中国医科大学病理学英文.ppt

2.Mediatorsfromplasma,ComplementS+kininS+ClottingS,1)kininsystem:releaseofthevasoactivenonapeptidebradykinin,IncreasesvascularpermeabilityCausescontractionofSMexceptBVSMVasodilationPain,2)ComplementSystem:,(1)Consistsof20componentproteintogetherwiththeircleavageproducts:presentasinactiveforms(C1C9)(2)Functions:Increasevasopermeability(C3a,C5a)Causevasodilation(C3a,C5a)Chemotaxist(C5a)Opsonization(C3b),C3a,5aincreasevascularpermeabilitycausevasodilationbyreleasinghistaminefrommastcellsC5aApowerfulchemotacticagentforneutrophilsbasophils,eosinophils,monocytesActivatesthelipoxygenasepathwayofAAmetabolisminmonocytes,neutrophilsreleaseofmediators,3)Clottingandfibrinolyticsystem,Activatedclottingsystem:i)Thrombinandfibrinopeptide:ThrombinpromotesleukocyteadhesionfibroblastproliferationFibrinopeptideincreasedVpermeabilitychemotacticactivityforleukocytes,ii)FactorXaincreasedVpermeabilityleukocyteexudationActivatedfibrinolyticsystemC3C3aincreasevpermeabilityvasodilationFibrintofibrinproducts:increasevpermeability,Sourcesofmediators,3.Summaryofinflammatorymediators,FunctionMajormediatorsVasodilationhistamine,bradykinin,PGI2,PGE2,NOPermeabilityhistamine,bradykinin,LTB4,C3a,C5a,PAFChemotaxisLTB4,C5a,cytokins,cationicproteinFeverIL-1,IL-2,TNFa,PGE2PainPGE2,bradykininTissuedamageoxyradical,Lysosomalenzymes,NO,V.Typesandmorphologyofacuteinflammation,AlterativeinflammationDegradation,necrosisAcuteseverehepatitis,encephalitisb,toxicmyocarditisExudativeinflammationSerousFibrinousPurulentHemorrhagicProliferousinflammationChronicinflammation,Serousinflammation1.CommonsiteslooseCT,serosamucosaandskin2.Lesions:Serousexudationbloodserum(main)secretionofmesothelialCLMalbumin:35%fibrin,neutrophils,epithelialcell,3.Commoncauses:,Rheumatism,TBinvolveserosaBurn,coldcatarrh4.Consequence:absorptionHarmfulseveredemainthroatstiflethoraciccavitypericardialcavity,dysfunction,Serousinflammationofskin,Serousinflammation.Low-powerviewofacross-sectionofaskinblistershowingtheepidermisseparatedfromthedermisbyafocalcollectionofserouseffusion.,Theskinblisterresultingfromaburnorviralinfectionrepresentsalargeaccumulationofserousfluid,eitherwithinorimmediatelybeneaththeepidermisoftheskin,Fibrinousinflammation,1.Lesions:ExudateswithalargeamountoffibrineosinophilicmeshworkofthreadsoramorphouscoagulumNecroticdebrisneutrophils2.Causesbacterial,virusinfectionintoxication:urea,mercury,3.Favorsitesandfeatures,(1)Mucosafibrinousinflammation:SitesupperrespiratorytractgastrointestinaltractFeature:pseudomembranousinflammationFibrin+necrotictissue+neutrophilsgray-white,membrane-shapedCommon:bacillarydysentery,diphtheria,Diphtheriaoftrachea,LarynxandTreacheaallrevealaroughcongestedmucosacoveredbyalayerofpseudomembrane.Adheretightlyonlaryngealregions,whilelooselyconnectedwiththesubmucosaoftrachea.,Mucosaofcoloniscoveredbyexudates.Bran-likesubstancessurfacethemucosalfoldsMucosaappearsthickenedduetoedemaConstitutesofthemixtureoffibrin,mucus,injuredtissue,neutrophils,RBCs,bacilli.,(2)Serosafibrinousinflammation:,Sites:pleura,pericardiumFeature:fibrinouspericarditiscorvillosumHairyheart,epicardiumiscoveredwithfibrinousexudateandformaheavyshaggycoatwithadhesionbetweenthelayersofthepericardium,Fibrinouspericarditis.Pericardialcavityhasbeenopenedtorevealafibriouspericarditiswithstrandsofstringypalefibrinbetweenviseralandparietalpericardium.Depositsoffibrinonthepericardium.Finevilloseformheavyshaggycoatonthsurface.,Fibrinouspericarditis,Apinkmeshworkoffibrinexudateoverliesthepericardialsurface.,(3)Lung:lobarpneumonia,thealveolarcapillariesappearcompressedalveolarspaces:progressivedisintegrationofneutrophilsalongwiththecontinuedaccumulationoffibrin,4.ConsequencesResolutionandabsorptionOrganization:lungcarnificationheartconstrictivepericarditisTheprocessofresolutionmayrestorenormaltissuestructure,butwhenthefibrinisnotremoved,itmaystimulatetheingrowthoffibroblastsandbloodvesselsandthusleadtoscarring.Conversionofthefibrinousexudatetoscartissue(organization),Suppurativeorpurulentinflammation,1.Concept:productionoflargeamountsofpusorpurulentexudateconsistingofneutrophilsnecrosiscellsandedemafluid.Pus,apurulentexudate,isaninflammatoryexudaterichinleukocytes(mostlyneutrophils),thedebrisofdeadcellsand,inmanycases,microbes.2.Causes:Staphylococcus,streptococcus,3.Types:,(1)SurfacepurulenceandempyemaConcept:purulentinflammationoccurringinmucosaandserosaFeatures:surfacepurulence:superficalinfiltrationofneutrophil(purulentcatarrh)empyema:pusdepositinthecavities(gallbladder,appendix),Purulentmeningitis,Athicklayerofsuppurativeexudatecoversthesurfaceofthebrainandthickenstheleptomeninges.Themeningealvesselsareengorgedandstandoutprominently.,Purulentmeningitis,Inflammatoryexudatesinthewidensubarachnoidspace.Composedofplentyofnutrophils,puscells,afewmonocyteandfibrin.BVareengorgedextensively.,(2)Phlegmonousinflammation,Concept:diffusepurulentinflammationoccurringinlooseconnectivetissuePathogen:hemolyticstreptococcusSites:skin,muscles,appendixLesionfeature:neutrophilsdiffuseinfiltration,Phlegmonousappendicitis,Appendixisswollen,withyellow-whitetotanexudatesandhyperemia,ratherthanasmooth,glisteringpaletanserosasuface.,Phlegmonousappendicitis,Mucosashowsulcerationandunderminingbyanextensiveneutrophilexudate.Thewallisthickenedbycongestionarereplacedbymonocytein2448hsii)Chronic:LC,PC,monocyteChemotacticfactors:C3a,PDGF,FibronectinFunctionsPhagocytosisTissuedamageFibrosis,Therolesofactivatedmacrophagesinchronicinflammation.Macrophagesareactivatedbycytokinesorbynonimmunologicstimuli.Theproductsmadebyactivatedmacrophagesthatcausetissueinjuryandfibrosisareindicated.,(2)Lymphocyte:,Chemotacticfactors:I(V)CAM,lymphotactinFunctions:Producelymphokines(IFN-)(3)Mastcell:DistributedinCTFunctionsproducecytokinescontributetofibrosisanaphylacticreactiontodrugs(4)Eosinophils:parasiteinfection,3)Somecharacteristicchanges:,(1)Inflammatorypolyp:Concept:underthestimulationofinflammatoryagentslocalmucosalepithelium,glands,GTproliferateformprotrudentmassCommonsitesnasalpolypcervicalpolypintestinalpolyp,Smoothmassoftissue(polyp)withstalksprotrudesoutwardsfromthesurfaceofintestinemucosa,Mucosalepithelium,gland&granulationproliferate,andtherearelymphocyte&plasmacellinfiltration,Nasalpolyp,(2)Inflammatorypseudotumor:,Concept:aclearedge,tumor-likemassformedbytissueinflammatoryproliferationoftenoccurineyesandlung.Lesions:Ineyes:largeamountsofLCproliferationInlung:GT,proliferativealveolarepi,MfoamC,infiltrativeLC,PC,2.ChronicspecificinflammationGranulomatousinflammation,1)Granulomatousinflammation:adistinctivechronicinflammationcharacterizedbyformationofgranuloma.Granuloma:ininflammatoryfocimacrophagesproliferateformclearnodularfocus.,2)Types,(1)Infectious(immune)granuloma:Concept:causedbyinsolubleparticlesthatarecapableofinducingacell-mediatedimmunereaction.Formation:MengulfinsolubleparticlespresentsomeofittoTCcytokines(IL-2,IFN-r)transformingMintoepithelioidCandmultinucleategiantC,Thecommondiseases:TB,leprosy,rheumatismtyphoidfever,syphilisForexample:TuberculosisCentral:caseousnecrosisPeripheryEpithelioidcellsLanghansgiantcellsLC,fibroblast,Tubercle,Tubercle,Thegranulomaisreferredtoasatubercle.centralcaseousnecrosisappearsaspink,amorphousgranlardebris,lossofallcellulardetail.,Theepitheliodcellshavepalepinkgranularcytoplasmwithdistinctcellboundaries,Nucleilongandstringy.EpitheliodcellsfusetoformLGCcontain10ormorenucleiarrangedperipherally,(2)Foreignbodygranuloma,Causes:foreignbody(talc,suture)LesionsForeignbodyEpithelioidcellForeignbodygiantcell,Foreignbodygranuloma,Foreignbodygaintcellsareseenwherethereischolesterolcrystal,thereralsoMC,fibroblasts.,Section4.Localmanifestationandgeneralreactions,I.Localmanifestation1.Redness:BVdilatinghyperemia(rubor)2.Swelling:congestion,edema,exudationchronicinflammationproliferation(tumor)3.Heat:hyperemiametabolismproducingheat(calor)4.PainswellingNendingpressedinflammatorymediator(dolor)5.Lossoffunctionreleasetoxicmetabolitesandproteases,II.Generalreactions,1.FeverExogenousF:toxin,virus,Ag-AbcomplexEndogenousF:cytokinesIL-1,TNFPGbeneficialandharmful2.Leukocytosis:Acutepurulentinfla:neutrophilsChronicorvirusinfection:LCAllergicdiseaseorparasite:eosinophilsleft-shift,SLEtyphoidfevervirusinfection,3.OthersMproliferation(liver,spleen,LN)lesionsofmesenchymalcells,Section5.Outcomesofacuteinflammation,1)ResolutionCompleteresolution:Smallarea:absorptionmorphologyandfunctionrecoveryIncompleteresolution:Largearea:GTfibrosisscar2)Progressionoftissueresponsetochronicacutechronic(prolongedduration),3)Extension