Asthma management 2

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Asthma management 2

  1. 1. Asthma Review of Pathophysiology and Treatment
  2. 2. Definition  It is a chronic inflamatory disorder due to hyperresponsiveness of airways characterized by dysponea, cough,wheezing and chest tightness with variable airway obstruction.
  3. 3. Types Early onset asthma Late onsetasthma  Nocturnal asthma Brittle asthma  Cardiac asthma Catamenial asthma  Cough variant asthma  Aspirin sensitive asthma  Occupational asthma 
  4. 4. Child-onset asthma – Associated with atopy – IgE directed against common environmental antigens (house-dust mites, animal proteins, fungi – Viral wheezing Infants/children, allergy/allergy history associated with continuing asthma through childhood
  5. 5. Adult-onset asthma – Many situations – Allergens important – Non-IgE asthma have nasal polyps, sinusitis, aspirin sensitivity or NSAID sensitivity – Idiosyncratic asthma less understood
  6. 6. Adult-onset asthma – Occupational exposure  animal products, biological enzymes, plastic resin, wood dusts, metal  removal from workplace may improve symptoms although symptoms persist in some
  7. 7. Pathophysiology Airway limitation usually reversible  Airway hyperreactivity  Airway inflamation   With increased severity and chronicity remodelling,fibrosis and fixed narrowing of airways and decreased response to drugs.
  8. 8. Airway Inflammation More often triggered by infections and chronic allergies. IgE mediated triggering mast cell release. Causes “fixed” obstruction not responsive to albuterol and more often has an inspiratory component. Strong genetic contribution. Needs steroids.
  9. 9. Airway hyperresponsiveness Primarily smooth muscle mediated. Can occur at any age. Reversible with albuterol. Primarily expiratory wheezes. Results in air trapping / obstruction (can be quantified on PFT’s). Variable throughout lungs. May cause atelectasis on xray. Primary process for wheezing due to cold air, exercise, pet allergens.
  10. 10. Airflow limitation – Acute bronchoconstriction IgE -dependent mediator release from mast cell (leukotrienes, histamine, tryptase, prostaglandins)  aspirin /NSAID  non-IgE response (cold air, exercise, irritants) 
  11. 11.  Airflow limitation – Chronic mucus plug formation  secretions & inspissated plugs  persistent airflow limitation in severe intractable asthma – Airway remodeling  irreversible component of airflow limitation secondary to structural airway matrix changes
  12. 12. A Closer Look
  13. 13. Etiology  Environmental(hygeine hypothesis)  Genetical
  14. 14. Common Triggers Infections: viral respiratory illness (rhinovirus, influenza, RSV, parainfluenz a, human metapneumovirus), sinus infections Allergens: seasonal allergens, indoor allergens, pets Irritants: cigarette smoke, wood smoke, other pollutants, weather changes
  15. 15. Diagnosis Compatible history plus either/or  FEV more than15% following bronchodilator therapy.  More than 20% diurnal variation on PEFR diary for 3 days a week for 2 weeks.  FEV more than 15% decrease after 6 minutes of exercise. 
  16. 16. Differential Diagnosis Upper RTI  Lower RTI  Systemic 
  17. 17. Asthma Classification  Mild intermittent Day symptoms < 2/week, Night symptoms < 2/month Normal FEV , FEV/FVC normal Mild persistent Day symptoms >2 per week but not daily, Night symptoms> 3-4/month Normal FEVFEV/FVC normal Moderate persistent Daily symptoms, affect activity, night symptoms > 1/weekFEV60-80% FEV/FVC reduced < 5% Continuous symptoms, limited activity, Severe persistent FEV <60%FEV/FVC reduced >5%.
  18. 18. Investigation Lab investigations  Radiology  Spirometry  PEFR recording 
  19. 19. Pharmacologic Therapy Long-term control medications  (Controllers)  Short term control medications  (Relievers)  – corticosteroids  inhaled form  systemic steroids used to gain prompt control of disease when initiating inhaled tx – cromolyn sodium or nedocromil  mild-to-moderate anti-inflammatory medications
  20. 20. Management AccordingtoGINA,NAEPP3,WHO,NHI,  NHLBI guidelines management should be in 4 steps.  Assess and monitor asthma severity and control  Patient education  Environmental control  Medical therapy 
  21. 21. Pharmacologic Therapy  Long-term control medications – corticosteroids  inhaled form  systemic steroids used to gain prompt control of disease when initiating inhaled tx – cromolyn sodium or nedocromil  mild-to-moderate anti-inflammatory medications (may be used initially in children)  preventive tx. prior to exercise or unavoidable exposure to known allergens
  22. 22. Relievers Beta adrenergic agonists.  Anticholinergic agents  Phosphodiesterase inhibitors  Corticosteroids  Antimicrobials 
  23. 23. Controllers Anti inflamatory agents (steroids)  Long acting bronchodilators     Mediator inhibitors Beta adrenergic agonists Phosphodiesterase inhibitors Leukotrienes modifiers  Desensitization drugs  Vaccinations  Miscellaneous agents 
  24. 24. Long-term control medications – Long-acting beta2-agonists  used concomitantly with anti-inflammatory meds for long-term symptom control especially nocturnal symptoms  prevents exercise-induced bronchospasm – Methylxanthines  sustained-release theophylline used as adjuvant to inhaled steroids for prevention of nocturnal symptoms
  25. 25. Long-term control medications – Leukotriene modifiers  zafirlukast - leukotriene receptor antagonist  zileuton - 5-lipoxygenase inhibitor is alternative therapy to low doses of inhaled steroids/nedocromil/cromolyn  alternative tx to low dose inhaled steroids/cromolyn/nedocromil  recommended for >12yrs with mild persistent asthma.
  26. 26. Quick relief medications – Short acting beta2-agonists - relief of acute symptoms – Anticholinergics - may provide additive benefit to beta2 drugs in severe exacerbation. May be alternative to beta2-agonists – Systemic steroids - moderate-to-severe persistent asthma in acute exacerbations or to prevent recurrence of exacerbations
  27. 27. Treatment/Long Term Control  Corticosteroids – Most potent and effective – Reduction in symptoms, improvement in PEF and spirometry, diminished airway hyperresponsiveness, prevention of exacerbations, possible prevention of airway wall remodeling – Suppresses: cytosine production, airway eosinophilic recruitment, chemical mediators
  28. 28. LABA  Long-acting beta-2 agonists – Relax airway smooth muscle – Duration of action >12 hrs – Not used in acute exacerbations – Adjunct to anti-inflammatory tx for longterm symptom control especially nocturnal symptoms
  29. 29. Methylxanthines – Provides mild-moderate bronchodilation – Low dose has mild anti-inflammatory action – Sustained release form used as alternative but not preferred to long-acting beta2 agonists to control nocturnal symptoms – Use may be necessary because of cost or patient compliance
  30. 30. Leukotriene modifiers – Leukotrienes are potent biochemical mediators released from mast cells, eosinophils, and basophils that:  contract bronchial smooth muscle  increase vascular permeability  increase mucus secretions  attract & activate inflammatory cells in airways
  31. 31. Leukotriene modifiers – Zafirlukast & zileuton (oral tabs)  improves lung fx and diminishes symptoms & need for short-acting beta2 agonists – Studies in mild-moderate asthma showing modest improvements – Alternative to low-dose inhaled steroids for pts. with mild persistent asthma – Further study in of other groups needed
  32. 32. Asthma Treatment/Quick Relief  Short-acting beta2 agonists – Relax airway smooth muscle and increase in airflow in <30 minutes – Drug of choice for treating symptoms and exacerbations and EIB – Use of >1 canister/mo indicates inadequate control and indicates need to intensify anti-inflammatory tx – Regularly scheduled use NOT recommended
  33. 33. Anticholinergics – Cholinergic innervation important in regulation of airway smooth muscle tone – Ipratropium bromide (quaternary derivative of atropine without its’ side effects) – Additive benefit with inhaled beta 2agonists in severe asthma exacerbations – Effectiveness in long-term management not demonstrated
  34. 34.  Systemic steroids – speed resolution of airflow obstruction – reduce rate of relapse  Medications to reduce oral steroid dependence – Troleandomycin, cyclosporin, gold, methotrexate, IV immunoglobulin, dapsone, hydroxychloroquine
  35. 35. Intermittent Asthma  Step 1 – Short-acting inhaled beta 2 agonists PRN  IF NEEDED >2 X/wk PATIENT SHOULD BE MOVED TO THE NEXT STEP OF CARE (exception is EIB or viral infections) – Viral infections  mild symptoms - beta 2 agonist Q 4-6 hr  moderate-to-severe symptoms - short course of systemic steroids recommended plus above
  36. 36. Persistent Asthma  Mild, moderate or severe – Daily long-term control recommended  Mild persistent asthma (step 2 care) – Daily anti-inflammatory meds - inhaled steroids (low dose) or cromolyn or nedocromil – Sustained release theophylline alternative but not preferred
  37. 37.  Moderate persistent asthma (step 3 care) – Increase inhaled steroids to medium dose OR – Add long-acting bronchodilator to a lowmedium dose of inhaled steroids OR – Increase to medium dose steroid then lower dose & add nedocromil (+/-)
  38. 38.  Moderate persistent asthma (if not adequately controlled) – Increase to high dose inhaled steroids & add long-acting bronchodilator (serevent or theophylline)
  39. 39.  Severe persistent asthma (step 4) – If not controlled on high dose of inhaled steroids and long-acting bronchodilator ADD oral systemic steroids on a regularly scheduled, long-term basis  use lowest dose  monitor closely  attempt to reduce or take off when control established
  40. 40. Complications Due to drugs  Due to disease 
  41. 41.

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