Bronchial asthma is an inflammatory disease\\r\\ncharacterized by an increase responsiveness of the\\r\\ntrachea and bronchi to various stimuli manifested by\\r\\na widespread narrowing of the airways that changes\\r\\nin severity either spontaneously or as a result of\\r\\ntherapy.1 Five characteristic structural alteration are\\r\\nusually observe in the preterminal and terminal\\r\\nbronchiole of fatal bronchial asthma. (a) Plugging of\\r\\nthe basophillic polysaccharide rich mucus blocking\\r\\nmany of the terminal bronchiole; (b) Goblet cells are\\r\\nincreased in size and number; (c) Marked thickening\\r\\nand irregularity of the basement membrane; (d)\\r\\nSmooth muscle of preterminal bronchiole are\\r\\nhypertrophied; (e) Inflammatory infiltrate composed\\r\\nof mononuclear cells, particularly eosinophillic\\r\\ngranulocytes is found in the submucosa and between\\r\\nthe hypertrophied muscle bundle.2\\r\\n
