Term
| norepinephrine (levophed) |
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Definition
adrenergic agonist
Potent vasoconstrictor and inotropic agent
L-isomer much more potent than d-isomer
More α than β activity
α activity produces increased peripheral vascular resistance, and increased systemic blood pressure and increased coronary artery blood flow
Some β1 activity: in lower doses, β1 cardiac stimulatory effects are seen, but with larger doses, vasoconstrictive effects (α1) are predominate cause of increased BP.
Like other catacholamines, NE increases cAMP in cells via β stimulation, and decreases cAMP via α stimulation.
Glycogenolysis, inhibition of insulin release and lipolysis is less than seen with EPI.
Reflexive vagal stimulation secondary to increased TPR and BP slows the heart and increases stroke volume.
Blood flow to abdominal organs and skeletal muscle is decreased, while coronary blood flow is increased indirectly due to a stimulation.
Does not increase myocardial O2 consumption.
Normally given only via IV, with rapid onset and short (1 - 2 minute) duration.
Does not cross the BBB.
Use limited, mainly used for shock and severe hypotension. |
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Term
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Definition
adrenergic agonist
Administered parenterally, via inhalation, or topically to eye.
Used as a cardiac stimulant and bronchodilator (anaphylactic shock).
Other uses in asthmatics is limited now due to more selective compounds.
Combined with other drugs (such as local anesthetics and topical eye preps) to prolong action by vasoconstriction, causing slower absorption and removal of the other agent from the site.
Ophthalmic use as a diagnostic aid.
Potent α and β agonist (non-selective adrenergic agonist).
α1 action leads to arteriolar vasoconstriction. α2 stimulation leads to decreased NE release from neurons.
β1 stimulation leads to increased chronotropic and inotropic activity. β2 stimulation leads to arteriolar vasodilation, bronchial smooth muscle relaxation and increased glycogenolysis.
Major therapeutic effects include: bronchodilation, cardiac stimulation, skeletal muscle vasodilation, and glycogenolysis.
Smooth muscle effects are varied and depend on receptor density and hormonal effects.
Lowers intraocular pressure (wide-angle glaucoma) and causes brief mydriasis.
Topical or local administration constricts blood vessels (hemostasis).
β2 stimulation also decreases mast cell histamine release.
Systolic pressure usually increased (due to increased inotropy) while diastolic is decreased (vasodilation).
Increases coronary artery vasodilation and stimulates increased myocardial O2 demand which has further local effect (via NO) to increased coronary vasodilation.
Increased risk of arrhythmias due to β1 activity.
At normal doses, some vasoconstriction, some dilation. Mostly constriction at higher doses.
α stimulation in liver increases gluconeogenesis and inhibits insulin release. β stimulation (β3) in adipose tissue causes catabolism and increased free fatty acids in plasma.
β2 stimulation at skeletal muscle and liver increases glycogenolysis.
Does not cross BBB well.
Duration varies with administrative route: IV – few minutes; IM - 1 - 4 hours; Inhalation - 1 - 3 hours
Uses include acute bronchospasm, anaphylaxis, asthma(??), cardiopulmonary resuscitation, glaucoma, surgical bleeding, ventricular fibrillation and asystole. |
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Term
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Definition
adrenergic agonist
Potent bronchodilator and inotrope.
Synthetic compound similar to EPI.
Potent β agonist (non-selective).
Not used much now due to more selective compounds.
Very little α activity at therapeutic doses.
Increases blood flow (vasodilation) and relaxes GI smooth muscles.
Oral (sublingual), inhalation and IV routes.
Sublingual onset - 30 minutes with 1 - 2 hour duration.
IV very rapid, but less than 1 hour duration.
Inhalational duration is 2 - 4 hours.
Used for acute bronchospasms, bradycardia, asthma, etc. |
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Term
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Definition
Parenteral inotrope.
Selective β1 agonist (minor β2 or α effects).
Stimulates rate and contraction of heart, increasing CO.
Systolic pressure is increased due to increased stroke volume, with little change in diastolic pressure.
Increased coronary blood flow and myocardial O2 demand seen.
Unlike DA, does not increase NE release from sympathetic nerves.
Plasma half-life approximately 2 minutes, so needs to be administered via constant IV infusion.
Uses include cardiac surgery, cardiogenic shock, and heart failure. |
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Term
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Definition
adrenergic agonist
Mimics action of endogenous DA, which is a precursor of EPI and NE.
Works at DA receptors to dilate renal arterioles and increase renal blood flow and GFR.
At low doses, causes much vasodilation in renal, mesenteric, coronary vessels.
At moderate doses, also stimulates β1 receptors, stimulating the heart (while maintaining vasodilation).
At high doses, α receptors also stimulated, increasing TPR.
Does not cross BBB.
Normally given via continuous IV infusion (half-life ~ 2 minutes).
Used for heart failure, shock. |
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Term
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Definition
adrenergic agonist
Synthetic compound similar in structure to isoproterenol.
More β2 selective than isoproterenol (but less than Albuterol).
Exclusively used as a bronchodilator.
Use declining due to better β2 agonists.
For COPD, asthma, chronic bronchospasms. |
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Term
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Definition
adrenergic agonist
Selective β2 agonist.
Indications - bronchospasm in patients with obstructive airway disease, asthma.
Adverse reaction - nervousness, tremor, tachycardia, palpitations. |
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Term
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Definition
adrenergic agonist
Relatively selective β2 agonist.
Structurally similar to Albuterol.
Used for asthma and bronchospasms. |
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Term
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Definition
adrenergic agonist
β2 agonist.
Much more selective for β2 than albuterol.
Note: many β2 receptors now known to be located on the heart. Their function is unclear at present.
For chronic treatment of asthma (BID dosing, due to longer half-life).
Side effects include tachycardia, palpitations, hypersensitivity, tremor, and headaches. |
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Term
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Definition
adrenergic agonist
β2 agonist.
Used for bronchospasms and asthma, emphysema.
Side effects include tremor, nervousness, tachycardia, palpitations, nausea and vomiting. |
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Term
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Definition
adrenergic agonist
Selective α2 agonist.
More CNS activity than peripheral.
α2 receptor stimulation in the CNS leads to decreased sympathetic outflow, increased parasympathetic outflow.
Indicated for control of hypertension.
Side effects include dry mouth, skin irritation |
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Term
| phenylephrine (neosynephrine) |
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Definition
adrenergic agonist
α agonist.
Used as vasoconstrictor to maintain blood pressure during surgery, decongestant, mydriatic (without cycloplegia).
Contraindicated in narrow angle glaucoma, ventricular tachycardia, aneurisms.
Side effects include bradycardia, decreased CO, arrhythmias, angina, dizziness, CNS excitation. |
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Term
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Definition
adrenergic agonist
A parenterally administered potent vasoconstrictor (α1).
Used to prevent surgical (spinal anesthesia) hypotension and shock.
Adverse reactions include anxiety, cardiac arrhythmias, and hypertension. |
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Term
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Definition
adrenergic agonists
Forms α-methyl NE - acts as a false transmitter - less potent than NE.
Used to treat hypertension.
Contraindicated in patients with hepatic disease.
Side effects include angina, congestive heart failure, orthostatic hypotension, bradycardia, many others! |
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Term
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Definition
adrenergic agonists
Inhibits amine re-uptake pump, thus causing increases stimulation. (Indirect effect).
Also has local anesthetic effects - blocks Na+ channels of nerve membranes.
Used for local (topical) anesthesia of mucous membranes in mouth, laryngeal and nasal cavities.
Side effects include vasoconstriction, mydriasis, nervousness, respiratory failure, cardiac arrest, general CNS stimulation. |
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Term
| indirect adrenergic agonists do what |
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Definition
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Term
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Definition
mixed- direct and indirect adrenergic agonist
Stimulates sympathetic neurons to release neurotransmitter.
Also has direct post-synaptic effect (mixed action).
Used for Narcolepsy, ADD, obesity.
Contraindicated in any cardiovascular disease, hypertension, hyperthyroidism.
Adverse reactions include: palpitations, tachycardia, increased blood pressure, psychoses, insomnia, headaches, tremor, general CNS stimulation. |
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Term
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Definition
mixed indirect adrenergic agonist
Stimulates both α and β receptors
Peripheral actions are due partly to norepinephrine release and partly to direct effect on receptors.
Therapeutic doses of ephedrine produce mainly relaxation of smooth muscle and, if norepinephrine stores are intact, cardiac stimulation and increased systolic and usually increased diastolic blood pressure.
Metabolized to a small extent, with remainder excreted unchanged in urine.
Available in oral and parenteral forms.
Much controversy over use, controlled to block Meth production (as is pseudoephedrine)
Fairly high abuse potential.
Many reported cases of cardiovascular events. |
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Term
| pseudoephedrine (sudafed) |
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Definition
mixed indirect adrenergic agonist
Potent sympathomimetic, they possess direct α1, β1 and β2 activity in addition to triggering the release of catacholamines from the nerve terminal (mixed effects).
Used mainly for asthma, stimulant (OTC) preps.
Contraindicated in CV disease, hypertension.
Side effects include: CNS excitation, tremors, insomnia, nervousness, palpitations, tachycardia, cardiac arrhythmias, headache, sweating. |
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Term
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Definition
indirect adrenrgic agonist
Tyramine (not used clinically)
Taken up into nerve terminal and converted to false transmitter that has less activity, leading to decreased sympathetic tone.
Slight direct α activity.
Also triggers release of neurotransmitter from neuron.
Found in some foods (Red wine, chocolate, cheese, etc.) and presents a potential interaction on patients taking monoamine oxidase inhibitors. |
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Term
| methamphetamine, methylphenidate, phentermine |
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Definition
| all indirect adrenergic agonists |
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Term
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Definition
α1 agonists
NE, EPI, DA (higher doses),Phenylephrine, Metaraminol
Effects: Increased arterial tone, increased TPR, increased diastolic pressure, decreased heart rate (reflex), increased venous tone. |
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Term
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Definition
α2 agonists
NE, EPI, Clonidine, α-methyldopa
Effects: Increased tone in large arteries, increased TPR (Post synaptic α2), increased coronary vasodilation. |
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Term
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Definition
β1 agonists
NE, EPI, ISO, DA, Dobutamine
Effects: Increased heart rate, increased O2 consumption, increased automaticity, conduction velocity, increased force of contraction, increased stroke volume and CO, decreased filling volume (in tachycardia), increased coronary vasodilation. |
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Term
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Definition
β2 agonists
Albuterol, Terbutaline, EPI, ISO
Effects: Decreased arterial tone, decreased TPR, decreased diastolic pressure, increased heart rate (reflexive). |
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Term
| phenoxybenzamine (dibenzyline) |
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Definition
alpha adrenergic anatgonists
α1 and α2 antagonist (‘irreversible’ - covalent binding).
Long lasting effects (at least three days).
Most effective at smooth muscle and exocrine glands.
Used for: pre-op treatment of pheochromocytoma to block potential hypertensive crisis during surgery, sweating and hypertension caused by pheochromocytoma, certain vasospastic disorders, and frostbite therapy.
Side effects include: dizziness, decreased ejaculation ability, fatigue, miosis, orthostatic hypotension, tachycardia.
Half-life is approximately 24 hours, and the drug takes several hours after initial dosing to see effects. Care must be taken with other drugs given even upon cessation of therapy, as blockade may still be present for 7 days after the last dose.
Oral dosing. |
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Term
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Definition
alpha adrenergic antagonist
α1 and α2 competitive antagonist.
Shorter duration of action of action than phenoxybenzamine.
Parenteral dosing.
Used for: pheochromocytoma diagnosis, pheochromocytomectomy, MAO induced hypertensive crisis, impotence.
Side effects include: dizziness, decreased ejaculation ability, flushing, hypotension, sinus tachycardia.
Given parenterally - short acting. |
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Term
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Definition
alpha adrenergic antagonist
Selective α1 antagonist.
For treating hypertension.
Side effects include: dizziness, headaches, drowsiness, palpitations, tachycardia, orthostatic hypotension.
Because it does not block α2 receptors, there is no excessive release of NE from neurons, and less of a risk of reflexive tachycardia seen with other α blockers.
Available as an oral dose form. |
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Term
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Definition
alpha adrenergic antagonist
Selective α1 antagonist.
Closely related to prazosin, but less potent.
More water soluble and higher bioavailability that prazosin, and also has a longer t1/2 (12 hrs), and can be used qD.
Used mainly for treatment of hypertension and benign prostatic hyperplasia (BPH).
Available as an oral dose form. |
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Term
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Definition
alpha adrenergic antagonist
Selective α1 antagonist.
Also closely related to prazosin.
Similar bioavailability as prazosin, but has a longer t1/2 (20 hrs), and can be used qD.
Used mainly for treatment of hypertension and benign prostatic hyperplasia (BPH).
Available as an oral dose form. |
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Term
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Definition
alpha adrenergic antagonist
Selective α1 antagonist.
Also closely related to prazosin.
Similar bioavailability as prazosin, but with a slightly longer t1/2 (3-5 hrs).
Used mainly for treatment of benign prostatic hyperplasia (BPH)- relaxes smooth muscle in bladder neck and prostate.
Available as an extended release oral dose form. |
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Term
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Definition
alpha adrenergic antagonist
Tamsulosin (Flomax)
Selective α1A antagonist (but limited α1B activity, which controls vascular smooth muscle).
Therefore, somewhat more selective at treating BPH, with little effect on blood pressure.
t1/2 of 5-10 hrs.
Metabolized mainly by P-450 system.
Available as an oral dose form. |
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Term
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Definition
alpha adrenergic antagonist
Selective competitive α2 antagonist.
Blocks central α2 receptors leading to increased blood pressure and heart rate (decreased parasympathetic outflow, and increased sympathetic outflow), possible aphrodisiac properties, due to peripheral α2 blockade and parasympathetic override.
Side effects include: antidiuretic effects, CNS excitation, hypertension, tachycardia, increased motor activity, nervousness, irritability, nausea and vomiting.
Local injections into penile shaft to increase erections. |
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Term
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Definition
beta adrenergic antagonists
Prototype β blocker.
Non-selective (blocks both β1 and β2 receptors).
Used for hypertension, ‘speakers’ nerves, angina, arrhythmias, migraines, pheochromocytoma.
Has membrane stabilizing effect (local anesthetic), which enhances its anti-arrhythmic effects (most b blockers share this property).
Contraindicated in shock, bradycardia, asthma, congestive heart failure.
Side effects include: bradycardia, congestive heart failure, hypotension, heart block, insomnia, hallucinations, bronchospasms. |
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Term
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Definition
beta adrenergic antagonist
Non-selective β antagonist.
For treating angina, hypertension.
Contraindicated in bradycardia, bronchial asthma, shock, heart block, myocardial infarction.
Side effects include: bradycardia, cardiac failure, conduction disturbances, arrhythmias, dizziness, bronchospasm, diarrhea, impotence, decreased libido, blurred vision. |
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Term
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Definition
beta adrenergic antagonist
Non-selective β antagonist.
For treating hypertension, ocular hypertension (wide angle glaucoma).
Contraindications include asthma, COPD, bradycardia, heart failure.
Side effects include fatigue, bradycardia, dizziness, cold hands and feet. |
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Term
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Definition
beta adrenergic antagonists
Non-selective β antagonist with some sympathetic agonist activity.
A vasodilatory β blocker (due to strong β2 agonist activity).
Also not as much bronchoconstriction as with other β2 blockers.
Used to treat hypertension.
Contraindications: bradycardia, COPD, heart failure.
Side effects include fatigue, dizziness, diarrhea, cardiac failure. |
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Term
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Definition
beta adrenergic antagonist
α1, β1 and β2 antagonist (non-selective).
Partial agonist at some β2 receptors.
For treating hypertension.
Contraindications: asthma, cardiac failure, severe bradycardia.
Side effects include postural hypotension, sweating, dizziness, nausea and vomiting, nasal stuffiness, bradycardia, impotence. |
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Term
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Definition
beta adrenergic antagonist
α1, β1 and β2 antagonist.
Higher β:α blockade than labetolol (and longer duration).
Indications: angina, heart failure (NYHA type II and III), hypertension.
Contraindications: bronchospasm, emphysema, COPD, asthma, bradycardia, diabetes mellitus, heart failure (NYHA type IV), liver disease, pheochromocytoma.
Adverse reactions: Bronchospasm, diarrhea, dyspnea, fatigue, headaches, hypotension, peripheral edema, bradycardia, syncope. |
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Term
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Definition
beta adrenergic antagonist
β1 antagonist.
Used to treat hypertension and angina pectoris.
Contraindications: bradycardia, heartblock, shock, myocardial infarction.
Side effects include dizziness, bradycardia, nightmares, congestive heart failure, peripheral edema, bronchospasms, nausea, diarrhea. |
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Term
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Definition
beta adrenergic antagonist
Mostly β1 blockade, but is also a partial sympathetic agonist (non-selective).
Low lipid solubility, so little CNS side effects.
Membrane stabilizing effect on the action potential is present, but less than propranolol.
Used in the reduction of hypertension and to control ventricular arrhythmias.
Does not cause as much bronchoconstriction as non-selective β blockers.
Less likely to cause bradycardia than other β1 blockers, due to its intrinsic sympathomimetic activity.
Side effects include: alopecia, dizziness, angina, fatigue, heart failure. |
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Term
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Definition
beta adrenergic antagonists
Blocks β1 mostly.
Used to treat hypertension, acute myocardial infarction, angina pectoris.
Contraindicated in bradycardia, heart block, shock, cardiac failure.
Adverse reactions include bradycardia, dizziness, fatigue. |
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Term
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Definition
beta adrenergic antagonists
β1 antagonist.
Given by IV infusion.
Used for atrial fibrillation or flutter, paroxysmal supraventricular tachycardia.
Contraindications: bronchospasms, bradycardia, shock.
Side effects: AV block, cardiac arrest, hypotension, bradycardia.
Half-life of only a few minutes (very short duration). |
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Term
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Definition
Metyrosine (Demser)
Inhibitor of tyrosine hydroxylase.
Used for pheochromocytoma.
Contraindicated in hepatic disease, Parkinson's disease.
Adverse reactions include anxiety, confusion, crystalluria, depression, Parkinsonism, salivation |
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Term
| 6-hydroxydopamine (experimental) |
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Definition
Taken up into adrenergic nerve terminals and destroys the cells.
Stimulates free radical production in cells, leading to cell death.
Therefore, removes adrenergic neurons (chemical sympathectomy). |
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Term
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Definition
| blocks catecholamine release from nerve terminal, used for v-tach, prophylaxis of v-fib, adverse reactions: hypotension, bradycardia |
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