adrenergic agonists and antagonists

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  1. What does the SNS control?
    visceral functions like BP, gastric motility, body temp, sweating, bladder emptying
  2. Where in the body causes activation of the SNS?
    brain stem, hypothalamus, and spinal cord
  3. In the SNS is the pre-ganglionic or post-ganglionic fiber longer?
  4. In the SNS what are the receptor types at the ganglion and at the end organ?
    • ganglion- nicotinic (cholinergic)
    • end organ- adrenergic
  5. Where do the SNS fibers originate in the spinal cord?
    • T1 to L2-3
    • called thoracoabdominal or thoracolumbar fibers
  6. In the PNS what are the receptor types at the ganglion and at the end organ?
    • ganglionic-  nicotinic (cholinergic)
    • end organ- muscarinic (cholinergic)
  7. In the PNS is the pre-ganglionic or post-ganglionic fiber longer?
  8. Where do the PNS fibers leave the CNS through?
    • cranial nerves 3,7,9,10 and also from the lowest part of the spinal cord through S2 and S3
    • -AKA craniosacral
  9. Where are the majority of the PNS fibers located?
    75% are in the vagus nerve
  10. What are the endogenous catecholamines?
    epi, norepi, and dopamine
  11. What are the synthetic catecholamine(s)?
  12. What are the synthetic non-catecholamines?
    ephedrine and neo
  13. Describe norepi synthesis.
    Where does this occur?
    • -tyrosine to dopa to dopamine to norepi
    • -occurs in the cytoplasm
  14. What are the 3 ways in which norepi's action is terminated?
    • 1) re-uptake into post-ganglionic nerve endings by active transport
    • 2) diffusion away from the receptor
    • 3) enzyme metabolism by MAO and COMT
  15. What happens to norepi in the adrenal medulla?
    80% of norepi is converted to dpi
  16. How is the majority of norepi inactivated?
    By reuptake into the adrenergic nerve endings. 50-80% is removed in this manor.
  17. What drugs can inhibit reuptake of norepi into the adrenergic nerve endings?
    tricyclics and cocaine
  18. What is the second most common way that norepi is removed from the site of secretion?
    diffusion away from the nerve endings
  19. What does stimulation of the alpha 1 receptor cause?  Is it pre or post synaptic?
    • -vasoconstriction, bronchoconstriction, and hypertension
    • -post-synaptic
  20. Where are the alpha 1 receptors located?
    smooth muscle throughout the body, eye, lung, blood vessels, uterus, gut, and GU
  21. What does stimulation of the alpha 2 receptor cause?  Is it pre or post synaptic?
    • -vasodilation, hypotension, sedation
    • -pre-synaptic
    • -negative feedback loop inhibiting norepi release
  22. What does stimulation of the alpha 2 subtype a cause?
    sedation, analgesia, and sympatholysis (hypotension)
  23. What does stimulation of the alpha 2 subtype b cause?
    vasoconstriction and hypertension
  24. What does stimulation of the alpha 2 subtype c cause?
    startle reflex
  25. What does stimulation of the beta 1 receptor cause?  Is it pre or post synaptic?
    • + chronotropic, dromotropic (increases conduction speed in the AV node), and inotropic effects
    • -post synaptic
  26. Where are the beta 1 receptors located?
  27. What does stimulation of the beta 2 receptor cause?  Is it pre or post synaptic?
    • -vasodilation, bronchodilation, glycogenolysis, lipolysis, insulin release
    • -post-synaptic
  28. Where are the beta 2 receptors located?
    smooth muscle and glands
  29. What is the characteristic catecholamine structure?
    3,4 dihydroxybenzene
  30. What is the characteristic chemical structure of the sympathomimetics?
  31. Direct acting sympathomimetic
    -stimulates the receptor itself
  32. What are examples of direct acting sympathomimetics?
    -epi, norepi, and neo
  33. Indirect acting sympathomimetic
    • -Causes release of a neurotransmitter (an endogenous catecholamine) which then stimulates the receptor
    • -Can displace stored catecholamines from nerve ending or can inhibit reuptake of an already release catecholamine
  34. What are examples of indirect acting sympathomimetics?
  35. Structurally what identifies a synthetic non catecholamine?
    Lacks 1 or more -OH (hydroxyl) groups
  36. How are synthetic non catecholamines metabolized?  How does this affect the rate of metabolism?  In what patients could these drugs have a prolonged effect?
    • -By MAO only, they are not effected by COMT.
    • -Metabolism is slower
    • -Pts taking MAOIs could have a prolonged effect from ephedrine or neo
  37. Of the synthetic non catecholamines, which is direct acting and which is indirect acting?
    • Neo is direct acting
    • Ephedrine is mixed
  38. What effect does increasing the size of alkyl substituents (number of carbons) on the amino group have on receptor affinity?  What's an example of this?
    • -Increases beta receptor activity.  
    • -Ex: epi has an extra methyl group compared to norepi, so epi has greater beta 2 activity
    • -Replacing the methyl group on epi with an isopropyl group to make isoproterenol further increases B activity
  39. Beta 2 selective drugs usually have a large amino substituent group which enhances their beta affinity, but how does this affect alpha affinity?
    Lower activity at alpha receptors
  40. What difference in the chemical structures of neo and epi accounts for the difference in potency?
    • -Drug potency is decreased if an -OH group is absent on the benzene ring (esp. at C-3)
    • -Neo has only 1 -OH group on the benzene ring, epi has 2 -OH groups
  41. What is the alpha carbon?
    The carbon closest to the amine group
  42. What effect does a substitution on the alpha carbon have?
    blocks oxidation by MAO so the DOA is prolonged
  43. What 2 drugs differ in their action due to substitution on the alpha carbon?
    • -Neo and ephedrine
    • -Neo has only H on the alpha carbon so acts directly only
    • -Ephedrine has a methyl group on the alpha carbon so can displace catecholamines from storage sites in the nerve endings (indirect action)
  44. What is characteristic of the chemical structure of direct acting agonists like epi, norepi, and isopreterenol?
    -OH group on the beta carbon
  45. Where is epi released from?
    adrenal medulla
  46. Which is more potent- epi or norepi?
    epi is 2-10x more potent than norepi
  47. What receptors does epi work at?
    potent alpha but also beta 1 and 2
  48. Major effects of epi
    • -moderate increase in HR
    • -mild increase in MAP
    • -moderate bronchodilation
    • -moderate increase in CO
    • -moderate decrease in renal blood flow
  49. What receptors does norepi work at?
    • -potent alpha agonist
    • -beta 1 (greater than or equal to epi)
    • -little to no effect at beta 2 (due to methyl group substitutions)
  50. Major effects of norepi
    • -mild decrease in HR
    • -marked increase in MAP
    • -no bronchodilation
    • -decreased CO
    • -marked decrease in renal blood flow
  51. What receptors does dopamine work at?
    • alpha 1 ++
    • alpha 2 ++
    • beta1 ++
    • beta 2 +
    • and dopamine +++
  52. Major effects of dopamine
    • -mild to moderate increase in HR
    • -mild increase in MAP
    • -marked increase in CO
    • -no bronchodilation
    • -marked increase in renal blood flow
    • -unique as it can increase GFR, Na+ excretion, and urine output
  53. T or F, randomized control studies show a a decrease in incidence of ARF with dopamine
  54. Risk associated with norepi (Sue told a story about this)
    -metabolic acidosis from hypoperfusion
  55. What receptors does dobutamine act at?
    • -beta 1 +++
    • -beta 2 +
    • -alpha 1 (its 2 isomers oppose each other at alpha receptors- so kind of cancels out)
  56. Major effects of dobutamine
    • -mild increase in HR and MAP
    • -marked increase in CO
    • -mild decrease in PVR (beta 2)
    • -mild increase in renal perfusion
    • -no bronchodilation
  57. What receptors does ephedrine act at?
    • alpha 1 ++
    • beta 1 ++
    • beta 2 +
  58. What is ephedrine's indirect effect
    release of norepi
  59. Major effects of ephedrine
    • -moderate increase in HR, MAP, and CO
    • -moderate increase in bronchodilation
    • -moderate decrease in renal blood flow
  60. What receptor does neo work at?
    • Alpha 1 +++
    • Alpha 2 +
    • Beta 1 + (but increased HR not usually seen)
  61. Major effects of neo
    • -marked increase in MAP and PVR
    • -mild decrease in HR and CO
    • -marked decrease in renal blood flow
  62. Phentolamine
    -competitive or non
    -reversible or non
    -major effects
    • -non selective alpha blocker
    • -competitive
    • -reversible
    • -peripheral vasodilation and hypotension
  63. phentolamine SE
    -Increased HR (baroreflex to compensate for hypotension)
  64. Phentolamine uses
    • -HTN from excess alpha stimulation
    • -clonidine withdrawal
    • -pheochromocytoma
    • -autonomic hyperreflexia
    • -treatment of sympathomimetic extravasation
  65. phenoxybenzamine
    -competitive or non
    -reversible or non
    -major effect
    • -non selective alpha blocker, alpha 1 blockade > alpha 2
    • -non competitive
    • -non reversible
    • -action can only be terminated by metabolism of the drug
    • -decreases BP
  66. phenoxybenzamine uses
    • -pre-op BP control for pt with pheo
    • -Raynaud's disease
  67. Are metoprolol, esmolol, and atenolol cardioselective?
  68. Esmolol metabolism and DOA
    • -metabolized by ester hydrolysis
    • -short DOA
    • -elim half time = 9 mins
    • -return of pre drug HR with in 15 mins of D/C
  69. Esmolol initial dose
    0.5 mg / kg but often start with less
  70. Esmolol indications
    • -brief stimulus
    • -laryngoscopy
    • -ECT
    • -pheo
    • -thyrotoxicosis
  71. Esmolol selectivity
    beta 1
  72. Labetalol receptor activity and uses
    • -alpha 1 selective blocker
    • -nonselective beta 1 and 2 blocker

    • -treats both HTN and tachycardia
    • -avoid in pts with reactive airway disease
  73. Elim half time of labetalol
    5-8 hours
  74. Esmolol onset
  75. Labetalol onset
    5-10 mins
  76. Indications for use of labetalol and esmolol intraop
    • -potential for SNS stimulation with endogenous catecholamine release
    • -pt pre-existing condition (risk for MI)
    • -to attenuate effects of exogenous catecholamines that might be used by the surgeon (ex: lido with epi or cocaine)
    • -not a substitute for light anesthesia!!!
Card Set:
adrenergic agonists and antagonists
2013-07-25 14:03:20
BC NU 493

adrenergic agonists and antagonists
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