Neurocognitive 2 - Parkinsons + Flashcards

1
Q

Parkinson’s disease

A

syndrome of resting tremor, rigidity, bradykinesia, postural instability

degeneration of dopaminergic neurons in basal ganglia

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2
Q

basal ganglia components

A

“middle manager”

composed of substantial migrant, striatum, gobs pallid us, subthalamic nucleus, thalamus

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3
Q

basal ganglia function

A

control and regulate activity of motor and premotor cortical ares so that voluntary movements are smooth

INHIBIT number of motor systems

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4
Q

Parkinson’s patho

A

loss of dopaminergic neurons in substantia nigra

loss of excitatory input from thalamus to cerebral cortex

increased inhibition to cerebral cortex form other nuclei in basal ganglia

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5
Q

etiologies of Parkinson’s

A

genetic (10%) - suspect if <50 @ diagnosis

environmental risk factors (rural environment, exposure to pesticides, well water)

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6
Q

Parkinson’s disease epidemiology

A

more common in older individuals, men > women

mc in white boys

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7
Q

Parkinson’s disease presentation

A

MC INITIAL IS RESTING asymmetric TREMOR of finger/thumb

rigidity, bradykinesia, postural instability, dystonia

general decreased dexterity

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8
Q

rigidity in PD

A

stiff limbs, poor mobilization of face

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9
Q

bradykinesia in PD

A

slowed movement BUT muscle strength is NOT weak on exam

facial (decreased blinking, drooling)

truncal (difficulty turning in bed, worse in small areas)

UE (micrographia)

LE (scuffing/dragging of feet)

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10
Q

dystonia

A

foot inversion or dorsiflexion

adduction of arm and Hand causing it to rest

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11
Q

other presenting symptoms of PD

A

decreased arm swing

soft voice, monotone, less distinct

decreased sense of smell

sleep disturbances

symptoms of autonomic dysfunction

weakness/malaise

depression or anhedonia

slowness in thinking/major neurocognitive dysfunction

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12
Q

cardinal signs of PD

A
  1. resting tremor (goes away with movement!!!)
  2. rigidity (resistance to moving wrist)
  3. Bradykinesia
  4. postural instability
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13
Q

dementia of PD

A

executive functioning, short term memory and visuospatial ability impaired

typically doesn’t occur right away (>1 yr following diagnosis)

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14
Q

making PD diagnosis

A

if pt presents with tremor = no workup

lack of tremor = imaging and lab work (will be normal)

MUST asses for depression (@ diagnosis and periodically)

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15
Q

meds used in PD tx

A

levodopa
MAO-B inhibitors
dopamina agonists

typically good for 4-6 yrs

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16
Q

drug class that will WORSEN PD symptoms

A

deplete central dopamine

antipsychotics, prochlorperazine, Reglan

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17
Q

levodopa/carbidopa

A

L = metabolic precursor of dopamine, but if given alone causes n/v

c= inhibits systemic breakdown of levodopa so more effective in CNS, can’t cross BBB

18
Q

levodopa/carbidopa ADRs + brand

A

orthostatic HoTN, syncope, dizziness, anorexia, n/v, confusion, dark urine

Sinemet

19
Q

why do we delay levodopa/carbidopa

A

delay use = delay onset of motor fluctuations

these are when pts wear off the med and have to continually increase dose to sustain normal function

20
Q

MAOIs used in PD

A

Selegiline (Eldepryl/Zelapar)

Rasagiline (Azilect)

21
Q

MAOIs use and Moa

A

initial or add on tx (can delay motor fluctuations)

block degradation of dopamine, extend action of L-Dopa

22
Q

MAOIs drug facts (ADRs_

A

excellent profiles, improved long term outcomes

nausea, confusion, hallucinations, HA, bitterness, orthostasis

23
Q

what meds are not good mixed w/ MAOIs

A

antidepressants, pain meds, cold and weight loss meds

esp. dextromethorphan, tramadol, methadone

24
Q

dopamine agonists used inPD

A

Ropinirole (Requip)

Pramipexole (Mirapex)

25
Q

dopamine agonists MOA

A

stimulate dopamine receptors in striatum

mono therapy in early dz or add on therapy in later PD

26
Q

why aren’t dopamine agonists mainstay of tx

A

cause increased ADRS such as somnolence, sudden onset sleep, halucinations, edema, impure control disorder

27
Q

amantadine

A

symmetrel

antiviral drug that has beneficial effects on PD thru mechanisms unknown

improves symptoms in mildly affected pts reduces motor fluctuations and dyskinesias in pts with advanced dz

28
Q

ADRs of amantadine and symmetrel

A
confusion 
hallucinations 
nausea 
HA
dizziness 
insomnia 
lived reticulars 
peripheral edema 
anticholinergics
29
Q

anticholinergics in PD

A

Benztropine mesylate (cognentin)

Trigexyphenidyl (artane)

benefit for tremor in 50% of pts, don’t improve bradykinesia or rigidity

avoid in pts > 70

30
Q

anti cholinergic side effects

A
dry mouth 
blurred vision
constipation
cognitive impairment 
hallucinations 
urinary retention
31
Q

Later stages of PD

A

over time, levodopa stops working (have to add on other medications or increase does)

will get peak dose dyskinesia

32
Q

COMT inhibitors

A

Catechol o methy transferase inhibitor

inhibits metabolism of dopamine so longer effects

may cause liver failure, removed from markets

33
Q

COMT inhibitors used in PD

A

entacapone (Comtan)

Carbidopa/levodopa.entacapone (Stalevo)

tolcapone (tasmar)

34
Q

surgical PD tx

A

create lesions in overactive part of brain to improve symptoms

can also implant DBS into a patient

35
Q

parkinsonian plus syndrome is suspected when

A

poor response to therapy with L dopa in patient who displays Parkinson’s syndrome

36
Q

Normal Pressure hydrocephalus

A

buildup of too much CSF in cranium when patient does not reabsorb CSF adequately or overproduce CSF

37
Q

NPH results in

A

transiently high pressure ad compression of brain and spinal cord

causing edema of brain

38
Q

NPH pathophys

A

enlarging ventricles to relieve pressure = shrinkage of brain parenchyma

may be 2/2 SAH, tumor, meningitis, head injury

39
Q

classic NPH symptoms

A
  1. abnormal gait (earliest, responds to tx)
  2. urinary incontinence
  3. dementia
40
Q

diagnosis of NPH

A

labs are normal

CT/MRI will show ventricular enlargement out of proportion to sulcus atrophy

41
Q

NPH tx

A

VP shunt to drain CSF from ventricle into the abdomen to be absorbed

risk of pump dysfunction and infection