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Pharmacology > Chapter 14: Parkinson's Disease > Flashcards

Chapter 14: Parkinson's Disease Flashcards

1
Q

the initiation and termination of movement is controlled by neural circuits in the ___

A

basal ganglia

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2
Q

many movement disorders have been attributed to disturbances in the ___

A

basal ganglia

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3
Q

the basic circuitry of the basal ganglia involves 3 interacting neuronal loops that include the ___, ___ and ___

A

cortex, thalamus, basal ganglia themselves s

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4
Q

balanced signalling between the ___ and ___ pathways of the basal ganglia circuits is what allows for smooth, coordinated muscle movement

A

direct and indirect

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5
Q

when any part of the basal ganglia circuit becomes disturbed, movements can become ___

A

jerky, uncoordinated and hard to control

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6
Q

___ is an essential regulatory component of the basal ganglia circuit

A

dopamine

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7
Q

Parkinson’s disease is a ___ disease

A

progressive neurodegenerative

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8
Q

what are the hallmark symptoms of Parkinson’s disease?

A

motor symptoms: rigidity, bradykinesia (slowness of movement and difficulty starting the movement), tremor

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9
Q

what are some cognitive symptoms of Parkinson’s that can. occur as the diseases progresses?

A

personality changes, anxiety, depression, confusion, cognitive impairment, ANS dysfunction

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10
Q

symptoms of Parkinson’s occur due to changes in ___

A

neuronal signalling in several regions of the brain

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11
Q

what is an ANS functions that may be distributed by Parkinson’s?

A

blood pressure

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12
Q

in many parts of the brain there is a balancing between what 2 NT?

A

dopamine and Ach

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13
Q

alternations in the neuronal circuits between the ___ and __ lead to motor symptoms that present in Parkinson’s

A

substantia nigra and striatum

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14
Q

dopamine and Ach signalling circuits travel ___ in many parts of the brain

A

together

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15
Q

Ach ___ GABA release and Dopamine ___ GABA release

A

increases; decreases

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16
Q

what 2 NT act to balance GABA release to control motor movements?

A

dopamine and Ach

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17
Q

in Parkinsons disease the dopaminergic neurons originating in the substantiated nigra begin to ___and ___(more/less) dopamine is released leading to imbalance of GABA that causes motor symptoms

A

degenerate; less

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18
Q

the therapeutic strategies to manage Parkinsons disease aim to restore the balance between ___ and __

A

dopamine and Ach

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19
Q

what are 2 strategies to rebalance Ach and DA in Parkinson’s?

A

increase DA signalling and decrease ach signalling

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20
Q

t/f anticholinergic drugs have been used in the past to treat Parkinson’s disease

A

t

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21
Q

Benzotriptine is an example of a ____ drug once used for Parkinson’s disease

A

anticholinergic

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22
Q

why are anticholinergic drugs not typically used in the treatment of Parkinson’s disease

A

they have an extensive array of systemic effects

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23
Q

what is the benefit and pitfall of targeting Ach GABA release for management of Parkinsons?

A

removes some muscle rigidity & helps tremors but does not tend to improve bradykinesia

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24
Q

which is the primary way to manage Parkinsons? Ach or DA management?

A

DA

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25
Q

what are the 3 ways to increase DA?

A
  1. add more
  2. decrease DA metabolsim
  3. activate DA receptors
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26
Q

where is dopamine made>

A

dopaminergic neurons

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27
Q

DA is made up of ___

A

tyrosine

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28
Q

___ is the immediate precursor to DA

A

L-Dopa (levodopa)

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29
Q

L-Dopa is a ____ converted to DA by the enzyme ___

A

amino acid; amino acid decarboxylase aka DOPA decarboxylase

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30
Q

the step of converting L-DOPA to DA is common to another pathway, with one more step, DA can become __

A

NE

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31
Q

metabolsim of DA occurs due to ___ and ___ enzyme which can be found in the CNS and periphery

A

monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT)

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32
Q

there are 5 subtypes of DA receptors, divided into 2 families, the ___ and ___ families

A

D1 and D2

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33
Q

the D1 family includes ___ and ___ receptors which are coupled to ___G proteins

A

D1 and D5; excitatory (Gs and Gq)

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34
Q

when Gs is activated it leads to an increase in ___ and when Gq is activated it leads to an increase in ___

A

cAMP; IP3 and DAG

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35
Q

the D2 family is coupled to ___ G proteins

A

inhibitory (Gi)

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36
Q

D2 receptors are expressed in the ___ and ___ of the brain and D3 receptors are highly expressed in the ____

A

substantia nigra and striatum; nucleus accumbens

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37
Q

which D receptors are the primary target for Parkinsons management?

A

D2 and D3

38
Q

does DA cross the BBB? why/why not?

A

not significantly, polar/water-soluble

39
Q

why can’t we just administer DA in the treatment of Parkinsons? what is a way around this?

A

it won’t cross the BBB enough; administering L-DOPA which will be turned into DA

40
Q

why can the L-DOPA precursor cross the BBB?

A

the BBB has transporters for brining in essential amino acids

41
Q

L-DOPA is administered by what route?

A

oral

42
Q

once L-DOPA enters the CNS after oral dosing, what happens to it?

A

taken up by dopaminergic neurons where it is converted to DA by DOPA decarboxylase

43
Q

what is yet another name for DOPA decarboxylase?

A

aromatic L-amino acid decarboxylase (AADC)

44
Q

L-DOPA enters the CNA via the ___ transporter

A

L-amin acid

45
Q

t/f L-DOPA can be metabolized and converted to DA in the periphery

A

t

46
Q

what are the 2 issues if L-DOPA is converted to DA in the periphery?

A
  1. DA has significant effects such as GI upset, tachycardia, vasodialtion
  2. peripheral metabolsim results in very little L-DOPA left to enter the CNS
47
Q

peripheral DOPA decarboxylase can be blocked by administering ___ along with L-DOPA

A

carbidopa

48
Q

if 100mg of L-DOPA is given alone, approximately ___ mg reaches the CNS

A

1

49
Q

when L-DOPA is given with carbidopa, only __mg are needed to achieve 1mg in the CNS

A

10

50
Q

does carbidopa cross the BBB? what is the advantage of this?

A

no; if it did, it would prevent the conversion to DA when it is needed

51
Q

when DA is metabolized by both or either MAO / COMT, ___metabolites are made which are excreted in the ___

A

polar; urine

52
Q

reducing the metabolsim of DA in the CNS allows it be ___ rather than ___

A

recycled; re-made

53
Q

tolcapone is a ___inhibitor in the treatment of Parkinsons

A

COMT

54
Q

Selegiline is a ___ inhibitor in the treatment of Parkinson

A

MAO

55
Q

MAO enzymes exist in 2 isoforms: __ and __

A

MAO-A and MAO-B

56
Q

MAO-A is important for the metabolism of monoamines from __ sources, done in the ___

A

food; GI tract

57
Q

MAO-A shows little preference for monoamine transmitters, metabolizing ___, ___ and __

A

5-HT, NE and DA

58
Q

accumulation of tyramine (if not metabolized by MAO) can lead to __ and __

A

hypertension and arrhythmia

59
Q

MAO-B prefers to metabolize ___

A

DA

60
Q

which is the better target for managing Parkinsons? MAO-A or MAO-B?

A

MAO-B bc it prefers to metabolize DA

61
Q

what are the side effects of inhibiting COMT / MAO?

A

sympathomimetic effects and those associated with increased DA (same as L-DOPA)

62
Q

Tolocane inhibits COMT in the CNS and periphery, which causes increased ___ and ___ and leads to many side effects (no longer used due to ___toxicity)

A

L-DOPA and DA; liver

63
Q

selginine is a selective ___ inhibitor

A

MAO-B

64
Q

t/f seleginine may be used as a mono therapy or with L-DOPA ro enhance DA actions

A

t

65
Q

when L-DOPA / enzyme inhibitors are used to increase DA, the DA levels will increase throughout the brain, what are some ADR of this?

A

hallucinations, delusions, mood/personality changes, poor impulse control, increased addictive activities (such as substances and gambling)

66
Q

is a patient who is taking Rx to increase their DA at higher risk for addictive tendencies such as gambling and using addictive substances? why?

A

yes; DA is involved in reward pathways in the brain

67
Q

persistent high levels of DA can cause ____ which are involuntary movements. why is this counterproductive?

A

dyskinesia; bc the medication is supposed to reduce involuntary movements (ataxia) caused by Parkinsons

68
Q

DA treatment in Parkinson’s disease can have ____ effects where as the time from last dose increases before next dose is given and in this time period control of movements can be lost

A

wearing-off effects

69
Q

what resolves the wearing-off effects of DA treatment?

A

the next dose bring the DA levels back up again

70
Q

____ phenomenon of DA treatment also involve a loss of controlled movement, but cannot be remedied by adding the next dose

A

on-off

71
Q

on-off effects of Parkinson’s tend to develop more as the disease progresses and there is further loss of dopaminergic neurons in the ____

A

dopaminergic neurones in the substantia nigra

72
Q

if there are no functional dopaminergic neurons in the ___ to convert L-DOPA to DA, the therapeutic effect may be lost

A

substantia nigra

73
Q

/t/f due to on/off effects, as Parkinsons progresses, other treatment may need to be used other than L-DOPA and enzymes

A

t

74
Q

what are 2 benefits of administering a DA receptor agonist instead of L_DOPA?

A
  1. doesn’t require selective metabolsim into metabolites

2. more selectively modulate DA R (less off-target effects)

75
Q

t/f when using a DA agonist there is no requirement for biosynthesis in functional neurons to create and release DA

A

t

76
Q

why may some patients be treated with DA agonists rather than L-DOPA in the early stages of parkinsons?

A

it has fewer off-target effects

77
Q

while DA agonists are more seletive and cause fewer off-target effects than L-DOPA, why is their specificity not absolute?

A

there are still DA receptor subtypes in many parts of the brain and periphery

78
Q

what are the 2 main regions of the brain where degeneration of DA neurons causes Parkinson’s? what are the 2 main types of DA receptors found here (the receptors most targeted by therapy)?

A

substantia nigra and the striatum; D3 and D2

79
Q

bromocriptine is a ___derivative of a natural product with has ____(agonist/antagonist) activity @ many receptor types in the CNS

A

agonist

80
Q

in the treatment of parkinsons, Bromocriptine acts as an agonist at ___ and ___ receptors

A

D2 and D3

81
Q

Bromocriptine was used extensively for Parkinsons in the past, but is now used less bc ___

A

it has many off-target effects bc of its ability t bind to so many different receptors

82
Q

besides its many off-target effects, what is another reason why Bromocriptine is not a great drug to use

A

it is metabolized by CYP3A4, which many drugs are metabolized by and this can result in interactions that increase or decrease metabolsim

83
Q

what are 3 ADR of Bromocriptine?

A
  1. hypotension
  2. hallucinations
  3. sudden onset of sleep
84
Q

Pramipexole is a DA receptor ___

A

agonist

85
Q

Pramipexole acts mostly on ___ receptors, but also has some activity on ___ receptors

A

D3; D2

86
Q

Pramipexole has fewer side effects than Bromocriptine , but can still cause ___

A

side effects relating to high DA, such as hallucinations

87
Q

t/f Pramipexole is not extensively metabolized, allowing it to have fewer drug interactions

A

t

88
Q

accidentally targeting 5HT can cause

A

sedation

89
Q

accidentally targeting Alpha 1 AR can cause

A

hypertension

90
Q

accidentally targeting peripheral DA and alpha2-AR causes

A

hypotension

91
Q

ADR of targeting central D2 receptors

A

hallucinations and delusions

92
Q

directly activating DA receptors is a more selective way to enhance DA signalling, however selectivity is relative and often lost at ___ concentrations

A

high

Pharmacology (49 decks)

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