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CVS II Pharmacology > Adrenoceptor Agonists/Antagonists > Flashcards

Adrenoceptor Agonists/Antagonists Flashcards

1
Q

what amino acid are catecholamines derived from

A

tyrosine

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2
Q

what is the order of epinephrine formation from tyrosine

A

tyrosine –> dopa –> dopamine –> norepinephrine –> epinephrine

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3
Q

what catecholamine is secreted by the adrenal medulla

A

epinephrine

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4
Q

What is the role of MAO and COMT

A

metabolism of catecholamines

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5
Q

where is COMT absent

A

intraneuronal

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6
Q

what is the MOA of cocaine

A

neuronal reuptake inhibitor (of NE and E)

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7
Q

what is the MOA of reserpine (no longer used clinically)

A

vesicular reuptake inhibitor

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8
Q

where is MAO-A located

A

adrenergic neurons, intestine, liver, kidney, and placenta

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9
Q

where is MAO-B located

A

dopaminergic neurons, brain, platelets, and liver

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10
Q

what is the MOA of clorgyline and moclobemide

A

MAO-A inhibitors

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11
Q

What is the most widely used MAO-B inhibitor and what is it used to treat

A

selegiline; Parkinson’s Disease

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12
Q

what is the role of alpha2 adrenergic receptor

A

inhibits further release of NE from presynaptic adrenergic neurons

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13
Q

what receptor does clonidine target

A

alpha 2

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14
Q

what receptor does terbutaline target

A

beta 2

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14
Q

what receptor does phenylephrine target

A

alpha 1

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14
Q

what receptor does dobutamine target

A

beta 1

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15
Q

what receptor does oxymetazoline target

A

alpha 1 and 2 (non-specific)

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16
Q

what receptor does isoproterenol target

A

nonspecific beta 1 and 2

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17
Q

what receptor does epinephrine target

A

all! alpha 1, 2 and beta 1, 2

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18
Q

what receptor does norepinephrine target

A

all except beta 2 (alpha 1, 2, and beta 1)

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19
Q

what is the MOA of amphetamines and tyramine

A

release/displace NE from vesicles of sympathetic nerve varicosities

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20
Q

what are some of the effects of phenylephrine

A

mydriasis, increased TPR, increased DBP, increased afterload, increased venous return and increased preload, increased glycogenolysis, and decreased renin release

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21
Q

what drug results in reflex bradycardia and why

A

phenylephrine; HR is decreased to compensate for the increase in peripheral vascular resistance and BP

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22
Q

What is the MOA of clonidine

A

alpha 2 selective agonist: decrease sympathetic outflow and suppress NE release

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23
Q

adverse effects of clonidine

A

dry mouth, sedation, nasal stuffiness, constipation, impotence (ed)

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24
Q

list common uses of clonidine

A

moderate HTN, prophylaxis of migraine, manage opiate, alcohol and nicotine withdrawal, menopause hot flashes, control diarrhea in diabetics w autonomic neuropathy

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25
Q

what is the MOA of tizanidine

A

centrally acting alpha-2 adrenoceptor agonist: presynaptic inhibition of motor neurons to decrease spasticity (used in MS)

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26
Q

what are the uses of albuterol, salmeterol, and terbutaline

A
  1. asthma relief (immediate)
  2. arrest uncomplicated premature labor
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27
Q

what are the adverse effects of beta2 selective agonists (albuterol, salmeterol, terbutaline)

A

tremors, palpitations, hypokalemia

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28
Q

what are the effects of beta-2 selective agonists

A

vasodilation, decreased TPR, decreased DBP, increased glycogenolysis, increased insulin secretion

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29
Q

what is mirabegron used to treat

A

overactive bladder (beta 3 selective agonist)

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30
Q

what are the clinical effects of dobutamine

A

as a selective beta 1 agonist, it will increase HR, conduction velocity, force of contraction, and renin release

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31
Q

why is dobutamine useful in heart failure

A

it increases CO and stroke volume without significantly increasing heart rate

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32
Q

what receptor is the primary target for epinephrine at low doses

A

beta 2 receptors

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33
Q

what receptor is the primary target for epinephrine at a moderate dose

A

beta 1

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34
Q

what receptor is the primary target for epinephrine at a high dose

A

alpha 1

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35
Q

what is the effect of epinephrine on SBP an DBP

A

overall increase in SBP and decrease in DBP

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36
Q

uses of EPI

A

anaphylactic shock, prolong duration of local anesthetic agents, control epistaxis and cardiac resuscitation

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37
Q

what are the adverse effects of epinephrine

A

angina, palpitation and arrhythmias, anxiety, tremors, headache, and cerebral hemorrhage

38
Q

list the contraindications of epinephrine

A

HTN, angina, hyperthyroidism, and concomitant use of MAO

39
Q

Epi/NE has poor beta2 action

A

NE

40
Q

how does NE differ from EPI with regard to SBP and DBP

A

NE: raises both SBP and DBP (via beta 1 and alpha 1)
E: raises SBP but lowers DBP

41
Q

list the uses of NE

A

cardiac arrest, hypotensive states in surgical shock and MI, alongside local anesthetics

42
Q

NE contraindications

A

may cause renal shutdown so dopamine is preferred in cardiogenic shock

43
Q

what receptors does dopamine work on

A

D1, D2, and B1 based on dosage (similar to that of epi)

44
Q

what is the dosage effect of dopamine

A

D1/D2 0.5-2mcg/kg/min
beta 1 2-10mcg/kg/min
alpha effect >10mcg/kg/min

45
Q

what is the effect of low dose dopamine (iv infusion)

A

increased urine output and renal blood flow

46
Q

what is the effect of moderate dose of dopamine

A

increased renal blood flow, CO, HR, and cardiac contractility

47
Q

what is the effect of high dose dopamine

A

increased BP and vasoconstriction

48
Q

list the uses of DA

A

cardiogenic shock, CCF, liver and renal failure, hypotensive states

49
Q

list the adverse effects of DA

A

nausea, tachycardia (high doses), hypertension, ectopic beats, arrhythmias

50
Q

what receptors does isoproterenol target?

A

beta 1, 2, 3 but no alpha action

51
Q

label the three graphs based on the drug its depicting

A

NE, E, ISO (L to R)

52
Q

explain Dale’s vasomotor reversal

A

its the effect of Epi when given after pretreatment of an alpha blocker: hypotension due to predominant beta2 effect

53
Q

what happens when epi is given after pretreatment of a beta blocker

A

accentuated hypertensive effect

54
Q

fill in the blank

A
55
Q

how can tyramine cause a “cheese rxn”

A

bc its metabolized by MAO so if a pt is on an MAO inhibitor, it can trigger a hypertensive crisis

56
Q

what is the common suffix of alhpa-1 selective antagonists

A

“zosin”
prazosin, terazosin, doxazosin, alfuzosin, tamsulosin

57
Q

phenoxybenzamine is an (alpha/beta) receptor antagonist

A

alpha; along with phentolamine

58
Q

what type of receptor antagonist is the drug phentolamine

A

non-selective alpha antagonist

59
Q

beta blockers typically have the suffix:

A

“olol”

60
Q

what are the effects of phenoxybenzamine

A

vasodilation, hypotension, tachycardia (reflex)
due to being a nonselective alpha antagonist

61
Q

what is phenoxybenzamine used to treat

A

pheochromocytoma, raynaud’s syndrome frostbite

62
Q

what are the adverse effects of phenoxybenzamine

A

postural hypotension, inhibition of ejaculation, sedation

63
Q

what is the MOA of phentolamine

A

competitive, reversible antagonist of alpha 1 and alpha 2

64
Q

what are the effects of phentolamine

A

vasodilation, decreased peripheral vascular resistance, hypotension, and reflex tachycardia

65
Q

what are the clinical uses of phentolamine

A

pheochromocytoma, peripheral vascular disease, and hypertensive crisis

66
Q

what is the MOA of prazosin

A

alpha-1 selective blocker

67
Q

what are the uses of prazosin

A

PTSD, nightmares, BPH, HTN, Raynaud’s syndrome

68
Q

what are the adverse effects of prazosin

A

postural hypotension, and the first dose phenomenon

69
Q

why are tamsulosin and silodosin more effective in BPH with little effect on BP?

A

because they are alpha 1 A antagonists which are specific to the bladder neck and urethra

70
Q

what are the adverse effects of tamsulosin and silodosin

A

abnormal ejaculation and floppy iris syndrome

71
Q

what’s the MOA of tamsulosin and silodosin

A

alpha 1A antagonists

72
Q

what is the MOA of yohimbine

A

alpha-2 antagonist

73
Q

what is the MOA of propranolol

A

nonselective beta blocker

74
Q

what are the effects of propranolol

A

bronchoconstriction (beta 2 block), decreased renin, decrease HR, B, contractility, CO, and velocity

75
Q

what are the cardiovascular uses of propranolol

A

CCF, angina pectoris (bc it decreases cardiac workload), Arrhythmias, and MI

76
Q
A
77
Q

list the adverse effects of propranolol

A

bronchoconstriction, bradycardia, cold extremities, hypoglycemia, fatigue, sleep disturbances, rebound hypertension, adverse lipid profile, sexual dysfunction

78
Q

what is the treatment for a pt with beta blocker toxicity

A

maintain ABC
IV fluid, ATROPINE
glucagon

79
Q

what is the MOA and clinical use of timolol

A

non-selective beta blocker; treats open angle glaucoma

80
Q

what is the MOA and clinical use of sotalol

A

non-selective beta blocker; class III anti-arrhythmic

81
Q

what beta blockers are safer in asthmatics

A

beta-1 selective blockers; esmolol and metoprolol

82
Q

what are the advantages of the beta-1 selective blockers, esmolol and metoprolol

A
83
Q

what is the MOA of labetolol

A

mixed alpha-1 and beta-1 antagonist

84
Q

what are the effects of labetolol

A

decrease BP, vaso and bronchodilation

85
Q

what are the clinical uses of labetolol

A

HTN, pheochromocytoma, and rebound HTN in clonidine withdrawal

86
Q

what are the adverse effects of labetolol

A

postural hypotension and heptotoxicity

87
Q

what is the MOA of Carvedilol

A

mixed beta-1, beta-2, and alpha-1 blocker (lesser alpha)

88
Q

what are the effects of carvedilol

A

inhibits free radical induced lipid peroxidation, inhibits smooth muscle mitogenesis, blocks L-type VGCa++ channels

89
Q

what are the clinical uses of carvedilol

A

CCF, HTN, angina

90
Q

what are the effector tissues for alpha-1 receptors and what do they cause

A

smooth muscles, eye, arterioles veins, vas deferens, liver, kidneys, pancreas
Gq (IP3/DAG)
increase Ca++, cause contraction
mydriasis, increased TPR, DBP, and Venous return; ejaculation, increased glycogenolysis and decreased insulin secretion

91
Q

what are the effector tissues for alpha-2 receptors and what do they cause

A

mostly nerve endings
Gi (decrease cAMP)
decrease transmitter release (nerves) by inhibiting further release of NE from presynaptic adrenergic neuron, inhibit digestive activity, and decrease insulin secretion and increase platelet aggregation

92
Q

what are the effector tissues for beta-1 receptors and what do they cause

A

cardiac muscle (SA and AV node), JG apparatus
Gs (increase cAMP)
increase HR, increase force/contractility, conduction velocity and increase renin release

93
Q

what are the effector tissues for beta-2 receptors and what do they cause

A

smooth muscle (blood vessels, uterus, bronchioles), pancreas, liver
Gs (increase cAMP)
relax smooth muscle, decrease TPR and DBP, uterine relaxation, bronchodilation, increase glycogenolysis and increased insulin secretion

94
Q

what are the effector tissues of beta-3 receptors and what do they cause

A

adipose cells
Gs
increase lipolysis

95
Q

what are the effector tissues of D1 receptors and what do they cause

A

smooth muscle
Gs (increase cAMP)
relax renal vascular smooth muscle, increases RBF and GFR

CVS II Pharmacology (9 decks)

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