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PHRM 845 > L42 patho and pharm of PD > Flashcards

L42 patho and pharm of PD Flashcards

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
Q

in the control of motor movement _______ is excitatory while _______ is inhibitory

A

ACh, Dopamine (IN THE INDIRECT PATHWAY (D2)

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26
Q

the loss of dopamine results in relative _____ of activity in _______ pathways

A

excess, cholinergic

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27
Q

what can partially compensate for the overactive activity of cholinergic pathways in the loss of dopamine?

A

a cholinergic antagonist

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28
Q

what is the antimuscarinic drug in the slide for the tx of motor symptoms in PD?

A

Benztropine (Cogentin)

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29
Q

What happens to cholinergic signaling when dopamine signaling is overactive?

A

it would go down

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30
Q

what is the “gold standard” for PD therapy?

31
Q

T or F: L-dopa is a precursor of dopamine

32
Q

T or F: L-DOPA is orally active and can enter the CNS

33
Q

why is there a difference in bioavailability between L-DOPA and dopamine

A

because DA (?) has a net positive charge at PH 7

34
Q

at high doses L-DOPA produces what 3 side effects?

A

nausea, hypertension (weird), and psychosis

35
Q

the dose of L-DOPA can be lowered (4x) by doing what?

A

co-administering with carbidopa

36
Q

a peripherally-acting DOPA decarboxylase inhibitor

37
Q

what is the combo drug called with L-DOPA and carbidopa?

38
Q

T or F: dopamine can go across the BBB with ease

A

False, it cant cross at all (which is super weird)

39
Q

where must L-DOPA be converted to dopamine?

A

in the SN, not in the periphery

40
Q

what structural feature keeps dopamine from crossing the BBB?

A

carboxyl group

41
Q

what happens physiologically that leads to us increasing the dose of DOPA?

A

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
Q

T or F: carbidopa passes the BBB

A

False, meaning it cannot inhibit DDC in the SN

43
Q

what can happen after several years of L-DOPA treatment? (highlighted red)

A

on/off oscillations

44
Q

adding carbidopa to L-DOPA accomplishes what main goal?

A

keeps L-DOPA from converting dopamine in the periphery

45
Q

______ and _____ are major problems in long term L-DOPA tx

A

dyskinesias and on/off effects

46
Q

how can the dyskinesias and on/off effects cause by LTT of L-DOPA be alleviated? (red text)

A

administering L-DOPA in a continuous manner (new liquid-based subq infusion)

47
Q

T or F: Dyskinesias are caused by Parkinsons

A

false, its the drugs

48
Q

another key limitation in L-DOPA therapy is?

A

prodrug conversion

49
Q

How do you address the challenge of prodrug conversion in L-DOPA tx?

A

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
Q

what drug is a mixed D1 and D2 agonist?

A

apomorphine

51
Q

what can be found in the apomorphine structure?

A

dopamine with catechol and aminoethyl groups

52
Q

Apomorphine administration

A

subq in late stage PD to provide rapid relief

53
Q

Why is the usefulness of Apomorphine limited?

A

potent emetic effects (puking)

54
Q

what are the 3 non-ergoline DA receptor agonists?

A

Ropinirole (requip), pramipexole (Mirapex), and rotigotine (neuropro)

55
Q

what kind of agonists are the non-ergoline DA agonist?

56
Q

T or F: Ergolines have less side effects than non-ergolines

A

False, ergolines have more side effects

57
Q

How are the non-ergoline drugs generally used?

A

as monotherapies for early-stage PD

58
Q

Which one of the following is a transdermal patch?
A. Ropinirole (requip)
B. pramipexole (Mirapex), C. rotigotine (neuropro)

A

C. rotigotine (neuropro)

59
Q

what drug class inhibits dopamine metabolism?

A

MAO-B inhibitors

60
Q

what are the two propargylamine MAO-B inhibitors?

A

Selegiline (deprenyl) and rasagiline (azilect)

61
Q

what structural significance do the propargylamines have? (-giline drugs)

A

triple bond

62
Q

how are MAO-B inhibitors generally used?

A

monotherapies to delay first use of L-DOPA BUT they can also be adjunct with L-DOPA

63
Q

what do MAO-B inhibitors inhibit?

A

oxidation of dopamine to DOPAL by monoamine oxidase-B (MAO-B)

64
Q

what is the reversible MAO-B inhibitor?

A

Safinamide (xadago)

65
Q

what makes Safinamide (xadago) reversible?

A

no propargylamine group

66
Q

how is Safinamide (xadago) generally used?

A

as adjunct to L-DOPA/Carbidopa (particularly during off episodes)

67
Q

what drug class ALSO inhibits dopamine metabolism that isnt the MAO-Bi’s?

A

COMT inhibitors

68
Q

what are the 3 COMT inhibitors?

A

entacapone (comtan)
Tolcapone (tasmar)
Opicapone (Ongentys)

69
Q

what do the COMTi’s inhibit?

A

the methylation of the 3-OH group of DA or L-DOPA by catechol-O-methyl transferase (COMT)

70
Q

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

A. Entacapone (comtan)
C. Opicapone (Ongentys)

71
Q

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)

A

B. Tolcapone (tasmar)

72
Q

T or F: COMT inhibitors increase the potency and duration of sinemet action

A

F, potency doesn’t change and it prolongs the duration

73
Q

the mixture of L-DOPA, carbidopa, and entacapone is called what

PHRM 845 (34 decks)

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