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  1. 1. Asthma John Noviasky, PharmD
  2. 2. Background <ul><li>At least 15 million Americans have asthma </li></ul><ul><li>Cost $12 billion annually </li></ul><ul><li>Leading cause of lost school days and common cause of lost workdays </li></ul>
  3. 3. Etiology <ul><li>Childhood asthma </li></ul><ul><ul><li>usually associated with IgE response </li></ul></ul><ul><ul><li>Common presentation - allergy to tree/grass pollen, house dust mites, pets, molds and family history asthma </li></ul></ul><ul><li>Adult asthma </li></ul><ul><ul><li>adults presenting with asthma may have atopy but may not have family history and negative allergy tests. </li></ul></ul><ul><ul><li>May have nasal polyps, asa sensitivity, sinusitis </li></ul></ul>
  4. 4. Etiology <ul><li>Adult asthma </li></ul><ul><ul><li>May have exposure to wood dusts, chemicals </li></ul></ul><ul><ul><li>Intrinsic Asthma </li></ul></ul><ul><li>Extrinsic Asthma - Atopic asthma </li></ul><ul><li>Risk Factors - atopy, chemical sensitizer exposure, viral infections, small size at birth, exposure to tobacco, pollutants </li></ul>
  5. 5. Etiology <ul><li>Hygiene Hypothesis </li></ul><ul><ul><li>Imbalance of TH2/TH1 T lymphocytes </li></ul></ul><ul><ul><li>TH1 (protective immunity) activators- older siblings, exposure to day care, childhood infections </li></ul></ul><ul><ul><li>TH2 (produces cytokines that mediate allergic inflammation) - antibiotic use, urban environment, Western lifestyle - more likely to develop asthma </li></ul></ul>
  6. 6. Pathophysiology <ul><li>Complex interaction between inflammatory cells and mediators </li></ul><ul><ul><li>Involves mast cells, eosinophils, T lymphocytes, neutrophils </li></ul></ul><ul><ul><li>TH2 cells release cytokines (IL4, IL5) that activate eosinophils </li></ul></ul><ul><li>Table 23-1 </li></ul>
  7. 7. Pathophysiology <ul><li>Airway remodeling </li></ul><ul><ul><li>structural changes, alteration in amount and composition of extracellular matrix in airway wall </li></ul></ul><ul><li>Hyperreactivity </li></ul><ul><ul><li>exaggerated response of bronchial smooth muscle to trigger stimuli </li></ul></ul><ul><ul><ul><li>to physical, chemical, immunologic, and pharmacologic stimuli (e.g. allergens, RSV, cold air, dry smoke, pollutants) </li></ul></ul></ul>
  8. 8. Pathophysiology <ul><li>Endogenous stimuli </li></ul><ul><ul><li>rhinitis, sinusitis, GERD, premenstrual asthma </li></ul></ul><ul><li>Primary Process in Bronchial hyperreactivity </li></ul><ul><ul><li>Inflammation </li></ul></ul><ul><li>Methacholine- can be used to measure hyperreactivity </li></ul>
  9. 9. Pathophysiology <ul><li>Pathologic changes secondary to chronic inflammation </li></ul><ul><ul><li>marked hypertrophy and hyperplasia of bronchial smooth muscle </li></ul></ul><ul><ul><li>mucus gland hypertrophy = excessive mucus secretion </li></ul></ul>
  10. 10. Symptoms <ul><li>Varied but can include </li></ul><ul><ul><li>Intermittent episodes of expiratory wheezing, coughing and dyspnea </li></ul></ul><ul><li>Severity of disease </li></ul><ul><ul><li>occasional, mild bouts of breathlessness </li></ul></ul><ul><ul><li>daily wheeze in spite of multiple medications </li></ul></ul><ul><ul><li>may be triggered by environmental factors (e.g. seasonal allergens) </li></ul></ul>
  11. 11. Symptom Classification <ul><li>Figure 23-3 </li></ul><ul><ul><li>Mild Intermittent </li></ul></ul><ul><ul><li>Mild Persistent </li></ul></ul><ul><ul><li>Moderate Persistent </li></ul></ul><ul><ul><li>Severe Persistent </li></ul></ul>
  12. 12. Symptom Classification <ul><li>Figure 23-3 </li></ul><ul><ul><li>Mild Intermittent </li></ul></ul><ul><ul><li>Mild Persistent->2 times/week, >2 nights/month </li></ul></ul><ul><ul><li>Moderate Persistent </li></ul></ul><ul><ul><li>Severe Persistent </li></ul></ul><ul><li>Frequency of symptoms is key component to asthma classification </li></ul>
  13. 13. Symptom Classification And Goals <ul><li>Figure 23-3 </li></ul><ul><ul><li>Mild Intermittent </li></ul></ul><ul><ul><li>Mild Persistent->2 times/week, >2 nights/month </li></ul></ul><ul><ul><li>Moderate Persistent </li></ul></ul><ul><ul><li>Severe Persistent </li></ul></ul><ul><li>Frequency of symptoms is key component to asthma classification </li></ul>
  14. 14. Diagnosis-History <ul><li>Based on intermittent symptoms of wheezing, chest tightness, shortness of breath, and coughing </li></ul><ul><li>May worsen seasonally-spring, fall </li></ul><ul><li>May worsen with exercise </li></ul><ul><li>Note any triggers </li></ul><ul><ul><li>cats, perfume, tobacco </li></ul></ul><ul><li>Family history </li></ul>
  15. 15. Pulmonary Function Tests-Spirometry <ul><li>Pulmonary disease affects volume of inhaled and exhaled air </li></ul><ul><li>Tidal volume </li></ul><ul><ul><li>volume of air inspired or expired during normal breathing </li></ul></ul><ul><li>Vital capacity </li></ul><ul><ul><li>volume of air blown off after maximal inspiration to full expiration </li></ul></ul>
  16. 16. Pulmonary Function Tests-Spirometry <ul><li>Residual volume (RV) </li></ul><ul><ul><li>volume of air left in lung after maximal expiration </li></ul></ul><ul><li>Total Lung capacity(TLC) </li></ul><ul><ul><li>Vital capacity plus RV </li></ul></ul><ul><li>Obstructive lung disease-difficulty with expiration </li></ul><ul><ul><li>decreased VC, increased RV, normal TLC </li></ul></ul><ul><li>Restrictive Lung Disease - </li></ul><ul><ul><li>Decrease in all lung volumes </li></ul></ul>
  17. 17. Pulmonary Function Tests-Spirometry <ul><li>FEV </li></ul><ul><ul><li>Patient exhales into spirometer as forcefully and completely as possible after maximal inspiration </li></ul></ul><ul><li>FEV1 </li></ul><ul><ul><li>is that volume of air exhaled in 1 second </li></ul></ul><ul><ul><li>Young adult male ~ 3-4L </li></ul></ul><ul><li>FVC </li></ul><ul><ul><li>Forced vital capacity - volume of air exhaled with maximal forced effort </li></ul></ul>
  18. 18. Pulmonary Function Tests (PFTs)-Spirometry <ul><li>FEV1:FVC ratio </li></ul><ul><ul><li>Most reproducible of the PFTs </li></ul></ul><ul><ul><li>measures the dynamic performance of the lung in moving air </li></ul></ul><ul><ul><li>Healthy individuals can exhale 75-80% of VC in 1 second and almost all in 3 seconds </li></ul></ul><ul><ul><ul><li>Normal ratio is 80% </li></ul></ul></ul><ul><ul><li>Patients actual ratio is compared against “predicted” based on age, race, gender, height and weight </li></ul></ul>
  19. 19. PFTs- Peak Expiratory Flow (PEF) <ul><li>Maximal rate of flow that can be produced during forced expiration </li></ul><ul><li>Can use handheld Peak Flow (PF) Meters </li></ul><ul><ul><li>Useful in ED, at home, at clinic </li></ul></ul><ul><li>Changes in PF usually correlate with change in FEV1 </li></ul><ul><ul><li>However, PEF is less reproducible than FEV1 </li></ul></ul><ul><li>Healthy young adult has PEF - 550-700L/min </li></ul>
  20. 20. Obstructive versus Restrictive Airway Disease <ul><li>Obstructive disease- limits airflow during expiration (e.g. bronchitis, asthma) </li></ul><ul><ul><li>narrow air passages, create air turbulence and increase resistance to airflow </li></ul></ul><ul><li>Restrictive disease - results from loss of elasticity (e.g. fibrosis, pneumonia) or physical deformity (kyphoscoliosis) which doesn’t allow lung expansion and reduces TLC </li></ul>
  21. 21. Reversible Airway Obstruction <ul><li>FEV1 is gold standard for determining reversibility of airway disease and bronchodilator efficacy </li></ul><ul><li>Significant Clinical Reversibility </li></ul><ul><ul><li>12% improvement in FEV1 after administration of bronchodilator </li></ul></ul><ul><ul><li>20% improvement in FEV1- noticeable subjective relief in most patients </li></ul></ul><ul><ul><li>IF patient with low FEV1 (e.g. <1L) improvement of 250ml may indicate benefit </li></ul></ul>
  22. 22. Limitations of Spirometry <ul><li>Patient cooperation </li></ul><ul><li>Can’t obtain in patients </li></ul><ul><ul><li>severely ill, Too old, Too young </li></ul></ul><ul><li>FEV1 and PEF relatively insensitive to small airway changes so may not detect mucus plugging and inflammation in small bronchioles </li></ul>
  23. 23. Blood Gas Measurments <ul><li>Best indicators of overall lung function are arterial blood gases </li></ul><ul><ul><li>PaO2, PaCO2, pH) </li></ul></ul><ul><li>Oxygen saturation (O2 sat) </li></ul><ul><ul><li>Quantity of O2 bound to Hg/ Quantity of O2 that could be bound to Hg </li></ul></ul><ul><ul><li>Normal O2 sat 97.5% </li></ul></ul>
  24. 24. Peak Expiratory Flow PEF <ul><li>Green - 80 to 100% of “personal best” </li></ul><ul><ul><li>good control </li></ul></ul><ul><li>Yellow - 50 to 79% of personal best </li></ul><ul><ul><li>use 2 puffs of B-agonist and call for medication adjustments if doesn’t improve </li></ul></ul><ul><li>Red - <50% of personal best </li></ul><ul><ul><li>call provider if use of B-agonist doesn’t bring you to yellow or green </li></ul></ul><ul><li>Crisis management plan </li></ul>
  25. 25. Final notes <ul><li>Asthma consists of bronchospasm and inflammation </li></ul><ul><ul><li>therapy should be directed at both </li></ul></ul><ul><li>The most common cause of death from asthma is undertreatment </li></ul><ul><li>For most asthmatics, this condition can be well controlled </li></ul>
  26. 26. Section 1 <ul><li>Asthma is an obstructive lung disease, this means that airflow is limited during inspiration or expiration? </li></ul><ul><li>Can increased wheezing occur during effective Asthma therapy? And why? </li></ul><ul><li>What might the coughing found in acute asthma attacks be due to? </li></ul><ul><li>What is atelectasis? Can it be mistaken for pneumonia? </li></ul>
  27. 27. Section 1 <ul><li>What symptoms result from feeling of suffocation during asthma? </li></ul><ul><li>What is pulsus paradoxus? </li></ul>
  28. 28. Section 2 <ul><li>What does a local decrease in breath sounds possibly indicate? </li></ul><ul><li>What is a disadvantage of PFT in acute asthma? </li></ul>
  29. 29. Section 3 <ul><li>What is most predictive test for asthma attack in determining outcome? </li></ul>
  30. 30. Section 4 <ul><li>What is first line of pharmacotherapy for acute asthma? </li></ul><ul><li>Why isn’t theophylline considered first-line? </li></ul><ul><li>Why isn’t ipratropium considered first-line? </li></ul><ul><li>Can ipratropium be added on to therapy? </li></ul>
  31. 31. Section 5 <ul><li>Is the parenteral route for B-agonist administration more effective than inhaled route? </li></ul><ul><li>Why shouldn’t B-agonist be given orally? </li></ul>
  32. 32. Section 6 <ul><li>In stable asthmatics, is there any advantage of nebulized versus metered-dose B-agonist? </li></ul><ul><li>What are some advantage of nebulized versus Metered dose inhaler? </li></ul>
  33. 33. Section 8 <ul><li>What is the difference between B2 specific agonists (albuterol) compared to nonspecific agonists (isopreoternol)? </li></ul><ul><li>What is levalbuterol? </li></ul>
  34. 34. Section 9 <ul><li>When should systemic corticosteroids be administered in asthma exacerbation? </li></ul><ul><li>Figure 23-17 </li></ul>
  35. 35. Section 10 <ul><li>What are some side effects from B-agonists? </li></ul><ul><li>Can Albuterol cause decrease serum potassium? Why? </li></ul><ul><li>What can we attribute tremor with use of B-agonist? </li></ul>
  36. 36. Section 11 <ul><li>Can tolerance to side effects of B-agonists occur? </li></ul><ul><li>Does tolerance to airway response occur with B-agonist use? </li></ul><ul><li>With long term use, does the intensity of response vary? The duration of response? </li></ul><ul><li>What are possible cause for variability of response? </li></ul>
  37. 37. Section 12 <ul><li>Do the NIH guidelines suggest addition of theophylline to acute management of asthma? Why or why not? </li></ul>
  38. 38. Section 14 <ul><li>How do corticosteroids (CS) work in relieving bronchial obstruction? </li></ul><ul><li>How long do CS take to work? </li></ul><ul><li>Can CS hasten recovery of acute exacerbations of asthma? </li></ul><ul><li>Once begun, how long should CS be continued for? </li></ul>
  39. 39. Section 15 <ul><li>Which is more effective to treat acute asthma </li></ul><ul><ul><li>high dose corticosteroids (CS) e.g. methylprednisolone 125mg q6h Versus low-dose CS e.g. methylprednisolone 40mg q6h? </li></ul></ul><ul><ul><li>IV CS or oral CS? </li></ul></ul><ul><li>When is methylprednisolone preferred over hydrocortisone? </li></ul>
  40. 40. Section 18 <ul><li>IS IV albuterol superior to inhaled albuterol in severe asthma? </li></ul><ul><li>Is inhaled ipraptropium useful in asthma? </li></ul><ul><li>IS IV or inhaled magnesium useful in severely ill patients? </li></ul>
  41. 41. Section 19 <ul><li>Which is more effective in increasing PEF, inhaled albuterol or IV aminophylline? </li></ul><ul><li>Does the addition of IV aminophylline produce a greater response than B2 agonist alone? </li></ul>
  42. 42. Section 25 <ul><li>After an acute asthma attack, how long should systemic corticosteroids be continued for? </li></ul>
  43. 43. Section 26 <ul><li>What adverse effects occur with steroids? </li></ul>
  44. 44. Section 27 <ul><li>Deaths in the Spitzer study were likely due to______? </li></ul><ul><li>What do most experts prefer? As needed short acting B2 agonists or scheduled B2 agonists? </li></ul><ul><li>When the patient needs B2agonist more than ____, the anti-inflammatory should be increased. </li></ul>
  45. 45. Section 33 <ul><li>Table 23-6 </li></ul><ul><li>At what dosage range is HPA suppression a concern? </li></ul><ul><li>Are there major differences between the various Inhaled corticosteroid (ICS)? </li></ul><ul><li>What is benefit to using a spacer with ICS? </li></ul><ul><li>Is there a link between prolonged high doses of ICS and cataracts and glaucoma? </li></ul><ul><li>Is there a concern with ICS and growth suppression in children? </li></ul>
  46. 46. Section 34 <ul><li>When should Inhaled corticosteroids (ICS) be initiated in patient also on systemic corticosteroids? </li></ul><ul><li>Which dosage for ICS is preferred, twice-daily or four times daily? </li></ul><ul><li>Is administration of ICS once daily an option? </li></ul>
  47. 47. Section 35 <ul><li>What is the most common local side effect with Inhaled corticosteroids (ICS)? </li></ul><ul><li>How can these be minimized/avoided? </li></ul>
  48. 48. Section 36 <ul><li>Has the leukotriene antagonist (e.g. montelukast) been shown to decrease utilization of Inhaled corticosteroids (ICS)? </li></ul><ul><li>Are leukotriene antagonist mentioned in NIH guidelines? </li></ul>
  49. 49. Section 44 <ul><li>Can emotional upset be a trigger for asthma? </li></ul><ul><li>Does inhaled anticholinergic (IAC) alter this response? </li></ul><ul><li>What considerations should be given to use of IAC rather than B2 agonist? </li></ul><ul><li>When can IAC be considered an alternative to B2 agonist? </li></ul>
  50. 50. Section 45 <ul><li>What are main mechanism to causing exercise induced asthma (EIA)? </li></ul><ul><li>What is the agent of choice for prophylaxis of EIA? </li></ul><ul><li>If using long acting B2 agonist (formoterol/salmeterol) for EIA prophylaxis, what considerations should be given? </li></ul>
  51. 51. Section 48 <ul><li>What is tendency for patients to mismanage ICS and B2 agonists? </li></ul><ul><li>In one study, what percentage of patients could not perform all MDI steps correctly? </li></ul><ul><li>Table 23-2 </li></ul><ul><li>What is the difference in speed of inhalation between turbuhaler, diskus, and MDI? </li></ul>