SMALL GROUP DISCUSSION (1).pptxppt..,...

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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`

10. 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

11. EMPHYSEMA

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

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

14. 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

15. 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

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

17. 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

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

19. 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

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

21. 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

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

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

24. Pathogenesis TH2 cell mediated

25. 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]

26. 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

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

28. 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

29. 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.

30. 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

31. 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