课件：哮喘的诊断和分级.ppt

* Asthma is a complex disease involving many different cells Current thinking on the pathophysiology of asthma regards it as a specific type of inflammatory condition, involving, in particular, mast cells, eosinophils and T lymphocytes, which release a wide range of inflammatory mediators These mediators act on cells in the airway, leading to contraction of smooth muscle, oedema due to plasma leakage and mucus plugging * * Asthma is a chronic inflammatory disease with episodic attacks, involving acute inflammation on top of chronically persistent inflammation Acute inflammation in asthma is associated with bronchoconstriction, plasma exudation / oedema, vasodilatation and mucus hypersecretion Chronic inflammation in asthma is associated with subepithelial fibrosis, smooth muscle hyperplasia / hypertrophy, mucus gland hyperplasia and new vessel formation If asthma remains uncontrolled or poorly controlled, the underlying persistent inflammation in the airways leads to structural changes (remodelling) that reduce the extent of FEV1 response to short courses of steroids * Slide 6 - The pathophysiogical consequences of airway inflammation is remodelling and airway narrowing, increased bronchial reactivity and reduced reversibility. This leads to the clinical manifestations of the disease - intermittent symptoms and prolonged periods of exacerbations. * 气流受限的形式 哮喘气流受限的反复发作有四种形式，均与气道炎症反应相关。 支气管痉挛 多种刺激因素可以导致急性支气管痉挛，如吸入变应原、运动、冷空气、烟雾、化学物质，以及强烈的情绪反应如哭泣、欢笑等。导致支气管痉挛的机制为支气管平滑肌收缩、炎症细胞释放以细胞因子为主的介质及局部和中枢神经反射的刺激作用等不同因素的综合结果。急性支气管痉挛导致的气流受限在吸入支气管扩张剂如短效β2激动剂时能很快得到缓解。 气道壁水肿 由于气道壁水肿，伴或不伴支气管平滑肌收缩（即支气管痉挛），均可产生气流受阻。支气管扩张剂可能缓解这种形式的气流受限，但抗炎药特别是糖皮质激素能更有效地逆转这种形式的气流受阻。 慢性粘液栓形成 粘液分泌增加、血浆蛋白渗出及细胞坏死碎片混合起来产生了粘稠的粘液栓，能阻塞周围气道，而且很难去除。 气道壁重塑 有时候即使使用糖皮质激素治疗也不能完全逆转气流受限。从细胞和分子生物学基础分析，可能与气道组织长期和严重的气道炎症而致结构改变有关。 * * * GINA：哮喘的临床诊断 不管是儿童还是成人，都有部分哮喘患者没有得到正确的诊断，因此治疗也不充分。很多患者在寻求医学帮助之前能忍受间歇的呼吸症状。而哮喘症状的瞬时特征使患者加强了对其认知。 通常根据阵发性气急、喘息及胸闷等症状做出哮喘的临床诊断。症状随季节变化，哮喘和过敏性疾病家族史阳性也有助于做出诊断。1 肺功能检查，特别是肺功能异常和可逆性的程度，能显著增加