Obstructive Lung Diseases Dr. Raid Jastania

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

Atelectasis

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

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

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

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

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

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

Bronchial Asthma

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

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

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

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

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 30-60 minutes – late phase 4-8 hours Mast cell degranulation (primary, secondary mediators) Para sympathetic broncho spasm Eosinophils

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

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

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

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

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

Chronic Obstructive Pulmonary Disease

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Bronchiectasis

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

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

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

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

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

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?