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Neuro Pharmacology > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

How common is PD?

A 
1. 2nd most common neurodegenerative disease. 
Prevalence increases w/ age
-1% of people older than 65
-2.5% of people older than 80 
-2:1 male to female ratio
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2
Q

What is the average age of onset for Parkinson’s

A

57

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3
Q

What is the etiology of Parkinson’s?

A

90% idopathic

10% Genetic

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4
Q

What are environmental positive risk factors for PD?

A
  1. Neurotoxin exposure
  2. Developmental exposure to pesticides
  3. Traumatic Brain injury.
  4. Latrogenic
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5
Q

What is drug-induce Parkinsonian syndrome caused by?

A
  1. DA receptor antagonists, no loss of DA just blocking of receptors that causes symptoms.
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6
Q

What has been shown to be protective against PD?

A
  1. Tobacco smoking (wtf)
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7
Q

What is the pathology of PD?

A
  1. Depigmentation of the Pars Compacta region of the Substantia Nigra associated w/ loss of DA producing neurons.
  2. Alpha Synuclein Dysregulation
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8
Q

When does PD occur per the clinical definition?

A
  1. Until about 70-80% of nigral DA levels are lost.
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9
Q

What is Alpha Syncuclein?

A

Involved w/ the formation of cortical and nigral lewy bodies.

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10
Q

Is PD a pre-synaptic or post-synaptic problem?

A

PRE-synaptic

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11
Q

What is the progression of PD?

A
  1. Pre-clinical (5years*)
  2. Honey-moon period (3 years)
  3. Wearing off (3-5 years motor complications)
  4. On-Off Dyskinesia (5-10 years)
  5. Levodopa Resistant symptoms/Cognitive Decline (10-20yrs+)
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12
Q

How is PD diagnosed?

A
  1. Resting Temor
  2. Cogwheel Rigidity
  3. Bradykinesia
  4. Postural Instability
  5. “pill rolling”
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13
Q

What is PD treated with?

A

Muscarinic Antagonists that cross the BBB b/c resting tremors seem to be a problem w/ muscarinic receptors.

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14
Q

What are two additional motor symptoms of PD that could be used as a diagnostic tool?

A
  1. Hypophonia (soft speaking voice)

2. Dysarthria (unclear pronunciation)

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15
Q

What are other motor symptoms involved in PD?

A
  1. Dysphagia
  2. Less desterity
  3. Difficulty arising from seat.
  4. Diminished arm swing during ambulation
  5. Festinating Gait
  6. “freezing” at movement initiation
  7. Hypomimia
  8. “mask” like facial features.
  9. Micrographia
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16
Q

What are the Autonomic and Sensory symptoms of PD?

A
  1. Fatigue
  2. Olfactory Disturbances
  3. Increased pain sensitivity
  4. Paresthesia
  5. Seborrhea
  6. Sexual dysfunction
  7. Mixed sympathetic/Parasympathetic effects.
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17
Q

What are Cognitive impairment symptoms of PD?

A
  1. Typically late onset
  2. Frontal cortex and other subcortical regions are thought to be involved.
  3. General mental slowness, lack of initiative, forgetfullness, visuospatial deficits, decreased executive functioning.
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18
Q

What are psychiatric symptoms of PD?

A
  1. Depression and Anxiety
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19
Q

What kind of therapy do PD patients require?

A

Extensive physical and speech therapy.

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20
Q

What are the goals of Pharmacotherapy for PD?

A
  1. Preservation of function & ability to perform activities.
  2. Improvement in mobility w/ minimal ADR’s.
  3. Improvement of non-motor symptoms.
  4. Delay Progression?
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21
Q

What are the Pharmacological Strategies in PD?

A
  1. Dopamine Replacement Therapy (L-DOPA)
  2. Direct acting DA receptor agonists
  3. Reduce the rate of DA catabolism
  4. Anti-Cholinergics (muscarinic antagonists)
  5. Amantadine (Symmetrel)
22
Q

How is Dopamine Replacement Therapy done?

A
  1. L-DOPA
    - Precursor to DA, DA does not cross the BBB, and only about 5% of L-DOPA crosses the BBB.
    - Oral Administration
    - Short t1/2 lead to “wearing off” Dose escalation req.
    - Typically used in combo w/ Carbidopa
    - 25/100 (25mg Carbidopa/100mg L-dopa) TID
23
Q

What does Carbidopa do?

A

Inhibit DD.

24
Q

What is Sinemet?

A

Regular & Controlled release CR

25
Q

What is Paropa?

A

Oral disintegrating formulation of L-DOPA.

26
Q

What are L-Dopa Enhancement Strategies?

A
  1. Prolong, and/ or enhance L-DOPA actions.
  2. Periphery
  3. CNS (Striatum)
27
Q

What strategies are used to enhance L-DOPA in the periphery?

A
  1. Entacapone/Tolcapone block COMT (L-DOPA to 3-O-MD)

2. Carbidopa blocks AADC (L-DOPA to DA)

28
Q

What strategies are used to enhance L-DOPA in the CNS?

A
  1. Selegiline (low dose)/Rasagiline Block MAO-B (DA to DOPAC)
  2. Tolcapone Blocks COMT (DA to 3MT)
29
Q

What is Selegiline (eldepryl)?

A

MAO-B inhibitor

-Orally disintegrating Selegiline (Zelpar)

30
Q

What are the COMT inhibitors (used w/ L-DOPA)?

A
  1. Tolcapone –> Risk for fatal hepatotoxicity
  2. Entacapone –> short half life
  3. Stalevo –> L-DOPA , Carbidopa, and Entacapone.
31
Q

What are the shortcomings of L-DOPA therapy?

A
  1. Peripheral catabolism by COMT
  2. ADRs
  3. Tolerance develops to movement improvements.
  4. Catabolism of DA increases the production of free radicals.
32
Q

What are the ADRs of L-DOPA?

A
  1. Nausea, Hallucianations, Insomnia, vivid dreams, postural hypotension.
33
Q

What are Non-Ergot D2 DA receptor agonists?

A
  1. Pramipexole
  2. Apomorphine
  3. Ropinirole
  4. Rotigotine
34
Q

What happens when Non-Ergot D2 DA receptor agonists are used as monotherapies?

A
  1. associated w/ much lower risk of developing motor complications compared to L-DOPA.

Preferred in younger people.

35
Q

Why is L-DOPA/Carbidopa preferred in older patients?

A
  1. Older people seem to suffer more from cognitive problems and hallucinations.
36
Q

What are the ADR’s of Non-Ergot D2 receptor agonists?

A
  1. Nausea, Hallucinations, Confusion, HA, Edema, sedation, Orthostatic Hypotension, Daytime sleepiness, “sleep attacks”, vivid dreaming.
37
Q

What is a concern w/ Non-ergot D2 receptor agonists?

A
  1. Gambling and other risk-taking behavior.
38
Q

What do Non-Ergot D2 Receptor Agonists not do?

A
  1. Dont Alter course of disease

2. Do NOT improve non-motor aspects of the disease.

39
Q

What are Ergot-Based D2 DA receptor Agonists obtained from?

A

The fungus “Claviceps Purpurea”

40
Q

What are the 3 Ergot-Based D2 receptor agonists?

A
  1. Bromocriptine
  2. Pergolide
  3. Cabergoline
41
Q

What is the efficacy of Ergot-Based D2 receptor agonists?

A
  1. Similar efficacy as non-ergot based, but more severe ADR’s and require special monitoring due to increased incidence of Cardiac Valvular Fibrosis.
42
Q

What are examples of M1 Muscarinic Receptor Antagonists?

A
  1. Benztropine (Cogentin)

2. Trihexyphenidyl

43
Q

Why are M1 muscarinic receptor antagonists used?

A
  1. DA tonically inhibits striatal ACh release
  2. Following death of DA neurons in the SN, there is increased striatal ACh release, which is thought to underline increased resting tremor in PD.
44
Q

How are M1 Muscarinic Receptor Antagonists used?

A

Adjuctively

45
Q

What are the ADR’s and Contraindications of M1 muscarinic receptor antagonists?

A

BLOCK 1

46
Q

What problems do Muscarinic Antagonists cause?

A

Cognitive Problems

47
Q

What is Amantadine?

A

NMDA antagonist

  • Originally anti-viral
  • Good approach for new patients w/ mild symptoms.
48
Q

What is the MOA of Amantadine?

A

Mixed Pharmacological Actions:

  • Enhances Presynaptic DA release
  • Blocks DAT
  • Some Anti-cholinergic properties.
49
Q

What risk is lowered with use of Amantadine?

A
  1. Development of dyskinesias compared to DA enhancing strategies.
50
Q

What are some Non-Pharmacological Approaches in PD?

A
  1. Deep brain stimulation in the Subthalmaic Nucleus.
    - Activating pathway
  2. Surgical Options
    - Pallidotomy, Thalamotomy, Subthalamotomy.
51
Q

What is GDNF?

A
  1. DA neuron growth factor.
  2. Which is selective and is infused into the striatum and goes through retrograde transport to the substantia nigra to have beneficial effect.
  3. most effort is to trick BBB to accept.
  4. Caffeine is an adenosine a2a antagonist.

Neuro Pharmacology (9 decks)

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