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RB Y3 1.2 Neurology > Idiopathic Parkinson's Disease > Flashcards

Idiopathic Parkinson's Disease Flashcards

1
Q

mean age of onset

A

65

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2
Q

more common in males or females

A

males

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3
Q

aetiology

A

not fully understood, genetic and environemental factors

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4
Q

which form of PD is more likely to have a genetic component

A

early onset (<40)

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5
Q

what is the most prominent risk factor

A

age - prevalence increases sharply with age

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6
Q

what is the location of teh dopaminergic neurons that are affected

A

in the pars compacta of the substantia nigra of the basal ganglia

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7
Q

outline the pathophysiology

A
  • progressive degeneration of dopaminergic neurons in PC of SN results in less dopamine being produced, other neurotransmitters are also affected, eg noradrenaline and ACh
  • this affects teh output of the BG - overactive GABA from the globus pallidus internus (output nuclei) results in excessive inhibition
  • there is decreased excitation of the motor cortex
  • –> smooth, coordinated and controlled movement is not produced
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8
Q

histology

A

Lewy bodies, these are eosinophilic alpha synculein inclusions

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9
Q

where are Lewy bodies found at the beginning and as disease progresses

A

initally in pars compacta of SN, they become more widespread as the disease progresses

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10
Q

which staging is used to classify pathology of PD and AD

A

Braak staging

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11
Q

when in the pathological timeline does the disease tend to present

A

presents insidiously, usually the pathological process starts years before symptoms develop and at time of presentation often around 70% of Dopaminergic neurons are already lost

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12
Q

which symtpoms develop first

A

prodromal premotor symptoms - around 7 years before motor symptoms

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13
Q

how many people get anosmia as part of teh premotor symptoms

A

90% - olfactory bulb is one of teh first structures to be affected

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14
Q

what is REM sleep behaviour disorder

A

vivid dreams and loss of normal muscle atonia during REM sleep - act out dreams

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15
Q

what other sleep related symptoms are seen

A

insomnia, sleep fragmentation, excessive daytime sleepiness

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16
Q

which autonomic features are seen

A

urinary urgency, hypotension

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17
Q

describe the pattern of body involvement of motor symptoms

A

almost always intially start on one side, eg arm, spread to ipsilateral leg, then finally to contralateral body

eventually involve axial muscles

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18
Q

describe the akinesia

A
  • The cardinal clinical feature of Parkinsonism and is the main cause of disability
  • Distinguished from other slowness of movement causes by a progressive fatiguing and decrement in the amplitude of repetitive movements
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19
Q

what actions can pt perform to demonstrate akinesia

A

repeatedly oppose fingers/pronate and supinate arm

–> result is fatiguing and amplitude of movement decreases

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20
Q

which part of the movement is found to be the most difficult

A
  • Initiating movement
  • Rapid dexterous movements impaired causing difficulty writing (micrographia) and e.g. doing up buttons or zips
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21
Q
A
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22
Q

what happens to facial expression

A

facial immobility - gives a mask ike semblance of depression

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23
Q

what happens to blinking

A

rate decreases - serpentine stare

24
Q

what happens to gait

A

decreased arm swing, small shuffling steps (festinating),

difficulty in first step or turning around - often freeze

25
Q

how does posture change

A

becomes flexed and stooped

26
Q

outline the progression of limb involvement in tremor

A

starts unilaterally in fingers, spreads to same leg and then opposite arm

27
Q

when is the tremor present

A

at rest, stops when hand is in motion

28
Q

how is the tremor classically described

A

pill rolling

29
Q

what can exacerbate tremor

A

stress or emotion - like most tremors

30
Q

how does rigidity rpesent

A

resistnace to passive movement around a joint - lead pipe

31
Q

what is cogwheel rigidity

A

a combination of rigidty and tremor that can be felt during rapid supinationa nd pronation

32
Q

what is the main danger with postural instability and balance disturbance

A

there is a greatly increased risk of falls - a late stage feature

this means that they may need assistance walking - impact QOL

33
Q

what happens to speech

A

quiet, indistinct and flat

34
Q

what changes happen to swallowing,and what problems does this cause

A

dysphagia - leads to drooling

diet chnages may be necessary

there is a risk of aspiration pneumonia

35
Q

what is the most common psychiatric disorder assoicated

A

depression - due to disease impact and involvement of serotonin and adrenaline pathways

36
Q

what cognitive and psychatric changes are seen and when

A

cognitive impairement, visual hallucinations, psychosis

late stage feature

37
Q

what cognitive impairement can develop in late stage disease

A

Parkiinsons dementia

38
Q

how do patients tend to first respond to treatment

A

dramatic improvement - honeymoon period

39
Q

what is the aim of pharmacological treatment

A

to supplement depleted dopamine stores in the SN

40
Q

what is the most effective drug in management

A

levodopa

41
Q

when should you start levodopa

A

when symptoms start to impact QOL - due to honeymoon period?

42
Q

describe how someone would respond to levodopa over time

A
  • at first - dramatic positive response - honeymoon period
  • doses wear off - duration of effectiveness of each dose becomes shorter - pt may experience akinesia (not enough Dopamine)
  • eventually, on-off phenomenon - sudden unpredictable transitions between akinesia and dyskinesia (too much Dopamine
  • basically, disease progresses, medications become less effective and complications develop
43
Q

what are teh long term effects of levodopa

A
  • Wearing off (motor fluctuations) – drug wears off and may experience akinesia/bradykinesia before next dose
  • Dyskinesia (overshoot – involuntary movements) reflects overstimulation of dopamine receptors à reduce dopaminergic supplementation
  • Impulsive and compulsive behaviour
  • Withdrawal symptoms if stopped suddenly (maybe because of impulsive/compulsive behaviour) – depression, anxiety, pain
  • Psychosis
  • Hallucinations
44
Q

is response ever lost to treatment

A

no

45
Q

why would one use dopamine agonists first in younger patients

A

younger pt are more susceptible to levodopa induced motor fluccutations and dyskinesia - better to use D2 agonist first line if they have mild symtpoms

46
Q

describe the mechansim of levodopa

A

it is a dopamine precursor that can cross the BBB and be convertef to dopamine in the CNS

47
Q

why is levodopa used with carbidopa

A

carbidopa prevents the peripheral conversion of levodopa to dopamine and thus reduces the side effects of peripheral circulating dopamine - nausea and vomiting

this also means more of the drug acts in the CNS - greater efficacy

48
Q

how many times a day is levodopa initally given

A

3

49
Q

describe the mechansim of dopamine agonists

A

act on the dopamine receptors directly - mimic dopamine

50
Q

compare dopamine agonists to levodopa

A

they are elss well tolerated and generally give less good symptoms control

however, they are assoicated with fewer motor complications in the long term (5 year period)

51
Q

what is the use of MOAB inhibitors and COMT inhibitors

A

they prevent the brain and peripheral (respectively) breakdown of dopamine - can extend therapeutic benefit as an add on therapy or be used as monotherapy

52
Q

which class of drugs shoudl someone with Parkinson’s avoid

A

anti dopaminergic - eg antipsychotics

53
Q

which anti psychotic can be given if one is necessary

A

quietapine - very little D2 receptor activity

54
Q

management of delirium in PD/LBD

A

quetiapine or lorazepam (short acting benzo, careful as can worsen delirium)

55
Q

if an anti emetic is needed, which one is preferred

A

domperidone, doesnt cross the BBB to block Dopamine receptors in CTZ

56
Q

how can motor complications be managed

A

increase dose frequency to challenge wearing ff

addition of COMT/MAOB to prolong action

slow release levodopa is available for overnight symptoms

57
Q
A

RB Y3 1.2 Neurology (23 decks)

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