Summary: The Adaptive Immune System

Asthma is a chronic inflammatory disorder of the bronchial mucosa and hyperreactive bronchial tubes. Its etiology has been linked to both genetic and environmental factors. Several genes, including those that influence the production of proteins and cells involved in the immune response (such as interleukins, eosinophils, mast cells) have been linked with asthma. A decreased number of T-regulatory cells is also associated with asthma. Environmental factors linked with asthma include exposure to allergens, urban residence, and smoking (or exposure to secondary smoke). Recurrent respiratory tract viral infections may also contribute to the development of asthma. Decreased exposure to certain infectious organisms during early childhood, and the consequent underdevelopment of the immune response, can also lead to the development of asthma--this is known as the hygiene hypothesis (McCance & Huether, 2014, p. 1263-4).

COPD is one of the greatest causes of disability and mortality in the twenty first century with future predictions painting an even graver story. Occupation, genome, and primarily smoking are the main causes of COPD. COPD is the third leading cause of death in America, claiming the lives of 134,676 Americans in 2010. Symptoms are typical of a constant smokers cough which progresses into the debilitating palliative stage of the disease; the development of co-morbidities exacerbates these symptoms. COPD has a complex pathophysiology involving hyperinflation, excessive mucus production and airway remodeling; diagnosis is through lung function tests. COPD is poorly managed with few effective treatments and a poor

The study included 100 patients with COPD. All patients fulfilled the inclusion and exclusion criteria. According to its demographic and clinical parameters and treatment groups differ among themselves. Completed the study, all patients included in the study. The therapy in all patients with a clinically meaningful improvement of symptoms was observed.

As you already know, Chronic Obstructive Pulmonary Disease (COPD), manifests itself when the passageway of air to the lungs is severely obstructed, thus preventing sufficient flow of oxygen into the bloodstream.1 The pathophysiology of COPD is a complex process that is the result of multiple airway diseases that simultaneously contribute to the impairment of airflow in the lungs.1 Specifically, the overlapping outcome of chronic bronchitis and emphysema is the pathogenesis of COPD.1 The risk factor for the COPD is influenced by the individual’s genetics, age, gender, exposure to air pollution, socioeconomic status, and the use of tobacco products.1 The use of tobacco products can increase the development of COPD.1 However, individuals that don’t smoke can also attain COPD.1 Therefore, COPD is not exclusive to individuals that smoke on a daily basis.1 In fact, genetics and the natural aging process plays a part in the development of pulmonary issues.1 For example, it has been proven that a deficiency in the alpha -1 antitrypsin gene is correlated with the development of COPD.1 The natural deterioration of lung tissue, coupled with the long term exposure to environmental elements, explains why the risk of attaining COPD increases as one progresses to the latter stages of their lives.1 In a healthy individual, goblet cells secrete about one liter of mucous that provides a moist surface over the lungs, trachea, and esophagus.1 The cilia on the pseuodocolumnar epithelial cells continuously sweep the mucus in the lungs in an upward motion.1 The cilia sweeps the mucosal trapped debris up, and removes pathogens and other foreign particles out the pulmonary tissue.1 In individuals with COPD, the pathogenesis of the disease creates structural modifications of the lung tissue, which result in deformed and nonfunctioning cilia.2 The lack of functioning cilia leads to the buildup of mucous, pathogens, and subsequent respiratory infections.2 Furthermore, the body tries to combat

Let us first discuss your recent diagnosis of COPD. You may have wondered what COPD is and what caused it. Excellent questions! COPD stands for chronic obstructive pulmonary disease (Mayo Clinic Staff, 2016). Chronic inflammation obstructs your airflow, resulting in trouble breathing and excess mucus production. So what exactly causes that chronic inflammation? Cigarette smoke and other noxious gases cause this inflammation in your lungs and airway (Mayo Clinic Staff, 2016). Not everyone who smokes gets COPD. Also, not everyone who has COPD smokes. Workplace exposure to noxious gases can also lead to COPD. Additionally, there is a genetic disorder that causes an underproduction of a lung protecting protein (Mayo Clinic Staff, 2016).

When the respiratory tissue damaged, the body’s inflammatory responses cause the lining of the airways to become swollen and thickened as a result of constant irritation that leads to an excessive mucus secretion in effort to protect the lungs from inhaled irritants such as cigarette smoking, air pollution, passive smoking, occupational dusts and chemicals (Currie 2009).

All over the world, chronic obstructive pulmonary disease (COPD) is a very significant and prevalent cause of morbidity and mortality, and it is increasing with time (Hurd, 2000; Pauwels, 2000; Petty, 2000). Due to the factor of COPD being an underdiagnosed and undertreated disease, the epidemiology (Pauwels, Rabe, 2004) is about 60 to 85 % with mild or moderate COPD remaining undiagnosed (Miravitlles et al., 2009; Hvidsten et al., 2010).

The World Health Organization (WHO) (2006A) defines COPD as a disease state characterized by airflow limitation that is not wholly reversible. The airflow limitation is usually both progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases. John's chronic bronchitis is defined, clinically, as the presence of a chronic productive cough for 3 months in each of 2 successive years, provided other causes of chronic cough have been ruled out. (Mannino, 2003). The British lung Foundation (BLF) (2005) announces that chronic bronchitis is the inflammation and eventual scarring of the lining of the bronchial tubes which is the explanation for John's dyspnea. The BLF (2005) believe that when the bronchi become inflamed less air is able to flow to and from the lungs and once the bronchial tubes have been irritated over a long period of time, excessive mucus is produced. This increased sputum results from an increase in the size and number of goblet cells (Jeffery, 2001) resulting in John's excessive mucus production. The lining of the bronchial tubes becomes thickened and an irritating cough develops, (Waugh & Grant 2004) which is an additional symptoms that john is experiencing.

According to the Australian Nurses’ Dictionary (King, J, et.al, 2012) COPD is defined as “A combination of chronic bronchitis and emphysema in which there is disruption of air flow into or out of the lungs. Dyspnoea, wheezing and cough predominate, often made worse by any exertion or pollution in any environment. Patients may be severely disabled and require oxygen for long periods of time.” The most common cause of COPD is chronic cigarette smoking, although only 25% of smokers will develop COPD of a moderate severity. Others may develop COPD as a result of a normal decline in lung function as age progresses, these patients may suffer airflow obstruction without abnormal inflammatory changes. The airflow limitation results in three different pathological mechanisms: thickening of small airways, emphysema and luminal obstruction with mucus and plasma exudate.

Chronic Obstructive Pulmonary Disease, also known as COPD, is the third leading cause of death in the United States. COPD includes extensive lungs diseases such as emphysema, non-reversible asthma, specific forms of bronchiectasis, and chronic bronchitis. This disease restricts the flow of air in and out of the lungs. Ways in which these limitations may occur include the loss of elasticity in the air sacs and throughout the airways, the destruction of the walls between air sacs, the inflammation or thickening of airway walls, or the overproduction of mucus in airways which can lead to blockage. Throughout this paper I am going to explain the main causes, symptoms, diagnosis, and ways to reduce COPD.

Chronic bronchitis, the fourth leading cause of death in the United States, is a main component of Chronic Obstructive Pulmonary Disease (COPD) that is characterized by airflow limitation that is irreversible. Clinically chronic bronchitis is defined as prolonged inflammation of the bronchi and bronchioles that leads to insistent coughing and overproduction of mucus recurrently for at least three months per year, two years in a row (Mannino, 2002). Inflammation decreases the diameter of both the bronchi and bronchioles and consequently makes breathing much more challenging. Smoking is the number one risk factor of chronic bronchitis. According to the

COPD has been considered primarily as a respiratory disease however the importance of extrapulmonary manifestations has not been acknowledged until recenty.64 Epidemiological studies and large clinical trials have helped us to understand the importance of co-morbidities.65 Pathophysiology of COPD focussed on the concept of systemic inflammation, has helped us to explain the higher frequency of major co-morbidities such as metabolic, cardiovascular, skeletal and nutritional disorders that would be seen in these patients in addition to the co-existing conditions that one would naturally expect in elderly patients.

Cigarette smoke is harmful and it contains over 60 known carcinogens particularly polycyclic aromatic hydrocarbons and nitrosamines. Cytochrome P450 enzymes metabolically activate these polycyclic aromatic hydrocarbons and nitrosamines, which can then bind to DNA leading to DNA adducts.(Br Med Bull (2010). These carcinogens are main reasons that a person who smokes a lot of cigarette is likely to get lung cancer, or that person may not cancer at all. Genetic studies have identified a nicotine dependence locus on chromosome 15q24-25, which includes the αα5-α3-β4 nicotinic receptor gene cluster. A polymorphism, which alters an amino acid in the αα5 nicotinic receptor subunit, also influences the risk for lung cancer, COPD and vascular disease (Br Med Bull (2010)).

Although asthma and COPD share some degree of clinical overlap, they are frequently viewed as separate diseases.[9] The most difficult group of patients in which to distinguish the 2 conditions are those who are current or former smokers with a 15- to 20-pack-year history. In smokers as young as 30 to 40 years, clinical and pathologic manifestations resembling early-stage COPD may be present, which is suggestive of a mixed or intermediary

Bronchitis is an inflammation and swelling of the respiratory tubes between the nose, throat and the lungs. These tubes include the trachea, the bronchi, and the bronchioles. Chronic Bronchitis is a serious long-term lung disease that can be caused by a long-term exposure to inhaled irritants such as cigarettes. Chronic Bronchitis is one of the conditions that correlates with Chronic Obstructive Pulmonary Disease (COPD). As the study shows M.K is noted to have a history of smoking for 22 years. Smoking is known to be the predominant cause associated with chronic bronchitis. Risk factors commonly lead to acute exacerbation and estimates suggest that cigarette smoking account for 85-90% of bronchitis and chronic obstructive pulmonary disease. Smoking impairs the ciliary movement, which obstructs the function of alveolar macrophages. M. K is also exhibiting chronic cough with severe sputum mainly in the morning. Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause coughing. The alveolar epithelium is both the target and the initiator of inflammation because the airway epithelial cells release inflammatory mediators in response to toxic, infectious, and inflammatory stimuli which decrease the release of regular products such as angiotensin-converting enzyme or neutral endopeptidase. As the patient experiences sputum production, the sputum becomes purulent because of the presence of neutrophils increases the quantity of sputum