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Ageing block > Intro to Parkinson's disease > Flashcards

Intro to Parkinson's disease Flashcards

1
Q

How does smoking/drinking affect PD?

A

-seems to be protective for PD

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2
Q

What are the characteristics of PD?

A
  • unilateral disease
  • symptoms start unilaterally then spread to the other side as the disease progresses
  • one side tends to be more affected than the other
  • people who live in the country side more likely to get it
  • People in the medical profession at increased risk
  • 2nd most common neurodegenerative disease
  • Mean age of onset=65 years
  • Men are 1.5times more likely to get it
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3
Q

What are the symptoms associated with PD?

A
  • Forward tilt of trunk
  • Rigidity and trembling of head & extremities
  • Reduced arm swinging
  • Shuffling gait with small steps
  • Bradykinesia
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4
Q

Outline the pathophysiology of PD

A

-Loss of dopamine neurons from substantia nigra
(so the black lines disappear)
-substantia nigra is a basal ganglia structure which is therefore part of the mid brain
-PD does NOT start in the non-dopinergic areas (EXTRANIGRAL)- IT IS SPECIFICALLY THE DOPAMINERGIC AREAS OF THE SN.

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5
Q

What is the function of the basal ganglia

A
  • Motor control region
  • Target of dopamine neurons
  • Control of voluntary movements
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6
Q

Parkinson’s patients tend to have Lewy bodies. What are they?

A
  • typical inclusion in their motor neurones (in substantia nigra)
  • They are mainly composed of a protein called alpha synuclein. This protein accumulates throughout the brain and causes neuronal damage which then causes the symptoms
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7
Q

Outline the two separate PD pathologies

A
  1. ) Early cell loss
    - Ventrolateral nigra
    - Pre SMA cortex
  2. ) Early alpha synuclein
    - Brainstem
    - Forebrain
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8
Q

Which neurochemical pathways are affected in PD?

A
  • Dopamine
  • Norepinephrine
  • Serotonin
  • Acetylcholine
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9
Q

What are the risk factors for PD

A
  • head injury
  • pesticide exposure
  • family history of PD
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10
Q

What are the major clinical manifestations of PD?

A
  • Cardinal features:tremor,rigidity,akinesia
  • Other motor features: gait& equilibrium,dysarthria, fix postures
  • Non-motor features: hyposmia (reduced ability to smell),depression, sleep alterations,cognitive impairment
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11
Q

What is unique about the tremor observed in PD

A

it is at REST

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12
Q

What are the 3 S’s observed in the motor symptoms in PD?

A
  • Shaking
  • Slowness
  • Stiffness
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13
Q

What is an important non-motor syndrome involving REM in PD

A
  • Rem sleep behaviour disorder (RBD)
  • Very specific for PD
  • can occur in some other diseases
  • acting out dreams in REM
  • may lead to physical injury to patient/partner
  • Associated with PD,synucleinopaty, narcolepsy, brainstem structural lesions
  • 40% risk of parkinsonian disorder or dementia after 5 years
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14
Q

Outline olfactory dysfunction in PD

A
  • 70-100% of pts
  • usually preserved in PARK2 (early onset genetic PD). psp/cbd, Vascular and drug induced parkinsonism, Mild OD in MSA & AD
  • Recommended for PD vs PSP
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15
Q

What is DaTSCAN used for?

A
  • SPECT imaging of membrane dopamine transporters
  • Detects degeneration of dopaminergic nigrostriatal pathway eg presynaptic parkinsonian syndromes
  • A scan
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16
Q

What are the motor symptoms of PD?

A

-resting tremor
-rigidity
-bradykinesia
-freezing
dyskinesia
-postural instability
-dystonia
-constipation
-bladder dysfunction
-daytime somnolence

17
Q

define dystonia

A

-A movement disorder in which the patients muscles contract uncontrollably

18
Q

What is freezing of gait?

A
  • phenomena in which people are ‘stuck to the floor’ and find it difficult to initiate their movement/gait
  • If you give them a visible cue eg lines on the floor they find it easier to initiate their movement
  • typical of PD but not every pt will have it
  • can also have freezing of the voice/freezing of other movements
19
Q

What does pulsatile delivery of traditional levodopa lead to?

A

Pulsatile stiumlation of dopamine receptors

20
Q

At what point can we diagnose PD

A

once people develop motor symptoms

  • The motor symptoms are related to a loss of dopamine-only occurs when the pathology of PD reaches the mesencephalon (mid-brain) so it takes a while before we can actually detect the symptoms
  • so people probs have PD few years before they came into clinic from motor symptoms
21
Q

What happens to gastric absorption in PD?

A
  • It is slowed

- and there is medication overload

22
Q

List the CDS treatment options for pts inadequately treated with traditional oral therapies

A
  • Duodenal carbidopa/levodopa gel infusion
  • Subcutaneous apomorphine infusion
  • Transermal Rotigotine ( dopamine agonist; leave the patch for about 24hrs; gives a stable level of DA in the blood; associated with less dyskinesia/less motor complications)
23
Q

outline the use of subcutaneous apomorphine infusion

A
  • DA agonist
  • Looks like DA but stimulates the DA receptors
  • comes in a fluid; attached to a pump which pumps the fluid with the apomorphine under the skin
  • small needle; allows for absorption of the fluid by the skin
  • stable level of DA so preventing the motor
  • symptoms but addresses the dyskinesia
  • Intra-jejunal levodopa infusion is similar system to the above
24
Q

Outline duodopa infusion therapy

A
  • Levodopa/carbidopa in gel suspension
  • 100ml cassette
  • PEG with duodenal tube
  • Ambulatory pump
  • Morning bolus dose
  • Continuous maintenance infusion over 16hr
25
Q

Outline the use of deep brain stimulation (DBS)

A

-sends electrical pulses to the brain to interfere with neural activity at the target site

26
Q

Outline the use of levodopa in PD

A
  • effective drug but only works for about 3-4 hours so need to keep taking more tablets a day, usually up to 6
  • Complications: because it is given several times a day so at some point people may develop side effects eg dyskinesia
  • motor fluctuations are exacerbated by intermittent levodopa dosing i.e if you dont take the med you are stiff and slow, then if u take it after a while you get dyskinesia
  • idea of ‘on/off’
  • the idea behind this is pulsatile treatment of PD
  • the process usually occurs after a few years of levodopa treatment and the threshold between on/off time decreases as progressive degeneration occurs so dyskinesias are related to disease duration
27
Q

What is the Parkinson’s disease sleep scale?

A

-A simple,validated screening instrument for evaluating nocturnal symptoms in PD

28
Q

What is significant and specific about the parkinsonia tremor

A

it occurs at REST

29
Q

what could be the cause of non-motor symptoms (NMS) in parkinson’s?

A

they could be disease or drug related

Ageing block (16 decks)

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