HEALTH&DISEASEPEACE&WAR炎癥與損傷的修復(fù)

InflammationandRepairByDr.S.J.YANGDepartmentofPatholgy,4thMilitaryMedicalUniversity學(xué)習(xí)內(nèi)容炎癥的概念(ConceptionofInflammation)病因(EtiologicAgents)局部表現(xiàn)和全身反應(yīng)(LocalandSystemicManifestations–Signs&Symptoms)炎癥的基本病理變化(MorphologicPatternsofInflammation)急性性炎癥類型及特點、發(fā)病機制(AcuteInflammation

andPathogenesis)損傷的修復(fù)(Repair)慢性炎癥及其類型和特點(ChronicInflammation)炎癥的結(jié)局(PrognosisofInflammation)AulusCorneliusCelsusJohnHunterRudolfVirchowElieMetchnikoffPaulEhrlichThomas,LewisHISTORICALHIGHLIGHTS:"BigRobbins"lists,ormighthavelisted

CorneliusCelsus(ancientRome)described

rubor

(redness),calor(heat--thisappliesonlytotheskin),dolor(pain),andtumor(whichthensimplymeant"swelling")asthe"cardinalsignsofinflammation".JohnHunter(thegreatearlysurgeon,*1793,*parodiedbyWilliamBlakeas"JackTearguts")firstcharacterizedinflammationasanonspecificbodyresponse.RudolfVirchowaddedfunctio

laesa(lossoffunction)asthefifthcardinalsignofinflammation,andhisstudent,JuliusCohnheim,providedthebasicstudiesofthepathologicmicroanatomyofinflammation.ElieMetchnikoff(*1892)wasthefirsttoobserveandstudyphagocytosis.(*ThisisthesameMetchnikoffwhopopularizedyogurtasa"healthandlongevityfood".Hediedatage70.)PaulEhrlichdevelopedtheideaofhumoralimmunityearlyinthiscentury.(ThisisthesameEhrlichwhodevelopedthe"magicbullet"forsyphilis,andmostofthestainswestilluse.)ThomasLewisdemonstratedthatinflammationisbroughtaboutbychemicalmediators,mostofwhichactlocally.Someonemaystillaskyouaboutthe"tripleresponseofLewis"toasuperficialscratch:(1)animmediateredscratchmark;(2)aredflarearoundthescratchmark;(3)aredswollenarea("wheal")aroundtheflare.(Tryit!)Dr.Lewisfoundthathecouldeliminatetheflare,butnottheothers,bycuttingtheautonomicnervesupply(i.e.,preventingthe"axonreflex").Thisexperimentledtothediscoveryofhistamine,whichmediatesevents1and3.Inflammation

Definition各種致炎因子引起機體的組織損傷所誘發(fā)的以防御為主的局部組織反應(yīng)。(第一版）具有血管系統(tǒng)的活體組織對損傷因子所發(fā)生的防御反應(yīng)。（第四版）Inflammationandrepair-Defensivereaction.Defensive?Defective?Definitionby

BigRobbins

“Inflammationisthereactionoflivingtissuestoallformofinjury.Itinvolvesvascular,neurologic,humoralandcellularresponseatthesiteofinjury”

（BasicPathology）

EtiologicAgentsofInflammation“Allthefactorsthatcaninjurythetissuesandcellscanalsocauseinflammationofthebody.Theyincludethephysical,chemicalbiological,andImmunologicalagentsetal.”炎癥的致病原因LocalandsystemicmanifestationsAcuteInflammation

CardinalSigns

(Celsus,1AD)

Redness(rubor)Swelling(tumor)Heat(calor)Pain(dolor)Lossoffunction(functio

laesa)(thefifthcardinalsignsupposedlyaddedbyVirchow)AcuteInflammation

CardinalSigns-Redness

AcuteInflammation

CardinalSigns-Swelling

AcuteInflammation

CardinalSigns-Pain

Inflammation

SystemicManifestationsofInflammationFever-clinicalhallmarkofinflammationEndogenouspyrogens:IL-1andTNF-aLeukocytosis-maybeneutrophils,eosinophils,orlymphocytesLeukopenia-rareAcutePhaseReactants-non-specificelevationofmanyserumproteins-willmarkedlyincreasethe“sedrate”LeukocytosisLinesofDefense

Inflammation

SystemicManifestationsofInflammationShock–mostcommoningram-negativesepticemia(bacteriainthebloodstream),althoughitcanoccurwithgram-positivebacteremiaLipopolysaccharide(endotoxin)ofgram-negativescanproducesymptomsofshockwheninjectedintoanimalsTNF-acanproduceasimilarsyndrome

三、炎癥的基本病理變化基本病變變質(zhì)：Alteration滲出：Exudation增生：Proliferation變質(zhì)和滲出出現(xiàn)于早期，而增生出現(xiàn)于晚期變質(zhì)（Alteration）1、概念：炎癥局部組織發(fā)生的變性和壞死2、原因：致病因子直接作用局部血液循環(huán)障礙免疫介導(dǎo)炎癥反應(yīng)產(chǎn)物的間接作用3、變質(zhì)的細(xì)胞的類型和形態(tài)變化實質(zhì)細(xì)胞變性：細(xì)胞水腫、脂肪變性壞死：凝固性和液化性壞死間質(zhì)細(xì)胞變性：黏液變性、玻璃樣變性壞死：纖維素樣壞死滲出(Exudation)1、概念：炎癥局部組織血管內(nèi)的液體成分、蛋白質(zhì)和各種白細(xì)胞通過血管壁進(jìn)入組織、體腔、體表和粘膜表面的過程，稱為滲出滲出是炎癥最重要特征性變化增生(Proliferation

)1、實質(zhì)細(xì)胞增生：肝炎時，肝細(xì)胞的再生慢性膽囊炎時粘膜上皮和腺體增生2、間質(zhì)細(xì)胞增生：包括巨噬細(xì)胞、血管內(nèi)皮細(xì)胞和成纖維細(xì)胞炎癥的類型Classification

ofinflammation臨床類型急性炎癥：病程短，幾天－1月，以變質(zhì)滲出為主慢性炎癥：病程長，數(shù)月－數(shù)年，以增生為主OUTCOMESOFINFLAMMATIONIncitingStimulusAcuteInflammation

Chronic-active

InflammationChronicInflammationResolutionAbscessResolution

withscarring**Thelongerthestimuluspersists,thegreaterthescarringwillbe.AdynamiccontinuumofchangeSpreadingBacteremiaToxemiaSepticemiaPyemiaStoryofmiceAcuteInflammationPathogenesisofAcuteInflammationTypeofAcuteInflammation急性炎癥

PHASESOFINFLAMMATIONInitiationAmplificationTermination

急性炎癥的類型病理分類漿液性炎纖維素性炎化膿性炎出血性炎

Inflammation

PhasesofAcuteInflammationInitiation(開始或啟動)

–

血管反應(yīng)為中心Stimulation(injury)withchangesinmicrovasculatureStructuralchangesleadingtoextravasationEmigrationofWBCstothesiteofinjuryAmplification(擴(kuò)大或進(jìn)展)*

-炎癥介質(zhì)和炎細(xì)胞的作用－BothsolublemediatorsandcellularinflammatorysystemsareactivatedandamplifiedTermination(終止)*

-再生、修復(fù)和愈合-

accomplishedbyspecificinhibitionordissipationofthemediators

急性炎癥的早期反應(yīng)

PhasesofAcuteInflammation-InitiationInitialvasoconstriction(secondstominutes),followedbyalongerperiodofvasodilationLeakageoffluidandplasmafromtheintravascularcompartment(increasedpermeability)Stasis,withtransmigrationofleukocytesanderythrocytesintoextravasculartissueTheTripleResponse-SirThomasLewis(1927)Normalregulationoffluidtransport

Extravascularfluid

(littleproteinorpressure)HydrostaticpressureOncoticpressure

EDEMA-TRANSUDATE(proteincontentlow-specificgravity<1.012)HydrostaticpressureOncoticpressureNon-InflammatoryEdemaIncreasedHydrostaticPressure

EDEMA-TRANSUDATE(proteincontentlow:specificgravity<1.012)HydrostaticpressureOncoticpressureNon-InflammatoryEdema

DecreasedOncoticPressureDecreasedOncoticPressure膠體滲透壓靜水壓

晶體滲透壓

EDEMA-EXUDATE

(proteincontenthigh:specificgravity>1.020)HydrostaticpressureOncoticpressureInflammatoryEdema

IncreasedVascularPermeabilityDiapedesis血球滲出

AcuteInflammation

PathogenesisofEdemaNon-inflammatoryedema,

e.g.:Pulmonaryedemaduetoheartfailure(increasedhydrostaticpressure)Nephroticsyndrome(decreasedoncoticpressure)Inflammatoryedema,either:Direct,irreversibleinjury-allvessels(burns)Transientincreaseinvascularpermeability,i.e.,theeffectofmediatorsonpost-capillary

venules漿液性炎Serousexudation–SerousinflammationSerousexudation–Serousinflammation漿液性炎Fibrinousexudation白喉纖維素性炎Fibrinous

exudattion白喉Fibrinous

exudattion絨毛心Pseudomembranous

enterocolitis假膜性炎Pseudomembranous

enterocolitis假膜性炎HemorrhagicInflammationHemorrhagicFeverwithRenalSyndrome出血性炎炎癥灶的血管損傷嚴(yán)重，滲出物中含有大量紅細(xì)胞。不是獨立的類型，常與其他類型合并存在，如纖維素性出血性炎常見于流行性出血熱、鉤端螺旋體和鼠疫等急性傳染病。急性炎癥擴(kuò)展

PhasesofInflammation-AmplificationPMNsandmacrophagesarerecruitedtothesiteofinjuryfromperipheralbloodbychemokines,principallyIL-8,plusc5a,TGF-b,andPlatelet-derivedGrowthFactorIL-1andTNFcausethereleaseofpost-mitoticreservegranulocytesfromthemarrow,plusinducetheproductionofColonyStimulatingFactors(CSF)ExudationofbloodcellsInflammation

Neutrophil

Inflammation

NeutrophilGranulesPrimary-containserineproteases,lysozymeandphospholipaseA2Secondary-similartoprimary,butalsocontainlactoferrinandcollagenaseTertiary-presentattheleadingedgeofmigratingPMNs,containgelatinasesthatarecapableofdegradingbasementmembraneInflammation

Eosinophil

Inflammation

MONONUCLEARPHAGOCYTES

Inflammation

LymphocyteInflammation

Plasmacell白細(xì)胞游出

LeukocyteExtravasationMargination,rolling,andadhesionTransmigration(diapedesis)MigrationtowardthesiteofinjuryalongachemokinegradientSequentialinvolvementof

adhesionmolecules

CentralAxialStreamRolling

Adhesion

TransmigrationSELECTINS(E&P)INTEGRINS&Ig-LIKEMOLECULES(ICAM,VCAM)QualitativeandQuantitativeEndothelialandPMNChangesInflammation

AdhesionMoleculeModulationP-selectinisredistributedtothecellsurfacefromtheWeibel-Paladebodiesduetostimulationbythrombin,histamine,andPlateletActivatingFactor(PAF)InductionofE-selectinonendotheliumbyIL-1andTNFIncreasedavidityofbindingofintegrins(conformationalchange)Inflammation

MarginationandPavementingInflammation

Transmigration趨化作用

ChemotaxisExogenousmediators,e.g.:N-formyl

methionineterminalaminoacidsfrombacteria Lipidsfromdestroyedordamagedmembranes(includingLPS)Endogenousmediators,e.g.:Complementproteins(C5a)Chemokines,particularlyIL-8Productsoflipoxygenase(LTB4)

炎細(xì)胞的作用

InflammatoryCellFunctionPhagocytosis

opsonizedbyIgG(subtypes1or3)orC3bLocalimmuneresponsebymonocytesandlumphocytesaswellascytokinesTissueinjurybyinflammatorycellsthoughtheproteinaseandinflammatorymediators吞噬作用、免疫作用、引起組織損傷

Inflammation

MononuclearPhagocytesNeutrophilingestionofbacteria,gramstain炎癥介質(zhì)

ChemicalMediatorsofInflammationVasoactiveaminesComplementsystemKininsystemCoagulationpathwayFibrinolyticpathwayArachodonicacidmetabolitesPlateletactivatingfactorCytokinesNitricoxide-以中性粒細(xì)胞滲出為主，并伴有不同程度的組織壞死和膿液形成。膿液：為膿性滲出物，外觀呈渾濁的凝乳狀液體，灰黃色或灰白色，稀薄或粘稠膿液的成分：膿細(xì)胞、細(xì)菌、壞死組織、漿液膿細(xì)胞：為變性壞死的中性粒細(xì)胞?；撔匝专C中性白細(xì)胞滲出

Purulentinflammation-ExudationofNeutrophil(1).表面化膿和積膿表面化膿-指發(fā)生于粘膜或漿膜的化膿性炎,黏膜的化膿性炎又呈膿性卡他性炎如化膿性尿道炎，中性白細(xì)胞向黏膜表面滲出，深部組織不明顯.積膿-當(dāng)化膿性炎發(fā)生于粘膜或漿膜時，膿液積聚于漿膜腔、膽囊和輸卵管腔內(nèi).(2).膿腫(3).蜂窩織炎（phegmonousinflammation）

疏松結(jié)締組織的彌漫性化膿性炎，常發(fā)生于皮膚、肌肉和闌尾。溶血性鏈球菌透明質(zhì)酸酶—降解結(jié)締組織基質(zhì)中的透明質(zhì)酸鏈激酶—溶解纖維素Acutemeningitis-Purulentexudate

表面化膿Acutesalpingitis-Purulentexudate

積膿Acutesalpingitis-Purulentexudate

Abscesss膿腫

Inflammation

TissueInjurybyInflammatoryCells膿腫Inflammation

AcuteInflammatorycellinfiltration彌漫性化膿

ActivatedoxygenspeciesCanmigratethroughintactplasmamembranesInitiatelipidperoxidationReactwithDNAOxidizesulfhydrylgroupsofproteinsDegradeextracellularmatrixcomponents炎癥引起組織損傷

TissueInjurybyInflammatoryCells

炎癥引起組織損傷

TissueInjurybyInflammatoryCellsLysosomalenzymesSincetheseenzymesareusedtodegrademicroorganismsinlysosomes,obviouslytheycoulddamagetissueintheextracellularenvironmentUsuallyproteaseactivityiscontrolledbyavarietyofanti-proteasespresentinplasma(a1-anti-trypsin,a2-macroglobulin,etc.)

炎癥引起組織損傷

TissueInjurybyInflammatoryCellsPhagocyticcelladherenceAdherencetobasementmembranes,othercomponentsoftheextracellularmatrixandothercellsbyphagocytesenhancesthedamagecausedbyreactiveoxygenspeciesandlysozyme,becausenormalinhibitorspresentinplasmacannotgainaccesstothatspacebyvirtueofthephagocyticcelladherence

炎癥引起組織損傷

TissueInjurybyInflammatoryCellsTherelativelyprimitiveandnon-specificimmuneeffectsofpolymorphonuclearleukocytesandmacrophagesuponinvadingmicroorganismsarealsocapableofdamagingthehostbytheextracellularreleaseofenzymesandactivatedoxygenspecies

Inflammation

TissueInjurybyInflammatoryCellsInflammation

Typhoidalulcers

Inflammation

TissueInjurybyInflammatoryCells損傷的修復(fù)

TissueRepair損傷的修復(fù)與愈合

Regeneration,

RepairandHealing修復(fù)（repair）：損傷造成機體部分細(xì)胞和組織喪失后，機體對所形成缺損進(jìn)行修補恢復(fù)的過程，稱為修復(fù)。方式再生性修復(fù),由周圍同種細(xì)胞增生修復(fù)纖維性修復(fù),由肉芽組織填補再生（Regeneration）：是指由同種細(xì)胞分裂增生來補充機體老化、消耗或壞死的細(xì)胞的過程。可分為：生理性再生：也稱為完全性再生。是指生理過程中老化、消耗的細(xì)胞由同種細(xì)胞分裂增生補充，如表皮角化層經(jīng)常脫落，由表皮基底細(xì)胞增生、分化，予以補充。病理性再生：也稱不完全再生。是指病理狀態(tài)下，組織細(xì)胞損傷后發(fā)生的再生，一般由纖維組織增生代替。再生修復(fù)

RepairbyRegenerationDefinition-RegenerationRegenerationisatypeofrepair.Thebestexampleofhealingbyregenerationinhumansoccursintheliver,whichhasincredibleregenerativeproperties.Itispossibletoresectvirtuallyanentirelobeofliver,andtheorganwillrepairitselfoveraperiodofmonthstocompletelyrecapitulateitspreviousstructure.（1）

不穩(wěn)定細(xì)胞（Labilecells）再生能力最強，如全身的上皮細(xì)胞、淋巴造血細(xì)胞等。（2）

穩(wěn)定細(xì)胞（Stablecells）損傷后，有較強再生能力。如肝、胰、內(nèi)分泌腺等腺上皮，成纖維細(xì)胞、血管內(nèi)皮細(xì)胞、骨細(xì)胞和原始間葉細(xì)胞等，平滑肌細(xì)胞也屬穩(wěn)定細(xì)胞，但再生能力弱。（3）永久性細(xì)胞（Permanentcells）幾乎沒有再生能力，受損傷后由結(jié)締組織增生修補，如神經(jīng)細(xì)胞、心肌細(xì)胞及骨骼肌等。細(xì)胞的再生能力

ClassificationofcellsbytheirproliferativepotentialCellclassificationLabilecells:Thissub-populationofcellsisconstantlyturnedover.Thebestexamplesarefoundintheepithelialcellpopulationoftheskinorgut,andthehematopoeticcellsofthebonemarrow.Thesecellshaveashort,finitelifespan,dieviaapoptosis,andarerapidlyreplaced.CellclassificationStablecells:Stablecellsareasub-populationofcellsthatarenormallyreplacedveryslowly,butarecapableofrapidrenewalaftertissueloss.Hepatocytesandtheproximalconvolutedtubulecellsofthekidneyaregoodexamples.

CellclassificationPermanentcells:Permanentcellsarefoundinthecentralnervoussystemandheart.Oncetheyaredestroyed,theycannotregenerate.Peripheralnervecellsarecapableoflimitedregenerationhasbeendemonstrated,but,forallpracticalpurposes,thoseoftheCNSarepermanentcells.損傷的修復(fù)

WoundHealing-Chickenpox

REGENERATION再生

ATN,regenerative(polyuric)phase.

Hyperplasia增生ChroniculcerativecolitiswithcryptabscessesSquamous

Metaplasia

化生

–UterineCervix

Dysplasia,cervix

不典型增生損傷的纖維性修復(fù)

Repairbyconnectivetissue

WoundHealingRepairGranulationtissueistheinitialresponsetoaninjury,andconsistsofrichlyvascularconnectivetissuewhichcontainscapillaries,youngfibroblasts,andavariableinfiltrateofinflammatorycellsDonotconfusewithGRANULOMA

Definition–FibroplasiaorFibrosisFibrosisisaalsoatypeofrepair.Thebestexampleofhealingbyfibrosisinhumansoccursintheheart,whichcontainspost-mitoticmyocytes.Necrotic(dead)myocytesarealwaysreplacedbycollagenousscarlaiddownbyfibroblasts,sincetheyareincapableofregeneration.

WoundHealingbyFibrosis

InductionofanacuteinflammatoryresponseFormationofnewbloodvessels(angiogenesis)MigrationandproliferationofbothparenchymalandconnectivetissuecellsSynthesisofextracellularmatrixproteinsRemodelingWoundHealing

byFibrosisRepairTheorderlyprocessbywhichawoundiseventuallyreplacedbyascarDestructionofepitheliumonlyistermedanerosion,andhealsexclusivelybyregenerationIfdestructionofthebasementmembraneoccurs(extracellularmatrix),thenascarwillform

Healinginspecifictissues(Skin)Definition-HealingHealingisaresponsetotissueinjury,andrepresentsanattemptbytheorganismtomaintainnormalstructureandfunction.Itoverlapstheinflammatoryprocess.愈合（Woundhealing）：是指組織遭受創(chuàng)傷進(jìn)行再生修復(fù)的過程。

WoundHealingPrimaryintention:theusualcasewithasurgicalwound,inwhichthereisacleanwoundwithwell-apposededges,andminimalclotformationSecondaryintention:whenwoundedgescannotbeapposed,(e.g.,followingwoundinfection),thenthewoundslowlyfillswithgranulationtissuefromthebottomupAlargescarusuallyresultsTissueRepair

PhasesofWoundHealing

FactorsthatinfluencewoundhealingType,size,andlocationofthewound(determinesprimaryorsecondaryintention)Vascularsupply(diabeticshealpoorly)Infection-delayswoundhealingandleadstomoregranulationtissueandscarringMovement-woundsoverjointsdonothealwell,duetotractionRadiation-ionizingradiationisbad,UVisgood

FactorsthatinfluencewoundhealingOverallnutrition:vitaminandproteindeficienciesleadtopoorwoundhealing,especiallyvitaminC,whichisinvolvedincollagensynthesisAge:youngerisdefinitelybetter!Hormones-corticosteroidsimpairwoundhealing,becauseoftheirprofoundeffectoninflammatorycellsComplicationsofWoundHealingDefectivescarformationExcessivescarformation(keloid)ContractionComplicationsofWoundHealingDefectivescarformationDehiscenceorulcerationisusuallydueto:Woundinfection(common)Malnutrition(scurvy-rare)Hypoxiawithulceration,usuallyduetoinadequatevascularityintheskinflap(common)ExcessiveScarFormation

Excessivescarformation(keloid).

Keloids(hypertrophicscars)aretheresultofover-exuberantproductionofscartissue,whichisprimarilycomposedoftypeIIIcollagen.Thecauseisthoughttobeduetogeneticfactors,perhapsduetolackofthepropercollagenasestodegradetypeIIIcollagen.Contraction

Keloid

Keloid(micro)

Contraction

Excessivecontractionofawoundisknownasacontracture.TheyareaspecialprobleminthetreatmentofextensiveburnsSeveraldiseasesofunknowncausearecharacterizedbytheformationofcontracturesPeyroniediseaseofthepenisDupuytrendiseaseofthepalms

Healinginspecifictissues(heart)Cardiacmyocytesarepermanentcells.Theydonotdivide,andtheheartthushealsbyresolution(deadmyocytesarephagocytizedbymacrophages)andcollagenousscarformation.

AcuteMI(gross)

AcuteMI(micro)

RemoteMI(micro)

Healinginspecifictissues(liver)Theliverhealsbyregeneration.Itcanregenerateperhaps75%ofitsvolume.Scarringoccurswhentheextracellularmatrixoftheliverisdamagedbyrepeatedorsevereinjury.Bileductsthenproliferate,regenerativenodulesform,andcollagenousscarsbecomeevident.Thisscarringprocessiscommonlycalledcirrhosis.

Inflammation

ChronicInflammation–Hepatitis

Cirrhosis,trichrome

Healinginspecifictissues(Bone)ChronicInflammation慢性炎癥

Inflammation

ChronicInflammationChronicinflammationmayoccurasasequeltoacuteinflammation,orasaprimaryimmuneresponsetoaforeignantigen(usuallyviral)Typeofchronicinflammationincludes:general,granulomatousinflammation,InflammatorypolypandpseudotumorACUTECHRONICVascularchangesCellularinfiltratesStromal

changesVasodilationandIncreasedpermeabilityPolymorphsNoreplicationMinimal-separationduetoedemaMinimalMononuclearReplicationCellularproliferationFibrosisInflammation

CharacteristicsofacuteandchronicinflammationInflammation

慢性炎癥(ChronicInflammation)病變特點

Histologicfeatures慢性炎細(xì)胞浸潤和組織細(xì)胞增生Mononuclearcells–macrophages,lymphocytes,andplasmacells.組織結(jié)構(gòu)破壞和瘢痕修復(fù)

Tissuedestructionbyongoinginflammation,thoughttobeduetocytokinesproducedlocallybythemononuclearcells.上皮細(xì)胞增生、化生和不典型增生

hyperplasia,metaplasiaandanaplasiaofparrenchymalcells.Inflammation

ChronicInflammationMonocyte/MacrophagesKeycellinchronicandgranulomatousinflammationReproducelocally,atthesiteofinjuryProducenumerouscytokines,whichcontinuetorecruitadditionalcells,includingmoremacrophagesMaypresentantigentoT-cells,producingspecifichypersensitivityreactions

ChronicInflammatoryInfiltrate

Inflammation

GranulomatousInflammationAcellularmechanismfordealingwithindigestiblesubstancesTheprincipalcellsinvolvedingranulomatousinflammationaremacrophagesandlymphocytesEpithelioid

histiocytesarethehallmarkofgranulomatousinflammation

Inflammation

GranulomatousInflammationImmunitymaybejudgedbyitseffectontheinvadingorganism,butanadverseeffectonthehostisgenerallytermedhypersensitivityDestructionoftissueisprimaryviatheactionofkillerTcells,directedbymacrophagesTheoldtermfortuberculosiswasconsumption,forgoodreason

GranulomatousInflammation

Langhanstypegiantcells

MultinucleatedGiantCells

Epithelioidcells

Inflammation

GranulomatousInflammationTuberculouslungInflammation

GranulomatousInflammationTuberculous

GranulomaInflammation

GranulomatousInflammationForeignbodygiantcellsinsuturegranulomaInflammation

GranulomatousInflammationCaseating

GranulomaNon-caseating

GranulomaCaseousNecrosisMacrophages,Epithelioid

Cells,andGiantCellsLymphocytesFibroblastsSarcoidosisInflammatoryPolypInflammatory