Parkinson's Disease/Test 3 Flashcards

1
Q

Etiology of Parkinson’s Disease:

A
  • Diagnosis increases with age, with peak onset being in 70’s.
  • Onset before age of 50 is likely r/t genetic defect
  • More common in men, ratio 3:2
  • *Dementia occurs in up to 40% of patients
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2
Q

Pathophysiology of Parkinson’s Disease:

A
  • Chronic, progressive, degenerative disorder
  • Affects dopamine-producing neurons in the brain
  • Caused by an imbalance of two neurotransmitters
  • dopamine
  • acetylcholine (ACh)
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3
Q

Symptoms of Parkinson’s do not occur until

A

80% of neurons in the substantia nigra are lost

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4
Q

Basal ganglia-

A
  • Refining motor skill
  • mass of gray matter or cell bodies deep within the cerebrum. Functions adjustment of posture and gross volunteer movement. Consists of putamen, caudate nucleus and globus pallidus.
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5
Q

Dopamine and acetylcholine are:

A

primary neurotransmitters responsible for controlling and refining motor movements and having opposite effects.

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6
Q

Dopamine has:

A

inhibitory effects

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7
Q

Acetylcholine has:

A

excitatory effects

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8
Q

At the cellular level-

A

impairment of the extra pyraminal tract (controls semiautomatic and coordinated movement Striatal degeneration destruction of dopaminergic neurons reduces availability of dopamine (inhibitory neurotransmittor)

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9
Q

Symptoms of Parkinson’s disease: Motor

A
  • Tremor at rest
  • Bradykinesia
  • Rigidity
  • Postural instability
  • Other (e.g. dysarthria (speaking difficulty due to mucle tone) shuffling gate, dystonia)
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10
Q

Symptoms of Parkinson’s disease: Nonmotor

A
  • Neurosychiatric (eg, dementia, cognitive decline, depression, anxiety, psychosis, apathy)
  • Sensory (eg, hyposmia, pain, paresthesias
  • Sleep disturbances (eg, RBD, RLS, sleep apnea, sleep attacks, daytime somnolence, insomnia)
  • Autonomic dysfunction
  • other. (eg. fatigue, weight loss)
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11
Q

Parkinson’s disease progression of movement disorder:

A
  • Onset is gradual and insidious, with a gradual progression and a prolonged course
  • May involve only one side of the body initially with mild tremor, slight limp, or decreased arm swing.
  • The classic manifestations of PD often include tremor, rigidity, and bradykinesia, which are often called the triad of PD.
  • Later signs may have shuffling, propulsive gait with arms flexed and loss of postural reflexes.
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12
Q

Clinical manifestations of Parkinson’s disease:

A

*Gradual and insidious progression and prolonged course

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13
Q

Classic symptoms: TRAP- T is for

A

Tremors: pill rolling

  • Most recognized and least disabling symptoms
  • rhythmic movement of thumb across the palm at rest but not during sleep- seen in limbs, jaw, lip, lower facial muscles and head.
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14
Q

R is for

A

Rigidity- muscles feel still and require increased effort to move, stiffness may have accompanying pain

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15
Q

A is for

A

Akinesis/bradykinesis
slow, can’t initiate movement. Difficulty initiating movement. Interferes with ADL’s. Predisposes to complication r/t constipation, circulatory stasis, skin breakdown, and other mobility issue

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16
Q

P is for:

A

Postural instability
Change in gait, unstable gate (shuffling, propulsive, festinating, loss of arm swing, stooped, righting reflex decreased or absent. Change in balance. Stooped arms semiflexed and do not swing when walking. Difficulty maintaining balance and sitting erect. Cannot brace self or prevent falling. “Cogwheel” ratchetlike rhythmic contractures of the muscle that occur when extremities are passively stretched.

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17
Q

Tremor is more prominent

A

at rest and is aggravated by emotional stress or increased concentration.

  • described as pill rolling because thumb and forefinger appear to move in rotary fashion.
  • Tremor can involve diaphragm, tongue, lips and jaw, dysarthria
  • Benign essential tremor, which occurs during voluntary movement, has been misdiagnosed as Parkinson’s
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18
Q

Rigidity is the

A

increased resistance to passive motion when the limbs are moved through their range of motion

  • Typified by a jerky quality when the joint is moved
  • Similar to intermittent catches in the movement of a cogwheel
  • complaint of soreness, feeling tired and achy
  • pain in the head, shoulder, neck, spine, hips or legs
  • *caused by sustained muscle contraction. Inhibits the alternating contraction and relaxation in opposing muscle groups, thus slowing movement.
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19
Q

Emotional Problems:

A

*non motor symptoms are common;
-depression
-insomnia
-mood swings
-hallucinations
-anxiety
-apathy
-fatigue
-pain
-impotence
-short-term memory impairment
Misc:
-excessive salivation, dysphagia, weight loss, micrographia, seborrhea, dandruff, excessive sweating, postural hypotension

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20
Q

How is PD diagnosed:

A
  • Facial appearance
  • Fine motor function
  • Speech problems
  • Autonomic disturbances
  • Dysphagia
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21
Q

Facial appearance:

A
  • expressionless
  • eyes are straight ahead; impaired upward gaze
  • much less blinking
  • mask like face
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22
Q

Fine motor function

A
  • micrographia
  • decreased manual dexterity
  • clummsiness and decreased cordination
  • decreased capacity to complete ADLs
  • freezing: sudden involuntary inability to initiate movement. Can occur during activity or inactivity.
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23
Q

Speech problems:

A
  • low volume
  • slurred, muffled
  • monotone voice
  • blepharospams; ivoluntary prol
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24
Q

Autonomic Disturbances:

A
  • constipation from hypomobility
  • prolonged gastric emptying
  • urinary frequency and hesitancy
  • orthostatic hypotension; dizziness, fainting, syncopy
  • dysphagia from neuromuscular incoordination
  • drooling from decreased swallowing
  • oily skin (seborrhea)
  • excessive perspiration
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25
Q

Dysphagia leading to malnutrition or aspiration:

A
  • mobility greatly decreased leading to constipation, ankle edema, contractures
  • posture
  • orthostatic hypotension resulting in falls/injuries
  • seborrhea
  • excessive sweating
26
Q

Collaborative Management:

A

*Supportive care is primarily directed at supporting independence in self care, developing coping resources, and ensuring safety.

27
Q

Drug program is designed to

A

reflect patient’s age, symptoms, severity and lifestyle

28
Q

Multi-discipline

A
  • Goal to create daily routine that is effective in slowing the rate of disability
  • physical
  • occupational speech.
29
Q

Medication Rational:

A
  • Replace depleted levels of dopamine
  • Stimulate the nerve receptors enabling neurotransmission
  • Increase the effect of dopamine on nerve receptors (agonist)
  • Counteract the imbalance of Ach and Dopamine
30
Q

Classes of drugs for Parkinson’s

A
  • Dopaminergic drugs (improving dopamine functioning)
  • Levodopa
  • Dopamine receptor agonists
  • Amantadine
  • Selective monoamine oxidase B inhibitors
  • Catechol-O-methyltransferase inhibitors
  • Anticholinergics (ACh inhibitors)
  • anticholinergic (for muscle rigidity)
31
Q

Collaborative care: Drug Therapy- aimed at

A

correcting an imbalance of neurotransmitters in the CNS

32
Q

Anticholinergics:

A

(for muscle rigidity) antagonize or block the effects of the overactive cholinergic neurons in the striatum. Antagonize the excitatory effects of the cholinergic neurons.

  • Trihexylphenidyl (Artane)
  • Benztropine (cogentin)
  • Orphenadrine (disipal)
  • Procyclidine (kemadrin)
33
Q

Dopaminergics

A

enhance the release or supply of dopamine

34
Q

Levadopa

A

Can cross the blood brain barrier

-Sinemet (levodopa-carbidopa combo)
*Levadopa- dopamine precursor and dopa decarboxylase inhibitor
*Carbidopa-prevents the conversion of levodopa in the peripheral tissue S/e orthrostatic B/P, vivid dreams
Toxicity-twitching muscle or eyelid need to report to Dr.

35
Q

Antiviral

A

Symmetrel (amantadine)- blocks reuptake of catecholamine and allows dopamine to accumulate in the synapse

36
Q

Dopamine agonist:

A

Help prevent or minimize the flucuations in motor response. Stimulates brain dopamine receptors.

Drugs:

  • pergolide (permax)
  • pramipexole (mirapex)
  • Ropinirole (requip)
  • Bromocriptine (parlodel)
37
Q

Levodopa (Madopar & Sinemet)

A
  • levodopa is a precursor of dopamine
  • blood brain barrier does not allow exogenously supplied dopamine to enter, but does allow levodopa
  • a natural amino acid that the brain converts into dopamine (replacement therapy) used since the 1960’s)
  • to make it slow release, combined with benserazide (an enzyme inhibitor) to create co-benserazide (an enzyme inhibitor) to create co-beneldopa or co-careldopa (Sinemet)
  • *Dose= 50, 100 or 200 mg (12.5, 25, or 50mg)
38
Q

Levodopa (Madopar and sinemet) is aimed at

A

increasing levels of dopamine as long as there are functioning nerve terminals remaining. Antagonizes or blocks the effects of ACh. Slows the progression of the disease.

39
Q

As PD progresses, it becomes

A

more difficult to control it with levodopa. Ultimately, levodopa no longer controls the PD, and the patient is seriously debilitated. This generally occurs between 5 and 10 years after the start of levodopa therapy.

40
Q

MAOIs break down

A

catecholamines in the CNS, primarily in the brain.

41
Q

Selective MAO-B inhibitors

A

Selegiline (Eldepryl) and rasagiine (Azilect)
-they cause an increase in levels of dopaminergic stimulation in the CNS. Do not elicit the “cheese effect” of the nonselective MAOIs used to treat depression (if 10mg or less is used)

42
Q

MAOIs and MAO-B inhibitors work in combination with

A

levodopa or carbidopa-levodopa- used as adjuncts when a patient’s response to levodopa is fluctuating . Allows the dose of levodopa to be decreased. Delay development of unresponsiveness to levodopa therapy

43
Q

Monoamine oxidase B inhibitors

A

-blocks/slow metabolism of dopamine
-targets the disease process and not just the symptoms
-neuroprotection
-durg:Eldepryl (selegline)
Adverse effect-vivid dreams

44
Q

Selective monoamine oxidase B inhibitors (selegiine/Eldepryl/Zelapar)

A
  • MoA- prolongs the effects of levodopa as MAO-B degrades dopamine.
  • Adverse effects: N, V, Dia, Constipation; dry mouth, sore throat; transient dizziness; insomnia, confusion and hallucinations.
  • Early stage- prescribed on its own to delay need for levodopa and there is good evidence for its slowing down of PD progression
45
Q

COMT Inhibitors:

A

Indirect acting- tolcapone (Tasmar), entacapone (Comtan)
Inhibit COMT, the enzyme responsible for the breakdown of levodopa, the dopamine precursor.
*Prolong the duration of action of levodopa; reduce wearing-off phenomenon

46
Q

tolcapone (Tasmar)

A
  • has caused severe liver damage
  • requires monitoring of liver enzymes
  • not used unless other drugs do not work
47
Q

amantadine (Symmetrel)

A
  • indirect acting
  • causes release of dopamine from storage sites at the end of nerve cells that are still intact
  • blocks reuptake of dopamine into the nerve endings, allowing more to accumulate both centrally and peripherally
  • does not stimulate dopamine receptors directly
  • used early in the course of the disease
  • usually effective for only 6 to 12 months
  • used to treat dyskinesia associated with carbidopa-levodopa
  • also used as an antiviral for influenza virus infection
48
Q

Adverse effects of Levodopa (Madopar and sinement)

A
  • As a result of the amount of peripheral dopamine levels:
  • N/V
  • postural hypotension
  • As a result of the amount of CNS dopamine levels
  • dyskinetic involuntary movements (face and neck)
  • hallucinations and confusion
49
Q

Dopamine receptor agonists-

A
  • Apopmorphine (APO-go):
  • SC administration
  • rescue therapy-rapid onset with a short duration of action (50 min)
  • Bramocriptine (Parlodel); Pergolide (Celance); Ropinirole (Requip)
  • helps prevent or minimize the fluctuations in motor response
  • stimulates brain dopamine receptors
  • longer lasting therapeutic effects that Levodopa
50
Q

Dopamine Receptor Agonists: Adverse Effects

A
  • Use gradual dose titration
  • N/V (Particularly apomorphine)
  • dyskinesia
  • hallucinations and confusion
  • peripheral vasospasm (Raynaunds)
  • respiratory depression (Apomorphine)
51
Q

Anticholinergics:

A

block the effects of ACh

  • used to treat muscle tremors and muscle rigidity associated with PD
  • these two symptoms are caused by excessive cholinergic activity
  • *Does not relieve bradykinesia (extremely slow movements)
52
Q

Anticholinergic Drugs:

A
  • Trihexyphenidyl (Broflex, Artane, Agitane); Benzotropine (Cogentin); Orphanadrine (Disipal); Procycline (Kemadrin, Arpicolin)
  • less common drugs but they affect Ach based interactions
  • Pharmacokinetics: fairly well absorbed, extensive hepatic metabolism, intermediate to long half-lifes
  • Adverse effects: dry mouth and confusion
53
Q

Anticholinergic Therapy:

A
  • benztropine mesylate (Cogentin)
  • also used to treat extrapyramidal symptoms caused by use of antipsychotic drugs
  • trihexyphenidyl (generic only)
54
Q

Antihistamines also have

A

anticholinergic properties

-diphenhydramine (benadryl)

55
Q

Symptom Management Drugs: PD is

A

multidimensional, therefore are a number of clinical presentations that require supplementary agents

  • drug-drug reactions is the problem
  • major area is depression
56
Q

Antidepressants:

A
  • Aminotriptyline (Tryptizol), imipramine (Tofranil), Nortriptyline (Allegron) lofepramine (Gamanil)
  • MoA:block re-uptake of noradrenaline and serotonin= >sedative actions, can help with drooling and loss of appetite.
  • Adverse effects: sleepiness, dry mouth, increased hunger, cardiac arrhythmias and changes in BP
  • can interfere with the effects of levodopa
57
Q

As disease progresses, combination therapy is

A

often required: Excessive amounts of dopaminergic drugs can lead to paradoxical effects and dyskinesias. (muscle and eye twitching)

  • **Common side effects
  • dyskinesias, akinesia
  • orthostatic hypotension
  • hallucinations
  • vivid dreams
  • weakness
58
Q

Collaborative Care: Deep Brain Stimulation (DBS)

A
  • involves placing an electrode in either the thalamus, globus pallidus, and subthamic nucleus
  • connected to a generator placed in the upper chest
  • device is programmed to deliver specific current to targeted brain location
  • less invasive and preferred over ablative or other surgical techniques
59
Q

Impaired physical mobility

A
  • promotion of physical activities to limit consequences of immobility
  • specific exercises to strengthen muscle involved with speaking and swallowing.
  • Safe transfer techniques- getting out of a chair by using arms and placing the back legs on small blocks. Consciously thinking about stepping over a line on the floor. Lifting toes when stepping.
  • Wide base stance helps maintain balance during ambulation. Holding hand clasped behind the back walking may help patient keep the spine erect and counter the problems created by the arms hanging stiffly by the sides.
60
Q

PD is risk for:

A
  • pneumonia
  • UTI
  • Skin breakdown
  • aspiration
  • Self Care Deficit
  • simplify clothing from buttons and hooks. Elevated toilet seats
  • Falls- remove rugs and excess furniture immobility
  • Constipation
  • Ankle edema
  • Contractures
61
Q

Imbalanced Nutrition: Less than body requirements-

A

r/t dysphagia, slowness in eating, impaired facial muscles

  • levodopa can be impaired by protein ingestion at same time as med adm.
  • dysphagia can lead to malnutrition
  • several small meals to prevent fatigue
  • provide ample time to avoid frustration
  • **Facial massage to decrease facial rigidity prior to meal times- chew better/swall better