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Asthma Chapter 33

Asthma Chapter 33. Chapter 28. Pharmacotherapy: A Pathophysiologic Approach The McGraw-Hill Companies. Abbreviations. Arg : arginine BHR: bronchial hyperresponsiveness CYP- cytochrome DPI: dry-powder inhaler FEV1: forced expiratory volume in 1 second FVC: forced vital capacity

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Asthma Chapter 33

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  1. Asthma Chapter 33 Chapter 28 Pharmacotherapy: A Pathophysiologic Approach The McGraw-Hill Companies

  2. Abbreviations Arg: arginine BHR: bronchial hyperresponsiveness CYP- cytochrome DPI: dry-powder inhaler FEV1: forced expiratory volume in 1 second FVC: forced vital capacity ICS: inhaled corticosteroid IgE: immunoglobulin E LABA: long-acting β2-agonist LTRA: leukotriene receptor antagonist MDI: metered-dose inhaler NAEPP: National Asthma Education and Prevention Program PEF: peak expiratory flow SABA: short-acting β2-agonist VHC: valved holding chamber

  3. Key Concepts • Asthma is a disease of increasing prevalence • caused by genetic & environmental factors • chronic inflammatory pulmonary disorder • No known cure or 1˚ prevention • Immunohistopathologic features include cell infiltration by eosinophils, neutrophils, T-helper type 2 lymphocytes, mast cells, epithelial cells

  4. Key Concepts • Intermittent or persistent airflow obstruction • inflammation & bronchial smooth muscle constriction • persistent changes in airway structure may occur • Inhaled corticosteroids have the greatest efficacy/safety profile for long-term management across all age groups • Bronchial smooth muscle constriction prevented/treated most effectively with inhaled β2-adrenergic receptor agonists

  5. Key Concepts • Variability in response to medications requires individualization of therapy • use lowest dose to maintain control • Ongoing patient education for a partnership in asthma care essential for optimal outcomes

  6. Asthma • Chronic inflammatory lung disease • reversible airflow obstruction • increase in bronchial hyperresponsiveness (BHR) • Recurrent symptoms • wheezing • breathlessness • chest tightness • coughing especially at night or early morning

  7. Epidemiology • Affects about 23 million Americans • most common childhood chronic disease • by early adulthood, 30 to 70% will markedly improve or be symptom-free • Higher prevalence in minorities • urbanization • poor access to care American Lung Association. Lung Disease Data: 2008. http://www.lungusa.org. Accessed 5-24.09.

  8. Epidemiology • Significant burden on healthcare system • 3rd leading cause of preventable hospitalization • > $19 billion direct & indirect costs • Can be life-threatening if not properly managed • nearly 4,000 asthma deaths per year • 80 to 90% preventable • education is key to prevention of death from asthma National Institutes of Health, National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Full Report of the Expert Panel: Guidelines for the diagnosis and management of asthma (EPR-3) 2007. http://www.nhlbi.nih.gov/guidelines/asthma American Lung Association. Lung Disease Data: 2008. http://www.lungusa.org

  9. Etiology • Genetic predisposition • atopy • linked with metalloproteinase genes • Environmental exposure • risk factors • socioeconomic status • family size • tobacco smoke • allergen exposure • urbanization • exposure to common childhood infectious agents • hygiene hypothesis

  10. Asthma Triggers DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM: Pharmacotherapy: A Pathophysiologic Approach, 7th ed. http://www.accesspharmacy.com

  11. Pathophysiology • Airway inflammation • BHR • Airflow obstruction • bronchospasm, edema, mucus hypersecretion • Airway remodeling • Mediated by eosinophils, T cells, mast cells, macrophages, epithelial cells, fibroblasts, bronchial smooth muscle cells

  12. Pathology Found in Asthmatic Bronchus Compared to Normal Bronchus

  13. Pathophysiology • Epithelial cells • release eicosanoids, peptidases, matrix proteins, cytokines, nitric oxide • epithelial shedding • Eosinophils • release inflammatory mediators • leukotrienes, granule proteins

  14. Pathophysiology • TH2 lymphocytes • produce cytokines that mediate allergic inflammation • TH1/TH2 imbalance • Mast cell degranulation • release histamine, leukotrienes, prostaglandins • Mucus plugs • epithelial & inflammatory cells • further airway obstruction

  15. ECP: eosinophil cationic protein; GM-CSF: granulocyte-macrophage colony-stimulation factor; IAR: immediate asthmatic reaction; IFN: interferon; IL: interleukin ; LAR: late asthmatic response; LT: leukotriene; MBP: major basis protein; PAF: platelet-activating factor; PG:prostaglandin DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM: Pharmacotherapy: A Pathophysiologic Approach, 7th ed. http://www.accesspharmacy.com

  16. Conditions Affecting Asthma Severity • Viral respiratory infections • Environmental/occupational triggers • Psychosocial stressors • Rhinitis/sinusitis • Gastroesophageal Reflux Disease (GERD)

  17. Clinical Presentation • No single test can diagnose asthma • careful patient history • spirometry demonstrates reversible airway obstruction • Symptoms • chronic asthma: dyspnea, chest tightness, coughing especially at night, wheezing • severe acute asthma: acute respiratory distress

  18. Aerosol Therapy

  19. Devices • Must determine which device is best for each patient • Metered-dose inhaler (MDI) • spacers • valved holding chamber (VHC) • Dry-powder inhaler (DPI) • Nebulizers • jet • ultrasonic

  20. Metered-Dose Inhaler

  21. Factors Determining Lung Deposition of Aerosols DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM: Pharmacotherapy: A Pathophysiologic Approach, 7th ed. http://www.accesspharmacy.com

  22. Patient Education • Appropriate inhalation technique is vital for optimal drug delivery and therapeutic effect • up to 30% cannot master MDI technique • Rinse mouth after inhaled corticosteroids (ICS) • < 4 years old usually need to attach a face mask to the inhalation device

  23. Steps for Using Your Inhaler • Remove the cap and hold inhaler upright • Shake the inhaler • Tilt your head back slightly and breathe out slowly • Position the inhaler • A or B is optimal • C is acceptable for those who have difficulty with A or B; required for breath-activated inhalers DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM: Pharmacotherapy: A Pathophysiologic Approach, 7th ed. http://www.accesspharmacy.com

  24. Steps for Using Your Inhaler Continued • Press down on the inhaler to release medication as you start to breath in slowly • Breathe in slowly (3 to 5 seconds) • Hold your breath for 10 seconds to allow the medicine to reach deeply into your lungs • Repeat puff as directed. Waiting 1 minute between puffs may permit second puff to penetrate your lungs better • Spacers/holding chambers are useful for all patients. Recommended for young children and older adults and for use with corticosteroids. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM: Pharmacotherapy: A Pathophysiologic Approach, 7th ed. http://www.accesspharmacy.com

  25. Steps for Using Your Inhaler Continued • Avoid common inhaler mistakes • breathe out before pressing your inhaler • inhale slowly • breathe in through your mouth, not your nose • press down on your inhaler at the start of inhalation (or within the first second of inhalation) • keep inhaling as you press down on inhaler • press your inhaler only once while you are inhaling (one breath for each puff) • make sure you breathe in evenly & deeply • Different type of inhalers require different techniques DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM: Pharmacotherapy: A Pathophysiologic Approach, 7th ed. http://www.accesspharmacy.com

  26. Severe Acute Asthma

  27. Goals of Therapy • Correct significant hypoxemia • Rapid reversal of airflow obstruction • Reduce likelihood of relapse or future recurrence of severe obstruction • Develop written action plan

  28. Treatment • Early recognition of deterioration & aggressive treatment are vital • patient/family education • Primary therapy • short-acting β2-agonist (SABA) • Additional therapy depending on severity • systemic corticosteroids • inhaled anticholinergic • O2

  29. Home Management of Acute Asthma Exacerbations

  30. Hospital Care of Acute Asthma Exacerbations Continued on next slide

  31. Continued from previous slide Hospital Care of Acute Asthma Exacerbations

  32. Special Populations • Children < 4 years old may have higher risk for respiratory failure • Require use of a face mask for aerosolized medication • appropriate size/fit • reduces drug delivery to lung by 50% • minimal dose is recommended vs weight based dose

  33. β2-Agonists • Mechanism: bronchodilator • smooth muscle relaxation • skeletal muscle stimulation • Aerosol route more bronchoselective

  34. Inhaled SABAs • Treatment of choice • most effective bronchodilator for severe acute asthma • Frequent administration • inhalations every 20 minutes • continuous nebulization • young children • unsatisfactory response to initial 3 doses of inhaled SABA • PEF or FEV1 < 30% predicted or personal best

  35. Inhaled Corticosteroids • Mechanism: antiinflammatory • reduce number of mast cells & eosinophils • increase number of β-adrenergic receptors, improve receptor responsiveness • reduce mucus production, hypersecretion • reduce BHR • reduce airway edema/exudation

  36. Pharmacokinetics of Inhaled Corticosteroids

  37. Systemic Corticosteroids • Use • incomplete response to initial inhaled SABA doses • Continue full dose until peak flow 70% of predicted or personal best • Adverse effects dependent on dose & duration • short “bursts” do not cause serious toxicities • adrenal suppression less common with shorter-acting corticosteroids (e.g. prednisone)

  38. Anticholinergics • Mechanism: bronchodilator • competitively inhibit muscarinic receptors • no effect on BHR • Less effective bronchodilator than β2-agonists • Not FDA approved for asthma • Available inhaled anticholinergics • ipratropium • tiotropium: studies inconclusive for use in asthma

  39. Ipratropium • Use • adjunct when incomplete response to SABA alone • Duration of action • 4 to 8 hours • duration/intensity of action dose dependent • Negligible systemic effects

  40. Clinical Controversy • Emergency department • unresponsive to standard doses of inhaled β2-agonists • treat with IV magnesium sulfate? • Magnesium sulfate • moderately potent bronchodilator • adverse effects include hypotension • some require dopamine to treat hypotension

  41. Clinical Controversy • Severe obstruction • response improves with ipratropium & continuous SABA nebulization • Subset analyses of 2 studies • less hospitalizations for magnesium versus placebo in patients with severe obstruction • Large randomized study did not find less hospitalizations even in severe subset Rowe BH, Bretzlaff JA, Bourdon C, et al. Intravenous magnesium sulfate treatment for acute asthma in the emergency department: A systematic review of the literature. Ann Emerg Med 2000;36:181-190.

  42. Clinical Controversy • Guideline recommendations • may consider IV magnesium sulfate in patients with severe exacerbations & poor response to initial inhaled β2-agonists

  43. Clinical Controversy • Inhaled β2-agonists administration • MDI plus VHC versus jet nebulization • treatment outcomes similar • is MDI plus VHC more cost effective? • no studies • Current practice should be based on comfort level of clinic staff Dolovich MB, Ahrens RC, Hess DR, et al. Device selection & outcomes of aerosol therapy: Evidence-based guidelines. Chest 2005;127:335–371. Dolovich MA, MacIntyre NR, Dhand R, et al. Consensus conference on aerosols and delivery devices. Respir Care 2000; 45:588–776

  44. Monitoring • Frequency dependent on exacerbation severity • lung function • spirometry • peak flow • O2 saturation

  45. Education • Self management plan • written action plan • peak flow monitoring • Asthma education • signs, symptoms of exacerbation • removal, avoidance of triggers

  46. Chronic Asthma

  47. Goals of Therapy • Reduce impairment • prevent chronic, troublesome symptoms • require infrequent use (≤ 2 days a week) of inhaled SABA for quick relief of symptoms • maintain (near-) normal pulmonary function • maintain normal activity levels • meet patients’ & families’ expectations of and satisfaction with care

  48. Goals of Therapy • Reduce risk • prevent recurrent exacerbations • minimize need for visits/hospitalizations • prevent loss of lung function • prevent reduced lung growth in children • minimal adverse effects of therapy

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