呼吸系统病理1（英文版）课件

Basic

PATHOLOGYRespiratory

DiseasesReview

ofthearchitectureoftherespiratorysystemPULMONARY

DUCTAlveolusBronchus BronchiolesAcute

bronchitisPULMONARY

ACINUSRespiratorybronchioles

Alveolar

duct Alveolar

cystEmphysemaChronic

bronchitisAsthmaBronchiectasisBronchiolar

pneumoniaLobular

pneumoniaSquamouscell

carcinomaAdenocarcinomaBronchioloalveolar

carcinomaPulmonary

tuberculosisPneumoniaPneumoniacanbeverybroadlyDefinedasanyinfectioninthelung.Pathologically,itmaybedefinedasanyinflammationof

lung.Classificationof

pneumonia1. Etiological

classification:bacterialpneumoniaviralpneumoniafungalpneumonia

etc.2.Anatomical

classification:lobarpneumonialobularpneumoniainterstitial

pneumonia.Clinically,etiologicalclassificationismorebeneficialtothe

treatment;buttheetiologicalclassificationusuallycannotbemade

readily.Theanatomicalclassificationmaygiveagreathelptotheetiologicaldiagnosis

sometimes.>90%:causedbyStreptococcuspneumoniae(pneumococcus)

;interstitialpneumoniaarecausedbyvirusor

mycoplasm.BacterialPneumoniaLobarpneumoniaDef.Inlobarpneumoniathecontiguousairspacesofpartorallofalobearehomogenouslyfilledwithanexudatesthatcanbevisualizedonradiographsasalobarorsegmentalconsolidationandisthussometimesreferredtoas“airspace”pneumonia.Thediseasewhichisoftenseeninpreviouslyhealthyyoungadultshasasuddenonset

andisaccompaniedbychills,fever,coughwithpink-foamsputaand

chest-ache.Etiologyand

pathogenesis>90% S.pneumoniaenterthelungsviathe

airwaysOccasionally otherorganisms(Klebsiellapneumoniae,staphylococci,streptococci,Haemophilus

influenzae).Lobarpneumoniaisinitiatedinperipheryacinus,fromtheretheexudativefluidcontainingetiologicagentflowsintotheadjacentairpassagetoinfectadjacentlobulesuntilasegmentorentirelobeis

infected.MorphologyForpurposesofdescription,itisconvenienttodividetheprocessintofourphases:CongestionRedhepatizatio

(consolidation)GrayhepatizationResolution1. Congestion

stage(1st-2nd

days)Theaffectedlobeisheavy,redandboggy.Afrothyblood-stainedfluid

canbesqueezedfromthecut

surface.Histologically,thereisvascularcongestionwithproteinaceousfluid,scatteredneutrophils,andmanybacteriainthe

alveoli.Clinically,theonsetissuddenwithfeverand

rigors.2.Redhepatization

stage(2nd-4th

day)Liver-likein

consistencySeptalcapillariesarecongested

markedlyAlveolarspacesarepackedwithmanyredcells,

andseveralneutrophils,

fibrin.Thepleurausuallydemonstratesafibrinousorfibrinopurulentexudates.3.Grayhepatization

stage(4th–8th

day)MoresolidinconsistencyPleuralsurfaceiscoveredwitha

confluentfibrinous

exudates.Thecutsurfaceisdryandgranularbutof

agrayish-white

color.Histologically,congestionofseptalcapillarieslightens.Thefibrinousexudatepersistswithinthealveoliandafibrinnetforms.There

are manyneutrophilsbutisrelativelydepletedofredcellsinthe

alveoli.4.Resolution

stage(8th-9th

day)Withtheeliminationofbacteria,theinflammation

subsides. Sincethereisnotissuedestructionthelungreturntonormalapartfromthe

pleura.X光肺叶密度增高肺叶实变Complications:1.Carnification:Organizationofintraalveolarfibrinousexudatesinsteadofresorptionmayconvertareasofthelungintosolid

fibroustissue.2.Tissuedestructionandnecrosismayleadtoabscessformation.3.Suppurativematerialmayaccumulateinthepleuralcavity,producingpurulentpleurisy

and empyema.4.Septicemiaor

pyemia:Bacteremicdisseminationmayleadtomeningitis,arthritis,orinfective

endocarditis.5. Infectiveshock:Failureofterminalcirculationandappearanceoftoxic

symptoms.BronchopneumoniaConception:Definedasanacutepurulentinflammationcharacterizedbydiffusepatchypneumonicconsolidation

often

with bronchiolitis

inits

center.Itisathreatchieflytothevulnerable

infants,theaged,andthosesufferingfromchronicdebilitatingillnessor

immuno-suppression.Children: Whoopingcoughandmeasles

areimportantantecedentsAdult:influenza,chronicbronchitis,alcoholism,malnutrition,andcarcinomatosisareallpredisposingconditions.Clinically,bronchopneumoniamayappearsasacomplicationofa

disease.HypostaticpneumoniaThepatientwithpulmonaryedemafromcardiacfailureorheavyuremia,etal,isparticularlyvulnerable,whoarenecessarytokeepthemselvesinbedinprolonged

time.AspirationpneumoniaThepatientincomaorapoplexy,

heavyanesthesiaandsoonisparticularly

vulnerable.Almostanyorganismmaycausebronchopneumonia,frequentoffendersarestaphylococci,streptococci,haemophilusinfluenza,proteusspecies

etc.EtiologyFociofinflammatoryconsolidationwithacenterofbronchiolitisaredistributedinpatchesthroughoneorseverallobes,mostfrequentlybilateral

andbasal.MorphologyWell-developedlesionsupto3or4cm(usually0.5-1cm)indiameterareslightlyelevated,dry,granular,gray-redtoyellowanddemarcated

distinctly.Thelungsubstanceimmediatelysurroundingareasofconsolidationisusuallyhyperemicandedematous,butthelargeinterveningareasaregenerally

normal.Histologically,thereactionconsistsofasuppurativeexudatesthatfillsthebronchi,bronchioles,andadjacentalveolarspaces.Hyperemia,edemaandinflammataryinfiltrationcanbeseeninthewallsof

bronchioles.ComplicationThesamecomplication,asinlobarpneumonia.ViralpneumoniaandmycoplasmalpneumoniaTheybothbelongtointerstitialpneumoniaDef. aninflammatoryprocessinvolvingtheinterstitialtissueofthe

lungs.Etiologyand

pathogenesisThecommonagentsarevirusesandmycoplasma.Attachmentoftheorganismstotherespiratoryepitheliumisfollowedbynecrosisofthecells

andaninflammatoryresponse.Then,theinflammationextendstotheinterstitialtissueincludingperibronchialconnectivetissueandinteralveolar

septa.MorphologyMacroscopically:red-blue,congested,andsubcrepitant.Becausemuchofthereactionisinterstitial,littleinflammatoryexudatesescapesonsectioningofthelung,althoughtheremaybe

slightoozingofred,frothy

fluid.Histologically,theinflammatoryprocessislargelyconfinedwithinthewallsofthealveoli.Theseptaarewidenedandedematous;theyusuallycontainamononuclearinfiltrateoflymphocytes,histiocytesandoccasionally

plasmacells.Invirusinfection,inclusionbodiesmaybeformedwithincytoplasmornucleusoftheepithelialcellsofbronchiolesand

alveoli.Inseverecasesalveolardamagewithhyalinemembranesmay

develop.A

TRYChronicobstructive

pulmonarydisease (COPD)chronic

bronchitisemphysemabronchial

asthmabronchiectasisChronic bronchitisDef.Apersistentproductivecough

foratleastthreeconsecutivemonthsinatleasttwoconsecutive

years.EtiologyandPathogenesissmoking,airpollution

(SO2,NO2)directlyor

throughneurohumoralpathwaysproliferation

ofbacteria↓hypersecretionofbronchialmucous

gland↓hypertrophyofmucousgland,Goblet

cellmetaplasiaof

bronchialepithelium↓chronic

bronchitis↙↙lossofciliatedepithelium↓retention

ofsecretion↓ ∣↖∣∣∣∣microbialinfectionMorphologyGrossly①mucosalliningofthelargerairwaysisusuallyhyperemicandswollen

by

edema fluid;②itiscoveredbyalayerofmucinousormucopurulentsecretions.Thesmallerbronchiandbronchiolesmayalsobefilledwith

similarsecretions.3.

病理变化部位主要特征眼观:

早期进展镜检:(1)腺体肥大, 分泌亢进后期腺体萎缩, 分泌耗竭(2)气管粘膜上皮细胞的损伤(3)支气管壁的病变Histologically:Hypertrophyofmucousglandandgobletcellmetaplasiaofbronchial

wall.①thediagnosticfeature:enlargementof

themucus-secreting

glands.Reidindex:theratioofthethicknessofthesubmucosalglandlayertothatofthe

bronchialwall

.Normal:

1:3Chronicbronchitis:usuallyexceeds

1:2.粘液腺肥大、增生;浆液腺发生粘液化生。粘液分泌亢进上皮鳞化粘液腺增生肥大②Increasednumberofgobletcellsintheliningepitheliumwithconcomitantlossofciliatedepithelial

cells.③squamousmetaplasiaofliningepitheliumfollowedbydysplasticchanges.④

Mucosalandsubmucosalliningofbronchiarehyperemicandswollen.inflammatoryinfiltration(lymphocytes,plasmacytes,sometimesadmixedwith

neutrophils).支气管粘膜慢性炎伴上皮鳞状化生ComplicationsEmphysemacor

pulmonalsBronchiectasisBronchopneumoniabronchogeniccarcinomaof

lungEmphysemaDef. characterizedbyabnormalpermanentenlargementoftheairspacedistaltothe

terminalbronchioleaccompaniedbydestructionoftheirwalls.Etiology1.Alveolarwalldestructionand

airspaceenlargementinvokesexcessproteaseorelastaseactivityunopposedbyappropriateantiproteaseregulation①IncreaseeitherthenumberofPMN

andMPinthe

lung②Increasereleaseofproteasefrom

PMNand

MP③

oxidantsincigarettesmokeandO

-2radicalssecretedbyPMN&MPinhibittheactiveofα1-ATanddecreasenetanti-elastaseactivityin

smokersDeficiencyPiMM/PiZZ

(Chr14)EmphysemAntiproteaseα1-antitrypsininhibition↗Smoking↓↑Protease

:elastasecollagenase↘←α1-antitrypsinDestructionofelastin

andcollagenofthe

lung↘→2.Obstructionofthe

bronchioles.AirenterintothealveolidistaltotheobstructedbronchiolethroughKohn’spore(interalveolarpore),andairistrappedduringexpirationbecausetheporeisclosed.Emphysemais

ended.（四） 病因与发病机理(1)病因(2)发病的二个基本环节细支气管阻塞和狭窄小气道及肺泡支撑组织的破坏Classificationand

MorphologyAlveolaremphysema:centriacinar

emphysemapanacinar

emphysemaperiacinar

emphysemaInterstitial

emphysema:Others:paracicatrical

emphysemabullaelungsenileemphysemacompensatory

emphysemaDiagramofthefundamentalunitofthelungcentriarclinalandpanacinar

emphysema.MorphologyThelesionsofcentriacinaremphysemaaremorecommonandsevereintheupperlobesparticularlyintheapical

segments.腺泡中央型肺气肿Panacinar

emphysema:pale,voluminous

lungs全腺泡型肺气肿Microscopic features:Thinninganddestructionofalveolar

walls.Adjacentalveolibecomeconfluent,creatinglargeairspaces.Capillariesinalveolarsepta

decreased.Terminalandrespiratorybronchiolesmaybedeformedbecauseofthelossof

septa.Bullous

emphysema囊泡型肺气肿（大泡直径3cm）Conditionsrelatedto

emphysema.Thereareseveralconditionsinwhichenlargementofairspacesisnotaccompaniedbydestruction;thisis

morecorrectlycalled

overinflation.CompensatoryemphysemaSenile

emphysemaInterstitialemphysemadesignatestheentranceofairintotheconnectivetissueof

thelung,mediastinumandsubcutaneous

tissue.Thismayoccurspontaneouslywithasuddenincreaseinintraalveolarpressure(as

withvomitingorviolentcoughing)thatcauseatear,withdissectionofairintothe

interstitium.Complications:Cor

pulmonalePneumothoraxRespiratory

failureBronchiectasisDef.Permanentdilatationofbronchiandbronchioleduetodestructionofthemuscle

andelasticsupporting

tissue.Thecharacteristic

symptom:coughandexpectorationofcopiousamounts

ofpurulent

sputum.Etiologyand

pathogenesisBronchialobstruction(tumor,enlarged

lymphnode,foreign

body)riseof

intrabronchialpressureduring

respirationbronchial

dilatationlossof

ciliatedepitheliumcongenit