Pathophysiology of asthma

Introduction, aetiology, pathophysiology of Bronchial asthma

1. Patho -physiology of Asthma

2. Asthma Bronchial asthma is chronic respiratory condition associated with inflammation of the airway wall. Associated with Hyper-responsiveness of tracheo -bronchial smooth muscles to a variety of stimuli/ Triggering factors. Intermittent Symptomatic episodes of Dyspnoea (shortness of breath) Wheezing (additional sound) Cough (persistent) Chest tightness Additionally: limitation of activity

3. Etiology/ Triggering factors Tobacco smoke Infections such as colds, flu, or pneumonia Allergens such as food, pollen, mold, dust mites, and pet dander Exercise Air pollution and toxins Weather, especially extreme changes in temperature Drugs (such as aspirin, NSAID, and beta-blockers) Food additives Emotional stress and anxiety Singing, laughing, or crying Smoking, perfumes, or sprays Acid reflux

4. Types of Asthma Extrinsic (atopic, allergic) Allergens: food, pollen, dust, etc. History of ` atopy ` in childhood Family history of allergies Positive skin test Raised IgE level Below 30 years of age Less prone to status asthmaticus Intrinsic (non-atopic) Initiated by infections, drugs, pollutants, chemical irritants No family history of allergy Negative skin test No rise in IgE level Middle age onset Prone to status asthmaticus

5. Pathogenesis Airflow limitation in asthma is recurrent and caused by a variety of changes in the airway: Airway inflammation (Mast cell degranulation , eosinophill infiltration ) Bronchoconstriction (tightening of muscles) Airway edema (Mucous hypersecretion ; Mucus plug formation) Bronchial hyperresponsiveness to various stimulii Airway remodelling (thickening of the sub-basement membrane, subepithelial fibrosis, airway smooth muscle hypertrophy and hyperplasia , angiogenesis and vasodilation , and mucous gland hyperplasia and hypersecretion ) Airflow obstruction (narrowing of air passage)

6. Inflammatory cells Lymphocytes : T-helper 2 cells (Th2 cells), activates eosinophillic inflammation by releasing cytokines(IL-4, IL-5 and IL-3) leads to: Eosinophill infiltration, Ig E overproduction, development of bronchial hyperresponsiveness . Mast cells: releases bronchoconstrictor mediators (histamine, cysteinyl-leukotrienes , prostaglandin D 2 ) Eosinophils : generates inflammatory enzymes and leukotrienes , most cases of asthma linked with increased number of eosinophills . Dendritic cells: These cells function as key antigen-presenting cells that interact with allergens from the airway surface and then stimulate Th2 cell production from naïve T cells Macrophages: Macrophages are the most numerous cells in the airways Neutrophils : Neutrophils are increased in the airways and sputum of persons who have severe asthma

7. Transverse section

8. Airway Narrowing Symptoms: Cough Dyspnoea (breathlessness) Wheezing Tightness of chest

9. Morphology Bronchial obstruction with overinflation Small areas of atelectasis (collapse) may be seen Inflammation & thickening of mucosa. Bronchial wall smooth muscle hypertrophy Thickening of bronchial basement membrane. Mucus plugging of bronchi Curschmann spirals : whorls of shed epithelium within mucus plugs Charcot-Leyden crystals : Within aggregates of eosinophils ;crystalloids of galectin-10 Lung Hyperinflation

10. Histological findings in Sputum

11. Summary

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