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Chapter: Medicine Study Notes : Respiratory

Chronic Obstructive Pulmonary Disease (COPD)

Increase resistance to air flow due to partial or complete obstruction at any level

Chronic Obstructive Pulmonary Disease (COPD)


·        = Increase resistance to air flow due to partial or complete obstruction at any level


·        = Permanent or minimally reversible obstruction of expiratory airflow caused by chronic bronchitis, emphysema or both


·        Lung Function results:

o   FEV1/FVC ratio < 70% with a concave expiratory loop

o   ­RV secondary to air trapping

o   ¯DL CO due to loss of parenchyma

o   Severity:

§  Mild: FEV1 > 50% predicted

§  Moderate: FEV1 35 – 49% predicted

§  Severe: FEV1 < 35% predicted

·        Chest Xray:

o   Emphysema: absent peripheral vessels, hypertranslucency, flattened diaphragm, bullous change

o   Bronchitis: thickened bronchial walls (especially end on)

·        Abnormalities in gas exchange:


·        Treatment:

o  Only smoking cessation and long term oxygen alters the natural course

o  No evidence that daily bronchodilators are beneficial in asymptomatic patients

o  20% benefit from oral corticosteroids. Should be used primarily for exacerbations. Inhaled steroids show no significant benefit

·        Management of an exacerbation:

o  Exclude differentials: PE, LVF, pneumothorax, hyperventilation

o  Is there an infective component: Upper or Lower RTI

o  Are there complications of COPD:

§  Cor pulmonale/pulmonary hypertension (look for signs of RH failure)

§  Polycythaemia secondary to chronic hypoxia

§  Low body weight/osteoporosis (from steroids and acidosis)

o  Investigations:


§  FBC (is Hb or WBC ­), U & E, Glucose

§  ECG

§  If Sats < 92% then ABG

§  CXR

§  Sputum microscopy, culture and sensitivity

§  Peak flow is asthmatic component

§  Spirometry when resolved

§  Echo if cor pulmonale or LVF suspected

o  Treatment:

§  O2 with goal of saturation 90 – 92% (beware CO2 narcosis)

§  Broncho dilation: Combivent 

§  Antibiotics: Usually oral. Augmentin, erythromycin, etc. Commonly H Influenzae or M Catarrhalis

§  Steroids: 30 – 40 mg/day, stepping down over around 2 weeks


Chronic Bronchitis


·        = Persistent cough with sputum for at least 3 months in 2 consecutive years


·        Follows prolonged exposure of the tracheobronchial trees to non-specific irritants ® hypersecretion of mucus and structural changes


·        Types:

o  Simple chronic bronchitis: no airway obstruction

o  Chronic asthmatic bronchitis: intermittent bronchospasm and wheezing

o  Chronic obstructive bronchitis: heavy smokers with chronic airways obstruction, usually with emphysema. Sputum will be clear/white, only occasionally will be infected (yellow/green)

o  [Cf Chronic infective bronchitis with green sputum Þ bronchiectasis]

·        Pathogenesis:


o  Chronic irritation (eg inhaled substances such as smoking) and microbiological infections ® hyper-secretion of mucus obstructing airways. Hypertrophy of submucosal glands in larger bronchi and hyperplasia of goblet cells in small airways.


o  Infection maintains the hyper-secretion and causes acute exacerbations

·        Macroscopic appearance: hyperaemia, swelling, mucopurulent secretions in the bronchi


·        Microscopic appearance: increased size of mucous glands. Reid index (ratio of mucous gland layer to thickness of epithelium to cartilage) greater than 0.4. Chronic inflammation ® metaplasia to squamous epithelium and dysplasia. Mucous plugging, inflammation and fibrosis. If severe ® luminal obliteration




·        Enlargement of air-spaces distal to terminal bronchioles and destruction of alveolar walls without fibrosis

·        Moderate to severe emphysema is rare in non-smokers

·        Aetiology:

o   Cigarettes: usually had a 20-pack year history.  Only 15 – 20% of smokers develop obstruction

o   Alpha-1 antitrypsin deficiency

o   Dusts: coal, gold mining, textile, cement and steel making

·        FEV1 best single indicator of prognosis


·        Pathogenesis: Disruption in balance of elastin synthesis: ­ in elastolytic activity from neutrophil elastase (smoking ® ­neutrophils) and ¯a1-antitrypsin (elastase inhibitor – oxidants in cigarette smoke inhibit a1-antitrypsin). Neutrophils also release free radicals that inhibit a1-antitrypsin


·        Types:


o   Centriacinar (Centrilobular): enlargement of respiratory bronchioles, distal alveoli are spared. (Small particles deposited here – don‟t make it right to the end). More severe in upper lobes. Blackened. Bronchi and bronchioles have chronic inflammation. Seen in smokers and coal workers pneumoconiosis


o   Panacinar (Panlobular): acinus is uniformly involved from respiratory bronchiole to terminal alveoli. Seen in a1-antitrypsin deficiency (ZZ or MZ alleles on chromosome 14) and as an extension of centrilobular emphysema in smokers. Mean age of onset is 45 – 50 years in non-smokers and 30 – 40 in smokers. Liver disease in 5 – 10 % of adults. Heterozygotes (MZ) predisposed to emphysema if they smoke. Treatment same as for smoking induced


o   Paraseptal (distal acinar): proximal acinus is normal, distal part affected. Most prominent sub-pleurally and next to interlobular septi. Often seen in cases of spontaneous pneumothorax in young people


o   Irregular emphysema: acinus irregularly involved.  Associated with scarring


·        Macroscopic appearance: voluminous lungs

·        Microscopic appearance: large abnormal airspaces, blebs and bullae.  Bronchitis and bronchiolitis

·        Clinical features:

o   60 years or older

o   Prolonged history of exertional dyspnoea

o   Minimal non-productive cough

o   Usually have lost weight

o   Use accessory muscles for respiration 

o   Prolonged expiration period (lungs collapse due to ¯elastin) 

o   Pink puffers: ­respiratory rate maintains O2. Xray: ­central pulmonary artery size, ¯peripheral vascular markings 

o   Blue bloaters: ­PaCO2, ¯PaO2, cyanotic, respiratory centre insensitive to CO2, instead rely on hypoxic drive to breathe. Dangerous to give O2 ® ¯ventilatory drive


·        Medical management:

o   Bronchodilators and inhaled corticosteroids: only if reversible obstruction

o   Smoking cessation (nicotine replacement doubles quit rate)

o   Antibiotics

o   O2 with care

o   Exercise/physio

o   Attention to nutrition




·        Chronic necrotising infection of bronchi and bronchioles (ie a pneumonia that doesn’t clear) ® abnormal airway dilation and destruction of bronchial walls ® obstruction due to inflammation, ulceration and distortion

·        = Chronic infective bronchitis

·        Pathogenesis:


o   Obstruction (especially during growth) due to tumour, foreign bodies, mucous impaction (eg in cystic fibrosis and immotile cilia)


o   Infection with bronchial wall weakening and atelectesis (eg in necrotising pneumonia). Especially Tb, pertussis, MAC


·        Macroscopic appearance: affects lower lobes, especially vertical airways and more distal bronchi. Airways may be cylindrical, fusiform or saccular


·        Microscopic appearance: Acute – inflammatory exudate with desquamation and ulceration of the epithelium. Chronic – peribronchial fibrosis


·        Clinical course: foul, bloody sputum, especially in the morning. (cf Clear sputum in chronic bronchitis). Repeated „bronchitis‟ with wheezing, haemoptysis, and dyspnoea. Coarse crepitations, wheezing, and clubbing.


·        Complications: obstructive ventilatory insufficiency ® dyspnoea and cyanosis. Rarely cor pulmonale, metastatic brain abscesses and amyloidosis


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