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NURS 2514 > Week 10 - Parkinson's Disease > Flashcards

Week 10 - Parkinson's Disease Flashcards

1
Q

what is parkinson’s disease

A
  • a progressive & neurodegenerative & movement disorder that involves degeneration of dopaminergic neurons in the substantia nigra
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2
Q

what two nt does parkinson’s disease effect? how?

A
  • causes an imbalance in nt dopamine & ach secreted in the basal nuclei
    = excessive Ach, dopamine deficiency
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3
Q

what is the fnxn of dopamine (3)

A
  • trunk support
  • voluntary motion
  • posture
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4
Q

what are movement programs from the motor cortex typically inhibited by

A
  • GABA secreted from the basal nuclei onto the thalamus
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5
Q

what effect does ach have on GABA? dopamine?

A
  • ach = excitatory hormone = increased secretion of GABA

- dopamine = inhibitory = decreased secretion of GABA

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6
Q

what effect does excessive ach have

A
  • excessive ach stimulated inhibition of the motor cortex = inhibition of movements

( why we get the rigidity, slowed movement, etc.

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7
Q

what is the most common cause of PD

A
  • most common cause is idiopathic
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8
Q

what are other causes of PD (4)

A
  • encephalitis
  • severe carbon monoxide poisoning
  • MPTP
  • neurleptic drug toxicity
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9
Q

what are risk factors of PD (4)

A
  • 60 years or older
  • FHx
  • history of head trauma
  • exposure to herbicides & pesticides
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10
Q

what are the 4 main symptoms of PD

A
  • tremor
  • rigidity
  • bradykinesia
  • postural instability
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11
Q

what other symptom may occur w PD

A
  • intellectual deterioration
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12
Q

what causes the tremor during PD to be more pronounced (4)

A
  • more pronounced at rest

- enhanced by stress, concentration, or anxiety

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13
Q

is the tremor uni or bilateral

A
  • usually begins in only one side of the body initially

- but can progress & be bilateral

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14
Q

what is the tremor during PD often described as

A

“pill rolling”

- looks like ur trying to roll a pill between the thumb & index finger

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15
Q

what affects does the tremor during PD have (2)

A
  • affect handwriting

- affect ADLs

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16
Q

what is rigidity

A
  • increased resistance to passive movement
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17
Q

what can rigidity during PD look like?

A

“cogwheel rigidity”

- watch video in notes as it is hard to explain

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18
Q

what can rigidity during PD cause

A
  • muscle soreness/fatigue due to the constant state of rigidity
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19
Q

what is bradykinesia

A
  • slow voluntary movements
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20
Q

what other effect can PD have on motor function (6)

A

can cause reduction in autonomic extrapyramidial movements –> does not execute involuntary movements such as:

  • blinking
  • swinging arms while walking
  • swallowing saliva = drooling
  • facial expressions
  • postural adjustments
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21
Q

what is meant by “masked face” during PD

A
  • way to describe the lack of facial expressions that occur w PD
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22
Q

what kind of posture is seen w PD

A
  • stooped or flexed posture
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23
Q

what is postural instability

A
  • flexed posture with “shuffling” steps
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24
Q

what can postural instability lead to (2)

A
  • instability

- falls

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25
Q

what is postural instability complicated by

A
  • slowed voluntary movements
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26
Q

describe the onset of PD

A
  • insidious & gradual
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27
Q

define akinesia

A
  • the loss of the ability to move muscle voluntarily

- absence of movement

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28
Q

define bradykinesia

A
  • slowness of movement
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29
Q

define dyskinesia

A
  • abnormal involuntary movement
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30
Q

what happens as PD progresses (6)

A

complications increase such as:

  • motor symptoms
  • weakness
  • akinesia
  • neuro problems
  • neuropyschiatric problems (depression, anxiety)
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31
Q

what changes in mental status might you see during assessment of PD (5)

A
  • depression
  • mood swings
  • flat affect
  • sleep disturbances
  • dementia (memory loss & confusion)
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32
Q

what changes in sensation might you see during assessment of PD

A
  • paresthesia

- loss of smell

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33
Q

what changes in balance/corrdination might you see during assessment of PD (5)

A
  • bradykinesia
  • shuffling gait
  • stooped posture
  • difficulty initiating movements
  • unable to stop themselves from going forward & backwards
34
Q

what changes in movement might you see during assessment of a pt with PD (7)

A
  • tremors (pill rolling)
  • rigidity (cogwheel)
  • jerky quality
  • muscle fatigure & soreness
  • difficulty executing involuntary movements
  • drooling
  • masked face
35
Q

which cranial nerves might be effected by PD

A
  • CN1
  • CN 2,3,4,6
  • CN 5, 7
  • CN 8
  • CN 9,10,12
  • CN 11
  • all of them
36
Q

what might the change in CN 1 cause

A
  • loss of smell
37
Q

what might the change in CN 2,3,4,6 cause (2)

A
  • visual changes

- difficulty w eye closure & blinking

38
Q

what changes in CN 5 and 7 might you see (2)

A
  • blank, expressionless face

- difficulty chewing

39
Q

what changes in CN 8 might you see (2)

A
  • hearing loss

- balance issue

40
Q

what changes in CN 9,10, 12 might you see (2)

A

-issues with speech & swallowing

41
Q

what changes in CN 11 might you see

A
  • issues w movement of head & shoulders
42
Q

_____ occurs in 40% of PD pts

A
  • dementia
43
Q

is there a diagnostic test for PD

A
  • no specific diagnostic test
44
Q

describe how diagnosis of PD is completed

A

based of manifestations & history

- must have 2/3 classic triad

45
Q

what is the PD traid

A
  • tremor
  • rigid
  • bradykinesia
46
Q

what can confirm the diagnosis of PD

A
  • positive response to antiparkinson meds
47
Q

what is a type of surgical care for PD

A
  • deep brains stimulation
48
Q

describe how deep brain stimulation works

A
  • involves placing an electrode in the thalamus, globus, pallidus, or subthalamic nucleus
  • connected to a generator in the upper chest
  • device is programmed to delivery specific current to targeted brain location
49
Q

what is the goal of treatment for PD

A
  • restoring the balance between ach and dopamine
50
Q

what 3 classes of meds are used for PD

A
  • dopaminergic agents
  • dopamine agonists
  • MAO inhibitors
51
Q

what are 2 types of dopaminergic agents for PD

A
  • levodopa

- levodopa/carbidopa

52
Q

what is the MOA of levodopa

A
  • crosses the BB and is converted to dopamine in the brain = increased lvls of dopamine
53
Q

what is a challenge w levodopa (2)

A
  • only a small part reaches the brain
  • bc most is metabolized in the body
    = difficult to achieve optimal dosages
  • also loses effectiveness over time
54
Q

what is the most effective drug for parkinsons

A
  • levodopa
55
Q

what are 4 adverse effects of levodopa

A
  • dyskinesias
  • postural hypotension
  • NV
  • psychosis
56
Q

what is dyskinesia

A
  • abnormal, involuntary, erratic movements of the face, arms, legs, or trunk
57
Q

how does levodopa cause dyskinesias

A

thru the on-off phenoneom:

  • too little dopamine = parkinson’s disease symptoms worsen
  • but too much due to the med = dyskinesia
58
Q

how can we prevent the NV associated levodopa? what is a con to this?

A
  • give w food

- but it will decrease absorption

59
Q

what needs to be done if levodopa causes psychosis

A
  • dose will need to be reduced
60
Q

what med is often given in combo w levodopa

A
  • carbidopa
61
Q

what is the MOA of carbidopa

A
  • no therapeutic effect on its own

- but it stops metabolism of levodopa in the body = increased amt of dopamine available to the brain

62
Q

list adverse effects of levodopa/carbidopa

A
  • decreased CVS effects (hypotension)
  • decreased NV side effect of levodopa
  • increased dyskinesias
63
Q

how does levodopa/carbidopa decrease the CVS and NV side effect associated w levodopa on its own

A
  • by decreasing the lvl of dopamine in the body
64
Q

how does levodopa/carbidopa increase the dyskinesias compared to levodopa on its own

A
  • by increasing the amt of dopamine in the brain
65
Q

what is a type of dopamine agonist used for PD

A
  • pramipexole
66
Q

what is the MOA of pramipexole

A
  • directly activates dopamine receptors
67
Q

describe the use of pramipexole

A
  • for mild to mod PD symptoms
68
Q

what are the effects of pramipexole

A
  • improved motor performance

- stabilized motor control in later disease when used w levodopa

69
Q

list s/e of pramipexole (6)

A
  • NV
  • dizziness
  • daytime somnolence
  • insomnia
  • hallucinations
70
Q

describe dyskinesia during pramipexole

A
  • does not cause dyskinesia
71
Q

what is one s/e associated w pramipexole if used with levodopa

A
  • high likelihood of postural hypotension (more than 50%
72
Q

what is an MAO-B inhibitor used for PD

A
  • selegiline (deprenyl)
73
Q

what is the MOA of selegiline

A
  • inhibits the enzyme monoamine oxidase B, which breaks down dopamine = more dopamine in brain
74
Q

describe the relation between selegiline and levodopa

A
  • prolongs the effects of levodopa bc it prevents the dopamine it is converted into from being inactivated so quickly
75
Q

what is a pro to selegiline

A
  • may delay disease progression
76
Q

what are 2 side effects of selegiline

A
  • insomnia

- postural hypotension

77
Q

what are 3 types of dyskinesia

A
  • akinesia
  • akathisia
  • dystonia
78
Q

what is akinesia

A
  • loss of voluntary motor function
79
Q

what is akathisia

A 
- having the urge to move, restlessness
ex:
- rocking while standing
- lifting feet as if marching on spot
- crossing & uncrossing legs while sitting
80
Q

what is dystonia

A
  • abnormal muscle tone leading to impaired or abnormal movements of head, neck, and tongue

NURS 2514 (75 decks)

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