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IC 1.0 > Adrenergic Pharmacology > Flashcards

Adrenergic Pharmacology Flashcards

1
Q

How do indirect sympathomimetic drugs function?

A
  • promote release of endogenous catecholamines
  • displace stored catecholamines
  • inhibit reuptake of catecholamines
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2
Q

Describe the selectivity for NE/Epi, distribution, associated intracellular cascade, and primary effect of a1 adrenergic receptors.

A
  • a1 are found in the peripheral vasculature
  • they have no selectivity with regards to NE v. Epi
  • activation results PLC activation, calcium mobilization, and PKC activation
  • in doing so, they stimulate contraction of smooth muscle and have a pressor effect (increasing BP)
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3
Q

Describe the selectivity for NE/Epi, distribution, associated intracellular cascade, and primary effect of a2 adrenergic receptors.

A
  • they are found on the adrenergic and non-adrenergic presynaptic cells
  • they have no selectivity with regards to NE v. Epi
  • they inhibit AC activity thereby decreasing cAMP levels and preventing a calcium influx
  • they inhibit further NT release by the presynaptic cell
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4
Q

Describe the selectivity for NE/Epi, distribution, and associated intracellular cascade of B-adrenergic receptors.

A
  • they are found in vasculature, lung, eye, and most other end-organs
  • B1 has equal affinity for the two agonists but B2 has higher affinity for Epi than NE
  • both activate AC, increasing cAMP levels in the post-synaptic cell
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5
Q

Through what intracellular cascade do a1, a2, B1, and B2 adrenergic receptors function?

A
  • a1 activate PLC
  • a2 inhibit AC
  • B1 activate AC
  • B2 activate AC
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6
Q

How do D1-type receptors compare to D2-type ones?

A
  • D1 stimulate AC

- D2 inhibit AC

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7
Q

What is phenylethylamine?

A
  • the parent compound for catecholamines

- a benzene ring with an ethyl amine side chain

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8
Q

What is the effect of sympathomimetic drugs on blood vessels?

A
  • alpha receptors increase arterial resistance in the periphery, particularly in the skin and splanchnic vessels, raising blood pressure
  • beta2 receptors relax vascular smooth muscle in skeletal muscles, increasing capacitance and O2 delivery to skeletal muscle
  • the net result is a shift in blood flow
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9
Q

What is the effect of sympathomimetic drugs on the heart?

A
  • B1 receptor activity dominates in the heart
  • activation results in increased calcium influx in cardiac cells, increasing positive inotrophy and chronotrophy
  • AV conduction velocity is increased and the refractory period is decreased
  • but keep in mind that with normal reflexes, heart rate is dominated by vagal tone and pulse will slow
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10
Q

What is the effect of sympathomimetic drugs in the eye?

A
  • alpha agonists contract the radial muscle, producing mydriasis, and slightly increase drainage of aqueous humor
  • beta agonists increase aqueous humor secretion
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11
Q

What is the effect of sympathomimetic drugs on the respiratory tract?

A
  • B2 receptors relax bronchial smooth muscle

- a1 receptors in blood vessels of the upper respiratory mucosa contract, producing decongestion

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12
Q

What is the effect of sympathomimetic drugs on the GI tract?

A
  • the primary GI effect is that alpha2 receptors decrease PNS drive on the enteric system
  • secondary to that, beta receptors have a direct relaxation effect on smooth muscle of the GI tract
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13
Q

What is the effect of sympathomimetic drugs on the GU tract?

A
  • alpha1 receptors contract the bladder base and urethral sphincter, promoting retention
  • beta2 receptors relax smooth muscle of the vessel wall, promoting retention
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14
Q

What is the effect of sympathomimetic drugs on exocrine glands?

A

alpha1 receptors on apocrine (stress) glands increase sweating on the palms of the hands, brow, and upper lip

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15
Q

What are the metabolic effects of sympathomimetic drugs?

A

shifts activity toward energy liberation and usage

  • beta receptors increase lipolysis, enhance glycogenolysis, increase glucose release, and increase insulin secretion (so released glucose can move into skeletal muscle)
  • alpha2 receptors decrease insulin release
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16
Q

a1 agonists have what effects?

A
  • increase arterial resistance in the periphery, particularly the skin and splanchnic vessels
  • inhibit renin release
  • contract radial muscle of the eye, producing mydriasis
  • constrict blood vessels of the upper respiratory mucosa, producing decongestion
  • contract bladder base and urethral sphincter to promote urine retention
  • activate apocrine sweat glands, producing sweating on the palms, brow, and upper lip
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17
Q

a2 agonists have what effects?

A
  • inhibit or diminish PNS tone on the enteric system, reducing GI motility
  • decrease insulin release
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18
Q

B1 agonists have what effects?

A
  • stimulate renin release
  • have a positive inotrophic and chronotrophic effect in the heart
  • increase aqueous humor secretion
  • relax GI smooth muscle
  • increase lipolysis, glycogenolysis, glucose release, insulin secretion
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19
Q

B2 agonists have what effects?

A
  • relax vascular smooth muscle in skeletal muscle, increasing capacitance
  • increase aqueous humor secretion
  • relax bronchial smooth muscle
  • relax GI smooth muscle
  • relax the detrusor muscle, promoting urinary retention
  • increase lipolysis, glycogenolysis, glucose release, insulin secretion
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20
Q

Which adrenergic receptors does epinephrine activate? Norepinephrine?

A
  • epinephrine: all adrenergic receptors

- norepinephrine: a1, a2, B1 > B2

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21
Q

Which is a more potent pressor, epinephrine or norepinephrine?

A

norepinephrine because it doesn’t activate B2 receptors very well and therefore, the vasodilation of vessels within skeletal muscle is limited

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22
Q

What is the effect of NE on heart rate?

A
  • at low dose, the vagal reflex overcomes NE’s chronotrophic effect
  • at high dose, it produces a tachycardia that overcomes the vagal reflex
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23
Q

What class of drug is isoproterenol? What are it’s effects?

A
  • it is a nonselective B-adrenergic receptor agonist
  • it has positive chronotropic and inotropic effects, which increases cardiac output
  • it also dilates certain vessels, decreasing both diastolic and mean arterial pressures
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24
Q

What class of drug is dobutamine? What are it’s effects?

A
  • a sympathomimetic drug with B1 and a1 activity
  • it therefore stimulates the heart (positive chronotropic and inotropic effects) while raising TPR
  • the effect is an increase in CO and MAP
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25
Q

Explain the effects of NE on peripheral resistance, blood pressure, and pulse.

A
  • stimulation of a1 receptors increase TPR
  • B1 activation has a positive inotropic effect
  • overall, then diastolic, systolic, and MAP all rise
  • it induces a bradycardia, however, because the vagal response overcomes the positive chronotropic effect of B1 stimulation
  • summary: TPR, MAP, diastolic BP, systolic BP all increase while HR decreases
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26
Q

Explain the effects of epinephrine on peripheral resistance, blood pressure, and pulse.

A
  • stimulation of a1 and B2 receptors results in a slight decrease in TPR
  • B1 activation has a positive inotropic effect
  • diastolic BP drops, systolic BP increases, and the MAP rises only slightly
  • the slight change in MAP isn’t enough to activate the vagal reflex, so B1 stimulation of the heart has a chronotropic effect and induces a tachycardia
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27
Q

Explain the effects of isoproterenol (B-receptor agonist) on peripheral resistance, blood pressure, and pulse.

A
  • stimulation of B2 receptors induces vasodilation within skeletal muscle, and TPR drops significantly
  • B1 activation has a positive inotropic effect
  • diastolic BP drops, systolic BP increases, MAP drops
  • the drop in MAP activates the sympathetic reflex, which releases NE on the heart, contributing to a tachycardia as does the isoproterenol stimulation of B1 receptors, so the increase is significant
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28
Q

What class of drug is phenylephrine? Describe it’s half life. What are it’s effects and uses?

A
  • the prototypic a1 agonist
  • not inactivated by COMT because it isn’t a catechol derivative, therefore it has a longer duration of action than catecholamines
  • it causes mydriasis, decongestion, and can raise BP
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29
Q

What is methoxamine?

A

an alpha1 receptor agonist

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30
Q

What is ephedrine?

A

the first orally active sympathomimetic drug

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31
Q

What is pseudoephedrine?

A
  • a sympathomimetic
  • a widely available OTC decongestant
  • has direct and indirect effect of releasing endogenous NE
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32
Q

Oxymetazoline

A

a direct a1 agonist used as a topical decongestant

33
Q

Xylometazoline

A

a direct a1 agonist used as a topical decongestant

34
Q

List the important alpha2-selective agonists and their uses. What is their primary side effect?

A
  • clonidine, methyldopa, guanfacine, guanabenz
  • they diminish SNS outflow and are therefore used as antihypertensives
  • may cause orthostatic hypotension
35
Q

What is dobutamine?

A

a sympathomimetic drug that serves as a B1, and to a lesser extent a1, agonist

36
Q

What is prenalterol?

A

a partial B1 agonist

37
Q

What is the clinical benefit of a B1 agonist?

A

it increases CO with less reflex tachycardia because it doesn’t induce B2-stimulated venous dilation

38
Q

List four important B2 agonists and their two most important clinical uses.

A
  • albuterol, salmeterol, terbutaline, and ritodrine

- used to treat asthma and for uterine relaxation in premature labor

39
Q

List the a1 selective agonists.

A
  • phenylephrine
  • methoxamine
  • oxymetazoline
40
Q

List the a2 selective agonists.

A
  • clonidine
  • methydopa
  • guanfacine
  • guanabenz
41
Q

List the B1 selective agonists.

A
  • dobutamine

- prenalterol

42
Q

List the B2 selective agonists.

A
  • albuterol
  • salmeterol
  • terbutaline
43
Q

List the indirect sympathomimetics.

A
  • ephedrine/pseudoephedrine
  • cocaine
  • tyramine
  • amphetamine
  • methamphetamine
  • methylphenidate
44
Q

Describe the action and effects of amphetamine. Compare it to methamphetamine.

A
  • it is an indirect sympathomimetic
  • stimulatant effects on mood and alertness but depressant effect on appetite
  • works by displacing stored catecholamines
  • methamphetamine is similar but with a higher ratio of central to peripheral actions
45
Q

What is methylphenidate? What is it used for?

A
  • a variant of amphetamine

- used in ADHD

46
Q

How does cocaine have it’s effects?

A

it is a sympathomimetic that blocks the activity of uptake 1

47
Q

Where is tyramine found? How does it function? What are it’s effects and side effects? What can be used to potentiate it’s effects?

A
  • found in fermented foods such as cheese
  • it has a high affinity for VMAT and blocks packaging of NE until it builds up and simply diffuses out
  • its effects can be potentiated by MAOIs
  • may produce a hypertensive crisis
48
Q

List the important clinical applications of sympathomimetic drugs.

A
  • hypotension, hypovolemic or cariogenic shock, cardiac insufficiency
  • hemostasis in surgery, reducing diffusion of local anesthetics
  • dobutamine can be used in heart failure
  • bronchial asthma or anaphylaxis
  • premature labor
  • narcolepsy
  • ADHD
49
Q

Describe sympathomimetic toxicity.

A
  • related to the extent of pharmacologic effects in the CV and CNS
  • include hypertension and tachycardia
  • as well as restlessness, tremor, insomnia, anxiety, and paranoia
50
Q

How does phentolamine compare to phenoxybenzamine?

A
  • they are both alpha-receptor antagonists
  • phentolamine is a competitive inhibitor while phenoxybenzamine has a long duration of action thanks to it’s irreversible inhibition of alpha receptors
51
Q

How do alpha receptor antagonists affect the CV system?

A
  • antagonism of a1 receptors in the periphery lead to vasodilation, a drop in TPR, and a lower MAP
  • also reduce ability to respond to postural changes so may cause orthostatic hypotension
  • vagal reflex is likely to initiate tachycardia
52
Q

How can an alpha antagonist be used in conjunction with epinephrine?

A
  • epinephrine is an a1/B2 agonist
  • adding an a1 antagonist can reverse the pressor effects associated with epinephrine
  • the result is essentially a B2 agonist
53
Q

Phentolamine

A
  • the prototypic alpha antagonist (non-selective)
  • works via competitive inhibition of receptors
  • reduces TPR and MAP, initiating a reflex tachycardia
54
Q

Tolazoline

A

an alpha antagonist very similar to the prototype phentolamine

55
Q

Phenoxybenzamine

A
  • an irreversible alpha receptor antagonist
  • moderate a1 selectivity (less than prazosin)
  • used in the treatment of pheochromocytoma
  • SEs include postural hypotension and tachycardia which limit it’s use
56
Q

Prazosin

A

a selective alpha1 receptor antagonist

57
Q

Doxazosin

A
  • a selective alpha1 receptor antagonist with long half-life

- used in the treatment of hypertension and BPH

58
Q

Tamsulosin

A
  • a competitive alpha1 inhibitor
  • slightly structural differences from other drugs provide it with good efficacy in BPH (perhaps more selective for a subtype of a1 receptors in prostate)
59
Q

Alfuzosin

A
  • a competitive alpha1 inhibitor
  • slightly structural differences from other drugs provide it with good efficacy in BPH (perhaps more selective for a subtype of a1 receptors in prostate)
60
Q

Yohimbine

A
  • a selective alpha2 antagonist

- no clinical role

61
Q

Reserpine

A
  • adrenergic antagonist
  • irreversibly blocks VMAT, inhibiting storage of all catecholamines, left unprotected they are metabolized by MAO and COMT in the cytoplasm
  • depletion on DA may lead to a drug-induced Parkinson’s
  • no clinical use, but helpful in establishing catecholaminergic models in the lab
62
Q

How are alpha receptor antagonists used int he treatment of hypertensive emergencies?

A
  • limited use

- direct vasodilators like nitrates are preferred

63
Q

How are alpha receptor antagonists used clinically?

A
  • useful for pheochromocytoma
  • limited used in hypertensive crisis
  • effective against chronic hypertension but may not prevent heart failure and are likely to come with orthostatic hypertension
  • used in the treatment of urinary obstruction due to BPH
64
Q

Esmolol

A

a beta receptor antagonist with an exceptionally short half life compared to the rest of the group due to it’s ester linkage, which is readily hydrolyzed by esterase in RBCs

65
Q

Propanolol

A
  • non-selective beta-receptor antagonist

- extremely low bioavailability due to extensive first-pass effect

66
Q

What is the effect of beta blockers on the CV system?

A
  • affect the heart, vasculature, and renin-angiotensin system
  • lower BP in those with hypertension but don’t often cause hypotension in normal subjects
  • have negative inotropic and chronotropic effects on the heart, reducing O2 demand of the myocardium; the result is that they are cardio protective and offer significant post-MI benefit
  • see slowed AV conduction and increased PR interval
67
Q

What is the effect of beta blockers in the respiratory tract?

A
  • B2 blockade increases airway resistance

- therefore they should be avoided in those with asthma (use selective B1 antagonists instead)

68
Q

What is the clinical used of beta blockers in the eye?

A

reduce intraocular pressure by reducing aqueous humor production

69
Q

What are the endocrine and metabolic effects of beta blockers? What cautions must be taken?

A
  • inhibit SNS stimulation of lipolysis and glycogenolysis
  • use with caution in insulin-dependent diabetics
  • chronic use may increase plasma VLDL or decrease HDL (unknown mechanism)
70
Q

Why are beta blockers with partial beta agonist activity clinically important?

A
  • may help limit the antagonism, thereby avoiding some of the side effects associated with pure antagonists
  • not as effective or cardioprotective post-MI
71
Q

Metoprolol

A

a selective B1 antagonist

72
Q

Atenolol

A

a selective B1 antagonist

73
Q

Nadolol

A

a beta antagonist with very long duration of action

74
Q

Timolol

A

a beta antagonist with very long duration of action

75
Q

Pindolol

A

a beta antagonist with partial agonist activity

76
Q

Labetalol

A
  • a reversible a1 antagonist with nonselective beta-adrenoceptor antagonist activity
  • produces hypotension with less tachycardia than alpha-blockers
77
Q

Butoxamine

A

a selective B2 antagonist with no clinical application

78
Q

What are the primary clinical uses of beta blockers?

A
  • effective and well-tolerated in those with hypertension
  • helpful in those with ischemic heart disease (reduce frequency of angina, improve exercise tolerance, decrease cardiac work, reduce myocardial O2 demand, prolong survival)
  • effective against supra ventricular and ventricular arrhythmias (increase AV node refractory period, slow ventricular response rates in atrial fibrillation, and reduce ventricular ectopic beats)
  • topical administration for glaucoma (particularly open-angle glaucoma)
  • useful in those with hyperthyroidism because it reduces distal tremor and tachycardia
79
Q

Beta Blocker toxicity

A
  • usually well tolerated
  • minor toxicity: rash, fever, sedation, depression
  • major toxicity: worsening of asthma, cardiac decompensation, supersensitivty with abrupt discontinuation after chronic use (gradual tapering necessary to prevent hypertensive crisis)
  • may exacerbate hypoglycemic episodes in diabetics

IC 1.0 (24 decks)

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