病理学十 结核(中英文)

Tuberculosis（结核）

IntroductionAchronicinfectiousdiseaseMycobacteriumTuberculosis☆PulmonaryTBisthemostcommontype.involveallorgans(rareinthyroid,pancreasandmyocardium)Characteristicchanges:

tuberculousgranuloma+caseousnecrosisEpidemiologyHistory☆Worldwide

1.7billioninfected8-10millionnewcases3milliondeathsChina0.55billioninfected0.13milliondeathsPredisposingfactorssocialfactors:poverty,crowding,agingchronicdebilitatingdisease:diabetesmellitus,hodgkindisease,pulmonarysilicosis,alcoholism,etalimmunitydeficiency:HIV

EtiologyRobertKoch24th,MarchPathogenspecies:

M.hominis(人型）M.bovine(牛型）M.avium(鸟型）M.piscium(鱼型)M.murium(鼠型)

humanHIVinfectedhostPathogenicity

Lipid:

mycolicacid（分枝菌酸）cordfactor（索状因子）WaxD（蜡质D）

phospholipid（磷脂）

mycosides（分枝菌糖苷脂）

Protein：结核菌素GlycogenEtiologytransmissionRespiratorytract(pulmonaryT.B):inhaletheairborneorganismsexposetocontaminatedsecretionsDigestivetract(intestinalT.B):

drinkinginfectedmilkSkininjury:

CongenitalBCG:nonpathogenic,livingT.B,undergoing230passages,13yrs）

mother placentafetusPathogenesis

infection≠disease★Onlyasmallfractionofthosewhocontractaninfectiondevelopactivedisease.

PathogenesisKochphenomenon:cellmediatedimmunity(CMI)accompaniedwithdelayedtissuehypersensitivity(DTH)PPDtestPPDtest

false-negativefalse-positivePathogenesisCMIandDTHaredifferentimmunoreactionsDifferentantigensDifferentTcellsubtypesTheamountoforganismsorantigenandTh1/Th2excursionDifferentCKsDifferentmethodstokillorganismsPathologicalchangesExudationdominantchanges:happenedinearlystageofinfectionordeteriorationofDis.

Predisposingfactors:suppressedimmunity,plentyofmycobacteriumT.BhighvirulenceandstrongDTHchanges:serousinflammation,serous-fibrinousinflammationlocation:pleura,meninges,peritoneumPathologicalchangesExudationdominantchanges:

development:unstableabsorbedwithoutanychangeschangeintoproliferationdominantornecrosisdominantchangeseasytofindorganismsProliferationdominantchange(Tubercleformation,granuloma)

Predisposingconditions:strongimmunityfewmycobacteriumlowvirulence

PathologicalchangesProliferationdominantchange(Tubercleformation,granuloma)

Changes:EpithelioidcellsLanghan’sgiantcellsLymphocytesdifficulttofindorganismsPathologicalchangesNecrosisdominantchangePredisposingfactors:weakenedimmunity,severehypersensitivitylargeamountofmycobacteriumT.B.highvirulenceChanges:caseousnecrosis（干酪样坏死)Gross:granular,cheesyappearance(richinlipid)LM:acidophiliagranularmaterialswithoutstructure

PathologicalchangesNecrosisdominantchangeeasytofindorganismsDevelopment:

Existforlong→timingbombTheamountofmycobacteriumwillincreasesharplywhenthediseasedeteriorateFibrosisPathologicalchangesPathologicalchangesexudationchangesgranulomalesioncaseousnecrosisConsequenceHealing

exudativelesion:absorptionproliferativelesion:fibrosisnoorganismsnecroticlesion:fibrosisandcalcification(calcificationfocimayharborviablebacilliforyears)Deterioration1.lesionenlarges,thediseaseprogressesgranuloma→exudationchangeexudation→caseousnecrosiscaseousnecrosisfocienlarge(infiltrativeprogressivestage)ConsequenceDeterioration2.CavitationandDisseminationcaseousmaterialsliquefynaturecanalcavitiesformationinoriginalsitesmycobacteriumdisseminatetomultiplesitesopenT.B

lymphaticcanal

bloodvessel

(disseminatedstage)ConsequencePulmonaryTuberculosis

PrimarypulmonaryT.B.SecondarypulmonaryT.B.PreviouslyunexposedMostinchildren,agedorimmunosuppressdpersons(HIV)ExogenousorganismPathologicalchange:GhonComplex（原发复合征)1-1.5-cmareaofgray-whiteinflammatoryconsolidation(lowerpartofupperlobeorupperpartoflowerlobe)TuberculouslymphatitisRegionalnodeinvolvement,oftenwithcaseatePrimaryPulmonaryTuberculosisGhonComplexChiefimplications:1.Itinduceshypersensitivityandincreasedresistance95%control2.ThefociofscarringmayharborviablebacilliforyearsnidusforreactivationPrimaryPulmonaryTuberculosisPrimaryPulmonaryTuberculosisDeteriorationandDissemination

B.

lymphaticsbronchial,trachealLN、

subclavical

LN、

mediastinal

LNretroperitoneal

LNC.bronchialspreading:uncommoninchildren.

A.bloodcirculation.acutemiliaryT.B.

subacuteorchronicmiliaryT.B.secondaryorextrapulmonaryT.B.(liedown)AcuteMiliaryT.B.SecondaryPulmonaryT.B.PreviouslyinfectedAdulttypePathogenesis<5%exogenous>95%endogenousseedingSomespecialpoints1.Location:apexoflobelowarterialbloodpressure,lessMΦ,lessventilation,highO2pressure2.Changes:caseousnecrosis---proliferationfocuslocalizationlesslymphaticandvascularspreadingmorebronchialdissemination3.Longcourseofdisease,complexchangesPathologicalchangesFocallesion:(局灶型）1.location:2~4cmbeneathapexoflobe2.pathologicalchanges:lessthan2cmindiametersingleormultiplefocusesproliferationdominant

caseousnecrosisincentralandaroundfibrosis3.development:healingbyfibrosisorcalcificationfewbecomeinfiltrativelesionPathologicalchangesInfiltrativelesion（浸润型）:1.source:focallesion2.location:apexorsubclavicalarea(subclavicularinfiltration)3.morphology:exudationdominant,caseousnecrosisincentral4.clinicalsymptoms

PathologicalchangesInfiltrativelesion（浸润型）:5.development:healingbyabsorb,fibrosis，calcificationdiseaseprogresses,acutecavitationmayoccur

caseouspneumoniaspontaneouspneumothorax

tuberculous

pyopneumothoraxchronicfibro-cavitativetypeChronicfibro-cavitativelesion(慢性纤维空洞型)1.source:infiltrativetypewithacutecavity2.Characters:☆singleormultiplechroniccavitiesthreelayers----inner:caseousnecroticmaterialsmid:tuberculousgranulationtissueouter:fibrousscar☆diversefoci☆fibrosis(cirrhoticpulmonarytuberculosis)PathologicalchangesChronicfibro-cavitativelesion(慢性纤维空洞型)

3.clinicalsymptoms

openT.B.(mycobacteriuminsputum)

emptysis,laryngealT.B.,IntestinalT.B.,cor

pulmonale

4.developmenthealing:smallcavity→scarhealinglargecavity→openhealingPathologicalchangesCaseousPneumonia(干酪样肺炎）

1.source:infiltrativelesionbronchialspreadingofacuteorchroniccavity2.modality:lobularorlobarcaseouspneumoniaacutecavity(localliquefaction).LM:caseousnecrosiswithserous-fibrinous

exudate3.Poorprognosis(百日痨or奔马痨)PathologicalchangesTuberculoma（结核球)1.source:fibrosisofcaseousnecrosisininfiltrativetypebronchiaclosureleadstocaseousmaterialsfillinthecavitycombinationofseveraltubercular2.pathologicalchanges:

gnosis:stabledeteriorationPathologicalchangesTuberculouspleuritis:wetanddrywettype----Exudativepleuritis：MostinyoungpeopleSource:mycobacteriadisseminationfromprimaryfocusorhilarlymphnodsDTHinducedbyproteinofmycobacteriainpleuraPathologicalchanges:serous-fibrinousinflammationClinicalsymptomsPrognosis:1.absorb2.richinfibrinmaycauseadhesionofpleuraPathologicalchangesdrytype----proliferativepleuritis：T.B.focusbeneathpleuraextendtopleuraMostinapexoflobe,localpleuraadhesionandthickeningCaseous

pleuritisrare

PathologicalchangesSecondaryPulmonaryT.B.Systemicsymptoms

responsetoT.B.“toxic”components

Localmanifestations:

coughhemoptysischestpainlowerrespiratoryfunctionCPCmalaise,weary,nightsweat,lowfeverintheafternoon,hecticrosycheeks,lossofappetiteHematogenictuberculosisResultfromPrimarytuberculosisorSecondarytuberculosissystemicmilitarytuberculosispulmonarymilitarytuberculosis

acutemilitarytuberculosissubacute/chronictuberculosisPrimaryPT.BSecondaryPT.B

InfectionpreviouslyuninfectedpreviouslyinfectedPatientchildrenadultsSpecialCMIandDTHoccurinthecoursepreexistPathologicalchangesGhoncomplexvariouschanges,localized,cavityOriginalfocuslowerpartofupperlobeapexoflobeupperpartoflowerlobeDominantchangesexudation,necrosisproliferation,necrosisDisseminationlymphaticandvascularbronchialCourseofdiseaseshort,self-controllong,fluctuant,clinicaltreatmentComparisonExtrapulmonaryTuberculosisInvolveallorgansReactivationoflatentfociPathologicalchangesandcharacteroforgansarecorrelativeIntestinalTuberculosisSourceofMycobacterium

primary:drinkinginfectedmilksecondary:

swollenmycobacteriumcontainedsputumLocation:

anysegmentofintestinemostcommonatileocecalsegment:1.richinlymphtissue,easytoinvade2.longtimeforfoodtostayinthissegmentUlcerativeintestinalT.B.

TuberclesinlymphtissuefusednecrosisulcerationFeaturesofulcer:

1.longaxisoftheulcerisverticaltolongaxisofintestine,becauseofthecircularlymphaticsofintestine

2.irregularmarginoftheulcer(rat-bite-like),

caseousbaseandtuberculargranulationtissuebeneath,fibrinexudateandmiliarytuberclesinserosaIntestinalTuberculosisUlcerativeintestinalT.B.3.IntestinalstraitnessafterulcerhealingFibrosisleadstoaadhesionamongserosaandadjacenttissuesHemorrhageandperforationareuncommonClinicalsymptoms:

chronicabdominalpain,intermittentdiarrheaandconstipation,tubuculartoxicsymptomsIntestinalUlcerativeT.B.ProliferativeintestinalT.B.

proliferativechangesdominant,causingthickeningofintestine,polyposis,leadingtoabdominalmassand/orileus※※※※※※※※IntestinalT.B.MesenteryT.B.Tuberculousperitonitis

wettypeperitonealtuberclegreenishyelloworhematicascites

drytypeperitonealtubercle,fibrinexudationextensiveadhesionandrubber-likeconsistencyofabdomenIntestinalTuberculosisTubercularMeningitisSourceofinfection:systemicdisseminationviabloodcerebralT.B.spreadtomeningesChanges:exudationdominantchangeTheexudationconsistsofserum,fibrin,lymphocytesandMΦgelatinousappearancecerebralinfarctionorsofteningOrganizationofexudateadhesiondisturbanceofCSFcirculationhydrocephalusRenalTuberculosisSourceofinfection:

systemicdisseminationviabloodChanges:

beginsfromtheborderofcortex&medull