儿童慢性咳嗽诊断 与治疗.pptVIP

Slide 13 Several pathophysiologic mechanisms have been proposed to explain the connection between allergic rhinitis and asthma. Aspiration of inflammatory secretions from the upper airway into the lower airway—Lower-airway symptoms can be provoked by the aspiration of secretions rich in inflammatory products from the upper airways. Evidence of this phenomenon is not conclusive, however, and the concept remains unproved.30 Shift from nasal to mouth breathing—The nose filters, warms, and humidifies air en route to the bronchial passages.4 Nasal blockage due to allergic rhinitis may lead to mouth breathing, which bypasses these nasal “air-conditioning” functions and exposes the lung to “unconditioned” air that may contain large amounts of allergen, during the pollen season, for example.4 Mouth breathing in asthmatic patients in a clinical study potentiated exercise-induced bronchoconstriction, possibly by exposing the lungs to cold, dry air or reducing natural bronchodilators (e.g., nitric oxide), or both.29-31 Nasobronchial reflex—Experimental evidence suggests the possibility of the existence of a “nasobronchial reflex” that may mediate lower-airway obstruction in patients with allergic rhinitis. This concept is under investigation.30 Systemic mediation of nasal and lower-airway inflammation—Inflammation produced by an allergic reaction in the upper airways may induce inflammatory events that alter the lower airways. Potentially, inflammatory cells and mediators could be absorbed from the nasal mucosa into the peripheral circulation, where they would eventually reach the lower airways.30 Ref 30, p 101, C2 ?1, L1-6,10-15, p 102, C1, L10-17 ?? Ref 4, p 535, C2,?3, L1-6 ? Ref 4, p 535, C2, ?3, L1-6, CMK ? Ref 29, p S603, C2, ?2, L1-5 Ref 30, p 100, C1, ?1, L1-9 Ref 31, p 71, C1, ?1, L1-8, p 72, C1, ?1, L2-10, 29-34 Ref 30, p 101, C1, L15-17, 20-23, C1, ?3, L1-2, C2, L1-4, 6-11,16-19 ? Ref 30, p 102, C1, ?1, L1-3, C2, ?1, L1-6, C12, Fig 3 caption 1、概念