Adrenergic Agonists B&B Flashcards
which 2 adrenergic agonists activate all receptor types?
epinephrine and dopamine - activate alpha1, alpha2, beta1, beta2
[note dopamine also activates D1 receptors in kidneys to increase renal blood flow]
which 2 adrenergic agonists activate just the beta receptor types (beta1 and beta2)? what is the key difference between them?
isoproterenol: beta1=beta2, so increases HR while lowering BP
dobutamine: beta1>beta2, but still increases HR while lowering BP
which 2 adrenergic agonists activate just the alpha receptors mostly (alpha1, alpha2)?
norepinephrine - but also binds beta1, beta2 (just not as much)
phenylephrine
therefore, it makes sense these are used as vasoconstrictors!
group the following adrenergic agonists into 3 groups and explain why:
a. epinephrine
b. norepinephrine
c. isoproterenol
d. dopamine
e. dobutamine
f. phenylephrine
activate all receptors (alpha1/2, beta1/2): epinephrine + dopamine
activate just beta receptors (beta1/2): isoproterenol (beta1=beta2) + dobutamine (beta1>beta2) —> raise HR, lower BP
activate just alpha receptors (alpha1/2): norepinephrine (also binds beta1/2 some) + phenylephrine —> vasoconstriction
which 2 adrenergic agonists would be best for raising HR and lowering BP?
isoproterenol and dobutamine: preferentially bind beta receptors (beta1, beta2)
[recall beta1 —> increase HR, beta2 —> vasodilation]
which 2 adrenergic agonists would be best for vasoconstriction in shock patients?
norepinephrine and phenylephrine: preferentially bind alpha receptors (alpha1, alpha2)
which receptors does epinephrine vs norepinephrine bind?
epinephrine: binds all adrenergic receptors well (alpha1/2, beta1/2)
norepinephrine: preferentially activates alpha receptors (alpha1/2) - great for vasoconstriction in shock patients
which receptors does dopamine vs dobutamine bind?
dopamine: binds ALL adrenergic receptors (alpha1/2, beta1/2)
dobutamine: preferentially binds beta receptors (beta1/2) —> raises HR while lowering BP
what is the effect of low vs medium vs high dose dopamine?
low dose = dopamine agonist —> binds D1 receptors in kidney to cause vasodilation
medium dose = beta1 agonist —> increased HR and contractility
high dose = alpha agonist —> vasoconstriction
DOES NOT CROSS BBB (NO CNS EFFECTS)
how big of a dose should you give of dopamine to achieve the following effects?
a. vasoconstriction
b. vasodilation in kidneys
c. increased HR and contractility
low dose = dopamine agonist —> binds D1 receptors in kidney to cause vasodilation
medium dose = beta1 agonist —> increased HR and contractility
high dose = alpha agonist —> vasoconstriction
DOES NOT CROSS BBB (NO CNS EFFECTS)
what is the effect of low vs high dose epinephrine?
epinephrine: binds all adrenergic receptors well (alpha1/2, beta1/2)
low dose: beta1 = beta2 —> increased HR and contractility + vasodilation (lower BP)
high dose: alpha agonist —> vasoconstriction
if you want to use epinephrine to treat a patient with anaphylaxis, what kind of dose should you give them?
epinephrine: binds all adrenergic receptors well (alpha1/2, beta1/2)
low dose: beta1 = beta2 —> increased HR and contractility + vasodilation (lower BP)
high dose: alpha agonist —> vasoconstriction - treats shock
to which adrenergic receptors do the following agonists bind? state the clinical use
a. pseudoephedrine
b. albuterol
c. salmeterol
d. terbutaline
e. ritodrine
a. pseudoephedrine: alpha1/2 —> nasal decongestant (constrict nasal vessels)
b. albuterol: beta2>1 —> tx asthma (bronchodilation)
c. salmeterol: beta2>1 —> tx COPD (bronchodilation)
d. terbutaline: beta2>1 —> decrease contractions (OB)
e. ritodrine: beta2 —> decrease contractions (OB)
what type of drug is pseudoephedrine, and what is its clinical use?
pseudoephedrine: alpha1/2 direct agonist
used as nasal decongestant via vasoconstriction in nose
direct agonist of alpha1&2 used as nasal decongestant
pseudoephedrine: alpha1/2 direct agonist
used as nasal decongestant via vasoconstriction in nose
to which adrenergic receptors do albuterol and salmeterol bind, and what are their respective clinical uses?
direct agonists of beta receptors (beta2>beta1) —> bronchodilation
albuterol - treats asthma
salmeterol - treats COPD
to which adrenergic receptors do terbutaline and ritodrine bind, and what is their clinical use? what is the difference between the two drugs?
terbutaline: direct agonist of beta2>beta1 receptors
ritodrine: direct agonist of beta2 receptors
both used in OB to decrease contractions
which of the following direct adrenergic agonists does NOT bind beta receptors?
a. albuterol
b. pseudoephedrine
c. terbutaline
d. salmeterol
e. ritodrine
a. pseudoephedrine: alpha1/2 —> nasal decongestant (constrict nasal vessels)
b. albuterol: beta2>1 —> tx asthma (bronchodilation)
c. salmeterol: beta2>1 —> tx COPD (bronchodilation)
d. terbutaline: beta2>1 —> decrease contractions (OB)
e. ritodrine: beta2 —> decrease contractions (OB)
what types of drugs are clonidine and methyldopa, and what is their clinical use?
direct alpha2 agonists used to treat hypertension
what kind of drug is apraclonidine, and what is its clinical use?
direct alpha2 agonist (with weak alpha1 activity) used in glaucoma to lower intraocular pressure
clonidine vs apraclonidine
clonidine: direct alpha2 agonist used to treat hypertension
apraclonidine: direct alpha2 agonist (with weak alpha1 activity) used in glaucoma to lower intraocular pressure
which of the following is used to treat HTN?
a. pseudoephedrine
b. albuterol
c. salmeterol
d. clonidine
e. terbutaline
f. ritodrine
g. apraclonidine
d. clonidine: direct alpha2 agonist used to treat hypertension
which of the following is used to treat COPD?
a. pseudoephedrine
b. albuterol
c. salmeterol
d. clonidine
e. terbutaline
f. ritodrine
g. apraclonidine
c. salmeterol: beta2>1 —> tx COPD (bronchodilation)
how do indirect adrenergic agonists work?
do not bind alpha or beta receptor to activate directly (that would be a direct agonist duh!)
instead, they increase the activity of norepinephrine either by promoting its release or blocking its reuptake
how do the following drugs act as indirect adrenergic agonists, and what are their respective clinical uses?
a. amphetamine
b. ephedrine
c. cocaine
a. amphetamine: blocks NE reuptake + promotes NE release —> stimulate to treat narcolepsy, obesity, ADHD
b. ephedrine: promotes NE release —> nasal decongestant, urinary incontinence
c. cocaine: blocks NE reuptake —> vasoconstriction, local anesthetic
which of the following drugs is used as a local anesthetic?
a. amphetamine
b. ephedrine
c. cocaine
a. amphetamine: blocks NE reuptake + promotes NE release —> stimulate to treat narcolepsy, obesity, ADHD
b. ephedrine: promotes NE release —> nasal decongestant, urinary incontinence
c. cocaine: blocks NE reuptake —> vasoconstriction, local anesthetic… however, note this is because of separate action of blocking Na channels in nerves!!!
ephedrine vs pseudoephedrine
pseudoephedrine: alpha1/2 direct agonist
ephedrine: indirect adrenergic agonist via promoting NE release
both used as nasal decongestant via vasoconstriction in nose
indirect adrenergic agonist used as nasal decongestant
ephedrine: promotes NE release
treats nasal congestion + urinary incontinence
[recall pseudoephedrine is a direct alpha1/2 agonist that treats nasal congestion]
what kind of neurotransmitters does cocaine act on? how does it exert this effect?
enhances monoamine [read: single NH2 group] neurotransmitter activity via blocking presynaptic reuptake pumps - dopamine, NE, serotonin
—> generalized sympathetic activation
cocaine intoxication induces massive alpha and beta stimulation —> HTN, tachycardia, coronary spasm (chest pain + increased O2 demand)
how does cocaine function as a local anesthetic?
aside from its action as indirect adrenergic agonist enhancing monoamine NT activity (dopamine, NE, 5-HT)…
… cocaine also blocks Na+ channels in nerves, allowing it to function as a local anesthetic
what is the treatment for cocaine intoxication, and how does it work? what drug should be AVOIDED?
cocaine: indirect adrenergic agonist via blocking monoamine NT reuptake - NE, dopamine, 5-HT
cocaine intoxication = massive alpha and beta receptor stimulation —> HTN, tachycardia, coronary spasm
tx: benzodiazepines - sedatives via GABA activation
AVOID beta blockers - this would cause unopposed alpha activation and SEVERE HTN
A college student presents to the ED with chest pain due to coronary spasms and HTN. It is discovered they are experiencing cocaine intoxication. Your fellow medical student on ED round is about to administer a beta blocker. You jump in just in time to stop them. Why? What will you do instead?
cocaine: indirect adrenergic agonist via blocking monoamine NT reuptake - NE, dopamine, 5-HT
cocaine intoxication = massive alpha and beta receptor stimulation —> HTN, tachycardia, coronary spasm
tx: benzodiazepines - sedatives via GABA activation
AVOID beta blockers - this would cause unopposed alpha activation and SEVERE HTN
what drug should you give?
5yo M presents with hives and wheezing following bee sting
anaphylaxis —> give epinephrine
alpha1/2 AND beta1/2 direct agonist = vasoconstrictor + bronchodilator
what drug should you give?
75yo M presents with pneumonia and hypotension
septic shock —> give norepinephrine OR phenylephrine
direct alpha1/2 agonists = vasoconstrictors
what direct adrenergic agonist should you give?
66yo M presents with massive myocardial infraction and hypotension
cardiogenic shock —> give dobutamine
direct beta1 agonist = increase cardiac contractility and HR
what adrenergic agonist should you give?
Pt is 10yo M with PMH of asthma presenting with wheezing and dyspnea
asthma flare —> give albuterol
direct beta2 agonist = bronchodilator
what direct adrenergic agonist should you give?
22yo M presents with runny nose
rhinitis —> give pseudophedrine OR phenylephrine
direct alpha1 agonists = vasoconstrictors
