Adrenergic agonists and antagonists

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Adrenergic agonists and antagonists
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2015-08-02 14:12:23
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  1. The sympathetic nervous system is also referred to as....
    • thoracoabdominal or thoracolumbar
    • - T1-L2-3
    • - Fibers originate in the spinal cord along with spinal nerves between T1 & L2-3 and then pass first into the sympathetic chain then to tissues and end organs
  2. The parasympathetic nervous system is also referred to as....
    • Craniosacral
    • Fibers leave the CNS through cranial nerves 3,7,9,10 & also from lowest part of the spinal cord through S2 and S3
  3. Norepinephrine synthesis...
    • Starts in the cytoplasm of terminal nerve endings then is completed in secretory vesicles
    • 1. Tyrosine --> dopa
    • 2. Dopa --> dopamine
    • 3. Transport of dopamine into vesicles
    • 4. Dopamine --> norepinephrine 

    *except the adrenal medulla were 80% of norepi --> epi
  4. Norepinephrine is removed from the site of secretion in 3 ways:
    • 1. Reuptake into the adrenergic nerve endings by active transport. Removes 50-80% of secreted norepi
    • 2. Diffusion away from nerve endings into surrounding body fluids and then into the blood (most of remaining norepi is removed this way)
    • 3. Breakdown of small amounts by tissue enzymes including MAO (in nerve endings) and COMT (diffusely present in all tissues)
  5. Alpha 1
    • Postsynaptic
    • Smooth muscle throughout body: eye, lung, blood vessels, uterus, gut and GU

    Stimulation causes vasoconstriction, bronchoconstriction and HTN
  6. Alpha 2
    Presynaptic

    Stimulation causes negative feedback inhibiting norepi release resulting in vasodilation, hypotension and sedation
  7. How does dexmetatomadine work
    • Causes hyper polarization because of potassium influx
    • Decreased firing neurons and decreased norepi release mediated by alpha 2 pre-synaptic receptors 
    • Up-regulation may occur with long term use so withdrawal will quickly cause HTN
  8. Alpha 2 subtypes
    • Alpha 2A: sedation, analgesia and sympatholysis (hypotension)
    • Alpha 2B: hypertension and vasoconstriction
    • Alpha 2C: startle reflex
  9. Beta 1
    Postsynaptic membranes in the heart

    Stimulation causes positive chronotropic, dromotropic and inotropic effects
  10. Beta 2
    Postsynaptic in smooth muscle and glands

    • Stimulation causes bronchodilation, vasodilation, glycogenolysis, lipolysis and insulin release 
    • Also activates Na/K pump so K goes INTO the cell and can induce hypokalemia and various arrhythmias
  11. Phenylethylamine structure is...
    • Parents compound for sympathomimetics!
    • Can have substitutions on the...
    • 1. Terminal amino group - NH2 group
    • 2. Benzene ring
    • 3. Alpha or beta carbons

    *these substitutions effect the affinity on the various receptors
  12. Substitution on the amino group
    • Increases size of alkyl substituents which increases beta receptor activity 
    • ex: putting methyl group on norepi to make epi enhanced B2 and replacing methyl on epi with isopropyl group to make isoproterenol enhance B activity even more
    • The larger the amino substituent group, the less alpha effect
  13. Substitution on the benzene ring
    • Max alpha and beta activity
    • If -OH group on C3 (especially) or C4 is missing, the potency of the drug is DRAMATICALLY reduced
    • Ex: Phenylephrine is much less potent than epi
  14. Substitution on the alpha carbon
    • Prolongs the duration of action by blocking oxidation by MAO
    • Ex: ephedrine has methyl group at alpha carbon - which means it can displace catecholamine from storage sites in nerve endings aka indirect mechanism of action
  15. Substitution on the beta carbon
    Direct acting agnostic typically have a eta hydroxyl group such as epi, norepi or isoproterenol
  16. Epinephrine - where it is released, receptors and potency
    • Prototype
    • Released from adrenal medulla
    • Most potent alpha activator but also B1 and B2
    • 2-10 times more potent than norepi
  17. Epinephrine is important for the regulation of...
    • Myocardial contractility
    • HR
    • Vascular and bronchial smooth muscle tone
    • Glandular secretions
    • Metabolism (lipolysis and glycogenolysis)
  18. Epinephrine effects on CV by dose!
    • @1-2mcg/min IV: stimulating mainly B2 receptors in peripheral vasculature 
    • @ 4mcg/min: beta 1 stimulation
    • @10-20mcg/min: both alpha and beta with alpha predomination
    • Rapid bolus of 2-8mcg IV causes cardiac stimulation lasting 1-5 minutes
  19. Epinephrine effects on BP, HR and vasculature
    • BP & HR
    • Incr SBP but modestly decreased DBP d/t vasodilation so MAP doesn't change much and baroreceptor mediated bradycardia doesn't occur
    • Tachycardia - due to accelerated rate of phase 4 depolarization
    • Increased likelihood of arrhythmias
    • Vasculature: constriction vs dilation depending on location 
    • Coronary flow ENHANCED
    • Renal perfusion DECREASED
    • Skeletal muscle vessels DILATE (B2)
  20. Norepinephrine release and receptors
    • Released from postganglionic sympathetic neurons
    • equal to epi for B1 stimulation but little/no B2
    • Potent Alpha agonist - VASOCONSTRICTION
    • No Bronchodilation
  21. Norepinephrine physiologic effects (SVR, BP, CO, HR)
    • INCREASES: SVR, SBP, DBP, MAP
    • DECREASES: venous return, HR (baroreceptor), CO
    • Metabolic acidosis may result from hypoperfusion 

    4-16mcg/min for refractory hypotension
  22. Dopamine basics
    • Immediate precursor for norepinephrine
    • NT in central and periph nervous systems
    • Stimulates alpha, beta and dopamine receptors 
    • UNIQUE: increases contractility, renal blood flow, glomerular filtration, sodium excretion and urine output
  23. Dopamine effects on CV
    • INCREASES: CO, HR, BP, SVR
    • Typically used for the increased CO effect
    • Increased inotropy is from the endogenous form, so if that's low, you might not see the same increase when giving dopa
  24. Dobutamine
    • Selective B1 agonist
    • - potent B1 at low dose and moderate vasodilation from B2
    • - higher doses the L isomer causes A1 stimulation to prevent further vasodilation
    • Isomers oppose each other at alpha receptors 
    • 2-10mcg/kg/min
    • Increases contractility - increases CO
  25. Ephedrine
    • Indirect and direct acting
    • Stimulates alpha and beta receptors directly
    • Causes release of norepi (indirect effect)
  26. Phenylephrine
    • Similar to norepi but much less potent
    • Mostly direct A1 activity 
    • Small indirect via release of norepi
    • Minimal beta stimulation
  27. Endogenous catecholamines
    • Epinephrine
    • Norepinephrine
    • Dopamine
  28. Synthetic catecholamines and non-catecholamines
    • Catacholamine: dobutamine
    • Noncatecholamines: ephedrine and phenylephrine
  29. Phentolamine basics
    • Nonselective alpha blocker
    • COMPETITIVE ANTAGONIST
    • REVERSIBLE BLOCKADE
    • Peripheral vasodilation and hypotension with tachycardia because of baroreflex
    • Risk for myocardial ischemia and arrhythmias
  30. Phentolamine uses, onset, duration
    • ONSET: 2 minutes
    • DURATION: 10-15 minutes
    • USES: clonidine withdrawal, phew, autonomic hyperreflexia and treatment for sympathomimetic extravasation (locally infiltrate 2.5-5mg/10ml)
    • BOLUS: 1-5mg (30-70mcg/kg)
  31. Phenoxybenzamine basics
    • Nonselective alpha blocker - A1 > A2
    • IRREVERSIBLE BLOCKADE - not competitive 
    • Action can only be terminated by metabolism
    • Only given orally
  32. Phenoxybenzamine uses, onset, duration
    • ONSET: up to 60 minutes
    • DURATION: with repeated doses can be up to 4 days because half time is so long
    • - Orthostatic hypotention, and patients can't compensation for hypovolemia/HoTN/decr SVR
    • USES: preop to control BP with pheo (blocks intense vasoconstriction to allow for increased intravascular volume and repletion) Raynaud's
  33. Esmolol: onset, receptor, half time
    • IV USE ONLY
    • Rapid onset, short acting
    • Beta 1 selective (HR)
    • Half time - 9 minutes (rapid hydrolysis by esterases)
    • Poor lipid solubility
  34. Esmolol indications and dosing
    • 0.5mg/kg IV: comes in 10mg/mL so usually just give 10mg and go up from there
    • Indications: transient events - laryngoscopy, ECT
  35. Labetolol receptors, halftime, dose
    • Selective alpha 1 and nonselective beta 1 and 2 blocker
    • *CAREFUL with reactive airways
    • Halftime: 5-8 hours
    • Max effect after about 5-10minutes 
    • 5mg/mL - start low and work up
  36. Labetolol is ______ as potent as phentolamine as an alpha blocker
    1/5th to 1/10th
  37. Labetolol is ______ as potent as propranolol as a beta blocker
    1/4 to 1/3
  38. For IV prep of labetolol the alpha:beta ratio is
    7:1

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