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Clinical Ageing > Parkinson's > Flashcards

Parkinson's Flashcards

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?

A

50%

22
Q

How common is depression among PD patients?

A

around 80%

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
Q

what happens during MSA?

A

cerebellum, pons and basal ganglia are affected

alpha synuclein pathology in neurones, oligodendrocytes+ astrocytes

26
Q

how many people in the UK have MSA?

A

3000

27
Q

how many progressive supranuclear palsy cases are there in the UK?

A

4000

28
Q

what pathology does PSP and CBD have?

A

tau

29
Q

What haplotype on the MAPT locus is associated with AD, PSP and CBD?

A

Hap1C

30
Q

what are classic clinical features of PSP?

A

downward gaze (damage to oculomotor nucleus), prominent stare, backward falls, neck hyperreflexia, dsyphonia, dsyphagia

31
Q

what are the classical features of corticobasal degeneration?

A

cognitive/ memory problems, apathy, anhedonia, phantom limb, paraesthesia, myoclonus movements, rapid decline

32
Q

how many cases of CBD are there in the UK?

A

200-500 cases

33
Q

what would tilavonemab do?

A

vaccination to clear protein accumulation - stop prions in LB and prevent tau in PSP, CBD

34
Q

what is hedonia?

A

excessive happiness which can block the feeling of pain

35
Q

what year is the study assessing levodopa and the progression of parkinsons?

A

2004

36
Q

how is parkinsons characterised by?

A

the loss of pigmented dopaminergic neurones in the substania nigra

37
Q

what is levodopa?

A

replacement therapy that ameliorates the symptoms of the loss of doperminergic neurones

37
Q

what is levodopa?

A

replacement therapy that ameliorates the symptoms of the loss of doperminergic neurones

38
Q

what was previously thought about levodopa and dopamine?

A

that the reaction between the two caused a build up of ROS and then quickened residual dopamine neuronal loss

39
Q

what did levodopa show within animal studies?

A

that it is non toxic and promotes functional recovery of damaged nigral neurones

40
Q

when did levodopa get approval to be used within the UK?

A

1988

41
Q

what did the 2004 study show about levodopa?

A

there was no clinical evidence suggesting that levodopa is associated with the worsening of the condition

42
Q

what is the glial repsonse?

A

source of trophic factors, protects against ROS and glutamate by deletrious events in the ROS production

43
Q

what are trophic factors?

A

they are helper molecules that allows a neurone to make connection’s

44
Q

how is glutamate linked to PD?

A

it is implicated in both motor and non-motor PD

45
Q

what happens after the death or impairment of dopamine producing cells in the substania nigra?

A

less dopamine produced - affects movement

46
Q

how many more males are affected than females in PD?

A

50% more

47
Q

how does noradrenaline link to PD?

A

due to the loss of nerve endings, there are less noradrenaline which causes fatigue and alters blood pressure

48
Q

what are the RF for PD?

A

age, toxin exposures such as pesticides, heavy metals, head injuries and being male

Clinical Ageing (10 decks)

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