PATHOGENESIS OF ASTHMA AND DISTIGUISHING ASTHMA FROM COPD: Asthma is a chronic disease charecterised by reversible expiratory airflow obstruction resulting from narrowing of the airways in response to various stimuli and a non specific hyperirritability of the Tracheobranchial tree. *COPD is charecterised by Mucous hypersecretion ,ciliary dysfunction,lung hyperinflation,and irreversible expiratory airflow obstruction. The underlying mechanism of both condition is thought to be CHRONIC AIRWAY INFLAMMATION. Bronchial biopsies of asthmetic reveal infiltration by inflammatory cells and epithelial shedding from the mucosa. *With Asthma, exposure to an initiating stimulus trigger inflammatory cells (Mast cells,Eosinophils, T lymphocytes, macrophages,Basophils,neutrophils and platelets)and structural cells (Epithelial cells,fibroblasts and airway smooth muscle cells) to release various mediators that lead to bronchospasm ,Vascular congestion,increased capillary permeability and thick tenacious secretions. The net result is a reduction in airway diameter ,an Increase in airway resistance, decreased force expiratory volumes and flow rates ,hyperinflation of lungs and thorax ,increased work of breathing,alternation in respiratory tract muscle function,mismatched ventilation /perfusion ,and altered blood gases. *IN COPD,Goblet cell hypertrophy, activated inflammatory cell (lymphocytes, neutrophils and macrophages )and alternation in function of structural cells leads to increased mucus production,airway fibrosis ,loss of alveolar attachments, and pulmonary vascular remodelling.The net result in hypersecretion of mucus ,emphysema with peripheral airway collapse, impaired gas exchange, Pulmonary hypertension and right ventricular dysfunction. The minority of COPD cases are a result of Genetic deficiency in antitrypsin level,leading to an imbalance between antiproteinases and increased lung parenchymal destruction.............................................................................................