Parkinsons Disease Flashcards

1
Q

What is the difference between Parkinsonism and parkinsons disease?

A

Parkinsonism - group of symptoms including rigidity, tremors and bradykinesia - umbrella for lots of different conditions
Parkinsons Disease - certain pathology that causes parkinsonism

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2
Q

What is parkinsons Disease?

A

Hypokinesia movement disorder
Caused by chronic + progressive degeneration of dopmainergic neurons in the brain, particularly between the SN and the dorsal striatum
Results in parkinsonism
Tends to be idiopathic

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3
Q

What is meant by Parkinson-Plus syndromes?
What are some examples?

A

Conditions that present with symptoms very similar to Parkinsons disease but also with additional features
Dementia with Lew Bodys
Multiple supranuclear palsy
Vascular Parkinsonism
Drug-Induced Parkinsonism

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4
Q

What is the key sign of dementia with lewy bodies as a Parkinson plus syndrome?

A

Significant cognitive decline

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5
Q

What are the key signs of Multiple system Atrophy as a Parkinson Plus syndrome?

A

Unsteadiness/Falls
Autonomic dysfuncation more prominent in early disease

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6
Q

What are the key features of Progressive supranuclear palsy as a PPS?

A

Unsteadiness
Dysphagia
Vertical supranuclear gaze palsy (voluntary eye movements)
More prominent in early disease.

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7
Q

What are the key signs of vascular parkinsonism as a PPS?

A

History of cerebrovascular disease and sudden onset symptoms

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8
Q

What are the key features of drug induced parkinsonism as a PPS?

A

Symptoms more likely to be bilateral than PD
Commonly caused by first gen antipsychotics (haloperidol) or antiemetics (prochlorperazine)

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9
Q

What are some risk factors for Parksinsons disease?

A

Male (1.5:1)
FHx of PD
Age - peak 60-70yrs
Suggestive of previous head injury

?? smoking is a protective factor

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10
Q

What are the key clinical features for diagnosis of parkinsons disease?

A

Bradykinesia plus at least one of:
Tremor
Postural instability
Rigidity

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11
Q

What are some additional motor symptoms of Parkinsons Disease?

A

Micrographia - small handwriting
Hypomimia - reduction in facial expressions
Quiet speech
Reduced arm swing when walking
Shuffling gait
Difficulty turning
Gait freezing.

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12
Q

What are some neuropsychiatric symptoms?

A

Apathy
Anxiety
Depression
Dementia
Loss of libido

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13
Q

What are some signs of autonomic dysfunction in Parkinsons Disease?

A

Constipation
Urinary Incontinence
Erectile Dysfuncation
Excessive sweating
Excessive salivation
Postural hypotension
Anosmia - loss of smell

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14
Q

What type of sleep disturbance can occur in Parkinsons Disease?

A

REM sleep disorder - acting out dreams
Vivid dreams
Daytime somnolence - sleep during day when bored/not paying attention

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15
Q

What areas in the history are important in a Parkinsons patient?

A

PMHx - known tremor or movement disorder, falls or cognitive impairment
HFx - first degree relative with PD
DHx - rule out drug-induced parkinsonism
SHx - smoking, alcohol (withdrawal can cause tremor), home environment (carers, baseline, ability to perform ADLs)

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16
Q

What is commonly seen on examination of a Parkinsons Patient?

A

TREMOR = Typically asymmetric resting “pill-rolling” tremor, may also have an action tremor
BRADYKINESIA - test for dysdiadochokinesia (finger tap)
RIGIDITY = cogwheel rigidity - intermittent increase in tone during movement
GAIT = abnormal
Ask to write a sentence - micrographia
Do up shirt button - struggle with dexterity

17
Q

What does the GAIT exam of a person with Parkinsons disease look like?

A

Struggles with Sit-to-Stand test (arms crossed)
Slow initiation
Reduced stride length
Reduced arm swing
Stooped posture
Impaired turning
Shuffling gait

18
Q

What investigations may be done to help diagnose a Parkinsons patient?

A

Bedside - LSBP, Congitive assessment (MMSE)
Bloods - no routine, may do a confusion screen.
Imaging - DaT scan (only if diagnostic uncertainty)

19
Q

How does a DaT scan show parkinsons disease?

A

Highlights areas of dopamine transporters
Healthy patient - comma shaped
Parkinsons patient - pupil shaped

20
Q

What are some key members of the MDT for a Parkinsons Patient?

A

Parkinsons Nurse Specialist
Physiotherapist
Occupational Therapist
Speech and Language Therapist

21
Q

What is the first line medication for Parkinsons Disease?

A

Levodopa/Carbidopa (co-careldopa)
Levodopa is a precursor to dopamine, cross BBB, converted to dopamine in neuron by dopa-decarboxylase.
Carbidopa is a dopamine decarboxylase inhibitor - prevents peripheral breakdown of Levodopa, can not cross BBB, increase amount of Levodopa that crosses the BBB
Reduces side effects of nausea and vomiting.

22
Q

What are the second line classes of medication that can be given to treat Parkinson Disease?
Examples

A

MAOinhibitors - selegiline
Dopamine agonists - rotigotine (act on post-synaptic neuron)
COMT inhibitors - entacapone - prevents dopamine breakdown in periphery - inc BBB crossing

23
Q

What are some common side effects of Parkinson Medication?

A

Levodopa - nausea and vomitting, long term use = dyskinesia,
Dopamine agonists - impulse control disorders, daytime sleepiness, lightheaded/low BP.
COMT inhibitors - red urine, saliva or tears

24
Q

What are the key rules regarding medications used in Parkinsons Disease?

A

Critical Medications - time sensitive
Must be given at specific times to avoid akinesia
If suddenly stopped can cause neuroleptic malignant syndrome.
Must be started by a specialist
Response to medication decreases over time meaning doses may need to be gradually increased - resulting in side effects.

25
Q

What is the use of deep brain stimulation in Parkinsons Patients?

A

Is a specialised management option
Reserved for patients with severe symptoms that are refractory to medical management.
Patients must be relatively fit with few co-morbidities.

26
Q

What symptoms of Parkinsons Disease tend to occur early or pre-motor?

A

Anosmia
REM sleep behaviour
Constipation
(mood changes)

27
Q

What is the cellular pathogenesis of Parkinsons Disease?

A

Progressive loss of dopaminergic neurons in the SNpc leads to dopamine deficiency in the striatum. (motor symptoms)
Mitochondrial dysfunction causes cell death in SNpc due to ROS and oxidative stress.
Protein oxidation leads to misfolding and aggregation - leads to accumulation of Lewy Bodies (misfolded alpha-synuclein protein)
These disrupt normal cellular functioning such as neuronal communication causing synaptic dysfunction.
Neuroinflammation can also occur as microglia are activated by abnormal protein aggregates.

28
Q

How are the basal ganglia impacted in Parkinsons Disease?

A