Chronic Airway Disease - Essay Example

of the Health Sciences and Medicine of the concerned 19 May Chronic Airway Disease 0 Introduction and ification of Diseases that affect lung function Diseases of lung can be classified depending upon the part of the respiratory system affected as well as the duration of the disease. Chronic diseases of lung can be further classified into obstructive and restrictive disorders. Restrictive lung diseases are characterised by restricted expansion of the lung or chest wall. Obstructive diseases are called obstructive because there is an obstruction to the egress or ingress of air through the airways (Hyatt, Scanlon & Nakamura 2009). Asthma and chronic obstructive pulmonary disease (COPD) form the majority of lung diseases typified by airflow limitation. Asthma is a distinct clinical entity, differentiated from COPD on the basis of onset at an early age, largely reversible airway obstruction and an associated history of allergy (Celli & MacNee 2004). The term COPD has traditionally included two components: chronic bronchitis and emphysema. Chronic bronchitis is epidemiologically defined as presence of cough and mucous production in at least 3 consecutive months for at least 2 consecutive years (Global Initiative for Chronic Obstructive Lung Disease 2011). Emphysema is characterised by the destruction of lung parenchyma distal to terminal bronchioles and loss of elastic recoil (Global Initiative for Chronic Obstructive Lung Disease 2011). However, recently it has been suggested that emphysema is a pathological not clinical diagnosis and that chronic bronchitis can occur even in the absence of airway limitation (Global Initiative for Chronic Obstructive Lung Disease 2011). Thus, COPD has been defined as a preventable and treatable disease which has progressive and irreversible airflow limitation associated with chronic inflammatory response and FEV1/FVC < 0.7(NICE 2010). 1.1 Epidemiology and prevalence of Chronic Obstructive diseases COPD most commonly affects the elderly population with smoking as the most important risk factor. In Great Britain, it causes more than 25000 deaths each year and the prevalence is estimated to be more than 1.5 million (Health and Safety Executive 2011). In terms of economic burden, direct and indirect costs due to COPD amount to nearly 50 billion dollars in United States alone (Global Initiative for Chronic Obstructive Lung Disease 2011). This is brought about by hospitalisation, oxygen and treatment costs as well as because of loss of productivity during acute exacerbations of the disease. 2.0 Historical Background Description of chronic bronchitis was first given by Badham way back in 1814 and Laennec described features of emphysema from the lungs of the patients which he dissected (Petty 2006). Since then, the history of COPD has evolved amidst spirometer, invented in 1846 and FVC proposed by Gaensler in 1950 (Petty 2006). Various consensus definitions have been proposed over years and now evidence based guidelines have been established by NICE, Global Initiative for Chronic Obstructive Lung Disease (GOLD) and American Thoracic Society and European Respiratory Society. 3.0 Signs and Symptoms of Chronic Obstructive Pulmonary Disease A patient of chronic obstructive pulmonary disease presents with long standing cough, dyspnoea, phlegm formation and easy fatigability. COPD is a progressive disease and decline in lung function usually starts long before the symptoms manifest (NICE 2010). Onset of symptoms is heralded by an accelerated impairment of lung function. 3.1 Shortness of breath COPD patients complain of marked shortness of breath (air hunger), tightness in the chest and uncomfortable awareness of one’s own breathing (dyspnoea). Dyspnoea is typically progressive and is aggravated with physical activity. Dyspnoea is objectively assessed using either Medical Research Council (MRC) Scale (Table 1) questionnaire as recommended by GOLD (2011) as well as NICE (2010) guidelines. Table 1 MRC dyspnoea scale Grade Degree of breathlessness related to activities 1 No breathlessness except on strenuous exercise 2 Short of breath when hurrying or walking up a slight hill 3 Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace 4 breathless after walking about 100 metres or after a few minutes on level ground 5 Too breathless to leave the house, or breathless when dressing or Undressing 3.2 Persistent and chronic Cough and phlegm formation Chronic cough which is persistent and may be productive or non-productive is the initial hallmark symptom of the disease. Rarely, cough may be absent in patients of with airflow limitation. Chronic bronchitis patients have, as their chief complaint, excessive mucous production associated with cough (Braman 2006). Infact, chronic bronchitis has been defined as a disease on the basis of sputum production. Respiratory infections are associated with purulent sputum, increased production and sometimes, haemoptysis. 3.3 Wheezing Audible and noisy breathing called wheezing is typically present in COPD. Adventitious lung sounds can also be auscultated over lung fields (Global Initiative for Chronic Obstructive Lung Disease 2011). It is produced because of increase in the velocity of airflow in the obstructed or thickened airways. 3.4 Fatigue Above mentioned symptoms are associated with marked limitation of exercise tolerance and decreased stamina which result in physical disability and decreased quality of life. Apart from these clinical features, history of exposure to risk factors such as tobacco smoke, dust and occupational exposure to pollutants may be elicited. Symptom history of associated co-morbidities such as cardiovascular disease, for example pedal edema because of cor pulmonale, may also be spelled out by the patient. Non specific features of a chronic disease like loss of weight and appetite are often present (Global Initiative for Chronic Obstructive Lung Disease 2011). So far as the signs are concerned, physical examination of patients with chronic bronchitis reveals use of accessory muscles of respiration, prominent supraclavicular fossae and tracheal tug on examination, and wheeze on chest auscultation. Wheeze may not be auscultated in emphysema but breath sounds are decreased and increase in antero-posterior diameter of the chest gives the appearance of a barrel-shaped chest. 4.0 Causes for Chronic Obstructive Pulmonary Disease COPD is believed to result from interaction between environmental and genetic factors. 4.1 Smoking Globally, cigarette smoking is the most important risk factor for the development of COPD. Smokers have a higher prevalence of disease as well as higher mortality rates (Global Initiative for Chronic Obstructive Lung Disease 2011). Both active and passive smoking and other forms of tobacco can cause COPD. In fact, it is the only risk factor whose removal has been associated with easing of decline in FEV1. Noxious chemicals present in cigarette smoke initiate a cycle of inflammation and oxidative damage which leads to pathological changes in the airways and lung parenchyma. 4.2 Pollutants and exposures due to Occupation Epidemiological association of occupation and COPD has been proved in up to 15% patients of COPD (Braman 2006). However, it is difficult to conclusively identify occupation as the causative factor because cigarette smoking is often a confounding factor. Common agents at work place which can cause respiratory symptoms are organic dusts, smoke, oil vapours, coal, silica, second hand smoke etc (Braman 2006). Indoor pollutants like smoke from wood fire, cow dung and coal are often ignored factors which are probably significant in view of their long term exposure. Outdoor pollution by exhausts and emissions from motor vehicles in heavily populated urban areas gives rise to respiratory symptoms as well as cause acute exacerbations in those with an already established disease(Global Initiative for Chronic Obstructive Lung Disease 2011). 4.3 Genetics In addition to environmental factors, genetic mechanisms have been proposed by which external stimuli are able to exert their action. Variations in genes concerned with antioxidant protective mechanisms have been implicated in the pathogenesis such as heme oxygenase (HMOX-1), glutathione S-transferase, microsomal epoxide hydrolase and matrix metalloproteinases (Molfino 2007). These lead to an accelerated decline in lung function. It has also been reported that acute exacerbations of COPD may be related to single nucleotide polymorphism of inflammatory mediator CCL 1gene (Takabatake et al 2006). In nearly 3% of COPD patients, proven genetic pattern of autosomal dominant inheritance is seen. These non-smoker individuals go on to develop emphysema because of deficient allele of alpha 1 antitrypsin (Lee, Gildea & Stoller 2002). 4.5 Autoimmune Disease That the inflammatory component of COPD has an autoimmune mechanism was suggested by Raj et al (2008). Autoimmunity is being explored as the possible reason why all smokers do not develop COPD. Recently, authors have linked an increased prevalence of COPD in patients with autoimmune diseases. However, more evidence is required to understand and conclusively demonstrate the relationship between autoimmunity and COPD (Hemminki et al 2011). 4.6 Other Risk Factors Age is obviously an important risk factor. Poor socio economic status, inadequate ventilation in cooking areas, recurrent respiratory infections and airway hyper-reactivity are some of the other risk factors (Celli & MacNee 2004). Gender, per se, is not a risk factor as the incidence of COPD has been increasing in women consistent with the increasing trend of smoking amongst women (Global Initiative for Chronic Obstructive Lung Disease 2011). 5.0 Pathophysiology and pathology of Chronic Lung Diseases Expiratory airflow obstruction, hyperinflation and air trapping are the pathophysiological manifestations of COPD. 5.1Chronic Bronchitis Increased number of inflammatory cells (neutrophils & macrophages) and pro-inflammatory cytokines (Interleukins 1, 6 & 8) are found in the sputum of COPD patients. Thus, airway inflammation is presumably the basic pathophysiology of COPD and is mainly triggered by smoking. Apart from inflammation, other factors incriminated in the pathogenesis of COPD are oxidative stress and altered balance between proteinase and antiproteinase activity (Celli &MacNee 2004). Pathological changes that develop as a result of inflammation and oxidative stress in the airways are mucosal oedema, smooth muscle and mucus gland proliferation, and resultant airway narrowing. Mucociliary abnormalities lead to pooling of mucous secretions leading to an increased bacterial count which depresses local immunity and results in creation of a vicious cycle (Braman 2006). As a result of above mentioned pathological changes, clinical features of persistent cough, airflow limitation, auto PEEP and air trapping, abnormalities in gas exchange and eventually pulmonary hypertension occur (Global Initiative for Chronic Obstructive Lung Disease 2011). 5.2 Emphysema Loss of lung parenchyma in emphysema basically occurs by proteinase and free radical activity. These are produced in the alveoli as a reaction to stimuli such as smoke. Other contributing factors that have been implicated are cell apoptosis and mechanical damage (Ingenito et al 2004). In long term, tissue remodelling and destruction occurs because of loss of structural proteins like collagen and elastin. End result is airflow limitation, hyperinflation, and loss of parenchyma and lung recoil (Ingenito et al 2004). Morphologically, emphysema can be divided into centriacinar, panacinar and distal acinar depending upon the part of acinus affected (Lee, Gildea & Stoller 2002). Centriacinar emphysema is predominantly seen in smokers, while panacinar emphysema is found in alpha1 antitrypsin deficiency (Lee, Gildea & Stoller 2002). Loss of pulmonary parenchyma gives rise to gas exchange abnormalities and pulmonary hypertension due to chronic hypoxia (Global Initiative for Chronic Obstructive Lung Disease 2011). 6.0 Diagnosis of Chronic Obstructive Pulmonary Disease COPD diagnosis is based on the assessment of clinical symptoms, presence of risk factors and spirometry criteria. 6.1 Spirometry Airflow limitation can be objectively measured with spirometry and it is used to support the clinical diagnosis of COPD (NICE2010 & Global Initiative for Chronic Obstructive Lung Disease 2011). FEV1/FVC fixed ratio of < 0.7 persisting after bronchodilator administration makes evident the irreversibility of airflow obstruction and hence, the diagnosis of COPD. Spirometry measures the Forced Vital Capacity (FVC) which is the volume of air exhaled with maximum effort after a forceful inspiration and Forced Expiratory Volume in 1st second (FEV1) which is part of FVC exhaled in the 1st second. The cut off point for the ratio of these two is 0.7. Reversibility testing should be performed if diagnostic doubt remains in differentiation of COPD from asthma. Apart from diagnosis, spirometry is useful in COPD for assessing severity of the disease, response to therapy and as a part of preoperative assessment of lung function (Karkhanis & Joshi 2012). 6.2 Other Tests such as blood tests, x-ray At the time of diagnosis, imaging studies, diffusion capacity of lungs, haematological investigations, sputum culture and exercise testing are also performed in addition to spirometry in COPD patients (NICE2010 & Global Initiative for Chronic Obstructive Lung Disease 2011). Imaging includes chest X-rays and CT chest depending upon the clinical profile of the patient. Alpha 1 antitrypsin assay can be carried out for patients who are non-smokers and the onset is at a younger age. ECG and echocardiogram are done if cor pulmonale is suspected (NICE 2010). 7.0 Management of Chronic Obstructive Pulmonary Disease 7.1 Risk factor reduction So far as the management of cough and mucous production part of symptoms is concerned, risk factor reduction is the best treatment. Avoiding exposure to noxious stimuli like smoke and pollutants prevents acute exacerbations as well as most effectively resolve the troublesome symptom of cough (Braman 2006). All COPD patients are encouraged to quit smoking but are unable to do so because of physical and psychological dependence issues (van der Valk et al 2004). Nicotine replacement therapy and behavioural support can be offered to those who wish to quit as appropriate (NICE 2010). Encouragingly, quit rates have been rising but whether this will translate into a lower incidence of COPD is yet to be seen (Pride 2001). Other modifiable risk factors are occupation, environmental pollution and recurrent infections (Celli & MacNee 2004). To prevent infections, it is advisable for the patients to get annually vaccinated against pneumococcus and influenza (NICE 2010). 7.2 Medication Drug therapy relieves the symptoms but has not been shown to halt the progression of disease (van der Valk et al 2004). Pharmacological management of stable COPD can be categorised into inhaled therapy, oral therapy and oxygen therapy. (NICE 2010). Inhaled therapy is favoured. Inhalational agents that are used are bronchodilators (short acting and long acting beta2 agonists, SABA & LABA respectively and anticholinergics), corticosteroids and combination therapy (Celli & MacNee 2004 & NICE 2010). To begin with, SABA is used for management of breathlessness and improves exercise tolerance. LABA delays the onset of acute exacerbations. In patients with unrelieved breathlessness and FEV1 Read More