Chronic obstructive pulmonary disease (COPD),sometimes known as chronic obstructive lung disease (COLD) or chronic obstructive airways disease (COAD), is the collective term for a number of chronic, slowly progressive conditions, most of which are either caused by tobacco smoking or are exacerbated by it. It has supplanted the term ‘chronic bronchitis’.
The conditions produce widespread, persistent airways obstruction that is largely irreversible but somewhat amenable to inhaled bronchodilator and corticosteroid therapy. The conditions can occur due to chronic inflammation and recurrent infection of the airways, and lead towards dyspnea and abnormal blood gas levels. The underlying casue in all of these is usually COPD or emphysema (or both) but chronic asthma could also present similarly. Bronchiectasis and cystic fibrosis are less frequent causes.
Definition of COPD:
‘Chronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. The disease is caused predominately by smoking.’
COPD is much more common in the UK and in Eastern Europe than in most developed countries. It was known in Western Europe as the ‘English disease’, a consequence of being the first intensively industrialized country at a time when the health hazards of environmental pollution and the effects of occupational exposure to airborne dusts and toxins were not appreciated. The overall prevalence of COPD in the UK is about 4% in men aged about 50 years, 9% at 60 years, 12% at 80 years, but only 3% in women.
This sex difference is wholly attributable to differences in smoking habits: in fact, the difference increases with advancing age because of the cumulative effects of long-term smoking in men. However, changes in smoking habits over the past 50 years, with an increasing proportion of girls and young women smoking cigarettes, may be expected to minimize the difference. These prevalence rates are about three times that for angina pectoris.
According to a national survey, in Pakistan, the prevalence of chronic bronchitis in the population over 65 years of age was 14% in rural females and 6% in rural males. In urban population, the prevalence was less than 2%in the age group of 15-24 and greater than 9% above 65 years of age, higher prevalence in female might be due to exposure to household smoke, use of biomass and wood as fuel.
COPD is responsible for considerable morbidity and time off work, and caused about 30 000 deaths in 1999 in the UK (male: female ratio about 5:1). Almost 30% of these deaths occur before retirement, although the death rate is declining with reduced smoking in men, less air pollution and better treatment. The disease is characterized by an insidious onset, starting with a ‘smoker’s cough’ that is usually disregarded. Significant symptoms may not appear until after some 20 years or more of smoking, by which time there is appreciable irreversible lung damage. There is then a progressive decline over 10–40 years with increasing dyspnea, exercise limitation, difficulty in expectoration and an increased frequency of alarming, acute infectious exacerbations, necessitating hospital admission. Occasionally, an acute respiratory infection is identified as the trigger for the initial onset of overt symptoms.
The prognosis can be related to the degree of exercise limitation: about 40% of patients with significantly reduced walking ability on the flat die within 5 years, usually of heart failure.
Etiology and histopathology:
The disease is multifactorial in origin, but prolonged bronchial irritation and damage is the major contributor.
The prime cause is cigarette smoking, and almost all clinical parameters, e.g. symptoms, work lost, hospital admissions and deaths, correlate with the extent of smoking. The death rate from COPD is increased about 10-fold for each 15 cigarettes smoked daily and regularly in the past. However, the statistic usually used is pack years.
Environmental pollution and some occupations (e.g. coal mining) potentiate the effect of smoking, and the effects of urbanization are very marked in smokers. However, the major improvement in urban pollution in the last 50 years means that there are now only very small effects in non-smokers unless it is extreme.
Climate plays a minor role, although morbidity is higher in the colder and wetter regions in the north and west of the UK, after allowing for the effects of urbanization. In Australia and New Zealand the age–mortality curve is displaced relative to that for the UK to higher age groups by about 10–15 years. This shift is due primarily to less urban pollution and differences in smoking habits. Also, the incidence of severe respiratory infections is lower in the better climate.
A low socioeconomic status predisposes to both morbidity and mortality. The mortality in Class V (unskilled) is six times that in Class II (administrative). This is related to differences in smoking habits, hygiene, nutrition, attitudes towards achieving a healthy lifestyle and usage of healthcare facilities. Educational and cultural differences lead to a lack of awareness in the lower socioeconomic groups of the importance of symptoms, or disregard of them, the need for medical care and the benefits that modern medicine can produce. Similar considerations apply to most diseases.
The cardinal early symptoms are as follows:
- ‘Smoker’s cough’: initially present on winter mornings, but later throughout the year.
- Sputum: usually copious and tenacious (mucoid). It may be yellow, green or khaki colored (mucopurulent) during infective exacerbations, but clear or greyish between the infective episodes, and occasionally streaked with blood.
- Dyspnea: as with all obstructive airways diseases expiration is the difficult phase.
- Fever and the usual signs of infection during exacerbations.
- In mild disease cough may be the only abnormality. Patients with moderate disease also have excess sputum, breathlessness (with or without wheezing), and a general reduction in breath sounds on auscultation (caused by total occlusion of some airways). In late-stage disease there is usually breathlessness at rest or on any exertion, together with a prominent wheeze and a productive cough. The following features may also be present:
- Cyanosis: if the respiratory deficit is severe; frank central cyanosis is discernible when there is about 5 g/dL of deoxygenated Hb in the blood.
- Heart failure and peripheral edema.
Tests and diagnosis:
- Chest X-ray. In a few people, a chest X-ray can show emphysema — one of the main causes of COPD. More importantly, an X-ray can help rule out other lung problems, such as lung cancer, or heart failure.
- Computerized tomography (CT). CT scans combine X-ray images taken from many different angles to create detailed, cross-sectional images of internal organs. A CT scan of your lungs can help detect emphysema and help determine if you might benefit from surgery for COPD.
- Arterial blood gas analysis. This blood test measures how well your lungs are bringing oxygen into your blood and removing carbon dioxide. The blood is usually drawn from an artery in your wrist.
- Sputum examination. Analysis of the cells in the mucus you cough up, which is known as sputum, can help identify the cause of your lung problems and help rule out some lung cancers. If you have a productive cough, identifying a bacterial pathogen and treating it before it causes pneumonia is good preventive medicine.
Pulmonary function tests:
Spirometry is the most common lung function test and the most important in diagnosing COPD and its stage. During this test, you’ll be asked to blow into a large tube connected to a spirometer. This machine measures how much air your lungs can hold and how fast you can blow the air out of your lungs. Spirometry can detect COPD even before you have symptoms of the disease. By repeating it at intervals, this test can also be used to track the progression of disease and to monitor how well treatment is working.
Treatments and drugs:
There’s no cure for COPD, and you can’t undo the damage to your lungs. But COPD treatments can control symptoms, reduce your risk of complications and exacerbations, and improve your ability to lead an active life.
The most essential step in any treatment plan for smokers with COPD is to stop all smoking. It’s the only way to keep COPD from getting worse — which can eventually result in losing your ability to breathe. But quitting smoking is never easy. And this task may seem particularly daunting if you’ve tried to quit before. Talk to your doctor about nicotine replacement products and medications that might help.
Doctors use several basic groups of medications to treat the symptoms and complications of COPD. You may take some medications on a regular basis and others as needed:
- Bronchodilators. These medications — which usually come in an inhaler — relax the muscles around your airways. This can help relieve coughing and shortness of breath and make breathing easier. Depending on the severity of your disease, you may need a short-acting bronchodilator before activities, a long-acting bronchodilator that you use every day, or both.
- Inhaled steroids. Inhaled corticosteroid medications can reduce airway inflammation and help you breathe better. But prolonged use of these medications can weaken your bones and increase your risk of high blood pressure, cataracts and diabetes. They’re usually reserved for people with moderate or severe COPD.
- Antibiotics. Respiratory infections — such as acute bronchitis, pneumonia and influenza — can aggravate COPD symptoms. Antibiotics can help fight bacterial infections, but are recommended only when necessary.
- Oxygen therapy. If there isn’t enough oxygen in your blood, you may need supplemental oxygen. There are several devices to deliver oxygen to your lungs, including lightweight, portable units that you can take with you to run errands and get around town. Some people with COPD use oxygen only during activities or while sleeping. Others use oxygen all the time.
- Pulmonary rehabilitation program. These programs typically combine education, exercise training, nutrition advice and counseling. If you are referred to a program, you’ll probably work with a range of health care professionals, including physical therapists, respiratory therapists, exercise specialists and dietitians. These specialists can tailor your rehabilitation program to meet your needs. Exercising regularly can significantly improve the efficiency of your cardiovascular system.
Surgery is an option for some people with some forms of severe emphysema who aren’t helped sufficiently by medications alone:
- Lung volume reduction surgery. In this surgery, your surgeon removes small wedges of damaged lung tissue. This creates extra space in your chest cavity so that the remaining lung tissue and the diaphragm work more efficiently. The surgery has a number of risks, and long-term results may be no better than for nonsurgical approaches.
- Lung transplant. Single-lung transplantation may be an option for certain people with severe emphysema who meet specific criteria. Transplantation can improve your ability to breathe and be active, but it doesn’t appear to prolong life and you may have to wait for a long time to receive a donated organ. So the decision to undergo lung transplantation is complicated.
Even with ongoing treatment, you may experience times when symptoms suddenly get worse. This is called an acute exacerbation, and it may cause lung failure if you don’t receive prompt treatment. Exacerbations may be caused by a respiratory infection, a change in outdoor temperatures or high air pollution levels. Seek medical attention if you notice more coughing or a change in your mucus or if you have harder time breathing.
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- Shapiro SD, Reilly JJ Jr., Rennard SI. Chronic bronchitis and emphysema. In: Mason RJ, Broaddus VC, Martin TR, et al.Murray & Nadel’s Textbook of Respiratory Medicine. 5th ed. Philadelphia, Pa: Saunders Elsevier; 2010:chap 39.
- Niewoehner DE, Erbland ML, Deupree RH, et al. Effect of Systemic Glucocorticoids on Exacerbations of Chronic Obstructive PUlmonary Disease. New England Journal of Medicine 1999; 340: 1941-7
- Dr Nasir Mehmood (Pharm D)
- Dr Ali Raza (Pharm D)
- Dr Salahuddin (Pharm D)
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