Tobacco-Related Respiratory Diseases - Assignment Example

Assignment 1: Tobacco Related Respiratory Diseases Name Institution Course Instructor Date Abstract Tobacco related respiratory diseases are associated with high morbidity and mortality rates. They have large costs of disease burden in Australia despite being preventable. The diseases include emphysema, chronic bronchitis and lung cancer. The pathogenesis of these diseases is discussed. The data that was used to generate content for the study was derived through secondary research methods. A search into PubMed, and other medicine and health websites as well as Australia’s national data on smoking related diseases was conducted. The data was analysed by appraising various articles and selecting those that helped to address the focus of the study. The data is also based on recent publications to ensure that the information is valid and reliable. Findings show that tobacco-related lung cancer is a major cause of death in Australia. The risks associated with smoking are also dependent on many factors including genetics, age, gender, socioeconomic implications and behavioural factors. Introduction Substantial evidence exists that smoking is associated with various respiratory diseases (Jeffrey & Teri 2009). The diseases compromise the health of an individual posing the risk of being affected by other chronic diseases, contributing to morbidity and mortality rates of the society (Verstappen et al. 2013). This paper discusses tobacco associated morbidity and mortality in Australia, pathogenesis of tobacco-related emphysema, chronic bronchitis and lung cancer. Finally, the paper discusses laboratory tests used in the screening, diagnosis and monitoring of smoking associated respiratory diseases. 1. General discussion a) Tobacco associated morbidity and mortality in Australia Australia experiences a smoking epidemic characterised by historic rate of prolonged, heavy smoking, and currently, low prevalence and cessation in the total number of smokers (Banks et al. 2015). Smokers are at a higher risk of a range of health problems including cancers, respiratory and cardiovascular diseases (Banks et al. 2015). Tobacco smoking was found to be the largest single risk factor for lung cancer in Australia, 90% in men and 65% in women. According to statistics from the Australian Government Department of Health (2015), tobacco smoking kills an estimated 15,000 Australians and costs the government $31.5 billion in health, social and economic costs. Statistics on tobacco smoking in Australia, and its associated morbidity and mortality is usually generated from national surveys conducted by the Australian Institute of Health and Welfare (AIHW) and the Australian Bureau of standards (ABS). According to AIWH (2014) tobacco smoking accounted for at least 25 percent of cancer cases in Australia in 2012. The current AIWH (2014) statistics shows that daily smoking among the general population declined between 2010 and 2013, and has reduced by almost half since 1991. This reduction is from 24.3% in 1991 to 12.8% in 2013. The reasons given for quitting or attempting to quit are the high costs and health concerns associated with smoking. The ABS (2014) showed tobacco sales decreased from $3.508 in December 2012 to $3.405 in March 2014. Smoking prevalence vary across various population groups. It is higher among Aboriginal and Torres Strait Islander Australians than non-indigenous Australians and also higher among people living in remote areas and people from low socioeconomic backgrounds (Furrukh 2013). b) Tobacco smoking and the pathogenesis of emphysema Emphysema manifests as an increase in size of the air spaces distal to the terminal bronchioles in the lungs, and the type of emphysema closely associated with tobacco smoking is centrilobular which results from the dilation or destruction of the respiratory bronchioles (Bhalla et al. 2009). The protease/antiprotease theory of emphysema pathogenesis suggests that tobacco smoke attracts alveolar macrophages to the distal terminal bronchioles (Bhalla et al. 2009). These bronchioles release neutrophil chemotactic factors which attract polymorphonuclear leucocytes to release serine protease -potent proteolytic enzymes. The enzymes work in addition to the alveolar macrophage protease and cleave all the macromolecules of the lung interstitium (Demkow & Overveld 2010). Thus a protease-antiprotease imbalance leads to emphysema. The imbalance is attributed the increased number of alveolar macrophages and neutrophilis. There is also the panlobular form of emphysema associated with alpha 1-antitrypsin (α1-AT) deficiency as α1-AT, a normal lung fluid constitute is antagonistic to serine elastatse (Demkow & Overveld 2010). However, α1-AT can be oxidised by oxidants in tobacco smoke and its deficiency therefore results in dilation or the destruction of the acinus. It is believed that genetic factors play a role in emphysema because not all tobacco smokers develop emphysema (Hecht 2012). c) Tobacco smoking and the pathogenesis of chronic bronchitis Chronic bronchitis is a type of chronic obstructive pulmonary disease (COPD) characterised by overproduction and hyper-secretion of mucous by goblet cells (Demkow & Overveld 2010). Clinically, the patient may have accelerated decline in lung function, greater airflow obstruction in smokers, increased frequency of severity and worse overall mortality (Gupta et al. 2013). The patient coughs and produces sputum due to an innate immune response to inhaled toxic particles in the tobacco smoke (Caminati et al. 2012). The airway inflammation is associated with increased mucus production, reduced mucociliary clearance and increased permeability of the airspace epithelial barrier (Demkow & Overveld 2010). Chronic hyper secretion of mucous contributes to airflow limitation in the later stages of the disease (Demkow & Overveld 2010). The process may be a reflection of an inflammatory response in the sub mucosal glands. The inflammatory cells produce serine proteases which are secretagogues for mucous (Demkow & Overveld 2010). The oxidants derived from the tobacco smoke and released from inflammatory leukocytes may also be involved in the overproduction of mucin through the induction of the MUC5AC gene (Furrukh 2013). d) Tobacco smoking and lung cancer Tobacco smoking is the most established cause of lung carcinogenesis and contributes to small cell lung carcinoma (SCLC) and squamous-cell carcinoma (SCC) (Furrukh 2013). Tobacco smoke has several compounds many of which are carcinogenic (Hecht 2012). Carcinogens present in tobacco products and their immediate metabolites can activate multiple signalling pathways leading to lung cancer carcinogenesis (Caminati et al. 2012). These carcinogens include the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and polycyclic aromatic hydrocarbons (PAH) which play a major role in lung cancer induction (Hecht 2012). They can also interact with the DNA and cause genetic changes (Furrukh 2013). The NNK and PAH carcinogens need metabolic activation to exert their carcinogenic effects (Furrukh 2013). The metabolic activation process leads to formation of carcinogenic DNA adducts which covalently bind to DNA Guanine or Adenine and cause mutation (Furrukh 2013). Apoptosis or programmed cell death can remove the damaged or mutated DNA. However, if the adducts escape the cellular repair mechanisms and persist, it leads to miscoding, which may results in a permanent mutation (Xue, Yang & Seng 2014). The occurrence of a permanent mutation in a critical region of an oncogene or tumour suppressor gene, it can cause the activation of the oncogene or deactivation of the tumour suppressor gene (Xue 2014). If such events are repeated severally, they cause aberrant cells with loss of normal growth control and ultimately to lung cancer (Xue, Yang & Seng 2014). e) Laboratory tests used in the screening, diagnosis and monitoring of smoking associated respiratory diseases Pulmonary function tests are usually used to screen, diagnose and monitor smoking associated respiratory diseases and the commonly used test is spirometry (Ranu, Wile & Madden 2011). The spirometry is a measure of lung volume against time and the values of respiration rate and lung volume can be used to screen for respiratory illnesses (Ranu, Wile & Madden 2011). The tests indicate clinical diagnostic symptoms and signs such as chest pain, cough, dyspenea, phlegm production, wheezing, crackles, and over inflation (Ranu, Wile & Madden 2011). The tests indicate abnormal laboratory tests including hypercapnia, hypoxemia, polycythemia and chest radiographs can be diagnosed by the spirometry (Gupta et al. 2013). The tests can help to monitor patients with known pulmonary disease for progreassion and response to treatment such as COPD, pulmonary vascular disease and interstitial fibrosis (Demkow & Overveld 2010). A single spirometry test cannot be counted upon to differentiate respiratory disease, hence the need for differential diagnosis (Price et al. 2010). Chest X-rays can be performed as a differential diagnosis for lung cancer or to rule out conditions such as tuberculosis (Wallace et al. 2009). Conclusion Tobacco smoking has contributed largely to the burden of diseases in Australia through high healthcare costs, morbidity and mortality of the population. Although many people have become aware and are practising cessation, the prevalence of illnesses associated with tobacco smoking is still high in the country. Tobacco related diseases include emphysema, chronic bronchitis and lung cancer. The pathogenesis follows through several mechanisms which entail inflammation of alveolar and obstruction of large and small airways, proteolysis of lung interstitium, and fibrosis, and DNA adducts formation from tobacco smoke metabolites which lead to tumour formation. Pulmonary function tests are used to assess patients with suspected or known smoking-related disease. Spirometery is a common test, a measure of lung volume against time and used to assess the rate of respiration. Further research is required to evaluate why not all smokers develop the discussed respiratory diseases while some non-smokers are affected by these diseases. References: Australian Bureau of Statistics 2014, Australian National Accounts: National Income, Expenditure and Product. Available from: http://www.abs.gov.au/AUSSTATS/abs@.nsf/DetailsPage/5206.0Mar%202014?OpenDocument [August 9 2015]. Australian Government Department of Health 2015, Key Facts and Figures on Tobacco Sales, Consumption and Prevalence. Available from: http://www.health.gov.au/internet/main/publishing.nsf/content/tobacco [August 9 2015]. Australian Institute of Health and Welfare/AIHW 2014, National Drug Strategy Household Survey Report 2013. Drug statistics series no. 28. Cat. No. PHE 183. Canberra: AIHW. Available from http://aihw.gov.au/alcohol-and-other-drugs/ndshs/ [August 9 2015]. Banks E, Joshy G, Weber M, Liu B, Grenfell R...2015, ‘Tobacco smoking and all-cause mortality in a large Australian cohort study: Findings from a mature epidemic with current low smoking prevalence’ BMC Medicine, vol. 13, no. 38, doi:10.1186/s12916-015-0281-z Bhalla D, Hirata F, Rishi A, & Gairola C 2009, ‘Cigarette smoke, inflammation, and lung injury: A mechanistic perspective. Journal of Toxicology and Environmental Health, vol. 12, no. 1 pp. 45-64. Caminati A, Cavazza A, Sverzellati N, & Harari S 2012, ‘An integrated approach in the diagnosis of smoking-related interstitial lung diseases’, European Respiratory Review, vol. 21, no. 125, pp. 207-217. Demkow U & Overveld, F 2010, ‘Roles of elastases in the pathogenesis of chronic obstructive pulomonart disease: Implications for treatment’, European Journal of Medical Research vol 15, no. 2, pp. 27-35. Furrukh M 2013, ‘Tobacco smoking and lung cancer’, Sultan Qaboos University Medical Journal, vol. 13, no. 3, pp. 345-358. Gupta D, Argawal R, Aggarwal A, Maturi V, Dhooria S...2013, ‘Guidelines for diagnosis and management of chronic obstructive pulmonary disease: Joint ICS/NCCP (I) recommendations’, Lung India, vol. 30, no, 3, pp. 228-267. Hecht S, 2012, ‘Lung carcinogenesis by tobacco smoke’, International Journal of Cancers, vol. 131, no. 12, pp. 2724-2732. Jeffrey G, & Teri F 2009, ‘Smoking-related lung disease’, Journal of Thoracic Imaging, vol. 24, no. 4, pp. 274-284. Price D, Yawn B, & Jones R 2010, ‘Improving the differential diagnosis of chronic obstructive pulmonary disease in primary care’, Mayo Clinic Proceedings, vol. 85, no. 12, pp. 1122-1129. Ranu H, Wile M, & Madden B 2011, ‘Pulmonary function tests’, Ulster Medical Journal, vol. 80, no. 2, pp. 84-90. Verstappen S, Lunt M, Luben R, Chipping J, Marshall T, Khaw K... 2013, ‘Demographic and disease-related predictors of abnormal lung function in patients with established inflammatory polyarthritis and a comparison with the general population’, Annals of the Rheumatic Diseases, vol. 72, no. 9, pp. 1517-1523. Wallace G, Winter JH, Winter JE, Taylor T, & Cameron R 2009, ‘Chest X-rays in COPD screening: Are they worthwhile?’ Respiratory Medicine, vol. 103, no. 12, pp. 1862-1865. Xue J, Yang S, & Seng S 2014, ‘Mechanisms of cancer induction by tobacco-specific NNK and NNN’, Cancers, vol. 6, no. 2, pp. 1138-1156. Read More