[Hyperreflectoric rhinopathy].
Research in molecular biology in the past few years offers new views on vasomotor rhinitis. The key role of mediator substances which contain the mast cell and which, after degranulation, are active immediately by histamine release or act in a delayed manner (eg. leucotriene), is discussed, as well as the "liberofunction" of the neurotransmitter acetylcholine. The contribution to vasomotor rhinitis of other humoral systems, the kinine system and complement factors are also taken into account. The biopharmacological actions of the effector systems of the nasal mucosa (vessels, exocrine glands, nociceptors) are also analyzed. Using clinical examples the differentiation between humoral or neural reflex mediated hyperreflexia is worked out related to the classic triad of sneezing, profuse nasal discharge, nasal obstruction. The causes of vasomotor rhinitis (exogenous endogenous and drugs) are examined in the light of their pathophysiological importance. The differential diagnosis must cover allergic rhinopathy as well as the different kinds of rhinitis medicamentosa, the most important of which are discussed. Drugs which can help are discussed as well as continuous physical therapy.
Terrahe
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D000109:Acetylcholine / Q000502:physiology; D003131:Combined Modality Therapy; D003937:Diagnosis, Differential; D006636:Histamine Release; D006801:Humans; D008407:Mast Cells / Q000502:physiology; D009297:Nasal Mucosa / Q000294:innervation / Q000503:physiopathology; D012018:Reflex / Q000502:physiology; D012223:Rhinitis, Vasomotor / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D011984:Sensory Receptor Cells / Q000503:physiopathology
D000109:Acetylcholine
Die hyperreflektorische Rhinopathie.