Rinitis alergica
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El documento proporciona información sobre la rinitis alérgica. Define la rinitis alérgica como una inflamación de la mucosa nasal asociada con estornudos, rinorrea, picor y congestión nasal. Explica que la rinitis alérgica es una de las enfermedades más comunes a nivel mundial y suele persistir de por vida. Detalla las diferentes clasificaciones de rinitis y sus síntomas, y señala que los corticoesteroides intranasales son el tratamiento médico de primera elección para la rinitis alérg
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Rinitis alergica
- 1. RINITIS ALERGICA LAURA VILORIA GÓMEZ SERVICIO DE PEDIATRIA 2019
- 3. The atopic march: current insights into skin barrier dysfunction and epithelial cell-derived cytokines. Immunol Rev. 2017 Jul; 278(1): 116–130
- 5. DEFINICIÓN RINITIS INFLAMACION DE LA MUCOSA NASAL ( RINORREA, ESTORNUDO, PICOR Y CONGESTION NASAL) ASOCIADO A NARIZ Y FOSAS NASALES COMPROMISO DE TODA LA MUCOSA DEL TRACTO RESPIRATORIO
- 6. EPIDEMIOLOGIA 0-40% 20- 25% 70% ASMA ADULTO NIÑOS is among the most common diseases globally and usually persists throughout life picor Estornudo Rinorrea congestion nasal
- 7. CLASIFICACION RINITIS RINITIS ALERGICA RINITIS LOCAL ALERGICA • NO EVIDENCIA ATOPIA SISTEMICA (-) TEST IgE (+) MUCOSA NASAL RINITIS AUTONOMICA RINITIS INFECCIOSA • RINOVIRUS RINITIS (IDIOPATICA)
- 8. CLASIFICACION RINITIS ALERGICA RINITIS AGUDA RINITIS CRONICA 2 > SINTOMAS POR AL MENOS 12 SEMANAS
- 10. RINITIS ALERGICA
- 12. RINITIS ALERGICA ( IRA)
- 14. DIAGNOSTICO
- 15. Facies adenoidea estigmas alérgicos (ojeras, líneas de Dennie, surco nasal) pliegue transverso en la nariz OBSERVAN : se puede ver una mucosa inflamada, pálida, gris- azulada, secreción cristalina, cornestes edematizados. Faringe congestiva, hipertrofia del anillo de Waldeyer o sin ella
- 17. TRATAMIENTO
- 21. Los corticoesteroides intranasales son el tratamiento médico de primera elección contra la rinitis alérgica moderada-severa
- 22. GRACIAS
Notas del editor
- The term “atopic march” (or “allergic march”) describes this developmental progression of atopic diseases.
- Allergic rhinitis (AR) is among the most common diseases globally and usually persists throughout life.1 The prevalence of self-reported AR has been estimated to be approximately 2% to 25% in children2 and 1% to greater than 40% in adults.1,3 The prevalence of confirmed AR in adults in Europe ranged from 17% to 28.5%. Recent studies show that the prevalence of AR has increased in particular in countries with initial low prevalence (for a discussion of prevalence of AR, see section 5.1-5.2 in Allergic Rhinitis and its Impact on Asthma [ARIA] 2008 Update1 ). Classical symptoms of AR are nasal itching, sneezing, rhinorrhea, and nasal congestion. Ocular symptoms are also frequent; allergic rhinoconjunctivitis is associated with itching and redness of the eyes and tearing. Other symptoms include itching of the palate, postnasal drip, and cough. AR is also frequently associated with asthma, which is found in 15% to 38% of patients with AR,4,5 and nasal symptoms are present in 6% to 85% patients with asthma.6-9 In addition, AR is a risk factor for asthma,4,9 and uncontrolled moderate-to-severe AR affects asthma control.10,11 Compared with other medical c
- RINITIS ALERGICA: • IgE-mediated infammation of the nasal mucosa, resulting in eosinophilic and Th2-cell infltration of the nasal lining • Further classifed as intermittent or persistent RINITIS IDIOPATICA: Etiology cannot be determined RINITIS AUTONOMICA: • Vasomotor • Drug-induced (rhinitis medicamentosa) • Hypothyroidism • Hormonal • Non-allergic rhinitis with eosinophilia syndrome (NARES) RINITIS INFECCIOSA: Precipitated by viral (most common), bacterial, or fungal infection. Human rhinovirus (more than 100 serotypes) is the most common cause, accounting up to 50% viral rhinitis episodes in children and adults; Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae are the most frequent micro-organisms in bacterial rhinosinusitis
- RINITIS ALERGICA: • IgE-mediated infammation of the nasal mucosa, resulting in eosinophilic and Th2-cell infltration of the nasal lining • Further classifed as intermittent or persistent RINITIS IDIOPATICA: Etiology cannot be determined RINITIS AUTONOMICA: • Vasomotor • Drug-induced (rhinitis medicamentosa) • Hypothyroidism • Hormonal • Non-allergic rhinitis with eosinophilia syndrome (NARES) RINITIS INFECCIOSA: Precipitated by viral (most common), bacterial, or fungal infection
- En la rinitis alérgica, numerosas células inflamatorias, incluidos los mastocitos, las células T CD4 positivas, las células B, los macrófagos y los eosinófilos, se infiltran en el revestimiento nasal tras la exposición a un alérgeno incitante (más comúnmente partículas fecales de ácaros del polvo en el aire, residuos de cucarachas, caspa de animales) , moldes y pólenes). En individuos alérgicos, las células T que se infiltran en la mucosa nasal son predominantemente de naturaleza T helper 2 (T2) y liberan citocinas (por ejemplo, interleucina [IL] -3, IL-4, IL-5 e IL-13) que promueven la inmunoglobulina Producción de E (IgE) por las células plasmáticas. La reticulación de IgE unida a los mastocitos por alergenos, a su vez, desencadena la liberación de mediadores, como histamina y leucotrienos, que son responsables de la dilatación arteriolar, aumento de la permeabilidad vascular, picazón, rinorrea, secreción mucosa y contracción del músculo liso en el pulmón. [1, 2]. Los mediadores y las citocinas liberadas durante la fase temprana de una respuesta inmune a un alérgeno incitante desencadenan una respuesta inflamatoria celular adicional durante las siguientes 4 a 8 h (respuesta inflamatoria de fase tardía) que produce síntomas recurrentes (generalmente congestión nasal) que a menudo persisten In allergic rhinitis, numerous infammatory cells, including mast cells, CD4-positive T cells, B cells, macrophages, and eosinophils, infltrate the nasal lining upon exposure to an inciting allergen (most commonly airborne dust mite fecal particles, cockroach residues, animal dander, moulds, and pollens). In allergic individuals, the T cells infltrating the nasal mucosa are predominantly T helper 2 (T2) in nature and release cytokines (e.g., interleukin [IL]-3, IL-4, IL-5, and IL-13) that promote immunoglobulin E (IgE) production by plasma cells. Crosslinking of IgE bound to mast cells by allergens, in turn, triggers the release of mediators, such as histamine and leukotrienes, that are responsible for arteriolar dilation, increased vascular permeability, itching, rhinorrhea, mucous secretion, and smooth muscle contraction in the lung [1, 2]. Te mediators and cytokines released during the early phase of an immune response to an inciting allergen trigger a further cellular infammatory response over the next 4–8 h (late-phase infammatory response) which results in recurrent symptoms (usually nasal congestion) that often persist