3rd Intrenational Conference on Chronic Obstructive Pulmonary Disease July 11-12, 2016 Brisbane, Australia

COPD is a disease that involves inflammation and thickening of the airways. It also involves destruction of the tissue of the lung where oxygen is exchanged. It is described by the Global Initiative for Chronic Obstructive Lung Disease as “a preventable and treatable disease…characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. This progressive and relentless loss of lung function is caused by emphysema due to destruction of lung parenchyma. Smoking(long term smokers), Chronic bronchitis, Inherited factors(genes) and by narrowing of small airways as a result of chronic inflammation and fibrosis and loss of elastic recoil. This results in progressive airflow limitation, air trapping, and progressive shortness of breath on exertion.

The current paradigm for the pathogenesis of chronic obstructive pulmonary disease is that chronic airflow limitation results from an abnormal inflammatory response to inhaled particles and gases in the lung. Airspace inflammation appears to be different in susceptible smokers and involves a predominance of inhaled irritants such as CD8⁺ T lymphocytes, neutrophils, and macrophages, B cells and macrophages to accumulate. When activated, these cells initiate an inflammatory cascade that triggers the release of inflammatory mediators such as tumour necrosis factor alpha (TNF-α), and leads   to   Structural changes.  Airway remodelling in COPD is a direct result of the inflammatory response associated with COPD and leads to narrowing of the airways. Three main factors contribute to this: peril bronchial fibrosis, build-up of scar tissue from damage to the airways and over-multiplication of the epithelial cells lining the airways. Parenchymal destruction is associated with loss of lung tissue elasticity, which occurs as a result of destruction of the structures supporting and feeding the alveoli. This means that the small airways collapse during exhalation, impeding airflow, trapping air in the lungs and reducing lung capacity.

Comorbidities such as cardiac disease, diabetes mellitus, hypertension, osteoporosis, and psychological disorders are commonly reported in patients with chronic obstructive pulmonary disease (COPD) but with great variability. Tobacco smoking is a risk factor for many of these comorbidities as well as for COPD, making it difficult to draw conclusions about the relationship between COPD and these comorbidities. Epidemiological studies and large clinical trials have helped us to understand the importance of comorbidities .However; recent large epidemiologic studies have confirmed the independent detrimental effects of these comorbidities on patients with COPD. Many of these comorbidities are now considered to be part of the commonly prevalent to COPD. The common ground between most of these extra pulmonary manifestations is chronic systemic inflammation.

Many treatments can help ease the symptoms and slow the progression of the illness. There are several paths for the treatment of chronic obstructive pulmonary disease. However, lifestyle changes and treatments can help you feel better, stay more active, and slow the progress of the disease. Health care provider may prescribe medications to control the symptoms of COPD like bronchodilators, anti-inflammatories, and antibiotics. The main therapeutic options for the management of COPD are inhaled corticosteroids and bronchodilators. Inhaled corticosteroids significantly reduce inflammatory cells in the lungs, as well as systemic inflammatory markers such as C-reactive protein, compared with placebo. The goals of COPD treatment include relieving symptoms, slowing the progress of the disease, preventing and treating complications, and improving overall health status. In patients with COPD bronchodilators improve lung function to some extent and relieve dyspnea. Within short-acting   bronchodilators, ipratropium is as effective as salbutamol (sympathomimetic agent) with fewer adverse effects. Presently, maintenance therapy is based on long-acting inhaled bronchodilators.

Assessment of patients with chronic obstructive pulmonary disease (COPD) is important to establish an accurate diagnosis, assist in making therapeutic decisions, measuring outcomes for clinical and research purposes. Assessment of patients with COPD for both clinical and research purposes should incorporate a variety of different outcomes. There are outcome measures that have been successfully incorporated in large clinical trials and the design and outcomes of these trials can be used to plan future clinical investigations in COPD. The most widely used current definitions of COPD are provided by two current clinical practice guidelines.

Clinical history and physical examination should help to determine the possible cause and site of respiratory disease. The results of the history, physical examination, and chest x-ray often suggest what additional testing may be needed to determine what is causing the person's symptoms.  A test for lung disorders is done by measuring the lungs' capacity. Transthoracic fine needle aspirates of lung often are useful in the diagnosis of fungal pneumonia but have lower yields in the definitive diagnosis of solitary pulmonary lesions. Solitary pulmonary masses often require transthoracic lung biopsy or surgical excision for definitive diagnosis. Transthoracic ultrasonography is a sensitive diagnostic tool for pleural disease (eg, pleural effusion, pneumothorax) and for parenchymal lung disease when lesions are adjacent to the pleural surface.

The aim of the present study is to manage the impact of COPD on health status by Characterization of human lung tissues by advanced molecular, biochemical, microbiological, and histo pathological methods. A better understanding of the cellular and molecular mechanisms that are involved in the underlying inflammatory and destructive processes has revealed several new targets for which drugs are now in development, and the prospects for finding new treatments are good. Research progress in COPD is hampered by a lack of fundamental knowledge regarding the pathology of this disease, particularly with regard to small airways. Changes with COPD in the structure, cellular composition, inflammatory status, and chemical milieu of the lung are poorly defined, as are the relationships of these changes to clinical manifestations of the disease. Characterization of lung tissues can now be performed with exquisite detail, using advanced methods of immunology. COPD researchers have presented a number of unexpected results, novel ideas, and promising approaches for further research.

Surgery is needed to take biopsies (tissue samples) of the lung for diagnosis. Recent advances in optic/video systems and endoscopic operating instruments have made thoracoscopic easier and more accurate than 20 years ago. The operative mortality rate was low (1%) and the diagnostic accuracy high (99%). Thoracoscopic has been performed at an increasing frequency in recent years because of its expanded applications, especially in the areas of therapeutic or operative procedures such as carbon dioxide laser treatment of spontaneous pneumothorax or diffuse bullous emphysema in the treatment of various airway diseases. Two common ways to do surgery on your lungs are thoracotomy and video-assisted thoracoscopic surgery (VATS). It involves passing a telescopic camera through small cuts in the chest to examine the lungs or pleura (linings of the lung) under video guidance.

People with COPD have difficulty clearing their lungs of bacteria, dusts and other pollutants in the air. This makes them at risk for lung infections that may cause further damage to the lungs. Historically, acute toxicity was associated with occupational exposures to concentrations of soluble beryllium salts greater than 100 mg/m³. With the advent of industrial control measures to minimize air levels, acute pulmonary syndromes have virtually disappeared. In addition to environmental exposure, genetic predisposition seems to have a major role in the development of CBD. A variant of the human leukocyte antigen (HLA-DPb1 [Glu69]) is found in 80% to 97% of patients with CBD and in only 30%