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B33CNS > Parkinson's Disease (Yvonne Mbaki) > Flashcards

Parkinson's Disease (Yvonne Mbaki) Flashcards

1
Q

What is the definition of Parkinsons?

A

Neurodegenerative; death of dopamine containing cells of the substantia nigra

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2
Q

What is the substantia nigra?

A

The origin of dopaminergic afferents implicated in Parkinson’s disease

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3
Q

What is the pathophysiology associated with Parkinson’s disease?

A

Domaine neurons in the substantia nigra in normal cells compared to the loss of noradrenergic and serotonergic neurons.

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4
Q

How do Lewy bodies form?

A

Aggregation of protein deposits in substantia nigra, locus coeruleus and other brain regions
Alpha-synuclein aggregation.

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5
Q

How is Parkinson’s disease linked to genetics?

A

The earlier the age of onset, the greater the familial occurrence
Odds of inheritance are increased if parent or sibling has PD

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6
Q

Which specific genes are the causative agents of PD?

A
  1. a-synuclein (autosomal dominant)
    Major constituent of Lewy bodies
    In familial Parkinson’s, too much or abnormal amounts of a-synuclein are produces.
    It is thought that it inhibits neurotransmitter release
  2. LRRK2 (autosomal dominant)
    Leucine-rich repeat kinase 2
    High prevalence in North African Arabs / Central/Eastern European Jews.
  3. Parkin (autosomal recessive)
    Juvenile parkinsonism - onset <30 yrs
    Acts as a ubiquitin-protein ligase; labels dead / damaged neurons to be cleared up
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7
Q

How can rural living increase risk of PD?

A

Some pesticides are known to be potent mitochondrial inhibitors
Mitochondrial complex 1 extracts energy from NADH; this complex is deficient in patients that have died from PD.
Infusion of insecticide rotenone in rats caused dopamingergic cell death, Lewy body formation and motor defecit.

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8
Q

How does mitochodrial inhibition cause PD?

A

Mitochondrial complex 1 extracts energy from NADH; this complex is deficient in patients that have died from PD.

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9
Q

Which insecticide has shown to cause PD effect in rats?

A

Rotenone

Dopaminergic cell death, Lewy body formation and motor defecit

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10
Q

Which two environmental factors can cause PD?

A

Pesticides that lead to mitochodrial inhibition

MPTP

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11
Q

What is MPTP?

A

MPTP (1- methyl - 4-phenyl - 1, 2, 3, 6 - tetrahydropyridine)

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12
Q

How was MPTP discovered?

A

By accident when synthetic heroin was the target
A student accidentally manufactured a neurotoxin MPTP
The student developed Parkinson’s disease smptoms but was responsive to treatment.
Autopsy showed destruction of substantia nigra but not Lewy body formation

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13
Q

What does increased prevalence of Parkinson’s Disease suggest?

A

Age is a factor associated with development of PD.
Loss of striatal dopamine (dopamine from the striatum) and dopamine cells in the substantia nigra
The precise role of aging is still unclear.

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14
Q

What are the motor symptoms associated with PD?

A

Bradykinesia: slowness of movement
Resting tremor: Shaking that disappears during active use of the affected body part
Rigidity: Increased resistance to passive movement
Postural instability: instability when standing, or impaired balance / coordination.

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15
Q

What other motor symptoms are included in PD?

A 
Drooling 
Fatigue 
Loss of facial expressions 
Speech problems 
Dysphagia
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16
Q

What are the non-motor symptoms / autonomic symptoms of PD?

A 
GI dysfunction 
Genitourinary dysfunction 
Cardiovascular dysfunction 
Cognitive dysfunction 
Sleep disorders 
Mood disorders
Pain
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17
Q

What GI dysfunction is associated with PD?

Parasympathetic NS

A

Constipation

Incomplete bowel evacuation / bowel incontinence

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18
Q

What genitourinary dysfunction is associated with PD?

A

Urinary urgency, frequency and incontinence

Sexual dysfunction presents in erectile dysfunction in men

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19
Q

What cardiovascular dysfunction is associated with PD?

A

Cardiac sympathetic denervation = loss of nerve supply
Responsible for light headedness and hypotension.
More commonly, postural hypotension related to medication for PD.

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20
Q

What cognitive dysfunction is associated with PD?

A

Slowness of thought and executive dysfunction

Parkinson’s Disease Dementia

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21
Q

What sleep disorders are associated with PD?

A 
Rapid eye movement disorder
Restless legs syndrome 
Periodic limb movement of sleep 
Insomnia 
Excessive daytime sleepiness
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22
Q

What are the mood disorders associated with PDD?

A

Depression
Psychosis (potentially due to too much dopamine as a result of Tx)
Anxiety - GAD, agoraphobia, panic disorder, social phobia

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23
Q

What are the pain symptoms associated with PD?

A

Muscoskeletal pain; cramping aching deformities
Radicular neuropathic pain; radiates into the lower extremity directly along the course of a spinal nerve root
Dystonic pain; pain in the neck muscles (effect of medication)
Centra/primary pain; stabbing burning scalding pain

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24
Q

What is the management strategy for treating PD?

A

Treat symptoms by replenishing dopamine

Prevent, delay, reverse neurodegeneration

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25
Q

What is the first line therapy for PD?

A

First line therapy is Levodopa

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26
Q

How does Levodopa treat PD?

A

Treats bradykinesia and rigidity

Mechanism of action - levodopa is converted to dopamine via DOPA-decarboxylase.

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27
Q

What is often concomittantly given with Levodopa and why?

A

Dopa-decarboxylase inhibitor such as carbidopa (Sinemet) or benserazide (Madopar)
Given in order to reduce peripheral side effects such as nausea, vomiting, cardiovascular

28
Q

What is the first line treatment in younger patients?

A

Dopamine agonists such as Ropinirole, Pramipexole, Rotigotine

29
Q

What is the factor that means young people have a different first line treatment?

A

They have fewer motor complications

30
Q

Which drugs are dopamine agonists?

A

Ropinirole, Pramipexole, Rotigone

31
Q

How do dopamine agonists work?

A

Agonists selective for D2 and D3 post synaptic receptors

32
Q

What can dopamine agonists be given in combination with?

A

Levodopa for effective treatment

33
Q

What are the side effects associated with dopamine agonists?

A

Nausea, sleepiness, dizziness, hallucinations and psychiatric disorders due to increased dopamine

34
Q

How do monoamine oxidase-B inhibitors treat PD?

A

Prevents the degradation of dopamine

35
Q

Which drugs are MAOi’s?

A

Selegiline, Rasagaline

36
Q

What are the side effects associated with MAOi’s?

A

Selegilline; excitement, anxiety or insomnia

Generally well tolerated

37
Q

What is the mechanism of action of amantadine?

A

Mechanism is unclear but has mixed dopaminergic and anti-glutamatergic effects

Initially used as an anti-viral

38
Q

Which drugs are COMT inhibitors?

A

Entacapone

39
Q

What is the mechanism of action of COMT inhibitors?

A

Prevents degradation of dopamine

40
Q

How can PD medication compliance be improved?

A

Levodopa + Carbidopa + Entacapone

                  Stalevo
41
Q

How can the cognitive function of PD be treated?

A

Rivastigmine for demention

Acetylcholinesterase inhibitor ; treats hallucinations more than amnesia

42
Q

How can mood orders be treated in PD?

A

Dopamine agonist - pramipexole

TCA SSRi

43
Q

How can pyschosis in PD patients be treated?

A

Atypical neuroleptics i.e clozapine (needs close monitoring due to bone marrow suppression).

44
Q

How can the cognitive function of PD be treated?

A

Rivastigmine for dementia

Acetylcholinesterase inhibitor ; treats hallucinations more than amnesia

45
Q

How can PD be managed surgically?

A

Deep brain stimulation

46
Q

What criteria must be met in order for deep brain stimulation to be suitable for patients?

A

Excellent response to levodopa
Younger age
No / mild cognitive impairment
Absence / well controlled psychiatric disease

47
Q

How does deep brain stimulation work?

A

Permanent implantation of leads into the subthalamic nucleus (basal ganglia) or globus pallidus
Leads deliver high frequency electrical impulses contolled by stimulator
Shown to alleviate motor problems
Presents opportunity to reduce levodopa dose

48
Q

What is cell replacement therapy?

A

No therapies currently available but current research focusses on embryonic, mesenchymal, neural, pluripotent stem cells

+long stability of grafted cells
+long lasting function recovery
+ effective restoration of dopamine release in vivo

49
Q

What lifestyle factor can help in management of PD?

A

Dance, martial arts are considered useful as an adjunct to medication.

50
Q

What vitamin is associated with the non-pharmacological treatment of PD?

A 
Vitamin D
Low in patients with PD
Related to bone health in PD
Appears related to severity of symptoms 
Neuroprotective role in animal studies
51
Q

What are the complication in treating PD with levodopa?

A

Dyskinesia
Fluctuations in clinical state
Nausea

52
Q

What is dyskinesia (complication of levodopa)?

How can it be treated?

A

Involuntary writhing which develops in most patients

Amantadine or clozapine to treat

53
Q

What are fluctuations in clinical state (complications in levodopa)?
How can it be treated?

A

Hypokinesia (reduced body movement) and rigidity worseding for a few minutes/hour then improving
Levodopa-SR or levodopa and COMT combined Tx

54
Q

How can nausea (induced by levodopa) be managed?

A

Administer levodopa with food; combination with carbidopa/benserazide
Domperidone anti-emetic (peripheral dopamine antagonist).

55
Q

What are the complications with treating PD with dopamine agonists?

A

Impulsive compulsive behaviour - exacerbated in a patient with a history of OCD, impulsive personality or addictive behaviour

56
Q

What action is taken when impulsive compulsive behaviour arises in people taking dopamine agonist medication for PD?

A

Reduce / discontinue dopamine agonists

Anti-convulsant zonisamide; reduces impulsive behaviour

57
Q

What are the benefits that arise in patients treating PD with clozapine?

A

Observed to improve psychosis

58
Q

What needs to be monitored in patients taking clozapine and why?

A

Agranulocytosis (lowered WBC count)

Blood monitoring is needed

59
Q

What are the co-morbities associated with Parkinson’s disease?

A

Depression, cognitive impairment, orthostatic hypotension

60
Q

How can PD related depression be treated?

A

SSRi and TCA

61
Q

How does depression present as a co-morbidity in PD?

A

Widespread in patients with early onset of PD

Abnormalities of serotenergic, noradrenerfic and dopaminergic function

62
Q

Why is it hard to diagnose depression in PD?

A

Challenging diagnosis due to symptoms overlapping e.g. weight loss and insomnia

63
Q

How does cognitive impairment arise in PD?

A

Cholinergic dysfunction observed in patients over time

64
Q

How can cognitive impairment be treated as a PD comorbitiy?

A

Clinical trials; acetylcholinesterase inhibitor (rivastigmine, donepezil)

65
Q

How does orthostatic hypertension manifest in PD patients?

A

Exists as manifestation of autonomic dysfunction or adverse effect of dopaminergic medication

66
Q

What medications are in clinical trials for PD related postural hypotension?

A

Corticosteroid; fludrocortisone
Cholinesterase inhibitor; pyridostigmine
NSAID; indomethacin
Domperidone

67
Q

What non-pharmacological advice can help alleviate orthostatic hypotension in PD?

A

Increase intake of fluid and salt –> Monitor for hypotension

B33CNS (20 decks)

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