病理学教学课件：呼吸系统疾病

呼吸系统疾病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终末细支气管AlveolarsacTerminalbronchiole

PulmonaryarteryTypeIIalveolarcellTypeIalveolarcellcapillaryAlveolarseptummacrophageBlood–airBarrierAlveolarpore(Kohn’spore)Heartfailurecell:Definition:Alveolarmacrophagescontaininghemosiderinareseenincardiacfailure.Thealveolarspacescontainmacrophageswhichshowbrownishdiscolorationoftheircytoplasmduetothehemosiderincontent.正常肺组织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气肿Pathogenesis

Etiology

CigarettesmokingObstructionofsmallairways

1-antitrypsin(

1-AT)geneticdeficiency

PulmonaryEmphysemaDegenerationofelastin

1－AT

Elastase&metallo-proteinases

MacrophageNeutrophilFreeradicals

Protease-antiproteaseimbalancehypothesisClassificaion&PathologicalChangeIntermsofanatomicdistribution

alveolar

emphysemacentriacinaremphysemapanacinaremphysemaperiacinaremphysemaOthertypes

Interstitial~,

Senile~Compensatory~ObstructiveOverinflationPulmonaryEmphysema腺泡中央型肺气肿呼吸性细支气管囊状扩张，而肺泡管、肺泡囊和肺泡不扩张因呼吸性细支气管位于肺腺泡的中央，故得名。正常肺腺泡中心型肺气肿吸烟者的肺气肿，腺泡中央型。全腺泡型肺气肿肺气肿均匀地累及全部腺泡呼吸性细支气管、肺泡管、肺泡囊和肺泡弥漫性扩张与

1-AT有关全腺泡型肺气肿全腺泡型肺气肿全腺泡型肺气肿腺泡周围型肺气肿也称隔旁肺气肿，因小叶间隔受牵拉或炎症所致；多累及邻近胸膜和小叶周边间隔的肺泡。腺泡周围型肺气肿间质性肺气肿由于肺泡间隔或细支气管壁破裂使空气进入肺间质所致；气体在小叶间隔和肺膜下形成囊球状小气泡。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小叶性肺炎：病灶坏死融合abscess小叶性肺炎ViralandMycoplasmalPneumonia

PrimaryAtypicalPneumonia

InterstitialPneumoniaDefinitionCharacterizedbyinflammatorychangesconfinedtothealveolarseptaandpulmonaryinterstitiumAtypicaldenotesthelackofalveolarexudateCausedbyvariableviruses,mycoplasmaanduncertainagentWithvarietypathologicalchangeandclinicalcourseInterstitialPneumoniaviralpneumoniaPathologicalChangeMicroscopicDependsontheseverityofthediseaseTheseptaarewidenedandedematous.Chronicinflammationconfinedwithinthewallsofthealveoli.Lymphocytesandmononuclearcellinfiltration,widenalveolarsepta.InterstitialPneumoniaPathologicalChangeMicroscopicAlveolarspacesareremarkablyfreeofcellularexudate.Inseverecases,diffusealveolardamagewithpinkhyalinemembranesmaydevelop.InterstitialPneumoniaViralInclusions:Affectedcellsarestrikinglyenlarged,andtheyshowcellularandNuclearpolymorphism,Prominentintranuclearbasophilicinclusionsspanninghalfthenucleardiameterareusuallysetofffromthenuclearmembranebyaclearhalo.PathologicalChange病毒包涵体是诊断病毒性肺炎的依据。在增生的支气管上皮细胞、支气管腺体上皮细胞、肺泡上皮细胞或多核巨细胞内见到的一种圆形或椭圆形红染球形小体，约红细胞大小，周围有透明晕。本质是多量病毒颗粒聚集而成。viralpneumonia呼吸道合胞病毒包涵体：在上皮细胞胞浆内呼吸道合胞病毒包涵体：在上皮细胞胞浆内麻疹病毒包涵体在细胞核和胞浆中禽流感病毒Tuberculosis黛玉题诗旧帕后自觉“通身燥热、腮上通红，自羡压倒桃花，却不知病由此萌”。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巨细胞由多个上皮样细胞融合而成，核排列在胞浆周围呈花环状、马蹄形或密集在胞体一端。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硬变性肺结核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免疫抑制剂治疗有效LargecellcarcinomaClinical:10%-20%oflungcarcinomasAnanaplasticcarcinomaStronglyassociatedwithsmoking.HighlymalignantLungcancerLargecellcarcinomaMacroscopic:Centralorperipheral.Typicallylarge,withpleuralinvasion.LungcancerLargecellcarcinomaSheetsandnestsgrowthpatternwithextensivenecrosis.Largecells,usuallyanaplastic,andhavelargevesicularnucleiwithprominentnucleoli.Lackdefinitiveevidenceofsquamousorglandulardifferentiationbylightmicroscope.Canhavegiantcell,clearcell,orspindlecellchanges.LungcancerLungcancerSmallcellcarcinoma

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