parkinson's Flashcards

1
Q

what is parkinson’s disease

A

progressive neurodegenerative disorder
starts slowly and progresses gradually
brain cells are lost due to abnormal protein aggregation (a-synuclein), mitochondrial dysfunction
dopaminergic cells in the brain (substantia nigra), other monoaminergic cells in brainstem
2nd most common neurodegenerative disorder after alzheimers disease

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2
Q

parkinson’s dsease is primarily caused by

A

loss of dopaminergic cells in the brain (substantia nigra), other monoaminergic cells in the brainstem also lost

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3
Q

cardinal features of parkinson’s disease

A
bradykinesia 
tremor 
rest 
posture and action 
regidity 
postural reflex impairment
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4
Q

pathogenesis of parkinson’s disease

A

toxic processes - oxidative stress, mitochodnrial dysfunction, toxins

gene mutations - a-synuclein, parkin

susceptibility - decreased expression of UPS components (age related), decreased UPS activity

leads to ubiquitin dependant proteasomal proteolysis system failure

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5
Q

staging of PD

A

stage 1 - dorsal motor nucleus of the vagal nerve, anterior olfactory structures
stage 2 - lower raphe nuclei, locus coeruleus
stage 3 - substantia nigra; anygdala; nucleus basilis of Maynert (clinical diagnosis)
stage 4 temporal mesocortex
stage 5 - temporral neocortex; sensory association and premotor areas
stage 6 - neocortex; primary sensory and motor areas

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6
Q

diagnosis of PD

A

mainly clinical - hisstory and examination
tests to rulle out other causes
- MRI scan of the brain
- metabolic/genetic testing in children/young adults
special tests if necesary
- DOPA PET, dopamine transporter scans
- MIBG heart scan

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7
Q

DAT scan

A

dopaminergic transporter scan

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8
Q

secondary parkinson’s

A

drugs, toxins, stroke, infections, head injury

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9
Q

parkinson-like tremors

A

essential tremork dystonic tremor

tremor due to drugs

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10
Q

symptoms of PD

A
motor (asymmetrical) 
- tremor, rigidity, bradykinesia
- posture, gait, balance 
- micrographia, hypophonia, facial expression 
non-motor 
- olfactory, RBD
- blood pressure, bladder, bowel, swallowing
- fatigue, pain, sleep
- attention, concentration, memory 
- mood, psychosis
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11
Q

prognosis of PD

A

most people with PD can live relatively normal lives in the first 5-10 years, many for over 15-20 years
life expectancy is reduced by up to 10%
disability in later stags

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12
Q

what responds best to drugs

A

rigidity and bradykinesia

tremor and gait

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13
Q

what does not respond optimally to drugs

A

balance, gait freezing

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14
Q

classes of drugs for parkinsons

A

L-Dopa
dopamine agonists
MAO-B inhibitors
amantadine, anticholinergics

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15
Q

L DOPA metabolism

A

converted to dopamine in the brain
prevented from turning into dopamine in the blood
MAO and COMT break down dopamine

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16
Q

non motor symptoms for parkinons

A
constipation 
urinary urgency and urge incontinence 
cognitive decline
psychosis, hallucinations, paranoia 
anxiety and depression 
pain and fatigue 
insomnia, daytime, sleepiness
17
Q

advrse effects of L DOPA

A

nausea, vomiting
dykinesia, motor fluctuation
dopamine dysregulation syndrome

18
Q

adverse effects of dopamine agonists

A

impulse control disorders, punding

sleepiness, pedal oedema

19
Q

adverse effects of all dopaminergic drugs

A

postural hypotension, hallucinations

20
Q

adverse effects of amentadine

A

confuson, leg swelling, livido-reticularis

21
Q

drugs than worsen symptoms in parkinson’s disease

A

antipsychotics
antiemetics
antihistamines
DDIs - selegeline and certain antidepressants

22
Q

surgery and parkinsons disease

A

PD is not a contraindication for any ssurgery or procedures
concern usually due to oral medictaion stoppage
no oral intake for any reason

23
Q

missing medication doses in PD

A

ok to miss 1 or 2 doses but more prologed periods without medications can worsen PD symptoms (and cause freezing)

24
Q

exercise for PD

A
maintains abilities 
strengthne muscles 
increase mobility in joints 
build up general fitness and health 
provides sense of achievemnt 
reduces feelings of sstress, anxiety and depression
25
Q

motor fluctuations

A

motor fluctaution, L-dopa induced dyskinesia, dystonia

releated to L DOPA and progression of disease

26
Q

continuous dopaminergic stimulation

A
too releive motor flucuations
subcutaneous apo-morphine infusion 
duodopa therapy 
deep brain stimulation (DBS) 
focused ultrasound
27
Q

deep brain stimulation

A

DBS
improvement of bradykinesia and rigidity, tremor
reduced levodopa induced dyskinesia
improvement in quality of life
improvement in bladder symptoms, sleep, constipation

28
Q

adverse effects of DBS

A
cognitive
mood - depression, hypomania, apathy 
weight gain 
dysarthria 
balance and falls 
eyelid opening apraxia
29
Q

late stage PD

A

relentlessly progresssive
within 15-20 years of disease onset mortality is 2-3 x the general population
currently no disease modifying treatment - unmet need in PD and most other neurodegenerative disorders

30
Q

treatment resistant problems

A
postural instability and falls 
speech and swalloing dyfunction 
autonomic symptoms 
psychosis 
dementia
31
Q

potential for disease modifying treatment

A

neuroprrotective drugs
stem cells
growth factors
gene therapy