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1.
Vestn Otorinolaringol ; 81(5): 73-76, 2016.
Artigo em Russo | MEDLINE | ID: mdl-27876743

RESUMO

The available literature data give evidence that viral infection is the main cause underlying the development of inflammatory nasopharyngeal pathology in the children. According to ICD-10, nether acute nor chronic adenoiditis should be considered as a self-consistent nosological entity. Acute adenoiditis is usually regarded as a form of acute nasopharyngitis (J02) or acute respiratory viral infection (J06.9) whereas chronic adenoiditis is commonly referred to as representing other chronic diseases of the tonsils and adenoids (J 35.8). The reactive changes in the nasopharyngeal tonsils begin to be manifested on days 3-5 after the onset of acute respiratory viral infection; thereafter, they persist and gradually disappear within the next 2-3 weeks. In the majority of the cases, acute adenoiditis is actually a physiological reaction of the nasopharyngeal tonsils as the organs of regional mucosal immunity to antigenic stimulation. There is no universally accepted opinion as regards the duration of the inflammatory process which would allow these pathological changes to be considered as turned into chronic ones. This condition is actually not a serious pathology provided it is not associated with the concomitant complications and produces no clinically significant effect on the child's quality of life. Under practical conditions, such children are most frequently treated with the use of irrigation therapy. Taking into account that otorhinolaryngologists all over the world do not consider chronic adenoiditis as an independent nosological entity but distinguish only hypertrophy of adenoid vegetations or chronic rhinosinusitis (in the presence of inflammatory changes in the nasopharynx), it appears correct to speak about chronic adenoiditis provided the clinical manifestations of the disease persist for more than 12 weeks. Based on the predominant etiological component, the viral, bacterial, and allergic forms of nasopharyngeal adenoiditis can be distinguished even though it is rather difficult to actually determine which etiological factor prevails in each concrete case. The aforedescribed situation poses a large number of questions pertaining to the choice of either systemic or topical antibacterial therapy.


Assuntos
Tonsila Faríngea/efeitos dos fármacos , Dexametasona/administração & dosagem , Nasofaringite , Fenilefrina/administração & dosagem , Polimixina B/administração & dosagem , Qualidade de Vida , Tonsila Faríngea/patologia , Tonsila Faríngea/fisiopatologia , Antibacterianos/administração & dosagem , Criança , Combinação de Medicamentos , Monitoramento de Medicamentos , Feminino , Glucocorticoides/administração & dosagem , Humanos , Masculino , Descongestionantes Nasais/administração & dosagem , Sprays Nasais , Nasofaringite/tratamento farmacológico , Nasofaringite/etiologia , Nasofaringite/fisiopatologia , Nasofaringite/psicologia , Resultado do Tratamento
2.
Ann Otol Rhinol Laryngol Suppl ; 163: 15-9, 1994 May.
Artigo em Inglês | MEDLINE | ID: mdl-8179263

RESUMO

A pathophysiologic model of otitis media with effusion secondary to IgE-mediated hypersensitivity is described. Specific mediators of inflammation are released by mucosal mast cells in the nasal mucosa following the interaction of antigen and specific IgE antibody. These mediators increase vascular permeability, mucosal blood flow, and, most important, mucus production. Furthermore, accessory cell types are recruited by colony-stimulating factors that in turn provide an autocrine-positive feedback for the influx of further inflammatory cells. The eustachian tube is then effectively obstructed by both intrinsic venous engorgement and extrinsic mucus plugs, isolating the middle ear space from the ambient environment. The net result is the increased exchange of nitrogen into the middle ear mucosa from the middle ear cavity. This causes the development of a significant middle ear underpressure that disrupts tight junctions and allows for transudation of fluids into the middle ear space. The prolonged obstruction of the eustachian tube with mucus results in middle ear inflammation, mucosal metaplasia, and increased glandular activities, all of which are hallmarks of chronic otitis media with effusion.


Assuntos
Orelha Média/imunologia , Orelha Média/fisiopatologia , Imunoglobulina E/imunologia , Otite Média com Derrame/imunologia , Otite Média com Derrame/fisiopatologia , Basófilos/imunologia , Pré-Escolar , Citocinas/imunologia , Tuba Auditiva/imunologia , Tuba Auditiva/fisiopatologia , Humanos , Lactente , Recém-Nascido , Mastócitos/imunologia , Nasofaringite/complicações , Nasofaringite/imunologia , Nasofaringite/fisiopatologia , Otite Média com Derrame/epidemiologia , Rinite Alérgica Perene/complicações , Rinite Alérgica Perene/imunologia , Rinite Alérgica Perene/fisiopatologia
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