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Management of asthma and copd
- 2. A chronic inflammatory disorder of the airway Infiltration of mast cells, eosinophils and lymphocytes Airway hyperresponsiveness Recurrent episodes of wheezing, coughing and shortness of breath Widespread, variable and often reversible airflow limitation
- 4. Predisposing Factors Atopy Causal Factors Indoor Allergens Outdoor Allergens Domestic mites Animal Allergens Cockroach Allergens Fungi Pollens Fungi Occupational Sensitizers Contributing Factors Respiratory infections Small size at birth Diet Air pollution – Outdoor pollutants – Indoor pollutants Smoking – Passive Smoking – Active Smoking
- 5. Environmental factors Mucosal inflammation Atopic sensitization Phenotype Genetic factors Structural changes
- 6. 1. Extrinsic or allergic: 1. History of `atopy` in childhood Family history of allergies Positive skin test Raised IgE level Below 30 years of age Less prone to status asthmaticus Intrinsic or Idiosyncratic: No family history of allergy Negative skin test No rise in IgE level Middle age onset Prone to status asthmaticus
- 7. CLASSIFY SEVERITY STEP 4 Severe Persistent STEP 3 Moderate Persistent STEP 2 Mild Persistent STEP 1 Intermittent Clinical Features Before Treatment Nighttime PEF Symptoms Symptoms Continuous <60% predicted Limited physical Frequent Variability >30% activity Daily Use β2-agonist daily Attacks affect activity a week >1 time but <1 time a day < 1 time a week Asymptomatic and normal PEF between attacks >1 time week >2 times a month <2 times a month >60%-<80% predicted Variability >30% >80% predicted Variability 2030% >80% predicted Variability <20% The presence of one of the features of severity is sufficient to place a patient in that category. Global Initiative for Asthma (GINA) WHO/NHLBI, 2002
- 8. GINA Guideline clearly states that THERE IS NO CURE FOR ASTHMA, But appropriate management most often leading to CONTROL of asthma
- 9. Relievers Preventers Peak Flow meter Patient education
- 10. - Rescue medications Quick relief of symptoms Used during acute attacks Action lasts 4-6 hrs
- 11. Short acting β 2 agonists Salbutamol Levosalbutamol Anti-cholinergics Ipratropium bromide Xanthines Theophylline Adrenaline injections
- 13. - Prevent future attacks Long term control of asthma Prevent airway remodelling
- 14. Corticosteroids Prednisolone, Betamethasone Beclomethasone, Budesonide Fluticasone Long acting β2 agonists Bambuterol, Salmeterol Formoterol Anti-leukotrienes Montelukast, Zafirlukast Xanthines Theophylline SR Mast cell stabilisers Sodium cromoglycate COMBINATIONS Salmeterol/Fluticasone Formoterol/Budesonide Salbutamol/Beclomethasone
- 15. SALBUTAMOL INHALER 100 mcg: 1 or 2 puffs as necessary LEVOSALBUTAMOL INHALER 50 mcg : 1 or 2 puffs as necessary
- 16. Formoterol ( fast relief and sustained relief ) + Budesonide ( twice or even once daily use ) Dose: 1- 4 puffs ( OD/BD ) Another combination Salmeterol + Fluticasone
- 17. Metered dose inhalers Dry powder inhalers (Rotahaler) Spacers / Holding chambers
- 18. Dry Powder Inhaler Metered Dose inhaler Spacer
- 20. Step I: When symptoms are less than once daily occasional inhalation of a short acting Beta-2 agonist – salbutmol, terbutaline. If used more than once daily – step II (Mild episodic asthma) Step II: Regular inhalation of low-dose steroids. Alternatively, cromoglycates. Beta-2 agonist as and whenever required (Mild chronic asthma) Step III: Inhalation of high dose of steroids (800 mcg) + Beta-2 agonist. Sustained release theophylline may be added. LT inhibitors may be tried instead of steroids (Moderate asthma with frequent exacerbations) spacers Step IV: Higher dose of steroid (800 to 200 mcg) + regular beta-2 agonist (long acting salmeterol) Additional treatment with oral drugs – LT antagonist or SR theophylline or oral beat-2 agonist
- 22. allergen allergen avoidance avoidance indicated indicated when possible when possible pharmacotherapy pharmacotherapy safety safety effectiveness effectiveness easy to be administered easy to be administered AR AR patient's patient's education education immunotherapy immunotherapy always indicated always indicated effectiveness effectiveness specialist prescription specialist prescription may alter the natural may alter the natural course of the disease course of the disease
- 23. Birth:TH2 Older siblings: Many infections [TH1 stimuli] Allergen Exposure TH1 No allergies Source: Busse WW, Lemanske RF. N Engl J Med 2001. Only child: Few infections Still TH2 Allergies
- 24. Patients diagnosed with allergic asthma Patients diagnosed with allergies such as hay fever Patients diagnosed with sinusitis that predisposes them to asthma Patients diagnosed with insect sting allergy
- 25. COPD is characterized by airflow limitation caused by chronic bronchitis or emphysema often associated with long term tobacco smoking This is usually a slowly progressive and largely irreversible process Consists of increased resistance to airflow, loss of elastic recoil, decreased expiratory flow rate, and overinflation of the lung. COPD is clinically defined by a low FEV1 value that fails to respond acutely to bronchodilators, a characteristic that differentiates it from asthma.
- 26. Chronic Bronchitis is characterized by Chronic inflammation and excess mucus production Presence of chronic productive cough Emphysema is characterized by Damage to the small, sac-like units of the lung that deliver oxygen into the lung and remove the carbon dioxide Chronic cough *Source: Braman, S. Update on the ATS Guidelines for COPD. Medscape Pulmonary Medicine. 2005;9(1):1.
- 28. Normal versus Diseased Bronchi
- 30. Night time waking with breathlessness or wheeze is common in asthma and uncommon in COPD. COPD is rare before the age of 35 whilst asthma is common in under-35.
- 31. Classification of COPD Severity by Spirometry Stage I: Mild FEV1/FVC < 0.70 FEV1 > 80% predicted Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus
- 32. Physical examination Signs of heavy smokers Observe for clubbing Distended neck vein on expiration The presence of barrel chest Observe for abdominal breathing The use of pursed lips breathing and chest movement Auscultate the chest& listen for musical wheezes characteristics of chronic bronchitis
- 34. Symptoms Physical examination Sample of sputum Chest x-ray High-resolution CT (HRCT scan) Pulmonary function test (spirometery) Arterial blood gases test Pulse oximeter
- 35. Give antibiotics to treat infection Give bronchodilators to relieve bronchospasm, reduce airway obstruction, mucosal edema and liquefy secretions. Chest physiotherapy and postural drainage to improve pulmonary ventilation. Proper hydration helps to cough up secretions or tracheal suctioning when the patient is unable to cough. Steroid therapy if the patient fails to respond to more conservative treatment.
- 36. Stop smoking Oxygenation with low concentration during the acute episodes In asthma adrenaline ( epinephrine) SC if the bronchospasm not relieved. Aminophylins IV if the above treatment does not help. IV corticosteroids for patients with chronic asthma or frequent attack. Sedative or tranquilizers to calm the patient. Increase fluids intake to correct loss of diaphoresis and inaccessible loss of hyperventilation. Intubations and mechanical ventilation if there is respiratory failure .
- 37. Oxygen therapy Used as long-term continuous therapy, during exercise, or to relieve acute dyspnea Improves survival in COPD patients with severe hypoxemia (partial pressure of oxygen [pO2] < 55 mm Hg or oxygen saturation [sO2] <88%) (Strength of Recommendation [SOR]: A) When used for >15 hours daily Does not improve survival in patients with moderate Cranston, 2008 hypoxemia or desaturation at night GOLD, 2009
- 38. Annual flu vaccine Reduces risk of flu and its complications Pneumonia vaccine Reduces risk of common cause of pneumonia
- 39. G lobal Initiative for Chronic bstructive O ung L isease D November 19, 2006 World COPD Day, Kyoto Japan
- 40. Revised 2006 Definition, Classification Burden of COPD Risk factors Pathogenesis, pathology, pathophysiology Management Practical Considerations
- 41. THANK YOU
Notes de l'éditeur
- Environmental and genetic factors lead to atopic sensitization, which may be asymptomatic. Together with local tissue factors it can develop to clinical disease. The balance between these factors is responsible for the allergic phenotype
- Atopy involves the capacity to produce IgE in response to common environmental proteins such as house dustmite, grass pollen, and food allergens. From the Greek atopos meaning out of place. A hereditary disorder marked by the tendency to develop immediate allergic reactions to substances such as pollen, food, dander, and insect venoms and manifested by hay fever, asthma, or similar allergic conditions. Also called atopic allergy. Atopy involves the capacity to produce IgE in response to common environmental proteins such as house dustmite, grass pollen, and food allergens. From the Greek atopos meaning out of place.
- This combination is available today in both metered dose and dry powder inhalers (Rotacaps). It is available in 3 different Rotacap strengths where the dose of formoterol remains constant but the budesonide dose varies according to the need (severity of asthma); i.e. 100, 200 and 400 mcg of budesonide in 3 different Rotacaps.
- One theory that might explain why we seem to be more vulnerable than ever to allergic disease is called the hygiene hypothesis. We’re all born with an abundance of TH2 immune cells designed to fight internal parasites. Exposure to infections triggers the development of TH1 immune cells, designed to fight bacteria and viruses, shown here on the left. Press space bar With no exposure to infections, the TH1 immune cells never take over, illustrated by the right arrow. Investigators theorize that with few parasites to conquer in the modernized West, TH2 immune cells might have turned on harmless allergens instead, resulting in more allergic disease. This hypothesis is based on studies showing lower asthma rates for children who live on farms, attend day care centers, have indoor pets or older siblings; all things that expose children to higher levels of bacteria and infection. Children who have delayed development of TH1 cells, possibly because they aren’t exposed to infections through contact with animals, dirt and other children, seem to have more allergies and might be more predisposed to asthma. Press space bar SOURCE: Busse WW, Lemanske RF. Advances in Immunology. NEJM. 2001 Feb; 344(5):350-362.
- So who can be helped by this treatment? Patients diagnosed with allergic asthma. Patients with allergies such as hay fever. Patients diagnosed with sinusitis that predisposes them to asthma. Patients diagnosed with an allergy to insect stings. Press space bar
- When used for more than 15 hours per day in patients with severe COPD (pO2 < 60 mm Hg), oxygen has been shown to increase survival. It doesn’t improve survival in patients with only moderate COPD or nocturnal desaturation only. Benefits on quality of life are unclear, but oxygen may improve general alertness and psychological state in some patients. Oxygen therapy can be used as long-term with continuous delivery, only during exercise, or to relieve acute dyspnea. GOLD, 2009; Rabe, 2007; Cranston, 2008