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116 Cards in this Set

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The main effects of the alpha 1 receptor are:
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
The main effects of the alpha 2 receptor are:
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
The main effects of the Beta 1 receptor are:
increased cardiac rate and force, increases renin release
The main effects of the Beta 2 receptor are:
bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis and skeletal muscle tremor
The main effects of the Beta 3 receptor are:
lipolysis
at low doses what affect does epinephrine have? why?
Vasodilation due to B2 receptors
which receptors respond the strongest to epinephrine?
B2, B1
at high doses, what affect does epinephrine have? why?
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.
at therapeutic doses, what affect does epinephrine have? why?
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
NE affects which receptors? which one predominates?
alpha 1 and 2, and Beta 1

alphas > beta1
what are the non-selective adrenergic agonists?
epinephrine, norepinephrine, isoproterenol, and oxymetazoline
what receptors are affected by isoproterenol?
Beta 1 and 2
which non-selective adrenergic agonists is an alpha agonist?
oxymetazoline (Alpha 1 and 2 receptors)
what are the clinical uses of epinephrine?
hypersensitivity reactions, cardiac resuscitation, relieve bronchospasm in asthma, dec IOP glaucoma, topical hemostatic, adjunct in local anesthetic
why can't epinephrine be given orally?
because it is rapidly inactivated by the Monoamine oxidases (MAO) and the catechol-methyl- transferases (COMTs).
epinephrine has a _____ onset of action and a ______ duration
rapid; short
what are the side effects of epinephrine?
HTN, tachycardia, reflex bradycardia, ventricular arrhythmias, tremor, hyperglycemia
what is the clinical use of NE?
reverses hypotension in shock
how is epinephrine and NE adminstered?
Intramuscularly or Subcutaneously
what is the clinical use of isoproterenol?
treatment of asthma and cardiac resusitation
is isoproterenol rapidly absorbed?
no, some tissues have a t 1/2 = 2 hours
what are the side effects of isoproterenol?
tachycardia, dysrhythmias, tremor
what is the clinical use of oxymetazoline?
nasal decongestant- short relief
what are the side effects of norepi?
same as epi: HTN, tachycardia, reflex bradycardia, ventricular arrhythmias, tremor, hyperglycemia.
what is the MOA of oxymetazoline?
constricts the small arterioles supplying the nasal mucosa, decreasing secretions.
T/F a pt can use oxymetazoline regularly without any change in the body's response
FALSE

you lose efficacy with chronic use: desensitization of alpha receptors
what are the side effects of oxymetazoline?
intense constriction can damage the nasal mucosa, rebound hyperemia and worsening of symptoms
what is the alpha 1 selective agonist?
phenylephrine
what are the clinical uses of pheynlephrine?
nasal decongestant, mydriasis (w/o loss of accommodation), short term hypotensive emergencies or to maintain BP during spinal anesthsia
what is the MOA of phenylephrine?
vasoconstriction in nasal mucosa, contraction of radial diameter
when is phenylephrine contraindicated?
narrow angle glaucoma
how does phenylephrine differ from epi and NE pharmacodynamically?
it is less potent, but has a longer duration of action than EPI and NE.
what are the alpha 2 selective agonists?
clonidine and apraclonidine
what are the clinical uses of clonidine?
hypertension and for addicts in withdrawal from alcohol, narcotics and tobacco.
what is the MOA of clonidine?
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).
T/F clonidine is a partial agonist
true
if clonidine is given via IV what is the result? what about orally?
IV- transient increase in BP
Orally- hypotensive agent
what makes clonidine dangerous? how do we avoid that?
it crosses the BBB. to avoid it we prescribe Transdermal patch in order to decrease CNS side effects
If you abruptly stop clonidine, what can you cause?
rebound hypertension
what are the side effects of clonidine?
dry mouth, sedation (in 50% of pts and generally only initially), bradycardia and sexual dysfunction
what is apraclonidine used for?
open-angle glaucoma
what is the MOA of apraclonidine?
constriction of blood vessels to eye --> decreased synthesis of aqueous humor
Apraclonidine is used in conjunction with 3 other drugs, what are they?
timolol followed by iopidine and pilocarpine
what are the B1 selective agonists?
dopamine and dobuatmine
what receptors do dopamine act on?
Beta 1 and Renal receptor D1
what is the clinical use of dopamine?
- improve cardiac and renal function in CHF and renal failure pts
- cardiogenic and septic shock: only after hypovolemia has been corrected
what is the MOA of dopamine?
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.
where is dopamine synthesized in the body?
in the proximal tubule of the kidney
what are the clinical uses of doputamine?
CHF, MI, short term management of cardiac decompensation after cardiac surgery
what is the MOA of dobutamine?
increase in CO and SV w/ o marked increase in HR or BP
what are the B2 selective agonists?
albuterol, salmeterol, ritodrine
what side effects do all B2 selective agonists cause?
tremor, decreased plasma K+ concentration, increased plasma glucose concentration
what are the clinical uses of albuterol?
symptomatic relief in asthma and COPD
what is the MOA of albuterol?
bronchodilation
how quickly does albuterol act? how long does it last?
acts w/n 15 min and persists 2-3 hours
what are the clinical uses of salmeterol?
symptomatic relief of bronchospasm in COPD - nocturnal asthma
what is the MOA of salmeterol?
bronchodilation, anti-inflammatory
how quickly does salmeterol act? how long does it last?
onset is slow (30min- 1hr), prolonged duration of action (>12 hours)
what is the clinical use of ritodrine? how is it given?
to arrest premature labor; IV
what is the MOA of ritodrine?
uterine relaxation
what are the non-selective A antagonists?
phenoxybenzamine and phentolamine
what are the side effects of all non-selective A antagonists?
orthostatic hypotension, tachycardia (increase NE release d/t presynpatic alpha 2 block), vertigo, sexual dysfunction
what is the clinical use of phenoxybenzamine?
tx of pheochromatocytoma (adrenal medulla cancer)
what is the MOA of phenoxybenzamine?
irreversible antagonist- decreased preload
what are the alpha 1 selective antagonists?
prazosin and tamsulosin
what are the clinical uses of prazosin?
HTN, CHF and BPH
what is the MOA of prazosin?
- 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)
why does prazosin evoke less reflex tachycardia?
lack of alpha 2 antagonism
what are the side effects of prazosin? how do you fix the problem?
1st dose phenomena: marked postural hypotension and syncope-minimize effect by limiting initial dose and give time for system to adapt.
what are the clinical uses of tamsulosin?
symptomatic relief of urethra obstruction in BPH (sx: weak stream, freq urination, nocturia)
what is the MOA of tamsulosin?
blocks A1 receptors on trigone, internal sphincter and prostate SM-- causing a relaxation of those muscles.
when are nonselective beta blockers contraindicated?
for asthma and COPD
what are the 1st generation non-selective B antagonists?
Propanalol and timolol
what are the clinical uses of propranalol?
tx: of HTN, exercise induced angina, arrhythmia, CHF, MI, thyrotoxicosis, migraine prophylaxis
what is the MOA of 1st generation non-selective B antagonists?
blocks sympathetic activation of the heart which decreases afterload and CO.
decreases renin release and Ang II in the kidneys.
what is the clinical use of timolol?
tx of open angle glaucoma
what is the MOA of timolol?
decreases IOP by decreasing aqueous humor production in the ciliary body
what is the B1 selective antagonist (2nd generation)?
atenolol
what are the clinical uses of atenolol?
treatment of heart stuff with less bronchoconstriction
what is a side effect of atenolol?
non-specific bronchoconstriction
what is the MOA of tamsulosin?
blocks A1 receptors on trigone, internal sphincter and prostate SM-- causing a relaxation of those muscles.
when are nonselective beta blockers contraindicated?
for asthma and COPD
what are the 1st generation non-selective B antagonists?
Propanalol and timolol
what are the clinical uses of propranalol?
tx: of HTN, exercise induced angina, arrhythmia, CHF, MI, thyrotoxicosis, migraine prophylaxis
what is the MOA of 1st generation non-selective B antagonists?
blocks sympathetic activation of the heart which decreases afterload and CO.
decreases renin release and Ang II in the kidneys.
what is the clinical use of timolol?
tx of open angle glaucoma
what is the MOA of timolol?
decreases IOP by decreasing aqueous humor production in the ciliary body
what is the B1 selective antagonist (2nd generation)?
atenolol
what are the clinical uses of atenolol?
treatment of heart stuff with less bronchoconstriction
what is a side effect of atenolol?
non-specific bronchoconstriction
what are the 3rd generation non selective Beta antagonist?
carvedilol, labetalol
what are the clinical uses of carvedilol and labetalol?
B-blockers with additional effects such as anti-oxidant, anti-inflammatory, anti-proliferative, membrane stabilizing properties (blocks Ca entry, opens K+ channels).
what is the MOA of carvedilol and labetalol?
B2 agonist properties, alpha 1 blockers
T/F 3rd generation nonselective B-antagonists show increase in morbidity and mortality?
FALSE

decreases
what are the 3rd generation B-selective antagonists?
betaxolol, celiprolol, nebiprolol
what are the drugs in the indirect sympathomimetics-amphetamines group?
desoxyn, dexedrine, and retalin
what are the clinical uses of desoxyn, dexedrine, and ritalin?
narcolepsy, ADHD, ADD, appetite suppressant
what is the MOA of desoxyn, dexedrine, and ritalin?
increase release of dopamine and other biogenic amines. It also inhibits dopamine vesicular transporters which inhibits uptake and inhibits MAO.
how do you administer desoxyn, dexedrine and ritalin? what makes these drugs potentially problematic?
orally. Can cross the BBB
what is the drug associated with the mixed acting sympathomimetics groups?
ephedrine
what receptors does ephedrine work on?
agonist at all adrenergic receptors
what are the clinical uses of ephedrine?
use in OTC cold medications
what is the MOA of ephedrine?
increases release of dopamine and NE
what is potentially problematic of ephedrine?
it crosses the BBB and is a potent CNS stimulant
what are the side effects of ephedrine?
arrhythmias, headache, hyperactivity, insomnia, nausea, and tremors
what are the two drugs that are grouped under the indirect sympatholytics?
methyldopa (aldomet) and alpha-methyl P tyrosine (metyrosine)
what is the clinical use of methyldopa?
hypertenstion in pregnancy
what is the MOA of methyldopa?
false transmitter precursors; turns into methyl-NE
how should methyldopa be administered? is it absorbed slowly or quickly?
orally; slowly and excreted slowly
what are the side effects of methyldopa?
hypotension, drowsiness, diarrhea, impotence, hypersensitivity rxns
what are the clinical uses of alpha-methyl p tyrosine?
anti-htn agent; occasionally in pheochromocytoma (adrenal medullary cancer)
what is the MOA of alpha-methyl p tyrosine?
inhibits tyrosine hydroxylase; inhibits NE synthesis
what are the side effects of alpha-methyl p tyrosine?
hypotension, sedation
what are the drugs that can inhibit catecholamine metabolism?
monoamine inhibitors and COMT inhibitors
what are the drugs that are characterized as MAOI?
phenelzine, tranylcypromine, selegiline

HINT: PHEel TRANscient SErenity

MAOIs are used to treat depression
what are the drugs that are characterized as COMTI?
entacopone and tolcapone

HINT: AL CAPONE caused the COps of MeTropolitan NY some issues