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Pharmacology > Parkinson Drugs > Flashcards

Parkinson Drugs Flashcards

1
Q

What are the signs of Parkisons Dz?

A

Bradykinesia; muscular rigidity; tremors; gait abnormalties; postural instability

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2
Q

What neurotransmitter pathway is affected in PD?

A

Dopaminergic pathway (inhibitory neurons) in the substantial nigra and corpus striatum (neurotransmitter ratio shifts toward the decreased DA and increased Ach)

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3
Q

What does increased levels of DA in the tuberoinfundibular tract lead to?

A

Decreased prolactin levels

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4
Q

What does increased levels of DA in the CTZ lead to?

A

increased emesis

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5
Q

What does increased levels of DA in the mesolimbic-mesocortical tracts lead to?

A

increased psychomotor activity; psychosis; schizophrenia; increased reinforcement

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6
Q

Which DA receptor subtype is implicated in PD?

A

D2 receptor subtype (inhibitory receptor subtype that decreases cyclic adenosine monophosphate [cAMP] levels in corpus striatum

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7
Q

Given the abnormal DA/ACh shift in the striatum, give two pharmacologic strategies in the treatment of PD?

A
  1. Medicaitons that will increase DA levels

2. Medications that will increase Ach

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8
Q

Do anti-parkinson meds effect pathology, symptoms or both?

A

symptoms

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9
Q

Name 2 antimuscarinic medications that are used in the treatment of PD:

A
  1. Benztropine

2. Trihexyphenidyl

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10
Q

Is benzodiazepine more or less lipid soluble than atropine?

A

More lipid soluble (therefore greater CNS penetration)

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11
Q

Which characteristic of PD is not affected by anticholinergics?

A

Bradykinesia

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12
Q

Is benzotropine useful in the treatment of tar dive dyskinesia?

A

No, it may actually exacerbate tar dive dyskinesia

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13
Q

What are the adverse effects of benzotropine & tihexyphenidyl?

A

Xerostomia; blurred vision; constipaiton;urinary retention; sedation; mydriasis

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14
Q

How does amantadine work in the treatment of PD?

A

May inhibit reuptake of DA into presynaptic neurons; may increase DArelease from presynaptic fibers

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15
Q

Amantadine is used to treat what condition other than PD?

A

Influenza A

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16
Q

What is the name of the dermatologic adverse effect caused by Amantadine?

A

Livedo reticularis

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17
Q

What is lived reticularis?

A

A network pattern discoloration of the skin cause dby dilation of capillaries and venules

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18
Q

Which characteristic is not affected by amantadine?

A

Tremors

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19
Q

Which selective MAO-B inhibitor is commonly used as first line treatment of PD?

A

Selegiline

20
Q

What is the MOA of Selegiline?

A

Inhibition of DA metabolism in presynaptic neurons located in the CNS via inhibition of MAO-B

21
Q

What are the two active metabolites of Selegiline?

A
  1. Amphetamine

2. Methamphetamine

22
Q

What are the main adverse effects of Selegiline?

A

Cardiovascular stimulation (hypertension, palpitations; arrhythmias; angina)

23
Q

Name two ergot derivatives that acts DA agonists in the nigrostriatal system:

A
  1. Bromocriptine

2. Pergolide*?

24
Q

Bromocriptine is used to treat what conditions other than PD?

A

Prolactin secreting microadenomas; NMS; acromegaly; postpartum lactation

25
Q

What are the adverse effects of bromocriptine?

A

Headache; dizziness; nausea; orthostatic hypotension; dyskinesia; hallucinations; confusion; psychosis

26
Q

Name two non-ergot DA agonists:

A
  1. Pramipexole

2. Ropinirole

27
Q

What are the adverse effects of non ergot DA agonists?

A

Sedation; syncope; nausea; vomiting; hallucinations; dyskinesia

28
Q

What is the mechanism of action of Tolcapone and entacopone?

A

Inhibition of peripheral catechol-O-methyltransferase (COMT), thereby increasing CNS uptake of L-dopa

29
Q

What reaction does COMT catalyze?

A

Conversion of L-dopa to 3-O-methyldopa (partial DA agonist) in peripheral tissues

30
Q

What are the adverse effects of COMT inhibitors

A

Orthostatic hypotension; headache; fatigue; nausea; diarrhea; anorexia; dskinesia; muscle cramps; brown-orange urine; discoloration; hallucinations; diaphoresis

31
Q

Which of the COMT inhibitors is hepatotoxic?

A

Tolcapone

32
Q

Are COMT inhibitors used as first line therapy, adjunctive therapy, or both in the treatment of Parkinsons?

A

Adjunctive therapy in combo with carbidopa/levodopa

33
Q

Are the non ergot DA agonist used as first-line therapy, adjunctive therapy, or both in the treatment of PD?

A

Both

34
Q

What is the precursor of DA?

A

Levodopa (L-dopa)

35
Q

What enzyme converts L-dopa to DA?

A

Dopa decarboxylase DDA

36
Q

Does DA cross the BBB

A

NO

37
Q

Does Levodopa cross the BBB

A

yes, it does and is subsequently converted to DA by dopaminergic neurons in the substance nigra

38
Q

Is levodopa effective in treating PD when all the dopaminergic neurons in the substantial nigra have been destroyed?

A

No, since dopinergic neurons in the substaia nigra are required to convert levodopa to DA

39
Q

What is the MOA of carbidopa

A

Inhibition of peripheral DDC, thereby increasing the amount of levodopa that is available to cross the BBB. this allows for lower doses of levodopa needed, thereby decreased levodopa adverse effects

40
Q

Does carbidopa cross BBB

A

no, so only inhibits peripheral DDC

41
Q

How does levodopa work in the treatment of PD

A

Decreases symptoms of PD such as rigidity bradykinesia and tremors

42
Q

What is the “on off phenomenon” of parkinsons

A

Levodopa has such a short half life (1-2 hours) that plasma concentrations may decline rapidly causing patient to experience sudden rigidity, bradykinesia, and tremors

43
Q

Which amino acids compete with levodopa for GI absorption

A

Isoleucine; leucine

44
Q

What are the adverse effects of levodopa

A

Anorexia; nausea; vomiting; tachycarida; hypotension; discoloration of saliva and urine; mydriasis; hallucinations; dyskinesia; incrased intraocular pressure; cardiac arrhythmias

45
Q

Why should vitamin B6 (pyridoxine) not be used in combo with levodopa?

A

pyridoxine enhance metabolism of levodopa.

Pharmacology (6 decks)

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