Free Essay About Effect Of Chronic Obstructive Pulmonary Disease (COPD) On The Lungs And The Body
Chronic obstructive pulmonary disease (COPD) is a disease of the lungs that is preventable and also treatable. COPD is a progressive disease that arises from chronic inflammation of the lung tissues due to irritation by noxious gases that leads to restricted airflow (Global Initiative for Chronic Obstructive Lung Disease [GOLD] 2015, p. 2). COPD is a blanket term that encompasses and is characterized by chronic conditions such as bronchitis and emphysema (Sherwood 2010, p. 474). COPD is the fourth leading cause of death in the world, killing 5% of the world population annually, and could become the third leading cause in another 5 years (Sethi et al. 2012, p. 1162). COPD results from many years of exposure to cigarette smoke and other irritants (Vestbo et al. 2013, p. 350) and is often underdiagnosed due to lack of clear clinical presentation (Currie 2011, p. 3). This paper will discuss the aetiology, normal lung physiology, diagnosis, treatment, management, prognosis, the mechanism of disease development, histopathological changes, systemic changes and comorbidities of COPD. Molecular and biochemical pathways of disease development are out of scope of this paper.
2. Aetiology of COPD
Smoking is one of the leading causes of development of lung disease, lung cancer and COPD, especially in the developed countries (Currie 2011, p. 3). It is estimated that 50% of the smokers develop some form of airway constricting and restricting disease while up to 20% develop COPD (Currie 2011, p. 3). Passive exposure to second hand tobacco smoke, smoking pipe, cigar and marijuana are some of the other risk factors associated with smoking. Occupational exposure to silica dust, asbestos, organic and other inorganic chemical dust, inhalation of smoke from coal burning, wood burning, animal dung, air pollution and genetic factors are some of the less common causes of COPD (Vestbo et al. 2013, p. 350).
3. Normal lung physiology and gaseous exchange
The act of breathing (pulmonary ventilation) is dependent on differences in the air pressure outside and inside the lungs. Pulmonary ventilation commences with the elevation of the rib cage facilitation by the external intercostal muscles, expansion of the diaphragm and consequently the expansion of the thoracic cavity (Sherwood 2010, p. 470). The air rushes inside the lungs (inspiration or inhalation) from a high pressure environment (the atmosphere) of 760 mm Hg into a low pressure area within the lungs. The expansion causes a drop in intrapleural pressure to -4 mm Hg. Intra-alveolar pressure is always equal to atmospheric pressure. The differences in pressure (partial pressure of oxygen and carbon dioxide) facilitates the exchange of gases between the alveoli and the pulmonary artery; the carbon dioxide moves from the high concentration area of the pulmonary artery into the low concentration area inside the alveoli and vice versa for oxygen (Martini, Nath and Bartholomew 2015, p. 859). The exchanged carbon dioxide is exhaled during which time intercostal muscles relax causing the rib cage to fall back into position and constriction of the diaphragm. This results in decrease in the volume of the thoracic cavity and forces air out due to increased air pressure within the lungs (Sherwood 2010, p. 470).
4. Pathophysiology of COPD and comorbidities
Over a period of many years, the constricted airway cause patients with COPD to develop tolerance for high levels of carbon dioxide within their system because of which the patient’s only drive to breathe is hypoxaemia, a condition caused by elevated concentrations of carbon dioxide in their body (Chang et al. 2006, p. 165). The body compensates for this by causing hyperventilation to increase the frequency of CO2 ventilation (Neighbors and Tannehill-Jones 2015, p.195). In patients with COPD, increased CO2 levels result in blood pH reduction and respiratory acidosis (Billings 2005, p. 316). Under normal circumstances such elevated CO2 would cause drowsiness, cyanosis, anxiety and irritability (Billings 2005, p. 315).
COPD clinically manifests as a combination of emphysema (changes in the alveolar parenchyma cells) and chronic bronchitis (airway obstruction due to inflammation caused by inhaling irritants). It is uncommon to see a COPD case with only one of these conditions. Anatomically, pulmonary emphysema is characterised by enlargement of the air space and destruction of the walls of the terminal bronchioles (Barbu, Iordache and Man 2011, p. 21). In centriacinar emphysema or centrilobular, the centre and the proximal acinus is damaged while the distal alveoli survive; COPD patients who are smokers but without α1-antitrypsin deficiency, are often afflicted with this type of emphysema. In panacinar or panlobular emphysema, the acinus is enlarged fully from the bronchiole right up the alveoli and often occurs in COPD patients who are smoker with α1-antitrypsin deficiency (Kumar, Abbas and Aster 2013, p. 464). Emphysema essentially reduces the surface area for proper gaseous exchange in the alveoli and hence causes the build-up in CO2 concentration in the blood (Barbu et al. 2011, p. 21). Post-mortem studies reveal that emphysema in smokers can occupy 70% of the lung space and 40% of non-smokers (Vestbo and Hogg 2006, p. 87).
Chronic bronchitis, the small and large airway disease of COPD, results from inhalation of noxious gases, which is thought to cause lung tissue modification by three inflammatory mechanisms, namely, oxidative stress, protease-antiprotease imbalance, production of inflammatory cells and mediators (GOLD 2015, p. 6). Oxidative stress could be due to release of reactive oxygen species in response to the COPD-associated cellular damage. The protease imbalance could be responsible for breakdown of tissue. The inflammatory response could be due to triggering of the immune system because of the irritants that lodge within the airways (GOLD 2015, p. 6). Large airway obstruction in chronic bronchitis is often marked by the accumulation of macrophages, B cells, neutrophils, eosinophils, CD4+ and CD8+ cells within the small airways (Adcock, Caramori and Barnes 2011, p. 266). The severity of COPD is directly proportional to the amount of neutrophils in the sputum of the patient (Rovina, Koutsoukou and Koulouris 2013, p. 2) because neutrophils secrete neutrophil elastase that destroy the alveolar structure and reduce elastic recoil of the lungs (Barnes, Shapiro and Pauwels 2003, p. 674; Sherwood 2010, p. 478). Such an accumulation causes the excessive mucous production and consequent thickening of the airways (Tuder and Petrache 2012, p. 2752). During an inflammatory response, the epithelial cells lining the airways produce tumour necrosis factor (TNF-) a, interleukin (IL) 1b, IL-8 and granulocyte-macrophage colony stimulating factor (GMCSF), which is thought to initiate collagen deposition (fibrosis) and mucous accumulation (Rovina et al. 2013, p. 2). As a result, the small airway lumen become a hub for bacterial colonisation and further sustenance of inflammation (Barnes et al. 2003, p. 673).
COPD’s manifestations are limited to the lungs, but the condition may progress to or give rise to diseases such as lung cancer in 40-70% of the patients (Tuder and Petrache 2012, p. 2752), cardiovascular disease owing to arterial stiffness and vasoconstriction (Barnes 2010, p. 1; GOLD 2015, p. 6), diabetes owing to chronic inflammation-mediated insulin resistance in 20% of the patients (Barnes 2010, p. 2), osteoporosis owing to chronic inflammation-induced cytokine production in 75% of the patients (Barnes 2010, p. 3) and psychiatric conditions such as anxiety and depression owing to reduced quality of life and social isolation in 20-40% of the patients (Barnes 2010, p. 3).
4. Clinical presentation and diagnosis of COPD
COPD is clinically represented by cough with or without sputum, wheezing, breathlessness, chest tightness, acid reflux, weight loss and high fat-free mass (Siafakas 2006, p. 7). Currently, the most reliable form of diagnosis is the assessment of COPD is using spirometry that calculates the severity of COPD using a ratio of 1% of forced expiratory volume (FEV1) to forced vital capacity (FVC). This test is often combined with α1-antitrypsin deficiency screening and exercise screening (GOLD 2015, p. 12). Differential diagnosis is performed to differentiate COPD from chronic asthma (Vestbo et al. 2013, p. 352).
5. Treatment, management and prognosis of COPD
Stable COPD is managed by reducing the risk factors such as smoking cessation, along with pharmaceutical drugs such as bronchodilators, inhaled corticosteroid and phosphodiesterase-4 (Sethi 2012, p. 1166). Physical activity and rehabilitation are some of the non-pharmacological therapies (Vestbo et al. 2013, p. 353). An exacerbation is an event that causes sudden worsening of the patient’s COPD symptoms that cripple’s the patient’s day-today activities (GOLD 2015, p. 40). The diagnosis is done purely based on the symptoms exhibited by the patient. Commonly used drugs during exacerbations are short acting bronchodilators, corticosteroids and antibiotics. In severe cases, controlled oxygen therapy and ventilator support are used (GOLD 2015, p. 42). Five year mortality rate of COPD is 50% and prognosis following hospitalization is poor (GOLD 2015, p. 41). Comorbidities affect the prognosis (GOLD 2015, p. 47).
COPD could be prevented by reducing exposure to noxious gases and irritants. COPD is difficult to diagnose until much later and therefore requires routine screening in susceptible populations. There is a need for a much accurate diagnostic method for detection of COPD is the early stages. There is also a dire need to educate people regarding the dangers of inhaling noxious gases and the poor quality of life conferred by COPD and other comorbidities.
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