Pharm Exam II.txt

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  1. Mechanisms of Adrenergic Receptor
    Activation by Agonist Drugs (4)
    • Direct Receptor Binding
    • Promotion of Norepinephrine (NE) Release
    • Inhibition of NE Reuptake
    • Inhibition of NE Inactivation-
  2. Mechanisms of Adrenergic Receptor Activation by Agonist Drugs:
    Direct Receptor Binding
    • Most common mechanism,activate peripheral adrenergic receptors.
    • Drugs mimic the actions of natural transmitters
  3. Mechanisms of Adrenergic Receptor Activation by Agonist Drugs
    Promotion of Norepinephrine (NE) Release-
    Acts on terminals of sympathetic nerves to cause NE release

    Example: amphetamines and ephedrine
  4. Mechanisms of Adrenergic ReceptorActivation by Agonist Drugs 

    Inhibition of NE Reuptake
    • Blocks NE reuptake, NEaccumulates in the synaptic space, increases receptoractivation
    • i.e. tricyclic antidepressants .
  5. Mechanisms of Adrenergic ReceptorActivation by Agonist Drugs
    Inhibition of NE Inactivation
    NE terminals can be inactivated by monoamine oxidase (MAO). Thereforedrugs that inhibit MAO can increase the amount of NEavailable i.e. MAOI’s
  6. Catecholamines and noncatecholamines differ in three respects:
    • Oral usability
    • Duration of action
    • Ability to act in the CNS
  7. Catecholamine's: (Epineherine, Norepinepherine)
    3 properties in common
    • Cannot be used orally
    • Brief duration of action
    • Cannot cross the blood-brain barrier
  8. Norepinephrine, dopamine, & dobutamine only work if
    given by continuous infusion
  9. Catecholamine’s are ____ _____, cannot cross the blood-brain barrier
    polar molecules
  10. Catecholamine's: IV solutions can turn pink or brown over time;
    Discard if discolored
  11. Adrenergic Agonists affect: (4)
    • alpha 1,
    • alpha 2,
    • beta 1 &
    • beta 2 adrenergic receptors
  12. Noncatecholamines (4)
    • can be given orally &
    • have longer half-lives
    • less polar,
    • can cross the blood brain barrier
  13. Alpha 1 Receptors :cause two responses
    • vasoconstriction (in blood vessels of skin, viscera, and mucous membranes) &
    • mydriasis (dilation of the pupil)
  14. Alpha 1 Activation
    Hemostasis
    Stop bleeding primarily in skin & mucous membranes (Epinephrine)
  15. Alpha 1 Activation
    Nasal Decongestion
    Relieve congestion by vasoconstriction of mucous membranes (phenylephrine & pseudoephedrine)
  16. Alpha 1 Activation
    Adjunct to Local Anesthesia-
    Combined with anesthetics to delay anesthetic absorption, vasoconstriction at the site.(Epinephrine)
  17. Alpha 1 Activation
    Elevation of BP-
    Vasoconstriction can elevate BP, ONLY usedwhen other therapies have failed
  18. Alpha 1 Activation
    Mydriasis-
    facilitates eye exams & ocular surgery
  19. Alpha 1 Adverse Effects (3)
    • Hypertension
    • Necrosis
    • Bradycardia
  20. Alpha 1 Adverse Effects 
    Hypertension
    • Widespread vasoconstriction can cause HTN, particularly parenteral administration IV:
    • Must monitor CV status continuously
  21. Alpha 1 Adverse Effects
    Necrosis
    Extravasation & necrosis with IV infiltrate,(intense vasoconstriction), alpha 1 blocker (antagonist) to minimize damage (phentolamine)
  22. Alpha 1 Adverse Effects
    Bradycardia
    Reflex response to increase in BP, cancause cardiac collapse & impaired tissue perfusion
  23. Alpha 2 Activation
    Peripherally inhibit NE release (but little clinical relevance)
  24. Alpha 2 Activation
    In CNS receptors cause
    • Reduction of sympathetic outflow to heart & blood vessels
    • Relief of severe pain
  25. Beta 1 Activation
    • Heart Failure
    • Shock
    • Atrioventricular (AV) Heart Block
    • Cardiac Arrest from Asystole
  26. Beta 1 Activation
    Heart Failure-
    Beta 1 receptors increase force of contraction (inotropic effect),improves cardiac Fxn
  27. Beta 1 Activation
    Shock
    - (Shock=profound hypotension) Beta 1’s increase heart rate (HR), force of contraction=increased cardiac output (CO), & improves tissue perfusion
  28. Beta 1 Activation
    Atrioventricular (AV) Heart Block-
    Beta 1’s enhance conduction through AV node (temporarily, until pacemaker )
  29. Beta 1 Activation
    Cardiac Arrest from Asystole-
    Beta 1’s can initiate acontraction in a heart that has stopped, (CPR & TXrequired, Epinephrine)
  30. Beta 1 Adverse Effects (2)
    • Altered Heart Rate or Rhythm
    • Angina Pectoris
  31. Beta 1 Adverse Effects
    Altered Heart Rate or Rhythm
    Overstimulation of beta 1’s can produce tachycardia & dysrhythmias
  32. Beta 1 Adverse Effects
    Angina Pectoris-
    Angina Pectoris- Beta 1’s increase cardiac oxygen demand, which can cause angina in pts with impaired coronary circulation
  33. Beta 2 Activation (3)
    • Limited to lungs and uterus
    • Asthma- Beta 2 receptors promote bronchodilation, Selective beta 2 receptors(albuterol) preferred, (Drugs that activate beta 1 receptors can stimulate tachycardia & angina).Most via inhalation to minimize adverse systemic effects, systemic toxicity with overdosing
    • Can Delay Preterm Labor- Relaxes uterine smoothmuscles
  34. Beta 2 Adverse Effects (2)
    • Hyperglycemia
    • Tremor
  35. Beta 2 Adverse Effects Hyperglycemia
    • (highest risk: diabetic pts)
    • beta 2 receptors stimulate breakdown of glycogen into glucose
  36. Beta 2 Adverse Effects
    Tremor
    Most common, beta 2;s in muscles cause enhanced contractions, fades over time, minimized by starting at low dose
  37. Dopamine Receptor
    • Activation of peripheral dopamine receptor causes dilation of renal vasculature
    • *Dopamine (the drug) used in shock to dilaterenal blood vessels & reduce risk of renal failure
    • Dopamine also enhances cardiac performance
    • Assess Urinary output (UOP), increases when kidneys are functioning, shock=no/low perfusion to kidenya and low UOP
  38. Epinephrine
    Receptor specificity:
    alpha 1, alpha 2, beta 1 and beta 2
  39. Epinephrine
    Therapeutic Uses:
    • Alpha 1-mediated vasoconstriction
    • Beta 1’s - to overcome AV heart block,
    • Beta 2’s: promotes bronchodilation
    • **Epinephrine is the Tx of choice for anaphylactic shock*
  40. Epinephrine Therapeutic Uses: Alpha 1-mediated
    vasoconstriction, used to delayabsorption of anesthetics, control superficial bleeding, &elevate BP. (Was used for nasal decongestion) Alsomydriasis.
  41. Epinephrine Therapeutic Uses: Beta 1’s -
    to overcome AV heart block, & restore cardiac function in pts experiencing cardiac arrest.
  42. Epinephrine Therapeutic Uses:Beta 2’s:
    promotes bronchodilation
  43. Epinephrine ROUTE:
    Topical, injection or IV administration only.
  44. Epinephrine  half-life
    Short (due to MAO and COMT)
  45. Epinephrine Adverse Effects:
    • Can cause Hypertensive Crisis-
    • Can cause Dysrhythmias-
    • Angina Pectoris-
    • Necrosis Following IV Extravasation-
    • Hyperglycemia
  46. Epinephrine Adverse Effects:Hypertensive Crisis
    Can cause Hypertensive Crisis- Alpha 1 stimulation,vasoconstriction, dramatic increase in BP (IV infusion)
  47. Epinephrine Adverse Effects: Dysrhythmias
    Can cause Dysrhythmias- Beta 1 stimulation
  48. Epinephrine Adverse Effects: Angina Pectoris
    Angina Pectoris- Beta 1 increases cardiac work & oxygendemand
  49. Epinephrine Adverse Effects: Necrosis
    Necrosis Following IV Extravasation-alpha-adrenergic antagonist can minimize (phentolamine)
  50. Epinephrine Adverse Effects:Hyperglycemia
    Hyperglycemia- beta 2’s, typically in diabetic pts only
  51. Epinephrine Drug Interactions: (5)
    • MAO Inhibitors
    • Tricyclic Antidepressants-
    • General Anesthetics-
    • Alpha-adrenergic Blocking Agents
    • Beta-adrenergic Blocking Agents-
  52. Epinephrine Drug Interactions:MAO Inhibitors-
    Prolong and intensify the effects ofepinephrine & other catecholamines
  53. Epinephrine Drug Interactions: Tricyclic Antidepressants-
    Block the uptake ofcatecholamines, so can intensify & prolong epinephrineeffects.
  54. Epinephrine Drug Interactions: General Anesthetics-
    Can cause tachydysrhythmias when used together
  55. Epinephrine Drug Interactions:
    Alpha-adrenergic Blocking Agents
    (antagonists) Can prevent receptor activation by epinephrine(*Phentolamine: antidote used to treat toxicity)
  56. Epinephrine Drug Interactions: Beta-adrenergic Blocking Agents-
    Can prevent receptoractivation by epinephrine, reduce adverse effectscaused by epinephrine
  57. Epinephrine
    Catecholamine or Noncatecholamine
    Catecholamine
  58. Norepinephrine (6)
    • Receptor specificity: Alpha 1, Alpha 2, Beta 1
    • Catecholamine
    • *Same as Epi, except no Beta 2 stimulation
    • Does not promote hyperglycemia
    • Typically only used in hypotensive states & cardiacarrest
    • IV infusion only
  59. Isoproterenol (3)
    • Receptor Specificity: Beta 1 and Beta 2
    • Catecholamine
    • *First beta selective medication
  60. Isoproterenol Therapeutic Uses:
    • Cardiovascular-overcome AV heart block, restart heart following cardiac arrest, increase cardiac output in shock 
    • Bronchospasm- Not used to treat asthma ONLY bronchospasm, (more selective medications treat asthma)
  61. Isoproterenol
    Adverse Effects:
    • Beta 1 activation- tachy-dysrhythmias & angina
    • Beta 2 activation- hyperglycemia
  62. Isoproterenol Drug Interactions:
    • Effects are enhanced by MAO Inhibitors andtricyclic antidepressants; Reduced by beta-blockers
    • Can cause dysrhythmias when given with inhaled anesthetics
  63. Inotropic drugs influence the
    • strength or contractilty of muscle tissue.
    • Increase the force of the heart's contractions
  64. Two types of Inotropic drugs
    Cardiac Gylcosides and phophodiesterase (PDE) inhibitors
  65. -Slow heart rate and slow electrical impulse conduction through the AV node.
    -Useful for pts who have artrial fibrillations.
    -Can help control HR and prevent it from becoming too fast
    - Incrs. perfusion of tissues improves function/help decrease edema (interstitial fld)
    Cardiac Glycosides
  66. Cardiac Glycosides Prototype
    Digoxin
  67. Digoxin Actions
    • Inhibits sodium-potassium- activated adenosine triphosphas: reg. amt. of Na and K+ inside the cell resulting in increased intracellular levels of Na and K.
    • Promotes the movement of Ca from extra cellular to intracellular cytoplasm and strengthens myocardial contraction
    • Acts on the CNS to enhance vagal tone, slowing contractions through the SA and AV nodes- provides an antiarrhythmic effect.
  68. Digoxin Indications (3)
    • heart failure
    • Atrial Fib. and flutter
    • Supraventricular tachycardia
  69. Digoxin Nursing Considerations
    • Monitor pt for adverse effects
    • W/hold if apical pulse is less than 60 bpm and notify prescriber
    • monitor serum K and digoxin levels
    • assess renal function
  70. Digoxin Pharmacokinetics
    • intestinal asbsorption varies greatly
    • cap. most efficent, then elixr then tabs
    • absorp. hightest concen. in heart musc., liver, and kideny
    • poorly bound to plasma protiens
    • Most is excrete from kid. unchanged
  71. Digoxin Pharmacodynamics
    • boost intracellular Ca at the cell membrane
    • enable stronger heart contractions
    • may enhance movement of Ca into myocardial cells and stimulate the release for block re-uptake of noreponephrine at the adrenergic nerve terminal
    • Works on CNS to slow HR
    • Increases refractory period
  72. Digoxin PK
    heart failure
  73. Digoxin ______ Cardiac Output:
    • Increased:
    • -Increases contractilityby restoring cardiac muscle fibers to near health,increases the stroke volume of failing heart =cardiac output rises
  74. Digoxin Three major secondary responses due to increased cardiac output:
    • – Decreased sympathetic tone
    • – Urine production increases
    • – Renin release declines
    • – These responses can reverse virtually all signs and symptoms of heart failure.
  75. Digoxin (Cardiac Glycoside)Adverse Effects 1:
    Cardiac Dysrhythmias
  76. Digoxin (Cardiac Glycoside) Adverse Effects 1: Cardiac Dysrhythmias:
    Digoxin: used in therapeutic doses to slow fastheart rates, but causes dysrhythmias if given inhigh doses or in the presence of hypokalemia
  77. Elevated digoxin levels- Narrow therapeutic window/Range:
    (0.5-0.8 ng/mL; variance among range, most state no higher than 1.5 ng/ml) levels slightly higher than therapeutic produce toxicity
  78. Managing Digoxin-Induced Dysrhythmias:–
    • Withdraw digoxin & potassium-wasting diuretics
    • – Monitor serum potassium
    • – Anti-dysrhythmic drug is sometimes needed (Lidocaine & phenytoin most effective for ventricular dysrhythmias, atropine for bradycardias)
    • – Can give reversal agent: Digibind or Digifab, Cost$2,000-$3,000, only use when severe (also can cause arrhythmias as it binds digoxin)
  79. Digoxin (Cardiac Glycoside) Adverse Effects 2: Non-cardiac Adverse Effects
    • **GI- anorexia, nausea, and vomiting
    • **CNS- Fatigue & visual disturbances (blurred vision, yellow tinge to vision, halos around dark objects)
  80. Digoxin (Cardiac Glycoside) Drug Interactions:
    • *Diuretics- Thiazide and Loop Diuretics promoteloss of potassium (increases risk of dysrhythmias)
    • ACE Inhibitors and ARBs- Can increase potassiumlevels (decreases digoxin levels)
    • Sympathomimetics- Can add to the inotropiceffects of digoxin
  81. Plasma Digoxin Levels:
    • Therapeutic Range: 0.5-0.8 ng/mL.
    • Anything over 1 ng/mL offers no additional benefit and increases the risk of toxicity.
  82. Herbs and Digoxin
    St. John's wort and ginseng can ^ levels of digoxin and  ^ risk of toxicity
  83. S/S of Digoxin toxicity:
    • slow to rapid ventricular rhythms
    • nausea and vomiting
    • blurred vision
    • anorexia
    • abdomin. discomfort
    • mental changes

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 Pharm Exam II.txt
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