1. Diseases of the Respiratory System Lu hua Dept. of Pathology Three Gorges University Medical College

2. Chronic Obstructive Pulmonary Disease （ COPD ） Pulmonary Infections Chronic bronchitis Bronchiectasis Emphysema Asthma P neumonia Lung Abscess Tuberculosis Pneumoconiosis Pulmonary tumors

3. The normal structure and function of Respiratory system The normal structure of Respiratory system includes nasopharynx, trachea and lungs.

4. The normal structure and function of Respiratory system The air passages portion Nasal cavity Pharynx Larynx Trachea Bronchia Small Bronchia Bronchiole No gas exchange function Keep airway unobstructed and purification of air inhaled

5. The respiratory portion Respiratory bronchiole Alveolar ducts Alveolar sac Pulmonary alveoli Arterial gas exchange

6. The normal structure and function of trachea and bronchia Mucosa Submucosa ----mucous glands----Secrete mucus Adventitia ---- hyaline cartilage ---- Keep elastic Pseudostratified ciliated columnar epithelium Goblet cell Elastic fibers Lymphoid tissue Cilium swings Secrete mucus Keep elastic Immunologic function

7. Function of Mucous--cilia system: Waterproof effect, can reduce moisture loss of respiratory tract. Constitutes a physical barrier between the irritants inhaled and mucosal cells. Foreign bodys can be adhered to mucus and pushed out the respiratory tract by cilium swings.

8. Pseudostratified ciliated columnar epithelium Elastic fibers Mucous glands Cartilage Smooth muscle

9. Bronchial epithelium Pseudostratified ciliated columnar epithelium

10. Electron microscope Goblet cell Cilium

11. Bronchial Submucosal Glands

12. Bronchia

13. Small Bronchia Cartilage

14. Bronchiole

15. The respiratory portion Distribution of the ending branches of pulmonary arteriole are all in the alveolar septum.

16. Pulmonary alveoli Arterial gas exchange Venous blood change to arterial blood

17. Chronic obstructive pulmonary disease, COPD COPD refers to a group of conditions that share a major symptom - dyspnea - and are accompanied by chronic obstruction to air flow within the lungs. These conditions-emphysema, chronic bronchitis, asthma and bronchiectasis -have distinct anatomic and clinical characteristics.

18. Chronic bronchitis

19. 一、 Chronic bronchitis Chronic bronchitis is a specific clinical name instead of referring to bronchial chronic inflammation. Chronic bronchitis is defined by Medical Research Council of England in 1965. It is present in any patient who has persistent cough with sputum production for at least 3 months in at least 2 consecutive years, in the absence of any other identifiable cause.

20. Pathogenesis 1.Smoking: The most commonly indentified factor implicated in causation of Chronic bronchitis. Morbidity: smoker/non-smoker=4-10 It impairs ciliary movement. It inhibits the function of alveolar macrophages (Phagocytosis ). It leads to hypertrophy and hyperplasia of mucus-secreting glands. It causes considerable obstruction of small airways. It stimulates the vagus and causes bronchoconstriction.

21. 2.Atmospheric pollution 3.Occupation 4.Infection:The role of infection appears to be secondary. It is not responsible for the initiation of chronic bronchitis but is probably significant in maintaining it and may be critical in producing acute exacerbations. It interferes with ciliary action of the respiratory epithelium, it may cause direct damage to airway epithelium, and it inhibits the ability of bronchial and alveolar leukocytes to clear bacteria. Viral infections can also cause exacerbations of chronic bronchitis. 5.Familial and genetic factors

22. Morphology: Chronic nonspecific inflammation 1. Damage of Mucous--cilia system : Ciliated columnar epithelium cells exhibit degeneration, necrosis, hyperplasia, regeneration, and even squamous metaplasia. Cilia exhibit adhesion, shorter, curly, broken or even fall off. Goblet cells proliferate and secrete exuberant.

23. 2. Hypertrophy and hyperplasia of Glands: Reid index :The ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage. The Reid index (normally 0.4) is increased in chronic bronchitis(0.55-0.79), usually in proportion to the severity and duration of the disease.

24. inner perichondrium basal lamina Chronic bronchitisNormal bronchus

25. 3. Inflammation of the bronchial wall: Congestion and infiltration of lymphocytes and plasma cells. Cartilage exhibit degeneration, atrophy and even calcification. Smooth muscle exhibit atrophy and fracture. Spread around to the closely tissue.

26. Hyperplasia of Mucus glands Normal

27. Squamous metaplasia

28. luminal and mucus chronic inflammation

29. Chronic bronchitis (degeneration, necrosis of the bronchial epithelium with loss of ciliated cells)

31. Clinical Features 1.Cough and sputum: Caused by the hypertrophy and hyperplasia of glands and proliferation of goblet cells. White frothy sputum. It can be converted into yellow purulent or yellow-green sputum. 2. wheeze Bronchospasm Edema of Bronchial mucosa leads to the thickness of wall increased. Sputum block the airway.

32. Complication: Bronchiectasis Emphysema Pulmonary heart disease Bronchial pneumonia

33. Bronchiectasis

34. 2.Bronchiectasis Bronchiectasis is a disease characterized by permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue, resulting from or associated with chronic necrotizing infections. The most characteristic clinical manifestation of bronchiectasis is persistent cough with expectoration of copious amounts of foul-smelling, purulent sputum. Post–infectious cases commonly develop in childhood and in early adult life.

35. Etiology and Pathogenesis Endobronchial obstruction and infection are the major influences associated with bronchiectasis. 1.Hereditary and congenital factors Congenital bronchiectasis caused by developmental defect of the bronchial system. Cystic fibrosis Hereditary immune deficiency diseases are often associated with high incidence of bronchiectasis. Primary ciliary dyskinesia Atopic bronchial asthma

36. Cystic fibrosis ----The primary defect in chloride transport leads to impaired secretion of chloride ions into mucus, low sodium and water content, defective mucociliary action, and accumulation of thick viscid secretions that obstruct the airways. This leads to a marked susceptibility to bacterial infections, which further damage the airways. With repeated infections, there is widespread damage to airway walls, with destruction of supporting smooth muscle and elastic tissue, fibrosis, and further dilatation of bronchi. The smaller bronchioles become progressively obliterated owing to fibrosis.

37. 2.Obstruction----by mucus impaction, tumors, or foreign bodies. Normal clearing mechanisms are impaired, there is pooling of secretions distal to the obstruction. 3.As secondary complication Necrotising pneumonias such as in staphylococcal suppurative pneumonias and tuberculosis may develop bronchiectasis as a complication. Endobronchial obstruction and severe infections of the bronchi lead to inflammation, often with necrosis, fibrosis, and eventually dilatation of airways.

38. Morphology The airways are dilated, sometimes up to four times normal size. Cylindrical bronchiectasis ----These dilations produce long, tubelike enlargements Saccular bronchiectasis ----These dilations cause fusiform or even sharply saccular distention. On the cut surface of the lung, the transected dilated bronchi appear as cysts filled with mucopurulent secretions.

39. Cut surface of lung shows markedly distended peripheral bronchi filled with mucopurulent secretions.

41. The bronchi are extensively dilated nearly to the pleura, there walls are thickened.

42. Desquamation of the lining epithelium and extensive areas of necrotizing ulceration. There may be hyperplasia of the columnar cells or squamous metaplasia of the remaining epithelium. In some instances, the necrosis completely destroys the bronchial or bronchiolar walls. Fibrosis of the bronchial and bronchiolar walls and peribronchiolar fibrosis develop in the more chronic cases, leading to varying degrees of subtotal or total obliteration of bronchiolar lumina Infiltrated by acute and chronic inflammatory cells.

43. Fibrosis of the bronchial and bronchiolar walls and peribronchiolar fibrosis. Exudate of muco-pus in the lumen (arrow).

44. Fibrosis of the bronchial and bronchiolar walls and peribronchiolar fibrosis.

45. Purulent exudation in the lumen Destruction of lining epithelium Scarring of the bronchial wall

46. Clinical features Bronchiectasis causes severe, persistent cough; expectoration of foul-smelling, sometimes bloody sputum; Dyspnea and orthopnea in severe cases; Occasional life-threatening hemoptysis. A systemic febrile reaction may occur when powerful pathogens are present. Cor pulmonale, metastatic brain abscesses, and amyloidosis are less frequent complications of bronchiectasis.