg daily
Usually administered in smaller divided doses to attempt to produce a ‘steady state’ plasma concentration, however does result in a higher tablet burden.
Modified release preparations can be used overnight.

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15
Q

Will all patients be on 800mg of Levodopa?

A

No whilst this is the maximum dose, patients may not be able to tolerate this dose due to side effects and therefore it is about titrating the dose according to Parkinson’s symptoms vs side effects of the medication.
Patients may have a ‘target’ dose, community pharmacies may be asked to titrate dose.

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16
Q

Should Levodopa be taken with food?

A

No proteins can inhibit the absorption of Levodopa and therefore wait 30-60 minutes after administration before eating.
However having a low protein snack such as a cream cracker can help to minimise nausea associated with the medication.

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17
Q

How should Levodopa be prescribed?

A

By brand to ensure consistent therapy

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18
Q

What underlying issues may affect absorption of Levodopa?

A

Constipation
Other drug interactions
Iron supplements wait a 2-3 hours afterwards

Also be mindful of dysphagia, advise to sit up.

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19
Q

What are the four preparations of Levodopa available?

A

Dispersible
Immediate release tablets/capsules
Modified release tablets/capsules
Intestinal gel for infusion

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20
Q

When are dispersible preparations appropriate?

A

Ensure the quickest onset/faster symptomatic relief
Also for administration via a feeding tube

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21
Q

What is the duration of action of immediate release tablets/capsules?

A

They have a slower onset than dispersible but a prolonged action of up to 3 hours

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22
Q

What is the duration of action of modified release tablets/capsules?

A

Slower onset
Sustained action of 4-5 hours

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23
Q

When is intestinal gel for infusion appropriate?

A

Administration via enteral tube

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24
Q

What are the two COMT inhibitors available?

A

Entacapone
Tolcapone

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25
Q

What drugs is Entacapone used alongside?

A

Entacapone can be added to either Co-Beneldopa or Co-Careldopa, or is also marketed as a combination product with Co-Careldopa known as by the brand name:
- Stanek
- Stavelo
- Sastravi

It is important to note that Entacapone is only an add on therapy and not used in isolation for the treatment of Parkinson’s disease.

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26
Q

What is the benefit of using Entacapone?

A

Reduces fluctuations in the plasma concentration of Levodopa.

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27
Q

Why is Tolcapone rarely used in therapy?

A

Risk of liver toxicity

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28
Q

What are some of the side effects of Entacapone?

A

Discolours the urine a bright red colour (harmless)
Diarrhoea, reduces with prolonged use
As it potentiates the effects of Levodopa - more likely to experience side effects

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29
Q

When are dopamine receptor agonists indicated?

A

Can be used as an alternative to Levodopa as first line monotherapy to delay the introduction to Levodopa
Or can be used as add on when the effects of Levodopa begin to wear off

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30
Q

Compare the side effect profile of dopamine receptor agonists with Levodopa.

A

Dopamine receptor agonists have fewer motor side effects in comparison to Levodopa and tend to see less fluctuations with symptoms
However on the other hand patients experience a poorer improvement in motor symptoms and there is a higher risk of neuro-psychiatric side effects

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31
Q

State the non-ergot derived Dopamine receptors agonists.

A

Ropinirole
Rotigotine
Pramipexole

32
Q

State the ergot derived Dopamine receptors agonists.

A

Bromocriptine
Cabergoline
Lisuride
Pergolide

33
Q

What limits the use of ergot derived Dopamine receptors agonists?

A

Although effective at treating Parkinson’s disease, it is limited by side effects such as causing nausea, fibrosis of the lungs and heart valves.

34
Q

With acknowledgement of the side effect profile of ergot derived Dopamine receptors agonists, when are they indicated?

A

Only when there is an adequate response to the non-ergot derived dopamine receptor agonists.

35
Q

What are some of the side effects associated with the non-ergot derived dopamine receptor agonists?

A

Although better tolerated, some side effects due to be linked to the reward function pathway includes hallucinations and compulsive behaviours such as gambling, sexual excess or over-eating.

36
Q

What is the dosing regimen for dopamine receptor agonists?

A

Due to having a short-half life of only 6-8 hours, three times daily dosing is required.
However sustained-release once daily preparation is also available.

37
Q

What is Rotigotine?

A

It is a newer drug of the non-ergot derived dopamine receptor agonist classification.

38
Q

What the benefits of using Rotigotine?

A

It is formulated as a transdermal patch and therefore useful for impaired oral intake, with often patients temporarily converted if acutely unwell for example to equivalent dose.

39
Q

What is the benefit of using dopamine receptor agonists alongside Levodopa?

A

Reduces the dose of dopamine required and the amount of ‘off’ time and improve motor function overall.

40
Q

Which Parkinson’s medications are associated with impulse control disorders?

A

Whilst all dopaminergic medication have the potential to cause impulse control disorders, dopamine receptor agonists pose the highest risk.

41
Q

Do impulse control disorders begin upon medication initiation?

A

No they can occur up to 4-5 years after beginning dopaminergic medication.

42
Q

What are the risk factors for experiencing impulse control disorders?

A

More likely to experience impulse control disorders as a side effect if you are:
- Male
- Younger age
- History of smoking/alcohol abuse

43
Q

What is the prevalence of impulse control disorders?

A

2.6 - 34.8% , big discrepancies in literature
But has a 58.3% prevalence in younger patients

44
Q

What behaviours are included in impulse control disorders?

A

Compulsive gambling
Hypersexuality
Binge eating
Obsessive shopping

45
Q

What are some of the effects of impulsive control disorders?

A

May be difficult to stop especially if patient tries to conceal their behaviours.
Can cause distress for both patients and carers and also lead to financial difficulties and criminal convictions.

46
Q

What is the appropriate pharmacological management for impulsive control disorders?

A

If patient is taking a dopamine receptor agonists, there should be a gradual dose reduction.
Monitor to assess whether the impulse control disorder improves and whether the patient has any symptoms of withdrawal.

47
Q

Why should Anti-Parkinson’s medications not be stopped abruptly?

A

Anti-Parkinson medication should not be stopped abruptly due to the small risk of neuroleptic malignant syndrome.

48
Q

If withdrawal of medication is not effective in improving impulse control disorders, what is the next line management?

A

Offering cognitive behavioural therapy targeted at impulse control disorders.

49
Q

Which monoamine oxidase B inhibitors are available?

A

Selegeline
Rasagiline

50
Q

When are monoamine oxidase B inhibitors indicated?

A

They are used alone or as adjunct to co-beneldopa or co-careldopa to reduce ‘end of dose’ deterioration - prevent clinical fluctuations.

51
Q

How do monoamine oxidase B inhibitors work?

A

Monoamine is responsible for the metabolism of dopamine. By inhibiting this enzyme therefore this increases the availability of dopamine in the brain for a longer period of time.

52
Q

What is the importance of these MAO inhibitors being selective for B type receptors?

A

MAO-A is responsible for the metabolism of tyramine. MAO-A inhibitors including anti-depressants therefore can result in tyramine accumulation due to inhibition of the enzyme. Tyramine accumulation can precipitate hypertensive crisis. MAO-B has no effect in tyramine metabolism and therefore selectivity for this enzyme does not cause accumulation of tyramine.

53
Q

What are the side effects of MAO-B inhibitors?

A

Nausea
Postural hypotension
Dyskinesia
Confusion in the elderly

54
Q

What is selegeline metabolised to?

A

Amphetamine and therefore can cause excitation, insomnia and anxiety.

55
Q

What are the benefits of Rasagiline use over Selegeline?

A

Is not metabolised to Amphetamine and therefore does not have the associated side effects (insomnia, excitability, anxiety).
Also thought as well as providing symptomatic relief can slow disease progression.

56
Q

What are the contra-indications to Selegiline?

A

Active duodenal ulceration
Active gastric ulceration
Avoid or use with great caution in postural hypotension (when used in combination with levodopa)

57
Q

What is the mechanism of action of Amantadine?

A

Categorised as an antidyskinetic its mechanism is not fully understood but does increase dopamine concentration perhaps by increasing dopamine release.

58
Q

When is Amantadine indicated?

A

Only as add on therapy for Parkinson’s.

59
Q

What is the effect of Amantadine?

A

It’s efficacy decreases after a couple of months, but by withdrawing the medication and then reintroducing it can still be effective.

60
Q

What are the side effects associated with Amantadine?

A

Psychological - hallucinations, delusions, paranoia, anxiety, impulse control disorders
Sleep disturbances
GI - nausea, vomiting, anorexia, weight loss, dry mouth
Hypotension
Palpitations

61
Q

What are the contra-indications of Amantadine?

A

Epilepsy and history of gastric ulceration

62
Q

What are the cautions of Amantadine?

A

Confused or hallucinatory states
Congestive heart disease (may exacerbate oedema)
Elderly;

63
Q

Compare use of Levodopa, Dopamine receptor agonists and MAO-B inhibitors in terms of improvement in motor symptoms.

A

Levodopa: GREATER improvement in motor symptoms
Dopamine receptor agonists: LESS improvement in motor symptoms
MAO-B inhibitors: LESS improvement in motor symptoms

64
Q

Compare use of Levodopa, Dopamine receptor agonists and MAO-B inhibitors in terms of improvement activities daily living.

A

Levodopa: MORE improvement in ADL
Dopamine receptor agonists: LESS improvement in ADL
MAO-B inhibitors: LESS improvement in ADL

65
Q

Compare use of Levodopa, Dopamine receptor agonists and MAO-B inhibitors in terms of motor complications.

A

Levodopa: MORE motor complications
Dopamine receptor agonists: LESS motor complications
MAO-B inhibitors: LESS motor complications

66
Q

Compare use of Levodopa, Dopamine receptor agonists and MAO-B inhibitors in terms of adverse effects.

A

Levodopa: FEWER specified adverse effects
Dopamine receptor agonists: MORE specified adverse effects
MAO-B inhibitors: FEWER specified adverse effects

67
Q

Compare use of Dopamine receptor agonists, MAO-B inhibitors, COMT inhibitors and Amantadine as potential add on therapy in terms of improvement in motor symptoms.

A

Dopamine receptor agonist: Improvement in motor symptoms
MAO-B inhibitor: Improvement in motor symptoms
COMT inhibitors: Improvement in motor symptoms
Amantadine: No evidence of improvement in motor symptoms

68
Q

Compare use of Dopamine receptor agonists, MAO-B inhibitors, COMT inhibitors and Amantadine as potential add on therapy in terms of improvement in activities of daily living.

A

Dopamine receptor agonist: Improvement in ADLs
MAO-B inhibitor: Improvement in ADLs
COMT inhibitors: Improvement in ADLs
Amantadine: No evidence of improvement in ADLs

69
Q

Compare use of Dopamine receptor agonists, MAO-B inhibitors, COMT inhibitors and Amantadine as potential add on therapy in terms of improvement in off time.

A

Dopamine receptor agonist: MORE off time reduction
MAO-B inhibitor: Off time reduction
COMT inhibitors: Off time reduction
Amantadine: No studies reporting this outcome

70
Q

Compare use of Dopamine receptor agonists, MAO-B inhibitors, COMT inhibitors and Amantadine as potential add on therapy in terms of adverse effects.

A

Dopamine receptor agonist: Immediate risk of adverse effects
MAO-B inhibitor: Fewer adverse effects
COMT inhibitors: More adverse effects
Amantadine: No studies reporting this outcome

71
Q

Compare use of Dopamine receptor agonists, MAO-B inhibitors, COMT inhibitors and Amantadine as potential add on therapy in terms of presence of hallucinations.

A

Dopamine receptor agonist: Higher risk of hallucinations
MAO-B inhibitor: Lower risk of hallucinations
COMT inhibitors: Lower risk of hallucinations
Amantadine: No studies reporting this outcome

72
Q

What are some of the effects of missing a dose of Parkinson’s medications?

A

Acute akinesia (inability to initiate movement)
Unable to communication
Inability to swallow, increasing the risk of aspiration
Increased risk of falls and hence fractures
Risk of neuroleptic-like malignant syndrome

73
Q

What are the causes of neuroleptic-like malignant syndrome?

A

It occurs when there is a sudden marked reduction in dopamine activity, either caused by sudden withdrawal of dopaminergic agents or blockade of dopamine receptors (often by anti-psychotics).

74
Q

What are some of the risk factors for neuroleptic-like malignant syndrome?

A

Although rare it is more common in those with severe Parkinson’s symptoms or on high doses of Levodopa.

75
Q

What are some of the symptoms of neuroleptic malignant syndrome?

A

Fever
Marked rigidity including affecting muscles that aid breathing resulting in hypoventilation
Altered consciousness
Leucocytosis
Elevated creatine kinase

76
Q

What is the GET IT ON TIME campaign?

A

Campaign helping to ensure that Parkinson’s patients receive their medication on time every time - aimed at ward staff, in care home and carers to reinforce this message.

Parkinson's (3 decks)

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