Notes in 14 Adrenergic Agonists & Antagonists

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Published	12/13/2023	{{c3::Acetylcholine}} is the neurotransmitter for {{c2::postganglionic sympathetic}} fibers at {{c1::eccrine sweat glands}} and some {{c1::blood …
Published	12/13/2023	Acetylcholine is the neurotransmitter released by {{c1::preganglionic sympathetic}} fibers and all {{c2::parasympathetic}} fibers.
Published	12/13/2023	Norepinephrine is primarily (80%) terminated via {{c1::reuptake}}.
Published	12/13/2023	The primary site of catecholamine metabolism is the {{c1::liver and kidneys}}.
Published	12/13/2023	α1 receptors → linked to {{c1::Gq}} proteins → activates {{c2::phospholipases}}
Published	12/13/2023	α2 receptors → linked to {{c1::Gi}} proteins → inhibit {{c2::adenylate cyclase}}
Published	12/13/2023	In the liver, sympathetic stimulation of α1 and β2 receptors {{c1::increases}} blood glucose via glycogenolysis and gluconeogenesis.
Published	12/13/2023	{{c4::α1}} receptor agonists cause {{c3::mydriasis}} due to {{c1::contraction::contraction/relaxation}} of the {{c2::radial}} eye muscles.
Published	12/13/2023	The primary vascular effect of α1 stimulation is {{c1::vasoconstriction}}.
Published	12/13/2023	Stimulation of presynaptic α2 receptors creates a {{c1::negative}} feedback loop that {{c2::inhibits::inhibits/activates}} further norepinephrine rele…
Published	12/13/2023	Smooth muscle contains postsynaptic α2 receptors that produce vaso{{c1::constriction::constriction/dilation}}.
Published	12/13/2023	Stimulation of β1 receptors in the heart result in:Positive {{c1::chronotropy}} → increased {{c2::heart rate}}Positive {{c1::dromotropic}} effect…
Published	12/13/2023	β2 receptor stimulation {{c1::relaxes::contracts/relaxes}} smooth muscle.
Published	12/13/2023	In pregnant patients, {{c2::β2}} stimulation causes uterine {{c1::relaxation}}
Published	12/13/2023	{{c1::Droperidol}} exerts its {{c2::antiemetic}} action via {{c3::D2}} receptors
Published	12/13/2023	Isoproterenol {{c1::increases}} the heart rate and {{c2::decreases}} the SVR.
Published	12/13/2023	Dobutamine produces a {{c1::increase::increase/decrease}} in heart rate via {{c2::β1}} agonism.
Published	12/13/2023	Catecholamines are metabolized by {{c1::monoamine oxidase (MAO)}} and {{c2::catechol-O-methyltransferase (COMT)}}.
Published	12/13/2023	Phenylephrine is a {{c1::noncatecholamine::catecholamine/noncatecholamine}} with selective {{c2::α1}}-{{c3::agonist::agonist/antagonist}} activity.&nb…
Published	12/13/2023	The primary effect of phenylephrine is peripheral vaso{{c1::constriction}}.
Published	12/13/2023	Phenylephrine administration can result in reflex {{c1::bradycardia::tachycardia/bradycardia}} causing {{c1::decreased::increased/decreased}} cardiac …
Published	12/13/2023	Reflex {{c2::bradycardia}} from phenylephrine is mediated by the {{c1::baroreceptor}} reflex .
Published	12/13/2023	Most (80%) {{c2::epinephrine::catecholamine}} is synthesized in the {{c1::adrenal medulla}}.
Published	12/13/2023	At higher doses, epinephrine stimulates {{c1::α1}} receptors.
Published	12/13/2023	Ephedrine is a {{c1::noncatecholamine::catecholamine/noncatecholamine}} sympatho{{c2::mimetic}}.
Published	12/13/2023	Norepinephrine directly stimulates {{c1::α1 and β1}} receptors.
Published	12/13/2023	{{c2::Norepinephrine}} is the vasopressor of choice in the management of {{c1::septic shock}}.
Published	12/13/2023	Dopamine at low doses ({{c2::0.5}} to {{c2::5}} mcg/kg/min) primarily activates {{c1::dopaminergic}} receptors.
Published	12/13/2023	At low doses, dopamine vasodilates the {{c1::renal}} and {{c1::splanchic}} vascular beds.
Published	12/13/2023	Dopamine at moderate doses ({{c2::5}} to {{c2::10}} mcg/kg/min) stimulates {{c1::β1}} receptors.
Published	12/13/2023	Dopamine at high doses ({{c2::10}} to {{c2::20}} mcg/kg/min) stimulate {{c1::α1}} receptors.
Published	12/13/2023	Isoproterenol is a pure {{c1::β}}-agonist.
Published	12/13/2023	The primary cardiovascular effect of dobutamine is a rise in {{c1::cardiac output}} as a result of increased {{c1::myocardial contractility}}.
Published	12/13/2023	Phentolamine causes a decrease in {{c2::blood pressure}} with reflex {{c2::tachycardia}} due to antagonism of {{c1::α2}} receptors in the heart.
Published	12/13/2023	IV extravasation of norepinephrine can be treated with local infiltration of {{c1::phentolamine}} {{c2::10}} mg in {{c2::10}} mL of normal saline…
Published	12/13/2023	Labetalol blocks {{c1::α1}}, {{c1::β1}}, and {{c1::β2}} receptors.
Published	12/13/2023	Labetalol has an α to β blockade ratio of approximately {{c1::1:7}} (in IV form)
Published	12/13/2023	Labetalol has both α and β effects, so it reduces blood pressure without reflex {{c1::tachycardia}}.
Published	12/13/2023	Atenolol is the only β-blocker eliminated primarily by {{c1::kidney excretion}}.
Published	12/13/2023	Esmolol is an an ultra-{{c1::short::long/short}} acting selective {{c2::β1}} {{c3::antagonist::agonist/antagonist}}.
Published	12/13/2023	Esmolol reduces {{c1::heart rate}} and {{c2::blood pressure}}.
Published	12/13/2023	Esmolol's short duration of action is due to rapid {{c1::redistribution}} and hydrolysis by {{c1::RBC esterase}}.
Published	12/13/2023	Esmolol's distribution half-life is {{c1::2}} minutes and its elimination half life is {{c1::9}} minutes.
Published	12/13/2023	Propranolol, carvedilol, and timolol are {{c1::nonselective}} β-blockers.
Published	12/13/2023	Ephedrine stimulates {{c1::α1}}, {{c1::β1}}, and {{c1::β2}} receptors.
Published	12/13/2023	The bolus dose of ephedrine is {{c1::0.1}} mg/kg, or in {{c2::5}} to {{c2::10}} mg pushes.
Published	12/13/2023	Ephedrine exerts its {{c1::indirect::direct/indirect}} action in the post-ganglionic adrenergic nerve by causing {{c2::catecholamine release}}.
Published	12/13/2023	The bolus dose of phenylephrine is {{c2::0.5}}-{{c2::1}} mcg/kg, or in {{c3::50}}-{{c3::100}} mcg pushes.
Published	12/13/2023	Esmolol primarily blockades {{c1::β1}} receptors, especially at lower doses.
Published	12/13/2023	The rate limiting step of catecholamine synthesis is the conversion of {{c1::tyrosine}} to {{c1::dopa}} by {{c2::tyrosine hydroxylase}}.
Published	12/13/2023	In catecholamine synthesis, {{c1::dopamine}} is converted to {{c1::norepinephrine}} by {{c2::dopamine β-hydroxylase}}.
Published	12/13/2023	In catecholamine synthesis, {{c1::dopa}} is converted to {{c1::dopamine}} by {{c2::dopa decarboxylase}}.
Published	12/13/2023	{{c1::Norepinephrine}} synthesis produces a negative feedback loop that inhibits {{c2::tyrosine hydroxylase::enzyme}}.
Published	12/13/2023	Norepinephrine is converted to {{c2::epinephrine}} by the enzyme {{c1::phenylethanolamine N-methyltransferase (PNMT)}}.
Published	12/13/2023	{{c3::Parasympathetic::Sympathetic/parasympathetic}} stimulation causes {{c2::miosis}} due to contraction of the {{c1::sphincter}} eye muscles.
Published	12/13/2023	{{c1::β2}} receptor stimulation of the {{c2::ciliary}} muscle of the eye causes {{c3::relaxation}} for far vision.
Published	12/13/2023	The primary vascular effects of β2 stimulation is coronary and skeletal {{c1::vasodilation}}.
Published	12/13/2023	{{c1::Sympathetic::Sympathetic/parasympathetic}} stimulation of the gastrointestinal system causes a general slowing in motility and digestion.
Published	12/13/2023	{{c1::β2}} receptor stimulation of the {{c2::detrusor}} muscle of the bladder causes {{c3::relaxation}}.
Published	12/13/2023	{{c1::α1}} stimulation of the {{c2::trigone and sphincter}} of the bladder causes {{c3::contraction}}.
Published	12/13/2023	In pregnant patients, {{c2::α1}} adrenergic receptor stimulation causes uterine {{c1::contraction}}
Published	12/13/2023	{{c1::α2}} stimulation of the pancreas {{c2::decreases::increases/decreases}} insulin secretion.
Published	12/13/2023	{{c1::β2}} receptor stimulation of the pancreas {{c2::increases::increases/decreases}} insulin secretion.
Published	12/13/2023	Dobutamine {{c1::decreases::decreases/increases}} systemic vascular resistance via β2 stimulation.
Published	12/13/2023	Inhibition of tyrosine hydroxylase produces sympatho{{c1::lytic}} effects.
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