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Bronchial Asthma

Bronchial Asthma. Nathir M Obeidat. Bronchial Asthma Definition. Bronchial asthma is a clinical syndrome characterised by recurrent episodes of airway obstruction , which resolve spontaneously or as a result of treatment.

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Bronchial Asthma

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  1. Bronchial Asthma Nathir M Obeidat

  2. Bronchial Asthma Definition Bronchial asthma is a clinical syndrome characterised by recurrent episodes of airway obstruction, which resolve spontaneously or as a result of treatment. The reversibility of the airway obstruction in asthma is the feature that distinguishes it from other forms of obstructive lung diseases.

  3. Definition of Bronchial Asthma • A chronic inflammatory disease of the airways in which many cells play a role, in particular, mast cells, eosinophils and T lymphocytes. • In susceptible individuals this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and or early morning. • These symptoms are associated with airflow limitation that is at least partially reversible either spontaneously or with treatment.

  4. Asthma Phenotypes

  5. Current Asthma Prevalence: United States, 2001-2010 Percent Total number of persons Year One in 12 people (about 26 million, or 8% of the U.S. population) had asthma in 2010, compared with 1 in 14 (about 20 million, or 7%) in 2001.

  6. Risk Factors for Developing Asthma Genetic characteristics Occupational exposures Environmental exposures

  7. Risk Factors for Developing Asthma: Genetic Characteristics Atopy The body’s predisposition to develop an antibody called immunoglobulin E (IgE) in response to exposure to environmental allergens Can be measured in the blood Includes allergic rhinitis, asthma, hay fever, and eczema

  8. Pathophysiology of Bronchial Asthma • It is a Complex interaction of cells and mediators, which lead to: 1- Inflammation 2- Bronchial hyperresponsiveness 3- Airflow limitation 4- Variability. 5- Reversibility

  9. Inflammation 1 • It is a result of interaction of Cellular changes which includes:1- Cells such as epithelial cells, mucous glands , endothelial cells andmyofibroblasts. 2- Resident cells such as bone marrow-derived mast cells and macrophages. 3- Infiltrating cells such as eosinophils, CD4 , neutrophils , basophilsand platelets.

  10. Inflammation 2 • The above cells will lead to generation of mediators that can induce bronchoconstriction. • These mediators includes histamine ,platelet activating factor, and some derivatives of arachidonic cascade such as PGD2 ,C4 ,D4, E4 (LTC4,LTD4 ,LE4). • Infiltration of airways by mast cells, eosinophils, activated T lymphocytes and neutrophils

  11. Inflammation 3 - Mast cells as aresult of IgE – Mediated stimulation also release mediators - Cytokines most of which are product of lymphocytes and macrophages - Edema of the airway mucosa is due to inflammation and increased capillary permeability.

  12. Inflammation 4 • Death from severe asthma usually occurs from blockage of airways by mucous plugging. • The presence of mucous plug is associated with hyperplasia and metaplasia of goblet cells

  13. Airway Hyper responsiveness - It is an exaggerated bronchoconstrictive response by the airways to a variety of stimuli such as histamine , methacholine ,cold air ,and environmental irritants. - It is not known whether bronchial hyperreacyivity ( BHR) is acquired or is present at birth. - it is thought that inflammation is the stimulus for BHR - The degree of BHR usually correlates with the clinical severity of asthma

  14. AIRWAY OBSTRUCTIONCauses - Acute bronchoconstriction - Mucous plugging of airways - Bronchial wall edema - Inflammatory cell infiltration - Airway wall remodeling - Smooth muscle hypertrophy

  15. Airflow limitation • Defined as FEV1/FVC <75%. • During remission this can be normal. • Age Dependent. • Needs spirometry for assement of severity of the disease.

  16. ATOPY • Defined as genetic susceptibility for developing immunoglobilinIgE directed to epitopes expressed on common environmental allergens such as dust mites , animal proteins, pollens, and fungi. • Atopic asthma has seasonal variation and avoidance of the offending antigens may result in dramatic improvement. • Atopy manifests as allergic asthma, allergic rhinitis , allergic sinusitis with eosinophilia and high serum IgE level

  17. Variability • Defined as a diurnal variation of PEEFR of 20%. • This is diagnostic for asthma. • The degree of variability is proportional to the severity of asthma. • A high degree of variability signals unstable asthma that demands increased medications

  18. Cost of asthma Direct Medical Care • Hospital stay • Intensive care • Emergency department • Primary care • Medications Indirect Costs • Social security • Loss of work output • Loss of school days • Impact on individual / family / society GINA Guidelines 2010

  19. Diagnosis • History • Physical Examination • PFT - Vitalogram - Spirometry - FVL - Lung Volumes - DLCO - PFM - ABG

  20. Diagnosis • CXR • IgE Level and Eosinophills

  21. FVL Location of the changes : - Above the line (Expiratory Arm) Or - Below the line (Inspiratory arm) Shape of the Loop

  22. SPIROMETRY  Volume-time tracing. Flow-volume tracing.

  23. Asthma: Treatment options & guidelines

  24. Goals of Treatment of Asthma • In spite of Immunotherapy, No real hope for cure of Bronchial Asthma. But • Treatment can achieve Asthma control and decrease exacerbations.

  25. Treatment objectives • No asthma attacks • No emergency visits • Minimal need for quick relief (as needed) ß2-agonist • Maintain normal physical activity including exercNo chronic symptoms ise • Maintain lung function as close to normal as possible • Minimal (or no) adverse effects from medicine GINA Guidelines 2010

  26. Domains of Asthma Control Impairment of Function : 1-Subjective Impairment: - Frequency and intensity of symptoms. - Limitations of daily activities. 2- Objective Impairment: - Variations and Severity of Impairment of lung function. Future risk: - Likelihood of exacerbations. - Progressive loss of lung function. - Adverse effects from medications.

  27. Control of airway inflammation BMJ. 2006 Apr 1; 332(7544): 767–771

  28. Is the Pathophysiological impact of Asthma limited to the Large Airways? Asthma Control Assessment Uncontrolled Poor Adherence Incorrect Diagnosis Incorrect Inhaler Technique Inadequate Treatment • Large vs Small Airway • Role of Small Airway Disease • Phenotypes Adapted from Haughney J, Price D, Kaplan A, et al.. Respir Med. 2008;102(12):1681-93.

  29. Pharmacological therapy Relievers • Inhaled fast-acting 2-agonists : • Albuterol • Fenoterol • Inhaled anticholinergics • Ipratropium bromide Controllers • Inhaled corticosteroids • Inhaled long-acting 2-agonists • Inhaled cromones • Oral anti-leukotrienes • Oral theophyllines • Oral corticosteroids

  30. The choice of treatment should be guided by: • Level of asthma control • Current treatment • Pharmacological properties and availability of the various forms of asthma treatment • Economic considerations Cultural preferences and differing health care systems need to be considered

  31. LEVEL OF CONTROL TREATMENT OF ACTION REDUCE maintain and find lowest controlling step controlled consider stepping up to gain control partly controlled uncontrolled step up until controlled INCREASE exacerbation treat as exacerbation REDUCE INCREASE TREATMENT STEPS STEP 1 STEP 2 STEP 3 STEP 4 STEP 5

  32. Beta 2-Adrenoceptor agonists are the most powerful known bronchodilators and play a pivotal role in every step of this algorithm. Hanania N. Current Opinion in Pulmonary Medicine 2010,

  33. Review Response and Adjusting the Dose 2-4 weeks after starting controller therapy. 1-3 months regular visit. 4-6 weeks regular visit in Pregnancy. within 1 week after exacerbation. The frequency of visits depends on: 1. Initial levelof control 2. previous response to treatment. 3. His ability and willingness to be engaged in self – management plan.

  34. Stepping Up Treatment Sustained step up every 2-3 months If symptoms persists or exacerbation in spite of 2-3 months controller therapy. Before stepping up consider: Incorrect Inhaler Technique Adherence Modified risk ( Smoking) Symptoms of comorbid condition(AR,GERD)

  35. Day to Day Adjustment By The Patient’s himself. Smart Symbicort.

  36. Stepping Down Approach When Asthma is controlled Well. Asthma controlled achieved for 3 months. You aim to find the lowest dose of treatment that maintain: symptoms free no exacerbation minimize side effects.

  37. Step down Technique Appropriate Timing ( no infection ,no travell no Pregnancy). Document the baseline , symptoms and PFT. Reduce ICS dose by 20-50% EVRY 2-3 months

  38. Treating Modifiable Risk Factoers Decrease Exacerbation Risk by optimizing medications. Self monitoring of symptoms and by using PEF. Avoid Tobacco smoke Exposure. Confirmed Food Allergy: Avoidance and availability of Epinephrine. For Severe Asthma : Refer to especial centre.

  39. Asthma Exacerbation • Exacerbations of asthma are episodes of progressive increase in shortness of breath, cough, wheezing, or chest tightness • Exacerbations are characterized by decreases in expiratory airflow that can be quantified and monitored by measurement of lung function (FEV1 or PEF) • Severe exacerbations are potentially life-threatening and treatment requires close supervision

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