Sinus anatomy and function(2)

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1、Sinus Anatomy, function, and evaluationAnatomic causes of nasal obstructionnThe trigeminal nerve endings provide the sensation of nasal airflownBlock these receptorsThe sensation of nasal obstructionAnatomic causes of nasal obstructionnEvaluation of the anatomic causes of nasal obstructionnHistory a

2、nd PEnSeek other causes:AR,sinusitisetcnAnt. rhinoscopy and nasal endoscopynObstruction that resolves with decongestion is caused by mucosal abnormalityAnatomic causes of nasal obstruction- Septal deviationnFrequently unilateralnPossibly with a distant history of nasal traumanKeenly aware of the nas

3、al cycleAnatomic causes of nasal obstruction- Septal deviationnAssessment of columella from the below helps evaluate caudal septal deflections, which can be underestimated on standard rhinoscopy.nPalpation of external nose and the septum test the support of the dorsum and the tipAnatomic causes of n

4、asal obstruction- Septal deviationnSeptoplastynSignificant improvement at 3 and 6 monthsnNo single test reliably predicts successful outcome preoperatively.nRhinomanometry:adjunctivenNot widely usedAnatomic causes of nasal obstruction- Septal deviationnThe location of deviation correlates with the s

5、urgical outcomenNasal valvenPosterior deviationAnatomic causes of nasal obstruction-Nasal Valve collapsenThe narrowest partnMost of the resistance to airflownA. DysfunctionnTurbinate hypertrophy and NSD:most commonly cause.Anatomic causes of nasal obstruction-Nasal Valve collapsenB. Collapse of the

6、structurenIatrogenic, congenitalnLong-term obstruction postrhinoplastynPhysical findings:nAn hourglass or pinched appearance of the middle segment of the nosenMedial collapse of the alar cartilage or deep alar groovesAnatomic causes of nasal obstruction-Nasal Valve collapsenPost-RhinoplastynAggressi

7、ve narrowing of the nasal tipnOverresection of the lateral crusnDisplacement of weak alar cartilagesnExcessive narrowing of the dorsumnOverresection of upper lateral cartilagenDisplacement of short nasal bones Anatomic causes of nasal obstruction-Nasal Valve collapsenSurgical techniquesnSpreader gra

8、ftnAlar batten graftnFlaring suturesnOverlay graftsnLateral suture suspensionAnatomic causes of nasal obstruction-Nasal Valve collapsenCottle maneuvernLateral traction on the cheeknNo specificnModified Cottle maneuvernEar curette separately supports the lower and upper lateral cartilageAnatomic caus

9、es of nasal obstruction-Turinate HypertrophynThe inf. TnThe degree of anterior turbinate engorgementnAnterior tip in nasal valve:n2/3 of upper airway resistancenRhinitis:inflammationnPersistent inflammation:nMucous gland grow in sizenCollagen accumulates beneath the basement membraneAnatomic causes

10、of nasal obstruction-Turinate HypertrophynMedical treatmentnAntihistaminenDecongestionnIntranasal corticosteroidnCorticosteroid turbinate injectionnMast cell stabilizersnImmunotherapynSurgical interventionnMinimize complications while restoring normal turbinate size and functionAnatomic causes of na

11、sal obstruction-Concha BullosanA pneumatized middle turbinatenMost common anatomic variations:25%nA lining of respiratory epitheilum and drains into frontal recess, lateral sinus, or hiatus semilunarisnFills the space between the lateral nasal wall and the septumnNasal obstructionnPredisposing to si

12、nus infection by blocking the OMGAnatomic causes of nasal obstruction-Concha BullosanEnlarged middle turbinatenCT:pneumatization of middle TnTreatmentnExcision of the lateral wallAnatomic causes of nasal obstruction-Choanal atresianRare cause:1/5000nFailure of the posterior choanae to develop proper

13、lynThe extent determines the severitynNewborn:obligate nose breathernBilateral atresia:severe N-O and airway distressnSuspected by the inability to pass a catheter or NG tube.Anatomic causes of nasal obstruction-Choanal atresianUnilateral atresianLate childhood or young adulthoodnUnilateral N-O, N-D

14、, OSAS.nEndoscopy and CTnLateral wall component of the atresiaAnatomic causes of nasal obstruction-Choanal atresianOther medical conditionnOMEnUpper and lower airway diseasenCardiac abnormaliesnGI disordernBilateral nCHARGE syndromen(Colobomas, heart defect, choanal atresia, retarded growth, genitou

15、rinary hypoplasia, and ear anomalies)nOSASnHematologic disordernFailure to thriveAnatomic causes of nasal obstruction-Choanal atresianTreatmentnTransnasal repair with / without stentnDilation of unilateral atresianTranspalatal repair with stentingnFibroblast-inhibiting topical mitomycin at the time

16、of surgeryAnatomic causes of nasal obstruction-Nasal polyposisnMultifactorial disordernAllergy, asthma, CRS, aspirin intolerance, and cystic fibrosisnPresence of edematous massesnTrigger drainage, smell loss, and obstructionAnatomic causes of nasal obstruction-Nasal polyposisnSinonasal inflammation

17、from any etiologies causes polyp increase in size and numbernNasal obstructionnSinus ostial blockagenIntranasal and systemic steroidnAntibiotics:purulent dischargenEndoscopic surgery:resistant to maximal medical therapyPhysiologynOlfactionnRespirationnProtectionnLarge surface areanThe mucosa lined,

18、moist, ciliated surfaceRespiratorynThe extensive vascular and secretory system:warm and humidifyn37n7L / minn85% humiditynBenefiting gas exchange in the lower airway.RespiratorynTurbulent airflow is central to the physiology of the nosenIncreases contact between inspired air and the nasal mucosanOcc

19、urs even at low air velocities and increases with higher velocitiesRespiratorynThe main airflownThe head of the MT-Middle meatusnMinor changes in flow pattern as velocity increasesnThe percentage of air passing through middle meatus increases with increased nasal congestionRespiratorynNasal airway r

20、esistancenThe nasal vestibule:n1/3 of nasal resistancenSusceptible to collapse from the negative pressurenFacial muscle contract during inspirationnThe nasal valve:highest resistancenThe turbinated nasal cavity:minimalRespiratorynThe nasal submucosa is rich in vasculaturenThe mucosa of inf. T contai

21、ns many small veins Venous sinusoids nExpansion CongestionRespiratorynSympathetic:Nasal airflownThe major control over venous sinusoidsndecrease the volume of bloodnParasympathetic:Nasal secretionnMinor controlnMore potent control of nasal secretionnWatery dischargeRespiratorynNasal cyclenHead and b

22、ody positionnExercisenNitric oxideRespiratorynNasal cycle:nspontaneous congestion and decongestion alternating between the two nasal passages.n80% nRepeats every 0.53 hoursnAirway resistance and nasal width changesnIn the decongestion passagesnResistance, Width Lower flow velocitiesnNot change the c

23、ombines resistance and total flowRespiratorynPosition changenChanges in relative venous pressurenExercise:nEpinephrine release decongestionnSex hormonesnPregnancy, puberty, and menstruation can lead to increased nasal obstructionRespiratorynNitric oxide:nBlood flow regulation and mucus productionnNO

24、 concentration:depends on airflow, not on cavitynAirflow:remove NO nFrom nasal cavities to the lung:vasodilator gasnHigh NO:nasal ciliary beat frequencynHelps protect the nasal airway during congested status as acute sinusitisRespiratoryRhinomamometrynMeasures airflow at a fixed pressurenMask:airflo

25、wnPressure detectors at different locationnAnterior:one nostrilnPosterior:both nostrilsnThe pressure-flow curveRespiratoryAcoustic rhinometrynNoninvasivenMeasure cross-sectional areanThe narrowest nasal valve usually lies within the first 2cm of the nasal cavitiesnThe head of inf. TnPoiseuilles law:

26、airflow is directly proportional radius to the fourth powerRespiratoryAcoustic rhinometrynCharacterizes the geometry of the nasal cavitiesnQuantifies nasal obstructionnMonitors results of treatmentnMost accurate for the anterior partnEspecially the nasal valve regionRespiratorynRhinomanometrynDeterm

27、ine resistancenHow hard?nAcoustic rhinometrynLocationnImpractical ?ProtectionNormal sinonasal mucosanEpithelial layer:nciliated, pseudostratified, columnar cellnVariable goblet cellnLamina proprianSubmucosanPeriosteumProtectionnTurbulent airflow forces all inspired air to contact mucosal surfaces be

28、fore passing to the lower airways.nCoarse nasal hairs and vibrissae filters out large particlesnSmall particles impact the mucosa as a result of turbulent airflown0.5 m passnMucociliary clearanceProtectionnGoblet cell produced glycoproteinsnGive the outer layer of nasal mucus its viscosity and elast

29、icitynOn the top of the nasal cilianInner layer: less viscosityProtectionMucociliary clearancenMaxillary sinus:begins at the floor and against gravitynAnt. ethmoid sinus:Middle meatusnPost. Ethmoid sinus:Superior meatusnFrontal sinus:drains toward the ostium only from the lateral sidenSphenoid sinus

30、:antigravitational into sphenoethmoidal recess Nasal cavities NasopharynxProtectionnThe mucous blanket cleared every 10-15 minutes by ciliary movementnCiliary activity impairednHumidity dropnTemperature decreasenCohesionnSaccharin test:20 minsProtectionCiliary dysfunctionnPrimary ciliary dyskinesia

31、(PCD):nAutosomal recessive disordernDefective ciliary structure and functionn50% have the Kartagener syndromenPanrespiratory diseasenClinical、NO concentration、Electron microscopenCystic fibrosis must be excluded in all casesProtectionCiliary dysfunctionnSecondary ciliary dysfunction(SCD)nUsually occ

32、urs during or after a respiratory infectionnOften ReversiblenLow percentage of anomalous ciliaProtectionThe innate immune systemnEpithelium:physical barriernMucosa:secrets enzymes and peptide antibioticsnNeutrophils and macrophagesnRecognize pathogen associated molecular patterns(PAMPs) and bind pat

33、hogensphagocytosisnTrigger the secretion of mediatorsnAffecting pathogen clearancenAttracting additional phagocytesProtectionThe acquired immune systemnDendritic cells (DCs):nAPCs in nasopharynx-associated lymphoid tissue(NALT)nSentinel functionnDistinguish invasive pathogen from commensal organismn

34、UnclearProtectionThe acquired immune systemnBegins with processing and presentation of antigen by DCs to Th cellsnPrimarily in NALTnThe effector response is heavily dependent on the strength of the PAMP stimulus and resulting cytokine millieu.ProtectionThe acquired immune systemnStrong PAMP stimulus

35、nTh1 response A cell-mediated response Macrophage-phagocytic activity and cell-mediated cytotoxicitynWeak PAMP stimulusnTh2 response IgE and secretory IgA Attraction of mast cell, basophilis, and eosinophilisnTh2 response also triggered by muticellular parasitesnTh2 response also mediate allergic di

36、sordersProtectionThe acquired immune systemnTh1 and Th2 responses reciprocally inhibit one anothernSome degree of Th1 and Th2 balance is necessaryProtectionAllergic rhinitis-Th2 responsenAllergens are typically protein antigen with weak PAMPs nFirst exposure Active Th2 cell Conversion of B cells to

37、plasma cells produce specific IgE Attach the surface of mast cell.nNext Exposure Allergen + IgE Ab Mast cell Inflammatory mediators Early phase symptoms of ARnThe late phase symptoms:infiltration of inflammatory cells Amplify the responseProtectionThe acquired immune systemnMany clinically allergen:

38、proteasesnAttack the epithelial barrier including tight juctions Increasing access to dendritic cells and sensitizied mast cellnSystemic IgEnCRS as an analogous to inflammatory bowel disease where the tolerance mechanisms toward commensal organisms are impairedProtectionnExotoxins secreted by colonizing S. aureus acts as a superantigensnBypassing APC DCsn30% by Superantigensn0.1% by conventional pathwaynOccurs in the nasal mucosa of CRS pt, at least in a subset of pt with polyps

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