Andrenergic Agonists, Andrenergic Antagonists, Indirect-Acting Antiandrenergic Agents

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Andrenergic Agonists, Andrenergic Antagonists, Indirect-Acting Antiandrenergic Agents
2013-10-26 17:07:46

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  1. Adrenergic agonists mimic the effects of ______
    sympathetic nervous system
  2. Most adrenergic agonists work by _______ receptor binding
  3. 3 indirect methods of binding by adrenergic agonists
    • promote release of NE
    • block NE reuptake
    • inhibit inactivation of NE
  4. Amphetamines and ephedrine work by which method of binding?
    promoting release of NE
  5. Cocaine and tricyclic antidepressants work by which method of binding?
    blocking reuptake of NE
  6. MAO inhibitors work by which method of binding?
    inhibiting NE inactivation
  7. 2 classes of Adrenergic Agonists
    • Catecholamines
    • Non-Catecholamines
  8. Three properties of catecholamines
    • Can't be taken orally
    • Brief duration of action
    • Can't cross BBB
  9. Why can't catecholamines be taken orally?
    Inactivated too quickly by liver and MAO/COMT (intestinal enzymes)
  10. Why is the duration of action for catecholamines brief?
    inactivated quickly by liver/MAO/COMT
  11. Why can't catecholamines cross the BBB?  What does this mean for their therapeutic use?
    • polar molecules
    • Don't affect CNS
  12. What color should catecholamines be?  what color can they turn, and what should you do if that happens?
    • should be colorless
    • turn pink/brown from oxidation
    • throw it away if it is discolored
  13. How do non-catecholamines differ from catecholamines?
    • Can take them orally
    • Metabolized slowly -> longer duration of action
    • less polar -> can cross BBB
  14. If the dose is high, will the drug be more or less selective?
    • Less
    • Low dose = more selective
  15. 2 therapeutic responses of activation of alpha1 receptors
    • vasoconstriction
    • -skin, viscera, mucous membranes
    • -most common use
    • mydriasis (pupil dilation)
  16. 3 drugs that activate alpha1 receptors
    epinenphrine, NE, dopamine
  17. Therapeutic effects of alpha1 activation
    • vasoconstriction:
    • stop bleeding in skin/mucous membranes
    • elevate BP
    • nasal decongestion
    • combined with local anesthetics to delay their absorption

    pupil constriction for eye exams/ocular surgery
  18. why use a1 agonists to delay absorption of anesthesia?  which drug is most commonly used?
    • prolong anesthesia
    • ->reduce dosage
    • ->reduce systemic effects

  19. clinical term for dilation of pupils
  20. Adverse Effects of a1 activation
    • hypertension
    • necrosis (lack of blood flow due to extreme vacoconstriction)
    • bradycardia (elevates BP -> triggers baroreceptor reflex -> heart rate declines)
  21. What does activation of alpha2 receptors do?
    inhibit NE release
  22. What drugs can activate a2 receptors?
  23. Clinical effects of activation of a2 receptors?
    • no therapeutic application
    • Some effects in CNS, discussed in later chapters
  24. Chronotropy
    change heart rate
  25. inotropy
    changes force of heart contractions
  26. dromotropy
    changes conduction velocity in heart
  27. lusitropy
    heart relaxation
  28. therapeutic responses of beta1 activation in kidneys
    none that are clinically relevant
  29. Drugs that can activate beta1 receptors
    E/NE, dopamine
  30. Therapeutic effects of beta1 activation in heart
    • -Positive chronotropy (increase heart rate)
    • -Positive inotropy (increase force of myocardial contraction)
    •  -> increased cardiac output
    • -positive dromotropy (increase speed of AV conduction)
    • -initiate contraction in cardiac arrest
  31. Adverse effects of beta 1 activation in heart
    • tachycardia/dysrhythmias
    • angina pectoris (chest pain)
  32. Drugs that activate beta2 receptors
    epinephrine, albuterol
  33. therapeutic effects of beta2 activation occur in which organs?
    • lungs
    • uterus
  34. therapeutic effects of beta2 activation in lungs
    how is it administered?
    • bronchodilation
    •      -treat asthma, coronary artery disease, tachycardia

  35. therapeutic effects of beta2 activation in uterus
    • relax uterine smooth muscle
    • -> delay preterm labor
  36. adverse effects of beta 2 activation
    • hyperglycemia (elevation of blood glucose)
    • -only in patients with diabetes

    • tremor
    • -b2 enhances skeletal muscle contraction
  37. what drug activates dopamine receptors?
  38. effect of dopamine receptor activation
    -used to treat what?
    dilation of renal blood vessels

    • used to treat shock (reduces risk of renal failure)
    • -also enhances cardiac performance
  39. Symptoms of anaphylactic shock
    • hypotension (widespread vasodilation)
    • bronchoconstriction
    • edema of glottis
  40. Drug used to treat anaphylactic shock
    activates which receptors?
    • epinephrine
    • activates a1, b1, b2
  41. Epinephrine activates which receptors?
    a1, a2, b1, b2
  42. Chemical classification of epinephrine
  43. effects of epinephrine

    pupil dilation (mydriasis)

    activate b1 receptors -> overcome AV heart block, restore cardiac function 

  44. Routes of administration for epinephrine
    • Oral inhalation (1%)
    • Subcutaneous, IM, Intraspinal ((0.1%)
    • IV, Intracardiac (0.01%)
    • In combination with local anesthetics (0.001%)
  45. adverse effects of epinephrine
    • hypertensive crisis
    • dysrhythmias
    • angina pectoris
    • necrosis following extravasation
    • hypergylcemia (in patients with diabetes)
  46. Adrenergic Antagonists affect which receptors?
    alpha and beta
  47. Two main categories of adrenergic antagonists
    • alpha-adrenergic blockers
    • beta-adrenergic blockers
  48. effects of Alpha1 antagonists
    • vasodilation -> reduce BP
    • bladder: promotes voiding

    Prostate: reduces contraction of smooth muscle in prostatic capsule and bladder neck
  49. Alpha1 antagonists can be used to treat which conditions?
    • hypertension
    • reverse toxicity from alpha1 agonists
    • Benign prostatic hyperplasia
    • Raynaud's disease
  50. Therapeutic effects of alpha2 antagonists
    no therapeutic application
  51. Adverse effects of alpha1 antagonists
    orthostatic hypotension

    reflex tachycardia 

    nasal congestion (vasodilation in nasal mucosa)

    inhibition of ejaculation

    sodium retention/increased blood volume
  52. how can a1 antagonists cause reflex tachycardia?
    vasodilation -> reduced BP -> baroreceptor reflex overcompensates -> tachycardia
  53. how can a1 antagonists cause increased blood volume?
    BP reduced 

    -> decreased renal blood flow, reduced perfusion

    -> less sodium and water excreted 

    -> retention of na+/h20 = elevated BP
  54. What can/should a1 antagonists be combined with when treating hypertension?
    • diuretic
    • so kidney doesn't "neutralize" hypotensive actions by retaining salt/water and raising BP again
  55. Most therapeutic effects of beta-adrenergic antagonists result from blocking ________ in the ______.
    beta1 receptors in the heart
  56. beta blockers can be used to treat which conditions?
    • angina pectoris
    • hypertension
    • cardiac dysrythmias
    • myocardial infarction
    • decrease risk of mortality in noncardiac surgery in high-risk patients
    • heart failure
    • hyperthyroidism
    • glaucoma
  57. what causes angina pectoris?

    how do beta blockers treat it?
    blood flow (oxygen supply) to heart is insufficient to meet cardiac oxygen demand

    decrease cardiac work, i.e. oxygen demand of heart, to match oxygen supply
  58. how do beta blockers treat cardiac dysrhythmias?
    suppress rate of SA node and AV conduction
  59. how can beta blockers treat heart failure?
    improve LV ejection fraction, increase exercise tolerance
  60. adverse effects of beta1 antagonists

    decreased cardiac output

    AV heart block (stops atrial impulses from reaching ventricles)

    heart failure

    • rebound cardiac excitation
    • -chest pain
    • -cardiac dysrhythmias
  61. what should you teach patients about regarding the adverse effects of beta1 blockers?
    early signs of heart failure (shortness of breath, night coughs, swelling of extremities)

    • warn against abruptly stopping treatment 
    • -sudden withdrawal can cause hypersensitivity to catecholamines -> sudden increase of cardiac activity
    • -carry adequate supply of beta blocker when traveling
  62. therapeutic effects of beta2 blockade
    no therapeutic application
  63. adverse effects of beta 2 blockade
    bronchoconstriction (opposite of activation of receptors which is sympathetic response -> dilation)

    hypoglycemia (activation causes glycogenolysis)
  64. Since beta2 blockers can cause bronchoconstriction and hypoglycemia, they are contraindicated in patients with which conditions?
    asthma, diabetes
  65. what the hell does an indirect-acting antiadrenergic do?
    prevents activation of peripheral adrenergic receptors by indirect methods
  66. 2 categories of indirect-acting antiadrenergics
    • central alpha2 agonists
    • adrenergic neuron blocking agents
  67. how and where do central alpha2 agonists work?
    • in CNS
    • reduce firing of sympathetic neurons
    • (less release of NE?)
  68. The effect of a central alpha2 agonist is similar to that of a _________
    direct-acting adrenergic receptor blocker
  69. In addition to treating hypertension, what is the other therapeutic use for central alpha2 agonists?
    block pain
  70. primary use of indirect acting central alpha2 agonists and targets
    • hypertension
    • heart and blood vessels
  71. how do central alpha2 agonists treat hypertension?
    • inhibit firing of sympathetic neuron
    • -> decrease release of NE
    • -> decrease in activation of adrenergic receptors in cardiovascular system
    • -> lowers heart rate and cardiac output
  72. Adverse effects of central alpha2 agonists
    Rebound hypertension (following abrupt withdrawal)

    drowsiness (from CNS repression)

    dry mouth (xerostomia)

    self-medication (euphoria, hallucination, etc)
  73. clinical term for dry mouth
  74. how do adrenergic neuron-blocking agents work?
    decrease release of NE
  75. therapeutic uses for adrenergic neuron-blocking agents?
    rarely used
  76. CNS drugs act on the ______ and ________
    brain and spinal cord
  77. what are the neurotransmitters for the peripheral nervous system?  how many are in the central nervous system?
    • PNS: aceytlcholine, E, NE
    • CNS: 21 neurotransmitters
  78. What is the function of the blood brain barrier?
    • impedes entry of drugs into brain
    • (protects brain from injury and potentially toxic substances)
  79. what drugs can cross the BBB?
    lipid-soluble and drugs with a transport system
  80. what drugs CAN'T cross BBB?
    protein bound drugs

    highly ionized drugs

  81. Describe the state/efficacy of BBB in infants
    • BBB is not fully developed yet
    • infants sensitive to CNS drugs
  82. 5 categories of CNS neurotrasmitters

    -for reference, with examples (not likely to memorize)
    Monoamines (MOA)-- E/NE, dopamine, seratonin

    Amino Acids, GABA

    Opioid peptides- 

    Nonopioid peptides- substance P, oxytocin

    Purines- Adenosine
  83. How much do we know about the mechanisms of action of CNS drugs?
    not much-- don't have enough definite understanding of brain or pathophysiology of CNS disorders

    most MOA's are proposed hypotheses
  84. CNS drugs may have altered effects as a result of _____ use
    • chronic (prolonged drug exposure)
    • --> adaptation
  85. three adaptations that may occur as a result of prolonged exposure to CNS drugs

    how do they occur?
    increased therapeutic effects- effects are produced as a result of CNS adaptation, take a few weeks to take place

    decreased side effects- brain adapts to side effects, they go away while therapeutic effects remain

    • tolerance/physical dependence- CNS adapts to drug, response to drug decreases
    • -abrupt discontinuation -> withdrawl