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Parkinson's Disease Flashcards

1
Q

What is Parkinson’s disease?

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2
Q

Why is PD often left undiagnosed & untreated?

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3
Q

Outline some PD statistics.

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4
Q

What are the four cardinal signs and symptoms of PD?

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5
Q

Outline the characteristic problems of PD.

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6
Q

Outline the epidemiology of PD

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7
Q

Parkinson’s disease is a result of…

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8
Q

What is the Substantia Nigra?

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9
Q

Why is it called the Substantia Nigra?

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10
Q

What are the two parts of the substantia nigra & their function?

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11
Q

What is the function of the Nigrostriatal pathway?

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12
Q

What is the function of the Putamen and Caudate nuclei?

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13
Q

What are the two types of medium-sized spiny GABAergic neurons?

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14
Q

What does the imbalance of the motor circuitry mean?

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15
Q

Why & how are Lewy bodies important in PD?/

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16
Q

Outline PET imaging techniques for PD.

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17
Q

Explain the pathophysiology of PD.

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18
Q

Outline the normal dopamine pathway vs PD dopamine pathway

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19
Q

Why is an abnormal protein build-up a problem in PD?

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20
Q

Describe the progression of neurofunction loss in neurodegenerative disorders

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21
Q

Pathophysiology of PD: Degeneration of Nigrostriatal Pathway

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22
Q

How do we diagnose PD? /Steps?

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23
Q

What are the motor signs and symptoms of PD?

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24
Q

What are the nonmotor signs and symptoms of PD?

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25
State the differential diagnosis of PD.
26
What is the Gold Standard of treatment?
27
What is the therapeutic challenge for L-DOPA?
28
What are the symptoms reduced by Levodopa?
29
Why is Levodopa effective at eliminating postural instability & shuffling gait?
30
What are the problems of Levodopa?
31
Outline the MOA of Levodopa?
32
What is the difference between noradrenergic and dopaminergic neurons?
33
What happens if we have more dopa decarboxylase?
34
Why is L-DOPA the cornerstone of PD therapy?
35
What are the two forms of L-DOPA?
36
Sinemet/Co-careldopa
37
Madopar/Co-beneldopa
38
Why is L-DOPA used alongside peripheral dopa decarboxylase inhibitors?
39
What are some additional issues with L-DOPA?
40
What should Pharmacists do if patients develop an impulse control disorder?
41
What is the current challenge in the treatment of PD?
42
How does levodopa therapy reduce morbidity/mortality in PD?
43
Describe the progress in the Pharmacotherapy of the symptoms of PD
44
What are the two types of dopamine agonists?
45
MOA of COMT Inhibitors?
46
MOA of MAO-B inhibitors?
47
How do these PD drugs work/site of action?
48
What are the main features of Dopamine agonists?
49
What are the Side effects of Dopamine agonists?
50
Give examples of Dopamine agonists/synthetic dopamine
51
What is the main issue with Dopamine agonists?
52
Outline Ergot agonist dosing examples
53
Outline Non-ergot agonist dosing examples
54
What are the two types of Monoamine oxidase?
55
MAO-A
56
MAO-B
57
- What is the role of Monoamine oxidase?
58
What are the features of Catechol-O-Methyl transferase (COMT)
59
How does Entacapone improve L-DOPA pharmacokinetics and Efficacy?
60
What is the effect of combing L-DOPA with Entacapone?
61
What is the effect of Entacapone on L-DOPA availability in the brain?
62
What are the problems with current treatment strategies?
63
What are the most important motor complications for Parkinson’s disease treatment?
64
Give examples of Antiparkinsonian agents used to treat motor fluctuations.
65
Why are there symptoms of re-emergence when Levodopa plasma levels fall?
66
What is Levodopa-induced dyskinesia?
67
What drug can control Levodopa-induced dyskinesia?
68
Features of Amantadine
69
What are the side effects of Amantadine?
70
Livedo reticularis
71
What are other problems with Amantadine?
72
Why is PD described as a multi-system disease?
73
What are the neuropsychiatric problems in PD?
74
What are the non-motor symptoms in PD?
75
How do non-motor symptoms help to identify motor symptoms?
76
Medication profile for PD drugs

ATI1 (20 decks)

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