Flashcards in Adrenergic Drugs Deck (49):
What is norepinephrine?
non-selective direct-acting agonist that hits alpha 1 receptors most (but also some alpha 2 and beta 1)
What will norepinephrine do to systolic and diastolic pressures?
raise both, therefore increasing MABP also!
What will norepinephrine do to HR?
keep it the same or DEcrease due to reflex bradycardia
When is norepinephrine used?
as a pressor in severe hypotensive states (EXCEPT if it is due to a loss of blood, because you will starve the kidneys where are already have reduced blood flow as that is a side affect of norepi)
What is phenylephrine?
selective alpha 1 direct-acting agonist used to increase BP (pressor) for hypotension, as a decongestant, or mydriatic (dilates pupils)
What is methoxamine?
slective alpha 1 direct-acting agonist used in hospital because it is I.V. only. This is a pressor, and also stimulates the release of NE.
What is pseudoephedrine (SUDAFED)?
selective alpha 1 direct-acting agonist used as a decongestant. Now controlled because people used it to make meth.
What are the adverse effects of alpha agonists?
anxiety, respiratory difficulty, forceful heart beat, headache (with overdose), severe hypertension, infiltration necrosis (I.V. drugs), and rebound nasal congestion.
What is clonidine?
selective alpha 2 direct-acting agonist that causes DECREASED sympathetic outflow and thus HYPOtension, sedation, and bradycardia. It does this by decreasing central outflow of impulses in the sympathetic nervous system by binding to a GPCR that is associated with the G-inhibitory subunit in the nucleus tractus solitatrius.
What mechanism functions with alpha receptors?
phosphatidylinosotol secondmessenger system. Agonist binds to alpha 1 receptor stimulating Gq to activate phospholipase C (or Gi for alpha 2; stopping sympathetic outflow), increasing intracellular IP3 and DAG. IP3 will free stored intracellular Ca++ to cause skin and splanchnic vessels along with iris to constrict causing pupil dilation and increased BP.
What is the mechanism for beta 1 receptors?
agonist binds to beta 1 receptor activating Gs protein, which uses GTP to activate adenylyl cyclase, which increases intracellular cAMP, activating PKA. This increases intracellular Ca++ in the HEART, thus increasing contractility and increased HR.
What are the the 2 beta 1 agonists?
1. dobutamine= B1
2. isoproterenol= B1, and B2
What does isoproterenol do?
because B1 and B2= smooth muscle relaxation, skeletal muscle vasodilation decreasing TPR, increases cardiac output, and stimulates glycogenolysis in skeletal muscles, and relaxes myometrial (uterine) muscles.
What does dobutamine do?
selective B1 agonist used to increase CO and SV w/o much change in HR. This is used short term during cardiac surgery, for CHF, or in acute MI
What are the two most common short acting B2 agonists?
terbutaline and albuterol for bronchodilation during asthma attacks.
What are the adverse effects of beta agonists?
skeletal muscle tremor (B2), tachycardia (B1), hyperglycemia (B2)
What is epinephrine?
non-selective direct-acting adrenergic agonist that hits all receptors but in dose dependent manner.
Low dose= beta
High dose= alpha (predominates) and beta
Used to relieve respiratory distress due to bronchospasm, or to prolong the action of a local anesthetic (by constricting the vessels around the nerve)
What is dopamine?
- low dose= activates the dopamine receptor (D1) causing vasodilation of renal, mesenteric, and coronary beds.
- moderate dose= hits B1 receptor
- high dose= release of NE
What is ephedrine?
mixed-acting adrenergic agonist that hits all receptors and used for nasal congestion, urinary incontinence, hypotension, and asthma.
For what are alpha adrenergic receptor antagonists (alpha blockers) used?
- decrease BP and TPR
- increase HR and CO (due to baroreceptor reflex)
- enhance release of NE
Are most alpha blockers competitive or non-competitive antagonists?
What is phenoxybenzamine?
IRREVERSIBLE non-selective alpha blocker that treats pheochromocytoma (tumor of the chromaffin cells of adrenal gland) by inhibiting uptake system. It will decrease BP and cause reflect tachycardia.
What are the side effects of alpha blockers?
postural (orthostatic) hypotension, tachycardia, inhibition of sperm production and inhibition of ejaculation.
What is phentolamine?
REVERSIBLE non-selective alpha blocker that is similar to phenoxybenzamine, but shorter acting and doesn't afffect ejaculation.
What are the uses for alpha 1-selective blockers?
(all names end with -osin)
primary systemic hypertension, but side effects follow first-dose phenomenon (postural hypotension and syncope, but tolerance develops).
What are prazosin, terazosin, doxazosin?
selective alpha-1 blockers that decreases TPR, thus decreasing preload and thus BP. There is NO effect on baroreflex.
What is Yohimbine?
selective alpha-2 blocker that will INCREASE BP (remember alpha-2 is opposite) and HR, but used to treat psychogenic impotence (i.e. ED).
*Side note: this is found in some supplements, so be sure to ask a pt. if they are taking any supplements that may contain this if they begin to experience cardiac symptoms.
What are the effects of beta blocking drugs?
(all names end with -olol)
- decrease HR and contractility, thereby decreasing CO and BP :)
- these also reduce O2 demand (increasing O2 supply) by decreasing the work of the heart
* Thus they increase the mechanical efficiency.
- they also influence rhythm by decreasing sinus (SA node) rate, decrease ectopic pacemakers, and decrease conduction in atria and AV node by increasing effective refractory period of the AV node.
* This is what gives beta blockers their antiarrhythmic efficacy :)
- they also attenuate release of renin (lowering BP)
- decrease release of NE
- decrease glycogenolysis (decrease glucose)
What are the non-selective beta blocking drugs?
propranolol, timolol, nadolol, pindolol, cartelol, and penbutolol
Would you use non-selective beta blocking drugs in an asthmatic?
no because it inhibits beta-2 receptors also (preventing bronchodilation).
What is unique about propranolol?
it is the most lipid soluble, has HIGHEST membrane stabilizing effect, and has no partial agonist activity.
What is unique about timolol?
NO intrinsic sympathomimetic activity (no partial agonist activity), NO membrane stabilizing effect, and used as ophthalmic solution to lower intraocular pressure in glaucoma.
What is unique about nadolol?
similar to timolol, but longer lasting.
What is unique about pindolol?
has intrinsic partial agonist (sympathomimetic) activity, like propranolol, but this one has LOW membrane stabilizing effect.
What is unique about carteolol and penbutolol?
they both have some intrinsic partial agonist (sympathomimetic) activity.
What makes beta-1 selective blockers better than non-selective?
These can be used with patients who have respiratory problems because they don't block bronchodilation.
What is metoprolol?
beta-1 selective blocker that has NO intrinsic sympathomemetic activity; complete blocking action. Also has low membrane stabilization.
*Most commonly used.
What is unique about atenolol?
beta-1 seletive blocker that has NO intrinsic sympathomemetic activity and NO membrane stabilization
What is unique about esmolol?
VERY FAST acting selective beta-1 blocker (I.V. only) for SVT emergencies.
What are the adverse effects of beta blockers?
occur when dose is too high: CHF, bradyarrhythmia, bronchoconstriction (non-selective), and blunt the recogonition of hypoglycemia (in diabetics) so they don't realize it, while delaying recovery from hypoglycemia.
What is Labetalol?
(notice spelling change -alol)
nonselective beta-blocker that ALSO blocks alpha-1 receptors allowing greater affects of BP reduction (I.V. in hypertensive emergencies) by relaxing arterial smooth muscle, and because of beta-1 blockade you won't see reflex tachy :)
What is reserpine? (old drug)
adrenergic neuronal blocker that depletes adrenergic nerve endings of catecholamines by blocking transport into storage vesicles and MAO metabolizes it within the cytoplasm.
What is guanethidine?
adrenergic neuronal blocker that blocks release of NE and thus NE will be metabolized by MAO (like reserpine). Very potent and used for sever hypertension.
What is bretylium?
prevents release of NE from terminal and used as an antiarrhthymic.
What is methyldopa?
DOPA with a methylated alpha carbon enters biosynthetic pathways forming methyl-NE which acts as a "false neurotransmitter." Acts like alpha-2 agonist.
What is tyramine?
displaces transmitter from axonal terminal acting as a sympathetic agonist.
What are the MAO inhibitors?
Pargyline, Tranylcypromine, and Phenelzine, which all irreversibly inactivate MAO, thus increasing levels of catecholamines and serotonin (5-HT).
They are used as antiparkinsonian drugs and to treat atypical depression (due to increased serotonin).
What is a major side effect of MAO inhibitors?
*Because many foods have tyramine in them, this will exacerbate this drug and therefore a dietician should be brought on board when using MAO inhibitors.