Parkinson's Disease Flashcards

1
Q

Define what is meant by Parkinsonism [1]

State the three main types [3]

A

Parkinsonism is any condition that causes movement abnormalities. Must have 2 symptoms from list of: Bradykinesia + muscle rigidity ro tremor or postural instability.
* Idiopathic PD
* Atypical Parkinson’s = Parkinson’s Plus Syndromes
* Secondary Parkinsonism

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2
Q

Describe the basic pathophysiology of PD

A

In Parkinson’s there is a deficiency of dopamine in the nigrostriatal pathway that links the substantia nigra to the basal ganglia, causing the basal ganglia to exert greater inhibitor effects on the thalamus and reduces excitatory input to the motor cortex

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3
Q

What’s the pathophysiological difference btw IPD and atypical PD? [1]

How do they manifest differently? [1]

A

IPD:
- Dopamine deficiency
- Later in disease: falling, dementia

Atypical PD:
- minimal to no dopamine deficiency
- early in disease: falling, dementia

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4
Q

Name 4 different classes of Parkinson’s Plus Syndromes [4]

State very basic manifestations of each

A

Progressive Supranuclear Palsy (PSP)
- often fall earlier in disease due to gaze restriction

Multiple Systems Atrophy (MSA) Early and more pronounced autonomic symptoms.
- MSA-P: more akin to PD but might have more autonomic symptoms than idiopathic PD. Often have dry eyes
- MSA-C: gait dysfunction; autonomic dysfunction required for dx

Corticobasal Degeneration (CBD)
- Apraxia, limb dystonia

Lewy Body Dementia (LBD)
- Fluctuating cognition, visual hallucinations, Parkinsonism, and sleep disorders.

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5
Q

Describe the difference between PD dementia and Dementia with Lewy body [1]

A

Parkinson’s disease dementia:
- dementia occurring in the setting of established Parkinson’s disease. This is defined as having Parkinson’s disease for more than one year before the onset of dementia.

Dementia with Lewy body:
- development of dementia and Parkinsonism concurrently. This is defined as developing dementia within one year of Parkinsonism features

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6
Q

What triad occurs in secondary parkinsonism due to normal pressure hydrocephalus? [3]

How do you treat? [1]

A

Triad:
- gait instability
- urinary incont
- cognitive decline

Tx:
- perform a LP and take out fluid
retest above
- put in LP shunt
(efficacy??)

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7
Q

Name 4 autonomic symptoms associated with Parkinsonism [4]

A

Autonomic symptoms:
* Orthostatic hypotension
* Constipation
* Urinary dysfunction
* Erectile dysfunction

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8
Q

How can DaT scans help differentiate between idiopathic PD and benign essential tremor? [1]

A

Essential tremor has normal levels of Da

PD has reduced

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9
Q

Describe the clinical motor features of PD [+]

A

Need a triad of following for a diagnosis:

Resting tremor
- exacerbated by rest / improves when engages in purposeful actions
- ‘pill-rolling’
- begins as an intermittent tremor, and as the disease progresses the tremor becomes more continuous
- starts unilateral can progress to bilateral

Muscle rigidity
- ‘cogwheel rigidity’
- muscular stiffness, stooped posture, and reduced arm swing when walking

Bradykinesia
- reduction in manual dexterity of finger movements
- difficulty standing from a seated position
- troubles when walking

Other characteristics:
- Postural instability
- Mask-like facies (hypomimia)
- Micrographia
- Dysphagia (due to bradykinesia of pharyngeal muscles)

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10
Q

Describe the clinical non- motor features of PD [+]

A

Mood disturbance
* Depression (50%)
* Apathy ( 40%)
* Anxiety (30%)

Psychiatric symptoms
* Psychotic episodes (may be due to dopaminergic medications, underlying Lewy-body dementia, or both)
* Visual hallucinations
* Paranoid delusions (typically patients have good insight)

Sleep dysfunction
* Frequently restless legs syndrome, insomnia and daytime somnolence
* Frequent awakening through the night and early morning waking are common, independent from depression

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11
Q

Why is it important to ask about sleep disturbance in a ptx with ? PD? [1]

A

When taking a Hx, important to ask if they have vivid dreams / fight or shout in their dreams - as could indicate they have a REM sleep behaviourr disorder (close indication between this & PD)

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12
Q

Describe the three step approach to diagnosing PD [3]

A

Step 1: triad of muscular rigidity; resting tremor (4-6 Hz frequency); postural instability

Step 2. :Exclusion of various criteria

Step 3: 3+ supportive criteria (in addition to step 1)
* Unilateral onset
* Resting tremor
* Progressive disease
* Persistent asymmetry, affecting initial side of onset most
* Excellent response (70-100%) to levodopa treatment
* Severe levodopa-induced chorea
* Levodopa response for greater than 5 years
* Clinical course of greater than 10 years

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13
Q

How do you differentiate between PD and essential tremor? [3]

A
  • An essential tremor worsens when holding the arms outstretched
  • An essential tremor worsens with activities such as writing, whereas the tremor associated with Parkinson’s disease improves with purposeful actions
  • Most often is symmetrical, however can sometimes be asymmetric
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14
Q

How do you differentiate between PD and MSA? [3]

A

In multiple system atrophy, there is usually a degree of cerebellar involvement (MSA-C), which is part of the exclusion criteria for Parkinson’s disease

Profound autonomic dysfunction leading to severe postural hypotension, urogenital dysfunction and a plethora of other features including cerebellar and corticospinal features.

Poor response to treatment

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15
Q

How do you differentiate between PD and PSP? [2]

A

PSP is characterised by vertical gaze dysfunction, dysarthria and cognitive decline.

Tremor is rare in this condition.

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16
Q

How do you differentiate between PD and LBD? [3]

A

Lewy-body dementia, the dementia usually occurs concomitantly with, or prior to, the development of parkinsonism

DLB is characterised by early onset dementia (< 1 year)

Characterised by a triad of visual hallucinations, fluctuating cognition, and parkinsonism

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17
Q

What is vascular parksinsonism caused by? [1]

How do changes usually occur? [1]

A

Vascular parkinsonism:
* Due to multiple infarcts affecting the basal ganglia
* Usually can be identified via a thorough history and radiological findings
* Probably step-wise progression rather than continuous

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18
Q

Describe the drug classes [3] and other management used in the tx of PD (name examples)

A

When first suspected by any medical professional, the NICE guidelines recommend that a person should be referred quickly and untreated to a specialist with Parkinson’s disease expertise first for assessment.

Levodopa (converted into dopamine for use within the brain by DOPA decarboxylase once it crosses the blood brain barrier) AND a DOPA decarboxylase inhibitor (DDCI) (to avoid peripheral conversion prior to passing BBB)

Monoamine oxidase B (MAO-B) inhibitors
- Inhibitors of MAO-B, which are responsible for degrading dopamine, therefore increasing the amount of dopamine available
- rasagiline and selegiline

COMT inhibitors
- Entacapone
- Inhibit the peripheral breakdown of levodopa by the COMT enzyme allowing more levodopa to cross the blood brain barrier

Anti-muscarinics
- e.g. procyclidine may be used although evidence is poor.
- Amantadine may be used as early monotherapy or late adjuvant to help with dyskinesia.

Non-selective dopamine agonists:
- Apomorphine
- generally reserved for advanced disease.
- It is given via subcutaneous injection/infusion, but can cause significant postural hypotension.

Dopamine agonists
- Mimic dopamine and bind to dopamine receptors to exert their effect
- Non-ergot (e.g. ropinirole, pramipexole)
- Ergot-derived dopamine agonists (e.g. bromocriptine, cabergoline)

Deep brain stimulation:
- For people whose symptoms are not adequately controlled by medical therapy
- This should never be used as first-line treatment

Adjuvant therapy:
- Physiotherapy (reduce falls)
- Speech therapy
- OT

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19
Q

qs about differentials between ps like ones.

A
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20
Q

Dopamine agonists are associated with side-effects and one particular issue is the development of []

A

Dopamine agonists are themselves associated with side-effects and one particular issue is the development of impulse-control disorders.

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21
Q

Describe how you create a management plan for a PD depending on their symptoms [+]

A

First-line treatment for early stage disease depends on the impact of the motor symptoms on the patient’s quality of life
- If motor symptoms IMPACT on quality of life - levodopa
- If motor DO NOT IMPACT - dopamine agonist, levodopa or MAO-B inhibitors

Whether it is a DA; MOABIn or levodopa - should be determined by:
- The patient’s current symptom profile
- Patient age
- Current co-morbidities and existing medications
- RIsks of meds

Deep brain stimulation:
- For people whose symptoms are not adequately controlled by medical therapy

22
Q

PD

According to the NICE guidelines, [drug class] should not be used first line, only if required as an adjunct or alternative after failure of initial therapy

A

According to the NICE guidelines, ergot-derived dopamine agonists (e.g bromocriptine, cabergoline) should not be used first line, only if required as an adjunct or alternative after failure of initial therapy

23
Q

Deep brain stimulation:

The two primary cortical structures to be targeted are the []

What is the aim of the procedure? [1]

A

The two primary cortical structures to be targeted are the globus pallidus interna and the subthalamic nucleus

This procedure aims to correct the imbalance created by reduced function of the substantia nigra, to improve the symptoms for patients

24
Q

Which aspects of PD does DBS help [2] but also cause a risk for [3]

A

The evidence suggests that this procedure improves motor function and movement abnormalities, however poses a risk of strokes, confusion and speech dysfunction

25
Q
A
26
Q

Describe the different complications that PD patients are at risk of

A

Autonomic dysfunction: abnormalities in the control of normal bodily homeostasis
- Postural hypotension
- Constipation
- Urinary dysfunction - increased frequency and urgency

Recurrent falls:

Cognitive impairment

27
Q

Dopamine-receptor agonists can help alleviate symptoms such as [3]

A

Dopamine-receptor agonists can help alleviate symptoms such as tremors, rigidity and bradykinesia.

28
Q

Ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide) have been associated with [3]

A

Ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide) have been associated with pulmonary, retroperitoneal and cardiac fibrosis.

29
Q

Levodopa usually combined with a decarboxylase inhibitor (e.g. [] or [])

There is usually reduced effectiveness with time (usually by [] years).

A

Levodopa usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide)

There is usually reduced effectiveness with time (usually by 2 years).

30
Q

Describe some of the adverse effects of levodopa therapy [+]

A

Unwanted effects:
Dyskinesia (involuntary writhing movements)
‘on-off’ effect
Dry mouth
Anorexia
Palpitations
Postural hypotension
Psychosis
Drowsiness

31
Q

Avoid levodopa treatment with [drug type / class] as they contraindicate the effects of levodopa

A

Do not use with antipsychotics as they contraindicate the effects of levodopa

32
Q

Why should patients avoid eating large amounts of cheese and alcohol if using a MAO-In inhibitor [1]

- Selegiline, Rasagiline

A

Hypertensive crisis may occur if large amounts of tyramine (an amine broken down by MAO) are consume so patient must cut down on aged cheeses and alcohol

33
Q

Name two drugs might use for a PD patient’s LUTS? [2]

A

Solifenacin, mirabegron

34
Q

If a patient has PD and is suffering from impulse control disorders, which drug class should you remove?

Dopamine agonists
Levodopa
COMTs
MAO-In

A

If a patient has PD and is suffering from impulse control disorders, which drug class should you remove?

Dopamine agonists
Levodopa
COMTs
MAO-In

35
Q

Why is not continuing PD tx / abruptly stopping PD treatment bad? [1]

A

Life threatening and potentially fatal Parkinsonism-hyperpyrexia syndrome

36
Q

Give two drugs that are contraindicated in PD [2]

A

Give two drugs that are contraindicated in PD. Metoclopramide and haloperidol

37
Q

Which of the following causes more risk of hallucinations if given after initial levodopa tx?

Dopamine agonists
Amantadine
MAO-B inhibitors
COMT inhibitors

A

Which of the following causes more risk of hallucinations if given after initial levodopa tx?

Dopamine agonists
Amantadine
MAO-B inhibitors
COMT inhibitors

38
Q

Consider [] to manage drooling of saliva in people with Parkinson’s disease.

A

Consider glycopyrronium bromide to manage drooling of saliva in people with Parkinson’s disease.

39
Q

Impulse control disorders have become a significant issue in recent years. These can occur with any dopaminergic therapy but are more common with:

Dopamine agonists
Amantadine
MAO-B inhibitors
COMT inhibitors

A

Impulse control disorders have become a significant issue in recent years. These can occur with any dopaminergic therapy but are more common with:

Dopamine agonists
Amantadine
MAO-B inhibitors
COMT inhibitors

40
Q

If a patient with PD continues to have postural hypotension which drug can be considered? [1]

A

If symptoms persist then midodrine (acts on peripheral alpha-adrenergic receptors to increase arterial resistance) can be considered.

41
Q

Vitamin [] supplementation is indicated in Parkinson’s disease.

Vitamin A
Vitamin B
Vitamin C
Vitamin D
Vitamin E

A

Vitamin [] supplementation is indicated in Parkinson’s disease.

Vitamin A
Vitamin B
Vitamin C
Vitamin D
Vitamin E

42
Q
A

Pyschosis

43
Q
A

palpitations

44
Q
A

Hypotension

45
Q
A

Hypotension

46
Q
A

Bromocriptine may cause pulmonary, retroperitoneal and cardiac fibrosis

47
Q
A

Antipsychotics may cause parkinsonism

48
Q
A

metoclopramide

49
Q
A

Parkinsonism, autonomic disturbance, cerebellar signs - multiple system atrophy

50
Q
A

MSA

51
Q
A

PSP

52
Q
A