COPD的定义及诊断.ppt

. 迷走神经分布于气道壁，其节后纤维终止于气道平滑肌和粘膜下腺。刺激迷走神经导致乙酰胆碱的释放，并与气道平滑肌细胞和粘膜下腺杯状细胞上的M3毒蕈碱受体相互作用。这继而导致平滑肌收缩和支气管狭窄以及粘液生成和分泌。 气道处于持续的低水平迷走神经刺激下，使得静息气道保持一定的“张力” 。 化学或机械刺激物的存在通过感觉性传入C-纤维会进一步刺激迷走神经。这些神经的刺激信号传输至CNS，并增强迷走神经刺激，从而导致支气管收缩和粘液分泌过多以防止刺激物深入到肺部。 * COPD的发病机制包括2种通路，气道炎症通路和迷走通路 在COPD中，烟草以及其他吸入型刺激性物质均可诱发炎症反应。COPD炎症反应以中性粒细胞为主，导致气道粘液过度分泌和肺泡壁损伤。 同时，吸烟可以刺激迷走神经引起乙酰胆碱释放，导致平滑肌收缩、气道痉挛、气道粘液过度分泌。 The animation begins with the alveolus fully inflated. Over the course of a normal exhalation, the alveolus fully deflates. With inhalation, the alveolus re-inflates. In COPD, irreversible damage causes the alveolar walls and supports to lose elasticity compared with the normal condition. The airways are partly collapsed and occluded, an effect made worse by reversible cholinergic constriction.1 As a result, deflation is slower, and so the alveolus only partly deflates over the course of an exhalation. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO workshop report. 2001. /workshop/toc.html. Accessed: 14 November 2003. In the normal state, inhalation is balanced by exhalation. There is no dynamic hyperinflation. COPD patients suffer from reduced expiratory flow. As a result, the lungs may not fully empty before the next breath begins. This is particularly likely if the patient has to breathe faster as a result of physical activity.1 Because the lungs do not fully empty, they become progressively over inflated with each breath. This process is known as air trapping, which leads to hyperinflation.1 Air trapping reduces the ability of the patient to breathe in, which causes the sensation of breathlessness that typifies the disease. ODonnell DE, Webb K. The etiology of dyspnea during exercise in COPD. Pulmonary and Critical Care Update 14, Lesson 15./downloads/education/online/Vol14_13_18.pdf. Accessed 24 February 2004. ? M Saetta Changes in large airways of COPD patients. The