A respiratory condition associated with the blockage of air passages and difficult breathing is termed as Chronic obstructive pulmonary disease (COPD).Obstructive airflow is progressive and causes the abnormal response of air sacs towards gases and noxious particles. It includes two states
- State of emphysema: in this state inhaled toxic chemicals or gases or smoke particles directly destroy the alveoli (functional unit of lungs).
- Chronic bronchitis: in this condition, the bronchial lining of the air passage got inflamed. This lining allows the air to pass from the mouth to the air sacs of the lungs. Due to inflammation patient feels difficulty in breathing. A patient with chronic bronchitis is observed with persistent cough with sputum.
These two states are observed together in a COPD patient and its severity varies from person to person.
COPD is a progressive disease and becomes severe if left untreated. Lifestyle changes and proper management makes a person less prone to COPD. (1)
Natural history of COPD.
The natural history of COPD is different and not all patients show the same course. Smoking is by far the most significant risk factor but only about 15-20% of individuals develop COPD. Smoking and recurrent chest infections during childhood and adulthood lead to impaired growth and dysfunction of the lungs. (2)
Signs and symptoms.
In most cases, the sign and symptoms of COPD are seen in the moderately advanced stage. It includes
- Shortness of breath or dyspneadue to inflamed air passages. The patient feels breathlessness more frequent during any physical activity
- Wheezing during breathing
- Persistent cough with phlegm production.
- Increased sputum production that may be yellow, white, or greenish
- Frequent chest infections
- Chest tightness
- Weight loss in advance stages
Due to non-compliance to treatment and poor management, symptoms do not improve and a patient suffers from the worst condition known as an exacerbation.
- COPD has been observed most commonly in tobacco users. Smoking is an underlying cause of COPD. People who directly smoke tobacco or work in a place where they are exposed to tobacco smoke are more prone to COPD. Some other irritants are also the cause such as pipe Smoke, air pollution, secondhand smoke, exposure to fumes, cigar smoke.
- Genetic susceptibility is another factor that increases the vulnerability of a person towards COPD
- Deficiency of alpha1. Antitrypsinis another cause of COPD. Due to some genetic disorders, individuals become deficient in protein Alpha 1 antitrypsin. This protein is secreted by the liver which plays an important role in the protection of the lungs. So deficiency of this protein can cause lungs or liver diseases both.
Pathology and pathophysiology.
In COPD, pathological changes occur in different compartments of the lungs.
- Peripheral airways
- Central airways
- Lung parenchyma
- Pulmonary vasculature
Inhaled smoking particles cause the inflammatory response of the lungs. In tobacco smokers, it becomes worst and causes COPD lesions. Oxidative stress, imbalanced proteinase, and antiproteinases also contribute to the pathogenesis of COPD. Different pathological mechanisms give rise to other physiological abnormalities such as ciliary dysfunction, hypersecretion of mucous, gaseous change abnormalities, hyperinflation, pulmonary hypertension, and systemic abnormalities.
- People who are smoking for the long term are at high risk of getting COPD. Moreover, the chances of COPD are high in labor working in tobacco making industries as they have more exposure to smoke and fumes.
- Asthmatic patients have already suppressed the immune system. These patients are at greater risk of getting COPD. Asthma and smoking, both increases the risk of COPD
- Individuals deficient in Alpha 1 AntiTrypsin can develop COPD more easily
Progressive COPD imparts disastrous influences on systemic physiology as well. COPD patients have comprised immune systems which make them more vulnerable to other infections such as common cold, pneumonia, and flu. These respiratory infections make it difficult to breathe and cause s more damage to pulmonary tissues. COPD increases the risk of getting a heart attack and the reason behind this is still not fully understood. Recurrent pulmonary infections elevate the chances of lung cancer. Due to obstruction in air pathways patient puts more effort into breath which produces tension in blood vessels ultimately causing high blood pressure.
Diagnosis of COPD is done by spirometry, evaluating body mass index (BMI), and dyspnea.
In spirometry, if the forced expiratory volume in one second (FEV1) / forced vital capacity (FVC) is less than or equal to 0.7 then it determines that airflow is not fully reversible. Spirometry I cannot tell the complexity and severity of COPD but still can predict mortality and health status.
Body mass index (BMI) can be calculated by dividing the body weight in Kg by height in m². The increased mortality rate is observed if the BMI value is less than 21kg/m².
With the help of the Research Council dyspnea scale, the functional dyspnea of the patient can be assessed.
Scale 0 shows that patient does not feel breathlessness unless he does strenuous exercise.
Scale 1 shows that patients can face shortness of breath just by walking up on a hill.
Patient showing scale 2 usually walks slower than the normal person of the same age and stops while walking to catch a breath.
Patients of scale 3 stop after every few minutes or covering a distance of 100m to regulate their breathing
Patients with scale 4 are too breathless to go outside the house.
Treatment of COPD
COPD treatment is done primarily through pharmacological agents. These agents minimize the symptoms, enhance the capacity to exercise, reduce exacerbation severity, and improves health status. Combination therapy imparts a noticeable improvement in symptoms and spirometry than monotherapy.
Anticholinergics, Beta-agonists, and methylxanthines are the bronchodilators. Although their mechanism of action is different their ultimate aim is to dilate the bronchial pathways and relaxes the smooth muscles. They aid in complete exhalation of air during tidal breathing.
Glucocorticoids acts within inflammatory cascade and cause an elevation in post-bronchodilator FEV1 and a decrease in bronchial activity in less severe COPD. Studies have shown a noticeable reduction in exacerbation and rate of health deterioration through inhaled glucocorticoids.