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SBL Pharm Week (EH) > Lecture 6: Adrenergic Drugs > Flashcards

Lecture 6: Adrenergic Drugs Flashcards

1
Q

The α1 AR is what type of GPCR?

What are the downstream effects?

A
  • Gq
  • Activates PLC; increased IP3, DAG; Ca2; activates PKC
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2
Q

The α2 AR is what type of GPCR?

What are the downstream effects?

A
  • Gi
  • Decreased cAMP
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3
Q

The β AR’s is what type of GPCR?

What are the downstream effects?

A
  • Gs
  • Increased cAMP
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4
Q

There are 5 dopamine receptors, what type of GPCR is each and what are the downstream effects of each?

A

D1 = Gs = Increased cAMP

D2 = Gi = Decreased cAMP

D3 = Gi = Decreased cAMP

D4 = Gi = Decreased cAMP

D5 = Gs = Increased cAMP

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5
Q

What are 4 major effects produced by stimulation of α1 AR’s?

A

1) Contraction of most vascular smooth muscle
2) Contraction pupillary dilatory muscle (dilates pupil)
3) Contraction of the prostate
4) Increases force and contraction of the heart

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6
Q

What are 4 major effects produced by stimualtion of α2 AR’s?

A

1) Aggregation of platelets
2) Inhibition of NT release at adrenergic and cholinergic nerve terminals
3) Contraction of some vascular smooth muscle
4) Inhibition of lipolysis in adipocytes

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7
Q

What is the major effect of stimulation of β1 AR’s on the heart and juxtaglomerular cells?

A
  • Increases force and rate of contraction
  • Increases renin release
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8
Q

What are the major effects of stimulation of β2 AR’s on the liver, skeletal muscle, and respiratory, uterine, and vascular smooth muscle?

A
  • Relaxation of respiratory, uterine and vascular smooth muscle
  • Promotes skeletal muscle potassium uptake
  • Activates glycogenolysis and gluconeogenesis in the liver
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9
Q

What is the major effect of stimulation of β3 AR’s on the bladder and fat cells?

A
  • Relaxes detrusor muscle in bladder
  • Activates lipolysis in adipocytes
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10
Q

What is the major effect of stimulation of D1 and D2 receptors?

A
  • D1 = dilation of renal blood vessels
  • D2 = modulation of transmitter release at nerve endings
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11
Q

What 2 drugs are direct adrenomimetic alpha agonists?

A

1) Phenylephrine - α1 > α2 >>>> β
2) Clonidine - α2 > α1 >>>>> β

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12
Q

What 2 drugs are direct adrenomimetic mixed alpha and beta agonists?

A

1) Norepinephrine - α1 = α2; β1 >> β2
2) Epinephrine - α1 = α2; β1 = β2

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13
Q

What 4 drugs are direct adrenomimetic beta agonists?

A

1) Dobutamine β1 > β2 >>> α
2) Isoproterenol β1 = β2 >>> α
3) Terbutaline β2 >> β1 >>> α
4) Albuterol β2 >> β1 >>>> α

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14
Q

What 2 drugs are direct adrenomimetic Dopamine agonists?

A

1) Dopamine D1 = D2 >> β >> α
2) Fenoldopam D1 >> D2

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15
Q

Which receptors does Norepinephrine act on?

A

α1 = α2; β1 >> β2

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16
Q

What are the major effects of Norepinephrine?

A
  • Potent cardiac stimulant, but reduces HR
  • Potent vasoconstrictor = increases peripheral vascular resistant and BP —> baroreflex will decrease the HR
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17
Q

Which receptors does Phenylephrine activate?

A
  • α agonist
  • α1 > α2 >>>> β
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18
Q

What is Phenylephrine used for and what are its effects?

A
  • Effective mydriatic (pupil dilator) and decongestant
  • Causes severe vasoconstriction, BP elevation and severe bradycardia
  • Role of baroreflex in the severe bradycardia
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19
Q

Which receptors does Clonidine activate most specifically?

A
  • Selective α2 agonist
  • α2 > α1 >>>> β
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20
Q

What are the central effects of Clonidine?

A
  • Act on α2 receptors in lower brainstem area
  • Decrease sympathetic outflow; reduction in BP; bradycardia
  • Local application produces vasoconstriction
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21
Q

Which receptors does Isoproterenol activate most specifically?

A
  • Non-selective beta agonist
  • β1 = β2 >>> α
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22
Q

What are the effects of Isoproterenol?

A
  • Non-selective beta agonist
  • Positive inotropic and chronotropic action, increases CO (β1)
  • Vasodilator, decreases arterial pressure (β2)
  • Bronchodilation (β2)
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23
Q

Which receptors does Dobutamine activate most specifically?

A
  • Selective β1 agonist
  • β1 > β2, α1
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24
Q

What is the effect of the (-) isomer vs. (+) isomer of Dobutamine on α1 receptors?

A
  • (-) isomer is an agonist
  • (+) isomer is an antagonist
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25
Q

What are the effects of Dobutamine?

A
  • Potent inotropic action
  • Less prominent chronotropic action as compared to isoproterenol
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26
Q

Which receptors do Terbutaline and Albuterol activate most specifically?

A
  • Selective β2 agonists
  • β2 > β1 >>>> α
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27
Q

What are the effects of Terbutaline and Albuterol?

A
  • Selective β2 agonists
  • Bronchodilation and relaxation of uterus
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28
Q

Where are there a high density of D1 receptors?

Activation by Dopamine causes?

A
  • Renal, cerebral, mesenteric and coronary vessels
  • Causes vasodilation
29
Q

Activation of presynaptic D2 receptors by dopamine causes what?

β1 receptors in heart?

α1 receptors of vasculature?

A
  • Suppresses NE release when D2 receptors activated presynaptically
  • At higher doses activates β1 receptors in heart
  • At even higher doses stimulates vascular α1 AR to cause vasoconstriction
30
Q

Which receptors does Dopamine effect most specifically?

A

D1 = D2 >> β1 >> α1

31
Q

What is the MOA of Ephedrine?

How is it classified?

A
  • Indirect adrenergic agonist
  • Released stored catecholamines w/ some direct action (similar to epinephrine in action)
32
Q

What is the clinical use of Ephedrine?

A
  • Nasal decongestant
  • Increases BP
  • Stress incontinence in women
33
Q

What is the MAO of Phenelzine and Selegiline?

How are they classified?

A
  • Indirect adrenergic agonist
  • Inhibitors of Monoamine oxidases (MAO)
  • Increase NE stores in CNS
  • Antidepressant action
34
Q

What is the MOA of Tyramine?

How is it classifed

A
  • Indirect adrenergic agonist
  • When administered parenterally releases stored NE from presynaptic adrenergic terminals (aka postganglionic sympathetic terminal)
35
Q

Administration of Tyramine may lead to marked increases in BP if given to patients taking what?

A

MAO inhibitors; since is metabolized by MAO in liver (first-pass effect)

36
Q

Tyramine is found in high concentrations in what types of food?

A
  • Smoked and pickled fish
  • Cheese
  • Cured meats
37
Q

Which 2 drugs would we use clinically to increase BP during hypotensive emergencies i.e., hemorrhagic shock, OD of antihypertensives, CNS depressants?

A
  • Norepinephrine (mixed alpha and beta agonist)
  • Phenylephrine (alpha agonist α1 > α2)
38
Q

Which drug would we use clinically to increase BP for chronic hypotension?

A

Ephedrine (indirect adrenergic agonist)

39
Q

Which 2 drugs would we use clinically to increase BP for cardiogenic shock (due to massive acute MI)?

A
  1. Dopamine
  2. Dobutamine
40
Q

What class of drugs would be used for long-term treatment of HTN?

A

Alpha-2 agonists (i.e., Clonidine)

41
Q

Which 3 adrenergic drugs would be used for Obesity?

A

1) Phentermine
2) Ephedrine
3) Amphetamines

42
Q

What are 2 adrenergic drugs that are beta-2 selective agonists used clinically for bronchial asthma?

A

1) Albuterol
2) Terbutaline

43
Q

Which 3 adrenergic drugs are used clinically for decongestion of mucous membranes?

A

1) Phenylephrine
2) Ephedrine
3) Pseudoephedrine

44
Q

Which drug is used clinically for examination of the retina due to its ability to induce mydriasis?

A

Phenylephrine (an α agonist - α1 > α2)

45
Q

Which class and 2 adrenergic drugs are used in the treatment of Glaucoma?

A
  • Alpha-2 selective agonists
  • Apraclonidine and Brimonidine
46
Q

Which class and what drug is used clinically for the suppression of pre-mature labor?

A

Beta-2 agonists (Terbutaline)

47
Q

What is the MOA of Metyrosine?

A
  • Indirect antiadrenergic drug
  • Inhibits tyrosine hydroxylase, which is a necessary enzyme in the synthesis of catecholamines
48
Q

What is the MOA of Guanethidine and what class does it belong to?

A
  • Prevents storage, depletes NE
  • Indirect antiandrenergic drug
49
Q

What are the 2 non-selective (α1 and α2) receptor antagonists?

A
  • Phentolamine
  • Phenoxybenzamine
50
Q

What are the 6 α1 receptor selective antagonists? (hint: the suffix is the same for all)

A

1) Prazosin
2) Terazosin
3) Tamsulosin
4) Doxazosin
5) Alfuzosin
6) Silodosin

51
Q

Phentolamine and Phenoxybenzamine are both non-selective (α1 and α2) receptor antagonists, but how do they differ in binding/enzyme kinetics?

A
  • Phentolamine is a reversible competitive α antagonist = non-covalent binding to receptor = shorter acting
  • Phenoxybenzamine is a irreversible non-competitive α antagonist = covalent binding to receptor = longer acting
52
Q

What are the adverse effects produced by alpha antagonists?

A
  • Decreased peripheral vascular resistance and BP
  • Postural hypotension
  • Reflex tachycardia
  • Retention of fluid and salt
  • Impaired ejaculation
  • Nasal stuffiness
53
Q

Which 2 drugs are used in the treatment of Pheochromocytomas?

A

1) Phentolamine
2) Phenoxybutamine

54
Q

Which 3 drugs are used clinically for chronic (essential) HTN?

A
  • Prazosin, Terazosin, and Doxazosin = α1 selective

*Non-selective α-blockers NOT used

55
Q

Which α receptor subtype is the most important in mediating prostate smooth muscle contraction?

Due to this what 2 drugs are used clinically for BPH?

A
  • α1A is the most important
  • Use Tamsulosin and Silodosin = greater selectivity for α1A
56
Q

Which beta-blockers are Antagonists?

Partial agonists?

Inverse agonists?

A

Antagonist: atenolol, nadolol, propranolol, and betaxolol

Partial: acebutolol, labetalol, penbutolol, pindolol

Inverse: carvedilol and metoprolol

57
Q

Which 4 beta-blockers are β1 selective?

A
  • Metoprolol
  • Acebutolol
  • Betaxolol
  • Atenolol

MABA - Make America Bitchin’ Again

58
Q

Which 4 beta-blockers are β1 and β2 (non-selective) blockers?

A
  • Propranolol
  • Pindolol
  • Penbutolol
  • Nadolol
59
Q

What are beta blockers w/ ISA (intrinsic sympathomimetic activity) and what do they do?

Why are they useful clinically?

A
  • Partial agonists at beta adrenergic receptors (i.e., Acebutolol, Labetalol, Penbutolol, Pindolol)
  • Block sympathetic effects BUT have submaximal effects of their own = a blunted sympathetic response
  • Less risk for bradycardia, increase in VLDL/HDL, amongst others
60
Q

What are the effects of beta-blockers on the heart?

A
  • Negative inotropic and chronotropic effect
  • Block AV node: slowed AV conduction and increased PR interval
61
Q

What is the effects of beta-blockers on the blood vessesl, both initially and after chronic use?

A
  • Initially –> rise in peripheral vascular resistance
  • Chronic use –> decrease in PVR (lowers BP in hypertensive individuals)
62
Q

What are the effects of beta-blockers on the RAAS, respiratory system, and eye?

A
  • RAAS –> inhibits renin release
  • Respiratory –> increase airway resistance
  • Eye –> reduce production of aqueous humor - reduce intraocular pressue
63
Q

What are the metabolic effects of beta blockers?

A
  • Inhibit lipolysis
  • Increase VLDL and decrease HDL, reduce HDL cholesterol/LDL cholesterol ratio
  • Inhibit glycogenolysis and gluconeogenesis in liver
64
Q

What are the 2 mixed (α and β) blockers?

A
  • Labetalol (β- and α1 antagonist)
  • Carvedilol (β- and α1 antagonist)
65
Q

How are beta-blockers used clinically for HTN?

A
  • Antihypertensive effect is delayed
  • Both beta-blockers and mixed α and beta-blockers (Labetalol) are used
66
Q

Which 4 heart conditions are beta-blockers used for?

A

1) Angina pectoris
2) MI –> long-term use in post-infarction period - prolong survival
3) Cardiac arrhythmias –> both ventricular and supraventricular arrhythmias
4) Heart failure –> only in chronic, not acute

67
Q

Which 3 beta-blockers can be used long-term post-MI and have been shown to prolong survival?

A
  • Timolol
  • Propranolol
  • Metoprolol
68
Q

Which 2 beta-blockers may be used for Glaucoma?

A
  • Timolol
  • Betaxolol

*Blockers w/o local anesthetic acitivity

69
Q

Which beta-blocker is used for Hyperthyroidism?

A

Propranolol

SBL Pharm Week (EH) (9 decks)

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