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2-Pharm Exam 3 > Sympathomimetics Part I > Flashcards

Sympathomimetics Part I Flashcards

1
Q

What is the overall MOA of beta agonists?

A

Relax bronchiole and uterine smooth muscles (tocolytics) (large concentrations can result in β-1 stimulation)

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2
Q

What is true about some beta agonists?

A

Selective agents resistant to methylation by COMT (longer action: intermediate versus long acting)

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3
Q

What is the preferred clinical use of beta agonists?

A

Preferred Tx of acute asthma, exercise induced asthma, also used with COPD, bronchospasm, and as tocolytics

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4
Q

How much of the inhaled route of beta agonists is administered through the inhaled route?

A
  • Inhaled route: only 12% reaches lungs.
  • ETT further decreased metered dose by 50-70%!
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5
Q

When is the best time to deliver beta agonists?

A

Best to deliver during inspiratory phase, need a dose 6-10 higher in nebulizer than metered dose to effect /delivery/bronchodilation

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6
Q

What is the main side effect of beta agonists?

A

main is tremor (β2 skeletal muscles)

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7
Q

What are some other general effects of beta agonists?

A
  • Increased heart rate less common
  • But may result in reflex tachycardia and vasodilation
  • Lactic acidosis
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8
Q

What are some metabolic effects of beta agonists?

A

Metabolically (short-term): hyperglycemia, hypokalemia, hypomagnesemia

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9
Q

What are the most frequently used beta agonists?

A
  • Albuterol (Ventolin)
  • Metaproterenol
  • Terbutaline
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10
Q

What is the most common clinical use for albuterol (Ventolin)?

A

acute bronchospasm due to asthma

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11
Q

What is the inhaler dose of Albuterol (Ventolin)?

A

100 mcg/puff (2 puffs q 4-6 h not to exceed 16-20 puffs/day)

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12
Q

What is the nebulized dose of Albuterol (Ventolin)?

A

Nebulized: 2.5-5 mg in 5 cc normal saline q 15 for 3-4 doses

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13
Q

What side effect can Albuterol (Ventolin) cause?

A

Tachycardia and hypokalemia with high doses

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14
Q

What is the dose for Albuterol (Ventolin) for tracheal intubation?

A

4 puffs to blunt airway responses to tracheal intubation

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15
Q

What can Albuterol (Ventolin) also be used as? What is the marketed name?

A

Also used as a tocolytic (marketed as Salbutamol)

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16
Q

What is the dose of Terbutaline?

A

SQ dose 0.25 mg

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17
Q

What is the response of Terbutaline?

A

produces responses similar to EPI but bronchodilation longer

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18
Q

What is the administration of Terbutaline? What does it temporary inhibit?

A

Administered as a single intravenous or subcutaneous dose for prompt but temporary inhibition of uterine activity (tocolytic)

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19
Q

What are the side effects of Terbutaline?

A
  • Tachycardia
  • hypotension
  • palpitations
  • shortness of breath
  • chest pain
  • pulmonary edema
  • hypokalemia
  • hyperglycemia
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20
Q

What drug class does digoxin belong to?

A

Cardiac Glycosides

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21
Q

Where does digoxin naturally occur?

A

Occurs naturally in foxglove plant

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22
Q

What is the indications for digoxin?

A

Slows conduction at AV node:

  • used to treat PAT
  • AFib
  • Aflutter (may be use in conjunction with a β-blocker)

Still used to treat some CHF.

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23
Q

What population is digoxin dangerous in?

A

patients with hypertrophic subaortic stenosis

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24
Q

What is the oral bioavailability of digoxin?

A

60-80% oral bioavailability

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25
Q

What is the peak of digoxin?

A

peaks in 1-3 hrs

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26
Q

What is the IV bioavailability, peak and onset of digoxin?

A

100% bioavailability after IV, onset 10-30 min, peak 2-4 hrs

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27
Q

What is the half life of digoxin?

A

Half live 1-2 days

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28
Q

What is the excretion of digoxin?

A

Renal excretion (inversely proportional with GFR, age, renal disease)

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29
Q

What is the metabolism of digoxin?

A

Only small fraction is metabolized by the liver and approximately 8% undergoes an enterohepatic cycle

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30
Q

What is the MOA of digoxin?

A

Selectively and reversibly inhibit the Na-K ATPase ion transport system located in sarcolemma of cardiac cells

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31
Q

What effect does digoxin binding to the alpha subunit of the ATPase enzyme?

A

thus interfering outward flow of Na+ from the cell: results in increase intracellular Na+ results in increased intracellular Ca++

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32
Q

What is the effet of increased intracellular Ca++ (Digoxin MOA)?

A

accounts for the positive inotropic activity

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33
Q

What is the inotropic activity of digoxin?

A

Increased inotropic activity without increase in HR yet decrease in LV preload, afterload, wall tension, and O2 consumption of a failing heart (decreases compensatory sympathetic activity)

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34
Q

What are the PNS effects of digoxin?

A
  • Enhanced parasympathetic effects
  • negative chronotropic and dromotropic effects
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35
Q

What are the EKG changes associated with digoxin?

A
  • Prolonged P-R
  • shortened QT
  • ST segment depression
  • diminished/inverted T waves
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36
Q

What is the therapeutic range of Digoxin?

A

Narrow therapeutic range (occur at 35% of fatal dose)

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37
Q

When does cardiac dysrhtymias with digoxin occur?

A

Cardiac dysrhythmias at 60% fatal dose

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38
Q

Digoxin Toxicity Attributed to the buildup in _________.

A

intracellular Ca++

39
Q

What is the biggest contributor to digoxin toxicity?

A
  • Hypokalemia biggest contributor to development of digoxin toxicity (hyperventilation, diuretics); others include hypercalcemia and hypomagnesemia
  • Increased K inhibits digoxin binding to ATPase enzyme
40
Q

Who is at higher risk for digoxin toxicity?

A

Elderly, renal dysfunction, hypoxemia (sympathetic stimulation)

41
Q

What is the theraputic range of digoxin?

A

Therapeutic range 0.5- 2.5 ng/ml (toxic > 3)

42
Q

What is the common manifestations of Digoxin Toxicity?

A

anorexia, N/V

43
Q

What is the most common EKG change associated with Digoxin Toxicity?

A

Atrial tach with block most common EKG but may see various dysrhythmias to complete heart block

44
Q

What is the typical cause of death associated with Digoxin Toxicity?

A

Cause of death: VF

45
Q

What is the treatment for Digoxin Toxicity?

A
  • correct underlying electrolyte or physiologic derangement (K+), medications such as phenytoin, atropine, lidocaine
46
Q

What is the dose of phenytoin and lidocaine for Digoxin Toxicity?

A
  • Phenytoin 0.5-1.5 mg/kg
  • Lidocaine 1-2 mg/kg
47
Q

What maybe required with digoxin toxicity?

A

may require pacemaker

48
Q

What is the principle action of Phosphodiesterase Inhibitors?

A
  • Competitive inhibitory action on phosphodiesterase enzyme
  • Various selective inhibitors
49
Q

What effect does PDE III have on cAMP?

A

PDE III decrease hydrolysis of second messenger cAMP (results in increased cAMP in myocardium and vascular smooth muscle)

50
Q

What effect do phsophodiesterase inhibitors have on the myocardium?

A
  • Increased intracellular Ca++ by stimulating protein kinases that phosphorylate the SR
  • Vascular smooth muscle: increased cAMP decreases Ca++ for contraction by facilitating Ca++ uptake by the SR
51
Q

What makes Phosphodiesterase Inhibitors an inodilator?

A

positive intropic effects with smooth muscle relaxation in both arterial or venous beds

52
Q

What effects do Phosphodiesterase Inhibitors have?

A
  • Increased contractility
  • CO
  • decreased LVEDP
  • decreased filling pressures
  • decreased venous return to the heart
  • diastolic relaxation (lusitropy)
53
Q

Where else do Phosphodiesterase Inhibitors exert there effects?

A

Work independently of β receptors (works with those β-blocked and refractory to catecholamine therapy

54
Q

What is the use for Phosphodiesterase Inhibitors?

A

Used for acute heart failure, cardiogenic shock

55
Q

What are contraindications to Phosphodiesterase Inhibitors?

A

Contraindications are severe obstructive cardiomyopathy, hypovolemia, tachycardia, and ventricular aneurysm

56
Q

What are some Phosphodiesterase Inhibitors?

A
  • Amrinone
  • Milrinone
57
Q

What is the new market name for Amrinone?

A

Inamrinone

58
Q

What is the MOA of Amrinone (Inamrinone)?

A

Selective PDE III inhibitor

59
Q

What are the effects of Amrinone (Inamrinone)?

A

dose dependent positive inotrope and vasodilator that increases CO, decreased LVEDP

60
Q

What is the formularies for Amrinone (Inamrinone)?

A

Be given oral or IV

61
Q

What is the dose of Amrinone (Inamrinone)?

A

Loading dose 0.5-1.5 mg/kg with infusion 2-10 mcg/kg/min

62
Q

What is the max dose of Amrinone (Inamrinone)?

A

Max daily dose 10mcg/kg

63
Q

What are the side effects of Amrinone (Inamrinone)?

A
  • hypotension, especially with rapid IV bolus
  • thrombocytopenia with long-term use
  • dose-related proarrhythmic potential
64
Q

What is the excretion of Amrinone (Inamrinone)?

A

26-40% excreted unchanged in urine (reduce dose with renal dysfunction)

65
Q

What is the inotropic effects of Amrinone (Inamrinone) compared to Milrinone?

A
  • 30 times the inotropic effects of amrinone
  • Replaced amrinone given less side effects
66
Q

What is the MOA of Milrinone?

A

Similar mechanisms of improved cardiac output due to positive inotropy and vascular smooth muscle relaxation

67
Q

What is the dose of Milrinone?

A

IV bolus 50 mcg/kg followed by infusion 0.375-0.75 mcg/kg/min

68
Q

What is the maximum dose of Milrinone?

A

not to exceed 1.3 mg/kg/day

69
Q

What is the protein binding of Milrinone?

A

70% protein bound

70
Q

What is the elimination half time of Milrinone?

A

2.7 hrs

71
Q

What is the excretion of Milrinone?

A

80% excreted unchanged in urine (decrease dose with severe renal dysfunction)

72
Q

What are some common clinical uses of milirone?

A
  • Acute LV dysfunction (post cardiac surgery)
  • Potentiate inotropic effect of adrenergic agents in CHF (sympathetically depleted)
  • Used for pulmonary HTN
73
Q

What is milirone not used for?

A

Not used for routine short-term acute exacerbation of chronic CHF but may provide a bridge to transplant

74
Q

What is Milrinone more effective in producing then dobutamine?

A
  • More effective that dobutamine in reducing cardiac filling pressures (rarely causes tachycardia and less cardiac O2 consumption)
75
Q

What populations is milirone most effective in?

A

patients with high filling pressures, elevated pulmonary pressures, need for continued β blockade, decreased responsiveness to catecholamines, increased risk for tachyarrhythmias

76
Q

What populations is dobutamine most effective in?

A

patients with significant vasodilation, renal dysfunction

77
Q

What properties can Milirone reverse?

A

vasospasm in arterial grafts and have anti-inflammatory effects

78
Q

What is the main side effect of Milirone?

A

Main side effect is hypotension with rapid administration, may increase ventricular automaticity in ischemic heart

79
Q

What is calicum important for (6)?

A
  • Neuromuscular transmission
  • Skeletal muscle contraction
  • Cardiac muscle contractility
  • Blood coagulation
  • Release of neurotransmitters (via exocytosis)
  • Principal component of bone
80
Q

Where is calicum stored?

A

Stored within cellular organelles such as mitochondria & sarcoplasmic reticulum of skeletal muscles

81
Q

Calicum is a __________.

A

Potent inotrope

82
Q

What is the use of exogenous calicum?

A

Exogenous administration (calcium chloride or calcium gluconate) commonly used to tx cardiac depression accompanying administration of inhaled volatile anesthetics, transfusion of citrated blood product, & following termination of CPB

83
Q

What is normal calicum range?

A

Plasma concentration of calcium is maintained between 4.3-5.3 mEq/L

84
Q

How is plasma concentration of calcium controlled?

A

by endocrine control of ion transport in the kidney, intestine, and bone

85
Q

What mediates plasma concentrations of calicum?

A

mediated by vitamin D, parathyroid hormone, and calcitonin

86
Q

What determines total plasma calicum?

A
  • Calcium bound to albumin
  • Calcium complexed w/citrate & phosphorus ions
  • Freely diffusible ionized calcium
87
Q

What causes total plasma calcium to decrease?

A

with low serum albumin & hypophosphatemia

88
Q

What type of calicum produces the physiologic effects of calicum?

A
  • Ionized calcium not total plasma calcium that produces physiologic effects of calcium – represents approx.
89
Q

How much of ionized calicum makes up total plasma concentration?

A

45%

90
Q

Hypoalbuminemia & hypophosphatemia typically not asso w/signs of __________.

A

Hypocalcemia

91
Q

What are large blood transfusions associated with?

A

acute hypocalcemia d/t binding of ionized calcium to citrate within blood products

92
Q

What effect does pH changes have on ionized fraction of calcium?

A
  • acidosis increases ionized calcium
  • alkalosis reduces ionized calcium
93
Q

Review doses of select vasoactive drugs.

A

2-Pharm Exam 3 (14 decks)

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