1. RINITIS NO ALERGICA
UNIVERSIDAD AUTONOMA 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
Rinitis no alérgica con eosinofilia
Rinitis hormonal
Rinitis por medicamentos
Rinitis atrófica
Rinitis Inducida por irritantes
Rinitis Vasomotora
Diagnostico
Tratamiento
3. Introducción
10% de la población
17 – 19 millones de Americanos
28 – 60% de paciente en ORL
AR : NAR 3:1
Mujeres 70%
Perenne
7. Fisiopatología
Función nasal e inervación
• T°
• Olfacción
• Filtración
• Humificación
Función
IgA
Proteínas
enzimas
Lubricación
• 15 batidas /
min
• 2,5-7,5
mL/min
Cilios
8. Fisiopatología
Función nasal e inervación
SNA
Simpático
Norepinefrina
Neuropeptido Y
Vasoconstricción
parasimpático
Acetilcolina
Péptido intestinal
vasoactivo
Secreción mucosa,
permeabilidad vasc.
-Vasculatura
-Act.
Glandular
Act. colinérgica
9. Fisiopatología
Función nasal e inervación
• Sensación nasal
PC V
• Epitelio
• Vasos
• Glándulas
N. etmoidal
• Dolor
• Temperatura
• Osmolaridad
• Relevantes en NAR
Fibras C
Histamina
Bradicinina
Aferencias
Aferencias
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 y seco
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
16. Clasificación
Rinitis no alérgica con eosinofilia
1981 Descrita por Jacobs et al. NARES
Perenne
Rinorrea
Prurito
Epifora
Estornudos
Reacción a alérgenos
negativos (piel, in vitro)
17. Clasificación
Rinitis no alérgica con 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.
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
Problemas que surgen de rinitis cornica
80% de las fatigas cronicas
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.
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.
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.
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
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.
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.
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
spicy foods, changes in temperature and humidity, environmental tobacco smoke, exercise, household cleaning products, perfumes and colognes, alcohol consumption, and bright lights
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
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
Through direct effects on the nasal mucosa, hormones may cause mucous gland hyperreactivity and increased rhinorrhea.1
PROLACTINA
Aumetno de flujo sistemico
semi-ischemic state results in rebound congestion from decreased vasomotor tone increased
parasympathetic activity, increased vascular permeability
Rinitis crónica inflamatoria caracterizada por atrofia de las estructuras nasales internas (cornetes, mucosa).
Incrementa con la edad
DE EPITELIO RESPIRATORIO CILIADO
SX NARIZ VACIA
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
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).
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
The incidence is estimated to be 5% to 15%, and it should be differentiated from occupationally induced AR or immunologic rhinitis.
Irritacion fibras C --- libera neuropeptidos, --- vasodilatación y edema -----
ALIVIO EN VACACIONES
Idiopathic or vasomotor rhinitis (VMR) is diagnosed when other identifiable causes have been excluded and no cytologic evidence of mucosal inflammation is found.
stos pacientes a menudo tienen una menor prevalencia de estornudos , prurito y conjuntival síntomas en comparación con el observado en pacientes CON AR
Negativas en NAR
Citilogia. Para ver si hay componenete inflamatorio
5 -25 comp con nARES
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,
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.
In addition to cleansing the nose, saline improves ciliary function and mucociliary clearance.
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
Perofacion y sist. Muy raro
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
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
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.
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.
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.