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What is Bronchial Asthma?

Bronchial asthma is a chronic relapsing inflammatory disorder of the airways characterized by paroxysmal reversible bronchospasm due to smooth muscle hypersensitivity or hyperactivity. There is increased high responsiveness of the tracheobronchial tree to various stimuli.

The major hallmarks of the disease are:

  • Increased airway responsiveness to a variety of stimuli, resulting in episodic bronchoconstriction or spasm.
  • Inflammation of the bronchial walls.
  • Increased mucus production.

Clinical manifestations

  • Episodic expiratory wheezing.
  • Nocturnal cough.
  • Increased anteroposterior diameter of the chest due to air trapping and residual volume.
  • The severe & constant form of the disease called status asthmaticus may be fatal.
    It affects all age groups people but nearly 50% of cases develop it before the age of 10 years.

Types of asthma:

  • Extrinsic asthma/atopic or allergic-type
  • Intrinsic (Non-atopic) asthma
  • Mixed type

Extrinsic asthma/atopic or allergic-type:

  • Immune-mediated disease
  • Most common type
  • It begins in childhood or early adult life.
  • A classic type I hypersensitivity (i.e., IgE mediated) caused this type of asthma.
  • Triggered by environmental antigens (for example, pollen, certain foods, etc.)
  • Most patients of this type have personal or family history of preceding allergic diseases such as rhinitis, urticaria, or infantile eczema.
  • Most of these allergens cause ill effects by inhalation like house dust, pollens, animal danders, molds, etc.
  • There is an increased level of IgE in the serum and positive skin test with inhaled antigen representing an IgE-mediated type I hypersensitivity reaction.

Intrinsic (Non-atopic) asthma

  • Non-immune type
  • It acts by stimulating the nerves of the airway passage.
  • This type of asthma mainly develops later in adult life with negative personal or family history of allergy, negative skin test, and normal serum levels of IgE.
  • It is associated with nasal polyp & chronic bronchitis.
  • Causative agents of intrinsic asthma are:
    • Aspirin
    • Pulmonary infections, Especially caused by viruses
      • Rhinovirus
      • Parainfluenza virus
      • Respiratory syncytial virus
    • Cold
    • Psychological stress
    • Exercise
    • Inhaled irritants (Cigarette smoke)
    • Ozone induced asthma

Mixed type

  • Many patients do not fit clearly into either of the above two categories and have mixed features of both.
  • Those patients who chance to develop asthma in early life have strong allergic components, while those who develop the disease late tend to be non-allergic.
  • Either type of Asthma can be precipitated by various stimuli such as cold, exercise, and emotional stress.

Pathogenesis

Extrinsic asthma (Atopic/Allergic type)

It is a Type I Hypersensitivity reaction with exposure to extrinsic allergens & develops in children with an atopic family history of allergies.

  1. Initial sensitization to an inhaled allergen
    • Stimulate induction of subset two helper T cells (CD4TH2) that release interleukin (IL)-4 and IL5.
    • Interleukin -4 (IL-4) stimulates isotype switching to IgE production.
    • Interleukin-5 (IL-5) stimulates the production and activation of eosinophils.
  2. Inhaled antigens cross-link IgE antibodies on mast cells on mucosal surfaces.
    • Release of histamine and other preformed mediators.
    • These mediators stimulate bronchoconstriction, mucus production, an influx of leukocytes.
  3. Late phase reaction (4-8 hours later)
    • Exotoxin produced which is Chemotactic for eosinophils and activates eosinophils.
    • Eosinophils release major basic protein (MBP) and cationic protein that damages epithelial cells and produce airway constriction.
  4. Other mediators involved in the pathogenesis
    • Leukotrienes LTC-D-E4 cause prolonged bronchoconstriction.
    • Acetylcholine causes airway muscle contraction.
  5. Genetic association of Asthma
    • Genetic associations have been made with:
      • Certain HLA alleles
      • Polymorphisms in IL-13, CD14, ADAM-33
      • Polymorphism in the beta two-adrenergic receptor, and the IL-4 receptor.

Morphology

Gross:

  • Lungs are overinflated with patchy atelectasis.
  • Mucus plugging of airways.
  • The cut surface shows characteristic occlusion of the bronchial area & bronchioles area by viscid mucus plugs.

Microscopy

  • There is submucosal glands hypertrophy as well as hypertrophy of the bronchial smooth muscle.
  • The bronchial wall shows thickened basement membrane of the bronchial epithelium, submucosal edema, and inflammatory infiltrate consisting of lymphocytes and plasma cells with a prominence of eosinophils.
  • Subepithelial fibrosis.
  • The mucus plugs contain normal or degenerated respiratory epithelium forming twisted strips called Curschmann‚Äôs spirals (Whorled mucus plugs).
  • The sputum generally contains numerous eosinophils cells & diamond-shaped crystals derived from eosinophils known as Charcot-Leyden crystals.

Laboratory findings

  • Pulmonary function test:
    • Initially develop respiratory alkalosis
    • Those patients work hard at air expelling through inflamed airways in the respiratory system.
    • It may progress (go forward) into respiratory acidosis if bronchospasm is not relieved.
  • FEV1 is the best measure of severity.
  • Others:
    • Eosinophilia, Positive skin test for allergens.

Status asthmaticus

  • Acute severe asthma (also referred to as status asthmaticus) is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and steroids.
  • Life-threatening condition.

Asthma PDF

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