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Block 9 Week 1 > Alpha and Beta Adrenergic Blockers - LeBlanc > Flashcards

Alpha and Beta Adrenergic Blockers - LeBlanc Flashcards

1
Q

Catecholamines causes peripheral (inhibition/excitation) on gut, bronchial, blood vessles supplying skeletal muscle SM

A

inhibitory

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2
Q

What are the effects on the heart of catecholamines?

A

increase in frequency and contractile force, increase conduction velocity

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3
Q

Regarding metabolism, what are the effects of catecholamines on fats and sugars?

A

glycogenolysis from liver and skeletal muscles

release of free fatty acids from adipose tissue

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4
Q

Which endocrine hormones do catecholamines regulate?

A

insulin
renin
pituitary hormones

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5
Q

What are the CNS effects of catecholamines?

A

wakefulness
appetite
resp. stim
psychomotor activity

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6
Q

What are the PREjunctional actions of catecholamines?

A

inhibition or facilitation of neurotransmitter release

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7
Q

describe the strength of Epi, NorEpi, and Iso on a1 receptors

A

Epi > NE&raquo_space; Iso

phenylephrine

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8
Q

describe the strength of Epi, NorEpi, and Iso on a2 receptors

A

Epi > NE»Iso

clonidine

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9
Q

describe the strength of Epi, NorEpi, and Iso on B1 receptors

A

Iso > Epi =NE

dobutamine

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10
Q

describe the strength of Epi, NorEpi, and Iso on B2 receptors

A

Iso > Epi&raquo_space; NE

terbutaline

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11
Q

describe the strength of Epi, NorEpi, and Iso on B3 receptors?

A

Iso = NE > epi

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12
Q

Wat is the a1 antagonist?

A

prazosin

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13
Q

What is the a2 antagonist?

A

yohimbine

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14
Q

What is the B1 antagonist?

A

metoprolol

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15
Q

which two receptors are found on smooth muscle?

A

a1

B2

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16
Q

which receptor is found on nerve terminals?

A

a2

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17
Q

Which receptor is found on cardiac muscle?

A

b1

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18
Q

which receptor is found on adipose tissue?

A

B3

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19
Q

What is the effect of stimulating a1 receptors?

A

contraction of SM

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20
Q

what is the effect of stimulating a2 receptors?

A

decreased transmitter release

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21
Q

wha is the effect of stimulating B1 receptors?

A

increase:
chronotropic
inotropic
dromotropic

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22
Q

What is the effect of stimulating b2 receptors?

A

SM relaxation (think albuterol inhalers)

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23
Q

what is the effect of stimulating b3 receptors?

A

lipolysis

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24
Q

what is the G protein assc’d with a1?

A

Gq

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25
Q

what is the G protein assc’d with a2?

A

Gi/o

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26
Q

what is the G protein assc’d with B receptors?

A

Gs

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27
Q

a1 directly stimulates (blank), which activates (blank) which converts PIP2 to IP3 and DAG

A

phospholipase

Protein kinase C

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28
Q

IP3 production allows for (blank) release from intracelllular stores which causes SM contraction

A

Ca

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29
Q

a2 stimulation blocks (blank) release from intracellular stores which blocks neurotransmitter release

A

Ca

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30
Q

A2 activation blocks (blank) activity which converts ATP to cAMP

A

adenylyl cyclase

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31
Q

cAMP production post A2 signaling has what effect on SM?

A

contraction

32
Q

B receptors activate adenylyl cyclase to produce cAMP which does what?

A

increase cardiac contractility
SM relaxation
glycogenolysis

33
Q

How does calcium release from intracellular stores actually get the cell to do things?

A

activates Ca dependent protein kinase

34
Q

which two receptors have competing action on adenylate cyclase?

A

a2 and B receptors

35
Q

Except for Phenoxybenzamine (PBZ) and related compounds, all α receptor antagonists are (blank) inhibitors

A

competitive

36
Q

where do we find the greatest affect of a-1 blockers?

A

smooth muscle; while present in CNS the effect is extremely small

37
Q

a2 receptors (inc/dec) intracellular calcium by decreasing cAMP levels

A

incerease intracell calcium

38
Q

a2 receptors (enhance/limit) sympathetic outflow

A

limit

39
Q

a2 receptors increase (blank) tone and therefore parasympathetic outflow

A

vagal tone

40
Q

what type of receptor increases PLT aggregation in the periphery?

A

a2

41
Q

a2 receptors decrease the release of which two neurotransmitters in the periphery?

A

NE and ACh

42
Q

What is the effect of a2 stimulation on insulin release and lipolysis?

A

decreases both

43
Q

T/F: a2 stimulation decreases lipolysis indirectly

A

false; directly acts on fat cells

44
Q

what receptor class increases insulin release?

A

b

45
Q

what do we use a1 blockers for?

A

decrease blood pressure

46
Q

is the decrease in BP from a1 blockers more noticeable when standing or lying down?

A

standing

47
Q

what can exacerbate the lowering of the BP after giving an a1 blocker?

A

hypovolemia

48
Q

what mechanism compensates for the lowering in BP from a1 blockers?

A

baroreflex:

increase HR and CO

49
Q

If an a1 blocker is mixed with a (blank) blocker, it can exaggerate the baroreflex by leading to the release of NE which activates B1 receptors

A

a2 receptors on a peripheral nerve ending

50
Q

a1 blockers will inhibit the effects of (blank) drugs adminstered externally

A

sympathomimetics; can use to reverse an adverse effect

51
Q

what is the pure a1 agonist and blocker?

A

agon: phenylephrine
blocker: prazosin

52
Q

what is the pure a2 agonist and blocker?

A

agon: clonidine
blocker: yohimbine

53
Q

what is the pure b1 agonist and blocker?

A

agon: dobutamine
blocker: metoprolol

54
Q

what is the pure b2 agonist and blocker?

A

agonist: terbutaline

no blocker

55
Q

t/f: a2 blockers target both the CNS and the periphery

A

true

56
Q

what are the effects of a2 blockers on the periphery?

A

increase release of NE from nerve endings

57
Q

what is the effect of a2 blockers on the CNS?

A

increase sympathetic outflow; increase BP

58
Q

which a1 and 2 blocker binds irreversibly via covalent modification?

A

PBZ/phenoxybenzamine

59
Q

what are the effects of phenoxybenzamine in the periphery?

A

block a receptor in SMC leads to decrease in peripheral resistance
enhanced baroreflex

60
Q

what are the effects of phenoxybenzamine in the CNS?

A

increase sympathetic outflow

tachycardia due to a2 block

61
Q

why would epi produce severe hypotension if given alongside phenoxybenzamine

A

PBZ blocks epi a action, therefore unapposed b2 action, therefore loooots of SMC relaxation

62
Q

why do you get hypotension when standing when taking PBZ?

A

lack of vasomotor reflex from baroreflex

63
Q

at high doses PBZ irreversibly binds to what three other neurotransmitters?

A

Serotonin
histamine
ACH

64
Q

what is the half life of PBZ?

A

less than 24 hours

65
Q

what is the use of PBZ?

A

pheochromocytoma: lots of catecholamines means HTN; PBZ lowers the BP by blocking cat. action

66
Q

what is the non-serious use for PBZ?

A

benign prostatic hypertrophy in men

67
Q

Besides postural hypotension, what are the other side effects of PBZ?

A

nasal stuffiness; miosis

sexual dysfunction in men

68
Q

which drug blocks a1 and a2 similarly via reversible competitive inhibition?

A

phentolamine; PTL

69
Q

what are the two “classic” a blockers?

A

phenoxybenzamine and phentolamine

70
Q

Beside the cardio effects of PTL (which are similar to PBZ), what are the other effects of PTL on other organ systems?

A

stimulates GI smooth muscle and enhances gastric acid secretion

71
Q

(phentolamine/phenoxybenzine) can be used to rapidly alleviate a hypertensive episode

A

phentolamine

72
Q

what happens when you get extravasation of phenyelephrine?

A

necrosis

73
Q

do you use PBZ or PTL for Raynaud’s?

A

PTL

74
Q

which a blocker do you give during rapid clonidine withdrawal or tyramine rich foods during MAOI Tx?

A

phentolamine

75
Q

what are the cardiac SE of phentolamine?

A 
hypotension
reflex tachycardia
arrhythmia
ischemic events
MI
76
Q

what are the GI SE of phentolamine?

A

abdominal pain
nauseua
PUD exacerbation

77
Q

what two conditions contraindicate the use of phentolamine?

A

PUD and CAD

Block 9 Week 1 (4 decks)

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