SPECIAL SELECTED TOPICS- RESPIRATORY SYSTEM DISORDERS-SSTRSDO-QAA 009

1. Define bronchial asthma and status asthmaticus.

Bronchial asthma is a chronic inflammatory disorder of the airways characterized by reversible bronchoconstriction, airway hyperresponsiveness, and increased mucus production.

Airflow obstruction is usually episodic and reversible either spontaneously or with treatment. Patients present with recurrent wheezing, cough, chest tightness, and breathlessness. Inflammation involves eosinophils, mast cells, lymphocytes, and airway epithelium.

Status asthmaticus is a severe, prolonged asthma attack that does not respond adequately to standard bronchodilator therapy. It causes persistent bronchospasm and severe airflow obstruction.

Patients develop profound hypoxemia and respiratory distress. Carbon dioxide retention indicates impending respiratory failure. Status asthmaticus is a medical emergency requiring immediate intensive treatment.

2. What are the main differences between extrinsic and intrinsic asthma?

Extrinsic asthma, also called atopic asthma, is mediated by IgE-dependent hypersensitivity reactions to environmental allergens. It commonly begins during childhood and is often associated with a personal or family history of allergy. Common allergens include pollen, dust mites, animal dander, and foods.

Intrinsic asthma is not associated with specific allergens or IgE-mediated reactions. It usually develops in adults after respiratory infections, stress, exercise, cold air, or exposure to irritants.

Skin allergy tests are positive in extrinsic asthma but usually negative in intrinsic asthma. Serum IgE levels are elevated in atopic asthma.

Both forms produce reversible airway obstruction and similar pathological changes. Clinical management is largely similar despite different initiating mechanisms.

3. What is the pathogenesis of atopic asthma?

Atopic asthma begins with sensitization to inhaled allergens in genetically susceptible individuals. Allergen exposure stimulates helper T lymphocytes to promote IgE production by B cells. IgE binds to mast cells present in the airway mucosa.

Re-exposure to the allergen causes cross-linking of IgE and mast cell degranulation. Histamine, leukotrienes, prostaglandins, and other mediators produce immediate bronchoconstriction. These mediators also increase vascular permeability and mucus secretion.

Eosinophils are recruited and release toxic proteins that damage airway epithelium. Chronic inflammation leads to airway remodeling with smooth muscle hypertrophy and subepithelial fibrosis.

Airway hyperresponsiveness persists even between acute attacks. The result is recurrent episodes of reversible airflow obstruction.

4. Describe the main differences between the acute and late-phase reactions in patients with bronchial asthma.

The acute phase begins within minutes after allergen exposure and is mediated primarily by mast cell degranulation. Histamine, leukotrienes, and prostaglandins cause immediate bronchospasm, edema, and mucus secretion.

Symptoms include sudden wheezing, cough, and breathlessness. The late-phase reaction develops approximately 4–8 hours later. It is characterized by infiltration of eosinophils, neutrophils, lymphocytes, and macrophages into the airway wall.

 These inflammatory cells release cytokines and toxic proteins that sustain airway inflammation. Airway edema and epithelial damage become more pronounced. Bronchial hyperresponsiveness increases during the late phase.

Repeated late-phase reactions contribute to chronic airway remodeling and persistent asthma.

5. What are the major mediators responsible for bronchospasm in patients with bronchial asthma?

Histamine released from mast cells is an important early mediator causing bronchoconstriction. Leukotrienes C4, D4, and E4 are among the most potent bronchoconstrictors and also increase vascular permeability. Prostaglandin D2 contributes to bronchospasm and vasodilation. Platelet-activating factor promotes inflammation and airway narrowing.

Cytokines such as IL-4, IL-5, and IL-13 stimulate IgE production and eosinophilic inflammation. Eosinophils release major basic protein and eosinophil cationic protein, damaging airway epithelium. Chemokines recruit additional inflammatory cells into the bronchi.

Acetylcholine released through parasympathetic pathways further enhances bronchoconstriction. Together these mediators produce airway hyperresponsiveness and recurrent asthma attacks.

6. What are the main pathologic characteristics of bronchial asthma?

The lungs are usually overexpanded because of air trapping during acute attacks. Bronchi and bronchioles are obstructed by thick mucus plugs. Mucus plugs contain Curschmann spirals and Charcot-Leyden crystals derived from eosinophils.

The bronchial mucosa is edematous and infiltrated by eosinophils, mast cells, and lymphocytes. Goblet cell hyperplasia causes excessive mucus production. The basement membrane becomes thickened because of subepithelial fibrosis. Smooth muscle hypertrophy contributes to airway narrowing.

Chronic inflammation produces airway remodelling and persistent hyperresponsiveness. Although airflow obstruction is usually reversible, long-standing disease may lead to partially irreversible changes.

These pathological findings explain the recurrent episodes of wheezing and dyspnea.

7. Discuss the clinical characteristics and prognosis of patients with bronchial asthma.

Bronchial asthma presents with recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night or early morning. Symptoms are often triggered by allergens, exercise, infections, cold air, or irritants. Airflow obstruction is usually reversible with bronchodilator therapy. Pulmonary function tests demonstrate variable airflow limitation.

Most patients achieve good symptom control with inhaled corticosteroids and bronchodilators. Acute severe attacks may progress to status asthmaticus requiring emergency treatment. Repeated uncontrolled attacks can lead to airway remodeling and persistent airflow limitation.

Mortality is low with appropriate management but increases in severe uncontrolled asthma. Avoidance of triggers and adherence to long-term therapy significantly improve prognosis.

Early diagnosis and regular follow-up help maintain normal lung function and quality of life.

---

DR.C.GANESAN M.D

PROFESSOR OF MEDICINE