Chronic Obstructive Airways Disease (COAD) Flashcards
Define Chronic Obstructive Airways Disease (COAD) and name its two primary pathological mechanisms.
✅ Answer: COAD is defined by expiratory airflow obstruction, with two main mechanisms:
Reduced functional airway diameter (e.g., Asthma, Chronic Bronchitis)
Reduced elasticity of parenchyma (e.g., Emphysema)
Name three conditions classified under COAD and specify their primary mechanism of obstruction.
Disease Mechanism
Asthma = Reduced airway diameter (bronchospasm, mucus)
Chronic Bronchitis = Reduced airway diameter (mucus, inflammation)
Emphysema = Reduced elasticity (alveolar wall destruction)
Describe the immunological process leading to atopic asthma.
✅ Answer:
Allergen exposure → Dendritic cells present antigen to Th2 cells
Th2 cells release IL-4, IL-5, IL-13
IL-4 stimulates B cells → IgE
IgE binds FcεRI on mast cells
IL-5 recruits eosinophils
Upon re-exposure → Mast cell degranulation, histamine release → bronchospasm, mucus, inflammation
What histopathological changes are observed in asthmatic bronchioles?
✅ Answer:
↑ Goblet cells and submucosal gland hypertrophy → excess mucus
Thickened basement membrane (epithelial turnover)
Eosinophilic infiltration
Smooth muscle hypertrophy and hyperplasia
Edema and mucus plugging
What causes wheezing in asthma?
✅ Answer: Wheezing is due to bronchospasm and airflow turbulence as air moves past narrowed and mucus-filled airways, especially during expiration.
What structural change defines emphysema?
✅ Answer: Abnormal enlargement of airspaces distal to terminal bronchioles due to destruction of alveolar walls, resulting in:
↓ Surface area for gas exchange
↓ Elastic recoil → airway collapse during expiration
Explain how smoking contributes to the pathogenesis of emphysema.
✅ Answer:
Smoking → ↑ recruitment of neutrophils and macrophages
These cells release elastase and collagenase
If α1-antitrypsin (protease inhibitor) is deficient or inhibited (by smoking), unchecked elastin degradation occurs → alveolar destruction
What are the clinical consequences of alveolar wall loss in emphysema?
✅ Answer:
↓ Gas exchange surface → hypoxia
Loss of capillaries → ↑ pulmonary resistance → right heart hypertrophy (cor pulmonale)
↓ Elastic recoil → air trapping and wheezing
How is chronic bronchitis clinically defined?
✅ Answer: A productive cough lasting ≥3 months per year for at least 2 consecutive years, often associated with infection and smoking.
Describe the histological features of chronic bronchitis.
✅ Answer:
↑ Goblet cells (metaplasia)
↑ Submucosal gland size (↑ Reid Index > 0.4)
Thickened basement membrane
Squamous metaplasia
Neutrophilic infiltration
Engorged blood vessels
Ciliary loss → impaired mucociliary clearance
What is the Reid Index and its diagnostic threshold?
✅ Answer: The Reid Index = thickness of submucosal glands / distance from epithelium to cartilage.
A value >0.4 suggests chronic bronchitis.
Compare asthma, emphysema, and chronic bronchitis based on cause and immune involvement.
Trigger, Immunity and key pathology Asthma: Allergen (Atopic) Type I hypersensitivity and Bronchospasm, mucus
Emphysema: Smoking, Protease imbalance, Alveolar wall loss
Chronic Bronchitis: Smoking / infection, Neutrophil-dominated inflammation, Mucus hypersecretion
What complications can arise from chronic COAD?
✅ Answer:
Pulmonary hypertension
Cor pulmonale (right heart failure)
Squamous cell carcinoma (due to metaplasia)
Recurrent infections
