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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
What is the peak of digoxin?
peaks in 1-3 hrs
26
What is the IV bioavailability, peak and onset of digoxin?
100% bioavailability after IV, onset 10-30 min, peak 2-4 hrs
27
What is the half life of digoxin?
Half live 1-2 days
28
What is the excretion of digoxin?
Renal excretion (inversely proportional with GFR, age, renal disease)
29
What is the metabolism of digoxin?
Only small fraction is metabolized by the liver and approximately 8% undergoes an enterohepatic cycle
30
What is the MOA of digoxin?
Selectively and reversibly inhibit the Na-K ATPase ion transport system located in sarcolemma of cardiac cells
31
What effect does digoxin binding to the alpha subunit of the ATPase enzyme?
thus interfering outward flow of Na+ from the cell: results in increase intracellular Na+ results in increased intracellular Ca++
32
What is the effet of increased intracellular Ca++ (Digoxin MOA)?
accounts for the positive inotropic activity
33
What is the inotropic activity of digoxin?
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)
34
What are the PNS effects of digoxin?
* Enhanced parasympathetic effects * negative chronotropic and dromotropic effects
35
What are the EKG changes associated with digoxin?
* Prolonged P-R * shortened QT * ST segment depression * diminished/inverted T waves
36
What is the therapeutic range of Digoxin?
Narrow therapeutic range (occur at 35% of fatal dose)
37
When does cardiac dysrhtymias with digoxin occur?
Cardiac dysrhythmias at 60% fatal dose
38
Digoxin Toxicity Attributed to the buildup in \_\_\_\_\_\_\_\_\_.
intracellular Ca++
39
What is the biggest contributor to digoxin toxicity?
* Hypokalemia biggest contributor to development of digoxin toxicity (hyperventilation, diuretics); others include hypercalcemia and hypomagnesemia * Increased K inhibits digoxin binding to ATPase enzyme
40
Who is at higher risk for digoxin toxicity?
Elderly, renal dysfunction, hypoxemia (sympathetic stimulation)
41
What is the theraputic range of digoxin?
Therapeutic range 0.5- 2.5 ng/ml (toxic \> 3)
42
What is the common manifestations of Digoxin Toxicity?
anorexia, N/V
43
What is the most common EKG change associated with Digoxin Toxicity?
Atrial tach with block most common EKG but may see various dysrhythmias to complete heart block
44
What is the typical cause of death associated with Digoxin Toxicity?
Cause of death: VF
45
What is the treatment for Digoxin Toxicity?
* correct underlying electrolyte or physiologic derangement (K+), medications such as phenytoin, atropine, lidocaine
46
What is the dose of phenytoin and lidocaine for Digoxin Toxicity?
* Phenytoin 0.5-1.5 mg/kg * Lidocaine 1-2 mg/kg
47
What maybe required with digoxin toxicity?
may require pacemaker
48
What is the principle action of Phosphodiesterase Inhibitors?
* Competitive inhibitory action on phosphodiesterase enzyme * Various selective inhibitors
49
What effect does PDE III have on cAMP?
PDE III decrease hydrolysis of second messenger cAMP (results in increased cAMP in myocardium and vascular smooth muscle)
50
What effect do phsophodiesterase inhibitors have on the myocardium?
* 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
What makes Phosphodiesterase Inhibitors an inodilator?
positive intropic effects with smooth muscle relaxation in both arterial or venous beds
52
What effects do Phosphodiesterase Inhibitors have?
* Increased contractility * CO * decreased LVEDP * decreased filling pressures * decreased venous return to the heart * diastolic relaxation (lusitropy)
53
Where else do Phosphodiesterase Inhibitors exert there effects?
Work independently of β receptors (works with those β-blocked and refractory to catecholamine therapy
54
What is the use for Phosphodiesterase Inhibitors?
Used for acute heart failure, cardiogenic shock
55
What are contraindications to Phosphodiesterase Inhibitors?
Contraindications are severe obstructive cardiomyopathy, hypovolemia, tachycardia, and ventricular aneurysm
56
What are some Phosphodiesterase Inhibitors?
* Amrinone * Milrinone
57
What is the new market name for Amrinone?
Inamrinone
58
What is the MOA of Amrinone (Inamrinone)?
Selective PDE III inhibitor
59
What are the effects of Amrinone (Inamrinone)?
dose dependent positive inotrope and vasodilator that increases CO, decreased LVEDP
60
What is the formularies for Amrinone (Inamrinone)?
Be given oral or IV
61
What is the dose of Amrinone (Inamrinone)?
Loading dose 0.5-1.5 mg/kg with infusion 2-10 mcg/kg/min
62
What is the max dose of Amrinone (Inamrinone)?
Max daily dose 10mcg/kg
63
What are the side effects of Amrinone (Inamrinone)?
* hypotension, especially with rapid IV bolus * thrombocytopenia with long-term use * dose-related proarrhythmic potential
64
What is the excretion of Amrinone (Inamrinone)?
26-40% excreted unchanged in urine (reduce dose with renal dysfunction)
65
What is the inotropic effects of Amrinone (Inamrinone) compared to Milrinone?
* 30 times the inotropic effects of amrinone * Replaced amrinone given less side effects
66
What is the MOA of Milrinone?
Similar mechanisms of improved cardiac output due to positive inotropy and vascular smooth muscle relaxation
67
What is the dose of Milrinone?
IV bolus 50 mcg/kg followed by infusion 0.375-0.75 mcg/kg/min
68
What is the maximum dose of Milrinone?
not to exceed 1.3 mg/kg/day
69
What is the protein binding of Milrinone?
70% protein bound
70
What is the elimination half time of Milrinone?
2.7 hrs
71
What is the excretion of Milrinone?
80% excreted unchanged in urine (decrease dose with severe renal dysfunction)
72
What are some common clinical uses of milirone?
* Acute LV dysfunction (post cardiac surgery) * Potentiate inotropic effect of adrenergic agents in CHF (sympathetically depleted) * Used for pulmonary HTN
73
What is milirone not used for?
Not used for routine short-term acute exacerbation of chronic CHF but may provide a bridge to transplant
74
What is Milrinone more effective in producing then dobutamine?
* More effective that dobutamine in reducing cardiac filling pressures (rarely causes tachycardia and less cardiac O2 consumption)
75
What populations is milirone most effective in?
patients with high filling pressures, elevated pulmonary pressures, need for continued β blockade, decreased responsiveness to catecholamines, increased risk for tachyarrhythmias
76
What populations is dobutamine most effective in?
patients with significant vasodilation, renal dysfunction
77
What properties can Milirone reverse?
vasospasm in arterial grafts and have anti-inflammatory effects
78
What is the main side effect of Milirone?
Main side effect is hypotension with rapid administration, may increase ventricular automaticity in ischemic heart
79
What is calicum important for (6)?
* Neuromuscular transmission * Skeletal muscle contraction * Cardiac muscle contractility * Blood coagulation * Release of neurotransmitters (via exocytosis) * Principal component of bone
80
Where is calicum stored?
Stored within cellular organelles such as mitochondria & sarcoplasmic reticulum of skeletal muscles
81
Calicum is a \_\_\_\_\_\_\_\_\_\_.
Potent inotrope
82
What is the use of exogenous calicum?
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
What is normal calicum range?
Plasma concentration of calcium is maintained between 4.3-5.3 mEq/L
84
How is plasma concentration of calcium controlled?
by endocrine control of ion transport in the kidney, intestine, and bone
85
What mediates plasma concentrations of calicum?
mediated by vitamin D, parathyroid hormone, and calcitonin
86
What determines total plasma calicum?
* Calcium bound to albumin * Calcium complexed w/citrate & phosphorus ions * Freely diffusible ionized calcium
87
What causes total plasma calcium to decrease?
with low serum albumin & hypophosphatemia
88
What type of calicum produces the physiologic effects of calicum?
* Ionized calcium not total plasma calcium that produces physiologic effects of calcium – represents approx.
89
How much of ionized calicum makes up total plasma concentration?
45%
90
Hypoalbuminemia & hypophosphatemia typically not asso w/signs of \_\_\_\_\_\_\_\_\_\_.
Hypocalcemia
91
What are large blood transfusions associated with?
acute hypocalcemia d/t binding of ionized calcium to citrate within blood products
92
What effect does pH changes have on ionized fraction of calcium?
* acidosis increases ionized calcium * alkalosis reduces ionized calcium
93
Review doses of select vasoactive drugs.

2-Pharm Exam 3 (14 decks)

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