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Pharmacology > Adrenergics > Flashcards

Adrenergics Flashcards

1
Q

Rate limiter in NE synthesis

A

conversion of tyrosine to DOPA

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2
Q

Dopamine is converted into…..

A

NE

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3
Q

Causes opening of vesicles to release NE

A

opening of Ca channels

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4
Q

NE Presynaptic receptor

A

a2 - Gi

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5
Q

Fates of NE

A

response on target organ- a or B
metabolized to inactive metabolites
reuptake

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6
Q

COMT

A

metabolizes NE into inactive metabolites

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7
Q

Reason for short half life of NE

A

rapid reuptake

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8
Q

Reason for short half life of Ach

A

rapid metabolism

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9
Q

a2 Agonist

A

more feedback

stops NE release

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10
Q

a2 Antagonist

A

more NE released

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11
Q

COMT Inhibitors

A

less metabolism, more NE available

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12
Q

Cocaine

A

blocks reuptake at Na/ K pump

more NE available

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13
Q

Imipramine

A

blocks reuptake

more NE available

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14
Q

MOAI

Monoamine oxidase inhibitor

A

increases recycling, more NE released

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15
Q

a1 Receptor

A

on target organ

use Gq

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16
Q

a2 Receptor

A

negative feedback presynaptic receptors

Gi

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17
Q

B Receptors

A

Gs

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18
Q

B1 has higher affinity for Epi or NE?

A

equal

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19
Q

B2 has higher affinity for Epi or NE?

A

Epi

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20
Q

Catecholamines

A

Epi, NE, dopamine

have short half lives

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21
Q

a1 Locations

A

vascular smooth muscle
pupillary dilator
prostate (a1A)

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22
Q

a1 Effects

A

muscle contraction
pupil dilation
prostate contraction; decrease urine output
raises blood pressure

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23
Q

Enlarged Prostate

A

a1A blocker to relax

avoid a agonists and M antagonists

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24
Q

a2 Locations

A

adrenergic presynaptic nerve terminals

pancreatic B cells

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25
Q

a2 Effects

A

negative feedback/ inhibit NE release

inhibits insulin release/ decreases storage

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26
Q

B1 Locations

A 
heart
juxtaglomerular cells (JGA)
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27
Q

B1 Effects

A

increase heart rate and force

stim renin release

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28
Q

B2 Locations

A

respiratory, uterine, vascular smooth muscle
liver
voluntary muscle

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29
Q

B2 Effects

A

relaxes smooth muscle- bronchodilation, stop premature labor, decrease BP
stimulates glycogenesis
causes tremor

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30
Q

How is B2 activated?

A

Epi in blood

not innervated

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31
Q

B3 Locations

A

fat cells

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32
Q

B3 Effects

A

stim lipolysis

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33
Q

Dopamine Receptor Locations

A

renal and blood vessels

34
Q

Dopamine Receptor Effects

A

relaxes renal and blood vessels - vasodilation

35
Q

CNS Effects

A

do not enter except for amphetamines

36
Q

Eye Effect

A

mydriasis (a1)

37
Q

Bronchi Effects

A

relax (B2)

38
Q

GI Effects

A

relax (B2)

39
Q

Urinary Effects

A 
contract (a1)
relax detrusor (B3)
40
Q

a1 Effects on Vascular System

A

increase pressure

reflex bradycardia

41
Q

B2 Effects on Vascular System

A

reduce pressure

reflex tachycardia

42
Q

Low Dose Dopamine

A

vasodilation of renal vessels (D1)

43
Q

Medium Dose Dopamine

A

has B1 effect on heart- increases rate

44
Q

High Dose Dopamine

A

acts on a1 to increase TPR and BP

45
Q

Direct Acting Adrenergic Agonists

NE

A

a1, a2, B1
increase TPR and BP
long term reflex bradycardia

46
Q

Direct Acting Adrenergic Agonists

Epi

A

a1, a2, B1, B2

47
Q

Direct Acting Adrenergic Agonists

Epi Low Dose

A

lowers BP and increases HR

48
Q

Direct Acting Adrenergic Agonists

Epi High Dose

A

increase BP

initial tachycardia followed by long term bradycardia

49
Q

Examples of Direct Acting Adrenergic Agonists

A

Isoproterenol
Phenylephrine
Albuterol
Mirabegron

50
Q

Isoproterenol

A

B1, B2 agonist

not used

51
Q

Phenylephrine

A

a1 agonist

mydriasis

52
Q

Albuterol

A

B2 agonist

53
Q

Mirabegron

A

B3 agonist for urinary incontinence

54
Q

Indirect Acting Adrenergic Agonists

A

don’t act on a or B receptors

go into nerve and release NE from vesicles

55
Q

Indirect Acting Adrenergic Agonists Examples

A

Amphetamine
Tyramine
Cocaine

56
Q

Amphetamine

A

increases NE release
a1 for vasoconstriction
B1 increased heart rate

57
Q

Tyramine

A

increases NE release
in ripe cheese and red wine
oxidized by MAO and normally has no effect

58
Q

Combining Tyramine and MOAI

A

hypertensive crisis

59
Q

Cocaine

A

blocks reuptake of NE
a1 vasoconstriction
B1 increased heart rate

60
Q

Ephedrine

A

mixed action adrenergic agonist
increases NE release
direct action on a and B like Epi

61
Q

Treating Anaphylactic Shock

A

Ephedrine

62
Q

Treating Acute Asthmatic Bronchoconstriction

A

B2 agonists

63
Q

Irreversible a-Adrenergic Blockers

A

long lasting

nonselective so blocks a1 and a2

64
Q

Phenoxybenzamine

A

Irreversible a-Adrenergic Blocker

lasts 48 hours

65
Q

Examples of Reversible a-Adrenergic Blockers

A

Zosins (a1)

mirtazapine (a2)

66
Q

a2 Block at Heart

A

increased levels of NE- tachycardia

67
Q

Pheochromocytoma

A

tumor of adrenal medulla
increases NE and Epi = increase BP
uses phenoxybenzamine before surgery (a1 block)

68
Q

Benign Prostatic Hyperplasia

A

enlarged prostate

treat with Zosins (a1A block)

69
Q

Hypertension Treatment

A

Zosins

a1 block

70
Q

a Blocker Toxicity

A

hypotension and reflex tachycardia

first dose should be slow

71
Q

B Blocker Examples

A

Olols

labetalol and carvedilol

72
Q

Nonspecific B Blockers Examples

A

N-Z Olols

73
Q

B1 Specific B Blockers Examples

A

A-M Olols

74
Q

a1 and B Blockers

A

labetalol

carvedilol

75
Q

B Blockers and Heart

A

blocks B1 for decreased rate

blocks B2 to prevent vasodilation

76
Q

B Blockers and Renal

A

block B1 to inhibit renin release

77
Q

B Blockers and Lungs

A

block B2 to cause bronchoconstriction

78
Q

B Blockers and Glucose Metabolism

A

block B2 causing decreased glycogenolysis and lowers blood glucose

79
Q

Glaucoma Treatment

A

B blocker decreases aqueous humor production

80
Q

B Blocker Toxicity

A

Hypotension, bradycardia
fatigue and sleep disturbance (CNS)
increase plasma lipids (decrease insulin)

Pharmacology (12 decks)

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