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116 Cards in this Set
- Front
- Back
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The main effects of the alpha 1 receptor are:
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vasoconstriction, mydriasis, relaxation of GI smooth muscle (except sphincters), thick viscid salivary secretions, hepatic glycogenolysis, decreases renin release, and ejaculation
HINT: Very Manly Guys Rarely Require Ejaculatory Training V- Vasoconstriction G- Glycogenolysis R- Relaxation R- Renin E- Ejaculation T- Thick |
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The main effects of the alpha 2 receptor are:
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inhibition of transmitter release (including NE and Ach relase from autonomic nerves), platelet aggregation, vasoconstriction, inhibition of insulin release and ejacultion
HINT: PIVIE P- Platelet I- Inhibits neurotransmitters V- Vasoconstriction I- Inhibits insulin E- Ejaculation |
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The main effects of the Beta 1 receptor are:
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increased cardiac rate and force, increases renin release
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The main effects of the Beta 2 receptor are:
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bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis and skeletal muscle tremor
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The main effects of the Beta 3 receptor are:
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lipolysis
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at low doses what affect does epinephrine have? why?
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Vasodilation due to B2 receptors
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which receptors respond the strongest to epinephrine?
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B2, B1
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at high doses, what affect does epinephrine have? why?
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vasoconstriction, mydriasis, relaxation of GI smooth much (except sphincters), thick viscid salivary secretions, and hepatic glycogenolysis, decreases renin release and ejaculation. ------ all of the main effects of alpha 1
This is because both alpha 1 and Beta 2 are activated, but the alpha effects predominant at high doses. |
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at therapeutic doses, what affect does epinephrine have? why?
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epinephrine increases blood flow to the skeletal muscle due to the powerful B2 mediated vasodilator action which is partially counteracted by vasoconstriction mediated by alpha receptors
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NE affects which receptors? which one predominates?
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alpha 1 and 2, and Beta 1
alphas > beta1 |
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what are the non-selective adrenergic agonists?
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epinephrine, norepinephrine, isoproterenol, and oxymetazoline
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what receptors are affected by isoproterenol?
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Beta 1 and 2
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which non-selective adrenergic agonists is an alpha agonist?
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oxymetazoline (Alpha 1 and 2 receptors)
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what are the clinical uses of epinephrine?
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hypersensitivity reactions, cardiac resuscitation, relieve bronchospasm in asthma, dec IOP glaucoma, topical hemostatic, adjunct in local anesthetic
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why can't epinephrine be given orally?
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because it is rapidly inactivated by the Monoamine oxidases (MAO) and the catechol-methyl- transferases (COMTs).
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epinephrine has a _____ onset of action and a ______ duration
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rapid; short
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what are the side effects of epinephrine?
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HTN, tachycardia, reflex bradycardia, ventricular arrhythmias, tremor, hyperglycemia
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what is the clinical use of NE?
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reverses hypotension in shock
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how is epinephrine and NE adminstered?
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Intramuscularly or Subcutaneously
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what is the clinical use of isoproterenol?
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treatment of asthma and cardiac resusitation
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is isoproterenol rapidly absorbed?
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no, some tissues have a t 1/2 = 2 hours
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what are the side effects of isoproterenol?
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tachycardia, dysrhythmias, tremor
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what is the clinical use of oxymetazoline?
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nasal decongestant- short relief
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what are the side effects of norepi?
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same as epi: HTN, tachycardia, reflex bradycardia, ventricular arrhythmias, tremor, hyperglycemia.
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what is the MOA of oxymetazoline?
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constricts the small arterioles supplying the nasal mucosa, decreasing secretions.
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T/F a pt can use oxymetazoline regularly without any change in the body's response
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FALSE
you lose efficacy with chronic use: desensitization of alpha receptors |
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what are the side effects of oxymetazoline?
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intense constriction can damage the nasal mucosa, rebound hyperemia and worsening of symptoms
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what is the alpha 1 selective agonist?
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phenylephrine
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what are the clinical uses of pheynlephrine?
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nasal decongestant, mydriasis (w/o loss of accommodation), short term hypotensive emergencies or to maintain BP during spinal anesthsia
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what is the MOA of phenylephrine?
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vasoconstriction in nasal mucosa, contraction of radial diameter
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when is phenylephrine contraindicated?
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narrow angle glaucoma
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how does phenylephrine differ from epi and NE pharmacodynamically?
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it is less potent, but has a longer duration of action than EPI and NE.
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what are the alpha 2 selective agonists?
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clonidine and apraclonidine
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what are the clinical uses of clonidine?
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hypertension and for addicts in withdrawal from alcohol, narcotics and tobacco.
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what is the MOA of clonidine?
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prevents increase in sympathetic activity and cravings: acts at PRESYNAPTIC A2 receptors --> decrease norepi synthesis --> DECREASE SYMPATHETIC TONE.
MAIN EFFECT= lower BP by acting at nuclei in the lower BRAINSTEM to decrease sympathetic outflow to the heart and to vasculature --> vasoconstriction (d/t cross talk of a1 at postsynapse). |
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T/F clonidine is a partial agonist
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true
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if clonidine is given via IV what is the result? what about orally?
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IV- transient increase in BP
Orally- hypotensive agent |
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what makes clonidine dangerous? how do we avoid that?
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it crosses the BBB. to avoid it we prescribe Transdermal patch in order to decrease CNS side effects
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If you abruptly stop clonidine, what can you cause?
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rebound hypertension
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what are the side effects of clonidine?
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dry mouth, sedation (in 50% of pts and generally only initially), bradycardia and sexual dysfunction
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what is apraclonidine used for?
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open-angle glaucoma
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what is the MOA of apraclonidine?
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constriction of blood vessels to eye --> decreased synthesis of aqueous humor
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Apraclonidine is used in conjunction with 3 other drugs, what are they?
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timolol followed by iopidine and pilocarpine
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what are the B1 selective agonists?
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dopamine and dobuatmine
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what receptors do dopamine act on?
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Beta 1 and Renal receptor D1
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what is the clinical use of dopamine?
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- improve cardiac and renal function in CHF and renal failure pts
- cardiogenic and septic shock: only after hypovolemia has been corrected |
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what is the MOA of dopamine?
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on B1: positive inotropy (increasing the strength of a muscle contraction)
on D1: inhibits Na pump and Na-H exchanger --> naturesis and dieresis also causes vasodilation via D1 in the renal, mesenteric and coronary vasculature. |
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where is dopamine synthesized in the body?
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in the proximal tubule of the kidney
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what are the clinical uses of doputamine?
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CHF, MI, short term management of cardiac decompensation after cardiac surgery
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what is the MOA of dobutamine?
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increase in CO and SV w/ o marked increase in HR or BP
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what are the B2 selective agonists?
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albuterol, salmeterol, ritodrine
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what side effects do all B2 selective agonists cause?
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tremor, decreased plasma K+ concentration, increased plasma glucose concentration
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what are the clinical uses of albuterol?
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symptomatic relief in asthma and COPD
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what is the MOA of albuterol?
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bronchodilation
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how quickly does albuterol act? how long does it last?
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acts w/n 15 min and persists 2-3 hours
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what are the clinical uses of salmeterol?
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symptomatic relief of bronchospasm in COPD - nocturnal asthma
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what is the MOA of salmeterol?
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bronchodilation, anti-inflammatory
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how quickly does salmeterol act? how long does it last?
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onset is slow (30min- 1hr), prolonged duration of action (>12 hours)
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what is the clinical use of ritodrine? how is it given?
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to arrest premature labor; IV
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what is the MOA of ritodrine?
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uterine relaxation
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what are the non-selective A antagonists?
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phenoxybenzamine and phentolamine
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what are the side effects of all non-selective A antagonists?
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orthostatic hypotension, tachycardia (increase NE release d/t presynpatic alpha 2 block), vertigo, sexual dysfunction
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what is the clinical use of phenoxybenzamine?
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tx of pheochromatocytoma (adrenal medulla cancer)
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what is the MOA of phenoxybenzamine?
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irreversible antagonist- decreased preload
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what are the alpha 1 selective antagonists?
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prazosin and tamsulosin
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what are the clinical uses of prazosin?
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HTN, CHF and BPH
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what is the MOA of prazosin?
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- blocks a1 in arteries and veins --> decreased preload
-in CNS suppresses sympathetic outflow (postsynaptic alpha 1 blocked). -favorable effects on lipid profile (decreased LDL and TG, incHDL) |
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why does prazosin evoke less reflex tachycardia?
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lack of alpha 2 antagonism
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what are the side effects of prazosin? how do you fix the problem?
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1st dose phenomena: marked postural hypotension and syncope-minimize effect by limiting initial dose and give time for system to adapt.
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what are the clinical uses of tamsulosin?
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symptomatic relief of urethra obstruction in BPH (sx: weak stream, freq urination, nocturia)
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what is the MOA of tamsulosin?
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blocks A1 receptors on trigone, internal sphincter and prostate SM-- causing a relaxation of those muscles.
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when are nonselective beta blockers contraindicated?
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for asthma and COPD
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what are the 1st generation non-selective B antagonists?
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Propanalol and timolol
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what are the clinical uses of propranalol?
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tx: of HTN, exercise induced angina, arrhythmia, CHF, MI, thyrotoxicosis, migraine prophylaxis
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what is the MOA of 1st generation non-selective B antagonists?
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blocks sympathetic activation of the heart which decreases afterload and CO.
decreases renin release and Ang II in the kidneys. |
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what is the clinical use of timolol?
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tx of open angle glaucoma
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what is the MOA of timolol?
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decreases IOP by decreasing aqueous humor production in the ciliary body
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what is the B1 selective antagonist (2nd generation)?
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atenolol
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what are the clinical uses of atenolol?
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treatment of heart stuff with less bronchoconstriction
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what is a side effect of atenolol?
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non-specific bronchoconstriction
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what is the MOA of tamsulosin?
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blocks A1 receptors on trigone, internal sphincter and prostate SM-- causing a relaxation of those muscles.
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when are nonselective beta blockers contraindicated?
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for asthma and COPD
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what are the 1st generation non-selective B antagonists?
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Propanalol and timolol
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what are the clinical uses of propranalol?
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tx: of HTN, exercise induced angina, arrhythmia, CHF, MI, thyrotoxicosis, migraine prophylaxis
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what is the MOA of 1st generation non-selective B antagonists?
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blocks sympathetic activation of the heart which decreases afterload and CO.
decreases renin release and Ang II in the kidneys. |
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what is the clinical use of timolol?
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tx of open angle glaucoma
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what is the MOA of timolol?
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decreases IOP by decreasing aqueous humor production in the ciliary body
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what is the B1 selective antagonist (2nd generation)?
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atenolol
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what are the clinical uses of atenolol?
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treatment of heart stuff with less bronchoconstriction
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what is a side effect of atenolol?
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non-specific bronchoconstriction
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what are the 3rd generation non selective Beta antagonist?
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carvedilol, labetalol
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what are the clinical uses of carvedilol and labetalol?
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B-blockers with additional effects such as anti-oxidant, anti-inflammatory, anti-proliferative, membrane stabilizing properties (blocks Ca entry, opens K+ channels).
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what is the MOA of carvedilol and labetalol?
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B2 agonist properties, alpha 1 blockers
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T/F 3rd generation nonselective B-antagonists show increase in morbidity and mortality?
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FALSE
decreases |
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what are the 3rd generation B-selective antagonists?
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betaxolol, celiprolol, nebiprolol
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what are the drugs in the indirect sympathomimetics-amphetamines group?
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desoxyn, dexedrine, and retalin
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what are the clinical uses of desoxyn, dexedrine, and ritalin?
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narcolepsy, ADHD, ADD, appetite suppressant
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what is the MOA of desoxyn, dexedrine, and ritalin?
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increase release of dopamine and other biogenic amines. It also inhibits dopamine vesicular transporters which inhibits uptake and inhibits MAO.
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how do you administer desoxyn, dexedrine and ritalin? what makes these drugs potentially problematic?
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orally. Can cross the BBB
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what is the drug associated with the mixed acting sympathomimetics groups?
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ephedrine
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what receptors does ephedrine work on?
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agonist at all adrenergic receptors
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what are the clinical uses of ephedrine?
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use in OTC cold medications
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what is the MOA of ephedrine?
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increases release of dopamine and NE
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what is potentially problematic of ephedrine?
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it crosses the BBB and is a potent CNS stimulant
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what are the side effects of ephedrine?
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arrhythmias, headache, hyperactivity, insomnia, nausea, and tremors
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what are the two drugs that are grouped under the indirect sympatholytics?
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methyldopa (aldomet) and alpha-methyl P tyrosine (metyrosine)
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what is the clinical use of methyldopa?
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hypertenstion in pregnancy
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what is the MOA of methyldopa?
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false transmitter precursors; turns into methyl-NE
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how should methyldopa be administered? is it absorbed slowly or quickly?
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orally; slowly and excreted slowly
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what are the side effects of methyldopa?
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hypotension, drowsiness, diarrhea, impotence, hypersensitivity rxns
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what are the clinical uses of alpha-methyl p tyrosine?
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anti-htn agent; occasionally in pheochromocytoma (adrenal medullary cancer)
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what is the MOA of alpha-methyl p tyrosine?
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inhibits tyrosine hydroxylase; inhibits NE synthesis
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what are the side effects of alpha-methyl p tyrosine?
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hypotension, sedation
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what are the drugs that can inhibit catecholamine metabolism?
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monoamine inhibitors and COMT inhibitors
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what are the drugs that are characterized as MAOI?
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phenelzine, tranylcypromine, selegiline
HINT: PHEel TRANscient SErenity MAOIs are used to treat depression |
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what are the drugs that are characterized as COMTI?
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entacopone and tolcapone
HINT: AL CAPONE caused the COps of MeTropolitan NY some issues |