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76 Cards in this Set

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