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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
what are the 3 ways to increase DA?
1. add more 2. decrease DA metabolsim 3. activate DA receptors
26
where is dopamine made>
dopaminergic neurons
27
DA is made up of ___
tyrosine
28
___ is the immediate precursor to DA
L-Dopa (levodopa)
29
L-Dopa is a ____ converted to DA by the enzyme ___
amino acid; amino acid decarboxylase aka DOPA decarboxylase
30
the step of converting L-DOPA to DA is common to another pathway, with one more step, DA can become __
NE
31
metabolsim of DA occurs due to ___ and ___ enzyme which can be found in the CNS and periphery
monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT)
32
there are 5 subtypes of DA receptors, divided into 2 families, the ___ and ___ families
D1 and D2
33
the D1 family includes ___ and ___ receptors which are coupled to ___G proteins
D1 and D5; excitatory (Gs and Gq)
34
when Gs is activated it leads to an increase in ___ and when Gq is activated it leads to an increase in ___
cAMP; IP3 and DAG
35
the D2 family is coupled to ___ G proteins
inhibitory (Gi)
36
D2 receptors are expressed in the ___ and ___ of the brain and D3 receptors are highly expressed in the ____
substantia nigra and striatum; nucleus accumbens
37
which D receptors are the primary target for Parkinsons management?
D2 and D3
38
does DA cross the BBB? why/why not?
not significantly, polar/water-soluble
39
why can't we just administer DA in the treatment of Parkinsons? what is a way around this?
it won't cross the BBB enough; administering L-DOPA which will be turned into DA
40
why can the L-DOPA precursor cross the BBB?
the BBB has transporters for brining in essential amino acids
41
L-DOPA is administered by what route?
oral
42
once L-DOPA enters the CNS after oral dosing, what happens to it?
taken up by dopaminergic neurons where it is converted to DA by DOPA decarboxylase
43
what is yet another name for DOPA decarboxylase?
aromatic L-amino acid decarboxylase (AADC)
44
L-DOPA enters the CNA via the ___ transporter
L-amin acid
45
t/f L-DOPA can be metabolized and converted to DA in the periphery
t
46
what are the 2 issues if L-DOPA is converted to DA in the periphery?
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
peripheral DOPA decarboxylase can be blocked by administering ___ along with L-DOPA
carbidopa
48
if 100mg of L-DOPA is given alone, approximately ___ mg reaches the CNS
1
49
when L-DOPA is given with carbidopa, only __mg are needed to achieve 1mg in the CNS
10
50
does carbidopa cross the BBB? what is the advantage of this?
no; if it did, it would prevent the conversion to DA when it is needed
51
when DA is metabolized by both or either MAO / COMT, ___metabolites are made which are excreted in the ___
polar; urine
52
reducing the metabolsim of DA in the CNS allows it be ___ rather than ___
recycled; re-made
53
tolcapone is a ___inhibitor in the treatment of Parkinsons
COMT
54
Selegiline is a ___ inhibitor in the treatment of Parkinson
MAO
55
MAO enzymes exist in 2 isoforms: __ and __
MAO-A and MAO-B
56
MAO-A is important for the metabolism of monoamines from __ sources, done in the ___
food; GI tract
57
MAO-A shows little preference for monoamine transmitters, metabolizing ___, ___ and __
5-HT, NE and DA
58
accumulation of tyramine (if not metabolized by MAO) can lead to __ and __
hypertension and arrhythmia
59
MAO-B prefers to metabolize ___
DA
60
which is the better target for managing Parkinsons? MAO-A or MAO-B?
MAO-B bc it prefers to metabolize DA
61
what are the side effects of inhibiting COMT / MAO?
sympathomimetic effects and those associated with increased DA (same as L-DOPA)
62
Tolocane inhibits COMT in the CNS and periphery, which causes increased ___ and ___ and leads to many side effects (no longer used due to ___toxicity)
L-DOPA and DA; liver
63
selginine is a selective ___ inhibitor
MAO-B
64
t/f seleginine may be used as a mono therapy or with L-DOPA ro enhance DA actions
t
65
when L-DOPA / enzyme inhibitors are used to increase DA, the DA levels will increase throughout the brain, what are some ADR of this?
hallucinations, delusions, mood/personality changes, poor impulse control, increased addictive activities (such as substances and gambling)
66
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?
yes; DA is involved in reward pathways in the brain
67
persistent high levels of DA can cause ____ which are involuntary movements. why is this counterproductive?
dyskinesia; bc the medication is supposed to reduce involuntary movements (ataxia) caused by Parkinsons
68
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
wearing-off effects
69
what resolves the wearing-off effects of DA treatment?
the next dose bring the DA levels back up again
70
____ phenomenon of DA treatment also involve a loss of controlled movement, but cannot be remedied by adding the next dose
on-off
71
on-off effects of Parkinson's tend to develop more as the disease progresses and there is further loss of dopaminergic neurons in the ____
dopaminergic neurones in the substantia nigra
72
if there are no functional dopaminergic neurons in the ___ to convert L-DOPA to DA, the therapeutic effect may be lost
substantia nigra
73
/t/f due to on/off effects, as Parkinsons progresses, other treatment may need to be used other than L-DOPA and enzymes
t
74
what are 2 benefits of administering a DA receptor agonist instead of L_DOPA?
1. doesn't require selective metabolsim into metabolites | 2. more selectively modulate DA R (less off-target effects)
75
t/f when using a DA agonist there is no requirement for biosynthesis in functional neurons to create and release DA
t
76
why may some patients be treated with DA agonists rather than L-DOPA in the early stages of parkinsons?
it has fewer off-target effects
77
while DA agonists are more seletive and cause fewer off-target effects than L-DOPA, why is their specificity not absolute?
there are still DA receptor subtypes in many parts of the brain and periphery
78
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)?
substantia nigra and the striatum; D3 and D2
79
bromocriptine is a ___derivative of a natural product with has ____(agonist/antagonist) activity @ many receptor types in the CNS
agonist
80
in the treatment of parkinsons, Bromocriptine acts as an agonist at ___ and ___ receptors
D2 and D3
81
Bromocriptine was used extensively for Parkinsons in the past, but is now used less bc ___
it has many off-target effects bc of its ability t bind to so many different receptors
82
besides its many off-target effects, what is another reason why Bromocriptine is not a great drug to use
it is metabolized by CYP3A4, which many drugs are metabolized by and this can result in interactions that increase or decrease metabolsim
83
what are 3 ADR of Bromocriptine?
1. hypotension 2. hallucinations 3. sudden onset of sleep
84
Pramipexole is a DA receptor ___
agonist
85
Pramipexole acts mostly on ___ receptors, but also has some activity on ___ receptors
D3; D2
86
Pramipexole has fewer side effects than Bromocriptine , but can still cause ___
side effects relating to high DA, such as hallucinations
87
t/f Pramipexole is not extensively metabolized, allowing it to have fewer drug interactions
t
88
accidentally targeting 5HT can cause
sedation
89
accidentally targeting Alpha 1 AR can cause
hypertension
90
accidentally targeting peripheral DA and alpha2-AR causes
hypotension
91
ADR of targeting central D2 receptors
hallucinations and delusions
92
directly activating DA receptors is a more selective way to enhance DA signalling, however selectivity is relative and often lost at ___ concentrations
high

.Pharmacology (55 decks)

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