L3. Parkinson's disease Flashcards

1
Q

what does the incidence of PD increase with

A

age

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2
Q

3 main features of PD

A

resting tremor
muscle ridigity
bradykinesia

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3
Q

what is the most common 1st sxs of PD

A

bradykinesia

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4
Q

4 other clinical feautures of PD

A
  1. postural instability
  2. depression
  3. autonomic NS dysfunction
  4. decreased cognitive impairment
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5
Q

give a few examples of autonomic dysfunction

A

impaired GI motility, bladder dysfunction, sialorrhoea, excessive head and neck sweating, orthostatic hypertension

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6
Q

give a few examples of decreased cognitive impairment

A

impaired visual-spatial perception and attendtion, slowness in motor tasks, impaired concentration, dementation

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7
Q

which part of the brain is involved in PD

A

substantia nigra

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8
Q

normal function of substantia nigra

A

allows smooth movements - regulation of posture and muscle tone

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9
Q

what is present in the substantia nigra in PD

A

lewy bodies and lewy neurites

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10
Q

what neurones are located in the substantia nigra?

A

dopamine

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11
Q

what is degraded in PD

A

substantia nigra

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12
Q

3 pathophysiological causes of PD

A
  1. loss of >80% dopamine
  2. loss of dopamine receptors in nigrostriatal pathway
  3. increase in acetylcholine in striatum
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13
Q

describe 4 steps in dopamine stimulation in a healthy individual

A
  1. DA stimulates basal ganglia
  2. basal ganglia has dampening effect on reticular formation - reducing unneccesary movements.Ach reduced
  3. rReticular formation sends motor info to spinal cord
  4. controlled smooth movement
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14
Q

describe 4 steps in dopamine stimulation in a person with PD

A
  1. lack of DA - basal ganglia not stimulated
  2. increase in ACh - inhibits smooth movement and dampening effect of RF
  3. info not sent to RG and therefore not sent to spinal cord
  4. increased muscle tension and tremor
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15
Q

what is parkinsonism

A

umbrella term used to describe conditions which have similar sxs to PD

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16
Q

what is the cause of PD

A

idiopathic

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17
Q

what 3 drugs can cause PD like sxs?

A

anti-psychotic drugs block DA receptors
MPTP
rotenone (pesticide)

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18
Q

what 5 things can cause secondary parkinsonism?

A
  1. drugs
  2. toxins
  3. neoplasms/strokes
  4. other neuronal system degenerations
  5. genetics
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19
Q

which 4 drugs can cause secondary parkinsonism?

A
  1. antipsychotics
  2. anti-emetics
  3. methyl-dopa (Anti-hypertensive)
  4. reserpine
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20
Q

what 2 toxins can cause secondary parkinsonism?

A

MPTP

carbon monoxide poisoning

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21
Q

strokes in what region of the brain can cause secondary parkinsonism?

A

nigrostriatal pathway

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22
Q

other neuronal system degenerations which can cause secondary parkinsonism?

A
  1. wilson’s disease - copper in brain
  2. progressive supranuclear palsy
  3. multiple-system atrophy
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23
Q

what is the only technique to differentiate PD and parkinsonism?

A

DAT scan (DA transporter scan)

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24
Q

what does the DAT scan image?

A

presynaptic DA transporter

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25
2 approaches to treatment of PD
dopamine and ACh
26
physiology of DA approach to treatment
increase DA conc in nigrostriatal system
27
physiology of Ach approach to treatment
decrease influence of ACh in striatum
28
4 drugs used in DA approach
1. MAO inhibitors 2. L-dopa 3. dopamine agonists 4. COMPT inhibitors
29
2 drugs used in Ach approach
1. anti-muscarinics | 2. amantadine
30
how does levo-dopa work?
it is a precursor for DA
31
why are peripheral decarboxylase inhibitors used with L-dopa?
can use lower L-dopa dose - decrease side effects; nausea and vomiting
32
3 acute side effects of L-dopa
1. hallucinations 2. confusion 3. dyskinesias
33
chronic side effect of L-dopa
benefits of the drug decline after 5 years - PD sxs reoccur
34
L-dopa can lead to the on-off effect. what is this?
as the drug has a short half-life, sxs reappear before taking the next dose
35
treatment for on-off effect
using modified release preparations (gel)
36
name for L-dopa + benserazide
Co-beneldopa
37
name for L-dopa + carbidopa
Co-careldopa
38
what are Co-beneldopa and Co-careldopa examples of ? which is this used in combo with?
PDI. | L-dopa
39
how does DA agonist work to treat PD?
stimulates D1 and D2 receptors
40
name 5 sxs of dopamine agonists
1. nausea 2. vomiting 3. hallucinations 4. narcolepsy 5. confusion 6. paranoia 7. postural hypotension 8. peripheral swelling
41
name 1 example of dopamine agonist
``` brocriptine pergolide pramipexol ropinirole cabergoline apomorphine ```
42
physiology of MAO inhibitors
inhibit MAO - which normally would break down DA. causing increase of DA in the synapse
43
1 example of MAO inhibitors
Selegiline | Rasagiline
44
what does COMPT inhibitors stand for?
catechol-o-methyl transferase inhibitors
45
physiology of COMPT inhibitors
prevent breakdown of L-dopa and DA
46
when are COMPT inhibitors used?
only in combo with L-dopa - used in advanced stages of the disease
47
1 example of COMPT inhibitor
entacopone | tolcapone
48
how do anti-muscarinic drugs work
block muscarinic receptors in striatum
49
what are anti-muscarinics useful in treating?
tremor
50
drug interactions of anti-muscarinincs
increase side effects of tricyclics
51
1 example of anti-muscarinincc
benzhexol benztropine procyclidine orphenadrine
52
physiology of amantadine
increases release of DA
53
2 side effects of amantadine
1. confusion | 2. tolerance may develop
54
describe 3 steps in syntheiss of DA
1. tyrosine 2. DOPA 3. DA
55
in the substantia nigra - why is DA not converted into NA?
the enzyme required is not present
56
2 moleucles which DA can be metabolised into
DOPAC and HVA
57
why may mild PD be left untreated/delayed treatment?
delay the use of L-dopa; to delay onset of its side effects
58
what 2 other neurological disorders are seen in PD?
depression and dementia
59
treatment for depression + PD
tricyclics or SSRIs
60
treatment for dementia + PD
reduce PD treatment dose -use clozapine
61
why can a vaccine which attacks alpha-synuclein be useful in treating PD?
alpha-synuclein is present in lewy bodies
62
what can glial cell line-derived neurotrophic factor possibly do?
stimulate growth of cells which are lost during PD