协和医学院病理呼吸系统课件

1PulmonarydiseaseInfectionsObstructivePulmonaryDiseaseRestrictivepulmonaryDiseaseTumors2ChronicObstructivePulmonaryDiseaseChronicbronchitisEmphysemaBronchiectasisasthma3Chronicbronchitispersistentcoughwithsputumproductionforatleast3monthsinatleast2consecutiveyears.4FormsofChronicbronchitissimplechronicbronchitisproductivecoughmucoidsputumnoairflowobstruction.ChronicasthmaticbronchitisChronicobstructivebronchitis5pathogenesisChronicirritation

Cigarettesmoking(最重要的病因)airpollutants(SO2,NO2)

MicrobialinfectionHypersensitivityOthers

67Chronicbronchitismorphology(与支扩比较)Bronchialepitheliumdegeneration：desquamation（脱落）,squamousmetaplasiagobletcellhyperplasia

mucousglandhyperplasia

inflammationFibrosisandsmoothmusclehyperplasiachronicbronchioles:

Gobletcellmetaplasia,mucousplugging,inflammation,andfibrosis.8Thedistinctivefeatureofchronicbronchitis:Hypersecretonofmucus:gobletcellhyperplasiamucousglandhyperplasia--Alsothemorphologicbasisofmuciodsputum（未感染的白色黏痰）9REIDINDEX=b-c/a-d>0.5(Normally0.4)1011InChronicobstructivebronchitis,themorphologicbasisofairflowobstruction:chronicbronchioles(smallairwaydisease):

gobletcellmetaplasiamucousplugging,inflammation,fibrosis.12Clinical:CoughmucoidsputumWheezing13Complications:Bronchiectasisemphysema（最主要的）chroniccorpulmonalebronchopneumonia14Emphysema

aconditionofthelungcharacterizedbyabnormalpermanentenlargementoftheairspacesdistaltotheterminalbronchiole,

accompaniedby

destructionoftheirwall.（过度充气+管壁破坏）

compensatoryEmphysemaSenile（老年性）EmphysemaOverinflation（过度膨胀）15TypeofEmphysemaAcinar(alveolar)EmphysemaobstructiveEmphysemaInterstitialEmphysemaParacicatrialEmphysemaBullaelung(>2cm)16TypeofAcinarEmphysemaCentroacinarEmphysema(Centrilobular)PanacinarEmphysema(Panlobular)PeriacinarEmphysema(Distalacinar)IrregularEmphysema17IrregularDistalpanacinarnormalcentral18阻塞性肺气肿的关键环节:小气道炎症肺泡间隔断裂1920Oxidant-antioxidantimblance21CentrilobularemphysemaLobularseptum22Longtimesmoker2324a1-ATdeficencyIntravenousdrugabuse252627Panacinaremphysema28Paraseptal(DistalAcinar)EmphysemaSubpleuralupperlobesFibrosisbullae29Clinical:dyspneabarrel-chested,breathsound↓,percussionnoteishyperreaonantX-ray:hyperinflation30Complications:chroniccorpulmonaleSpontaneouspneumothoraxAcuteinflammatory31chroniccorpulmonale

--pulmonarymorphologySmallerarteriesandarteriolesthickeninginternal/medialhypertrophyLuminanarrowmuscularizationofarterioles

32chroniccorpulmonale33Bronchiectasis

Bronchiectasisisthepermanentdilatinofbronchiandbronchiolescausedbydestructionofthemuscleandelasticsupportingtissue,resultingfromorassociatedwithchronicnecrotizinginfections.34Twoprocessesarecrucialandintertwinedinthepathogenesisofbronchiectasis:obstructionandchronicpersistentinfection.35BronchiectasisoriginsBronchialobstructionTumorsForeignbodiesOccasionallymucousimpactionCongenitalorhereditaryconditionsCysticfibrosisImmotileciliaandKartagenersyndromesNecrotizingorsuppurativepneumonia36Bronchiectasis（与慢支不同点）LowerlobesEpitheliumdamageBronchial/bronchiolarwalldestruction,fibrosis

DuctirregulardilatationPeribronchiolarfibrosisChronicandactiveinflammation3738Bronchiectasis39Bronchiectasis40Bronchiectasis41Clinical:1.Episodic2.Severe,persistentcoughCopiousamountsofpurulentsputum(fetid)Hemoptysis3.Clubbingofthefingers42Pulmonaryinfections43LobarpneumoniaAcutebacterialinfectionInitiallyfromalveoli,involvessegamentaloranentirelobe.DiffusefibrinousexudateinfectionMale>Female,30-50yearsAbruptmalaise,fever,chestpain,coughproductiveofBrownsputum44LobarPneumoniaEtiologyLobarpneumonia,90-95%arecausedbypneumococciMostcommonaretypes1,3,7and2.Type3causesaparticularlyvirulentformoflobarpneumonia.Occasionally,Klebsiellapneumoniae(肺炎克雷伯杆菌),staphylococci（葡萄球菌）,streptococci（琏球菌）,H.influenzaeandsomeofthegram-negativeorganisms.45Lobarpneumonia(morphology)adiffusefibrinousexudateinfectionthatleadstospreadthroughtheporesKohnconsolidationoflargeareas&evenlobesofthelung.46fourstagesofthehistopathology

1.congestion(1-2days)2.redhepatization(3-4days)3.grayhepatization(5-10)4.resolution(10-days)471.Congestion此期细菌大量繁殖1-2daysLobeisheavy,redandboggyVascularcongestionProteineousfluid（浆液性渗出）,scatteredneutrophilsandredcellsinthe

alveoliManybacteria482.redhepatization纤维素通过肺泡间孔相连，限制细菌扩散3-4daysLobe（s）isheavy，darkred，liver-likeconsolidationVascularcongestionAlveolarspacesarepackedwithmanyneutrophils,redcellsand

fibrin

Manybacteria493.Grayhepatization无菌，病人自觉症状减轻，咳铁锈色痰，胸痛5-10daysLobe(s)islarge、dry、grayandfirmVascularcompressed（毛细血管受压充血消退，菌不入血）Redcellsarelysed,fibrinpersistswithsinthealveoli.Bacteriadisappear504.resalutionAfter10daysLobe(s)issoftasnormalAlveolarexudatesareenzymaticallydigested,resorbedandingested.51lobularuniformlyconsolidationgrayhepatization525354Clinical:Abruptmalaise,fever,X-ray：consolidation

Cyanosiscough

Brownsputumchestpain55Complications(lobarpneumonia)OrganizingpneumoniaPulmonarycarnificationAbscessesExudativepleuritisEmpyema56Bronchopneumonia

(lobularpneumonia)It’saninflammationthatoriginatesinbronchiolesandextendsintothesurroundingalveoli.Childrenorelderperson

57Bronchopneumonia

OftenmixedBacterialinfection:staphylococci,streptococci,pneumococci,H.InfluenzaeInhalationofnoxiousgasesanddustsAspirationoffluidandsolidcontentsofthealimentarytract58MorphologyofBronchopneumonia

Patchyconsolidation

（实变灶大小不等，散在多发，不规则）Onelobe/multilobar,frequentlybilateralandbasalpartofthelung（分布）Thelesionsare3-4cmindiameter,slightlyelevated？

,dry,gray-redtoyellow,poorlydelimitedatthemargins（病灶直径，颜色，边界）59Bronchopneumoniahistology

Asuppurative,neutrophil-richexudatethatfillsthebronchi,bronchioles,andadjacentalveolarspaces60616263Complicationsofbronchopneumonia

LungabscessesEmpyemaSuppurativepericarditisBacteremiawithmetastaticabscessformationinotherorgansandtissueinthebody64Legionellapneumonia

Anoutbreakofseverepneumoniaaffected180ofabout4400personsattendingtheAnnualConventionofAmericanLegionnairesinPhiladolphia,USAduringJuly1976,causing29deathes.Gram(-)fibrinopurulentbronchopneumoniaabundantfibrin,variablemacrophageandneutrophils65AtypicalpneumoniaUsualyabsenceofphysicalfindingsofconsolidationandonlymoderateelevationofwhitecellcountApulmonaryinflammatorylargeconfinedtoalveolarseptaandpulmonaryinterstitium,Lackofalveolarexudate(interstitialpneumonia)Commonlycausedbymycoplasma,viruses…mycoplasmapneumoniaviralpneumonias66Histologically:

theinflammatoryreactionislargelyconfinedwithinthewallofthealveoli.67Clinically,respiratorydistressseeminglyoutofproportiontothephysicalandradiographicfindings68Severeacuterespiratroysyndrome(SARS)Coronavirus(SARS-CoV)InfectthelowerrespiratorytractandinduceviremiaThehistopathologyoflungofSARSusuallydemonstratedDiffusealveolardamagePneumocystis（卡氏肺孢菌）pneumoniaP.cariniiAnopportunisticinfectionsoccurredinimmunocompromisedpersonAIDSOrgantransplantationchemotherapymalnourishedchildren

70PulmonarytuberculosisachronicgranulomatousdiseasecausedbyM.tuberculosis,usuallyaffectingthelungs,butvirtuallyanyextra-pulmonaryorgancanbeinvolvedbyisolatedtuberculosis.71Characteristictubercle–-----

tuberculousgranuloma（即结核结节tubercle）

Centralcaseousnecrosis以及四种细胞成分epithelioidcellsMultinucleatedgiantcellsLymphocytesFibroblasticcell73PrimarypulmonarytuberculosisChildrenTheformofdiseasethatdevelopsinapreviouslyunexposed,unsensitizedpersonItbeginsasasinglegranulomatouslesion(Ghonfocus即原发灶),subjacenttothepleuraintheinferiorupperlobe/superiorlowerloberegions.Thespreadtodrainingbronchialandhilar（门）nodes即引流到支气管和肺门淋巴结CombinationoflungandlymphnodelesionscalledtheGhoncomplex74Primarypulmonarytuberculosis,Ghoncomplex原发灶，淋巴管炎，肺门淋巴结结核HilarLN7576Ziehl-Neelsenstain77Finalresultsoftheprimarytuberculosis

abenign,self-limiteddisease,Inducehypersensitivity/resistance--自限resultsinlocalscarringandcalcification,mayreactivation--局限progressiveprimarytuberculosis--进展Throughthelymphohematogenousroutes,distantorgansmaybemiliarydisseminatedtuberculosisorisolatedorgantuberculousinfection--播散78Progressiveprimarytuberculosisbronchopneumonia79SecondarytuberculosisAdultInapreviouslysensitizedhostReinfectionMostcasesadultorsecondarypulmonarytuberculosisrepresentreactivationofanold,possiblysubclinicalinfection.80SecondarytuberculosisClassicallylocalizedtotheapexofoneorbothupperlobesCavitationoccursreadilyDisseminationalonetheairways81SecondarytuberculosisMorphologyLesionisalmostinvariablylocatedintheapexofoneorbothlungs.（位置）Asmallfocusofconsolidation,usuallylessthan3cm.Indiameterwithin1or2cm.Oftheapicalpleura.（大小）Thefociarefairlysharplycircumscribed,firm.gray-whitetoyellowareasthatagreaterorlessercomponentofcentralcaseationandperipheralfibrousinduration（边界清，质实，灰白到黄，伴不同程度的干酪样坏死和硬化）.8283SecondarytuberculosisHistologicallygranulomas,withnecrosis(caseation)Theprogressivelesions,moretuberclescoalescetocreateaconfluentareaofconsolidatonThefavorablecase,isconvertedtoafibrocalcificscar.Mayprogressalongseveraldifferentpathways8485CavitaryfibrocaseoustuberculosisThecavityremainslocalizedtotheapexislinedbyayellow-graycaseousmaterialismoreorlesswalledoffbyfibroustissueThrombosedarteriesmaytraversethesecavitiestoproduceapparentfibrousbridgingbands.Theinfectivematerialmaydisseminatethroughtheairways.86Secondarytuberculosis:bilateralcavitarylesions8788MilitarytuberculosisLymphhematogenousdisseminationmaygivetomilitnarytuberculosislymphaticsmajorlymphaticducts/venous

rightoftheheartlungPulmonaryvenoussystemiccirculation

distantseeding89Militarytuberculosisofspleen90Secondarymilitarytuberculosis91TuberculousbronchopneumoniaHighlysensitizedTuberculousinfectionmayspreadrapidlyadiffusebronchopneumoniaorlobarpneumonia(gallopingconsumption奔马痨)Histologicalfeatures:exudates,caseation,numerousTBbacilli9293Pneumoconiosis-silicosisPneumoconiosesencompassagroupofchronicfibrosingdiseasesofthelungresultingfromexposuretoorganicandinorganicparticulates.Silicosisiscausedbyinhalationofcrystallinesilicondioxide(silica),isthemostcommonPneumoconiosisintheworld.94SilicosisDusts5nosecavity3-5bronchialcavity2alveoliPhagocytosis(macrophages)Resp