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Parkinson's Disease Flashcards

1
Q

What is Parkinson’s Disease?

A

a progressive degenerative disease caused by death of dopaminergic neurons primarily in the substantia nigra pars compacta

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2
Q

What does PD actually begin with?

A

loss of noradrenergic input into the dorsal motor nucleus of X
loss of noradrenergic neurons of the locus coeruleus

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3
Q

What is seen in the SNc with normal aging?

A

a loss of dopaminergic neurons (50% decrease ages 20-60)

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4
Q

Besides the SNc, what is another area that experiences a decline in DA?

A

mesolimbic system.

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5
Q

What is the mesolimbic system?

A

it includes projections from the ventral tegmental area to the amygdyla,
nucleus accumbens,
prefrontal cortex,
and hippocampus via medial forebrain bundle (MFB)

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6
Q

With continued development of Parkinson’s, there is a continued decline and loss of connections within the PFC, limbic cortex, and hippocampus. what symptoms does this cause?

A

loss of cognitive skills
memory loss
higher associative cognitive functioning

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7
Q

What are cardinal signs of Parkinsons?

A
  • resting tremor
  • bradykinesia
  • rigidity
  • postural instability
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8
Q

What is resting tremor characterized by?

A

4-6 Hz resting “pill rolling” tremor which begins in peripheral extremities but progresses proximally

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9
Q

What are the 3 components of bradykinesia?

A

Hypokinesia
Bradykinesia
Akinesia

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10
Q

Hypokinesia?

A

paucity of movement

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11
Q

Bradykinesia?

A

slow movement

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12
Q

Akinesia

A

problem initiating movement

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13
Q

What is rigidity?

A

increased muscle tone and resistance to movement

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14
Q

What are the two types of rigidity common in PD?

A

Lead pipe- continuous rigidity making joints stiff

Cog-wheel- interposition of rigidity and breaking of rigidity when limbs are passively moved

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15
Q

What is postural instability in PD?

A

slowing of postural reflexes.

posture and rigidity make pt more unstable and increased risk of falling

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16
Q

What are the gait abnormalities associated with PD?

A

slow shuffle
no arm swing
retropulsion (stepping backward)
festinating gait (rapid short steps)

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17
Q

2 other S/S with PD?

A

Dysarthria and dysphagia

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18
Q

What are 6 nonmotor impairments common in PD?

A
  • cognitive decline (up to 80%)
  • postural hypotension
  • hallucinations
  • autonomic changes
  • fatigue and sleepiness
  • pain
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19
Q

in most cases there is no known cause of the degeneration of DA neurons, but some cases might have what involved?

A

environmental or genetic causes

20
Q

What are a few pharmacological management approaches to PD?

A
  • replacement therapy
  • dopamine agonists
  • blocking enzymatic breakdown of DA
  • anticholinergic interventions
21
Q

What is used in replacement therapy for PD?

A

Levodopa (L-Dopa)
Levorotatory 3, 4 dihydroxyphenylanaline
(metabolic precursor to DA because it cannot cross BBB)

22
Q

Why is L-Dopa rapidly metabolized peripherally? how can we fix this?

A

because there are a large # of DA neurons in the gut area.

typically co administered with carbidopa

23
Q

what is carbidopa?

A

blocker of DOPA decarboxylase

24
Q

What is the combination of carbidopa and L-Dopa called?

25
What does the use of L-Dopa require?
intact DA neurons (therefore with the progression of the disease, L-Dopa becomes less effective because it might have intact dopaminergic neurons,
26
What might pts on L-Dopa experience?
On-Off sudden shifts of symptoms late in therapy
27
How do we get extension of the action of L-DOPA?
sustained release Sinemet-CR
28
What symptom could be caused by an effect of dosing of L-DOPA and the rapid metabolism of it?
considerable dyskinesias
29
Why might L-DOPA accelerate DA neuron cell death?
increased free radicals or metabolic stress. | this is why some neurologists might suggest shifting medications
30
What are some advantages of DA receptor agonists rather than L-Dopa?
- no requirement for DA neurons, so there longer effect over the course of the disease - slower rate of metabolism (longer half life effectiveness) - more selective action (D1 or D2) - less dyskinesias - not accelerate SNC cell death
31
What are adverse reactions of DA agnoists and L- DOPA?
dyskinesias- choreoform movements abnormal thinking- hold onto false beliefs hallucinations addictive behaviours constipation - due to action on DA neurons of enteric nervous system
32
What is used for PD that is inhibiting the DA metabolism?
Monoamine oxidase inhibitors (MAOI) | Catechol-O-methyl transferase inhibitors (COMT)
33
What is one of the oldest therapies for PD?
anticholinergic agents (before L-DOPA
34
Why would blocking muscarinic receptors reduce PD symptoms?
because there is a large # of cholinergic striatal interneurons and PPN afferents to the substantia nigra
35
What is wrong with anticholinergic agents?
strong autonomic adverse reaction
36
What is amantadine?
used for PD | antiviral that may also effect catecholamine pathways
37
Why would anti depressants be used in pts with PD?
other than MAOI, probably have no direct effect per se but used for depression symptoms
38
why are newer NMDA receptor antagonists being used?
slow cell degeneration (apoptosis)
39
What is a surgical approach for PD?
pallidotomy- lesion of the GPi. use stereotaxic device to localize GP and stabilize pt.
40
what does a pallidotomy do?
reduces tremor and rigidity but not other symtpoms
41
What is a ventrolateral thalamotomy?
lesion of the VL nucleus
42
What is deep brain stimulation?
involves the implantation of leads to different brain regions along with implanted pacemaker unit
43
What does the deep brain stimulator target?
thalamus, subthalamus, GPi
44
Which intervention does the PD pt show remarkable improvement?
deep brain stimulation | improve in tremor and other symptoms (but sometimes there are behavioral adverse reactions)
45
What is fetal nigral ttransplation?
adverse reactions noted in young pts.

Neuroanatomy (14 decks)

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