Adrenergics Flashcards

1
Q

SA node - B1 - __________

A

increased rate

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2
Q

AV node - B1 - __________

A

increased conduction

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3
Q

Ventricles - B1 - __________

A

increased contractility

Increased automaticity

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4
Q

Blood vessels in skin/mucosa - a1 - _________

A

constriction

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5
Q

Blood vessels in skeletal muscle - B2 - ________

A

dilation

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6
Q

Blood vessels in skeletal muscle - a1 - __________

A

constriction

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7
Q

Blood vessels in abdominal viscera - a1 - _________

A

constriction

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8
Q

Blood vessels in abdominal viscera - B2 - __________

A

dilation

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9
Q

Blood vessels in lungs - a1 - __________

A

constriction

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10
Q

juxtaglomerular apparatus - B1 - __________

A

renin release

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11
Q

GI - B2 - ___________

A

decreased motility

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12
Q

GI - a1 - ___________

A

sphincter contraction

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13
Q

Bladder - B3 - ________

A

detrusor relaxation (prevent urination)

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14
Q

Bladder - a1 - _________

A

sphincter contraction (urine retention)

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15
Q

Sex organs - a1 - ___________

A

ejaculation/orgasm

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16
Q

uterus - a1 - ____________

A

contraction in pregnancy

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17
Q

uterus - B2 - ___________

A

relaxation (pregnant or non pregnant)

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18
Q

prazosin

A

selective, reversible alpha 1 blocker

hypertension
PTSD
BPH

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19
Q

phentolamine

A

nonselective alpha blockers, reversible

pheochromocytoma

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20
Q

phenoxybenzamine

A

alpha blocker, somewhat alpha1 selective, IRREVERSIBLE

BPH

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21
Q

postural hypotension

reflex tachycardia (esp non-selective)

nasal conjestion

anorgasmia

ARE ADVERSE EFFECTS OF

A

ALPHA BLOCKERS

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22
Q

EPI reversal

A

giving epi + alpha blocker reduces blood pressure

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23
Q

lungs - B2 - ___________

A

bronchodilation

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24
Q

propranolol

A

nonselective beta blocker.
(but beta-2 blockade is overcome by beta-1 block)

antihypertensive
migraine ppx
performance anxiety
early in MI

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25
Q
heart block
hypoglycemia in DM
dyslipidemia
bronchoconstriction
CNS depression, lethargy
SIDE EFFECTS OF
A

beta-blockers

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26
Q

timolol

A

non-selective beta blocker

eye drops, for glaucoma

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27
Q

atenolol

A

selective beta-1 blocker

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28
Q

esmolol

A

selective beta-1 blocker

8 minute half life for emegency procedures

29
Q

benefit of selective beta-1 blockers for treating hypertension

A

less risk of respiratory effects

30
Q

enters via NET
concentrates in vesicle
slowly kicks out NE which is metabolized by MAO

A

guanethidine

historically used for HTN

31
Q

enters terminal and blocks vesicle, which prevents entry of NE into vesicle
depletes NE over time

A

reserpine

historically used for HTN

32
Q

clonidine

A

direct alpha-2 agonists

inhibit NE presynaptic release
decrease sympathetic outflow

33
Q

a-methyldopa

A

metabolized to a-methyl-NE

which acts as a2-agonist

34
Q

pregnant patient with essential hypertension can take:

A

a-methyldopa

35
Q

patient with opioid withdrawal symptoms might benefit from:

A

clonidine

36
Q

how does a-2 agonist treat glaucoma?

A

decreases production of aqueous humor

37
Q

treats ADHD

A

clonidine
guanfacine
(sympatholytic in brain)

38
Q

dry mouth
sedation
hypertensive crisis after abrupt withdrawal

A

clonidine

39
Q

dry mouth
sedation
autoimmune response (+ Coombs test)

A

a-methyldopa

40
Q

dexemedetomide (Precedex)

A

a2 agonist

41
Q

rhinitis

A

phenylephrine

42
Q

bronchial asthma

A

terbutaline

43
Q

cardiogenic shock

A

dopamine

44
Q

heart failure

A

dobutamine

45
Q

precursor to dopamine

A

tyrosine

46
Q

dopamine –> ________ –> epinephrine

A

norepinephrine

47
Q

most CIRCULATING epinephrine is metabolized by _____________.

A

monoamine oxidase (MOA) and catechol-o-methyl-transferase (COMPT)

48
Q

NE levels WITHIN the terminal are regulated by ___________

A

monoamine oxidase

49
Q

About 90% of released NE is recycled via _________

A

re-uptake by the presynaptic neuron at NET (NE transporter)

50
Q

taken up by NET and vesicle in presynaptic neuron,

this rapidly kicks NE out of the vesicle which then diffuses into the terminal

A

amphetamine

increases BP and HR

51
Q

reversing action of the NET and increasing NE in the terminal is generally called:

A

FACILITATED EXCHANGE DIFFUSION

52
Q

normally metabolized by MOA in the gut

goes through NET and kicks NE out of presynaptic neuron –> hypertension

A

tyramine

53
Q

blocks NET (reuptake of NE) leading to rapid increase of NE in the synapse

A

cocaine
imipramine
atomoxetine

54
Q

phenylephrine

A

a1 agonist

in nasal spray, constricts blood vessels in nose

55
Q

chronic use of an adrenergic agonist causes ______ of receptors

A

desensitization and down regulation

except nicotine at nicotinic receptors

56
Q

chronic use of adrenergic antagonist causes _______ of receptors

A

super sensitization and up-regulation

57
Q

NE is released by______

A

postganglionic sympathetic neurons

58
Q

NE likes to bind to ________ receptors

A

a1 and B1

59
Q

Isoproterenol selectively binds to _______ receptors

A

Beta (1 and 2)

60
Q

Epinephrine binds to _______ at low concentrations, but binds to ______ at high doses.

A
beta receptors (1 and 2)
alpha
61
Q

Dopamine binds to _______ most, but also binds ______ at low doses and ______ at high doses.

A
dopamine receptors
beta receptors
all receptors (promiscuous!)
62
Q

Dobutamine preferentially binds to _______ receptors.

A

beta-1

at high doses will bind to anything

63
Q

Which drug stimulates contractility without affecting HR?

A

dobutamine

64
Q

B1 receptors prefer __________ over _______ and ______.

A

isoproterenol

epi = NE

65
Q

B2 receptors prefer ________ over ________ over ______.

A

isoproterenol > epi&raquo_space; NE

NE likes the 1s

66
Q

a1 receptors prefer _________ over _______ over _________.

A

epi > NE&raquo_space; isoproterenol

iso likes beta

67
Q

Drugs without hydroxyl groups get into the brain easily. These include:

A

phenylephrine
ephedrine
amphetamine

68
Q

Which adrenergic agonist cannot be metabolized by MOA?

A

amphetamine

69
Q

no reflex tachycardia

A

alpha-2 agonists