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Published in Ken Addley, MCQs, MEQs and OSPEs in Occupational Medicine, 2023
COPD is typically caused by inhalation of dusts, gases and vapours which produces inflammation in the airways and/or structural damage to the lung. The main risk remains smoking, though smoking and working in higher risk occupations (e.g., welding) can have an additive effect. Studies which excluded smokers and those with a history of asthma have found that all of the above workers had an increased risk of developing COPD.
Chest
Published in Henry J. Woodford, Essential Geriatrics, 2022
Long-term oxygen (more than 15 hours per day) increases survival in people with severe resting hypoxaemia (not exercise-induced desaturation alone). It is recommended when arterial blood gas analysis shows PaO2 < 7.3 kPa or 7.3 to 8.0 if there is evidence of pulmonary hypertension, peripheral oedema or polycythaemia.28 There is a risk of burns/fire if there is a current smoker within the residence (i.e. not recommended of people who continue to smoke). There is a risk that the person may trip over the oxygen tubing. Long-term non-invasive ventilation may be considered for people with hypercapnia. People with COPD should maintain or increase physical activity where possible. Pulmonary rehabilitation is beneficial in moderate to advanced disease; especially if there is evidence of deconditioning, weight loss, depression and social isolation. It can result in increased muscle mass and exercise tolerance, with reduced breathlessness, which can improve quality of life, functional capacity and reduce anxiety and depression. The effects in older people seem to be similar to those seen in younger age groups.56 An optimal benefit is obtained with programmes lasting six to eight weeks, occurring at least twice weekly.
Respiratory
Published in Kristen Davies, Shadaba Ahmed, Core Conditions for Medical and Surgical Finals, 2020
Chronic obstructive pulmonary disease (COPD) is a chronic progressive respiratory disorder characterised by airway obstruction with little to no reversibility. It is an umbrella term that describes the damage to the airway caused by chronic bronchitis and emphysema.
Identification of cancer risk assessment signature in patients with chronic obstructive pulmonary disease and exploration of the potential key genes
Published in Annals of Medicine, 2022
Qingzhou Guan, Peng Zhao, Yange Tian, Liping Yang, Zhenzhen Zhang, Jiansheng Li
COPD is a common disease with severe health consequences. It is also a high-risk factor for lung cancer. For the non-cancer patients with COPD, it would be significant if their cancer incidence-risk could be assessed. Considering the unique merits of qualitative transcriptional characteristics (also called the within samples REOs of genes), which are insensitive to batch effects and could be used for the analysis of individual patients, a qualitative signature was identified to predict the lung cancer incidence-risk for non-cancer patients with COPD. Key genes for COPD were further identified, optimized by correlation analysis with COPD stage, and filtered in COPD rat model data. The genes that occurred in reverse fashion when the COPD rat model was treated with some TCM were further identified. In summary, the qualitative transcriptional signature circumvented problems associated with batch effects and is suitable for the individualized diagnosis of single samples, making it feasible for application in clinical settings for the surveillance of non-cancer patients with COPD. The value of COPD key genes in both TCM treatment of COPD and cancer prevention should be further explored.
Advances in phosphoproteomics and its application to COPD
Published in Expert Review of Proteomics, 2022
Xiaoyin Zeng, Yanting Lan, Jing Xiao, Longbo Hu, Long Tan, Mengdi Liang, Xufei Wang, Shaohua Lu, Tao Peng, Fei Long
Chronic obstructive pulmonary disease (COPD) is characterized by not fully reversible airflow limitation, varying with cough, phlegm, wheezing, breathlessness, and comorbidities in clinical manifestations. The typical COPD phenotype is mainly chronic airway inflammation, and emphysema type, while special patients will have a more refined inflammatory phenotype. Fibrotic lesions can be found in the small airways and can contribute to small airway obstruction in COPD [4]. This can cause difficulties in breathing and can lead to more severe symptoms of COPD. Different phenotypes of patients have different degrees of expiratory airflow limitation [5]. Asthma is characterized by airway narrowing due to bronchoconstriction and airway inflammation. Asthma may be a risk factor for COPD. In severe asthma, structural changes such as airway remodeling can lead to airway obstruction and a narrower inner diameter of the airway. Approximately 15–20% of COPD patients have features of both of these diseases [6], which is termed asthma-COPD overlap (ACO). Whether COPD, asthma, or ACO, they are all characterizes as heterogeneous diseases, which means more disease burden and challenges to current diagnostic and therapeutic strategies.
Role of RAGE and its ligand HMGB1 in the development of COPD
Published in Postgraduate Medicine, 2022
Lin Chen, Xuejiao Sun, Xiaoning Zhong
Chronic Obstructive Pulmonary Disease (COPD) is projected to become the third leading cause of death worldwide by 2030 [1]. Smoking is the main risk factor, but only 20–25% of smokers eventually develop COPD [2].Interestingly, up to 25% of COPD patients have never smoked [1]. Environmental exposure and genetics also play an important role in COPD pathogenesis [1,3]. COPD is characterized by a progressive and irreversible airflow limitation [1]. Common COPD symptoms include dyspnea, cough and/or sputum production. Post-bronchodilator ratio of forced expiratory volume in the first second to forced vital capacity (FEV1/FVC) < 70% is required for a diagnosis of COPD. The small airway diseases (increased bronchial hypersecretion, narrowing and disappearance of small airways, persistent chronic airway inflammation, etc.) and the parenchymal destruction play a role in the pathogenesis of COPD and cause chronic airflow limitation [4]. To date, long-acting inhaled bronchodilators and anti-inflammatory therapies have been the mainstay of COPD therapy, but can’t stop COPD progression, so far, any therapeutic approach of COPD can’t significantly decrease mortality rate [5]. This may reflect the fact that there is still a poor understanding of the underlying disease mechanisms and new molecular targets are urgently needed to deal with this challenge.