Andrenergic Agonist and Antagonist Flashcards
Isoproterenol
M: non-selective beta agonist
CA: emergency arrythmias and bronchospasm
AE: HTN, palpitations, tremor
TCo:
Dobutamine
M: B1 agonist with potent inotrope but mild chronotropic effects
CA: management of acute heart failure and cardiogenic shock; dobutamine stress echocardiogram
AE:
TCo: short half life due to COMT metabolism
Albuterol
M: B2 agonist causing bronchodilation
CA: asthma and COPD
AE: tachycardia, tremors, restlessness, apprehencion, anxiety
TCo: short acting (15min)
Salmeterol & Formoterol
M: B2 agonist to prevent bronchoconstriction
CA: asthma and COPD
AE: tachycardia and tremors
TCo: long acting 12-24 hours
Phenylephrine
M: selective A1 agonist causing vasoconstriction
CA: nasal decongestant, mydriatic, increase BP in hypotension from septic shock, anesthesia, or episodes of supraventricular tachycardia
AE: bradycardia when given parenterally
TCo: HTN
What are the A2-selective adrenergic agonist?
Clonidine, Methyldopa, Brimonidine
Clonidine
M: partial A2 agonist
CA: centrally acting antihypertensive (reduces sympathetic outflow)
AE: lethargy, sedation, xerostomia
TCo:
Methyldopa
M: converted to alpha-methylnorepinephrine which activates central A2-receptors
CA: DOC for HTN during pregnancy
AE: sedation, impaired mental concentration, xerostomia
TCo:
Brimonidine
M: highly selective A2 agonist
CA: lower intraocular pressue in glaucoma (reduces aqueous humor production and increased outflow)
AE:
TCo:
What are the indirect-acting adrenergic agonists that act as releasing agents?
Amphetamine, Methylphenydate, Tyramine
Amphetamine
M: cause relase of norepinephrine from presynaptic terminals
CA: ADHD, and narcolepsy
AE:
TCo: centrally stimulatory action, can increase blood pressure by A-agonist action on vasculature as well as B-stimulatory effects on heart
Methylphenydate
M: causes release of norepinephrine from presynaptic terminals
CA: ADHD
AE:
TCo: structural analogue of amphetamine
Tyramine
M: causes relase of norepinephrine from presynaptic terminals
CA:
AE: normally oxidized by MAO but if pt is taking MAO inhibitors it can precipitate as serious vasopressor episodes causing headache
TCo: found in fermented foods (cheese, wine)
What are the uptake inhibitors?
Cocaine, Atomoxetine, Modafinil
Cocaine
M: blocks monoamine reuptake causing monoamines to accumulate in synaptic space
CA: potentiation and prolongation of their central and peripheral actions
AE:
TCo:
Atomoxetine
M: selective inhibitor of the norepinephrine reuptake transporter
CA: ADHD
AE:
TCo:
Modafinil
M: not fully known but inhibits norepinephrine and dopamine transporters
CA: treats narcolepsy
AE:
TCo: increase synaptic concentrations of norepinephrine, dopamine, serotonin, and glutamate; decrease in GABA levels
What are the mixed-acting adrenergic agonists?
Ephedrine and Pseudoephedrine
Ephedrine
M: activate andrenergic receptors to induce relase or norepinephrine
CA: myasthenia gravis and used as a pressor (during spinal anesthesia)
AE:
TCo:
Pseudoephedrine
M: activate adrenergic receptors to induce release of norepinephrine
CA: decongestant
AE:
TCo: one of four enantiomers
What are the non-selective alpha-andrenergic blockers?
Phenoxybenzamine and Phentolamine
Phenoxybenzamine
M: irreversible non-selctive alpha-adrenergic blocker
CA: DOC for pheochromocytoma prior to surgical removal of tumor and for chronic management of inoperable tumors
AE: postural hypotension, nasal stuffiness, nausea, vomiting, inhibit ejaculation
TCo: contraindicated in pts with decrease coronary perfusion because of reflex tachycardia
Phentolamine
M: reversibly blocks alpha receptors
CA: HTN crisis due to stimulant drug overdose, control HTN during surgery of Pheochromocytoma, diagnoses of pheochromocytoma (phentolamine blocking test), pevent dermal necrosis
AE: postural hypotension, arrythmias, angina
TCo: contraindicated in pts with decrease coronary perfusion due to reflex tachycardia
Explain epinephrine reversal?
- When alpha-andrenergic blockers are present there will be no effect on the alpha receptors by epinephrine so vasodilation by B2 receptors will be predominant leading to decrease in blood pressure (reflex tachycardia)
What are the alpha-1 selective andrenergic blockers?
- Prozosin
- Terazosin
- Doxazosin
- Tamsulosin
Prazosin
M: alpha-1 selective blocker
CA: DOC for BPH; HTN
AE: first does must be 1/3 or 1/4 normal because of exaggerated hypotensive response can cause syncope
TCo: Prazosin is the prototype and has short half-life
Terazosin and Doxazosin
M: alpha-1 selective blocker
CA: DOC for benign prostatic hypertropy (BPH), HTN
AE: first does must be 1/3 or 1/4 normal because of exaggerated hypotensive response can cause syncope
TCo: prazosin analogs with longer half life
Tamulosin
M: alpha-1A selective blocker (alpha-1A receptor predominant in GU smooth muscle)
CA: BPH
AE: less likely to cause orthostatic hypotension
TCo: little effect on blood pressure
What are the nonselective beta-blockers and name there cardiovascular, respiratory, and metabolic effects?
Propranolol, Nadolol, Timolol
CVS: slow heart rate and decrease myocardial contractility
Respiratory: can precipitate a respiratory crisis in pts with COPD or asthma
Metabolic: decrease glycogenolysis and decrease glucagon secretion
Atenolol and Metoprolol
M: beta-1 selective adrenergic antagonist
CA: tx HTN in pts with impaired pulmonary function and diabetics who are receiving insulin/oral hypoglycemic agents
AE:
TCo:
Esmolol
M: B1 selective andrenergic antagonist
CA: rapid control of ventricular rate in pts with atrial fibrillation or atrial flutter
AE:
TCo: ultra-short acting, half life 10 minutes, IV
Labetalol
M: alpha-1 and beta blockers
CA: HTN
AE:
TCo: more potent as a beta antagonist
Carvedilol
M: alpha-1 and beta-blockers
CA: HTN and CHF
AE:
TCo: also has antioxidant properties
Pindolol
M: partial beta-agonist
CA:
AE:
TCo: preferred in individuals with diminished cardiac reserve or a propensity to bradycardia
What are the uses of beta blockers?
- HTN: lower blood pressure by decreasing CO
- Glaucoma: diminishig intraocular pressure (timolol)
- Migraine: prophylaxis
- Hyperthyroidism: blunt sympathetic stimulation
- Angina Pectoris: decrease O2 requirement of heart
- Atrial Fibrillation: contral ventricular rate
- MI: protective effect on myocardium
- Performance Anxiety: stage fright
- Essential Tremor: most commonly used drug
What are the adverse effects of beta blockers?
- Hypoglycemia: blockade of beta-2 receptors in liver
- Lipid metabolism: inhibit relase of free FA from adipose tissue, both non-selective and B1 blockers increase TG and reduce HDL, lipids unaffected by labetalol and pindolol
- CNS: sedation, dizziness, lethargy, fatigue
What are the warnings and precautions of beta blockers?
- should not be withdrawn abruptly (especially pts with CAD) because of gradually tapered to avoid acute tachycardia, HTN, and/or ischemia due to up-regulation of beta receptors
alpha-Methyltyrosine (Metyrosine)
M: competitive inhibitor of tyrosine hydroxylase
CA: management of malignant Pheochromocytoma and used preop during resection of Pheochromocytoma
AE:
TCo:
Reserpine
M: irreversibly blocks VMAT so vesicles cannot store norepinephrine and dopamine (depletion of norepinephrine because of MAO in cytoplasm)
CA: HTN (used in the past)
AE:
TCo: gradual decrease in BP and slowing of cardiac rate
Tetrabenazine
M: reversible inhibitor of VMAT causing presynaptic depletion of catecholamines
CA: chorea associated with Huntington’s Disease
