chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough
triad of intermittent and reversible airway obstruction, chronic bronchial inflammation with eosinophils, and
bronchial smooth muscle cell hypertrophy and hyperreactivity
increase in airway responsiveness (bronchospasm)
Types:
extrinsic or atopic: due to IgE and TH2-mediated immune responses to environmental antigens
intrinsic or non-atopic: triggered by non-immune stimuli such as aspirin; viruses; cold; psychological stress; exercise; and inhaled irritants
Drug-Induced Asthma: eg aspirin, probably because it inhibits the cyclooxygenase pathway without affecting the lipoxygenase route
Occupational Asthma: eg, fumes (epoxy resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene)
Atopic Asthma- Pathogenesis:
Triggering factors: dusts, pollen, animal dander, and foods
Associated with other atopic manifestations like allergic rhinitis, urticaria, or eczema.
hypertrophy of bronchial smooth muscle and deposition of subepithelial collagen; aka airway remodeling
excessive TH2 reaction against environmental antigens.
Cytokines produced by TH2 cells account for most of the features of asthma-IL-4 stimulates IgE production, IL-5 activates eosinophils, and IL-13 stimulates mucus production
Atopic Asthma:
Acute attack consists of
immediate response: Exposure of IgE-coated mast cells to the same antigen causes cross-linking of IgE and release of mediators like Leukotrienes C4, D4,E4, Acetylcholine, Histamine, Prostaglandin D2: which cause bronchoconstriction, increase vascular permeability, and increase mucin secretion
late-phase reaction: Eosinophils are particularly important in the late phase, as they can amplify and sustain the inflammatory response without additional exposure to the triggering antigen by releasing different chemical mediators themselves
status asthmaticus:
may last for hours and even days
hypercapnia, acidosis, and severe hypoxia may be fatal
Maynot respond to bronchodilators
May need artificial ventilatory support under sedation and paralysis
Morphology:
lungs are overdistended because of overinflation, and there may be small areas of atelectasis
occlusion of bronchi and bronchioles by thick, tenacious mucus plugs
M/E:
whorls of shed epithelium (Curschmann spirals)
Numerous eosinophils
Charcot-Leyden crystals (made of eosinophil proteins)
Airway remodeling: includes:
thickening of the basement membrane
Edema and prominence of eosinophils and mast cells
increase in the size of the submucosal glands
Hypertrophy of the bronchial muscle walls.
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