Parkinson's Flashcards

(49 cards)

1
Q

what is alpha- synuclein responsible for?

A

Parkinson’s
Dementia with Lewy Bodies
Multi System Atrophy

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2
Q

what is Tau responsible for?

A

Progressive Supranuclear Palsy

Corticobasal degeneration

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3
Q

what are the fundamentals of PD?

A

clinical presentation depends on the population of neurones affected
progressive
aggregates of misfolded proteins and protein deposition

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4
Q

What is the UK incidence of PD?

A

0.1-0.2% of the UK pop

roughly 145,000

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5
Q

how many people does PD affect globally?

A

5 million

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6
Q

what are the complications of PD?

A
motor impairment
autonomic dysfunction
cognitive impairment
sleep disturbance
GI problems
incontinence
pain
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7
Q

what happens in the substania nigra (with LB)

A

severe neuronal loss

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8
Q

what are the symptoms of PD?

A

resting tremor, rigidity, bradykinesia, gait disturbance, masked face, less blinking, freezing gait, micrography

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9
Q

what does MRI/ CT show?

A

can show the disturbances

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10
Q

what happens when there is a dopamine deficiency?

A

overactivity of indirect pathway and more GABA - excessive inhib of motor thalamus

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11
Q

what are the three pharmacological options for treatment

A

L -DOPA (4x daily)
carbidopa ( inhib peripheral metabolism of levodopa)
MAO-B inhib (selegiline, rasagiline) - prvents L- DOPA removal

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12
Q

what happens over long periods of time using pharmacological treatment

A

it wears off and gradually becomes more ‘off’

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13
Q

what are the side effects of PD treatment?

A

dskinesia (invol movement), hedonia, impulsivity, freezing of gait

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14
Q

what surgical interventions can be used to treat PD?

A

subthalamic deep brain stimulation

globus pallidus DBS

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15
Q

what happens during rapid eye movement sleep disorder?

A

dream enactment
excessive daytime sleepiness
increased psych problems

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16
Q

how many PD patients experience rapid eye movement sleep disorder?

A

15-35%

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17
Q

what happens during autonomic disorders?

A

orthostatic hypotension

GI disturbances

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18
Q

how many people are affected with autonomic disorders?

A

50-85%

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19
Q

how mnay PD patients experience a lower UTI?

A

20-60%

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20
Q

what are the side effects of anticholinergics?

A

‘turn off all the taps’

- dizziness, light headed, dry mouth, blurred vision, urinary retention

21
Q

what percentage of PD patients experience memory problems within 5yrs of diagnosis?

22
Q

How common is depression among PD patients?

23
Q

what types of PD are classed as atypical?

A

multi-system atrophy (MSA)
progressive supranuclear palsy
corticobasal degeneration

24
Q

what are the features of atypical PD?

A
gait dsyfunction/ postural instability
axial rigidity
no tremor
prominent autonomic dysfunction
poor response to L- DOPA
early speech problems - dysphonia
25
what happens during MSA?
cerebellum, pons and basal ganglia are affected | alpha synuclein pathology in neurones, oligodendrocytes+ astrocytes
26
how many people in the UK have MSA?
3000
27
how many progressive supranuclear palsy cases are there in the UK?
4000
28
what pathology does PSP and CBD have?
tau
29
What haplotype on the MAPT locus is associated with AD, PSP and CBD?
Hap1C
30
what are classic clinical features of PSP?
downward gaze (damage to oculomotor nucleus), prominent stare, backward falls, neck hyperreflexia, dsyphonia, dsyphagia
31
what are the classical features of corticobasal degeneration?
cognitive/ memory problems, apathy, anhedonia, phantom limb, paraesthesia, myoclonus movements, rapid decline
32
how many cases of CBD are there in the UK?
200-500 cases
33
what would tilavonemab do?
vaccination to clear protein accumulation - stop prions in LB and prevent tau in PSP, CBD
34
what is hedonia?
excessive happiness which can block the feeling of pain
35
what year is the study assessing levodopa and the progression of parkinsons?
2004
36
how is parkinsons characterised by?
the loss of pigmented dopaminergic neurones in the substania nigra
37
what is levodopa?
replacement therapy that ameliorates the symptoms of the loss of doperminergic neurones
37
what is levodopa?
replacement therapy that ameliorates the symptoms of the loss of doperminergic neurones
38
what was previously thought about levodopa and dopamine?
that the reaction between the two caused a build up of ROS and then quickened residual dopamine neuronal loss
39
what did levodopa show within animal studies?
that it is non toxic and promotes functional recovery of damaged nigral neurones
40
when did levodopa get approval to be used within the UK?
1988
41
what did the 2004 study show about levodopa?
there was no clinical evidence suggesting that levodopa is associated with the worsening of the condition
42
what is the glial repsonse?
source of trophic factors, protects against ROS and glutamate by deletrious events in the ROS production
43
what are trophic factors?
they are helper molecules that allows a neurone to make connection's
44
how is glutamate linked to PD?
it is implicated in both motor and non-motor PD
45
what happens after the death or impairment of dopamine producing cells in the substania nigra?
less dopamine produced - affects movement
46
how many more males are affected than females in PD?
50% more
47
how does noradrenaline link to PD?
due to the loss of nerve endings, there are less noradrenaline which causes fatigue and alters blood pressure
48
what are the RF for PD?
age, toxin exposures such as pesticides, heavy metals, head injuries and being male