病理學(xué)教學(xué)課件：呼吸系統(tǒng)疾病

呼吸系統(tǒng)疾病DiseasesofRespiratorySystemAnatomyandHistology

TheUpperRespiratoryTract

thenose,pharynxandlarynx

Cricoidcartilage

TheLower

RespiratoryTract

thetrachea,bronchiandlungsTrachea

Bronchus

Lobarbronchus

Segmentalbronchus

Bronchiole

Terminalbronchiole

Respiratorybronchiole

Alveolarduct

Alveolarsac

Alveolus

Trachea&BronchialtreeLobuleAcinusLobeTracheaEpitheliumLaminapropriaSubmucosaAdventitiaBrushcell

Gobletcell

basalcellciliatedcell

smallgranularcellPseudostratifiedciliatedcolumnarepithelium0.5-2cmLobuleLungPulmonaryveinRespiratorybronchioleAlveolarductAlveolarsac

Pulmonaryalveolus終末細(xì)支氣管AlveolarsacTerminalbronchiole

PulmonaryarteryTypeIIalveolarcellTypeIalveolarcellcapillaryAlveolarseptummacrophageBlood–airBarrierAlveolarpore(Kohn’spore)Heartfailurecell:Definition:Alveolarmacrophagescontaininghemosiderinareseenincardiacfailure.Thealveolarspacescontainmacrophageswhichshowbrownishdiscolorationoftheircytoplasmduetothehemosiderincontent.正常肺組織DiseasesofRespiratorySystem1）ObstructiveLungDiseases:Chronicbronchitis,Emphysema,BronchiectasisAsthma2）RestrictiveLungDiseases：

acute—ARDS

，chronic—Silicosis3）Chroniccorpulmonale4）PulmonaryInfections:

Community-Acquired—AcuteandAtypicalpneumoniasTuberculosis

—Primary,Secondary5）Tumor：Lungcancer,NasopharyngealcarcinomaAgroupofdiseasescharacterizedbylimitationofairflow,usuallyresultingfromanincreaseinresistancefrompartialorcompleteobstructionatanylevelMajorsymptom–dyspneaMajordisordersChronicbronchitisEmphysemaBronchiectasisAsthmaObstructiveLungDiseasesDefinition:apersistentproductivecoughforatleast3consecutivemonthsinatleast2consecutiveyearsThediagnosisismadeonclinicalgroundsAcommondiseaseinmiddle-agedheavysmokersMayprogresstoemphysemaandchroniccorpulmonaleChronicBronchitisEtiology&PathogenesisChronicirritationbyinhaledsubstancesCigarettesmoking—predisposestoinfectionInterferewithciliaryactionCausedirectdamagetoepitheliumInhibitleukocytesfunctionAirpollutants（SO2,NO2)ColdairMicrobiologicinfectionsRecurrentviralinfectionsSecondarybacterialinfectionsChronicBronchitisPathologicalChangeFromtracheatobronchiandbronchiolesDamageofepithelium:ciliumSquamousmetaplasiaGobletcellhyperplasiaMucousglandshyperplasiaandhypertrophyChronicinflammatorycellsinfiltrationSmoothmusclehypertrophy(asthmatic)Fibrosisofbronchiolarwall(persistent)ChronicBronchitisSquamousmetaplasiaSquamousmetaplasiaMucousglandshyperplasiaandhypertrophyChronicbronchitis

GobletcellhyperplasiaClinicalCourseMiddle-agedheavysmokersPersistentcoughproductiveofcopioussputumWheezinginasthmatictypePulmonaryfunctiondamagewithcomplicationLeadtoemphysema,corpulmonalewhenpersistChronicBronchitisPulmonaryEmphysema

DefinitionApathologicalconditionofthelungcharacterizedbypermanentenlargementoftheairspacesdistaltotheterminalbronchiole,accompaniedbydestructionoftheirwalls,andwithoutobviousfibrosis.PulmonaryEmphysema正常肺腺泡中心型肺氣腫Pathogenesis

Etiology

CigarettesmokingObstructionofsmallairways

1-antitrypsin(

1-AT)geneticdeficiency

PulmonaryEmphysemaDegenerationofelastin

1－AT

Elastase&metallo-proteinases

MacrophageNeutrophilFreeradicals

Protease-antiproteaseimbalancehypothesisClassificaion&PathologicalChangeIntermsofanatomicdistribution

alveolar

emphysemacentriacinaremphysemapanacinaremphysemaperiacinaremphysemaOthertypes

Interstitial~,

Senile~Compensatory~ObstructiveOverinflationPulmonaryEmphysema腺泡中央型肺氣腫呼吸性細(xì)支氣管囊狀擴(kuò)張，而肺泡管、肺泡囊和肺泡不擴(kuò)張因呼吸性細(xì)支氣管位于肺腺泡的中央，故得名。正常肺腺泡中心型肺氣腫吸煙者的肺氣腫，腺泡中央型。全腺泡型肺氣腫肺氣腫均勻地累及全部腺泡呼吸性細(xì)支氣管、肺泡管、肺泡囊和肺泡彌漫性擴(kuò)張與

1-AT有關(guān)全腺泡型肺氣腫全腺泡型肺氣腫全腺泡型肺氣腫腺泡周圍型肺氣腫也稱隔旁肺氣腫，因小葉間隔受牽拉或炎癥所致；多累及鄰近胸膜和小葉周邊間隔的肺泡。腺泡周圍型肺氣腫間質(zhì)性肺氣腫由于肺泡間隔或細(xì)支氣管壁破裂使空氣進(jìn)入肺間質(zhì)所致；氣體在小葉間隔和肺膜下形成囊球狀小氣泡。PathologicalChangeGrossExaminationThebasisofdiagnosisandclassificationPaleandvoluminouslunginadvancedcasesPanacinartypemorevoluminousthancentriacinartypeUpper2/3oflungmoreseverelyaffectedPulmonaryEmphysemaasmoker,centriacinaremphysemaPanacinaremphysemaPeriacinaremphysemaMicroscopicexaminationDestructionofalveoliwallsAdjacentalveolifuseDeformationorcompressionofvasculatureoflungWithorwithoutbronchitisorbronchiolitisPathologicalChangePulmonaryEmphysemaPulmonaryEmphysemabullaelung>2cmindiameterAdjacenttopleuraCausespontaneouspneumothoraxinyoungadultsPulmonaryEmphysemaPathologicalChangeClinicalCourseProgressivelydyspneawithprolongedexpirationBarrel-chestPulmonaryfunctiondamage:slowingofforcedexpirationRecurrentinfectioninpatientswithchronicbronchitisComplication:pneumothorax,corpulmonalePulmonaryEmphysemaBronchiectasisDefinition:

achronicnecrotizinginfectionofthebronchiandbronchioleleadingtopermanentdilationoftheseairways

Clinicalmanifestation:coughwithlargeamountsoffoul-smellingpurulentorbloodysputumBronchiectasisEtiologyBronchialobstructionDiffusedobstructivelungdiseasesTumorForeignbodiesNecrotizingorsuppurativepneumoniaCongenitalorhereditaryconditionsCysticfibrosisImmunodeficiencyKartagenersyndromeBronchiectasisObstructionChronicpersistentinfectionPermanentdilationofbronchiandbronchiolesPathogenesisPeribronchialfibrosisandscarringtractiononthewallBronchialwallsdamageClearancemechanisms

AccumulationofexudatePathologicalChangeLowerlobes,bilateralCylindroidandsacculardilatedairwaysDilatedairwaydirectouttothepleuralsurfacesDamageofepitheliumAirwaywallsdestructionandfibrosisAcuteandChronicinflammatoryexudationBronchiectasisBronchiectasisMacroscopic:Diffuseorlocalizedenlarged,fibroticcartilaginousairwaysDilatedairwaysextendtopleuralsurfaceCommonlyfilledwithmucopurulentmaterialMicroscopicEctatic,dilatedairwaysChronicallyinflamedwallFollicularbronchitismaybepresentAcuteandorganizingpneumoniaiscommonBronchiectasisBronchiectasis

Definition:Asthmaischaracterizedbyepisodic,reversiblebronchospasmresultingfromanexaggeratedbronchoconstrictorresponsetovariousstimuli.Clinicallymanifestedbyepisodicdyspnea,coughandwheezingTypesExtrinsicasthmaIntrinsicasthmaBronchialasthmaBronchialasthmaEtiology&PathogenesisEtiologyVariousstimuliExaggeratedbronchoconstrictorresponsePathogenesisImmediatereactionLate-phasereactionBronchialasthmaBronchialasthma

ImmediatereactionAntigen-inducedcross-linkingofIgEBronchospasmlast-phasereactionRecruitedinflammatorycellsDamagetotheepitheliumPathologicalchangesOverdistentionofthelungsBronchiandbronchiolesOcclusionbythick,tenaciousmucusplugsCharcot-LeydencrystalsCurschmannspiralsEdemaandinflammationin

wallswithprominenteosinophilsPatchynecrosisandsheddingofepitheliumcellsHyperplasiaofmucousglandsorincreasednumbersofgobletcellsThickenedbasementmembraneHypertrophyandhyperplasiaofthesmoothmuscleBronchialasthmaBronchialasthmaMacroscopicMucouspluggingofairwaysOverdistentionwithabundantairtrappingRestrictiveLungDiseasesCharacterizedbyreducedcomplianceInterstitialfluidorfibrosisproduceda“stifflung”Abnormalitiesintheventilation-perfusionratioTypesAcute:AdultRespiratoryDistressSyndrome(ARDS)ChronicOccupationalandEnvironmental—silicosisDrugortreatmentrelatedImmunologic—sarcoidosisIdiopathic—idiopathicpulmonaryfibrosis(IPF)AdultRespiratoryDistressSyndrome(ARDS)(DiffuseAlveolarDamage)Definition

AsyndromecausedbydiffusealveolarcapillarydamageCharacterizedclinicallybyacutelife-threateningrespiratoryinsufficiency,severearterialhypoxemiathatisrefractorytooxygentherapyandthatmayprogresstoextrapulmonarymultisystemorganfailure.Synonyms

Shocklung/Traumaticwetlungs/AdultrespiratoryfailureARDSEtiology&PathogenesisARDSDirectlunginjuryEndothelialand/orepithelialinjuryVascularpermeability

Imbalanceofproinflammatoryandanti-inflanmmatorycytokinesIL-8,IL-1,TNF,TGF,PDGFIndirectlunginjuryLossofdiffusioncapacityAlveolarfloodingNeutrophils¯ophagesactivationHyalinemembranesformationPathologicalChangeGrosslyAcuteedematousstage(0-7days)heavy,firm,red,boggy,airlessProliferativephase(1-3weeks)FibroticphaseARDSMicroscopicCongestion,edemaandfibrinexudationHyalinemembranes

Fibrin-richedemafluid&RemnantsofnecroticepitheliumsProliferationoftypeIIpneumocytesphagocytosisofhyalinemembranesbymacrophagesOrganizationandpulmonaryfibrosisARDSPathologicalChangeAcuteedematousstageProliferativephaseSilicosisDefinition:

Alungdiseasecausedbyinhalationofcrystallinesilicondioxide(silica,SiO2),characterizedbyprogressivesilicoticnodulesanddiffusepulmonaryfibrosis.

Currentlythemost

prevalentchronicoccupationaldiseaseintheworldPneumoconiosis

includesdiseasesinducedbyorganicparticulatesandchemicalfumesandvaporsSilicosisInvolvingpulmonarytissue,pleuraandlymphnodesSilicoticnodule2-3mm,round,well-demarcatedcollagenousscarswithcentralcavityProgressivemassivefibrosisSilicosisPathologicalChangePathologicalChange

SilicoticnoduleconcentriclayersofhyalinzedcollagenPolarizedmicroscopy:birefringentsilicaparticlesDiffusedinterstitialfibrosisSilicosisChroniccorpulmonaleDefinition

Corpulmonaleisthediseaseoftheright-sidedcardiacchamberscausedbypulmonaryhypertensionresultingfromchronicpulmonaryparenchymalorpulmonaryvasculardisease.MaybeacuteorchronicTheaverageincidenceis0.46%CorpulmonaleDisordersthatpredisposetocorpulmonaleChroniclungdiseasesCOPD:mostcommonChronicrestrictivelungdiseasesDiseasesofpulmonaryvesselsPulmonaryembolism:acutePrimarypulmonaryarteryhypertensionDisordersaffectingchestmovementCorpulmonalePathologenesisCorpulmonalePulmonaryresistanceArteriolarspasmDecreaseincapillarybedRemodelingofvascularstructureThrombosisRestrictionofchestmovementPulmonaryhypertensionPathologicalChangeRightventricular(and/oratrium)progressivelyhypertrophy(compensation)&dilation(decompensation)HeartenlargementwithbluntingoftheapexWeight>300gRightventricularwall>0.5cmCorpulmonalePathologicalChangePrimarypulmonarydiseasesThickeningAlterationsofpulmonaryarteriolewallIntimalhyperplasiaMedialhypertrophySecondarythrombosisandorganizationCorpulmonaleClinicalCourseThesymptomsandsignsofprimarychronicpulmonarydiseasesRespiratoryfailureRight-sidedcongestiveheartfailureHepaticcongestionAscitesEdemaofthelowerextremitiesComplication

PulmonaryencephalopathyCorpulmonaleCorpulmonalePneumoniaDefinition:

AcuteExudativeinflammationoflung,CommonlyseenEtiologyInfective:Bacterial/Viral/Fungal/MycoplasmalPhysical/Chemical/AllergicPathologicalchange1)Location:Alveolar/Interstitial2)Range:Lobar/Segment/Lobular3)Feature:Serous/Fibrinous/Suppurative/Hemorrhagic/GranulomaPneumoniaPneumoniaLobarPneumoniaAnacutebacterialinfectionofalargeportionofalobeoranentirelobeCausedbystreptococcuspneumoniaeCharacterizedbydiffusedfibrinousexudativeinflammationofalveoli.CommoninyoungmenClassiccaseisnowinfrequentowingtoeffectiveantibioticsapplication.LobarPneumoniaDefinitionAnacutebacterialinfectionofalargeportionofalobeoranentirelobe

EtiologyandPathogenesisEtiologicagentStreptococcuspneumonia(type1，3，7)90-95%,Predisposedagent(Impariedresistanceofairway)Smoking,Flu,Alcoholic,Fatigue,ImmunodeficiencyAlobardistributionappearsmerelytobeafunctionofthevirulenceoftheorganismandthevulnerabilityofthehostLobarPneumoniaPathologicalChangeWide-spreadFibrinousinflammationofalveoliwithinanentirelobeFourstages:ConsistencyofexudationCongestion(1-2days)RedhepatizationGrayhepatizationResolution(7-10days)LobarPneumonia3-7daysRedhepatizationGrayhepatizationCongestionGrosslyHeavy,BoggyandRedMicroscopicSerousexudationwithfewneutrphilsVascularengorgementNumerousbacteriaLobarPneumoniaRedhepatizationGrosslyRed/Firm/AirlessLiver-likeMicroscopicMassiveconfluentexudationfillingthealveolarspaces

Redcells/Neutrophils/Fibrin

LobarPneumoniaGreyhepatizationGrosslyGrayishbrownDrysurfaceLiver-likeMicroscopicDisintegrationofredcellsPersistenceoffibrinosuppurativeexudationLobarPneumoniaResolutionGrosslySoftenofconsolidationMicroscopicGranular,semifluiddebrisinalveoli

Theexudateisresorbed,ingestedbymacrophages,orcoughedupNostructuredamageLobarPneumoniaYoungmen,Malaise,feverCoughproductiveofsputumPleuriticpain(accompaniedbypleuritis)Characteristicradiology:radiopaque,well-circumscribedlobeClinicalpictureissignificantlymodifiedbytheadministrationofantibioticsClinicalCourseLobarPneumoniaComplicationCarnificationPulmonaryabscessPurulentpleuritisSepticemiaInfectiveshockLobarPneumoniaPulmonaryCarnificationAdhesivepleuritisPurulentpleuritisabscessLobularPneumoniaBronchopneumonia0.5-2cmlobuleDefinitionAcutesuppurativeinflammationofbronchioleandaroundpulmonarytissueGenerallybilateral,multilocated,basedonlobuleCommonlyseeninchildrenandoldpeopleEtiologyandPathogenesisEtiologicagentStaphylococci/pneumococci/Streptococci/H.influenzaePredisposedagentImpairedresistanceofairway,commonlyseenasacomplicationUsuallysecondarytopre-existingdisease.LobularPneumoniaBronchopneumonia

Grossly

bilateral,multilobarbasal,patchydistributionconsolidation1-2cmindiameterCentredonbronchiolesorbronchiPathologicalChangeLobularPneumoniaBronchopneumoniaLobularPneumoniaBronchopneumoniaPathologicalChangeMicroscopicSuppurativeinflammationofbronchioles

Neutrophil-richexudationwithinalveolarspacesDestructionofalveolarwalls

LobularPneumoniaBronchopneumoniaMicroscopicVariableexudation

Neutrophils,Serousfluid,fibrin,macrophage,RBC小葉性肺炎：病灶壞死融合abscess小葉性肺炎ViralandMycoplasmalPneumonia

PrimaryAtypicalPneumonia

InterstitialPneumoniaDefinitionCharacterizedbyinflammatorychangesconfinedtothealveolarseptaandpulmonaryinterstitiumAtypicaldenotesthelackofalveolarexudateCausedbyvariableviruses,mycoplasmaanduncertainagentWithvarietypathologicalchangeandclinicalcourseInterstitialPneumoniaviralpneumoniaPathologicalChangeMicroscopicDependsontheseverityofthediseaseTheseptaarewidenedandedematous.Chronicinflammationconfinedwithinthewallsofthealveoli.Lymphocytesandmononuclearcellinfiltration,widenalveolarsepta.InterstitialPneumoniaPathologicalChangeMicroscopicAlveolarspacesareremarkablyfreeofcellularexudate.Inseverecases,diffusealveolardamagewithpinkhyalinemembranesmaydevelop.InterstitialPneumoniaViralInclusions:Affectedcellsarestrikinglyenlarged,andtheyshowcellularandNuclearpolymorphism,Prominentintranuclearbasophilicinclusionsspanninghalfthenucleardiameterareusuallysetofffromthenuclearmembranebyaclearhalo.PathologicalChange病毒包涵體是診斷病毒性肺炎的依據(jù)。在增生的支氣管上皮細(xì)胞、支氣管腺體上皮細(xì)胞、肺泡上皮細(xì)胞或多核巨細(xì)胞內(nèi)見到的一種圓形或橢圓形紅染球形小體，約紅細(xì)胞大小，周圍有透明暈。本質(zhì)是多量病毒顆粒聚集而成。viralpneumonia呼吸道合胞病毒包涵體：在上皮細(xì)胞胞漿內(nèi)呼吸道合胞病毒包涵體：在上皮細(xì)胞胞漿內(nèi)麻疹病毒包涵體在細(xì)胞核和胞漿中禽流感病毒Tuberculosis黛玉題詩舊帕后自覺“通身燥熱、腮上通紅，自羨壓倒桃花，卻不知病由此萌”。EpidemiologyItisestimatedthat1.7billionindividualsareinfectedworldwide,with8to10millionnewcasesand3milliondeathsperyear.TheWorldHealthOrganizationestimatesthattuberculosiscauses6%ofalldeathsworldwide,makingitthemostcommoncauseofdeathresultingfromasingleinfectiousagent.DefinitionEtiologyBasicpathologicalchangesClassificationandfeaturesDefinitionAcommunicablediseasecausedbyMycobacteriumtuberculosisCaninvolveanyorgans,esp.lung,skin,lymphnodesTypicalpathologicalchangeistuberculousgranulomaswiththecentersofcaseousnecrosisEtiologyMycobacteriumtuberculosisSlenderrodsObligateaerobesGrowthinhibitionLowpHLong-chainfattyacidsO2deficiencytuberculosisProliferativechange(Tubercle,Tuberculousgranuloma)

NecroticchangeExudativechange(Caseousnecrosis)(Serum/fibrin)BasicPathologicalChangeDependsonthenumber,thevirulenceofbacteria,individualimmunityandallergyresponsesNecroticchange(Caseousnecrosis)Acombinationofhypoxiaandfreeradicalinjuryleadstoacentralzoneofnecrosis.Exudativechange(Serum/fibrin)Proliferativechange(Tubercle)TubercleChronicinflammationcharacterizedbyaggregatesofactivatedmacrophagesthatassumeaepithelioidappearance.Activatedmacrophagesingranulomashavepink,granularcytoplasmwithindistinctcellboundaries.TubercleTheaggregatesifepithelioidmacrophagesaresurrounedebyacollaroflymphocytessecretingthecytokinesresponsibleforongoingmacrophageactivation.TubercleOldergranulomasalsodevelopasurroudingrimoffibroblastsandconnectivetissue,duetocytokineselaboratedbytheactivatedmacrophages.TubercleMultinucleatedgiantcells40-50μmindiameterarealsofoundingranulomas.Theyconsistofalargemassofcytoplasmandmultiplenucleiandderivefromthefusionof20ormoremacrophages.Acentralzoneofcaseousnecrosis.Langhans巨細(xì)胞由多個(gè)上皮樣細(xì)胞融合而成，核排列在胞漿周圍呈花環(huán)狀、馬蹄形或密集在胞體一端。PathologicalClassificationPulmonarytuberculosisPrimarypulmonarytuberculosisSecondarypulmonarytuberculosisFocalpulmonarytuberculosisInfiltrativepulmonarytuberculosisChronicfibro-cavitativepulmonarytuberculosisCaseouspneumoniaTuberculomaTuberculouspleuritisExtrapulmonarytuberculosisClinicalFeaturesPrimaryinfection(exogenicorganism)AlmostalwaysbeginsfromthelungsCommonlyseeninchildren95%recoverTheresttransformintoothertypesPrimarypulmonarytuberculosisPathologicalChangePrimarycomplex(dumb-bellform)GhonfocusLower(upper)partofupper(lower)lobeClosetopleura,1-2cmCentralcaseousnecrosisInflammationoflymphaticvesselsoflungTuberculosisofHilarlymphnodes146primarypulmonarytuberculosisPathological&ClinicalFeaturesSecondaryinfectionCommonlyseeninadultsCoursesofdisease:reinfectionorreactivationInitiallesionstartsfromtheapexoflungVariablepathologicalchanges(6types)SecondarypulmonarytuberculosisPathologicalClassificationFocalpulmonarytuberculosisInfiltrativepulmonarytuberculosisChronicfibro-cavitativepulmonarytuberculosisCaseouspneumoniaTuberculomaTuberculouspleuritisFocalpulmonaryTBGrossappearanceApexoflung,1-2cmtoapicalpleuraLessthan2cmSharplydefined,grey-whiteMicroscopicappearanceTBGranulomaPrognosisFibrousencapsulationCalcificationInfiltrativepulmonaryTBInfiltrativepulmonaryTBGrossappearanceBeneaththeapexNotwelldemarcatedAcutecavitiesMicroscopicappearanceGranulomaExudationNecrosisPrognosisFibrousencapsulationChronicfibro-cavitativepulmonaryTBCaseouspneumoniaChronicfibro-cavitativepulmonaryTBGrossappearanceChroniccavitieswiththickfibrouswallCoexistenceoffreshandoldlesionsSclerosisoflungMicroscopicappearanceGranulomaExudationNecrosisPrognosisCaseouspneumoniaRespiratorydysfunctionChroniccorpulmonaleSecondarydigestivetractTB硬變性肺結(jié)核x片secondarypulmonarytuberculosisCaseouspneumoniaGrossappearanceLobarorlobularconsolidationAcutecavitiesMicroscopicappearanceExtensivecaseousnecrosisExtensiveexudationBadprognosisRespiratoryfailureCaseouspneumoniaTuberculomaGrossappearanceSolitarynodule,2~5cmWell-demarcatedSatellitenodulesMicroscopicappearanceCentralcaseousnecrosisPeripheralthickfibroustissuePrognosis:CalcificationExtensionofcaseousnecrosisTuberculouspleuritisGrossappearanceThickstickyhydrothoraxPleuraadhesion/sclerosisMicroscopicappearanceAcute:serum,fibrinexudationChronic:pleurasclerosisPrognosisRespiratorydysfunctionLungcancerGrosslyCentraltype>50%casestakeoriginfromfirsttothird-orderbronchiLungcancerPathologicalChangeLungcancerCentraltypeLargesquamouscellcarcinomaextendingintothepleuraandassociatedwithcentralcavitation.PathologicalChangeGrosslyPeripheraltype30-40%Ariseintheperipheryofthelungs,fromthealveolarcellsorterminalbronchiolesLungcancerGrosslyDiffusetype2-5%LungcancerPathologicalChangeHistologicalChangeClassification

Squamouscarcinoma:25-30%Adenocarcinoma:30-35%Largecellcarcinoma:10-15%Smallcellcarcinoma(SCLC):20-25%LungcancerMostcommoninmenCloselyrelatedwithsmokingCentraltypeVaryfromsmalltolarge,obstructivelesions,commonlycavitate.Usuallyfoundinsegmentalorsubsegmentalbronchi.Incidence:1/3SquamouscellcarcinomaLungcancerOrigin:SquamousmetaplasiaAtypicalhyperplasiaInsitucarcinomaHistologically,thesetumorsrangefromwell-differentiatedsquamouscellneoplasmsshowingkeratinpearlsandintercellularbridgestopoorlydifferentiatedneoplasms.SquamouscellcarcinomaAdenocarcinoma

Mostcommoninwomen

PeripheraltypeDesmoplasiacanbeprominent(“scarcarcinomas”)PrognosisworsethanSC80%containmucinIncidence:1/3LungcancerGlandulardifferentiationpresentDifferentgrowthpatterns:LepidicPapillaryAcinarmicropapillarySolidAdenocarcinomaMicroscopicPrimarypulmonaryadenocarcinomawithsignetringcells,amostunusualfindinginthislocation.

ALK免疫抑制劑治療有效LargecellcarcinomaClinical:10%-20%oflungcarcinomasAnanaplasticcarcinomaStronglyassociatedwithsmoking.HighlymalignantLungcancerLargecellcarcinomaMacroscopic:Centralorperipheral.Typicallylarge,withpleuralinvasion.LungcancerLargecellcarcinomaSheetsandnestsgrowthpatternwithextensivenecrosis.Largecells,usuallyanaplastic,andhavelargevesicularnucleiwithprominentnucleoli.Lackdefinitiveevidenceofsquamousorglandulardifferentiationbylightmicroscope.Canhavegiantcell,clearcell,orspindlecellchanges.LungcancerLungcancerSmallcellcarcinoma

Youngormiddle-agedmenStrongrelationshiptosmokingarisefromKulchitskycellsIncidence:1/4Highlymalignant,withearlymetastases;chemotherapyresponsive.Lungcan