Descargado 49 veces
Subido porAngel Castro Urquizo
Rinitis no alergica
Este documento trata sobre la rinitis no alérgica, clasificándola en varios tipos como la rinitis no alérgica con eosinofilia, rinitis hormonal, rinitis inducida por medicamentos y rinitis atrófica. Explica la fisiopatología de la rinitis no alérgica y los factores asociados. Finalmente, detalla el diagnóstico y tratamiento de esta condición, incluyendo corticoesteroides tópicos nasales, antihistamínicos y cirugía en algunos casos.
Más contenido relacionado
Similar a Rinitis no alergica
Más de Angel Castro Urquizo
Rinitis no alergica
- 1. RINITIS NO ALERGICA UNIVERSIDADAUTONOMA DE SINALOA HOSPITAL CIVIL DE CULIACAN CENTRO DE INVESTIGACIÓN Y DOCENCIA EN CIENCIAS DE LA SALUD OTORRINOLARINGOLOGIA Y CIRUGIA DE CABEZA Y CUELLO DR. ANGEL CASTRO URQUIZO R1 ORL CULIACAN SINALOA AGOSTO 2016
- 2. Temas a tratar Introducción Fisiopatogenia Rinitisno alérgica con eosinofilia Rinitis hormonal Rinitis por medicamentos Rinitis atrófica Rinitis Inducida por irritantes Rinitis Vasomotora Diagnostico Tratamiento
- 3. Introducción 10% dela población 17 – 19 millones de Americanos 28 – 60% de paciente en ORL AR : NAR 3:1 Mujeres 70% Perenne
- 4. Introducción *Rinosinusitis *Pólipos *Disfunción eustaquiana *Disfunción laríngea *OMC *Hipoacusia *Trastorno del sueñoy respiratorio *Trastorno olfatorio *Fatiga
- 6. Introducción Síntomas de AR+ pruebas negativas Rinitis crónica (rinitis vasomotora) Rinitis no alérgica
- 7. Fisiopatología Función nasal einervación • T° • Olfacción • Filtración • Humificación Función IgA Proteínas enzimas Lubricación • 15 batidas / min • 2,5-7,5 mL/min Cilios
- 8. Fisiopatología Función nasal einervación SNA Simpático Norepinefrina Neuropeptido Y Vasoconstricción parasimpático Acetilcolina Péptido intestinal vasoactivo Secreción mucosa, permeabilidad vasc. -Vasculatura -Act. Glandular Act. colinérgica
- 9. Fisiopatología Función nasal einervación • Sensación nasal PC V • Epitelio • Vasos • Glándulas N. etmoidal • Dolor • Temperatura • Osmolaridad • Relevantes en NAR Fibras C Histamina Bradicinina Aferencias Aferencias
- 10. Fisiopatología Función nasal einervación • Hiperinervación • Inflamación nerv. • Fibras amielinicas • Neuropeptidos • Calcitonina gen • Irritantes • Tracto sup e inf. interconectados• PG, leucotrienos Cascada inflamatoria Vía aérea unida NeuromediadoresProinflamatorios
- 11. Fisiopatología Prueba de provocación Metacolina •Intranasal • Actividad glandular aumentada Histamina • Aumento permeabilidad vasc. • NAR en menor grado Capsaicina • Estimula fibras C • Independiente de Histamina • Selectivo de NAR
- 12. Fisiopatología Aire frio yseco Resequedad en mucosa Induce síntomas Incremento de tono y osmolaridad -Mediadores -Estímulos aferentes -Parasimpatico Perdida de agua hiperosmolaridad Estimulación nerviosa Activación mast cells Daño epitelial Disminuir osmolaridad -Alteración vascular -Alteración glandular
- 13. Fisiopatología Hiperreactividad nasal Respuesta a Estímulos Reactividadincrementada de la mucosa nasal resultando en síntomas. Daño epitelial Incremento de la permeabilidad Alteración glandular Alteración Vascular Alteración sensitiva
- 14. Fisiopatología Componente alérgico IgE en mucosanasal Sin atopia sistémica NARES
- 16. Clasificación Rinitis no alérgicacon eosinofilia 1981 Descrita por Jacobs et al. NARES Perenne Rinorrea Prurito Epifora Estornudos Reacción a alérgenos negativos (piel, in vitro)
- 17. Clasificación Rinitis no alérgicacon eosinofilia Citología nasal Eosinofilia Parte de RNS crónica 1/3 de forma aislada Mecanismos poco claros IgE-Mastocitos- Disfunción neural NARES No hay mediación de IgE.
- 18.
- 19. Clasificación Rinitis hormonal Rinitis embarazo 22% 69% en fumadoras Congestión, rinorrea Progesterona relajación vascular
- 20.
- 21. Clasificación Rinitis atrófica Previamente asociadacon Klebsiella ozaenae Resultado de múltiples agresiones Cirugia, trauma, Granulomatosas, cocaína, radioterapia. Epitelio no funcional, no ciliado Metaplasia escamosa Edad Perdida de limpieza mucociliar y regulación neurologica
- 22.
- 23. Clasificación Rinitis atrófica Tratamiento Insatisfactorioy limitado Antibióticos Lavados nasales Humidificación
- 24. Clasificación Rinitis inducida porirritantes Presión barométrica Alimentos Aire frio- seco Irritantes inhalados Clima Altitud Rinitis gustativa
- 25. Clasificación Rinitis inducida porirritantes Pruebas cutáneas negativas Estimulación nerviosa Activación parasimpática
- 26. Clasificación Rinitis ocupacional Incidencia5 al 15% Síntomas típicos NAR Trastorno olfatorio Epistaxis Costras Reducción mucociliar Hiperreactividad nasal
- 27.
- 28. Clasificación Rinitis idiopática (Vasomotora) Forma de NAR mas común Exclusión Sin evidencia citológica inflamatoria
- 29. Clasificación Rinitis idiopática (Vasomotora) Imbalance autonómico •>Parasimpático •< Simpático “Blockers” “Runners” • Obstrucción • Rinorrea Menores síntomas de AR
- 30.
- 32.
- 34. Diagnostico Pruebas diagnosticas IgE séricoPruebas cutáneas Citología nasal 5-25 eosinofilos por campo NARES Exposición aire frio y seco
- 35.
- 36.
- 38.
- 39. Corticoesteroides tópicos nasales Efectosadversos Irritación septal Resequedad nasal y costras Resequedad de garganta Cefalea Perforación septal Efectos sistémicos
- 40.
- 42.
- 43.
- 44. Transantral Transpalatino Transetmoidal Endoscopica transnasal
Notas del editor
- #2 CAP 43 CM 371 BLY
- #4 10% of the population is affected by chronic or recurrent nasal symptoms, with an estimated 17 to 19 million Americans affected by nonallergic rhinitis. In many instances, AR and NAR are often indistinguishable and coexist
- #5 Problemas que surgen de rinitis cornica 80% de las fatigas cronicas
- #6 These symptoms often interfere with school or work performance, and a lack of productivity is worsened by the need for frequent doctor visits. In a recent survey of rhinitis patients, one fourth noted restricting their choice of occupation or residence to reduce their symptoms In addition, medications, although usually helpful, may elicit undesirable side effects such as drowsiness, epistaxis, palpitations, and nasal dryness, which compound the overall impact of NAR.
- #7 Most commonly a patient will complain of rhinorrhea, nasal congestion, and sneezing despite a negative allergic history and negative skin testing and nasal cytology. Unfortunately, after allergy has been ruled out as the cause of the rhinitis, these patients may be diagnosed with vasomotor rhinitis, a blanket term used to diagnose affected patients Chronic rhinitis has been described in the literature using many terms. Historically, the term vasomotor rhinitis has been favored, but distinct vascular or motor nerve dysfunction has been difficult to identify.
- #8 The effects of NAR cannot be fully appreciated without a brief review of nasal function, which includes temperature regulation, olfaction, filtration, and humidification of inspired air. The nasal lining also produces secretions that contain immunoglobulin A, protein, and enzymes to provide lubrication and protection. Secretions trap particulate matter, and nasal cilia propel the matter toward the natural ostia. This occurs at a frequency of 10 to 15 beats/min, and the mucous blanket streams at a rate of 2.5 to 7.5 mL/min.
- #9 N. eferentes.. Mitad simpáticos y mitad para Regulation of mucosal vasculature and glandular secretions is controlled by the autonomic nervous system. The sympathetic nerves form one half of the efferent nasal reflex arc. Once stimulated, sympathetic nerves release norepinephrine and neuropeptide Y, which cause vasoconstriction of the nasal vasculature. The parasympathetic nerves comprise the other half of the efferent nasal reflex arc. After they have been stimulated, parasympathetic nerves release acetylcholine, norepinephrine, and vasoactive intestinal peptide. Cholinergic neuropeptides and neurotransmitters stimulate the serous glands of the nasal mucosa and increase mucus secretion. Unilateral stimulation of the efferent reflex arc leads to a bilateral response
- #10 Nasal sensation primarily originates from the trigeminal nerve. Afferent ethmoidal nerves provide sensory innervation to the epithelium, vessels, and glands. C fibers are unspecialized afferent sensory nerves that react to pain and changes in temperature and osmolarity, and they are the most relevant type of sensory fibers in NAR.
- #11 DESORDE DE CALQIER COMPONENTE DE LA MUCOSA TE PUEDE DAR NAR The nonspecific and variable symptoms of NAR are confounding, which compounds the difficult task of identifying the exact pathophysiologic source.
- #12 METACOLINA: ACT. AUMENTADA EN AR Y NAR. NO ES PARA DIFERENCIARLAS Agonista colinérgico. receptor muscarinicos Histamine provocation increases vascular permeability, causing sneezing, pruritus, rhinorrhea, and nasal obstruction
- #14 spicy foods, changes in temperature and humidity, environmental tobacco smoke, exercise, household cleaning products, perfumes and colognes, alcohol consumption, and bright lights
- #15 recently showed a subgroup of NAR patients who also produced local IgE upon nasal provocation testing. This has also been studied and shown in a clinical study performed by Wedbeck and colleagues in 2005. These results suggest that a subgroup of NAR patients may have an allergic disease pathway, while still exhibiting negative systemic atopy; this group could possibly be those with NAR with eosinophilia NARES
- #18 The majority of patients deny specific triggers, although some complain that weather changes or exposure to irritant chemicals are troublesome. Cytologic examination of nasal secretions shows marked eosinophilia. This reaction may occur as part of a continuum of chronic rhinosinusitis with and without nasal polyps, and Samter triad, or may occur as an isolated disorder in up to one third of patients with NAR. However, as noted above, studies have shown that mast cells, IgE-postive cells, and eosinophils are increased in the nasal mucosa of AR and NAR patients, possibly as a consequence of localized IgE-mediated reactions. Along with this possible allergic component, nasal neural dysfunction has also been described to contribute to the symptomatology in NARES patients
- #19 Through direct effects on the nasal mucosa, hormones may cause mucous gland hyperreactivity and increased rhinorrhea.1 PROLACTINA
- #20 Aumetno de flujo sistemico
- #21 semi-ischemic state results in rebound congestion from decreased vasomotor tone increased parasympathetic activity, increased vascular permeability
- #22 Rinitis crónica inflamatoria caracterizada por atrofia de las estructuras nasales internas (cornetes, mucosa). Incrementa con la edad DE EPITELIO RESPIRATORIO CILIADO SX NARIZ VACIA
- #23 Crusting, fetor, mucosal atrophy, and widely patent nasal cavities are seen in patients who complain of nasal congestion.54 The normal pattern of airflow is changed, which likely contributes to the sensation of congestion and obstruction in addition to
- #25 Temperature changes, alterations in barometric pressures, ingested foods, and inhaled irritants are other inciting causes of NAR. Physical stimuli such as cold air and weather changes are known triggers. As mentioned earlier, cold, dry air is a known factor in the development of profuse rhinorrhea.27,55 Altitude and pressure changes result in facial pressure, headaches, and nasal symptoms in susceptible individuals (e.g., those who work in the aviation field).
- #26 AUSENCIA DE RESULTADOS EN PRUEBAS CUTANEAS Stimulation of afferent sensory nerves is the most likely pathophysiologic mechanism; this activates the parasympathetic nerves that supply the nasal mucosal glands and could also explain the sweating and epiphora that sometimes accompany this reaction.57
- #27 The incidence is estimated to be 5% to 15%, and it should be differentiated from occupationally induced AR or immunologic rhinitis.
- #28 Irritacion fibras C --- libera neuropeptidos, --- vasodilatación y edema ----- ALIVIO EN VACACIONES
- #29 Idiopathic or vasomotor rhinitis (VMR) is diagnosed when other identifiable causes have been excluded and no cytologic evidence of mucosal inflammation is found.
- #30 stos pacientes a menudo tienen una menor prevalencia de estornudos , prurito y conjuntival síntomas en comparación con el observado en pacientes CON AR
- #35 Negativas en NAR Citilogia. Para ver si hay componenete inflamatorio 5 -25 comp con nARES
- #36 Patient education is of utmost importance in treating NAR. Patients frequently are not aware of the specific trigger that incites their symptoms, but a thorough and accurate history can often elucidate the cause. After being informed, patients can take an active role in their health care and control their environment. Avoidance of inciting factors such as perfumes, tobacco smoke, cleaning supplies, and certain foods or wines can usually be accomplished without great difficulty. If a change in environment is not feasible, exposures can be limited; for example, occupational exposures can be reduced or eliminated by using masks and protective coverings, and medications associated with symptoms can be discontinued or changed. Exercise is an important and frequently overlooked adjunct to therapy; vigorous exercise decreases nasal congestion by stimulating adrenergic receptors in the nasal mucosa. Unfortunately, in many circumstances, inciting exposure cannot be avoided,
- #37 Decongestants, either topical or systemic, can be used to decrease mucosal edema and assist with the initiation of topical nasal steroid application. After the topical steroids consistently and successfully reach the nasal mucosa, decongestants should be tapered and discontinued. Physiologically normal saline is another useful adjunct to therapy, and rinsing with this substance increases steroid efficacy at the mucosal level. In addition to cleansing the nose, saline improves ciliary function and mucociliary clearance. topical medications must reach the nasal mucosa to be effective.
- #38 In addition to cleansing the nose, saline improves ciliary function and mucociliary clearance.
- #39 Fluticasone propionate and beclomethasone are currently the only topical steroid preparations with a U.S. Food and Drug Administration (FDA) indication for treating NAR, because they have both been found to be effective in patients with NAR.79,80 Budesonide has also shown good efficacy and is currently the only topical nasal steroid that has a pregnancy category of B, whereas all others are C.81,82 On the other hand, mometasone did not show better efficacy than placebo in reducing rhinitis symptoms in perennial NAR patients over a 6-week period in a separate study
- #40 Perofacion y sist. Muy raro
- #41 Azelastine is an H1-receptor antagonist. In addition, it inhibits the synthesis of leukotrienes, kinins, and cytokines and also inhibits the expression of intercellular adhesion molecules and prevents the generation of superoxide free radicals --- se ha mostrado que ayda en OBSTRUCCION, RINORREA, EDEMA
- #42 Azelastine is an H1-receptor antagonist. In addition, it inhibits the synthesis of leukotrienes, kinins, and cytokines and also inhibits the expression of intercellular adhesion molecules and prevents the generation of superoxide free radicals
- #43 Para rinorera Alternatively, ipratropium bromide, which is a topical anticholinergic, acts locally and blocks parasympathetic input to the nasal mucosa glands only. Systemic side effects are uncommon with intranasal ipratropium bromide; epistaxis and nasal dryness may occur, but they are rarely intolerable, and they decrease in incidence with prolonged use of the medication.
- #44 Nasal polyps, hypertrophic inferior turbinates, and septal spurs or deviation CON EL FIN DE QUE EL ESTEROIDE LE PEGUE MAS ALA MUCOSA Nervio petroso superficial mayor (rama colateral de nervio facial). - Nervio petroso profundo mayor (rama colateral del nervio glosofaríngeo). steroid injection, electrocautery, laser ablation, microdebrider resection, submucosal resection, lateral displacement, partial turbinectomy, and radiofrequency ablation.
- #45 La inervación parasimpática se origina en el núcleo salivar superior o lagrimonasal y sigue el nervio facial hasta el ganglio geniculado. Aquí las fibras parasimpáticas se separan del facial para formar el nervio petroso superficial mayor, que sale del hueso temporal a través del hiato facial en la superficie anterior del peñasco donde recibe una anastomosis del petroso profundo mayor. Este tiene su origen en el nervio de Jacobson, que a su vez es rama del glosofaringeo, quedando formado así el nervio vidiano, el cual al penetrar por el agujero rasgado posterior recibe otra anastomosis del plexo simpático paracarotídeo; después atraviesa la base de la apófisis pterigoides y al final de un trayecto muy corto termina en el ganglio esfenopalatino, en la extremidad anterior dilatada del canal vidiano. Conduce estímulos parasimpáticos secretorios de la mucosa nasal, con vasodilatación del lecho vascular.