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PT 10111 MedSurg 2 > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Rising neurological disorder

A

Parkinson’s disease

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2
Q

Life expectancy for Parkinson’s

A

68-69 males
75-76 females

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3
Q

Broader term for PD

A

Parkinsonism

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4
Q

Parkinsonism is a combination of (3)

A

Rest tremor, rigidity, bradykinesia

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5
Q

Parkinson’s takes up how many percent of Parkinsonism?

A

77%

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6
Q

Parkinson plus syndromes take up how many percent of Parkinsonism?

A

12%

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7
Q

Drug induced, extrapyramidal symptoms take up how many percent of Parkinsonism?

A

5%

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8
Q

Classification of Parkinsonism (4)

A

Primary/Idiopathic Parkinsonism
Secondary Parkinsonism
Heredodegenerative Parkinsonism
Multiple-System Degeneration / Parkinsonism-Plus

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9
Q

Types of Primary / Idiopathic Parkinsonism (2)

A

Parkinson’s disease
Juvenile parkinsonism

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10
Q

Types of Secondary Parkinsonism (2)

A

Infectious, Drugs, Toxins, Vascular, Trauma
Stroke, TBI

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11
Q

Types of Heredodegenerative Parkinsonism (2)

A

Huntington’s
Wilsons

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12
Q

Types of Multiple-System Degeneration / Parkinsonism-Plus (4)

A

PSP (progressive supranuclear palsy aka Steele Richardson Olszewski)

CBD (corticobasal degeneration)

LBD (lewy body dementia)

Multisystem atrophy
○ Striatonigral degeneration
○ Olivopontocerebellar atrophy
○ Shy Drager syndrome

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13
Q

Described by James Parkinson in 1817 as “the shaking palsy”

A

Parkinson’s disease

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14
Q

PD is a ____ disorder of the CNS

A

Chronic progressive disorder

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15
Q

PD results from degeneration of ____ producing cells in the substantia nigra

A

Dopamine-producing cells

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16
Q

Substantia nigra is located where?

A

Midbrain

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17
Q

T/F: PD is the 2nd most common neurodegenerative disease after Alzheimer’s Disease

A

True

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18
Q

T/F: PD is the 2nd most common neurodegenerative disease after Alzheimer’s Disease

A

True

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19
Q

T/F: PD is age related, progressive disorder

A

True

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20
Q

___ is markedly decreased in PD

A

Dopamine

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21
Q

Famous people with PD (7)

A

Muhammad Ali
George Bush
Yasser Arafat
Mao Zedong
Pope John Paul II
Michael J. Fox
Adolf Hitler

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22
Q

Prevalence of PD

A

100-180 in a million
4-20 per 100,000
Rising with age
Male:female 3:2

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23
Q

Myths of PD (3)

A

Not true:
Only old people get PD
The only thing that people have with PD is shaking
Only the person with PD is a ffected by the disease

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24
Q

Parkinson’s disease is a neurodegenerative disease associated with _____ of the substantia nigra and loss of dopaminergic input to the basal ganglia (extrapyramidal system)

A

Depigmentation

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25
Q

T/F: In healthy individuals, dopamine is produced by neurons that project from the substantia nigra to the neostriatum (which include caudate and putamen) and globus pallidus

A

True

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26
Q

The loss of dopamine-producing neurons in the substantia nigra results in the ______ between _____, and the excitatory neurotransmitter ______

A

Imbalance between dopamine (an inhibitory neurotransmitter) and acetylcholine

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27
Q

T/F: Even if there is a normal rate of production of Acetylcholine but diminished dopamine secretion (less inhibition), it will be a balance state thus more kinetic movement

A

False: imbalance

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28
Q

Medication is also given to combat PD or reduce activity of the cholinergic system

A

Anticholinergic medication

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29
Q

Medication is also given to combat PD or reduce activity of the cholinergic system

A

Anticholinergic medication

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30
Q

Etiology of PD (3)

A

Unknown

Proposed etiology
○ Influence of aging
○ Environmental toxins
○ Genetic susceptibility

Oxidative stress

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31
Q

Alterations in the substantia nigra of patients w/ PD suggestive of oxidative damage

A

Oxidative Stress Theory

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32
Q

Evidences that supports oxidative damage (6)

A

Increased iron levels

Lack of compensatory rise in isoferritins

Increased aluminum levels

Reduced glutathione levels

Selective defect in complex I of mitochondrial
respiratory chain

Evidence of oxidative damage to
■ Lipids, DNA, Proteins, Tyrosine-containing molecules

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33
Q

Genetics of PD: Onset

A

Young onset PD, onset <40 y.o.
Juvenile onset PD, onset <20 years old

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34
Q

Major cause of young onset autosomal recessive PD and isolated juvenile PD

A

Parkin mutation

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35
Q

Mutations in autosomal dominant PD

A

ɑ synuclein and ubiquitin carboxyhydrolase

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36
Q

T/F: Mutations give rise to problems in protein clearance, accumulation of excessive protein that can be harmful to the neurons

A

True

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37
Q

Loss of dopaminergic (DA) cells located in substantia nigra; most symptoms do not appear until striata DA levels decline by at _______

A

70%-80

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38
Q

Pathophysiology of PD

A

Use of SPECT (single-photon emission computerized tomography) & PET (positron emission tomography) Scan for research purposes

Degeneration of substantia nigra

Reduced production of dopamine
○ Commonly used for research purposes

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39
Q

Clinical manifestations of PD (TRAP)

A

Tremor (most common: rest tremors)
Rigidity
Akinesia/Bradykinesia
Postural instability

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40
Q

Characteristics of Tremors (5)

A

4-6 Hz
Resting (disappears with voluntary movement, sleep)
Accentuated by stress and anxiety
Pill rolling (at rest)

Additional:
Essential Tremor & Physiologic Tremors are 8-12 Hz
and are kinetic and/or postural (during movement)

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41
Q

Resistance to passive movement of limbs
Involuntary hypertonia of skeletal muscles

A

Limb rigidity

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42
Q

Manifestations of limb rigidity

A

Cogwheeling
Not spastic (like a swiss knife initial resistance upon opening but then “gives”)

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43
Q

Decreased speed and amplitude of complex voluntary movement
Slowness in initiating and sustaining movement
Fragmented

A

Bradykinesia

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44
Q

How to elicit bradykinesia

A

Micrographia: asking them to write where writing becomes smaller over time

Tapping fingers: compare the left and right; will get slower

Twiddling of Hands: will present unilaterally then bilaterally

Pinching and Circling

Tapping with the Heel

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45
Q

How to elicit limb rigidity

A

When extending limb, there’s rigidity but not spastic
Rigid over the ROM, can slowly extend extremity

46
Q

Tendency to fall, keel balance to one side → fractures
● Prone to falls & fractures (humerus, hip, femoral)

Initial phase of PD: others may think it is normal and
only part of aging

Develop stoop posture, angle worsens over time

A

Postural instability

47
Q

Major symptoms of PD (5)

A

● Bradykinesia - slowness in initiation and execution of voluntary movements

● Rigidity - increase muscle tone and increase resistance to movement (arm and legs are stiff )

● Tremor - At rest, when person sits, arm shakes, tremor stops when person attempts to grab something

● Postural Instability - stoop when standing, equilibrium, and righting reflex, lose balance

● Gait Disturbance - Shuffl ing Feet

48
Q

Hitler’s condition

A

Micrographia

49
Q

Diagnosis of PD

A

Diagnosis depends on clinical findings

Tests to rule out secondary parkinsonism

PET to visualize dopamine in substantia nigra and basal ganglia

SPECT for dx essential tremor, Parkinsonian syndromes or Non-parkinsonian

50
Q

Clinical criteria of PD (5)

A
  1. Presence of at least 2 of the 3 cardinal features of parkinsonism: Tremor, rigidity, bradykinesia
  2. Presence of at least two of the following:
    ○ Marked response to levodopa
    ○ Asymmetry of signs
    ○ Asymmetry of onset
    ○ Symptoms usually starts unilaterally
  3. Evidence of disease progression
  4. Absence of clinical features of alternative diagnosis
  5. Absence of etiology known to cause similar features
51
Q

Stage of PD: No clinical signs evident

A

Stage 0

52
Q

Stage of PD: Unilateral involvement, including the major features of tremor, rigidity, or bradykinesia; minimal functional impairment

A

Stage 1

53
Q

Stage of PD: Bilateral involvement but no postural abnormality

A

Stage 2

54
Q

Stage of PD: mild to moderate bilateral disease , mild postural imbalance, but still able to function independently

A

Stage 3

55
Q

Stage of PD: Bilateral involvement with postural instability; patient requires substantial assistance

A

Stage 4

56
Q

Stage of PD: Severe disease; patient restricted to bed or
wheelchair unless aided

A

Stage 5

57
Q

Differential Dx:
Gradual onset; tremor; gait disturbance; slowed movements (bradykinesia)

Resting tremor (limbs), Cogwheel rigidity (limbs)

A

Idiopathic PD

58
Q

Differential Dx:
Exposure to haloperidol or metoclopramide

Similar to idiopathic to PD

A

Drug induced Parkinsonism (secondary)

59
Q

Differential Dx:
Present for many years; + family history

Tremor w/ arms raised; head involved

A

Essential tremor

60
Q

Differential Dx:
Parkinsonism w/ autonomic system dysfunction

Orthos. hypotension (syncope), skin changes

A

Multisystem atrophy

61
Q

Differential Dx:
Involuntary movement cognitive or behavioral problem

Chorea; loose tone, early dementia

A

Huntington’s Disease

HCC: Huntington-Chorea-Cognitive

62
Q

Exercise, rehabilitation, intervention, nutrition

A

Non-pharmacological approach

63
Q

Giving of drugs that can protect the neurons in
the brain

A

Pharmacological approach

64
Q

MAO B (Monoamine oxidase-B) such as selegiline
and tocopherol (Vitamin-E) acts as a scavenger
of free radicals

Dopamine agonists serve as scavengers of free
radicals; decrease dopamine turnover, there are increases in oxidative stress
■ Helps in treating PD but also contributed to oxidative stress in the long run

A

Neuroprotective treatment

65
Q

Four classes of drugs available (A, P, D, I)

A

Anticholinergics (good for treating rest tremors)

Precursor of dopamine (Levodopa, Carbidopa)

Direct-acting dopamine agonists (Bromocriptine, Perogoiide)

Indirect-acting dopamine agonists
-Decrease re-uptake (amantadine)
-Decrease metabolism (selegiline)

66
Q

Drug Therapy for treating associated symptoms (e.g. pain, mood problems) (3)

A

○ Tricyclic antidepressants
○ Beta-Blockers
○ Antihistamines

67
Q

Treatment Plan (4)

A

● Age
● Severity of Sx
● Cognitive function
● Comorbidities
○ Medications are already prescribed and may interact with anti-PD medications

68
Q

Treatment Strategies (2)

A

● Symptomatic treatment - look at the 4 classes of drugs
○ Levodopa
○ Amantadine
○ Anticholinergics
○ COMT inhibitors
○ Surgery

● Symptomatic with Neuroprotection
○ Dopamine agonists ○ Selegiline

69
Q

Gold standard for PD

A

Levodopa

70
Q

To reduce peripheral conversion of levodopa so that more amount of levodopa can enter the CNS and cross the BBB

A

Carbidopa-levodopa combination

71
Q

Taken up by dopamine nerve terminals in the striatum

Converted to dopamine by dopa decarboxylase

Released and acts at the dopamine receptors

A

Levodopa

72
Q

E ffects and Precautions of Levodopa

A

○ Mainstay of therapy

○ Produce immediate symptomatic response thus
being part of the diagnostic criteria for clinical
diagnosis of PD

○ Long-term use leads to dyskinesias and motor
response fluctuations (“on-off ” phenomenon)

○ Development of nonlevedopa-responsive
features (freezing, autonomic dysfunction)

○ May induce oxidative stress due to increased
dopamine turn over and free radical formation

○ Major side e ffects: Nausea, hallucinations,
orthostasis (drop in BP)

73
Q

Block muscarinic cholinergic receptors

A

Anticholinergic

74
Q

Block muscarinic cholinergic receptors

A

Anticholinergic

75
Q

Purpose of anticholinergic

A

Restore motor function by reducing acetylcholine in
the setting that dopamine is already reduced in PD
→ less hyperkinesis

76
Q

Effects and precautions of anticholinergic

A

○ Can be effi cacious for tremor and dystonia

○ May be used as a secondary pharmacologic
option

○ Peripheral side e ffects - dry mouth, blurred
vision, urinary retention, constipation

○ Central nervous system side eff ects - confusion,
memory loss (one of the long term e ffects)

77
Q

Indirect dopamine agonist

A

Amantadine

78
Q

Discovered serendipitously because it is originally an
antiviral medication

A

Amantadine

79
Q

E ffects and Precautions of Amantadine

A

○ Improves bradykinesia and tremor

○ Can be used as monotherapy or as adjunct
therapy to levodopa

○ Antiparkinsonian mode of action is not
completely understood

○ Short term benefits

○ Adverse e ffects include: restlessness, confusion,
depression, nausea, hypotension

80
Q

● Popular drug before
● Monoamine oxidase-B (MAO-B) inhibitor
● Reduces dopamine metabolism
○ Less breakdown of dopamine
○ Has neuroprotective eff ects
○ Gone down in popularity d/t many
contraindications with other drugs

A

Selegiline

81
Q

E ffects and Precautions of selegiline

A

Postulated to have neuroprotective eff ect
■ Reduce oxidative stress
■ Reduce free radical production

○ No benefit in reducing levodopa-induced motor fluctuations
○ Has mild symptomatic e ffects
○ Nausea, hallucinations

82
Q

● Catechol-O-methyl-transferase
● Reduces dopamine breakdown
● Not very popular in the market d/t limited
improvement but it can be used in conjunction with
levodopa

A

COMT inhibitor

83
Q

Effects and Precautions of COMT inhibitor

A

○ Increases the bioavailability of levodopa → good
to be combined
○ Useful adjunct in early stage of PD and in
patients w/ mild response fluctuations → delays
onset of more severe PD
○ Downside:
■ Reported cases of rare hepatocellular injury*
■ Possible neurotoxicity in PD**

84
Q

Effects and Precautions of COMT inhibitor

A

○ Increases the bioavailability of levodopa → good
to be combined
○ Useful adjunct in early stage of PD and in
patients w/ mild response fluctuations → delays
onset of more severe PD
○ Downside:
■ Reported cases of rare hepatocellular injury*
■ Possible neurotoxicity in PD**

85
Q

No longer available in the market

A selective and reversible inhibitor of COMT and
is used as an adjunct to levodopa/carbidopa
therapy

Inhibits COMT both peripheral and centrally

A

Tolcapone

86
Q

T/F: COMT is the main enzyme responsible for peripheral and central metabolism of catecholamines, including levodopa. Addition of a COMT inhibitor results in the doubling of the elimination half-life of levodopa and in increased oral bioavailability of levodopa by 40-50%

A

True

87
Q

Surgical options for PD

A

● Pallidotomy
● Thalamotomy
● Thalamic stimulation
● Transplantation of fetal cells
● All of which showed mild improvement in the Sx of PD

88
Q

A pallidotomy entails the surgical resection of
parts of the globus pallidus

Improves contralateral dyskinesia

A

Globus pallidus internus (Gpi) Pallidotomy

89
Q

High-frequency stimulation that induces functional inhibition of target regions of the brain by implanting an electrode into a target site and connecting the lead to a subcutaneously placed pacemaker

Pt can control it to stimulate the areas and regulate the abnormal Sx of PD

Quite expensive (1-2M pesos)

A

Deep Brain Stimulation

90
Q

Implantation of embryonic dopaminergic cells
into the denervated striatum to replace degenerated neuronal cells

DID NOT REALLY SHOW any strong evidence that it
can help in the improvement of Sx

A

Fetal nigral transplantation

91
Q

Nonpharmacological management (4)

A

Education
Support
Exercise
Nutrition

92
Q

Education

A

Early stage:
● Selective information
● Aimed at promoting general health
● Refer to PD organization
● Referred to PT early on

Advanced stage:
● Problem oriented

93
Q

Support

A

Early stage:
● Emotional needs assessment
● Support network assessment
● Financial / occupational counseling

Advanced stage:
● Psychological counseling (d/t PD dementia or depression)
● Respite care
● Need assistance

94
Q

Exercise

A

Early stage:
● Aerobics, stretching
● Improves mood, mobility
● Improves postural equilibrium reaction

Advanced stage:
● Physiotherapy referral
● PD exercise group
● Energy conservation techniques

95
Q

Nutrition

A

Early stage:
● Balanced diet
● Fibers and fluids vs constipation (caused by meds)
● Calcium vs increased bone mass loss

Advanced stage:
● Dietetic referral
● Help preparing food
● Meal deliveries
● End stage → tube fed (nasogastric or gastrostomy tube)

96
Q

Secondary effects of PD (4)

A

● Cardiovascular e ffects
○ Including orthostatic hypotension and arrhythmia

● Gastrointestinal eff ects
○ Including constipation and hypersalivation

● Genitourinary e ffects
○ Including increased urinary frequency, impotence

● Central nervous system e ffects
○ Including hallucination, depression, and psychosis, dementia

97
Q

PD late disabilities divided into two groups

A

Levodopa-related Disabilities
Non-levodopa-related Disabilities

98
Q

■ Include MOTOR fluctuation, dyskinesia, neuropsychiatric toxicity (hallucinations, psychosis), and reduced response

■ Too much MOVEMENTS, orofacial movements, chewing or tongue movements, dystonic movements

A

Levodopa-related disabilities

99
Q

Include COGNITIVE impairment, instability
resulting in more frequent falls, gait disturbance, incontinence, dysphagia (di fficulty swallowing so they choke a lot), and speech disturbance, pneumonia.

A

Non-levodopa related disabilities

100
Q

Urinary urgency

A

oxybutynin

UO: urgency-oxibutynin

101
Q

Urinary retention

A

apomorphine (not readily available in PH)

RA: retention-apomorphine

102
Q

Constipation

A

increased fiber diet, polyethylene glycols, laxatives

103
Q

Tenesmus (feeling the need to pass stools even if bowel is empty)

A

clonazepam, apomorphine, relaxants like
benzodiazepines

104
Q

Hypersalivation

A

antihistamine, anticholinergic

105
Q

Dysphagia

A

liquid levodopa (not available in PH),
gastrostomy or nasogastric tube feeding

106
Q

Sweating crises

A

3-blockers, anticholinergic agents

107
Q

Daytime sleepiness

A

Selegiline

SS: sleep-selegiline

108
Q

Nightmares

A

amitriptyline (antidepressant), clonazepam (benzodiazepine)

109
Q

Panic attacks and depression

A

liquid levodopa, amitriptyline, SSRIs for mood problems

110
Q

Orthostatic hypotension

A

domperidone, desmopressin (available in PH)

HDD: hypotension-domperidone-desmopressin

111
Q

Dysphonia

A

reduce levodopa dosage, speech therapy

112
Q

Pain

A

amitriptyline, fluvoxamine (not used that much anymore), pregabalin

PT 10111 MedSurg 2 (3 decks)

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