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INTERGRATED STUDIES IN MENTAL HEALTH > Parkinsons > Flashcards

Parkinsons Flashcards

1
Q

What is the definition of Parkinson’s

A

A neurodegenerative, progressive disease.

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2
Q

What is PD characterised by

A

Bradykinesia
Rigidity
Tremor
Postural instability

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3
Q

What percentage of people develop Parkinson’s Disease

A

At age 60: 1%
At age 80: 4%

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4
Q

What age range does early onset occur and what is it linked to

A

Ages 21-40

Genetic component links

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5
Q

What is Parkinsonism

A

A neurological syndrome characterised by tremor, bradykinesia and rigidity

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6
Q

What causes Parkinsonism

A

-Drugs: Antimycotics, Metoclopramide, TCA and MPTP (Toxin for dopamine neurons)
-Vascular disease
-Trauma
-Parkinson’s plus syndrome
-Multiple system atrophy
-Progressive supranuclear palsy
-Corticobasal degeneration
-Lewy-body dementia

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7
Q

Parkinsonism is not reversible. TRUE or FALSE

A

FALSE

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8
Q

What is the classic TRIAD that is used to diagnose

A

BRADYKINESIA / slowness
RIGIDITY / stiffness / increased tone
TREMOR / pill rolling / 4-6 Hz /resting
AND
Postural instability

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9
Q

What are the initial symptoms of Parkinson’s

A

-Persistent mild fatigue
-Handwriting becomes shaky
-Becoming unbalanced or have difficulty performing sit-to-stand
-Agitation, irritability , depression and anxiety
-Masked face

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10
Q

List the motor symptoms of Parkinson’s

A

-Hand tremors
-Rigidity/ resistance
-Spontaneous movement become slower
-Imbalance: Vulnerable to falls
- Tiled forward
- Head down

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11
Q

List some non motor symptoms

A

Depression
Emotional changes
Memory loss
Swallowing difficulties and Lewy bodies -> Dementia
Speech problems
Bladder/Bowel disorders
Excessive sweating
Sleep disturbances

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12
Q

What are Lewy bodies

A

Insoluble aggregates in neurons

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13
Q

Describe the pathology of PD

A

1- Degeneration of pigmented neurones in the pars compacta of the substantia nigra.
2- Lewy Bodies
3- Degeneration of brainstem nuclei

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14
Q

What are Lewy bodies composed of

A

Aggregates containing Alpha-synuclein

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15
Q

In healthy humans what is Alpha-synuclein used for

A

To control NT release

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16
Q

Describe the neurobiological of the motor system

A

The Basal ganglia pathway is involved in regulating movement (Extrapyramidal motor system)

GABA cell increased activity due to death of Dopaminergic substantial nigra cells to the striatum

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17
Q

What brain regions are involved in non-motor symptoms and what happens to those regions

A

Cell death in the:

-Locus coeruleus degeneration
-Nucleus Basalis
-Enteric nervous system NT release

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18
Q

What effect does cell death in the locus coeruleus have on non-motor symptoms

A

Emotional changed
Anxiety
Stress

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19
Q

What effect does cell death in the Nucleus Basalis have on non-motor symptoms

A

Memory decline
Cognition decline

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20
Q

What effect does enteric nervous systems NT release degeneration have on non-motor symptoms

A

Constipation
Swallowing
Drooling

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21
Q

What are the causes PD

A

Unknown
Genetic (AS)
Environmental factors- toxins such as MPTP
Oxidative stresses - Free radical dopamine are cytotoxic

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22
Q

List the 4 types of pharmacotherapeutic strategies

A

peripheral dopa decarboxylase inhibitor
to increase the amount that is delivered to the brain

Reduces peripheral side effects

23
Q

Name 2 dopamine replacement medication and which type of dopa decarboxylase inhibitor that they contain

A

Co-Beneldopa: Benzerazide
Co-Careldopa: Carbidopa

24
Q

Side effects of L-DOPA

A

GI side effect
Cardiovascualr S/E
Postural hypotension
Behavioural
Abnormal involuntary movement (Dyskinesia)
On-Off symptoms

25
Q

List the some DA receptor modulators

A

Amantadine
Dopaminergic agonists

26
Q

Which adjuvant is given along side L-dopa and why

A

peripheral dopa decarboxylase inhibitor
to increase the amount that is delivered to the brain

Reduces peripheral side effects

27
Q

What is Amantadine

A

An Antiviral agent that has anti-parkinsonian activity

28
Q

What is the mechanism of action of Amantadine

A

Releases dopamine from intact dopamine terminal in the striatum

29
Q

List some dopamine receptor agonist (Dopaminergic agonists)

A

Bromocriptine
Pergolide
Pramipexole
Ropinirole
Apomorphine

30
Q

Which dopamine agonists bind to D2 receptors

A

Bromocriptine
Pergolide
Ropinirole

31
Q

Which dopamine agonists bind to D1 receptors

A

Pergolide

32
Q

Which dopamine agonists bind to D3 receptors

A

Pramipexole

33
Q

what are the benefits of pergolide

A

More effective than Bromocriptine so therefore a lowered dose of L-dopa

34
Q

Cautions associated with Pergolide

A

Valvular heart disease so is less favourable than newer agents

35
Q

List the benefits of Pramipexole

A

Effective as a monotherapy for mild PD
Effective as co-therapy with L-dopa in advanced PD
May reduce affective symptoms of PD
Potential Neuroprotective effect

36
Q

List the Benefits of Ropinirole

A

Effective as monotherapy in mild PD
Effective “smoothening” the response to L-dopa

37
Q

What form is Apomorphine administered

A

Subcutaneously

38
Q

What is Apomorphine used for

A

Advanced cases that are unresponsive to other therapies to refractory motor fluctuation

39
Q

What types of medication stops the breakdown DA

A

MAOI -Mono amine oxidase inhibitors
COMT- catechol-o-methyl transferase inhibitors

40
Q

How many types of MOAs are there and what do they metabolise

A

2 types
MAO-A: Metabolises NA and 5-HT
MOA-B: Metabolises DA

41
Q

List the 2 MOAIs used for PD

A

Selegiline
Rasagiline

42
Q

What is the mechanism of MAOI for PD

A
  • Binds irreversibly to MA0-B
  • Prevents the breakdown of DA and prolongs antiparkinsonian effect of L-dopa
  • Lower dose of L-dopa needed
43
Q

What are the disadvantages of selegiline

A

Does not have any therapeutic effects

44
Q

what is the benefit of Rasagiline over Selegiline

A

Rasagline is more potent

45
Q

List the name of come COMT inhibitors

A
  • Entacapone
  • Tolcapone
46
Q

What is the mechanism of COMT Inhibitors

A

Prolong the activity of of L-dopa by preventing peripheral breakdown.

47
Q

List the antimuscarinic drugs of PD

A

Benztropine
Orphenadrine

48
Q

How do anti-muscarinic drugs help with PD

A

In PD there is an overexcitation of cholinergic neurons

the antimuscarinic drugs will block cholinergic receptor

49
Q

In which cases are anti-muscarinic drugs used

A

When the PD is drug induced NOT primary PD

50
Q

What are some none medical treatments for PD

A

Brain Graphs

Stem cell therapy

Deep brain stimulation

51
Q

Why is administering Parkinson’s medication, on time vital

A

Because the therapeutic window for the drug reduces over time, the dose must be given so that the persons symptoms does not appear.

52
Q

What adjunct treatments to Levo-dopa

A

Dopamine agonist: Non ergot then ergot derived

MAO-B inhibitors

COMT inhibitors

Then if the above doesn’t work use Amantadine

53
Q

When should the dose of Dopamine agonist be reduced

A

When there are impulse disorders.

INTERGRATED STUDIES IN MENTAL HEALTH (16 decks)

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