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
dopamine agonists MOA
stimulate dopamine receptors in striatum mono therapy in early dz or add on therapy in later PD
26
why aren't dopamine agonists mainstay of tx
cause increased ADRS such as somnolence, sudden onset sleep, halucinations, edema, impure control disorder
27
amantadine
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
ADRs of amantadine and symmetrel
``` confusion hallucinations nausea HA dizziness insomnia lived reticulars peripheral edema anticholinergics ```
29
anticholinergics in PD
Benztropine mesylate (cognentin) Trigexyphenidyl (artane) benefit for tremor in 50% of pts, don't improve bradykinesia or rigidity avoid in pts > 70
30
anti cholinergic side effects
``` dry mouth blurred vision constipation cognitive impairment hallucinations urinary retention ```
31
Later stages of PD
over time, levodopa stops working (have to add on other medications or increase does) will get peak dose dyskinesia
32
COMT inhibitors
Catechol o methy transferase inhibitor inhibits metabolism of dopamine so longer effects may cause liver failure, removed from markets
33
COMT inhibitors used in PD
entacapone (Comtan) Carbidopa/levodopa.entacapone (Stalevo) tolcapone (tasmar)
34
surgical PD tx
create lesions in overactive part of brain to improve symptoms can also implant DBS into a patient
35
parkinsonian plus syndrome is suspected when
poor response to therapy with L dopa in patient who displays Parkinson's syndrome
36
Normal Pressure hydrocephalus
buildup of too much CSF in cranium when patient does not reabsorb CSF adequately or overproduce CSF
37
NPH results in
transiently high pressure ad compression of brain and spinal cord causing edema of brain
38
NPH pathophys
enlarging ventricles to relieve pressure = shrinkage of brain parenchyma may be 2/2 SAH, tumor, meningitis, head injury
39
classic NPH symptoms
1. abnormal gait (earliest, responds to tx) 2. urinary incontinence 3. dementia
40
diagnosis of NPH
labs are normal CT/MRI will show ventricular enlargement out of proportion to sulcus atrophy
41
NPH tx
VP shunt to drain CSF from ventricle into the abdomen to be absorbed risk of pump dysfunction and infection