Hypersensitive pulmonary diseases. Bronchial asthma. Eosinophilic pneumonia. Allergic granulomatosis (Churg-Strauss syndrome)
Asthma
Asthma is a chronic inflammatory bronchial disease characterised by reversible obstruction of the airway. It causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, often at night or early morning. It is a hypersensitive disorder, where inflammatory cells over react to antigens such as house dust mites (dust), irritants such as smoke, stress or exercise.
Asthma can be atopic (allergen sensitization, often with eczema, allergic rhinitis etc) and nonatopic, although bronchospasm can be caused by any of the antigens above, atopic types tend towards type 1 hypersensitivity reactions (re-exposure reaction with Ig E antibodies).
Pathogenesis
- Inflammation involves many cell types and inflammatory mediators but helper T (type 2) cells are of critical importance
- The atopic type sees an overaction of TH2 cells against environmental antigens, which triggers a chain reaction stimulating B cells to produce Ig E antibodies, this in turn triggers bronchoconstriction and increased mucus production.
- Atopic Asthma has a significant genetic component, as well as environmental (60% genetic link)
- Non-atopic asthma does not have evidence of allergen sensitization and a FH is less prevalent, generally respiratory infections due to viruses and inhaled air pollutions are the culprits.
Pathology
- Bronchi show edema, hyperemia of mucosa and infiltration of mucosa by mast cells, eosinophils and lymphocytes (TH2).
- Airway is thickened by deposition of type III and type V collagen below basement membrane in chronic cases, this causes bronchial airway remodelling
H&E, asthma: mucus plug in a bronchus packed with eosinophils; the slender pink needle-shaped structures are Charcot-Leyden crystals.
Image: “Charcot-Leyden crystals in airway- Asthma” by Yale Rosen, CC BY-SA 2.0, via Wikimedia Commons.
Remember: classic findings in asthmatic airways and sputum: Curschmann spirals (whorled mucus plugs containing shed epithelium), Charcot-Leyden crystals (crystallised galectin-10 from eosinophils) and numerous eosinophils. Remodelling also includes goblet cell hyperplasia, enlarged submucosal glands and hypertrophy of bronchial smooth muscle.
Treatment:
- Two aspects, control of symptoms (rescue treatments) and prevention of exacerbations.
- Rescue treatments - taken as required in flare up
- Beta adrenergic agents
- E.g. albuterol
- Anticholinergics
- E.g. Ipratropium bromide
- Controller treatments - taken daily to prevent flare ups
- Inhaled corticosteroids
- E.g. beclomethasone, budesonide, fluticasone
- Antileukotrienes
- Long acting beta-agonists
- Theophylline
- Systemic corticosteroids
- Monoclonal antibody treatment
Treatment for Status Asthmaticus goes beyond the scope of this document, see Internal Medicine: Pulmonology