Chronic Obstructive Pulmonary Disease

 

 

 

 

 

 

 

Chronic Obstructive Pulmonary Disease

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Summary

Chronic obstructive pulmonary disease (COPD) refers to emphysema and chronic bronchitis. The conditions are the fifth killer in UK. COPD mechanism is recognized as an imbalance between the protective antiproteases and destructive proteases. It is primarily caused by smoking. The smoke from cigarette inactivates α1-antitrypsin and damages anti-proteases such as elafin, leukoprotease. The causation of COPD is explained on the antioxidant and oxidative activities collectively referred to as oxidative stress. Tar and cigarette smoke have a high concentration of oxidants such as nitrogen dioxide, ozone and diesel particulates which needs to be eliminated by the lung antioxidants. Consequently, the antioxidant defense system in the lung is overwhelmed. The diagnosis of COPD is done on patients with sputum production and dyspnoea in the cough, or historical factors of being exposed to the disease risk factors. The diagnosis involves the application of a spirometry, used in confirming the presence of irreversible airflow limitation. The condition has been implicated in having various systemic effects such as skeletal muscle dysfunction, weight loss, depression, cardiovascular disease and osteoporosis. The treatment of emphysema may involve liver implantation when the patient is young, and the condition diagnosed at an early stage. Lung transplantation is considered when lungs are examined to be affected. Alpha-1 emphysema is also treated by administration of the missing α1 antitrypsin. The most cost effective treatment of COPD is ensuring that the patient stops smoking. Bronchodilators are also provided to assist in opening the airways and lower breath shortness. In addition, steroids assist in decreasing inflammations of airways while bacterial infections are treated with antibiotics.

Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) refers to two lung diseases: emphysema and chronic bronchitis. The two conditions cause airflow obstruction, thus, interfere with normal breathing. The conditions coexist in patients making the term COPD frequently used by physicians. COPD is the fifth the killer in the United Kingdom, and the second most common cause of hospital admission. There are over 3.7 million persons currently suffering from the disease in UK. The condition leads to more than twenty-five thousand deaths yearly. However, only close to nine thousand patients have been diagnosed with the condition, which is an indication that 2.8 million people are unaware of having the disease. In Scotland, 3.8 percent of adults are already diagnosed with COPD. The disease is prevalently high in women than in men with a percentage of 4.2 percent compared to 3.3 percent.

The COPD hotspots in Scotland include Lanarkshire and Greater Glasglow (4.4 percent). In England, areas most affected include inner city areas and ex-industrial areas in Yorkshire, North West, and North East and Humberside. There are some incidences reported in Dagenham and Barking and in areas with high populations such as East Anglia and South Coast of England. In Wales, the most affected areas are Welsh valleys and Blaenau Gwent while in Ireland the most affected areas are Londonderry and Belfast. Most of the areas affected in Scotland and other parts of the United Kingdom are associated with unemployment and high levels of deprivation.

According to World Health Organization (WHO), the main primary cause of COPD is tobacco smoking. Smoking is argued to be responsible for up to 90 percent of all the COPD cases in Scotland and other areas in the United Kingdom. Tobacco smoke inflames and permanently damages the lining of the airways. More than 25 percent of smokers are at risk of developing COPD. In addition, passive smoking as well increases the risk of COPD in their victims. COPD is also explained to be caused by exposure to certain types of chemicals and dust at workplaces. Such chemicals and dust include coal, isocyanate, grains, and cadmium. The risk is heightened by breathing in these dust and chemicals by tobacco smokers. COPD is also thought to be caused by air pollution, especially by indoor air pollutants. However, the present statistics are not conclusive.

An existence of an imbalance between the protective antiproteases and destructive proteases has for a long time recognized for the potential COPD mechanism. The smoke from cigarette inactivates α1-antitrypsin and damages other anti-proteases such as elafin, leukoprotease. The smoke as well impairs secretory metalloproteinase. The increased amount of protease destroys collagen and alveoli, whereas neutrophil elastase increases the secretion of mucus by goblet cells. This may increase the victims’ susceptibility to gram-negative bacterial infection and induce expression of interleukin-8. This is a better explanation to the airway obstruction caused by airway collapse and mucus, and the loss of elasticity of the lungs. Consequently, COPD becomes characterized by poorly reversible obstruction to airflow. The condition is also characterized by an abnormal inflammatory reaction in the lungs. All smokers have inflamed lungs; however, those who develop COPD have an abnormal response to inhaling toxic substances. The amplified response result to mucous hypersecretion leading to chronic bronchitis, tissue destruction as in emphysema, the disruption of defense and repair mechanism that causes airway inflammation and bronchitis.

COPD causation is explained on the antioxidant and oxidative activities termed oxidative stress. Tar and cigarette smoke have a high concentration of oxidants such as nitrogen dioxide, ozone and diesel particulates. The antioxidant defense system in the lung becomes overwhelmed by the added oxidants since it already works on the bodily produced oxidants such as hydroxyl radicals, superoxide dismutases catalases, mucin, glutathione and ascorbic acid. The resultant oxidative stress damages lung’s elastin and cells while the increased activity of the nuclear factor-kβ causes the damage through the production of cytokines and epithelial cells apoptosis.

The diagnosis of the condition is considered in patients with sputum production and dyspnoea in the cough, or historical factors of being exposed to the disease risk factors. The diagnosis involves the application of a spirometry, which confirms the presence of irreversible airflow limitation. It should be done on persons exposed to cigarettes or occupational pollutants. A single measurement of forced expiratory volume per second (FEV1) is not enough to represent the sophistication of COPD clinical consequences. Therefore, it is desirable to have a multi-stage examination system that would provide a portrayal of the severity of the condition.

Smoking is the leading risk factor in the causation of COPD. Other factors include second-hand smoke and exposure to air pollution, heredity and a history of childhood infection. Particulates of air pollution and smoke are related to lung damage as discussed above. Particulates with diameters between 2.5 to 10.0 microns are of particular concern. Large particles are easily trapped in the throat or nose as smaller particulates readily drawn into small air passages. Particulates of diameter less than 2.5 microns provide the most serious threat since they may pass to the bloodstream.

COPD has been implicated in having various systemic effects such as skeletal muscle dysfunction, weight loss, depression, cardiovascular disease and osteoporosis. 50 percent of the patients with severe COPD experience unexplained weight loss. Weight loss is also experienced in about 15percent of patients with moderate or mild condition. Weight loss highlight poor prognosis.

The treatment to a young person diagnosed with emphysema at an early stage requires liver implantation. In case of an evidenced lung disease, lung transplantation is considered. Alpha-1 emphysema can also be treated by administration of the missing α1 antitrypsin protein on a weekly basis for life. Although COPD lung damage is irreversible, particular treatment are given to enhance the quality of life of the patient. One such treatment is stopping smoking, which is the most cost effective treatment in slowing the progression of COPD. Bronchodilators are given to assist in opening the airways and decrease breath shortness. Steroids can assist in lowering inflammations in certain patient’s airways while infections are treated with antibiotics.

List of references

Agusti, A. (2007) Systemic Effects of Chronic Obstructive Pulmonary Disease. Proc Am Thorac Soc 4, 522-525.

American Lung Association Lung Disease Data. (2008). Chronic Obstructive Pulmonary Disease. [Online] Available at:   http://www.lung.org/assets/documents/publications/lung-disease-data/ldd08-chapters/LDD-08-COPD.pdf [Accessed June 13, 2015].

British Lung Foundation. (2007) Invisible Lives: Chronic Obstructive Pulmonary Disease (COPD) finding the missing millions. [Online] Available at: http://www.blf.org.uk/Files/94ff4ae1-1858-485f-ae85-a06200ded618/Invisible-Lives-report.pdf [Accessed June 13, 2015].

Cell, B. Macnee, W. (2004) Standards for the diagnosis and treatment of patients with COPD. ERS Journal, 23, 932-946.

Prosser, T. and Bollmeier, S. () Chronic Obstructive Pulmonary Disease. Pharmacotherapy Self-Assessment Program, 6th Edition.[Online] Available at: https://www.accp.com/docs/bookstore/psap/p6b06sample01.pdf [Accessed June 13, 2015].

WHO. (2015) Chronic Respiratory Diseases: Causes of COPD. [Online] Available at: http://www.who.int/respiratory/copd/causes/en/ [Accessed June 13, 2015].

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