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PHRM 845 > L42 patho and pharm of PD > Flashcards

L42 patho and pharm of PD Flashcards

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1
Q

T or F: The ratio for PD is 2:1 female:male

A

F, males twice as likely

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2
Q

PD results from a neurological deficit in the ___________ system.

A

extrapyramidal, (noncortical voluntary motor control)

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3
Q

PD sxs acronym

A

TRAP
- resting Tremor
- Rigidity
- Akinesia/bradykinesia
- Postural instability

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4
Q

other sxs of PD not related to motor fxn (3)

A

speech difficulties, cognitive deficits, depression

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5
Q

PD is characterized by a loss of _______ ________ in the _______ ________

A

dopaminergic neurons, substantia nigra

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6
Q

Some studies suggest that __% of the nigral dopamine neurons, or -% of the nerve terminals in the striatum, are lost before patients present with motor symptoms.

A

50, 70-80

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7
Q

In PD, ther loss of neurotransmission is through what system?

A

nigrostriatal

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8
Q

Lewy bodies are enriched with fibrillar forms of what protein?

A

protein a-synuclein

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9
Q

surviving neurons in PD pts have dense, spherical protein deposits called?

A

lewy bodies

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10
Q

T or F: Lewy bodies are found intracellularly

A

True

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11
Q

If you see braak stages what should you think of?

A

A-synuclein

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12
Q

At which Braak stage are there lewy bodies in the SN?

A

Stage 3

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13
Q

lewy bodies move from where to where as the braak stages go up?

A

lower structures and move up towards cortex

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14
Q

what structure in the brain undergoes neurodegeneration?

A

SN pars compacta

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15
Q

what structure do the caudate nucleus and putamen make up?

A

striatum

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16
Q

direct pathway (simple pathway)
A. D1 striatal neurons receptor pathway
B. D2 striatal neurons receptor pathway

A

A. D1 striatal neurons receptor pathway

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17
Q

Indirect pathway (complicated pathway)
A. D1 striatal neurons receptor pathway
B. D2 striatal neurons receptor pathway

A

B. D2 striatal neurons receptor pathway

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18
Q

SNpc ->striatum -> Gpi/SNpr -> thalamus -> cortex

A

simple pathway, D1 pathway

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19
Q

SNpc -> striatum -> Gpe -> STN -> Gpi/SNpr -> thalamus -> cortex

A

imdirect/complicated pathway, D2 pathway

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20
Q

what is the result of SNpc releasing dopamine to either pathway?

A

increased signaling from thalamus to the cortex -> increased proper motor function

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21
Q

what signaling is favored in the signaling from the SNpc to D1 or D2 receptors?

A

thalamocortical signaling, this effect is disrupted in PD

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22
Q

what is globus pallidus?

A

two versions, internal and external, both are downstream of striatum

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23
Q

what do antimuscarinics treat in PD?

A

adjunct therapy for tremor and motor symptoms

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24
Q

T or F: Antimuscarinics are used only in high doses to ensure treatment of motor symptoms

A

False, they are used in low doses because of side effects

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25
in the control of motor movement _______ is excitatory while _______ is inhibitory
ACh, Dopamine (IN THE INDIRECT PATHWAY (D2)
26
the loss of dopamine results in relative _____ of activity in _______ pathways
excess, cholinergic
27
what can partially compensate for the overactive activity of cholinergic pathways in the loss of dopamine?
a cholinergic antagonist
28
what is the antimuscarinic drug in the slide for the tx of motor symptoms in PD?
Benztropine (Cogentin)
29
What happens to cholinergic signaling when dopamine signaling is overactive?
it would go down
30
what is the "gold standard" for PD therapy?
L-Dopa
31
T or F: L-dopa is a precursor of dopamine
true
32
T or F: L-DOPA is orally active and can enter the CNS
tru
33
why is there a difference in bioavailability between L-DOPA and dopamine
because DA (?) has a net positive charge at PH 7
34
at high doses L-DOPA produces what 3 side effects?
nausea, hypertension (weird), and psychosis
35
the dose of L-DOPA can be lowered (4x) by doing what?
co-administering with carbidopa
36
a peripherally-acting DOPA decarboxylase inhibitor
carbidopa
37
what is the combo drug called with L-DOPA and carbidopa?
sinemet
38
T or F: dopamine can go across the BBB with ease
False, it cant cross at all (which is super weird)
39
where must L-DOPA be converted to dopamine?
in the SN, not in the periphery
40
what structural feature keeps dopamine from crossing the BBB?
carboxyl group
41
what happens physiologically that leads to us increasing the dose of DOPA?
LDOPA is converted in a decarboxylation reaction in the periphery, this leads to a loss of LDOPA that is supposed to go into the CNS leading to more dopamine in the periphery that we do not want
42
T or F: carbidopa passes the BBB
False, meaning it cannot inhibit DDC in the SN
43
what can happen after several years of L-DOPA treatment? (highlighted red)
on/off oscillations
44
adding carbidopa to L-DOPA accomplishes what main goal?
keeps L-DOPA from converting dopamine in the periphery
45
______ and _____ are major problems in long term L-DOPA tx
dyskinesias and on/off effects
46
how can the dyskinesias and on/off effects cause by LTT of L-DOPA be alleviated? (red text)
administering L-DOPA in a continuous manner (new liquid-based subq infusion)
47
T or F: Dyskinesias are caused by Parkinsons
false, its the drugs
48
another key limitation in L-DOPA therapy is?
prodrug conversion
49
How do you address the challenge of prodrug conversion in L-DOPA tx?
use dopamine receptor agonists- this is reasonable bc the postsynaptic dopamine receptors are still present in the striatum (this was red so read it twice)
50
what drug is a mixed D1 and D2 agonist?
apomorphine
51
what can be found in the apomorphine structure?
dopamine with catechol and aminoethyl groups
52
Apomorphine administration
subq in late stage PD to provide rapid relief
53
Why is the usefulness of Apomorphine limited?
potent emetic effects (puking)
54
what are the 3 non-ergoline DA receptor agonists?
Ropinirole (requip), pramipexole (Mirapex), and rotigotine (neuropro)
55
what kind of agonists are the non-ergoline DA agonist?
D2 and D3
56
T or F: Ergolines have less side effects than non-ergolines
False, ergolines have more side effects
57
How are the non-ergoline drugs generally used?
as monotherapies for early-stage PD
58
Which one of the following is a transdermal patch? A. Ropinirole (requip) B. pramipexole (Mirapex), C. rotigotine (neuropro)
C. rotigotine (neuropro)
59
what drug class inhibits dopamine metabolism?
MAO-B inhibitors
60
what are the two propargylamine MAO-B inhibitors?
Selegiline (deprenyl) and rasagiline (azilect)
61
what structural significance do the propargylamines have? (-giline drugs)
triple bond
62
how are MAO-B inhibitors generally used?
monotherapies to delay first use of L-DOPA BUT they can also be adjunct with L-DOPA
63
what do MAO-B inhibitors inhibit?
oxidation of dopamine to DOPAL by monoamine oxidase-B (MAO-B)
64
what is the reversible MAO-B inhibitor?
Safinamide (xadago)
65
what makes Safinamide (xadago) reversible?
no propargylamine group
66
how is Safinamide (xadago) generally used?
as adjunct to L-DOPA/Carbidopa (particularly during off episodes)
67
what drug class ALSO inhibits dopamine metabolism that isnt the MAO-Bi's?
COMT inhibitors
68
what are the 3 COMT inhibitors?
entacapone (comtan) Tolcapone (tasmar) Opicapone (Ongentys)
69
what do the COMTi's inhibit?
the methylation of the 3-OH group of DA or L-DOPA by catechol-O-methyl transferase (COMT)
70
Inhibition of COMT by which of the following decreases metabolism of L-DOPA in the periphery A. Entacapone (comtan) B. Tolcapone (tasmar) C. Opicapone (Ongentys)
A. Entacapone (comtan) C. Opicapone (Ongentys)
71
inhibition of COMT by which of the following in the CNS allows levels of CNS dopamine to remain higher and increased the dopamine elimination time by 30-50% A. Entacapone (comtan) B. Tolcapone (tasmar) C. Opicapone (Ongentys)
B. Tolcapone (tasmar)
72
T or F: COMT inhibitors increase the potency and duration of sinemet action
F, potency doesn't change and it prolongs the duration
73
the mixture of L-DOPA, carbidopa, and entacapone is called what
Stalevo

PHRM 845 (34 decks)

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