1. Obstructive Lung Diseases
Dr. Raid Jastania

2. Respiratory System Components Upper Respiratory tract
Lower Respiratory tract
Lungs:
Airways
Interstitium
Blood vessels
Pleura

3. Atelectasis

5. Atelectasis (Collapse)
Atelectasis is loss of lung volume by decreased expansion of the airspaces
Types
Resorption atelectasis (obstruction)
Obstruction followed by resorption of air – collapse
Causes: Post operative, Asthma, Chronic bronchitis, aspiration of foreign body, tumor

6. Atelectasis (Collapse)
Types:
Compression Atelectasis:
Fluid, blood or air in the pleural cavity
Contraction Atelectasis:
Fibrosis of lung and pleura
Micro atelectasis:
Generalized loss of lung volume and expansion
Loss of surfactant

7. Clinical Correlation
25 year old man presented to the emergency room with sudden, severe dyspnea. He is previously healthy, and has no previous episode of dyspnea.
He also describes mild vague chest discomfort (pain) in the right side of the chest.
On examination: RR is 30/minute, he has deviated trachea to the left side, decrease breathing movement of the right side, decreased vocal tactile fremitus on the right side, hyper resonance percussion on the right side, and decreased breath sound on the right side.
X-ray shows air in the right chest with collapse of the right lung

8. Questions
What is the differential diagnosis of lung collapse (atelectasis)?
What is diagnosis in this young man?
How do you manage his case?

9. Obstructive and Restrictive Lung Disease
Obstructive: Limitation of airflow due to increase resistance
Asthma, emphysema, chronic bronchitis, bronchiolitis, bronchiectasis, cystic fibrosis
FEV1/FVC is low
Restrictive: Reduced expansion of the lung
Both FEV1 and FVC are low (normal ratio)
Extrapulmonary: severe obesity, kyphoscoliosis, neuromuscular disorder
Interstitial lung disease: acute: acute respiratory distress syndrome ARDS, pneumoconiosis, sarcoidosis, idiopathic pulmonary fibrosis

10. We will discuss: Bronchial Asthma
Chronic Obstructive pulmonary disease
Emphysema
Chronic Bronchitis
Bronchiectasis

11. Bronchial Asthma

12. Bronchial Asthma Reversible, episodic bronchospasm
Due to bronchial hypersensitivity to stimuli
Persistent bronchial inflammation
Chronic inflammatory disease of airways
Episodic dyspnea, cough, wheeze
5% of adult, 7-10% of children

13. Bronchial Asthma
Classified on the basis of presence or absence of immune disorder
Extrinsic Asthma (immune disorder)
Type I hypersensitivity
Exposure to extrinsic antigen
Atopic: young people, severe attacks, associated with other allergies, family members involved, high eosinophils, high IgE
Occupational
Allergic bronchopulmonary aspergillosis

14. Bronchial Asthma
Classified on the basis of presence or absence of immune disorder
2. Intrinsic Asthma (non immune)
Aspirin, infections, stress, exercise
No family history
No allergies
Normal IgE

15. Bronchial Asthma Pathogenesis:
Bronchoconstriction (hyper responsiveness)
Bronchial inflammation
Type I hypersensitivity Reaction

16. Bronchial Asthma Extrinsic Asthma
Allergen – Immune response – sensitized T cell, Th2 – Re exposure – IL-4, IL-5, IL-13 – IgE, mast cells, eosinophils – Early phase minutes – late phase 4-8 hours
Mast cell degranulation (primary, secondary mediators)
Para sympathetic broncho spasm
Eosinophils

17. Bronchial Asthma Extrinsic Asthma Early phase Late phase:
Lukotrienes C4, D4, E4: Bronchoconstriction, increase vascular permeability, increase mucin
Prostaglandins D2, E2, F2: bronchoconstriction, vasodilatation
Histamine: bronchospasm, increase permeability
Late phase:
Leukotriene B4: chemotactic agent
IL-4, IL-5: enhance IgE production
TNF

18. Bronchial Asthma Extrinsic Asthma Inflammatory cells
Chemical mediators
Epithelial cell injury
Eosinophils: major basic protein, eosinophil peroxidase

19. Bronchial Asthma Intrinsic Asthma Not well understood
? Viral infection, inhaled pollutant
Similar to extrinsic asthma
Respiratory syncytial virus

20. Bronchial Asthma Morphology: Hyperinflated lungs Areas of atelectasis
Edema, hyperemia, inflammatory cells, eosinophils, mast cells, macrophages, lymphocytes, plasma cells
Increase in mucus glands
Mucus plugs, Curschmann spirals
Epithelial injury and necrosis
Increase collagen (fibrosis)
Hypertrophy and hyperplasia of smooth muscle

22. Bronchial Asthma Asthmatic attack Status asthmaticus
Wheeze, dyspnea, dry cough, tachycardia
Prolonged expiration
Use of accessory muscles
Hyperinflated chest
Severe attack: exhaustion and fear, inability to speak, drowsiness, cyanosis, tachycardia, reduced breath sounds, “silent” chest

23. Chronic Obstructive Pulmonary Disease

24. Chronic Obstructive Pulmonary Disease (COPD)
10% of US adults
4th leading cause of death
Definition:
Pulmonary function test: Persistent irreversible airway obstruction
Chronic bronchitis and Emphysema: may be pure or co-existence of both

25. Chronic Obstructive Pulmonary Disease (COPD)
The diagnosis is often based on three findings:
History of heavy smoking
Previous diagnosis of COPD or emphysema
Reduced breath sounds

26. Emphysema
Permanent enlargement of airspaces distal to terminal chronchioles, with destruction of the alveolar wall
In contrast, hyperinflation is enlargement with no destruction

27. Emphysema Types: Centrilobular (centriacinar) Panacinar (Panlobular)
The central part of the acini (respiratory bronchioles) is affected
Affect upper lobes
Cigarette smoking
Panacinar (Panlobular)
Uniform enlargement from the level of respiratory bronchioles
Common in lower zones
Alpha1- antitrypsin deficiency
Paraseptal (Distal Acinar)
Distal near pleura and septae
In areas of fibrosis and scarring
Bullae formation

31. Emphysema Incidence: common disease 50% of autopsies
Common in heavy smokers

32. Emphysema Pathogenesis Protease – antiprotease imbalance:
Oxidant – antioxidant imbalance
Protease – antiprotease imbalance:
Like alpha1 antitrypsin deficiency
It is enzyme in serum and macrophages
In any inflammation there protease activity (eg. Neutrophils attracted by nicotine)
Elastic destruction

33. Emphysema Pathogenesis Oxidant – Antioxidant
Protease – antiprotease imbalance
Oxidant – antioxidant imbalance
Oxidant – Antioxidant
Normal antioxidant: superoxide dismutase, glutathione
Smoke contains oxygen free radicals
Deletion of antioxidant

34. Emphysema Morphology: Large lung, pale
Thinning, destruction of alveolar walls
Large spaces
Airway collapse in expiration
Fibrosis (minimal) of respiratory bronchioles

36. Emphysema
Clinical:
Dyspnea: progressive, pursed lip breathing, use of accessory muscles
Weight loss
FEV1/FVC low
Barrel chest
Reduced chest expansion
Hyper resonance on percussion
Decreased breath sounds, Prolonged expiration
Gas exchange is adequate (till late in disease)
Pink Puffers
Secondary pulmonary hypertension due to
Hypoxia-induced vascular spasm
Loss of capillaries
Death: pulmonary failure, cor pulmonale

37. Emphysema
Morphologic definition
Acinus involved (distal to terminal bronchioles)
Chronic Bronchitis
Clinical definition
Involves small and large airways

38. Chronic Bronchitis 20-25% of men 40-65 year of age Cigarette smokers
Chronic bronchitis is persistent productive cough for at least 3 consecutive months in at least 2 consecutive years

39. Chronic Bronchitis Different forms Simple chronic bronchitis
No airway obstruction
Chronic mucopurulent bronchitis
Associated with infection
Chronic asthmaticus bronchitis
Chronic obstructive bronchitis

40. Chronic Bronchitis Airflow obstruction is due to:
Inflammation, fibrosis, narrowing of bronchioles (chronic bronchiolitis)
Co-existent emphysema

41. Chronic Bronchitis Pathogenesis:
Smoking – increase mucus secretion – inflammation – epthelial injury – metaplasia and hypertrophy of mucus glands

42. Chronic Bronchitis Morphology: Enlarged mucus gland, endema
Squamous metaplasia, dysplasia
Inflammation
Chronic bronchiolitis
Goblet cells in small bronchioles, inflammation, fibrosis, smooth muscle hypertrophy

44. Chronic Bronchitis Clinical: Cough and sputum Cyanosis, “blue bloater”
Hyerinflated chest
Reduced expansion
Increased resonance on percussion
Reduced breath sounds with end expiratory wheeze
Right ventricular failure

45. Bronchiectasis

46. Bronchiectasis
Bronchiectsis is permanent dilatation of bronchi and bronchioles caused by destruction of muscle and elastic tissue as a result from chronic necrotizing infection.
It is secondary condition (not primary disease)
Diagnosed by history of persistent cough and purulent sputum and imaging (x-ray) showing dilated bronchi and bronchioles

49. Bronchiectasis Predisposing conditions
Bronchial obstruction: like tumors or foreign body
Congenital and hereditary conditions
Cystic fibrosis, immunodeficiency, Kartagener syndrome (autosomal recessive of abnormal cilia)
Necrotizing, suppurative pneumonia
Staph, Klebsiella

50. Bronchiectasis Pathogenesis
Obstruction – infection – destruction of the wall – inflammation – fibrosis – permanent dilatation of the bronchi and bronchioles

51. Bronchiectasis Morphology: Lower lobes bilaterally
Acute and chronic inflammation
Bronchial wall destruction, ulceration
fibrosis

52. Bronchiectasis Clinical: Fever, cachexia, sinusitis
Persistent cough with large volume of mucopurulent, foul smelling sputum
Clubbing of fingers
Cyanosis if severe
Coarse Inspiratory crackles
Cor pulmonale

53. Homework To be delivered in paper on 26/2/1429
Compare between atelectasis and brochiectasis (definition, causes, clinical presentation, significance)
List the clinical features of bronchial asthma. (presentation, symptoms and signs)
Compare between emphysema and chronic bronchitis (definition, causes, pathogenesis, clinical presentation, and significance). What is their relation to COPD?
What is chronic asthmatic bronchitis?