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
Q

State the differential diagnosis of PD.

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26
Q

What is the Gold Standard of treatment?

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27
Q

What is the therapeutic challenge for L-DOPA?

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28
Q

What are the symptoms reduced by Levodopa?

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29
Q

Why is Levodopa effective at eliminating postural instability & shuffling gait?

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30
Q

What are the problems of Levodopa?

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31
Q

Outline the MOA of Levodopa?

32
Q

What is the difference between noradrenergic and dopaminergic neurons?

33
Q

What happens if we have more dopa decarboxylase?

34
Q

Why is L-DOPA the cornerstone of PD therapy?

35
Q

What are the two forms of L-DOPA?

36
Q

Sinemet/Co-careldopa

37
Q

Madopar/Co-beneldopa

38
Q

Why is L-DOPA used alongside peripheral dopa decarboxylase inhibitors?

39
Q

What are some additional issues with L-DOPA?

40
Q

What should Pharmacists do if patients develop an impulse control disorder?

41
Q

What is the current challenge in the treatment of PD?

42
Q

How does levodopa therapy reduce morbidity/mortality in PD?

43
Q

Describe the progress in the Pharmacotherapy of the symptoms of PD

44
Q

What are the two types of dopamine agonists?

45
Q

MOA of COMT Inhibitors?

46
Q

MOA of MAO-B inhibitors?

47
Q

How do these PD drugs work/site of action?

48
Q

What are the main features of Dopamine agonists?

49
Q

What are the Side effects of Dopamine agonists?

50
Q

Give examples of Dopamine agonists/synthetic dopamine

51
Q

What is the main issue with Dopamine agonists?

52
Q

Outline Ergot agonist dosing examples

53
Q

Outline Non-ergot agonist dosing examples

54
Q

What are the two types of Monoamine oxidase?

55
Q

MAO-A

56
Q

MAO-B

57
Q
  • What is the role of Monoamine oxidase?
58
Q

What are the features of Catechol-O-Methyl transferase (COMT)

59
Q

How does Entacapone improve L-DOPA pharmacokinetics and Efficacy?

60
Q

What is the effect of combing L-DOPA with Entacapone?

61
Q

What is the effect of Entacapone on L-DOPA availability in the brain?

62
Q

What are the problems with current treatment strategies?

63
Q

What are the most important motor complications for Parkinson’s disease treatment?

64
Q

Give examples of Antiparkinsonian agents used to treat motor fluctuations.

65
Q

Why are there symptoms of re-emergence when Levodopa plasma levels fall?

66
Q

What is Levodopa-induced dyskinesia?

67
Q

What drug can control Levodopa-induced dyskinesia?

68
Q

Features of Amantadine

69
Q

What are the side effects of Amantadine?

70
Q

Livedo reticularis

71
Q

What are other problems with Amantadine?

72
Q

Why is PD described as a multi-system disease?

73
Q

What are the neuropsychiatric problems in PD?

74
Q

What are the non-motor symptoms in PD?

75
Q

How do non-motor symptoms help to identify motor symptoms?

76
Q

Medication profile for PD drugs