Respiratory Medicine: Asthma and COPD

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Respiratory Medicine: Asthma and COPD Dr Rickbir Singh Randhawa FY1

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Respiratory Medicine: Asthma and COPD. Dr Rickbir Singh Randhawa FY1. Definition: Asthma. Chronic inflammatory airway disease characterised by reversible airway obstruction , airway hyper-responsiveness and bronchial inflammation. Three factors contribute to reversible airway narrowing: - PowerPoint PPT Presentation

Transcript of Respiratory Medicine: Asthma and COPD

Respiratory Medicine: Asthma and COPD

Respiratory Medicine:Asthma and COPDDr Rickbir Singh RandhawaFY1Definition:AsthmaChronic inflammatory airway disease characterised by reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation. Three factors contribute to reversible airway narrowing:1. Bronchial smooth muscle contraction triggered by a variety of stimuli2. Mucosal swelling/inflammation caused by mast cell and basophil degranulation- release of inflammatory mediators3. Increased mucus production Definition:COPDChronic progressive lung disorder characterized by airway obstruction with little or no reversibility. It includes the following:Emphysema: defined histologically as permanent destructive enlargement of air spaces distal to the terminal bronchiolesChronic Bronchitis: defined clinically as a chronic cough with sputum production on most days for 3 months per year over 2 successive years.AetiologyAsthmaGenetic factors-+VE family Hx, atopic (eczema, allergic rhinitis), linkages to multiple chromosomal locations genetic heterogeneityEnvironmental triggers-Allergens (House dust mite, pollen, pets (fur)), cigarette smoke, viral URTI, occupational allergens (isocyanates-spray paints, epoxy resins-adhesives/fibreglass fabrics)

PathophysiologyAsthmaType 1 hypersensitivity reaction in atopic asthmaEarly phase (up to 1 hour) After exposure to inhaled allergen in a presensitized individual results in cross linking of IgE antibodies on the surface of mast cells. Release of inflammatory mediators-bronchial smooth muscle contraction (bronchoconstriction), mucous hyper secretion and airway oedema and obstruction. Late phase (after 6-12 hours)Recruitment of eosinophils, basophils,neutrophils and Th2 lymphocytes results in the perpetuation of the airway inflammation and bronchial hyper-responsiveness.

Aetiology/Risk factorsCOPDBronchial and alveolar damage due to environmental toxins- smoking (cigarette smoke)Indoor air pollution (such as solid fuel used for cooking and heating)Outdoor air pollutionOccupational dusts and chemicals (vapours, irritants, and fumes)Frequent lower respiratory infections during childhood.Rare cause is 1-antitrypsin deficiency (35 years (Rare cause is 1-antitrypsin deficiency (50-75% of best or predictedNo features of severe asthmaSevere exacerbation:Unable to complete sentences in one breathPEF 33-50% of best or predictedRR 25/minHR 110/min

Severity of AsthmaLife threatening attack: Any ofPEF