Introduction
Chronic obstructive pulmonary disease is normally characterized by breathlessness, coughing and a wheezing sound that is normally heard when somebody breaths. These symptoms are caused by either chronic emphysema or bronchitis (Løkke, 2006 p.10). Patients with emphysema are normally plagued with persistent short breath where as those with chronic bronchitis produce excess sputum with some cough.
Symptoms
Chronic obstructive pulmonary disease normally exhibits signs of breathlessness, cough and sputum production by the patients. Before the symptoms become full blown the lung may considerably lose its functions. Patients normally have a tendency to seek medical help when the disease has reached advanced stages.
Patients with chronic respiratory disease normally complain of having difficulty in inhaling. Because COPD makes the airways to be fixed, it makes the patients unable to fully use their inspiratory reserve volume. Breathing problems are normally worsened by the hyperinflation of the lungs characterized by the trapping of air in the alveoli that necessitate increase in residual volume at instead of inspiratory reserve volume (Hogg, 2004 p.709).
Emphysema characterized by dynamic airway collapse aggravates breathlessness because it causes further air trapping. Diaphragms can flatten when the lungs become hyperinflated. COPD also do have problems with bending.
Cough may come before problems with breathing are exhibited or they may take place concurrently. The cough becomes more serious in the morning hours, but as opposed to asthma victims, COPD patients rarely stay awake at night. Expectoration normally relieves the tightness of the chest and morning cough (Gorska, 2004 p.89). Many COPD patients do produce sputum but this symptom is not so universal. The sputum is normally white or grey but with exacerbations, the sputum may have characteristic green or yellow.
Wheezing sound is normally very common in both asthma and OCPD, but COPD patients normally experience the wheeze when they walk into wind hanging out when it is cold. This does not happen when they are sleeping. Patients rarely stay awake due to the wheeze.
Risk factors
Smoking of tobacco is a major risk factor to the development of chronic obstructive pulmonary disease. People who smoke tobacco without developing such conditions may have other factors involved that prevent them from developing COPD. Cigarette smoking is a major risk factor to the development of chronic obstructive pulmonary disease (Crapo, 2010 p.8503). Other risk factors include pipe smoking and cigar smoking. Passive smokers like individuals who inhale smoke fumes smoked by other people do also develop respiratory symptoms. Scavenger cells are normally depressed by the smoke. Smoke also interferes with ciliary cleaning procedures of the respiratory tract. The cilia help in keeping the respiratory passages free of bacteria and other irritants. When ciliary cleaning procedures has been interfered with by smoking air flow is impaired as the air get obstructed.
The alveoli become distended leading to decrease in the capacity of the lungs. Goblet cells and mucous glands also do get irritated by the smoke (Maclay, 2009 p.513).
Irritation of mucous glands by smoking contributes to accumulation of mucus. This can lead to the damage of the lungs (Willemse, 2005 p.835). Carbon monoxide that is normally produced when smoking reacts with hemoglobin to produce carboxyhemoglobin. The compound makes it difficult for hemoglobin to help in transportation of oxygen to various parts of the body.
The nature of job that one does may also make him or her to develop COPD. Cadmium is normally implicated in the development of COPD as it is normally found in high concentration in emphysematous lungs. A study commissioned to look at the pulmonary function abnormalities among workers exposed to cadmium has suggested a fibrotic reaction amongst workers subjected to higher levels of cadmium in contrast to workers exposed to low levels of cadmium (Sabit, 2007 p.1259).
Emphysema may occur early in life due to glycoprotein alpha 1- antitrypsin deficiency. Both the male and the female are at 50-50 chances of developing emphysema due to such deficiencies. This makes alpha 1 antitrypsin a genetic risk factor. Alpha antitrypsin deficiency is the most common killer deficiency among the Caucasians. The United States has a stunning 25 million carriers of the defect. Genetically susceptible population is very sensitive to risk factors like smoke and air pollutants and allergens (Alford, 2010 p.7485).
Current medical treatment of COPD and assessment measures
Many stakeholders in medical field have always advocated for the use of bronchodilators in treatment of severe chronic obstructive respiratory disease. However, anticholinergics are normally used in initial treatment regimes in different countries. COPD patients who are symptomatic are normally given bronchodilators to relieve them of the persistent symptoms like dyspnea realized by COPD victims at the time of training. The long term beta-adrenoreceptor was at first used in treating asthma of the bronchus. They are promising as they reduce the number of exacerbations. Beta adrenergic receptor agonists are normally used in bronchodilation. However, they are not effective in bronchodilation in COPD as they do with asthma. Inhalation of beta receptor agonists by patients with COPD enable them show some improvement in FEV1. Beta agonists initiate an enzymatic pathway that increases intracellular cAMP that initiates bronchodilation. They also help in clearing the airways by ciliatory mechanisms. They in deed improve airflow. They can only last for 3 hours on the maximum hence patients have to take them several times in a day.
A reliable indicator of severity of the disease is spirometry. However, FEV1 is the best abnormality indicator. Deterioration of FEV1 is a viable prognostic indicator. Dyspnea only shows extent of obstruction of air flow.
Preoperative Spirometry
Accuracy of spirometry has been enhanced by calculation of postoperative predicted values in spirometric raw numbers and percentage predicted values. Calculation is done by estimating functional lung segment numbers. A quantitative ventilation perfusion scan assesses functions of the lungs regionally. This procedure helps in calculation of postoperative spirometric functions in COPD patients (Celli, 2004 p.932).
Conclusion
Chronic Pulmonary Obstructive Disease symptoms are normally occasioned by either chronic bronchitis or emphysema. The symptoms are exhibited in the form of breathlessness, coughing and production of wheezing sound. Predisposing factors include smoking and occupational hazards. It can also be genetically instigated.
Reference list
Alford, S.K, van Beek, E.J.R., McLennan, G., Hoffman, E.A. (2010) Heterogeneity of pulmonary perfusion as a mechanistic image-based phenotype in emphysema susceptible smokers. Proc Natl Acad Sci USA 107:7485–7490.
Celli, B.R. et al (2004). Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J, 23:932- 946.
Crapo, J.D. (2010).Preclinical vascular disease identifies smokers at risk for COPD. Department of medicine, National Jewish Health, 107 (19), 8503-8504.
Gorska, K., Maskey-Warzechowska, M., Krenke, R. (2010). Airway inflammation in chronic obstructive pulmonary disease. Curr Opin Pulm Med 16:89–96.
Hogg JC (2004) Pathophysiology of airflow limitation in chronic obstructive pulmonary disease. Lancet 364:709–721
Løkke A, Lange P, Scharling H, Fabricius P, Vestbo J (2006) Developing COPD: A 25 year follow up study of the general population. Thorax 61:935–939.
Sabit R, et al. (2007) Arterial stiffness and osteoporosis in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 175:1259–1265.
Maclay JD, et al. (2009).Vascular dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 180:513–520.
Willemse, B.W.M., et al. (2005) Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers. Eur Respir J 26:835–845.