COPD Sheet PDF

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) A morning cough, occurring well before the diagnosis of chronic obstructive pulmonary disease, is ignored by many smokers as it is taken to be quite normal. The cough is due to the irritant caused by smoking and the resultant mucus that forms...

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) A morning cough, occurring well before the diagnosis of chronic obstructive pulmonary disease, is ignored by many smokers as it is taken to be quite normal. The cough is due to the irritant caused by smoking and the resultant mucus that forms. Irritation and mucus production ultimately lead to damage of the airways. Hence the cough associated with chronic obstructive pulmonary disease is referred to as a ‘smoker’s cough’. Chronic Obstructive Pulmonary Disease (COPD sometimes referred to as COAD – chronic obstructive airways disease) is an umbrella term which is characterised by obstruction to airflow especially during expiration. The terms Chronic Bronchitis and Emphysema have been used. These two chest diseases are different in presentation but their cause, management and outcomes are similar. Most patients with COPD suffer from a mixture of the two but one usually predominates. Unlike asthma, the changes that cause airflow limitation are fixed rather than reversible. Patients with COPD do not, therefore, respond with an increase in spirometry (FEV1 or PEFR) following inhaled doses of bronchodilators. For this reason they are termed ‘irreversible’. There are some that do respond but this improvement is usually less than 15%. Patients with chronic bronchitis are referred to as blue bloaters and those with emphysema as pink puffers. In COPD the changes which give rise to chronic bronchitis lead to hypersecretion of mucus and an impaired respiratory drive The net effect of these symptoms is to reduce oxygen concentrations in the blood and increase carbon dioxide. The fall in oxygen causes the body to produce more haemoglobin. All these combine to provide a ‘blue’ appearance. Many of these patients are also obese hence the term ‘bloater’ The changes in the airways that give rise to emphysema are more related to destruction especially of the elastic recoil of the lungs. Due to this decrease in the elastic recoil secondary forces develop to pull open the airways. These cause the total capacity of the lungs to increase (hyperinflation). These subjects have a high respiratory drive (rate) to maintain normal blood gases Their tidal volume is at the top of their total lung capacity which, when combined with their respiratory drive, causes them to breathe with a pursed lip appearance (‘puffer’). Breathing in this manner is very difficult and strenuous; hence they look pink in appearance. The process by which they breathe requires a lot of work and energy that decreases appetite and burns fat. The pink puffer is therefore usually thin COPD is a very slow progressive degeneration of the lungs and the primary cause is smoking. 1 In those susceptible to COPD smoking starts to damage the lungs soon after starting. The main symptoms are cough with increased sputum production (especially in the morning). Breathlessness especially during exercise is slow and progressive and thus is not usually noticeable. This Figure shows how stopping smoking can halt the speed of lung function deterioration. The rate in the fall in lung function after stopping smoking is similar to that of a non-smoker. Pathophysiology The internal diameter of the airways can be narrowed (bronchoconstriction) by: (a) secretions, usually mucoid in nature, in the lumen 2 (b) thickening of the airway wall by mucous gland hypertrophy, inflammation and oedema (c) loss of elastic recoil. Chronic bronchitis The irritant effects of smoking (and other inhaled pollutants) cause hypertrophy of the mucus glands. This results in a thickening of the airway walls which decreases the internal diameter of the airways. Furthermore cigarette smoke damages the cilia and the build up of mucus on top of the cilia causes damage. The net effect of these is the inability to get rid of all the mucus thereby making the patient prone to chest infections which themselves will cause damage to the airway and linings. Irritation from smoke leads to an inflammatory process especially in small bronchioles (bronchitis) and alveoli (alveolitis). As a result of this macrophages and neutrophils infiltrate the epithelium. Although these are not as destructive as eosinophils (in asthma) they will cause some inflammation and its resulting oedema which will further restrict the airway lumen. Emphysema Cigarette smoking has been shown to inhibit ά1-antitrypsin, the main protective factor which inhibits proteolytic enzymes in the lungs and so prevents damage. 3 Women are less likely to experience decreased ά1-antitrypsin production because oestrogen stimulates its production. ά1-antitrypsin is essential for the production of elastin which maintains the elastic recoil in the lungs. The macrophages and neutrophils which are stimulated due to the inflammatory effects of smoking release lysosomal enzymes such as elastase which destroy the connective tissues in the lungs especially when the elastase levels exceed those of ά1- antitrypsin. Thus elastic recoil is destroyed. Management of patients with COPD The goals of management of the COPD patient are:  Smoking cessation  Improve the chronic obstructive state  Arrest the rate of progression of the disease  Improve the physical and psychological well-being of the patient  Reduce working days lost  Reduce hospitalisation  Reduce mortality Management of patients with COPD 1. Smoking cessation Smoking as a cause of disease, Smoking cessation is an effective way to reduce mortality and morbidity. 2. Drug treatment of COPD (I)Anticholinergics Inhaled anticholinergics are more useful bronchodilators in patients with COPD than in those with asthma. They cause bronchodilation by blocking the vagal cholinergic tone of airway smooth muscle. Other studies have shown that they also have an inhibiting effect on airway mucus hypersecretion. It is now recognised that there are at least four sub-types of muscarinic receptors in the airways. Ipratropium bromide and oxitropium bromide are non-selective.  Ipratropium bromide: MDI:- 40mg 3-4 times a day is most widely used Nebuliser:- 500mg 3-4 times a day  Oxitropium bromide: MDI:- 200mg 2-3, (up to 4) times a day (200mg of oxitropium is equivalent to 80mg of ipratropium) Tiotropium bromide is a selective M3-receptors blocker it reported to have a long duration of bronchodilatory effect in patients with COPD. The greatest density of the cholinergic receptors is situated on the upper parts of the airways and thus easier to target in COPD. This may be the reason why these drugs are more beneficial than β2-agonists.  Tiotropium bromide - 18g daily using a handihaler (single capsule DPI) (II) ß2- agonists These are more beneficial when given with anticholinergics. 4 Salmeterol and Formeterol have a longer duration of action and thus should be more beneficial especially for those who find night-time symptoms a problem. (III) Corticosteroids Their mode of action in COPD is not as well understood as it is for asthma. Some believe that patients with COPD can be divided into steroid responsive and non- responsive groups. It has been suggested that when stabilised a patient with COPD should be given a trial of 40 mg oral prednisolone per day and the lung function measured 10 days later - those that respond should be given maintenance inhaled steroids. (IV) Xanthines In COPD theophylline is usually used as one of the last resorts but there may be a case to introduce this before corticosteroids. The theophylline bronchodilation action is well-known but recent studies suggest that long term use of theophylline in patients with COPD may go beyond bronchodilation. (V) Oxygen therapy Long term treatment with supplementary oxygen in selected patients according to their response reduces mortality in these patients. A trial of oxygen is given and the patient’s blood oxygen values have to increase by predetermined values. Patients who fit this criteria benefit from both 15hrs/day and 24hrs/day oxygen therapy. 24 hour continuous oxygen has been shown to increase survival in COPD patients more so than 15 hour therapy. Long term oxygen in patients meeting the criteria for therapy has been shown to increase their life span by 6-7 years compared to others who do not meet the criteria. 5