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The prevalence of PD increases with...?
age
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In people with PD, there is a lack of _______ in the brain.
Dopamine
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A lack of dopamine in the brain can cause:
- -relay of messages is disturbed
- -problem with control of movement
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Causes of Parkinson's Disease?
- -idiopathic
- -genetic
- -environmental
- -viruses
- -oxidative stress
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Describe the genetic cause of Parkinson's Disease
- -mutation of alpha-synuclein gene
- -some of the brain cells contained clumps of alpha-synuclein protein (Lewy bodies)
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Name some risk factors of PD
- a positive family hx
- male gender (2:1 female)
- head injury
- exposure to pesticides
- rural living
- comsumptions of well water
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Factors associated with a REDUCED incidence of PD
- coffee drinking
- smoking
- use of NSAIDs
- estrogen replacement in postmenopausal women
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4 characteristics that a patient will present to diagnose with PD
- Tremor at rest
- Rigidity
- Akinesia or Bradykinesia
- Postural instability
- ***diagnosis of PD requires identifying 2 of these 4 features***
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Define tremor:
- most specific feature of PD
- improves with intentional movement or sleep
- usually the symptom that causes people to seek attention
- involve the thumb and forefinger and appear as a "pill rolling" tremor
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Define rigidity:
- muscles remained constantly tensed and contracted, resistant to movement
- becomes obvious when another person tries to move the patient's arm, which only moves in short, jerky movements, "cogwheel rigidity"
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Define akinesia or bradykinesia:
- slowing down of loss of spontaneous and automatic movement
- cannon rapidly perform routine movement
- simple activities may take hours (dressing, washing)
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Define postural instability:
- impaired balance
- a stooped posture in which the head is bowed and the shoulders are dropped
- diagnostic test for PD- pull on patient's back and try to make them fall
- cane, walker, or wheelchair to prevent falls
- physical therapy for gait training
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Name the 5 drug classes that can be used to treat PD
- levodopa
- MAO-B inhibitors
- Dopamine agonists
- COMT inhibitors
- Anticholinergics
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Which is the single most effect agent in PD, but has greater incidence of motor fluctuations?
Levodopa
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Which class may provide initial symptomatic treatment in order to confer mild benefit prior to the institution of dopaminergic therapy?
MAO-B inhibitors
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Which class have less motor complications, but more dose-related adverse effects?
dopamine agonists
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Why is levodopa generally given with carbidopa?
Carbidopa helps get more levodopa to the brain which prevens N/V because you have less dopamine floating around in the body.
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T/F: All carbidopa/levodopa doses need to be titrated?
True
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How often do dose adjustments need to be made in titrating carbidopa/levodopa?
every 2 to 3 days
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Name adverse effects of carbidopa/levodopa
- nausea
- anorexia
- vomitting
- choreiform movements (caused by excess dopamine)
- dyskinesias(dance-like movements)
- orthostatic hypotension
- psychotic episodes
- depression
- hallucinations
- constipation
- blepharospasm (contraction of eye lids, could mean dopamine toxicity)
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Drug interactions with carbidopa/levodopa?
- antihypertensive drugs (decreased bp)
- iron salts (separate 2 hours)
- MAOI's (serotonin syndrome, NMS)
- metoclopramide (can cause parkinson-like symptoms)
- do not take with high-protein foods (reduce absorption and effectiveness)
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Name 2 MAO-B inhibitors:
- selegiline (Eldepryl)
- rasagiline (Azilect)
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MOA of MAO-B inhibitors:
inhibit the enzyme MAO-b which breaks down dopamine in the brain. MAO-B inhibitors cause dopamine to accumulate in surviving nerve celss and reduce the symptoms of PD.
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Adverse effects of MAO-B inhibitors:
- nausea
- postural hypotension
- headache
- dizziness
- confustion, hallucinations
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Adverse effects of selegiline:
do not take HS!! metabolized to an amphetamine-like compound cause insomnia
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Adverse effects of rasagiline:
dyskinesias more common, should avoid caffeine, tyramine
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MAO-B drug interactions:
- CNS stimulants
- analgesics (serotonin syndrome)
- anesthetics
- cyclobenzaprine
- MAOIs
- serotonin modulators
- tca's
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Name some dopamine agonists:
- apomorphine injection (Apokyn)
- pramipexole (Mirapex)
- Ropinorole (Requip)
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MOA of dopamine agonists:
stimulate dopamine receptors (mimic the effect of dopamine in the brain)
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Is it necessary to taper with dopamine agonists?
yes
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Dopamine agonists adverse effects
- anorexia
- nausea
- vomitting
- vivid dreams
- hallucinations
- delusions
- dyskinesias
- dry mouth
- constipation
- insomnia
- "sleep attacks"
- impulse control symptoms
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Dopamine agonists drug interactions
- dopamine antagonists (phenothiazines, butyrophenones, thioxanthines)
- non-specific MAO inhibitors
- metoclopramide
- ropinirole
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MOA of COMT inhibitors:
reversible inhibitor of COMT, an enzyme responsible to breaking down levodopa in ther peripheral circulation
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Name COMT inhibitiors
- entacapone (Comtan)
- carbidopa/levodopa/entacapone (Stavelo)
- tolcapone (Tasmar)
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T/F: withdrawal may lead to worsening of PD symptoms?
True, tapering may not help
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Common adverse effects of COMT inhibitors:
- nausea, diarrhea, dyskinesia, orthostatic hypotension
- tolcapone: excessing dreaming, hallucinations
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What is the black box warning for tolcapone?
risk of potentially fatal, acute fulminant liver failure
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MOA of amantadine (Symmetrel)
- blocks the reuptake of dopamine into presynaptic neurons or increases dopamine release from presnaptic fibers
- smoothing out the fluctuations in movement
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adverse effects of amantadine
- agitation
- anxiety
- nausea
- dizziness
- insomnia
- ****experience a fall-off effectiveness after a few months****
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Name some anticholinergics used in PD and their MOA
- benztropine (Congentin)
- trihexyphenidyl (Artane)
tend to diminish the characteristic tremor associated with PD
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MOA of bromocriptine
directly stimulates dopamine receptors
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name some treatment strategies for PD
- -early symptomatic therapy to preserve activity level
- -no evidence that early medical therapy accelerated disease progression
- -continuous dopaminergic stimulation may avoid long-term motor fluctuations
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T/F: Patients with younger onset of PD symptoms are probably at increased risk of the development of motor fluctuations due to dopamine
true
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Treatment strategies for motor fluctuations:
- more frequent, smaller doses of levodopa
- use of longer-acting levodopa
- addition of dopamine agonist
- COMT inhibitors
- MAO-B inhibitors
- use of amantadine
- deep brain stimulation
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Tremor vs. dyskinesia: which has a rhythmic oscillation?
tremor
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tremor vs. dyskinesia: which could indicate a medication dose increase is needed?
tremor
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tremor vs. dyskinesia: which is jerky and not rhythmic?
dyskinesia
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tremor vs. dyskinesia: which could indicate a dose decrease is needed?
dyskinesia
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What are preferred treatments for tremor?
- amantadine
- anticholinergics
- may be used with or without levodopa
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name some non-motor symptoms
- depression
- psychosis
- dementia
- constipation
- dry mouth
- exercise
- weight loss
- sleep disorders
- emotional changes
- difficulty with swallowing/chewing
- speech changes
- muscle cramps/dystonias
- ED
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Tx of depressoin from PD
- amitriptyline
- clozapine (Clozaril) highest level of evidence
- quetiapine (Seroquel)
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Tx of dementia with PD
- Donepezil (Aricept)
- rivastigmine (Exelon)
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Tx for constipation in PD
- increase fiber
- increase fluid intake
- polyethylene glucol
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Tx of dry mouth with PD
- chewing gum, hard candy
- fluids
- regular dental visits
- good oral hygeine
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sleep disorders in PD
- restless sleep
- REM behavior disorder
- difficulty staying asleep at night
- nightmares and emotional dreams
- sdden sleep onset during the day
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tx of ED in PD
sildenafil
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