Tuesday, February 5, 2013

CHRONIC OBSTRUCTIVE AIRWAYS DISEASE


CHRONIC OBSTRUCTIVE AIRWAYS DISEASE 
Table of contents
1). Introduction……………………………………………………………………………….4
2 Pathophysiology and pathology…………………………………………………………….4
i) Pathophysiology…………………………………………………………………….4
ii) Mechanisms responsible……………………………………………………………6
a) Smoking…………………………………………………………………….6
b) Industrial exposures………………………………………………………...6
c) Air pollution………………………………………………………………...7
d) Genetic factor……………………………………………………………….7
e) Autoimmunity………………………………………………………………8
iii) Clinical characteristics……………………………………………………………..8
a) Symptoms…………………………………………………………………...8
3) Medical management……………………………………………………………………….9
i) Diagnosis……………………………………………………………………………9
a) Patient’s medical history……………………………………………………9
b) Chronic smoking……………………………………………………………9
c). X-ray and CT scans……………………………………………………….10
d) Pulmonary function tests………………………………………………….10
e) Carbon dioxide and oxygen levels in the blood…………………………...11
f) 6MWT……………………………………………………………………..11
ii) Historical development of therapeutics/medical treatments………………………11
iii) Current management practices/therapies…………………………………………12
a) Smoking cessation…………………………………………………………12
Benefit………………………………………………………………..12
Limitation…………………………………………………………….12
b) Medications………………………………………………………………13
Benefits……………………………………………………………...13
Limitations…………………………………………………………...13
c) Oxygen therapy……………………………………………………………13
Limitation…………………………………………………………….14
Benefit………………………………………………………………..14
iii) Development of new therapies and future perspectives………………………….14
4) Conclusion………………………………………………………………………………...14
5) References…………………………………………………………………………………15
6) Appendices………………………………………………………………………………...16
















1. Introduction
Chronic obstructive airways disease refers to the incidence of chronic bronchitis or emphysema. These two are common diseases affecting the lungs that most of the times coexist making the airways to get narrowed. A person suffering from this disease has limitation in the amount of air flowing to and from his or her lungs, resulting in breath shortness, also known as (dyspnea). In medical practice, the disorder, the definition of the disorder is through its typically low flow of air into the lung. As opposed to other related conditions such as asthma, the limitation resulting from this disorder is inadequately reversible and tends to get worse over time. According to Simpson, Hippisley-Cox and Sheikh (2010), in the United Kingdom it is approximated that 842,100 of 50 million individuals are diagnosed with the disorder. Internationally, chronic obstructive airways disease was ranked among the six major causes of death in the year 1990. Projections reveal that it might be the fourth major cause of death by 2030 because of the higher rates of smoking as well as demographic changes in the world.
2. Pathophysiology and pathology
i) Pathophysiology
In an event where one is suffering from COAD, the normal functioning of the lungs is affected. The lung is the body organ that is responsible for gaseous exchange. It is responsible for ensuring that there is enough air rich in oxygen entering the body and that air rich in carbon dioxide is exhaled from the body. COAD affects the optimal exchange of these gases. There are various risk factors for the disorder that affect the lungs and tampers with the smooth exchange of gases in and out of the body. However, research has not completely revealed the process that take place to cause the damage to the lungs by smoke and other pollutants. However, some of the known processes that result in the damage to the lungs include: oxidative stress generated by high levels of free radicals in smoke; release of cytokine because of inflammation in the lungs due to the response by the body to particles in the airways; the functioning of antiprotease enzymes like alpha 1-antitrypsin is affected by the irritants (Simpson, Hippisley-Cox and Sheikh, 2010).
Following the damaging of the lungs and the airways, there is reduction in the rate of flow of air to and from the alveoli. With the effects of the disorder, higher reductions in the rate of flow of air happen when one is breathing out. This is due to the fact that the force in the chest compresses instead of expanding the lungs. Theoretically, the rate of the flow of air is enhanced when one breathes with a lot of force, augmenting the force of the chest while the air is being breathed out. With individuals suffering from the disorder, there is normally a restriction in the manner in which the pressure can augment the flow of air. Calverley and Koulouris (2005) refer to this situation as expiratory flow limitation. In case of very low rate in breathing, an individual may fail to complete the expiration before the need to catch another breath. Hyperinflation, an increase in the amount of air inside the lungs, resulting from some of the air from the preceding breath is left in the lungs when the next is begun.
Shortness of breath also results from the decrease in the surface area in the people suffering from the disorder. There is a limit in the amount of surface area available for gaseous exchange with emphysema. The effect of the loss of surface area lowers the speed of exchange between the lungs and the atmosphere and can result to higher CO2 and lower O2 levels. Such a situation may require more rapid and deep breathing to make up for the insufficiency of oxygen, which can be hard because of the limitation in the flow. Some of the patients may manage to breathe faster and deeper to make up, but dyspnea may develop as a result. For others, it is possible to have less shortness in breath, tolerate high levels of carbon dioxide and low levels of oxygen in the body, but may suffer other compilations such as headaches, drowsiness and even heart failure. The disorder can cause complications in other parts of the body like cachexia or weight loss, pulmonary hypertension and cor pulmonale or right-sided heart failure.
ii) Mechanisms responsible
a) Smoking
The primary risk factor for COPD is chronic smoking. It is estimated that about 80-90 percent of he disorder is as a result of chronic smoking. The measurement of the exposure to cigarette smoking is done in pack-years. This is by taking the average number of cigarette packs used in a day and multiplying the number by the number of years the person has been smoking. The chances of getting the disorder increase as the person ages as well as increasing exposure to smoke. According to Rennard and Vestbo (2006), approximately every one of life-long cigarette smokers will get the disorder provided other extrapulmonary disorders (cardiovascular, diabetes, cancer) related to smoking do not kill the person ahead of time.
b) Industrial exposures
Another risk factor for the disorder is industrial exposure. Extreme and long-drawn-out exposure to work-related dust and other pollutants present in gold-mining, coal-mining and textile industries as well as chemicals like isocyanates, cadmium, and fumes resulting from welding have been suggested to increase the chances of developing the disorder. Obstruction of airways results under these kinds of exposures even among people who do not smoke (Rennard and Vestbo, 2006). Those who work in these kinds of environment and also smoke are at a higher risk of developing the disorder. Severe exposure to silica dust has been known to cause silicosis, which is a limiting lung disorder that is different from COAD, but exposure to less severe silica dust has been related to incidences of COAD-like conditions. Nevertheless, the risk of exposure to industrial dusts has been found to be less significant compared to the risk resulting from cigarette smoking.

c). Air pollution
Researchers have suggested air pollution as another risk factor for COAD. Studies have showed that those who reside in large cities are at a greater risk of developing the disorder compared to those who reside in rural regions (Halbert, et al 2006). This is because air pollution in the large cities is a contributing factor for the disorder. It is suggested that the pollution affects the ordinary development of the lungs. However, there has not been thorough research to establish this relationship. Research carried out on work-related waste gas as well as COAD/asthma-aggravating compounds, sulphur dioxide, and the opposite connection to the occurrence of the blue lichen Xanthoria have suggested that combustive manufacturing activities do not assist those suffering from COAD. In the developing world, air pollution happening indoors such as smoke from cooking fire is related to the occurrence of the disorder, particularly among women.
d) Genetic factor
Genetic predisposition is a factor that has been found necessary to cause the disorder in addition to heavy smoking. It has been established that the disorder is common among individuals with a family history of the disorder. This is because of the genetic dissimilarities that render some lungs vulnerable to the effects of cigarette smoke and other pollutants. However, these genetic differences are not very well known. Insufficiency in Alpha 1-antitrypsin is a genetic factor that has been showed to be responsible for approximately 2 percent of the suffering from the disorder. Individuals with this genetic predisposition have their bodies failing to produce protein, alpha 1-antitrypsin. This chemical offers protection to the lungs from being damaged by protease enzymes, like elastase and trypsin, which can be produced as a response of inflammatory reaction to smoke (Mahler, 2006).


e) Autoimmunity
Studies have suggested that there might be an autoimmune element to the development of the disorder, set off by life-long cigarette smoking (Mahler, 2006). Most of the people suffering from the disorder who have quit smoking tend to have active lung inflammation. Because of the continuing inflammation on the lungs, the disease may continue worsening even after one quits smoking. Autoantibodies and autoreactive T cells are suggested to be the mediating factors of the ongoing inflammation (Mahler, 2006).
iii) Clinical characteristics
Past studies have revealed dual character of the pathology. Additionally, more recent studies have showed that a patient diagnosed with the disorder could be categorized as having a principally bronchial or emphysematous phenotype. This is through the analysis of medical, functional, and radiological results or carrying out studies on remarkable biomarkers (Kitaguchi et al 2006).
a). Symptoms
According to Kitaguchi et al (2006), essentials of diagnosis of COAD include: a long history of smoking; chronic cough accompanied by sputum production; dyspnea; rhonchi which is the decrease in the strength of breath sounds, as well as long-drawn-out expiration on physical test; and limitation in the flow of air revealed on lung function test. The limitation should be poorly reversible and progressing over time.
The most common indication of the disorder is shortness of breath, also known as dyspnea. Individuals with the disorder normally describe this occurrence as: “My breathing requires effort,” “I feel out of breath,” or “I can't get enough air in” (Mahler, 2006: 234-235). Such people notice this symptom (shortness of breath) following long and vigorous activities as this is where the demand of air to the lung is highest. As it progresses with time, it gets worse such that patients can experience shortness of breath even folk owing minor activities, even household chores. In the advanced stages of the disorder, the problem can worsen such that it happens even when one is resting and is constantly present.
There are other symptoms of the disorder such as persistent coughing, production of mucus or sputum, wheezing, tightness of the chest, and tiredness. Respiratory failure has been noted among individuals during the advanced stages of the disorder or for people with severe COAD. This can be indicated by cyanosis. Cyanosis refers to a bluish staining of the lips as a result of the inadequacy of oxygen reaching the blood. Headaches, twitching (asterixis) or drowsiness can result from the increase of carbon dioxide levels in the blood. Cor pulmonale is a complication that happens at the advanced stage of the disorder which is a staining of the heart because of the extra demand in pumping blood through the affected lungs. Some of the symptoms of this complication include dyspnea and peripheral edema, indicated by the swelling of ankles (Kitaguchi et al, 2006).
3) Medical management
i) Diagnosis
a) Patient’s medical history
The disorder is normally diagnosed based on the patient’s medical history. Such history forms the basis for disclosing various symptoms of the disorder. The signs of the disorder are disclosed through physical tests. Some of the tests that diagnose the disorder include chest X-ray, CAT or CT chest scan, lung function test and tests to measure the levels of oxygen and carbon dioxide levels in the blood (Rabe et al 2007).
b) Chronic smoking
Doctors normally suspect COAD in smokers exhibiting signs such as shortness of breath, in the presence or absence of exertion, those with chronic unrelenting cough producing sputum, and recurrent lung infections like bronchitis or pneumonia. Some cases of the disorder are diagnosed in patients developing respiratory infections requiring hospitalization. Practically, the disorder to be suspected in all chronic smokers whether or not they have the symptoms as some of the symptoms of the disorder appear after significant lung damage. Some of the physical findings that are used in the diagnosis of the disorder are wheezing and enlargement of the chest cavity. A stethoscope is used in listening to the chest where faint and distant breath can be heard (Rabe et al 2007).
c). X-ray and CT scans
According to Mahler et al (2006), the X-ray on the chest can reveal enlargement in chest cavity and enlarged lung markings among patients with principally emphysema, revealing damaging of tissues in the lungs and increase in air-sacs. The X-ray reveals an increase in lung markings for patients suffering from chronic bronchitis only. CT or CAT chest scan can more accurately than X-ray reveal damages in lung tissue and airways in a patient with the disorder. X-rays and CT scans are used as a way of ruling out other lung infections with similar symptoms as COAD. However, CT scans are not required for regular tests and management of the disorder, but they are important in the evaluation of the level of change in emphysematous and in detecting initial stages of lung cancer.
d) Pulmonary function tests
According to Nathell et al (2007) lung or pulmonary function tests are also useful in the diagnosis of COAD. One such test is spirometry, which is a test that quantitates the level of the obstruction of the airway. The test is used in determining the severity of the disorder (see appendix 1).  During the test, the individual is asked to take complete breath and exhale rapidly and vehemently into a tube. The tube is normally attached to a machine used for measuring the amount of exhaled air. The volume of air exhaled per second (the FEV1) has proven a reliable and significant measure of the amount of obstruction in the flow of air. The normal ratio of FEV1 to the FVC is typically 70 percent. There is reduction in the ratio where there is occurrence of obstruction. The test is normally repeated after treatment using bronchodilators. Improvement in the second test reveals that the obstruction of the airway is reversible (Mahler et al 2006).
e) Carbon dioxide and oxygen levels in the blood
Samples of blood drawn from the patient’s artery are used in testing the level of carbon dioxide and oxygen in the blood. Pulse oximetry is an alternative to inserting a needle into the artery to draw blood. This test operates from the point of view that the extent of redness of the haemoglobin is relative to the level of oxygen. This means that the blood becomes redder with the amount of oxygen present. The patient has a probe (oximeter) put around his or her finger. Different shades of red are transmitted through the tip of the finger on the basis of the amount of oxygen present in the blood (Rabe et al 2007).
f) 6MWT
Nathell et al (2007) posits that 6MWT or six minute walking test is a simple and effective test for the disorder. This is where the individual is required to take a six minutes walk on a level ground at his own speed. A standard script is used by the healthcare worker performing the test. Besides being kept up to date on the amount of time remaining to complete the task, there is no other kind of engorgement given. The patient is allowed to stop and take a rest at any point. There is measurement of distance covered. It is normally an extremely precise index (Rabe et al 2007).
ii) Historical development of therapeutics/medical treatments
Research has been carried towards the development of treatment for COAD, but there is still no cure for the disorder. However, the years of research have produced preventive and treatment methods for managing it. Research on COAD and its treatment can be traced back to the 18th century with descriptio of cases where the lungs did not function optimally. Contemporary diagnosis started with the development of the stethoscope by René Laennec in 1837. However, thorough research and understanding of the disorder did not start until the past century.
iii) Current management practices/therapies
According to Rabe et al (2007) the main present directions of the management of the disorder are assessment and monitoring of the disease in order to lower the risk factors, management of stable COAD, prevention of acute damage and management of comorbidity. Two measures have been found to lower mortality, which are smoking cessation and supplemental oxygen.
a) Smoking cessation
This ha been revealed to be the most effective factor in reversing the progression of the disorder once diagnosed. Even at the advanced stages, quitting smoking can lower the rate of damage to the lungs, thus delaying the start of disability or death. This process starts with a personal decision to quit smoking. There are other management therapies that involve the use a second or third party in helping the individual to quit smoking. Such strategies that can help include social support, smoking cessation programme. Medications like nicotine replacement therapy, varenicline and bupropion can also be used. Reduction or elimination of workplace exposure would decrease the risk of developing COAD and can also lower the progression of the disorder for those who are already diagnosed (Paoletti et al 2009).
Benefits: The main benefit of this method is reduction in the rate of progression of the disorder once it is diagnosed. Those people who are diagnosed early and quit smoking on time tend to have higher chances of longer life than those who continue to smoke. Studies show that long-term sustained smoking cessation can cause a decrease in the progression of the disorder. Reduction or elimination of industrial exposure also works in the same wary.
Limitations: Particularly for individuals living in an environment that encourages smoking it is hard to avoid or quit smoking. Even if cessation, even following many years of smoking, lowers the risk of developing COAD, ex-smokers never reasonably lower their risk when compared to non-smokers. Additionally there is the risk of relapse. For industrial exposure it is hard to avoid toxins while working in industries where they are produced. Additionally, some people are forced to loose their source of income to manage the disorder (Rabe et al 2007).
b) Medications
There are various medications that are used in the treatment and management of the disorder. Bronchodilators are drugs used for the relaxation of smooth muscle in the airways, thus improving the flow of air. Normally used with inhaler or through a nebulizer. Two kinds of bronchodilators are presently used: β2 agonists and anticholinergics. Anticholinergics medications block the stimulation of cholinergic nerves causing relaxation of airway muscles (Paoletti et al 2009).
Benefits: Medications are used to lower the symptoms of the disorder such as shortness of breath, wheeze as well exercise limitation. They help in enhancing the quality of life for those with the disorder. Ipratropium has been linked to higher cardiovascular morbidity.
Limitations: Drugs are known to cause other negative side effects such as cardiovascular problems. Additionally, the drugs used in the management of the disorder help in alleviating the symptom and the patient may have to use them for a long time without the possibility of being cured of the disorder.
c) Oxygen therapy
The current research is centred on the use of oxygen in therapy. People with low oxygen in the body are given supplementary oxygen.  Some of the equipments that can be used include oxygen cylinder or oxygen concentrator. This is important in allowing individuals with the disorder to carry on with their daily duties (Rabe et al 2007).
Benefits: Oxygen therapy has been proven to improve the ability of the patient to carry on with the normal duties without suffering shortness of breath. It has also been known to increase the chances of survival in the patient.
Limitations: A high level of oxygen supplementation is capable of causing accumulation of carbon dioxide as well as respiratory acidosis for a number of individuals with the disorder.
iii) Development of new therapies and future perspectives
The current development is headed towards development of pulmonary rehabilitation which will combine exercise program, disease management with the use of the other kinds of therapies, and counseling, all coordinated to for the good of the patient. This will provide a sense of control for the patient in addition to improving the quality of life and chances of survival.
4) Conclusion
Chronic obstructive airways disease has been defined as the occurrence of chronic bronchitis or emphysema. It is a common disease especially among cigarette smokers. Various advancements have been made in the diagnosis and management of the disorder, but there is still no cure. All the therapies and treatment programs that are currently available are used in the management of the symptoms and slowing down the progression of the disorder. it is thus important that more research is made into more effective treatments or therapies, possibly those that can cure the disorder.






5) References:
Calverley PM, Koulouris NG (2005). "Flow limitation and dynamic hyperinflation: key
concepts in modern respiratory physiology". Eur Respir J 25 (1): 186–199.
Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (September 2006).
"Global burden of COPD: systematic review and meta-analysis". Eur. Respir. J. 28 (3): 523–32.
Kitaguchi Y, Fujimoto K, Kubo K, Honda T (October 2006). "Characteristics of COPD
phenotypes classified according to the findings of HRCT". Respir Med 100 (10): 1742–52.
Mahler DA (2006). "Mechanisms and measurement of dyspnea in chronic obstructive
pulmonary disease". Proceedings of the American Thoracic Society 3 (3): 234–8.
Nathell, L.; Nathell, M.; Malmberg, P.; Larsson, K. (2007). "COPD diagnosis related to
different guidelines and spirometry techniques". Respiratory research 8 (1): 89.
Paoletti M, Camiciottoli G, Meoni E, et al. (December 2009). "Explorative data analysis
techniques and unsupervised clustering methods to support clinical assessment of Chronic Obstructive Pulmonary Disease (COPD) phenotypes". J Biomed Inform 42 (6): 1013–21
Rabe KF, Hurd S, Anzueto A, et al. (2007). "Global Strategy for the Diagnosis, Management,
and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary". Am. J. Respir. Crit. Care Med. 176 (6): 532–55.
Rennard, S. I.; Vestbo, J. R. (2006). "COPD: the dangerous underestimate of 15%". The
Lancet 367 (9518): 1216.
Simpson CR, Hippisley-Cox J, Sheikh A (2010). "Trends in the epidemiology of chronic
obstructive pulmonary disease in England: a national study of 51 804 patients". Brit J Gen Pract 60 (576): 483–488.

6) Appendices

Severity of COPD (GOLD scale)
FEV1 % predicted
Mild (GOLD 1)
≥80
Moderate (GOLD 2)
50–79
Severe (GOLD 3)
30–49
Very severe (GOLD 4)
<30 or chronic respiratory failure symptoms

Appendix 1