2.9 Neurological and Sensory PARKINSON'S Flashcards

1
Q

Parkinson’s disease

PATHOPHYSIOLOGY

A

PATHOPHYSIOLOGY
Chronic & gradually progressive; classed as movement disorder but sensory S/S occur
Genetic, environmental, and lifestyle factors –cause not understood
Risk factors: age, exposure to toxins, head injury, sex
Accumulation of Lewy bodies
Neurotransmitter problem: death of dopaminergic neurons in substantia nigra
dopamine deficit
lose balance of acetylcholine (excitatory) & dopamine (inhibitory) stimulation of neurons
movement, mood, behavior, & cognitive change
Diverse disorder –individual clinical picture
1 million people in the US

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2
Q

Parkinson’s disease

Dopamine

A

Dopamine is a chemical messenger (neurotransmitter) that is primarily responsible for controlling movement, emotional responses and the ability to feel pleasure and pain. In people with Parkinson’s, the cells that make dopamine are impaired. As Parkinson’s progresses, more dopamine-producing brain cells die. Your brain eventually reaches a point where it stops producing dopamine in any significant amount. This causes increasing problems with movement.

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3
Q

Parkinson’s disease
Manifestations
MOVEMENT SYMPTOMS

A

Manifestations
MOVEMENT SYMPTOMS:
Bradykinesia- slow movements

Rigidity – stiffness “cogwheel rigidity”

Tremors - resting (various areas “pill rolling”)

Postural instability

Additional motor manifestations:
Stooped posture & Gait disturbances –no arm swing, shuffling, festinating (tendency to speed up when performing repetitive movements
Dyskinesia, dystonia (involuntary muscle contractions that cause slow repetitive movements or abnormal postures)
Freezing
Facial masking, swallow problems, & drooling – staring & lack of blinking
Micrographia (small handwriting)
Dysphonia (soft, hoarse voice)

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4
Q

Parkinson’s disease
Cramping
Drooling

A

Cramping (dystonia: involuntary muscle contractions that cause slow repetitive movements or abnormal postures):sustained or repetitive twisting or tightening of muscle.

Drooling (sialorrhea):while not always viewed as a motor symptom, excessive saliva or drooling may result due to a decrease in normally automatic actions such as swallowing.

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5
Q

Parkinson’s disease
Dyskinesia
Festination

A

Dyskinesia:involuntary, erratic writhing movements of the face, arms, legs or trunk.

Festination:short, rapid steps taken during walking. May increase risk of falling and often seen in association with freezing.

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6
Q

Parkinson’s disease
Freezing
Masked face

A

Freezing:gives the appearance of being stuck in place, especially when initiating a step, turning or navigating through doorways. Potentially serious problem as it may increase risk of falling.

Masked face (hypomimia):results from the combination of bradykinesia and rigidity.

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7
Q

Parkinson’s disease
Micrographia
Shuffling gait
Soft speech

A

Micrographia:small, untidy and cramped handwriting due to bradykinesia.

Shuffling gait:accompanied by short steps and often a stooped posture.

Soft speech (hypophonia):soft, sometimes hoarse, voice that can occur in PD

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8
Q

Parkinson’s disease
Manifestations
NON-MOVEMENT SYMPTOMS:

A

NON-MOVEMENT SYMPTOMS:
Cognitive changes: attention, planning, language, memory, dementia

Constipation

Fatigue

Loss of taste or smell

Urinary urgency, frequency, & incontinence

Sleep problems

Mood disorders: depression, anxiety, apathy, irritability

Early satiety (feeling of fullness after eating small amounts), weight loss

Orthostatic hypotension, dizziness

Vision problems, especially when attempting to read items up close

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9
Q

Parkinson’s disease

diagnosis

A

diagnosis
No specific test – must have 2 of the 4 symptoms: tremor, bradykinesia, rigidity, postural instability
Neurologist movement disorders specialist – challenging dx, pt’s have variable symptoms
Rule out other conditions that mimic PD
Tests:
-CT scan
-MRI
-DatScan SPECT: shows density of dopamine transporter, qualitative
-PET scan

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10
Q

Parkinson’s disease

DaT scans

A

The new DaT scans use a substance that “tags” a part of a neuron in the brain where dopamine attaches to it, thus showing the density of healthy dopamine neurons. Thus, the more of the picture that “lights up”, the more surviving brain cells. Dark areas could mean either Parkinson’s disease or parkinsonism.

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11
Q

Parkinson’s disease

Treatment

A

Treatment
No cure, meds & treatments control symptoms, eventually not effective

Medications
Dopamine replacement – levodopa/carbidopa levodopa converts to dopamine in brain
(carbidopa delays breakdown & ↓N & V;) levodopa can cause dyskinesias; wearing off”

Sometimes give COMT inhibitors to prolong levodopa by blocking its metabolism (entacapone)

Surgical insertion in intestine of gel delivery system for pts with “wearing off”

Dopamine agonists – stimulate the areas of brain where dopamine works (pramipexole, ropinirole)

Anticholinergics – treat tremor by blocking acetylcholine

MAO inhibitors – prevent breakdown of dopamine
Medical marijuana

Surgery – deep brain stimulator

Therapy

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12
Q

Parkinson’s disease

Nursing care

A

Nursing care
Safety – balance, gait problems, coordination problems

Psychosocial – depression, loss of independence, isolation

Nutrition & fluid balance – swallowing, chewing problems, utensils, soft foods

Risk of aspiration
Impaired mobility – specialized assistive devices
https://www.youtube.com/watch?v=J6g-OjBJ5c0

Education managing freezing episodes (laser point walker)

Constipation/bladder problems
Medication education – strict schedules, foods, side effects, peak

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13
Q

Parkinson’s disease

Deep brain stimulator

A

The deep brain stimulation system consists of four parts: Leads (thin insulated wires) that end in electrodes that are implanted in the brain, A small pacemaker-like device, called a pulse generator, that creates the electrical pulses

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