COPD should be suspected in any patient over the age of 40 years who presents with symptoms of chronic bronchitis and/or breathlessness. Depending on the presentation, impoant differential diagnoses include chronic asthma, tuberculosis, bronchiectasis and congestive cardiac failure. Cough and associated sputum production are usually the first symptoms, and are often referred to as a 'smoker's cough'. Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigation. Breathlessness usually prompts presentation to a health professional. The level should be quantified for future reference,often by documenting what the patient can manage beforestopping; scales such as the modified Medical Research Council (MRC) dyspnoea scale may be useful . Inadvanced disease, enquiry should be made as to the presence of oedema ( which may be seen for the first time during an exacerbation) and morning headaches (which may suggest hypercapnia). Physical signs are non-specific, correlate poorly with lung function, and are seldom obvious until the disease is advanced. Breath sounds are typically quiet; crackles may accompany infection but, if persistent, raise the possibility of bronchiectasis. Finger clubbing is not a feature of COPD and should trigger fuher investigation for lung cancer or fibrosis. Right hea failure may develop in patients with advanced COPD paicularly if there is coexisting sleep apnoea or thromboembolic disease ('cor pulmonale'). However, even in the absence of hea failure, COPD patients often have pitting oedema from salt and water retention caused by renal hypoxia and hypercapnia. The term 'cor pulmonale' is a misnomer in such patients, as they do not have hea failure. Fatigue, anorexia and weight loss may point to the development of lung cancer or tuberculosis, but are common in patients with severe COPD and the body mass index (BMI) is of prognostic significance. Depression and anxiety are also common and contribute to morbidity. Two classical phenotypes have been described: 'pink puffers' and 'blue bloaters'. The former are typically thin and breathless, and maintain a normal PaCO2 until the late stage of disease. The latter develop (or tolerate) hypercapnia earlier and may develop oedema and secondary polycythaemia. In practice, these phenotypes often overlap. Investigations Although there are no reliable radiographic signs that correlate with the severity of airflow limitation, a chest X-ray is essential to identify alternative diagnoses such as cardiac failure, other complications of smoking such as lung cancer, and the presenceof bullae. A blood count is useful to exclude anaemia or document polycythaemia, and in younger patients with predominantly basal emphysema a1-antitrypsin should be assayed. The diagnosis requires objective demonstration of airflowobstruction by spirometry and is established when the post- bronchodilator FEV1/FVC is <70%. The severity of COPD may be defined in relation to the post-bronchodilator FEV1 . Measurement of lung volumes provides an assessment of hyperinflation. This is generally performed by helium dilution technique; however, in patients with severe COPD, and in paicular large bullae, body plethysmography is preferred because the use of helium may under-estimate lung volumes. The presence of emphysema is suggested by a low gas transfer . Exercise tests provide an objective assessment of exercise tolerance and provide a baseline on which to judge the response to bronchodilator therapy or rehabilitation programmes; they may also be valuable when assessing prognosis. Pulse oximetry may prompt referral for a domiciliary oxygen assessment if less than 93%. The assessment of health status by the St George's Respiratory Questionnaire (SGRQ) is commonly used for research. In practice, the COPD Assessment Test and the COPD Control Questionnaire are easier to administer. HRCT is likely to play an increasing role in the assessment of COPD, as it allows the detection, Ref Davidson edition23rd pg 575