The Physical and Psych impact of PD Flashcards
Hallmark signs of PD
-Tremors
-Bradykinesia
-Muscular rigidity
-Postural instability
Autonomic nervous system symptoms of PD
Postural Hypotension
-Dysphagia
-Urinary dysfunction
-Constipation
Dopamine in PD
Dopamine levels decrease
Acetylcholine in PD
As a result of decreasing dopamine there is increased Ach released into the synapse increasing excitability leading to movement issues
Braak stages of PD (Stage 1)
Oldfactory bulb is affected
-Nuclei 9 and 10 in medulla is affected
Braak stages of PD (Stage 2)
Intermediate reticular zone,
Lower raphe, coeruleous complex
-Cellular level
Braak stages of PD ( Stage 3)
-Substantia nigra, amgydala, hippocampus
-Motor deficits become present
Braak stages of PD ( Stage 4)
Temporal mesocortex and allocrtex
Further degeneration of motor, and cognition and emotion
Braak stages of PD ( Stages 5-6)
-High order sensory association areas of neocortex and prefrontal cortex
Stages in PD based on symptoms progression ( Stage 1)
Mild , unsevere symptoms
-Tremors on ONE SIDE and postural changes are observed
Stages in PD based on symptoms progression ( Stage 2)
Moderate symptoms with facial modifications
-Tremors on both sides and postural changes are observed
-mask like face,shuffling gait
Stages in PD based on symptoms progression ( Stage 3)
Progression of disease occured
-Imbalance of body and improper reflexes are observed
-postural instability
Stages in PD based on symptoms progression ( Stage 4)
Drastic change is observed, decrease in tremors however there is increased amines is and rigidity
-Personal assistance is required in simple tasks
Stages in PD based on symptoms progression ( Stage 5)
Advanced stage with aggressive symptoms, may not be able to walk. Would need care for every daily task
-Hallucinations and spasm occur in this stage
Why is the scale based on symptoms progression favored over the Braak stages in the clinical practice
The former is easier to detect on clinical practice as it relates directly to their symptoms
Acetycholine
Excitability
Young onset PD
-Rare, occurs in ages 20-40
-Micheal J fox
Idiopathic PD
Occurs later in life
-More common
-Progresses faster in older patients
_Muscular rigidity is already present
-Cardinal signs
-Tremors at rest
-Bradykinesia
-Muscular rigidity
Drug induced PD
-Some drugs block or limit dopamine
-this is REVERSIBLE, just stop giving the drug
-Mostly antipsych
Common drugs that cause drug induced PD
-Lithium
-Haldol (Haloperidol)
-Thorazine (Chlorpromazine)
-Reglan (Metoclopermide)
-Phenergan (Promethazine)
-Methyldopa (Aldomet)
PD occurs more in males (T/F)
True, however postmenopausal women also have an increased rate in comparison to those prior to menopause
Age of onset for PD
40-70
Environmental exposure in relation to PD
-Occupational: Lead exposure
-Exposure to toxins
-Exposure to pestisides
-Exposure to heavy metals
-Drinking well water
Dopamine
Inhibition of muscle fibers
Diagnosis of PD
-Diagnosis of occlusion, no definite test
-Hallmark signs
-Levodopa challange
-Smell test
Neuro imaging
-MRI, PET, SPET
Levodopa challenge
-Giving a small dose of levodopa and seeing if there is improvement
Smell test
-Old factory is one of the first to be affect by PD and can be an early indication with a smell test
Which cranial nerves are affected by PD
-Oldfactory
-Ocular-motor, decreased blinking, impairment of upward gaze
Motor disturbances in PD
-Shuffling Gait (Cant pick up feet due to decreased muscle control)
-Stooped posture
-Decreased arm swing
-Rigidity
-Cog-wheeling (Arms move up jumpy like a robot)
True or false those with early PD with tremors, the tremors are always present
False, the can go away with movement and when sleeping, later into the disease it will be present even with movement
Bradykinesia
-Slowness of voluntary movement
-Reduced automatic movements
-Difficulty with initiation with movement, impacting fine motor control.
-Micrographia
-Soft voice or monotone
-Example, Issues with buttoning with the shirt
Autonomic (Non-motor) disturbances
-Dizziness or vertigo
-Orthostatic hypotension
-Drooling
-Constipation
-Sweating
-Erectile dysfunction
Mask like face
Symptoms with PD, Affect becomes flat, they cannot smile or frown.
-Voice becomes soft and quiet
Pill rolling
Symptom with PD which a person looks like they are rolling a marble in their hands
Tremors in PD
-Rhythmic movement of a limb
-Usually the presenting symptom
-Most reliable sign of degeneration of substantia nigra
-Pill rolling
-Usually arm before leg
-Finger shaking to entire hand shaking
-More noticeable under stress
-Can disappear with activity or sleep
Micrographia
occurs with PD, hand writing becomes tiny, linked to decreased fine motor control
Muscular rigidity
-Stiffness of the muscles
-Felt with passive ROM (Cog wheel, jumpy movement)
-Affects both extensors and flexors
-Resistance is felt when they are relaxed, lead pipe
Postural instability
Dopamine is responsible for inhibition, leading to smooth movement, with PD this is interfered
-Control over pace is worsened, can have periods where they increase pace and decrease pace (Racing baby steps)
-Wide base, dont wanna fall
-FALL RISK
Racing baby steps
Going fast and then slow, they cant control pace
Orthostatic hypotension
-Disorder of the autonomic nervous system
-Failure of arterial baro-receptors (Cant regulate BP effectively)
-Criteria
-SBP decrease of 20 mmHg with change of position
-DBP decrease of 10 mm Hg with change of position
Dysphagia
Difficulty swallowing
-Later complication of neurologic degeneration
-CN 9,10,12 regulate tongue and swallowing
-Drooling, inability to automatically swallow saliva
Issues with urinary dysfunction
-Frequency, urgency, incontinence
-UTI
-FUNCTIONAL incontinence related to mobility issues
Constipation in PD
-ANS dysfunction (Decreased Motility)
-Decreased physical activity (shuffling doesnt move as much bowels)
-Anticholinergic meds (Dries you out)
-Other constipating meds
-Decreased oral intake, cannot swallow as well
Collaborative problems
-Physical S+S of PD
-Seborrhea (Over-secretion of oils)
-Corneal abrasions
-Lewy body dementia
Dopaminergic agents
-Acts to increase dopamine within the basal ganglion
-Essentially artificial dopamine
-There is increased tolerance and drug metabolism over time,
-Wearing off effect leading to returning symptoms
-Short half life (90-120 min) needs like 3-6 doses a day
-Tolerance is frequent
-Need to administer between meals for adequate absorption
side Effects of Dopaminergic agents
-Increased restlessness (Too high of a dose)
-Dyskinesia
-Orthostatic hypotension
-Mental disturbances
-Insomnia
Levo-dopa/ Carbidopa
-Gold standard of PD treatment
-Most potent anti-PD agent
-Precursor to dopamine, develops into dopamine in circulation
-Carbidopa blocks PNS inhibition
-Sinemet (Combo of the drugs) only works on the CNS
Dopamine agonist
-Acts to release dopamine, more dopamine in the synapse
-More effective when used in combination with dopaminergic drugs
-Side effects: Orthostatic hypotension, Dyskinesia, Hallucinations
bromocroptine (Paradol)
Dopamine Agonist
Ropinirole (Requip)
Dopamine agonist
Pramipexole (Mirapex)
Dopamine Agonist
Carbidopa
Dopaminergics agent, that acts to reduce metabolism of levodopa
Anti-cholinergic agents
-Decreases Ach, which decreases the excitability
-Helps to control tremors and rigidity
-Drys you out
-Used also in treatment of tardive-dyskinesia
-Side effects: Dry mouth, Constipation, Urinary retention, Confusion
Benztropine (Cogentin)
Anti-cholinergic agent
Trilhexyphenidyl (Artane)
Anti-Cholinergic agent
Catechol O-Methyltransferace Inhibitor (COMT)
-Prevents the breakdown of Levodopa, leaving more dopamine in the receptor
-Works best when combined with dopaminergic and dopamine agonist agents
-Side effects: Monitor for dyskinesia when given with levodopa
-Diarrhea
-Causes the urine to turn dark
Entacapone (Comtan)
COMT
Monoamine Oxidase Type B (MAO-B) Inhibitors
-Inhibits Monoxidase B activity, Increasing activity levels
-Reduces “Wear off” effect of levodopa when given with levodopa
*Need to avoid foods with tyramine, can cause hypertensive crisis
Selegiline
MAO-B inhibitor
Rasagine
MAO-B inhibitor
Foods rich with tryamine
-Aged cheese, Cured meats, red wine, broad beans, ripened fruit
-Smoked and old stuff
Anti-virals medications
-Stimulates release of dopamine and prevents reuptake
-We dont know why it works
-Side effects: Anxiety, confusion, anticholinergic effects (Dry)
Amantadine (Symmetrel)
Anti-viral
Deep brain stimulation
-Invasive, electrode implanted into thalmus, and shock is delivered to interfere with tremor cells and reduces tremors
-Monitor for infection, hemorrhage or stroke
Stereotactic pallidotomy
-Destroy a chunk of the brain, (Globus pallidus)
-Insert probe through probe hole (Destroys that area of the brain as well), to provide electrical stimulation to destroy part of globus pallidus and thalamus (Decreasing motor symptoms
-Improves: Tremor, muscle rigidity, bradykinesia, dyskinesia
-Need to assess for neurologic deficits and brain hemorrhage and infection post op,
-destroying a part of the brain you need to monitor to make sure you didnt destroy something important
Complications of PD/Collaborative problems:
-Decreased Mobility
-Falls
-Dysphagia
-Weight loss
-Aspiration pneumonia
-Urinary/retention/UTI/ Incontinence
-Bowel obstructions
-Self care Deficits (Loss of independence)
-Altered cognition: Lewy body Dementia
Psychosocial impact of PD (Depression): Physiological causes
-imbalance of serotonin
-Sleeping disturbances
-Sexual dysfunction
Psychosocial impact of PD (Depression) Cognitive causes
1/3 of persons with PD develop cognitive impairment and dementia (Lewy body)
Psychosocial impact of PD (Depression) Psycho-social
-Adaptation to chronic and slowly debilitating illness
-Personality changes, becomes more withdrawn
-Mood changes
-Lewy-body Type: hallucinations/anger/agitation
Which protein is responsible for Lewy body dementia
alpha synuclein
Lewy Body dementia
Alpha-synucle is a protein that clumps up in large deposits occluding transmission of chemicals
-Results in deficits in Thinking, Movement, Behavior, Mood
-Lots of psychosis
-Doesnt respond to dementia drugs
Fetal Stem cell transplant
Implantation of cells which develop into dopamine producing cells
-Sucks, because initially it releases too much dopamine
-Also sucks because those new cells become diseased over time
Where is dopamine stored in the brain
Substantia Nigra, and when it becomes dmg it leads to decreased dopamine levels
