HAND OUT Chapter 5: Bronchodilators – Flashcards

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Define key terms relative to bronchodilator pharmacotherapy.
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1.
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Describe the neurologic control of bronchial smooth muscle, including the sympathetic and parasympathetic nerves, their chemical mediators, and how bronchodilation is achieved.
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2.
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Differentiate bronchospasm and bronchoconstriction.
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3.
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Describe three pharmacologic methods for bronchodilation (sympathomimetic, anticholinergic, and xanthine) and the mode of action of each.
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4.
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State the indications, contraindications, adverse reactions, onset of action, and dosage range for each bronchodilator.
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5.
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Recommend appropriate bronchodilator therapy for various patient situations, including drug, dosage, frequency, and route of delivery.
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6.
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Describe appropriate techniques for monitoring the patient's response to bronchodilator therapy.
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7.
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This is the phenomenon of increasing incidence of and mortality from asthma in recent years despite a better understanding of the pathophysiology and improved drugs for treatment of asthma. The reasons for the asthma paradox are still open to debate
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Asthma paradox
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A drug that combines with a ?-receptor and stimulates the activity of that receptor
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Beta-agonist (?-agonist)
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Narrowing of the bronchioles due to swelling, mucus obstruction, or spasm of the smooth muscle of the airway
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Bronchoconstriction
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Narrowing of the bronchioles due to contraction of the smooth muscle surrounding the airways
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Bronchospasm
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Enzyme produced when ?2-receptors are stimulated; it affects the activities of a variety of cells, including the relaxation of bronchial smooth muscle
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Cyclic AMP
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Enzyme that has the opposite effect of cyclic AMP, causing bronchoconstriction
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Cyclic GMP
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The long-term process of decreasing the sensitivity of ?-receptors to ?-agonists because of a reduction in the number of receptors
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Downregulation
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Labored or difficulty breathing
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Dyspnea
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Also called adrenaline, it is a hormone produced by the adrenal medulla. It acts as the circulating neurotransmitter for the sympathetic nervous system, stimulating both ?- and ?-receptors. It is also a poteen catecholamine, administered for its effects on the sympathetic nervous system.
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Epinephrine
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Pulmonary function test that measures the volume of air forcefully exhaled in one second
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Forced Expiratory Volume in 1 second (FEV1)
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Medications that provide long-term control of symptoms, such as shortness of breath and wheezing; usually taken daily
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Maintenance therapy
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Measurement of maximum flow rate generated during a force exhalation; used to indicate the degree of air-flow obstruction
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Peak Expiratory Flow Rate (PEFR)
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Potentially serious abnormal heartbeats that originate in the ventricles
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Premature Ventricular Contraction (PVC)
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Rapid-acting medications used to provide prompt relief of symptoms, such as shortness of breath and wheezing in asthma
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Rescue Therapy
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The strength of the stimulus to breathe, controlled by the CNS; influences the rate and depth of breathing
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Ventilatory drive
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Bronchospasm Edema Secretions
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A.Bronchoconstriction versus bronchospasm
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Fight-or-flight Physiologic response
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A.Sympathetic nervous system
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Sleep and eat Physiologic response
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B.Parasympathetic nervous system
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Acetylcholine Norepinephrine Acetylcholinesterase
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C.Chemical mediators of neural transmission
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Alpha Beta Dopamine
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D.Sympathetic nervous system receptors
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Neuronal receptors Hormonal receptors Catecholamines
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E.The sympathetic nervous system in the lung
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? effects ?1 effects ?2 effects
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A.Sympathomimetic (adrenergic) bronchodilators
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G-protein Adenyl-cyclase cAMP Phosphodiesterase
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B.Mechanism of action
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Racemic epinephrine and epinephrine COMT MAO
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A.Catecholamines
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Terbutaline
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B.Resorcinols
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Albuterol Pirbuterol Levalbuterol Salmeterol Formoterol Brovana® Olodaterol
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C.Saligenins
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Tachyphylaxis Desensitization Downregulation Asthma paradox Tachycardia Tremor Nausea
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D.Side effects of ?-agonists
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SABA
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1.
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Rescue therapy
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2.
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LABA
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3.
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Maintenance therapy
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4.
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Anticholinergic (Parasympatholytic) Bronchodilators
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V.
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Mechanism of action
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A.
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GTP
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1.
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cGMP
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2.
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Inhibition of acetylcholine to stop GTP to cGMP
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3.
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Atropine sulfate
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B.
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Prototypical parasympatholytic
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1.
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Used for symptomatic bradycardia
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2.
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Ipratropium bromide
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C.
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Nebulizer
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1.
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MDI
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2.
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Combination medications
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3.
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SAMA
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4.
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Tiotropium bromide
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D.
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LAMA
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1.
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DPI
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2.
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Aclidinium (Tudorza ® Pressair®)
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E.
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LAMA
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1.
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DPI
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2.
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Monitoring Outcomes of Inhaled Bronchodilator Therapy
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VI.
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Methylxanthines
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VII.
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Mechanism of action
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A.
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Weak bronchodilator
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1.
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Phosphodiesterase inhibitor
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2.
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Nonbronchodilating effects of theophylline
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B.
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Ventilatory drive
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1.
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Summary
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VIII.
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Three Mechanisms of bronchoconstriction
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A.
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Bronchospasm
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1.
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Secretions
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2.
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Inflammation
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3.
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Understanding what causes the bronchoconstriction will dictate the type of treatment you use for the patient.
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B.
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The longer the amine side chain, the more specific a medication is to the receptor
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C.
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Bronchodilation can be achieved with sympathomimetics, anticholinergics, and methylxanthines.
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D.
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There are different classifications of bronchodilators.
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E.
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LAMA
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1.
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SAMA
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2.
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LABA
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3.
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SABA
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4.
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It is imperative to understand the normal function of the sympathetic nervous system.
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F.
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It is imperative to understand the normal function of the parasympathetic nervous system.
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G.
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Realize that there are different names that mean essentially the same thing when referring to sympathetic and parasympathetic system.
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H.
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Why are catecholamines stored in dark containers?
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They degrade in the presence of light.
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What advantages do the resorcinols have over the catecholamines?
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4.They are longer acting because they are resistant to COMT and can be taken orally.
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Contrast rescue versus maintenance bronchodilator therapy.
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Rescue drugs must have a rapid onset to relieve acute symptoms. Maintenance drugs should have a long duration to prevent the occurrence of symptoms.
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Why is atropine contraindicated in cystic fibrosis patients who have thick tenacious secretions?
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Atropine reduces mucociliary clearance and inhibits mucus production, which causes mucus to be very thick.
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List the positive clinical responses to bronchodilator therapy.
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Improved appearance, decreased dyspnea, decreased accessory muscle use, improved vital signs, productive cough, decreased wheezing, improved air entry, improved oxygenation, and increased forced expired volume (FEV1) and PEFR
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(b) It is potent, it is fast acting, and it has few side effects.
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1.
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(b) Ipratropium does not have the parasympatholytic effect of drying secretions as atropine does.
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2.
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(d) Salmeterol is a long-acting maintenance drug that should work overnight to reduce morning symptoms. It should always be combined with or added to an inhaled corticosteroid therapy.
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3.
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(c) Monitoring blood levels is critical because many factors influence theophylline concentrations and put a patient at risk of toxicity when above therapeutic levels.
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4.
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(d) This is explained in Question 6.
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5.
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The R-isomer is more potent.
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6.
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(d) The treatment should not continue with this adverse reaction.
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7.
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(c) Serevent® and tiotropium are available in DPI form.
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8.
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(c) Salmeterol would not be indicated because it is a long-acting maintenance drug.
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9.
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(b) Spiriva® and Serevent® are both long-acting medications.
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10.
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(d) PEFR, FEV, and the use of accessory muscles monitor the effectiveness of bronchodilator therapy.
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11.
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Change to the HFA formulation.
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12.
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A bronchodilator may not be helpful due to swelling in the upper airway above the glottis. Racemic epinephrine may be more beneficial because of its vasoconstricting associated with its stimulation of the alpha1 receptor.
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13.
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