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All rights reserved. healthpermissions@elsevier.comhttp://www.medicinejournal.co.uk/article/PIIS1357303912000680/abstract?rss=yesContents10.1016/S1357-3039(12)00068-0Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5OFCOFChttp://www.medicinejournal.co.uk/article/PIIS1357303912000709/abstract?rss=yesEditorial Board10.1016/S1357-3039(12)00070-9Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5iihttp://www.medicinejournal.co.uk/article/PIIS1357303912000333/abstract?rss=yesAbstract: Asthma is a syndrome of variable airflow obstruction. It is characterized pathologically by bronchial inflammation and remodelling changes, physiologically by bronchial hyperresponsiveness, and clinically by cough, chest tightness and wheeze. Cytokines secreted by CD4+ Th2 type T cells play a major role in coordinating asthmatic bronchial inflammation, while other effector cells, such as myofibroblasts, epithelial cells, smooth muscle cells and endothelial cells (activated partly by Th2 type cytokines and partly by other mediators), play an intermediary role in airways damage and remodelling. Although the pathological changes in the airways in association with asthma are now well described, there is a gap in our understanding of precisely how these changes cause clinical symptoms. A key aetiological trigger factor for asthma is exposure to environmental antigens, in particular inhaled allergens, including occupational allergens and infectious agents, which are probably a major drive to T cell activation in asthma. Genetic factors governing the production of T cell cytokines and their actions on target cells, as well as variability in the structure and development of the mesenchymal elements of the bronchial mucosa influence the risk of developing asthma. Many other environmental agents exacerbate asthma, but the evidence that they cause disease is much less clear.Mechanisms of asthmaChris Corrigan10.1016/j.mpmed.2012.02.007Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Principles of asthma223227http://www.medicinejournal.co.uk/article/PIIS135730391200028X/abstract?rss=yesAbstract: Drugs for obstructive airway diseases include relievers and controllers. Inhaled β2-agonists are the most effective bronchodilators. Short-acting inhaled β2-agonists are used for symptom relief, whereas long-acting inhaled β2-agonists may be added to inhaled corticosteroids if asthma control is poor in those taking low doses of inhaled corticosteroids and are conveniently taken as a fixed combination inhaler. Long-acting β2-agonists are also effective bronchodilators in chronic obstructive pulmonary disease (COPD). Inhaled anticholinergics are the bronchodilators of first choice in COPD and tiotropium once daily is preferred. Inhaled corticosteroids are the first-line controller treatment for chronic asthma, but are much less effective in COPD. Anti-leukotrienes may be used as an add-on therapy in patients with asthma that is not controlled by inhaled corticosteroids, but are less effective than adding a long-acting β2-agonist and the response is unpredictable. Theophylline is a useful add-on therapy in severe asthma and COPD. Anti-immunoglobulin E (anti-IgE) antibody (omalizumab) reduces exacerbations in patients with severe asthma not controlled by maximal does of inhaled therapy, but response is unpredictable and the treatment is very expensive. Roflumilast is an oral phosphodiesterase-4 inhibitor that may be added in patients with severe COPD and frequent exacerbations.Drugs for airway diseasePeter J. Barnes10.1016/j.mpmed.2012.02.002Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Principles of asthma228237http://www.medicinejournal.co.uk/article/PIIS1357303912000308/abstract?rss=yesAbstract: Childhood asthma has a very high disease burden measured in financial and social terms. Wheezing in the preschool age has increased but prediction of long-term symptoms is difficult. The mechanisms causing inflammation are now better understood. Guidelines for management are well established but the use of measures for inflammation, such as exhaled nitric oxide, are less clinically helpful than expected. Tertiary asthma clinics have been established nationwide to manage very severe asthma. Recent tobacco laws will help with long-term management of asthma and there may be emerging evidence that asthma control is generally improving. There are few new medications for asthma management but leukotriene receptor antagonists in young children, combination therapy in school age and omalizumab in very severe asthma show encouraging results.Asthma in childrenWarren Lenney10.1016/j.mpmed.2012.02.004Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Asthma in children238242http://www.medicinejournal.co.uk/article/PIIS1357303912000345/abstract?rss=yesAbstract: Asthma is a disorder of the airways that is characterized by typical symptoms arising from a complex interplay between chronic inflammation and disordered airway function. Worldwide disease prevalence continues to rise steadily and the condition contributes to significant morbidity and preventable mortality. The goals of treatment in asthma are to achieve control of symptoms and to prevent exacerbations. Important non-pharmacological measures include patient education, avoidance of triggers and smoking cessation. Pharmacological management involves the stepwise titration of β-agonist bronchodilators and inhaled corticosteroids according to symptoms. Although satisfactory control of asthma is achieved in primary care for a large proportion of patients, between 5 and 10%, with so-called ‘refractory asthma’, remain poorly controlled and contribute disproportionately to asthma-related morbidity and mortality. The reasons for this are complex and multifactorial and many patients with refractory asthma require referral to specialist centres.Diagnosis and management of adult asthmaPranabashis Haldar, Ian D. Pavord10.1016/j.mpmed.2012.02.008Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Adult asthma243251http://www.medicinejournal.co.uk/article/PIIS1357303912000369/abstract?rss=yesAbstract: Acute severe asthma represents a common medical emergency accounting for over 75,000 UK hospital admissions each year and asthma still accounts for approximately 1500 UK deaths annually. Risk factors for fatal asthma include poorly controlled disease, inappropriate medical management, and adverse behavioural and social factors. Asthma is characterized by chronic airways inflammation, resulting in periodic wheeze, cough and breathlessness. A variety of triggers can precipitate an exacerbation; viral respiratory tract infections are the most common. Exacerbations are identified by an increase in asthma symptoms and fall in lung function. National and international acute asthma management guidelines highlight best practice. All patients presenting with poorly controlled asthma symptoms should be examined and peak expiratory flow (PEF) or forced expiratory volume in 1 second (FEV1) recorded. Patients with a PEF less than 50% of baseline/predicted have a severe exacerbation and should be referred to hospital. Treatment aims to rapidly relieve bronchoconstriction and halt airways inflammation; oxygen, systemic corticosteroids and inhaled bronchodilators represent first-line treatments. Patients with features of life-threatening asthma should receive magnesium sulphate and be discussed with intensive care. Prior to discharge, patients’ medications should be reviewed, asthma self-management plan agreed and early follow-up should be arranged.Acute severe asthma in adultsHannah K. Bayes, Neil C. Thomson10.1016/j.mpmed.2012.02.010Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Adult asthma252256http://www.medicinejournal.co.uk/article/PIIS135730391200031X/abstract?rss=yesAbstract: Chronic obstructive pulmonary disease (COPD) is a physiological diagnosis made on the basis of airflow obstruction. It develops when a genetically susceptible individual encounters a sufficient environmental trigger. Genetic susceptibility is complex and determined by multiple alleles, aside from the model of emphysema caused by α-1 anti-trypsin deficiency. Cigarette smoke is the usual trigger in the developed world but globally the burning of biomass fuel in under-ventilated space is important. In those subjects genetically susceptible to the effects of smoke, there is an airway inflammatory response that is qualitatively and quantitatively different from non-susceptible subjects, predominantly composed of neutrophils, macrophages and CD8+ lymphocytes. Once established, the inflammation can persist even after exposure to smoke has ceased. Airflow obstruction in COPD results from a combination of the airway wall inflammatory response, luminal mucus, and loss of alveolar–airway attachments from co-existent emphysema. Although progressive airflow obstruction is the hallmark of COPD, it is now recognized that there are other important outcomes in this condition, notably exacerbations and the development of co-morbidities.Chronic obstructive pulmonary disease: aetiology, pathology, physiology and outcomeRohit Chitkara, John R. Hurst10.1016/j.mpmed.2012.02.005Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Chronic obstructive lung disease257261http://www.medicinejournal.co.uk/article/PIIS1357303912000357/abstract?rss=yesAbstract: Chronic obstructive pulmonary disease (COPD) is the disease that has been described as the epidemic of our time. Cigarette smoking is the major cause of the disease and smoking cessation is the most effective intervention in both preventing disease development and progression. Once established, COPD causes irreversible airways obstruction that often results in breathlessness. The management of this condition involves initially an accurate diagnosis and a clinical and functional assessment. The primary confirmatory investigation is spirometry, although other tests such as chest X-ray are helpful in excluding other diseases. Treatment is aimed at preventing acute attacks (exacerbations) of disease and stopping disease progression. After smoking cessation, the most effective therapy is pulmonary rehabilitation, a multidisciplinary series of exercise and education sessions, which have been shown to be clinically and cost effective. Drug therapy reduces breathlessness and reduces attack rates. An effective approach to COPD requires cooperation of all healthcare providers working across primary and secondary care boundaries. Many agencies will and should be involved, including GPs, palliative care services, district nurses, hospital specialist services and social services. Patients can be educated about their disease and empowered to self manage, so that they can use health service providers in a more effective manner.Chronic obstructive pulmonary disease: management of chronic diseaseRichard Russell, Jayne Norcliffe, Mona Bafadhel10.1016/j.mpmed.2012.02.009Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Chronic obstructive lung disease262266http://www.medicinejournal.co.uk/article/PIIS1357303912000291/abstract?rss=yesAbstract: Bronchiectasis is defined as irreversible, abnormal dilatation of one or more bronchi, with chronic airway inflammation, associated chronic cough and sputum production, recurrent chest infections and airflow obstruction. The diagnosis of bronchiectasis is made clinically and confirmed by high-resolution computed tomography (HRCT) of the chest. Patients with a diagnosis of bronchiectasis should be referred to a specialist unit for investigation and management. This article deals with non-cystic fibrosis (CF) bronchiectasis. Bronchiectasis is a common structural endpoint that can be reached by several pathological routes from foreign body obstruction to post-infectious damage (tuberculosis), genetic defects (cystic fibrosis), abnormal host defence (ciliary dyskinesia and hypogammaglobulinaemia) and autoimmune disease (rheumatoid arthritis and ulcerative colitis). About half of all cases are called idiopathic since no known underlying cause is identified following detailed investigation. These patients typically have bilateral, predominantly lower lobe disease, and chronic rhinosinusitis. The underlying pathogenesis of bronchiectasis is not known. Innate and adaptive immune mechanisms have been implicated. There appear to be two stages to the disease process: an initial insult followed by a continuing inflammatory process encompassing recurrent infection and progressive lung damage. Abnormalities in immune regulation may predispose to bronchiectasis, both at the time of the initial insult that sets off the disease and during the on-going inflammatory process that ends in progressive lung damage. Immunogenetic evidence suggests a link between the extent of natural killer (NK) cell activation and disease susceptibility. Further evidence for adaptive immune mechanisms includes a genetic association with HLA-DR1, DQ5 and increased susceptibility to idiopathic bronchiectasis.BronchiectasisRosemary J. Boyton10.1016/j.mpmed.2012.02.003Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Bronchiectasis267272http://www.medicinejournal.co.uk/article/PIIS1357303912000321/abstract?rss=yesAbstract: Cystic fibrosis (CF) is the most common lethal genetic disease in the Caucasian population. Survival has improved dramatically with expected median survival in the UK now 41.4 years. In CF, a vicious cycle of mucus stasis, chronic inflammation and recurrent infection leads to respiratory failure and death in the majority of patients. CF is a multisystem disease with pancreatic exocrine insufficiency occurring in the majority of patients.Treatment involves airway clearance techniques, inhaled muco-active therapies and the prevention and control of respiratory infection. Pseudomonas aeruginosa is the most common respiratory pathogen.In 2011, a mutation-specific therapy (VX-770) demonstrated efficacy for the first time. A number of other similar compounds are in the pipeline. With these treatments we are potentially entering a new era of CF care in which we may expect even longer survival.Cystic fibrosisKatharine Hurt, Diana Bilton10.1016/j.mpmed.2012.02.006Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Cystic fibrosis273276http://www.medicinejournal.co.uk/article/PIIS1357303912000679/abstract?rss=yesThis CPD section was prepared by Eric Beck FRCP FRCP(Ed) FRCP(Gl) We hope you enjoy the CPD section. Let us know your views by email to: medicine@medicinepublishing.co.ukSelf-assessment/CPD10.1016/j.mpmed.2012.03.015Medicine 40, 5 (2012)2012-05-01Medicine2012-05-01405S1357-3039(12)X0004-5Self-assessment277278