Parkinson's Disease Flashcards

1
Q

what is parkinsons

A

a progressive, degenerative disorder of the basal ganglia function
- characterized by tremor, rigidity, bradykinesia

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2
Q

what is the basal ganglia

A

function of the cerebellum to make smooth coordinated movements
- part of the basal ganglia is the substantia nigra where dopamine is produced

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3
Q

what is primary parkinson’s disease

A

idiopathic
- genetic and sporadic
* damage to dopamine producing cells*

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4
Q

what is secondary parkinson’s

A

acquired
- infection
- intoxication
- trauma
- drug induced (antiemetics/depressions will interfere with dopamine transmission)
alter production of dopamine

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5
Q

what are the risk factors for parkinson’s

A

age (70s)
more likely men
genetics
anxiety/depression
head trauma
hysterectomy
coffee consumption (protective)

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6
Q

what is dopamine

A

NT that is both inhibitory and excitatory
- in parkinson’s it is inhibitory
- helps muscles work smoothly, controllably, and without unwanted movements
* inhibits unnecessary movement

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7
Q

what is ACh

A

an excitatory NT that works in conjunction with the dopamine system
- prevents unwanted movements
- must be balanced, if one goes up then one must come down

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8
Q

what is the pathogenesis of parkinson’s

A
  • destruction of substantia nigra in basal ganglia
  • dec levels in dopamine
  • imbalance between dopamine and ACh
  • relative excess of ACh
  • loss of controlled movements and balance
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9
Q

what are the clinical manifestations

A
  • bradykinesia (slowness of movements)
  • cog wheel rigidity (stiffness)
  • resting tremor
  • shuffling gait
  • mask like expression
  • postural instability
    *gradual onset and progression, typically one side of body first *
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10
Q

what is the classic triad of manifestations of parkinson’s

A

tremor
rigidity
bradykinesia

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11
Q

what are the characteristics of tremors in parkinson’s

A
  • often first sign
  • affects handwriting
  • more prominent at rest
  • aggravated by stress or concentration
  • pill roll
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12
Q

what are the two types of tremors

A

parkinsons
essential

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13
Q

what is an essential tremor

A

results form faulty neurological impulses w fine motor movements
- occur with motor function
- no other sx of parkinsons

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14
Q

what is the parkinson’s tremor

A

results from a dopamine def
- occur with rest and improve with movements
- other symptoms of parkinsons

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15
Q

what is rigidity

A

resistance to passive movements
- cog wheel rigidity –> movements are jerky and slow
- sustained muscle contractions
- too much ACh
- associated complaints are muscle soreness, aches, pain

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16
Q

what is bradykinesia

A

loss of automatic movements
- no blinks, swinging of arms, swallowing saliva, no self expression with hands and face
–> results in drooling, flat face
overall lack of spontaneous movement

17
Q

what are complications of parkinson’s

A

dementia
depression/anxiety
decreased mobility –> malnutrition, aspiration, pneumonia, UTIs, skin breakdown
drug related complications

18
Q

what are the goals of pharm of parkinsons

A

maintain independence and dec sx that are associated

19
Q

how do parkinson’s drug work

A

correct the imbalance btw dopamine and ACh
- enhance dopamine (dopaminergic) or block ACh (anticholinergic)

20
Q

what is levodopa/carbidopa

A

most effective drug for parkinson’s that is a combo drug

21
Q

what is the moa of levodopa

A

converts dopamine in the brain and activates dopamine receptors

22
Q

what is the moa of carbidopa

A

blocks destruction of levodopa

23
Q

what is the disadvantage of levodopa/carbidopa

A

takes several months to see improvement
does not work long term
- dose eventually wears off so may need shorter dose intervals
- abrupt loss of effect calles the on off phenomenon that can occur at anytime (off periods will inc over time) (can be reduced w drugs and avoid high protein meals)

24
Q

what are the adverse effects of levadopa

A

N/V (give low doses, take w food)
dyskinesias (range from annoying to disabling)
postural hypotension
dysrhythmias
psychosis: hallucinations, nightmares, paranoia
darken sweat and urine
activate malignant melanoma

25
Q

what interactions dec levodopa

A

vit B6
antipsychotics
protein

26
Q

what interactions inc levodopa

A

carbidopa
anticholinergics
MAOi –> can cause toxicity

27
Q

what is a duopa

A

carbidopa-levodopa infusion that can be
- instilled into a feeding tube into the small intestine
- gel form suspension
- continuous infusion for continuous blood levels up to 16 hrs/day

28
Q

why is dopa used

A

for pts who respond to drugs but response fluctuates
- more consistent levels of drug in the body

29
Q

what is important info to know about duopa

A

major drug interactions
- anti htn
- mao i
- antipsychotic
- metoclopramide
- isoniazid
- iron
- vitamins (B6)
- high protein

30
Q

what are the side effects of duopa

A
  • falling asleep without warning
  • orthostatic hypotension
  • hallucinations
  • unusual urges
  • depression
  • dyskinesia
  • side effects related to placement of tube (infection, dislodge)*
31
Q

what is the class of pramipexole

A

dopamine receptor agonist

32
Q

what is the moa of pramipexole

A

binds with D2 receptors –> stimulates dopamine receptors

33
Q

what are the indication for pramipexole

A

mono therapy in early PD (younger pts)
combined with carbidopa-levodopa in advanced PD
restless leg syndrome (inhibits dopamine receptors to block sensation)

34
Q

what are the side effects of pramipexole

A

N
sleep attacks
pathologic gambling and other compulsive behaviors
when combined with levodopa
- orthostatic hypotension.
- dyskinesia
- hallucination risk doubles

35
Q

what is the class of ropinirole

A

dopamine receptor agonist –>idiopathic PD

36
Q

what is the moa of ropinirole

A

unknown
- thought to inc nerve impulses within the substantia nigra

37
Q

what are the effects of ropinirole

A

adverse effects similar to PD drugs
- long term use may be inc risk of DM and acromegaly

38
Q

what are other dopamine agonists

A

ritgotine: daily patch
apomorphine: short acting sub q for fast relief of sx used in the “off” phase