Presentation on theme: "Chronic Obstructive Airways Disease Gerard Flaherty B.Sc.(Hons.), M.B., B.Ch., B.A.O., M.R.C.P.I. Specialist Registrar in General Medicine/Endocrinology."— Presentation transcript:
Chronic Obstructive Airways Disease Gerard Flaherty B.Sc.(Hons.), M.B., B.Ch., B.A.O., M.R.C.P.I. Specialist Registrar in General Medicine/Endocrinology
Lecture Outline Definition of COAD Diagnostic criteria Classification of severity Epidemiology Chronic bronchitis Emphysema Bronchiectasis Bronchial asthma
Definition of COAD COAD is a disease state characterised by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
Epidemiology of COAD Prevalence and morbidity data greatly underestimate the total burden of COAD. Prevalence of 9.34/1,000 in men and 7.33/1,000 in women (Global Burden of Disease Study, 1990). Morbidity increases with age and is greater in men than in women. Currently the 4 th leading cause of death in the world. Economic burden: per capita cost of COAD in UK of US$65 (1996).
Risk Factors for COAD Host factors Alpha-1-antitrypsin deficiency Asthma and airway hyperresponsiveness Disordered lung development Environmental factors Tobacco smoke Occupational dusts/chemicals Air pollution Childhood infections Lower socioeconomic status
Diagnosis of COAD Considered in patients with cough, sputum production, or dyspnoea +/- risk factors. Confirmed by spirometry. FEV 1 /FVC <70% + postbronchodilator FEV 1 <80% of predicted value. A low peak expiratory flow has poor specificity for the diagnosis of COAD.
Spirometry Normal flow-volume loop Flow-volume loop in severe COAD
Classification of Severity StageCharacteristics 0: At Risk Normal spirometry Cough, Sputum I: Mild COAD FEV 1 /FVC <70% FEV 1 ≥ 80% II: Moderate COAD FEV 1 /FVC <70% FEV 1 50-80% III: Severe COAD FEV 1 /FVC <70% FEV 1 30-50% IV: Very Severe COAD FEV 1 /FVC <70% FEV 1 <30%
Respiratory Failure Results when gas exchange is inadequate, resulting in hypoxia with PaO 2 <8kPa. Type I: Hypoxia with normal/low PaCO 2. Caused by ventilation/perfusion mismatch, e.g., Life- threatening asthma, Emphysema. Type II: Hypoxia with hypercapnia (PaCO 2 >6.5kPa). Caused by alveolar hypoventilation, e.g., Chronic bronchitis. Oxygen therapy must be controlled in type II respiratory failure due to the risk of further hypercapnia if the hypoxic drive to ventilation is abrogated by excessive oxygen.
Chronic Bronchitis Persistent cough with sputum production for at least 3 months in ≥ consecutive years Simple / Chronic asthmatic / Obstructive Most frequent in middle-aged men Higher incidence in urban dwellers May coexist with emphysema Presents with exertional dyspnoea and frequent respiratory tract infections
Chronic Bronchitis Pathogenesis Chronic irritation by inhaled substances Respiratory infections 4-10 times more common in heavy smokers Hypersecretion of mucus in large airways Submucosal gland hypertrophy Increase in goblet cells in small airways Excessive mucus → airway obstruction Cigarette smoke predisposes to infection
Chronic Bronchitis Morphology Gross Hyperaemia and oedema of mucous membranes Excessive secretions +/- casts Histology Hypertrophy of submucosal smooth muscle Hyperplasia of submucosal glands of trachea/bronchi Increased Reid index (>0.4) Squamous metaplasia and dysplasia of epithelium Loss of ciliary activity Narrowing of bronchioles +/- bronchiolitis obliterans
Emphysema Abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls Types: (1) centrilobular (2) panlobular (3) paraseptal (4) irregular Associated with heavy cigarette smoking
Emphysema Presents with progressive dyspnoea, reduced exercise tolerance, wheeze and weight loss Signs of hyperinflation Loss of elastic support → Airways collapse on expiration → Obstructive pattern on spirometry Respiratory acidosis Cor pulmonale (rarely) Pneumothorax
Emphysema Pathogenesis Protease-antiprotease hypothesis Homozygous alpha-1-antitrypsin deficiency is associated with panlobular emphysema, especially in smokers Emphysema results from the destructive effect of high protease (elastase) activity in patients with low antiprotease activity Smoking stimulates release of elastase from neutrophils
Bronchiectasis A chronic necrotising infection of the bronchi and bronchioles associated with abnormal permanent dilation of these airways Presents with cough, productive of large amounts of foul-smelling, purulent sputum, hamoptysis and digital clubbing Pooled secretions in lower lobes → respiratory tract infections
Bronchiectasis Pathogenesis Bronchial obstruction → Atelectasis Dilatation of walls of patent airways Infection → Bronchial wall inflammation → weakened walls → further dilation Cystic fibrosis: squamous metaplasia with impaired mucociliary action, infection, necrosis of bronchial and bronchiolar walls Kartagener’s syndrome: absent dynein arms in cilia → lack of ciliary activity
Bronchiectasis Morphology Gross Usually both lower lobes May be localised Dilated airways Cylindroid Fusiform Saccular Cystic pattern on cut surface of lungs Histology Acute and chronic inflammation Desquamation of epithelium Necrotising ulceration Squamous metaplasia Necrosis → lung abscess Fibrosis