Intro To Adrenergic Drugs - More Detailed Flashcards
Phenylephrine CLASS: MOA: SE: CI:
Phenylephrine
CLASS: a1 agonist (a1>a2»B)
MOA: Causes a decrease in Bronchial Mucous Secretion, an Increase in Blood Pressure, and Mydriasis
SE: Bradycardia (BR Reflex), Severe Vasoconstriction w/ elevated BP
CI: HTN
Clonidine
CLASS:
MOA:
SE:
Clonidine
CLASS: Selective a2 agonist (a2>a1»B)
MOA: Decreases release of NE at synaptic terminals where a2 receptors are found in the Brainstem -> decreasing Sympathetic Outflow -> Decreased BP and Bradycardia.
Local (peripheral) Application causes Vasoconstriction.
Isoproterenol
CLASS:
MOA:
SE:
Isoproterenol
CLASS: Non-Selective B agonist (B1 and B2)
MOA: Increased HR/CO (B1) and Bronchodilation & Vasodilation (B2)
SE: Slight decrease in BP, BUT substantial Tachycardia
Albuterol
CLASS:
MOA:
Albuterol
CLASS: Selective B2 agonist
MOA: Increases Bronchodilation and Uterine Relaxation
Dobutamine
CLASS:
MOA:
Dobutamine
CLASS: Selective B1 Agonist
MOA: Increase in Heart Contractility -> Increased CO
Epinephrine
CLASS:
MOA:
Epinephrine
CLASS: Endogenous NT, Mixed a & B Agonist
MOA: Increase in CO/HR, Vasodilation -> Slight Increase in BP & Tachycardia; Bronchodilation and Decreased Mucous Secretion; enhances glycogenolysis and gluconeogenesis; increases Renin levels; increases K+ reuptake
Norepinephrine
CLASS:
MOA:
Norepinephrine
CLASS: Endogenous NT, Mixed a & B Agonist (except B2)
MOA: Potent Cardiac stimulant; Increases HR and BP, BUT BR corrects this -> Bradycardia;
Dopamine
CLASS:
MOA:
Dopamine
CLASS: Endogenous NT, Dopamine Receptor Agonist
MOA: D1 Receptors cause vasodilation and D2 Receptors suppress NE release (at physiological levels) -> decreased BP
At higher levels DA activates B1 receptors -> Increased CO/HR
At even higher levels DA activates a1 receptors -> Vasoconstriction and Increased BP
Cocaine
CLASS:
MOA:
SE:
Cocaine
CLASS: Indirect AR Agonist (Sympathomimetic)
MOA: Cocaine inhibits the reuptake of DA and NE into the presynaptic terminal via NET, thus enhancing their activity
SE: Has the potential to induce Hemorrhagic stroke and/or death
Phenelzine, Selegiline
CLASS:
MOA:
Phenelzine, Selegiline
CLASS: Indirect AR Agonist (Sympathomimetic)
MOA: inhibits MOA (Monamine Oxidase) from breaking down E, NE, and DA, increasing their stores in the CNS
Amphetamines, Methylphenidate
CLASS:
MOA:
SE:
Amphetamine, Methylphenidate
CLASS: Indirect AR Agonist (Sympathomimetic) may have a small direct effect as well
MOA: Stimulates the release of NE and DA, and inhibits their reuptake, increasing their overall activity. Creates a stimulant effect.
SE: Decreased appetite
Ephedrine
CLASS:
MOA:
Ephedrine
CLASS: Indirect AR Agonist (Sympathomimetic) but has some direct activity
MOA: Non-selectively releases stored catecholamines with a long duration of action. Increases BP. Mildly Stimulating.
Tyramine CLASS: MOA: Rx: Other:
Tyramine
CLASS: Indirect AR Agonist (Sympathomimetic)
MOA: Releases NE stored in Pre-Synaptic Terminals if administered Parenterally.
Rx: Can cause a marked increase in BP in Patients taking a MOA Inhibitor
Other: Pdt of Tyrosine metabolism found in cheese, cured meats, & smoked and pickled fish
What Adrenergic Agonists might you use to treat CHF?
Dobutamine (B1 Agonist) - may be used short-term to treat Acute HF as it increases CO
Dopamine - may be used to treat Severe Congestive HF with reduced Renal perfusion as D1 Receptors will induce Renal A. Vasodilation
What Adrenergic Agonists might you use to treat Hypertension?
Clonidine or another a2 agonist may be used as they work in the brainstem to inhibit catecholamine release and reduced Sympathetic outflow
What Adrenergic Agonists might you use to treat a patient in Hypotensive Emergencies such as Hemorrhagic Shock, OC of Anti-Hypertensives, or CNS Depressants?
Epinephrine or Norepinephrine, both of which will increase Sympathetic activity and functions to increase CO/HR (B1) and BP (a1)
What Adrenergic Agonists might you use to treat Chronic Hypotension?
Ephedrine would be a likely drug to use due to the fact that it is plant-based, and thus not a Catecholamine, so it will have a longer duration of action as opposed to other Adrenergic Agonists we have discussed. It increases BP by stimulating Catecholamine Release
What Adrenergic Agonists might you use to treat a patient in Cardiogenic Shock due to a Massive Acute MI?
Dopamine (enough to stimulate B1 receptors) or Dobutamine (B1) could both function to increase CO
What kind of Adrenergic Agonists might you use for Emergency treatment of a complete AV Block and Cardiac Arrest?
Epinephrine or Isoproterenol could be used as both function to increase HR (B1)
What kind of Adrenergic Agonist might you use to treat Narcolepsy?
Amphetamines or Methylphenidate could be used as either function to increase sympathetic outflow by increasing Catecholamine release and inhibiting their uptake, and function as a stimulant