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Pharmacology > Adrenergic Agonists and Antagonists > Flashcards

Adrenergic Agonists and Antagonists Flashcards

1
Q

Catecholamines

A

Epinephrine, norepinephrine, isoproterenol, dopamine

  1. High potency
  2. Rapid inactivation: metabolized by COMT (gut wall) and MAO (liver and gut wall). Given orally is useless
  3. Poor penetration into the CNS because they are polar
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2
Q

Non catecholamines

A

Phenylephrine, Ephedrine, Amphetamine
lack the -oh catechol, longer half lives, not inactivated by COMT. Better penetration into CNS, some may cause release of catecholamines.

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3
Q

Direct Acting Agonists

A

Epinephrine, NE, Dopamine, Isoproterenol, Dobutamine, Terbutaline, albuterol, salmeterol, formoterol, phenyephrine, colnidine, Methyldopa, Brimonidine

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4
Q

Indirect Acting Agonists

A

amphetamine, methylphenidate, tyramine, cocaine, atomoxetine

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5
Q

Mixed acting Agonists

A

Ephedrine, Pseudoephedrine

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6
Q

Adrenergic Antagonists

A

Phenoxybenzamine, phentolamine, Prazosin, Terazosin, doxazosin, tamsulosin, yohimbine, propranolol, Nadolol, Timolol, Atenolol, metoprolol, esmolol, labetalol, carvedilol

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7
Q

Partial Adrenergic agonists

A

pindolol

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8
Q

Drugs that act presynaptically

A

metyrosine, reserpine, guanethidine

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9
Q

Epinephrine

*FYI: Blood Vessels: B2 has a lower threshold to be activated than A1. So at low concentrations B2 wins. At high doses both are activated and A1 is stronger.

A

Agonist at alpha and beta receptors. Created from Tyrosine. metabolized to metanephrine and vanillylmandelic acid (VMA).
Uses: anaphylactic shock, asthma attacks, cardiac arrest, local anesthetics. Rapid onset and brief duration
Adverse effects: CNS disturbances: fear, anxiety, tension, HA, tremor. Hemorrahage in brain due to increased blood pressure. Cardiac arrhythmias escpecillay if patient is on digitalis, pulmonary edema.
Interactions: Hyperthyroidism: there is a hypersensative response due to increased receptors
Cocaine: prevents reuptake of catacholamines and so it can produce its effects longer
Beta-blockers: these prevent epinephrine activation fo B receptors. Leads to increased peripheral resistance and blood pressure

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10
Q

Epinephrine effects on Cardiovascular System

A

Increases contractility of myocardium B1
Increases contraction rate B1
CO increases and increase in O2 demand B1
Increases Renin Release B1
Constricts arterioles in skin, mucus membranes, and visera A1
Low dose dilation of blood vessels going to the skeletal muscle and liver B2

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11
Q

Epinephrine effects on SM

A

powerful bronchodilation by acting directly on bronchial smooth muscle B2
Relaxes GI smooth muscle A1,2 B2
Sphincter contraction A1
Detrusor muscle relaxaxation B2 and trigone and sphincter contraction A1

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12
Q

Epinephrine on the CNS

A

may cause restlessness, apprehension, HA and tremor in many persons. these are probably secondary effects because it can’t cross BBB very well because its too polar

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13
Q

Epinephrine on metabolism

A

Hyperglycemia: B2. hyperglycemia due to glucagon release in the alpha cells and also glycogenolysis in the liver. Insulin secretion is inhibited because A2 will inhibit it and is stronger than B2
Lipolysis: activates B3 so FFA will be high in blood

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14
Q

Norepinephrine

A

At the adrenergic nerves. the alpha receptor is most affected A1 and 2. Can also activate B1 but NOT B2
Cardiovascular effects: Vasoconstriction due to A1 both systolic and diastolic increase. Reflex bradycardia counters the B1 stimulation. CO unchanged. Unlike epinephrine, NE can cause vasodilation at small doses because that is a B2 process
USES: treat shock, beause it increases peripheral resistance

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15
Q

Dopamine

A

immediate metabolic precursor to NE and epi. Destroy by MOA and COMT.
Cardiovascular effects: at low concentrations D1 is dominant in renal, mesenteric, coronary beds activating cAMP to lead to vasodilation, increase in GFR, RBF and Na excretion. If these systems are causing low CO then DA can fix it. DA at high concentraitons can act on B1 receptors. DA also causes NE to be released from nerve terminals. Usually increases Systolic blood pressure only. Total peripheral resistance is unchanged. At high concentraiton D1 can cause vasoconstriction acting on A1. Cant cross BBB very well.
USES: Drug of choice for cardiogenic shock and septic shock
Adverse: overdose leads to same effects as Epi. Also metabolized to homovanillic acid to produce nausea, HTN, Arrhythmias. good thing it that this effect is short lived.

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16
Q

Fenoldopam

A

D1 receptor selective agonist. Selective leads to peripheral vasodialtion in some vascular beds. Treat severe HTN in the short term. Give by continuous IV infusion. Bolus dose should not be used

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17
Q

Isoproterenol

A

Non selective B agonist. Stimulates both B1 and 2ff
Cardiovascular effects: stimulate the heart B1, treatment of AV block or cardiac arrest, dilates arterioles of skeletal muscle B2 to decrease peripheral resistance. It may increase systole a little but it really decreases diastolic and mean arteriole pressure.
-Bronchdialtion B2. GI is relaxed, Just as strong as epinephrine is createing FFA but causes less hyperglycemia than epi
Uses: can be used to stimulate the heart in emergency situations
Pharmacokinetics: absorbed systemically by sublingual mucosa, more reliably absorbed when given parenterally or as inhaled aerosol. Marginal substrate for COMT and stable to MOA action.
Adverse: similar to epi

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18
Q

Dobutamine

A

Selective for B1 agonist. Administered as racemic mixture consisting fo the + and - isomers. - isomer is A1 agonist and weak B1 agonist. + is A1 antagonist and potent B1 agonist. Net result is B1 agonist
Uses: increase CO for acute management of heart failure. Increases CO with little change in heart rate and doesnt incre o2 demand of myocardium. THis is the major advantage over other sympathetic drugs.

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19
Q

Terbutaline and Albuterol

A

Short acting B2 agonist. bronchodilator for asthma and terbutaline can also reduce uterine contractions in premature labor

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20
Q

Salmeterol and formoterol

A

B2 agonist. long acting bronchodilators of about 12 hours as a result of high lipid solubility. slow onset of action not useful for quick attacks of bronchospasms.

Adverse effects: tremors, restlessness, apprehension, anxiety and eventhough it is B2 there is slight B1 activation so it can cause tachycardia. Adverse effects are less likely than with inhalation therapy than parental or oral

21
Q

phenylephrine

A

A1 agonist. vasoconstrictor. raises both systolic and diastolic. no direct effect on the heart but does ccause reflex bradycardia
USES: nasal decongestant. they cause vasoconstrion in nasal vessels decreaseing space used in the airway.
Used as mydriatic, increases BP for hypotension and septic shock or someone under anasthesia

22
Q

Clonidine

A

A2 agonist. Major antiHTN drug. acts on the cardiovascular control in the CNS. It suppresses the sympathetic signal coming from the brain.
IV infusion (not oral) of clonidine causes brief increase in BP due to the A2 in vascular SM. It will lead to a more prolonged hypotensive response (CNS)
Adverse: sedation, xerostomia, lethargy

23
Q

Methyldopa

A

A2 Agonist, anti HTN. taken up by Noradrenergic neurons and metabolized to alpha-methylnorepinephrine which then activates A2 much like clonidine. This is the drug for treating hypertension during pregnancy because it is effective and safe for both parties involved.
Adverse: sedation, mental lassitude, impaired mental concentration, dry mouth

24
Q

Brimonidine

A

A2 highly selective administered ocularly to lower intraocular pressure in glaucoa.

25
Q

Amphetamine

A

Indirect acting adrenergic agonist. displaces endogenous catacholamines from storage vescicles. weak inhibitor of MAO and blocks the catacholamine reuptake.

  • can bind postsynaptic A and B but has little effect but can still cause increase in BPt hrough A1 and B1
  • increase alertness, decrease fatigue, deptressed appetitie and insomnia. treat depression following the period of central stimulation
26
Q

Methylphenidate

A

structural analogue of amphetamine. widely used to treat attention-deficit hyperactivity disorder in children

27
Q

Tyramine

A

NOT CLINICALLY USEFUL! found in fermented foods like cheese and wine. normally oxidized by MAO. IF the patient is taking MAO inhibitors, it can precipitate serious vasopressor episodes. can act like amphetamine

28
Q

Cocaine

A

Reuptake inhibitors. most potent for inhibiting DA reuptake. higher concentration inhibits Serotonin transporter and NE transp. Catacholamines remain in the synaptic cleft
-tachycardia, HTN, pupillary dilation adn peripheral vasoconstriction. Produces a big euphoria. Can be used as a local anethetic becasue it blocks Voltage gated Na channels

29
Q

Atomoxetine

A

Uptake inhibitor. Selective for NE transport Treats ADHD

30
Q

Ephedrine

A

mixed acting adrenergic agonist. induces release of NE.
activates A and B. poor substrate for COMT and MAO. long duration of action. Excellent oral absorption. penetrates CNS.
-Increases systole adn diastole BP by vasoconstriction and cardiac stimulation, causes bronchodilation, used with anticholinesterases may treat myasthenia gravis, improves athletic performance, and can stimulate the CNS to cause alertness, decrease fatigue, and prevents sleep.
USES: can be used for asthma but not frequently

31
Q

Pseudoephedrine

A

1 of 4 ephedrine enantiomers. used as nasal decongestion. found with H1 histamine antagonsit

32
Q

Phenoxybenzamine

A

Non selective alpha adrenergic blocker. irreversibly binds to A. also blocks H1, muscarinic and serotonin receptors and inhibits reuptake of NE by presynaptic adrenergic nerve terminal.
It blocks A so stops vasoconstriction and decreases preipheral resistance. Blockinh A2 in heart leads to increased CO
USES: Pheochromocytoma: to block the effects of the hormones it pumps out. Used preoperative period to help control HTN and sweating. *May need to give B blockers but don’t give before having A bllockade since unopposed B blockade could cause BP elevation due to increased Vasoconstriction
Adverse Effects: Postural Hypotension, nasal stuffiness, nausea and vomiting, inhibit ejaculation, tachycardia, mediated by the baroreceptor reflex and is contraindicated in patients with decreased coronary perfusion

33
Q

Phentolamine

A

reversible non selective adrenergic blocker. causes postural hypotension. blocks serotonin receptors and H1,2 receptors. trigger arrhythmias, anginal pain. contraindicated in patients with poor coronary perfusion
USES: Prevent HTN episodes in patients with pheos. Use it to diagnose pheo.
**with alpha blockers, Epi still has B agonist effects. And most of NE effects are diminished.

34
Q

Prazosin

A

Alpha 1 selective adrenergic blockers. it decreases vascular resistance and lowers arterial BP by relaxation of arterial and SM so NO REFLEX TACHYCARDIA. may act on CNS to decrease sympathetic outflow. Decrease LDL and TAG is plasma. Approved for HTN

35
Q

Terazosin and Doxazosin

A

A1 antagonist. structural analogs of prazosin. these agents have a longer half life than prazosin allowing less frequent dosing. Approved for HTN and BPH.

36
Q

Tamsulosin

A

A1 blockers. little effect on BP. USeful for BPH. decrease orthostatic hypotension.

37
Q

Yohimbine

A

A2 blocker. used to treat erectile dysfunction but its been replaced. It can reverse antihypertensive effects of an A2 agonist like clonidine.

38
Q

Propranolol

A

B1,2 blocker

  • Slow the heart, peripheral resistance increases, decreases BP
  • Treat Glaucoma to diminish intraocular pressure
  • treat anxiety, after a MI, Headache
  • Bronchoconstriction so don’t give to COPD or asthma patients
  • decreased glycogenolysis and decreases glucagon secretion so you can give to Type 1 Diabetic and so they don’t have too much Glucose. But watch glucose levels carefully.
39
Q

Adverse effects of non selective B blockers

A
  • bronchoconstriction (bad for asthma)
  • cause hypoglycemia
  • masks tachycardia seen in hypglycemia so there is no warning
  • reduction of HDL, increase LDL and increase Triglycerides.
  • sedation, dizzinenss, lethargy fatigue, depression
  • **Do not remove B blockers abruptly. Gradually wean them so you can prevent tachycardia, HTN, ischemia. During long term use there may be an upregulation of B reeceptors due to long term therapy with B blockers.
40
Q

Nadolol

A

non selective B blocker

  • long duration of action
  • indication for the long term management of patients with angina pectoris
  • Indicated for the management of HTN
41
Q

Timolol

A

Non selective B blocker.

  • Treats HTn
  • prophylaxis of migraine headache
  • Treats open angle glaucoma
42
Q

Atenolol and Metoprolol

A

B1 selective antagonists

  • Treat HTN, Especially usefull in patients with impaired pulmonary function, and diabetic patients on insulin
  • long term treatment for angina pectoralis, also useful in acute MI patients to reduce cardiovascular mortality.
  • you should still avoid with patients with asthma because it may still act on B2
43
Q

Esmolol

A

-B1 selective antagonist
-Ultra short acting half life=10minutes
-given by IV infusion
USES: safer to use than longer lasting antagonists in critically ill patients who need B antagonist. USeful in controlling supraclavicular arrhythmias, arrhytmias associated with thyrotoxicosis, perioperative HTN, and mycardial ischemia in acutely ill patients.

44
Q

Labetalol

A

B and A1 antagonist. Much more potent as B blocker than A.
-reduces BP
-oral for longer term HTN
-IV for emergency HTN
Adverse: orthostatic HTN and dizziness associated by A1 blockade. Hepatic injury insome patients

45
Q

Carvedilol

A

A1 and B blocker.
more potent for B blocking.
-has antioxidant properties.
-used to reduce HTN and in patients with CHF

46
Q

Pindolol

A

Partiall B Agonist. Used to treat HTN

-produce smaller reduction in Heart rate and BP

47
Q

Alpha-methyltyrosine (Metyrosine)

A

competititve inhibitor of tyrosine hydroxylase. interferes with synthesis of DA which eventually effects NE and Epi.
-used with phenoxybenzamine and other alpha blockers for the management of pheochromocytomas and during preoperative preparation for its removal

48
Q

Reserpine

A

Irreversibly damages VMAT so vsecicles cant concentrate and sore NE and Epi. depleation of NE becaue MAO has access to degrade it. Slow onset, long duration. Decrease heart rate, BP

49
Q

Guanethidine

A

Transported through NET. It is then pumped into vesicles to displace NE. essentialy it inhibits NE release into nerve endings. AntiHTN
Adverse: orthostatic HTN and interferes with male sexual function

Pharmacology (9 decks)

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