COPD诊断和治疗进展演示文稿.ppt

* n为均值，用药前小于用药后，是由于有些患者早晨没有用药，身体不适，或者需要急救等原因，没有参加肺量计，而用药后病情稳定，所以参加了用药后的肺量计检测 * * * * * * * 肺部炎症溢出导致细胞因子进入血液循环，引起全身炎症，使得诸如CRP等急性时相蛋白增加。全身炎症可以导致骨骼肌萎缩、恶液质，还可以引起或加重合并症。全身炎症液可以促进肺癌的形成。 * * ? GlaxoSmithKline * Changes in large airways of COPD patients. The epithelium often shows squamous metaplasia and there is goblet cell and submucosal gland hyperplasia, resulting in mucus hypersecretion. The airway wall is infiltrated with macrophages and CD8+ lymphocytes, whereas neutrophils predominate in the airway lumen and around submucosal glands. Airway smooth muscle and basement membrane are minimally increased compared to the findings in asthma. * Changes in small airways in COPD patients. The airway wall is thickened and infiltrated with inflammatory cells, predominately macrophages and CD8+ lymphocytes, with increased numbers of fibroblasts. In severe COPD there are also lymphoid follicles. The lumen is often filled with an inflammatory exudate and mucus. There is peribronchial fibrosis and airway smooth muscle may be increased, resulting in narrowing of the airway. * Changes in the lung parenchyma in COPD patients. There is loss of elasticity and alveolar wall destruction, and accumulation of inflammatory cells, predominantly macrophages and CD8+ lymphocytes. The destructive changes reduce the pulmonary capillary bed. The left panel shows a scanning electron micrograph of a patient with emphysema demonstrating the enlargement of alveoli and destruction of the alveolar walls. * Changes in pulmonary arteries in COPD patients. There is dysfunction of endothelial cells (reduced vasodilator release), intimal thickening, hyperplasia of smooth muscle and infiltration with inflammatory cells, predominantly macrophages and CD8+ lymphocytes. * Pathogenesis of COPD, illustrating the central role of inflammation * Inflammatory cells involved in COPD. Cigarette smoke activates macrophages and epithelial cells to release chemotactic factors that recruit neutrophils, monocytes and CD