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IP1 > E1: Powerpoints > Flashcards

E1: Powerpoints Flashcards

1
Q

N_M

A

post-junctional; skeletal neuromuscular junction

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2
Q

N_N (N_2)

A

Autonomic ganglia, adrenal medulla

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3
Q

M1

A

sympathetic post-ganglionic; some pre-synaptic, lungs

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4
Q

M2

A

myocardium, smooth muscle, some pre-synaptic sites, lungs

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5
Q

M3

A

lungs, urinary bladder

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6
Q

M4, M5

A

No pharmacologic agents

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7
Q

Predominant tone of the SNS (2 locations/actions)

A

Arteries: vasoconstriction
Kidney: renin secretion

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8
Q

Predominant tone of PNS (2)

A

Detrusor muscle (bladder)
Resting state

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9
Q

Spinal efferents of SNS

A

Thoracic and lumbar
Paravertebral ganglion

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10
Q

Spinal efferents of PNS

A

Cranial, cervical, sacral (ganglion in organs)
Vagus nerve (cranial nerve X, 75% of all PNS activity)

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11
Q

What agents are not use clinically but block the uptake of choline

A

Hemicholinium and vesamicol

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12
Q

What disrupts SNAPS to prevent the release of Ach into the synaptic cleft

A

botulinum toxin derivatives

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13
Q

alpha-1 locations
Alpha-1A locations

A

arteries smooth muscle
Alpha-1A: prostate, urethra

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14
Q

beta-1

A

heart muscle

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15
Q

beta-2

A

lung, heart

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16
Q

beta-3

A

fat cells, urinary bladder (detrusor)

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17
Q

what is the rate limiting enzyme of the adrenergic nerve terminal and what does it do

A

tyrosine hydroxylase, converts Tyr to DOPA

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18
Q

How does NE get degraded in the synaptic cleft

A

by COMT

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19
Q

what influences neurotransmitter release (2)

A

autoreceptors and heteroreceptors

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20
Q

where are autoreceptors found and what do they do

A

alpha2, decrease NE release

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21
Q

what are heteroreceptors? what NT do they affect

A

receptors with the ability to influence neurotransmitter release but have less profound effects than autoreceptors
they act on muscarinic receptors to inhibit NE release and on AT1 to stimulate NE release

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22
Q

Metryrosine-Demser

A

TH inhibitor (decrease NE synthesis)

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23
Q

Reserpine

A

VMAT inhibitor (inhibits NE storage)

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24
Q

Bretylium

A

SNAP inhibitor (inhibit NE release)

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25
Q

Phenylzine-Nardil

A

MAO inhibitor (increase NE in nerve terminal)

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26
Q

Cocaine

A

inhibits NET; increase NE in synaptic cleft by inhibiting its reuptake

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27
Q

what type of receptors are at the neuromuscular junction

A

The ach receptors are only nicotinic (N_M)

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28
Q

phenylephrine is a __________ agonist

A

alpha-1 agonist

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29
Q

clonidine-Catapres is a ________ agonist

A

alpha-2 agonist

30
Q

methyldopa-Aldomet is a ______ agonist

A

alpha-2 agonist

31
Q

what agent is a non-selective alpha agonist

A

oxymetazoline

32
Q

what agent is a beta-1 agonist

A

dobutamine-Dobutrex

33
Q

albuterol-Ventolin is a ______ agonist

A

beta-2 agonist

34
Q

mirabegron-Myrbetriq is a _______ agonist

A

beta-3

35
Q

what agent is a non-selective beta-1, beta-2 agonist

A

isoproterenol

36
Q

what agent is a non-selective adrenergic agonist

A

epinephrine

37
Q

what agent is a indirect acting adrenergic agonist that causes the release of NE

A

pseudoephedrine

38
Q

what agent is a mixed acting adrenergic agonist so it targets alpha-1, alpha-2, beta-1, beta-2 agonist and causes the release of NE from the nerve terminal

A

ephedrine

39
Q

dopamine is a ______ agonist

A

dopamine (beta-1 and DA-1)

40
Q

fenoldopam-Corlopam is a _____ agonist

A

dopamine agonist (beta-1, DA-1)

41
Q

what agent is used for hypotension/shock (IV)

A

phenylephrine

42
Q

what agent’s MOA is to selectively bind to alpha-1 adrenergic receptors post-synaptically in effector cells

A

phenylephrine

43
Q

what agent’s pharmacologic effect is causing vascular smooth muscle receptor stimulation to cause vasoconstriction in blood vessels, arteries throughout the body and vagal afferent induced decrease in HR

A

phenylephrine (indication is hyPOtension/shock, MOA to bind to alpha-1 adrenergic receptors (located in blood vessels))

44
Q

what 3 systems does phenylephrine have potential ADR

A

CV, CNS, endocrine

45
Q

what are the CV ADR(s) of phenylephrine

A

Increased BP

46
Q

what are the CNS ADR(s) of phenylephrine

A

nervousness, excitability, insomnia

47
Q

what are the endocrine ADR(s) of phenylephrine

A

hyperglycemia
alpha1 receptors in liver increase glucose production and secretion
possible decreased insulin secretion that increases blood glucose

48
Q

what are the warnings/precautions of phenylephrine

A

patients w/hypertension, ischemic heart disease, diabetes mellitus

49
Q

what agent is an alpha-2 adrenergic agonist with a TTS patch available

A

clonidine (Catapres)

50
Q

what alpha-2 adrenergic agent is indicated for HTN and ADHD (ER-Kapvay)

A

clonidine (Catapres)

51
Q

what alpha-2 adrenergic agent is indicated for HTN in pregnancy

A

methyldopa (Aldomet)

52
Q

what is the MOA for clonidine (Catapres)

A

alpha2a receptor stimulation presynaptically (autoreceptor)/ post-synaptically (CNS) decreasing sympathetic tone
overall decrease in sympathetic impulses in CNS

53
Q

what 3 things does the presence of phenols/catechols on a benzene ring do

A

1: decrease lipophilicity
2: decrease CNS penetration
3: more likely to be metabolized by COMT

54
Q

Which confers to beta-2 receptor selectivity? 3,4 or 3,5 dihydroxy

A

3,5

55
Q

If you substitute/replace the OH on the ring _______ _______ receptor selectivity

A

increase Beta-2

56
Q

Substitution on ____ carbon blocks oxidation by MAO and prolongs duration of action

A

alpha

57
Q

what type of compounds are more likely to cause release of NE from storage since they stay in the nerve terminals longer

A

alpha-methyl compounds

58
Q

what group does Clonidine have on its structure that increases its CNS penetration

A

halogens which increase lipophilicity

59
Q

Catapres is 300x more active on _____ than ____

A

more active on alpha 2 than alpha 1

60
Q

substitution on ____ carbon increases activity at both alpha and beta adrenergic receptors

A

beta

61
Q

hydroxyl groups decrease actions within the CNS therefore decreasing lipid solubility when there are substitutions on ___ _______

A

beta carbon

62
Q

If there is a methyl substitution on the amine the compound reacts with which receptors
Give an example

A

alpha-1, beta-1, beta-2
Epinephrine, the small methyl groups allows it to retain the alpha1 receptor affinity

63
Q

If there is an isopropyl, t-butyl, or other bulky group substitution on the amine, the compound will react with

A

beta1 and beta2 if isopropyl group
only beta2 if t-Bu or larger (double activity)

64
Q

Loss of ____ binding increases with nitrogen substitution

A

alpha

65
Q

what is the order of increasing potency in which catecholamines stimulate beta-adrenoreceptors

A

norepinephrine < epinephrine < isoproterenol

66
Q

MAO metabolism occurs at _____

A

amines

67
Q

_____ are more susceptible to MAO metabolism, why

A

primary amines; large substitution decreases MAO metabolism

68
Q

where does COMT metabolism occur on a structure

A

OH on a benzene ring

69
Q

which metabolism takes place orally resulting in rapid inactivation in intestine and liver

A

COMT metabolism

70
Q

what are the 4 criteria for high agonist activity

A

1) primary or secondary amine
2) amine separated by 2 carbons from benzene ring (ethyl)
3) hydroxyl group on B carbon
4) 3,4 di-OH for alpha and beta receptor activity

IP1 (23 decks)

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