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Patho > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

0
Q

Describe what happens in the substantia nigra neurons

A
  • Tyrosine is HYDROXYLATED to become L-dopa
  • L-dopa is decarboxylated to become dopamine
  • Dopamine is packaged into vesicles
  • Ca2+ influx stimulates the exocytosis of the vesicles
  • DA crosses the cleft and goes to the putamen neurons in the striatum
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1
Q

Descibe the epidemiology of parkinson’s disease.

A
  • 4 million people affected worldwide
  • incidence increases with age (around 60)
  • affects males to females 2:1
  • development of IPD inversely related with smoking and caffeine consumption
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2
Q

What signals the Ca2+ channels to open?

A
  • the arrival of the AP to the presynaptic terminal

- influx causes the release of the NTs (Dopamine)

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3
Q

What is the basal ganglia composed of?

What does it control?

A

Composed of:

  • substantia nigra
  • striatum
  • subthalamic nucleus

The basal ganglia controls complex motor movements and plays a part in motor learning

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4
Q

Where is the substantia nigra located?

What is its role?

A
  • located in the midbrain

- important role in reward, addiction and movement

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5
Q

What is the striatum composed of?
Where is it located?
Name its receptors.

A
  • putamen neurons
  • located below the cortex of cerebrum
  • D1 and D2 neuron
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6
Q

What does VLT stand for?
What is its role?
What is its mechanism?

A
  • Ventrolateral thalamus
  • role is to control the motor cortex for movement
  • DA stimulates putamen neurons, PNs then act on the VLT to produce movement
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7
Q

What happens in the motor cortex?

A
  • input signals are converted to output which produces movement
  • located in frontal cortex of brain
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8
Q

Why does smoking help with Parkinson’s?

A

because it releases DA

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9
Q

What brain functions involve DA?

A
  • reward
  • voluntary movement
  • motivation
  • cognition
  • learning
  • mood
  • attention
  • sleep
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10
Q

How is DA related to Parkinson’s?

A

A parkinson’s pt has insufficient DA, which leads to loss of the ability to execute smooth controlled movements

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11
Q

Parkinson’s disease manifests when _______ of DA function has been lost.

A

~ 80%

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12
Q

Ach is excitatory, DA is inhbitory.

Thus, this makes these NTs ______________ ______________.

A

antagonistic neurotransmitters

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13
Q

What happens when there is an excess of Ach?

A
  • overactivity of cholinergic neurons
  • muscles contract
  • due to decreasing levels of Ach, muscles stay contracted
  • pt becomes “locked in stone”
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14
Q

In normal motor systems, how is GABA release regulated?

A

By the binding of DA to receptors

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15
Q

How does a decrease in DA levels affect GABA?

A
  • Decreased DA increases GABA
  • too much GABA doesn’t allow the VLT to be stimulated
  • no movement
  • pt becomes partially or totally paralyzed
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16
Q

What receptor does DA bind to on the direct movement pathway?

A

D1 on putamen neurons

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17
Q

What happens in a normal pt when DA binds the the D1 receptor?

A
  • causes an initial increase in GABA, putamen neurons can’t fire
  • since PNs produce GABA, levels will decrease
  • less inhibition to VLT
  • body movement
18
Q

What happens to the direct pathway in PD pts?

A
  • insufficient DA
  • DA doesn’t bind to D1 receptors
  • GABA will decrease
  • Firing of D1 neurons increases
  • D1 neurons release GABA, less VLT transmission to motor cortex
19
Q

What is IPD?

What is its etiology?

A
  • idiopathic Parkinson’s disease
  • AKA primary PD
  • caused by the degeneration of DA in the substantia nigra

Genetics factors
Oxidative Stress
- free radicals generated from DA metabolism
- lack of antioxidant defense
Excitotoxicity
- nerve cells are damaged or killed due to excess glutamate
- DA not present to inhibit glutaminergic stimulation

20
Q

What is secondary PD?

Causes?

A
  • inability to produce DA
  • inability to secrete DA
  • inability of DA to bind to receptors on putamen neurons
  • drugs
  • toxins
  • infections
  • head trauma
21
Q

Describe the mechanism of drug-induced PD.

A
  • certain drugs are DA antagonists
  • they block DA receptors and output from the substantia nigra
  • onset is abrupt, sx symmetrical
  • cause Parkinson’s signs (rigidity, hypokinesia, resting tremor)

ex. antipsychotics, CCBs

22
Q

How do CCBs cause drug-induced PD?

A
  • Ca2+ is needed to release the DA vesicles from substantia nigra
  • if blocked, no DA binds to putamen neurons
  • no movement
23
Q

How do toxins contribute to secondary PD?

A
  • pesticides or heavy metals (iron and manganese) can cause irreversible damage to the dopaminergic neurons in the SN
24
Q

How do infections contribute to secondary PD?

A

Post-encephalitic syndrome

  • due to viral illness
  • causes degeneration of the nerve cells in SN
  • follows encephalitis lethargica –> brain inflammation
  • leaves patient speechless and statue-like
25
Q

How does head trauma contribute to secondary PD?

A
  • lesions to SN, striatum causes hematoma
  • ventricular outflow is obstructed –> pressure on the brain
  • lesions and pressure affect dopaminergic cells –> parkinson’s signs
26
Q

What are the primary sx of PD?

A
  • resting tremor
  • hypokinesia
  • cogwheel rigidity
  • postural instability
27
Q

What are the secondary motor sx?

A
  • decreased blink rate
  • hypomimia (reduced facial expression)
  • monotonous speech
  • hurried, slurred speech
  • micrographia
  • drooling
28
Q

What are the autonomic secondary sx?

A
  • uncontrolled sweating
  • drooling
  • lacrimation (tearing)
  • impaired thermal regulation
  • constipation
  • incontinence
  • impotence
  • sexual dysfunction
29
Q

What are the psychological secondary sx?

A
  • dementia (~20% of patients)
  • anxiety
  • depression (endogenous, exogenous)
  • psychosis
  • sleep disturbances
30
Q

What is Huntington’s disease?

A
  • hyperkinetic movement disorders
  • progressive atrophy of indirect pathway and basal ganglia
  • onset 30-50 years
  • sx: fidgets, tics, chorea
31
Q

Why is diagnosing IPD so difficult?

A

because the early stages of IPD resemble sx that occur in the natural aging process

32
Q

How is a diagnosis made for PD?

A
  • clinical examination

- complete medical history to rule out secondary parkinson’s

33
Q

How can you tell the difference between IPD and other types of PD?

A
  • give the pt L-dopa

- IPD pts respond well to L-dopa treatments, other types don’t

34
Q

How is IPD confirmed after death?

A
  • with the presence of Lewy bodies in the substantia nigra
35
Q

What pharmacologic management can be used for PD?

A
  • DA replacement
  • COMT inhibitors
  • MAO-B inhibitors
  • dopamine agonists
  • amantidine
  • anticholinergics
36
Q

Why is levodopa administered instead DA?

A
  • because can’t cross the BBB

- also, DA in the periphery causes serious side effects (nausea, vomiting)

37
Q

Why is COMT inhibitors good for PD?

A
  • increases L-dopa in the blood and CNS

- higher chance of it being converted to DA

38
Q

Are MAO-B inhibitors a good treatment for PD?

A
  • yes, because less DA will be converted in the CNS

- therefore, more DA to be utilized

39
Q

How does amantidine work to help PD?

A

presynaptically:

  • increases release of DA
  • blocks reuptake of DA

postosynaptically:

  • acts directly on receptors
  • up regulates D2 receptors
  • Improves motor fluctuations and tremors
40
Q

Describe the non-pharms for PD.

A
  • education
  • support groups
  • therapies (OT, PT)
  • diet and nutrition
  • deep brain stimulation
41
Q

What are the side effects of DA agonists?

A
  • dyskinesia
  • motor fluctuations
  • hallucinations
  • postural hypotension
  • confusion
  • sleep disorders
  • impulsive behaviors
  • leg edema
42
Q

What are the side effects of anticholinergics?

A
  • urinary retention
  • blurred vision
  • constipation
  • tachycardia
  • confusion
  • memory loss
  • restlessness
  • hallucinations

Patho (15 decks)

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