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(UNI) Neuropharmacology (3rd Year) > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Define Parkinson’s disease.

A

Parkinson’s is a progressive, neurodegenerative disorder characterised by muscle rigidity, akinesia/dyskinesia (caused by difficulties in initiating movement), resting involuntary tremor (characteristic pill rolling of the thumb and forefinger), and a slow shuffling gait.

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2
Q

What are the symptoms of Parkinson’s disease?

A

muscle rigidity, akinesia/dyskinesia (caused by difficulties in initiating movement), resting involuntary tremor (characteristic pill rolling of the thumb and forefinger), and a slow shuffling gait. Progression can be followed by the patients writing getting smaller as the disease progresses. Progression of the condition can be associated with dementia (PDD/DLB).

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3
Q

What percentage of the total population suffers from Parkinson’s disease?

A

0.1%.

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4
Q

After the age of 50, what percentage of people suffer from Parkinson’s disease?

A

1%.

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5
Q

What is the mean survival time after diagnosis of Parkinson’s disease?

A

10 Years.

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6
Q

Do patients die of Parkinson’s disease?

A

Patients don’t die of Parkinson’s, they die of complications related.

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7
Q

What changes occur in the brain when one develops Parkinson’s disease?

A

Physiologically, Parkinson’s disease is a specific loss of the dopaminergic cells in the substantia nigra pars compacta which in turn leads to the loss of the dopaminergic nigrostriatal pathway.

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8
Q

How can the brain slices of Parkinson’s patients be identified?

A

This can be seen, in brain slices, as a loss of the dark dopaminergic cells; these cells are dark because they contain melanin and as the cells die, the melanin goes with them.

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9
Q

What can cause Parkinson’s disease?

A

Idiopathic, stroke, viral infection, genetics, environmental causes.

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10
Q

What does the term Parkinsonism refer to?

A

The term Parkinsonism refers to drug-induced Parkinsonian symptoms; this can be caused by drugs such as amphetamines or neuroleptics.

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11
Q

When and how was MPTP discovered?

A

It was discovered in California in the 1980s when heroin addicts were being found ‘frozen’ after using designer drugs which they thought were heroin.

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12
Q

How does MPTP act to cause Parkinsonian symptoms?

A

MPTP is metabolised into MPP+ by MAO B and is taken up by specific DA transporter systems. It inhibits mitochondrial oxidation reactions, putting the neurones under oxidative stress eventually killing them.

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13
Q

Despite its dangerous effects, how has MPTP been used usefully?

A

This has been a useful experimental tool for inducing Parkinsonism in laboratory animals.

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14
Q

In early-onset Parkinson’s (<40 years), what is the main cause?

A

A genetic factor. This mutation leads to the presence of Lewy bodies which contain α-synuclein.

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15
Q

What are the specific genes related to early onset Parkinson’s?

A

Parkin, Ubiquitin, LRRK2, PINK.

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16
Q

What nuclei make up the basal ganglia?

A

Striatum, external globus pallides, internal globus pallides, subthalamic nucleus, substantia nigra pars compactum, substantia nigra pars reticulara.

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17
Q

What is the function of the basal ganglia?

A

The basal ganglia integrate motor and sensory information from the cortex before relaying it back to the cortex via the thalamus.

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18
Q

What controls output from the basal ganglia?

A

The output from the basal ganglia are controlled by two parallel but opposing pathways which are modulated by dopamine.

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19
Q

How does motor impairment arise in Parkinson’s?

A

Motor dysfunction arises through an imbalance between the direct and indirect pathways. In Parkinson’s the loss of the nigrostriatal dopaminergic pathway leads to excessive inhibition of the thalamocortical pathway.

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20
Q

What methods of assessment are there for assessing ones Parkinson’s?

A

UPDRS III, the unified Parkinson’s disease rating scale, is a 5-section system of evaluation of a person’s Parkinson’s. There are also carer assessments and ADL (activities of daily living (self-reported)) rating systems.

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21
Q

Why is the UPDRS III Parkinson’s rating scale not very good?

A

Due to its subjectivity.

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22
Q

What surgical interventions are available for the treatment of Parkinson’s?

A

Pallidotomy, Subthalmotomy (Thalamotomy), Deep Brain Stimulation.

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23
Q

What is a pallidotomy/thalamotomy?

A

This involves the insertion of electrodes into the sub-thalamic nuclei and the use of electricity to kill the cells here. The aim was to prevent the massive inhibition of the thalamocortical motor loop.

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24
Q

What is the major risk associated with a pallidotomy/thalamotomy?

A

This had the chance of causing massive haemorrhage and death due to the nucleus’ close proximity to a major blood vessel.

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25
Q

What is deep brain stimulation?

A

This is electrical stimulation of the subthalamic nucleus at a frequency of 130Hz. This is used to provide stimulation to override the dysfunction of the pathways here; providing optimal action of the thalamocortical motor loop.

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26
Q

What other surgical interventions for treating Parkinson’s disease have been proposed?

A

Direct, non-invasive stimulation of the motor cortex is the next aim for researchers however this has proved hard to achieve and as of yet hasn’t been developed to a point where it can be used.

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27
Q

What is the primary aim of most drug therapies for Parkinson’s disease?

A

Most therapies are aimed at replacing or replenishing dopaminergic neurotransmission or reducing ACh action at muscarinic receptors.

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28
Q

What determines the choice of drug therapy for the treatment of Parkinson’s disease?

A

The choice of therapy depends on the patients’ age, symptoms, cognitive impairment, and other illnesses.

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29
Q

What antimuscarinics are used in the treatment of Parkinson’s disease?

A

Benztropine, Biperiden.

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30
Q

Why should antimuscarinics be avoided in elderly patients?

A

They have potentially troublesome side effects.

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31
Q

How are antimuscarinics used in the treatment of Parkinson’s disease?

A

These drugs are used in the early-mid stage of the disease and are helpful for the treatment of tremor, however, have no effect on hypokinesia or rigidity.
They are useful in secondary Parkinsonism such as neuroleptic-induced Parkinsonism (D2 receptor antagonist-induced, can’t give L-DOPA as this exacerbates psychosis).

32
Q

What is the first line pharmacological treatment for Parkinson’s disease?

A

L-DOPA.

33
Q

How does L-DOPA work to treat Parkinson’s disease?

A

It is given orally and crosses the BBB to be metabolised into dopamine, replenishing the brain’s stores of the neurotransmitter.

34
Q

What is the dosage regimen for L-DOPA in Parkinson’s disease?

A

It is given in doses of 250mg to 8g per day, split into 3 doses per day. So much is given so frequently as the drug has a short half-life of 1.5 hours and constant coverage is needed.

35
Q

What adjunct treatment is L-DOPA often given with?

A

The peripheral dopa decarboxylase inhibitor carbidopa; at a dose of 500mg-1g two or three times a day. Brands of this include Sinemet and Sinemet CR.

36
Q

How effective is L-DOPA treatment?

A

Initially, about 80% of patients show improvement with drug therapy and 20% become ‘normal’ although normal is subjective.

37
Q

What treatment is given to Parkinson’s patients who are resistant to drug therapy?

A

Surgical interventions.

38
Q

What are the side effects of L-DOPA?

A

Dyskinesia, wearing off effects, progressive on-off swinging, neuropsychiatric effects, nausea and vomiting, anorexia, hypotension.

39
Q

One of the side effects of L-DOPA is progressive on-off swinging; define this.

A

On periods complicated by dyskinesias and off periods being seriously akinetic.

40
Q

One of the side effects of L-DOPA is neuropsychiatric effects; define this.

A

Schizophrenic symptoms i.e. hallucinations.

41
Q

What adjunct therapies is L-DOPA often given with?

A

DOPA-decarboxylase inhibitors, dopamine agonists, COMT inhibitors, MAO-B inhibitors, DA releasers, ACh antagonists.

42
Q

Give examples of DOPA-decarboxylase inhibitors.

A

Carbidopa, benserazide.

43
Q

Give examples of dopamine agonists.

A

Bromocriptine, pramipexole, apomorphine.

44
Q

Give examples of COMT inhibitors.

A

Entacapone.

45
Q

Give examples of DA releasers.

A

Amantadine.

46
Q

Give examples of MAO-B inhibitors.

A

Selegiline.

47
Q

Give examples of ACh antagonists.

A

Benzotropine.

48
Q

Apomorphine is a dopamine agonist used in the treatment of Parkinson’s disease. How is it used?

A

This is a dopamine agonist that is administered by injection on a when required basis by the patient. It is used as a rescue treatment for sudden on/off periods and works within 5-15 minutes.

49
Q

What class of drugs may be an alternative to L-DOPA in young Parkinson’s patients?

A

Dopamine agonists.

50
Q

How to COMT inhibitors act to help treat Parkinson’s disease?

A

COMT inhibitors are used as an adjunct therapy and work to prolong the half-life of L-DOPA by blocking the metabolic action of COMT. They also reduce the plasma concentration fluctuations, which as shown above contribute to the dyskinesia associated with L-DOPA use.

51
Q

What are the side effects of COMT inhibitors?

A

The side effects associated with COMT inhibitor use are diarrhoea and discoloured urine.

52
Q

At what daily dose is the MAO-B inhibitor selegiline given?

A

5-10mg.

53
Q

What are the side effects of selegiline?

A

Hallucinations and confusion.

54
Q

What drugs should selegiline not be given with and why?

A

Opioids = fatal interactions. TCAs and SSRIs = selegiline is a mild antidepressant.

55
Q

How do dopamine releaser work in the treatment of Parkinson’s?

A

They enhance dopamine release and block re-uptake.

56
Q

What is amantadine useful for treating in terms of Parkinson’s?

A

Amantadine is useful in early treatment for rigidity and end-stage dyskinesia.

57
Q

What are the side effects of amantadine?

A

Confusion, lightheadedness, red spiders web mottling of the legs.

58
Q

How does amantadine impair a patients cognition?

A

It is antagonistic against NMDA receptors.

59
Q

What alternative therapies may be used to treat Parkinson’s?

A

Foetal nigrostriatal transplantation, green tea, smoking, cannabis, ecstasy, use of stem cells, gene therapy.

60
Q

What is the most common Levodopa-induced side effect?

A

Vomiting and nausea.

61
Q

Is levodopa given alone?

A

No.

62
Q

What enzyme rapidly metabolises dopamine in the periphery?

A

Dopa decarboxylase.

63
Q

When titrating doses of antiparkinsonian medication, what form should be used and why?

A

Immediate release medications as modified release medications have less predictable release profiles and can lead to dose accumulation and the sudden emergence of levodopa-induced dyskinesias.

64
Q

Define dystonias.

A

Abnormal muscle contractions.

65
Q

One of the most common problems associated with levodopa therapy is the emergence of ‘end of dose’ tail off. What is this?

A

A phenomenon that after several years of therapy. Patients begin to notice re-emergence of motor symptoms before the next dose is due.

66
Q

What can the ‘end of dose’ tail off associated with levodopa therapy progress into?

A

It can ultimately progress into ‘on-off’ phenomenon; where patients switch between symptom control (on) and total freezing (off).

67
Q

When ‘end of dose’ tail off is seen in patients with Parkinson’s disease, why is simply increasing the dose not necessarily the best solution?

A

Because it can lead to an increased likelihood of the patient developing dyskinesias during peak plasma levels.

68
Q

Compared to immediate release medications, what is the bioavailability of CR antiparkinsonian medications?

A

60-70%.

69
Q

What is the best solution for treating a patient who has Parkinson’s disease and is experiencing ‘end of dose’ tail off (not including the use of CR formulations)?

A

Often the best solution is reducing the dosing interval but maintaining the same daily dose.

70
Q

The latency of CR antiparkinsonian medications is considerably longer than that of immediate release medications. What does this mean for the dosage regimen of a patient on such formulations?

A

It is sometimes necessary to ‘kick start’ a patient in the morning with a standard release preparation.

71
Q

How should a patient with early-stage Parkinsons be counselled to take their Levodopa in relation to food?

A

They should take their Levodopa with food to avoid nausea.

72
Q

How should a patient with late-stage Parkinson’s be counselled to take their Levodopa in relation to food?

A

They should take their Levodopa 30 minutes before food as dietary proteins can critically interfere with absorption.

73
Q

What patient group is most likely to benefit from the use of Dopamine Agonists?

A

Patients with early-onset Parkinson’s.

74
Q

What form can rivastigmine be given in to help with the administration to patients with swallowing difficulties?

A

A transdermal patch.

75
Q

What are the symptoms of impulse control disorder (also known as dopamine dysregulation disorder)?

A

Pathological gambling, hypersexuality, binge eating.

76
Q

What drug can be used to manage nausea and vomiting associated with dopamine agonist use?

A

Domperidone.

(UNI) Neuropharmacology (3rd Year) (20 decks)

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