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76 Cards in this Set
- Front
- Back
impairment?
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frequency and intensity of symptoms and functional limitations the patient is experiencing currently or has recently experienced
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risk?
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likelihood of either asthma exacerbations, progressive decline in lung function (or lung growth in children), or risk of adverse effects from the medication
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what are initial management decisions for asthma based on?
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categorization of asthma severity
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after initial management decisions for treatment of asthma, what are subsequent decisions based on?
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assessment of asthma control
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asthma control?
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degree to which manifestations of asthma are minimized
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why is it important to separate the two concepts of asthma severity and control?
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dispels the common misconception that well-controlled asthma is synonymous with mild asthma and that poorly controlled asthma is synonymous with severe asthma
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responsible for early reaction of asthma?
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mast cells
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responsible for late reaction of asthma?
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leukocytes
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allergen-induced acute bronchoconstriction results from?
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IgE-dependent release from mast cells of histamine, tryptase, leukotrienes, and prostaglandins which directly control airway smooth muscle
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airway hyperresponsiveness?
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important to the pathogenesis of asthma and level of airway responsiveness usually correlates with the clinical severity of asthma
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non-antigenic stimuli for asthma?
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exercise
cold air environmental pollutants |
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contributors to bronchial asthma?
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mediator-release pathways
neural/humoral pathways both |
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neural pathway contributing to asthma?
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sensory receptors can activate vagal afferents leading to increased output of vagal effects resulting in ACh release and bronchoconstriction
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goals of asthma pharmacologic therapies?
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prevent and control symptoms
reduce frequency and severity of exacerbations reverse airflow obstruction |
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drugs of choice for long-term control of asthma?
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inhaled corticosteroids
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inhaled corticosteroids?
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budesonide
fluticasone mometasone |
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budesonide?
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inhaled corticosteroid
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fluticasone?
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inhaled corticosteroid
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mometasone?
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inhaled corticosteroid
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inhaled corticosteroids mechanism?
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block late reaction to allergen
reduce airway hyperresponsiveness |
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clinical effects of inhaled corticosteroids?
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reduction in severity of symptoms;
improvement in peak expiratory flow and spirometry; diminished airway hyperresponsiveness; prevention of exacerbations; possibly prevention of airway wall remodeling |
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when is maximal improvement in lung function seen with inhaled corticosteroids?
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may not occur for several weeks
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local adverse effects to inhaled corticosteroids?
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thrush
hoarseness |
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potential systemic adverse effects of inhaled corticosteroids?
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impaired linear growth in children
bone metabolism/osteoporosis disseminated varicella dermal thinning, increased ease of bruising hypothalmic-pituitary-adrenal axis suppression |
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what vaccine should those on corticosteroids receive?
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varicella vaccine (if not had clinical varicella)
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systemic corticosteroids?
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prednisone
others |
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clinical use of systemic corticosteroids for asthma?
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in severely uncontrolled asthma for long-term prevention (>2 weeks), suppression and control of symptoms and reversal of inflammation
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mechanism of inhaled cromolyn sodium and nedocromil?
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inhibition of activation and release of mediators from mast cells, eosinophils, etc (do not degranulate);
inhibit early and late asthmatic response |
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why are inhaled corticosteroids preferable to inhaled cromolyn sodium or nedocromil?
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must be given prophylactically
administered 4x a day response is generally less predictable not as effective at reducing bronchial hyperreactivity |
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clinical uses of inhaled cromolyn and nedocromil?
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alternative med for mild persistent asthma;
preventative prior to exercise or unavoidable exposure to known allergens; reduce need for quick relief β agonists |
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adverse effects of cromolyn and nedocromil?
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virtually no systemic toxicity
transient cough |
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other preparations of cromolyn and nedocromil have uses in what other conditions?
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vernal conjunctivitis
allergic conjunctivitis allergic rhinitis |
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contraindicated for monotherapy of persistent asthma?
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LABAs
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pharmacologic therapy for controlling moderate asthma?
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LABA + inhaled corticosteroids is considered more effective than raising the dose of corticosteroids, although this may be necessary as well
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clinical use of LABAs?
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concomitant use with inhaled corticosteroids for long term control of moderate to severe asthma, including nocturnal symptoms;
prevent exercise induced bronchospasm; NOT monotherapy or for acute exacerbations |
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why are LABAs and inhaled corticosteroids available in fixed combinations?
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more convenient
enhance compliance eliminate risk of use of LABA as monotherapy |
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revised FDA labeling for LABAs in 2006?
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associated with possible increased risk of bronchospasm in some people;
although decrease frequency of asthma episodes, may increase chance of severe asthma episodes and death when these episodes do occur |
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main advantage to theophylline?
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oral asthma drug
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theophylline mechanism?
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not definitively established
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clinical use of theophylline?
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adjuvant to inhaled corticosteroids for prevention of nocturnal asthma symptoms;
alternative for long-term preventive therapy (issues with cost or adherence) |
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use of low-dose theophylline?
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revived interest as maintains full anti-inflammatory/immunomodulatory effects without potential for toxicities
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adverse effects of theophylline?
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narrow TI necessitating monitoring
>15 microg = anorexia, n/v, nervousness, insomnia, tremor, aggravation of ulcer or reflux, increase in hyperactivity in some children and possible difficulty in urination in elderly males with BPH; >40 microg = seizures and cardiac arrhythmias possible |
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leukotrienes?
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potent biochemical mediators;
released from mast cells, eosinophils, basophils; contract airway smooth muscle; increase vascular permeability; increase mucus secretion; attract and activate inflammatory cells in airways |
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systemic leukotriene modifiers?
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montelukast
zileuton |
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clinical considerations with leukotriene modifiers?
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considerable variability in response
less effective as add on therapy than LABAs not useful for acute asthma attack |
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clinical indications for leukotriene modifiers?
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alternative monotherapy for mild persistent asthma;
concomitant with inhaled corticosteroids for moderate persistent asthma; exercise induced asthma (especially in children who may not have access to SABAs when needed) [indications for responders] |
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leukotriene modifiers effects?
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improve lung function;
diminish symptoms; diminish need for short acting β agonists; reduction in inhaled corticosteroid dosage |
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montelukast mechanism?
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leukotriene CysLT1 receptor antagonist
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agonists for leukotriene CysLT1 receptor?
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LTC4
LTD4 LTE4 |
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clinical use of montelukast?
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asthma
allergic rhinitis |
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adverse effects of montelukast?
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neuropsychiatric events
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zafirlukast drug interactions?
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increased half-life of warfarin
decreased bioavailability with meals |
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zileuton mechanism?
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inhibits 5-lipoxygenase enzyme to inhibit synthesis of all leukotrienes
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additional benefit of zileuton over other leukotriene modifiers?
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capable of attenuating bronchoconstriction from exercise and from aspirin in aspirin-sensitive individuals
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adverse effects of zileuton?
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liver toxicity
avoid in pregnancy |
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zileuton drug interactions?
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metabolized by CYP3A4, 1A2, 2C9
inhibit warfarin, theophylline metabolism |
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omalizumab?
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monoclonal IgG tha interacts with Fc of IgE to neutralize and prevent its binding to mast cells and basophils
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administration of leukotriene modifiers?
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oral
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administration of omalizumab?
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subcutaneous
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effect of omalizumab?
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limits release of mediators
downregulation of FcI receptors on basophils |
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omalizumab indications?
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adults and adolescents with severe persistent asthma;
symptoms inadequately controlled with inhaled corticosteroids, LABAs, and leukotriene modifiers |
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how long must patients be treated with omalizumab before efficacy is assessed?
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at least 12 weeks
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omalizumab adverse reactions?
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malignancies
anaphylaxis (contraindication) |
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why are systemic corticosteroids important in treatment of severe exacerbations despite slow onset?
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prevent progression of exacerbation
speed recovery prevent early relapses |
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use of quick relief medications?
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prompt relief of bronchoconstriction, cough, chest tightness, and wheezing
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mechanism of SABAs?
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β2 stimulation (functional antagonism)
inhibit function of inflammatory cells |
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therapy of choice for acute symptoms and prevention of exercise induced bronchoconstriction?
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SABAs
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frequency of SABAs use?
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regularly scheduled is not recommended;
use can be used as barometer of disease activity |
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SABAs adverse effects?
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sympathomimetic effects (tremor, anxiety, heart pounding, tachycardia, small increases in K+ and Mg2+);
possible tolerance |
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SABAs?
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albuterol
levalbuterol |
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inhaled anticholinergics?
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tiotropium
ipratropium |
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tiotropium mechanism?
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competitive inhibitors of M1 and M3 to inhibit bronchoconstriction and secretory effects of ACh
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clinical uses of ipratropium?
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bronchospasm in chronic bronchitis, COPD;
bronchospasm due to β-blocker therapy; allergic rhinorrhea |
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tiotropium clinical uses?
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COPD
offlabel for refractory severe asthma or those that cannot tolerate β2 agonists |
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side effects of inhaled anticholinergics?
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drying of mouth
bitter tast constipation tachycardia blurred vision narrow angle glaucoma |
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clinical use of systemic corticosteroids?
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severe exacerbations unresponsive to bronchodilators to speed recovery and prevent recurrence of exacerbations;
gain prompt control of disease when initiating long term therapy with inhaled corticosteroids |