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Pharm > Antiparkinsonian Drugs > Flashcards

Antiparkinsonian Drugs Flashcards

1
Q

What are the four key characteristics of Parkinson’s?

A
  1. Bradykinesia
  2. Muscular rigidity
  3. Resting tremor
  4. Postural instability
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2
Q

What are the proteins that are deposited in Parkinson’s?

A

Lewy bodies

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3
Q

What is the cause of parkinson’s?

A

Progressive loss of dopaminergic neurons in the basal ganglia

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4
Q

What happens to Parkinsonian pts without treatment?

A

rigid, akinetic state, leading to secondary complication like pneumonia or PE

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5
Q

What is the goal of pharmacologic treatment of Parkinson’s?

A

Improve functionality

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6
Q

Where is the loss of dopaminergic neurons in Parkinson’s greatest? What other brain regions are affected?

A

Basal ganglia

Brainstem
Hippocampus
Cerebral cortex

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7
Q

What are the 3 main characteristics of Neurodegenerative disorders?

A
  1. Progressive and irreversible loss of neurons
  2. Etiology relates to specific neuronal loss
  3. Aggregation of misfolded proteins
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8
Q

What is the neuron/neurotransmitter lost in AD?

A

Ach in hippocampal areas

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9
Q

What is the protein that is accumulate in Parkinson’s? Where?

A

Alpha-synuclein in intracytoplasmic aggregates

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10
Q

What is the protein that is accumulate in AD? Where?

A

Extracellular beta-amyloid plaques, and intracellular neurofibrillary tangles

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11
Q

What is the protein that is accumulated in Huntington’s disease?

A

Intranuclear Huntingtin protein

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12
Q

What age does Parkinson’s usually start?

A

50 and 60s

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13
Q

What are the non-motor effects of PD?

A

Cognitive decline
Affective disorder
Sleep disorders
Personality changes

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14
Q

Resting tremor = what dysfunction?

A

Basal ganglia (PD)

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15
Q

Why is it that cerebellar dysfunction are usually ipsilateral to the lesion?

A

Crosses twice

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16
Q

What part of the basal ganglia specifically, is affected by PD?

A

Substantia nigra

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17
Q

What are the components of the motor loop?

A

Cortex
Striatum
Pallidum
Thalamus

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18
Q

What is the principal input structure of the basal ganglia? Where does this receive input from? What kind of input?

A

Striatum, receives excitatory input from the cortex

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19
Q

What is the neurotransmitter used in the striatum?

A

Dopamine

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20
Q

What are the two pathways from the striatum?

A

Direct pathway = striatum to substantia nigra pars reticularis and GP

Indirect = From the striatum through the GP and subthalamic nucleus (GABA links)

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21
Q

What is the primary defect in PD?

A

Destruction of the dopaminergic neurons of the substantia nigra pars compacta

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22
Q

What are the neurotransmitters from the cerebral cortex to the striatum?

A

Glu (+)

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23
Q

What are the neurotransmitters from the striatum to the globus pallidus?

A

GABA (-)

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24
Q

What is the neurotransmitter from the globus pallidus to the subthalamic nucleus?

A

GABA (-)

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25
Q

What is the neurotransmitter from the globus pallidus to the substantia nigra?

A

Glu (+)

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26
Q

What is the neurotransmitter from the substantia nigra to the VA/VL thalamus?

A

(GABA) (-)

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27
Q

What is the neurotransmitter from the thalamus, back to the cortex?

A

Glu (+)

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28
Q

Draw out the neurotransmitter/ basal ganglia relationship pathway (pg 4 of the handout).

A

Draw, and mark the pathway destroyed in PD

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29
Q

What is the net effect off the loss of dopaminergic neurons in the basal ganglia?

A

neurons in
the SNpr and GPi become more active. This leads to
increased inhibition of the VA/VL thalamus and
reduced excitatory input to the cortex

30
Q

Which BG pathway is overactive and which is under active in PD?

A

Indirect is overactive

Direct in not active

31
Q

What pathway is increased in PD? What is the neurotransmitter here?

A

Direct–ACh

32
Q

What is the major effect of alpha synuclein accumulation?

A

ROS generation

33
Q

What are the three net effects of degeneration of the direct pathway?

A
  • Increased VA/VL thalamus
  • Reduced excitatory input to the cortex
  • Diminished execution of motor movement
34
Q

What do the interneurons of the corpus striatum use for a neurotransmitter? What inhibits these interneurons?

A

ACh

Normally, dopaminergic neurons from the SN inhibit these, but in PD there is none.

35
Q

What is the basis for treating PD with ACh antagonists?

A

Interneurons of the Striatum which secrete ACh to stimulate the pallidus, are normally inhibited by dopaminergic neurons from the substantia nigra. Antagonizing these will reduce the ssx of parkinson’s

36
Q

What are the five treatment strategies for PD?

A
  1. DA replacement
  2. DA receptor agonists
  3. L-DOPA degradation inhibitors
  4. Increase DA release
  5. Anticholinergic agents
37
Q

What is the MOA of L-DOPA? Why not just use dopamine?

A

replaces dopamine in the brain–dopamine itself cannot cross the BBB

38
Q

What is the major drawback of using L-DOPA?

A

Tolerance builds up over years

39
Q

What is the MOA of carbidopa? What is the benefit of administering it with L-DOPA?

A

Inhibitor of decarboxylase in the periphery

Reduces the amount of L-DOPA needed to have an effect

40
Q

What are the major side effects of L-DOPA?

A

Dyskinesias
Wearing off (end of dose akinesia)
Postural hypotension
Behavioral disturbances

41
Q

What vitamin can enhance the therapeutic effect of L-DOPA metabolism?

A

B6

42
Q

Can carbidopa cross the BBB? How, then, does it work?

A

No–reduces the metabolism of L-DOPA in the periphery

43
Q

What are the GI problems with L-DOPA?

A

n/v

44
Q

What are the cardio effects of L-DOPA?

A

Hypotension

Cardiac dysrhythmias

45
Q

What are the behavioral disturbances associated with L-DOPA?

A

Depression/anxiety
Insomnia
Agitation and confusion

46
Q

What is the interaction of MAO-A inhibitors and L-DOPA?

A

hypertensive reaction d/t increase norepi levels

47
Q

What is the interaction of L-DOPA with antipsychotics

A

DA receptor blockade

48
Q

What is the interaction of L-DOPA and protein-rich meals?

A

Competition for GI and BBB absorption

49
Q

What is the MOA of pramipexole?

A

Direct agonist preferentially at dopamine D3 receptors; nonergot

50
Q

What are the effects of pramipexole?

A

Reduces PD symptoms

51
Q

What are the side effects of pramipexole?

A

impulse control

Psychotic episodes

52
Q

What is the MOA of ropinirole?

A

D2 agonist

53
Q

What is the use of apomorphine?

A

Rescue treatment for L-DOPA induced dyskinesias

54
Q

What part of the brain is affected by dopamine agonists, and cause impulse control?

A

Reward pathway

55
Q

What is the MOA of Rasagiline?

A

MAO-B inhibitor, causing an increase in dopamine. At higher doses, also inhibits MAO-A

56
Q

What is the use of Rasagiline and selegiline?

A

PD adjuvant to levadopa

57
Q

What are the two major categories of drugs that Rasagiline reacts with?

A

SSRIs and TCAs

58
Q

What is the MOA of Selegiline?

A

MAO-B inhibitor, causing an increase in dopamine. At higher doses, also inhibits MAO-A

59
Q

What is the MOA of entacapone?

A

Inhibits COMT in the periphery; does not enter CNS. Reduces the metabolism of L-DOPA

60
Q

What are the side effects of entacapone?

A

dyskinesias

Confusion

61
Q

What is the MOA of Tolcapone?

A

COMT inhibition in the CNS and in the periphery

62
Q

What is the main difference between Tolcapone and entacapone?

A

Tolcapone works in the CNS and periphery

Entacapone works only in the periphery

63
Q

Why is Entacapone preferentially used over Tolcapone?

A

Entacapone it has not been associated with hepatotoxicity

64
Q

What is the MOA of amantadine?

A

Antiviral agent that has antiparkinsonian properties. MOA unclear

65
Q

What is the half life of amantadine?

A

Short

66
Q

What are the side effects of Amantadine?

A 
Restlessness
Depression
Irritability
Insomnia
Hallucinations
67
Q

What is the livedo reticularis associated with Amantadine?

A

Blotchy reddend pattern, usually on the legs, clears w/in 1 month after stopping

68
Q

What is the MOA of benztropine?

A

Antagonist at M receptors in basal ganglia

69
Q

What is the MOA of Trihexyphenidyl?

A

Antagonist at M receptors in the basal ganglia

70
Q

What are the main pharmacological effects of Benztropine and Trihexyphenidyl on PD?

A

Reduces tremor and rigidity; little effect on bradykinesia

71
Q

What are the surgical techniques used to treat PD? (2)

A

Stimulate subthalamic nucleus or globus pallidus by an implanted electrode and stimulator

Transplant of dopaminergic tissue

Pharm (73 decks)

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