The document discusses obstructive airway diseases, focusing on chronic obstructive pulmonary disease (COPD), asthma, and bronchiectasis, detailing their clinical presentations, pathogenesis, and morphology. It emphasizes the risk factors for COPD, such as smoking and environmental pollutants, as well as distinguishing features of emphysema and chronic bronchitis. Additionally, it outlines the mechanisms of asthma and bronchiectasis, including inflammation, mucus secretion, and infection-related causes.

1. SMALL GROUP DISCUSSION
OBSTRUCTIVE AIRWAY DISEASES

2. Obstructive lung diseases
• Chronic obstructive pulmonary disease
• Asthma
• Bronchiectasis

3. CASE 1
• 66 year old man with a smoking history of one pack per day for past
47 years presents with progressive shortness of breath and chronic
cough productive of yellowish sputum for the past 2 years. On
examination he appears cachectic and in moderate respiratory
distress and has pursed lip breathing. Lung examination reveals a
barrel chest and poor air entry bilaterally with moderate inspiratory
and expiratory wheezing

4. • Diagnosis ?
• Chronic obstructive pulmonary disease
• Risk factors?
• Smoking
• Poor lung development early in life
• Exposure to environmental and occupational pollutants
• Airway hyperresponsiveness
• genetic

5. • 2 major clinicopathological manifestations?
• Emphysema
• Chronic bronchitis

6. EMPHYSEMA
Irreversible enlargement of air
spaces distal to terminal bronchiole
accompanied by destruction of their
walls

7. TYPES ??
• Centriacinar
• Panacinar
• Paraseptal
• Irregular

8. Centriacinar emphysema
• Most common
• Central or proximal parts of the acini affected
• More common in Upper lobes-apical segment

9. Panacinar emphysema
• Associated with alpha 1 antitrypsin deficiency
• Uniformly enlarged from respiratory bronchiole to terminal alveoli
• More common in lower zones and in anterior margins`

11. Distal acinar emphysema
• Distal part of acini predominantly involved
• More severe in upper half
• Multiple enlarged airspaces <0.5 to >2 cm
Irregular emphysema
• Irregular involvement of acini
• Associated with scarring

12. EMPHYSEMA

14. Pathogenesis
• Toxic injury and inflammation
• Protease antiprotease imbalance
• Oxidative stress
• Infection

16. Morphology
• Voluminous lung overlapping heart anteriorly
• Large alveoli seen on cut surface of fixed lungs

17. Microscopy
• Abnormal large alveoli separated by thin septa with focal centriacinar
fibrosis
• Loss of attachment between alveoli and outerwall of small airways
• Decrease in capillary bed area

18. Chronic bronchitis
Persistent cough with sputum
production for atleast 3 months in at
least 2 consecutive years in the
absence of any other identifiable
cause

19. Pathogenesis
• Exposure to noxious or irritating inhaled substances
• Mucus hypersecretion-earliest feature-airway obstruction
• Acquired CFTR dysfunction
• Inflammation
• infection

20. Morphology
• Hyperemia,swelling, and edema of mucus membrane with excess
mucinous or mucopurulent secretions
Microscopy
• Chronic inflammation of airways
• Thickening of bronchiolar wall
• Deposition of extracellular matrix in the muscle layer
• Peribronchial fibrosis
• Goblet cell hyperplasia
• Enlargement of mucous secreting glands

21. Reid index
• Ratio of thickness of
mucous layer to the
thickness of wall between
epithelium and cartilage
• Increased in chronic
bronchitis

22. Clinical features
• Pink puffers- emphysema dominates
• Barrel chest
• Dyspnoea
• barrel chest
• Pursed lip
• Blue bloaters-pure chronic bronchitis
• Persistent productive cough
• Hypercapnia
• Hypoxemia
• Mild cyanosis

23. Treatment
• Smoking cessation
• Oxygen therapy
• Long acting bronchodilator
• Antibiotics
• Physical therapy
• Bullectomy

25. ASTHMA
• Chronic disorder of conducting airways caused by immunological
reaction, marked by episodic bronchoconstriction due to increased
airway sensitivity of stimuli
• Inflammation of bronchial walls
• Increased mucus secretion

26. Clinical features
Recurrent episodes of:
• Wheezing
• Breathlessness
• Chest tightness
• Cough
• At night/early morning
• Acute severe asthma [Status asthmaticus]

27. Atopic asthma
• Allergen sensitization
• IgE mediated
Non atopic asthma
• No evidence of allergen sensitization
• Virus- Rhinovirus, Parainfluenza , RSV
• Air pollutants

29. Pathogenesis
• TH2 cell mediated

31. Morphology
• Occlusion of bronchi, bronchioles – thick mucus plugs
• Curschmann spirals in sputm or bronchoalveolar lavage- mucus plugs
• Eosinophils and Charcot leyden crystals [composed of eosinophil
protein –Galactin 10]

33. Microscopy
Airway remodeling
• Thickening of airway wall
• Subbasement membrane
fibrosis – collagen I & III
• Increased vascularity
• Increase in size of submucosal
glands and number of airway
goblet cells
• Hypertrophy/hyperplasia of
bronchial muscle

34. BRONCHIECTASIS
• Destruction of smooth muscle and elastic tissue by chronic
necrotizing infections
• Lead to permanent dilation of bronchi & bronchioles

35. Causes
• Congenital or hereditary conditions -cystic fibrosis, intralobar
sequestration of the lung, immunodeficiency states, primary ciliary
dyskinesia, and Kartagener syndrome.
• Severe necrotizing pneumonia caused by bacteria, viruses, or fungi
• Bronchial obstruction, due to tumor, foreign body, or mucus
impaction
• Immune disorders, including rheumatoid arthritis, systemic lupus
erythematosus, inflammatory bowel disease, and the posttransplant
setting (chronic rejection after lung transplant)
• 50% of cases are Idiopathic

36. Pathogenesis
• Obstruction and infection are the major conditions associated with
bronchiectasis.
• Infections due to defect in airway clearance.
• Sometimes this defect stems from airway obstruction, leading to
distal pooling of secretions.

37. Morphology
• Bronchiectasis usually affects the lower lobes bilaterally
• Esp air passages that are vertical
• Most severe in the more distal bronchi and bronchioles
• The airways are dilated, sometimes up to four times normal size
• Cut surface of the lung, the dilated bronchi appear cystic and are
filled with mucopurulent secretions

39. • Acute and chronic inflammatory exudation within the walls of the
bronchi and bronchioles
• Desquamation of the lining epithelium and extensive ulceration
• There also may be squamous metaplasia
• Lung abscess
• Haemophilus influenzae
• Pseudomonas aeruginosa