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中国医科大学病理学英文课件6中国医科大学病理学英文课件61Section1.Introduction
1.Definition:
1)Inflammation:adefensivereactioninlivingtissuewithvascularsystemtoinjuriousstimuli.2)ReactionofBVsisthecentrallinklimitingandkillinginjuredfactoreliminatingandabsorbingnecrotictissue3)TheinflammatoryresponsesiscloselyintertwinedwiththeprocessofrepairSection1.Introduction
1.D2最新病理学英文课件63最新病理学英文课件64最新病理学英文课件65最新病理学英文课件66最新病理学英文课件67最新病理学英文课件68Section2.AcuteinflammationTwomajormechanismsofhostdefense:AntibodyLeukocytesmajorcomponents:1)Changesofhemodynamics
2)Fluidexudation3)LeukocyteextravasationandphagocytosisagainstmicrobesSection2.AcuteinflammationT9最新病理学英文课件610I.Changesofhemodynamics1.Alterationinvascularflowandcaliber
1)Transientvasoconstrictionofarterioles:lastingforafewseconds.2)Vasodilationandincreasedbloodflow(1)ArteriolardilationopeningofnewcapbedsincreasedbloodflowinflammatoryhyperemiaI.Changesofhemodynamics1.A11(2)Relatedtothefactorsof:Bodyfluid:chemicalmediatorNervous:axonreflection3)Slowingofbloodflow:increasedpermeabilityofthemicrovasculatureoutpouringoffluidintoextracellulartissuesconcentrationofRBCandincreasedviscosityofbloodstasisofbloodflow(2)Relatedtothefactorso12NormalbloodflowVasodilationincreasedbloodflowSlowingofbloodflowStasisofbloodflowExtravasation(fluidandleukocyte)NormalbloodflowVasodila132.IncreasedvascularpermeabilityIncreasedpermeability→themostimportantcauseresultinginexudationoffluidandprotein
MechanismofIncreasedpermeability1)ECretraction
FormationofendothelialgapsinvenulesImmediatetransientresponse:occursrapidlyafterexposuretothemediatorandisusuallyreversibleandshort-lived(15to30minutes)mostcommonmechanismofvascularleakageandiselicitedby:histamine,bradykinin,substanceP,leukotriene2.Increasedvascularpermeabi142)CytoskeletalreorganizationDelayedprolongedresponseinducedbycytokines(IL-1,TNF,IFN-γ),increasedpermeabilityafteradelayof4to6hourslastingformorethan24hoursinvolvesvenulesaswellascap.theendothelialcellsretractfromoneanother3)IncreasedtranscytosisacrosstheendothelialcytoplasmBytranscytoplasmicchannelVEGF,histamine,bradykinin,Increasingthenumberandthesizeofchannels2)Cytoskeletalreorganization154)DirectendothelialinjuryImmediatesustainedresponse:
severeburn,purulentBacteriaresultinECnecrosisanddetachmentleakagestartsimmediatelyafterinjurysustainedatahighlevelforseveralhoursuntildamagedBVthrombosedandrepaired4)Directendothelialinjury165)Leukocyte-mediatedendothelialinjuryMild-to-moderatethermalinjury,toxin,x-radiatonincreasedleucocyteinfiltration
involvesvenulesaswellascap.LeukocyteadheretoECactivatedReleasingtoxicspeciesandproteolyticenzymes5)Leukocyte-mediatedendothel176)Highpermeabilityofnewcapsduringrepair,endothelialcellsproliferateandformnewbloodvessels①NewvesselssproutsremainleakyuntilECsdifferentiateandformintercellularjunctions.②Certainfactorsthatcauseangiogenesis(VEGF)increasepermeability③Increaseddensityofreceptorforvasoactive
mediatorsinthesurfaceofEC6)Highpermeabilityofnewca18DiagrammaticrepresentationoffivemechanismsofincreasedvascularpermeabilityininflammationDiagrammaticrepresentationof19II.Fluidexudation1)Majorcauses:①Increasedvascularpermeability→escapeofaprotein-richfluidintotheinterstitium②Thelossofprotein
reducesintravascularcolloidosmoticpressureincreasesthecolloidosmoticpressureoftheinterstitialfluidII.Fluidexudation1)Majorc20Bloodpressureandplamacolloidosmoticforcesinnormalandinflammedmicrocirculation.Bloodpressureandplamacollo21exudation:Theescapeoffluid,proteins,andbloodcellsfromthevascularsystemintotheinterstitialtissueorbodycavities.
Exudate:aninflammatoryextravascularfluidthathasahighproteinconcentration,cellulardebris,andahighergravity.Itimpliessignificantalterationinthenormalpermeabilityofsmallbloodvesselsintheareaofinjury.Transudate:afluidwithlowproteincontent(mostofwhichisalbumin)andalowergravity.Itisessentiallyanultrafiltrateofbloodplasmathatresultsfromosmoticorhydrostaticimbalanceacrossthevesselwall.exudation:Theescapeoffluid222)Distinguishbetweenexudateandtransudate
TransudateExudateVascularpermeabilityNormalIncreasedProteinconcentration<30g/L>30g/LProteintypeAlbuminKindsofproteinRivaltatestNegative(-)Positive(+)FibrinNoHaveSpecificgravity<1.018>1.018Cellnumber<300×106/L>1000×106/LAutoagglutinationNoYesAppearanceClear
Cloudy2)Distinguishbetweenexudate233)Functionsofexudate:(1)Dilutelocaltoxins→reducetheinjurytotissue(2)Bringinthenutritionalsubstanceforleukocytescarryoffthemetabolicproductsininflafoci(3)killthepathogen:Ab,complement(4)Fibrinmesh:limitthespreadingofpathogenicorganismslimittheremovingofMφ3)Functionsofexudate:(1)Di24III.Leukocyteextravasation
andphagocytosis1)Leukocyteextravasation:leukocytepassthroughvascularwallintothesiteofinjury.
Dividedintofollowingsteps:
MarginationandrollingAdhesionTransmigrationandchemotaxisIII.Leukocyteextravasation
25
(1)Marginationandrolling
leukocyteincentralaxialcolumnBVdilation,speedofbloodflow↓marginationrollingpavementingappearance(1)Marginationandroll26Leukocyticemigration
Leukocyticemigration27(2)Adhesion:a.Bybindingofcomplementaryadhesionmoleculesontheleukocyteandendothelialsurfacesb.Adhesionmolecules:
Theimmunoglobulinfamily:I(V)CAM-1Integrinsselectins(2)Adhesion:a.Bybindingof28c.Mechanismsofadhesiveprocess:i)Redistributionofadhesionmoleculestothecellsurface:
Forexample:P-selectin
NormallypresentinW-PbodyofECHistaminethrombin,PAFRedistributedtothecellsurfaceBindingtothereceptorofleukocytec.Mechanismsofadhesiveproc29ii)InductionofadhesionmoleculessynthesisSomeinflammatorymediators,(IL-1,TNF)inducedthesynthesisandsurfaceexpressionofendothelialadhesionmoleculesForexample:InnormalECNoexpressionofE-selectinIL-1TNFSynthesisandexpressE-selectinii)Inductionofadhesionmole30iii)IncreasedavidityofbindingForexample:
LFA-1
Presentonneutrophils,monocyte,LCNotadheretoitsligandICAM-1onECowingtoleukocyteactivationLFA-1convertedfromastateoflow-affinitybindingtohighaffinitybinding
towardICAM-1iii)Increasedavidityofbind31Regulationofendothelialandleukocyteadhesionmolecules.A,RedistributionofP-selectin.B,Cytokineactivationofendothelium.C,IncreasedbindingavidityofintegrinsRegulationofendothelialand32(3)Transmigrationandchemotaxis①Injuredvenulesorcaps,leukocytesinsertpseudopodsintojunctionbetweenECssqueezethroughinterendothelialjunctionssecretecollagenase→decomposetheBMescapeintointerstitialtissue(3)Transmigrationandchemota33pseudopodpseudopod34AdhensionandtransmigrationAdhensionandtransmigration35最新病理学英文课件636②Redcelldiapedesis:
apassiveprocess,determineinjuredextent③Thetypeofleukocytevarieswiththeageofinflammatorylesion:i)Acute:neutrophilspredominateduringthefirst6~24hs;arereplacedby
monocytein24~48hsii)Chronic:
LC,PC,monocyteLCPCNeutrophilsMC②Redcelldiapedesis:LCPCNeu37Basophil12-15μmEosinophil12-15μmNeutrophil12-15μmMonocyte14-20μmLmphocyte6-8μmRBC7.5μmBasophilEosinophilNeutroph38最新病理学英文课件639④Thetypeofemigratingleukocytevarieswiththetypesofstimulus:i)Viralinfection:LC→firstCtoarriveii)HypersensitivityreactionParasiteinfectioniii)Bacterialinfection:neutrophilsEosinophils④Thetypeofemigratingleuko40⑤Chemotaxis:afterextravasationleukocytesemigratetowardthechemicalmediatorsalongachemicalconcentrationgradient.
Chemotacticagent:
Exogenous:bacterialproductsEndogenous:complements(C5a)leukotrieneB4(LTB4)cytokines:chemokine⑤Chemotaxis:afterextravasat41ChemotaxisChemotaxis42(4)Therolesofleukocytes
Acriticalfunctionofinflammationistodeliverleukocytestothesiteofinjuryandtoactivatetheleukocytestoperformtheirnormalfunctionsinhostdefense.
Phagocytosis(ingestoffendingagents)Immunologicalfunction(killbacteriaandothermicrobes,andgetridofnecrotictissueandforeignsubstances)Leukocyte–inducedtissueinjury(4)Therolesofleukocytes
A43Phagocytosis:Leukocyteemigratetoinflammatoryfocusengulfandkillordegradatethepathogenicorganismandtissuedebris.Phagocytosis:44a.Typesofphagocytes①Neutrophils:10~12umi)Azurophilicgranules:NeutralproteinaseandacidichydrolaseDigestanddegradatedebris,deadbacteriaMyeloperoxidase,phospholipaseA2,lysozyme,andcationprotein→killthebacteriaa.Typesofphagocytes①Neutro45ii)Specificgranules:Lysozyme,lactoferrin,Alkaliphosphatase,phospholipaseA2②Macrophage:12~24umi)SitedistributedinCT,liver(kupfferC)spleen,LN,lunginflammatoryfocus:derivedfrombloodmonocytekillbacteriaii)Specificgranules:Lysozyme46ii)Functions:
Phagocytosis→eliminatethedeadbacteria,cells,debris,foreignbodiesthatcan’tbedigested
ii)Functions:P47b.Processofphagocytosis:Involvesthreesteps:
RecognitionandattachmentEngulfmentkillingordegradationb.Processofphagocytosis:48①Recognitionandattachment:i)Opsonins:akindofproteininserumwhichenhancestheefficiencyofphagocytosisii)Opsonization:microorganismcontactwiththeserumcontainedopsoninsandarecoatediii)MajoropsoninsFcfragmentofIgGC3b
collectins①Recognitionandattachment:i49②EngulfmentBindingofopsonizedparticletotheFcreceptorofphagocyticleukocytePseudopodstocreateadeeppocketcompleteenclosureoftheparticlewithinaphagosomecreatedbytheplasmamembraneofthecellThelimitingmembraneofthisphagocyticvacuolethenfuseswiththelimitingmembraneofalysosomalgranuleresultingindischargeofthegranule'scontentsintothephagolysosome.②EngulfmentBindingofo50ProcessofphagocytosisOpsonizationattachmentEngulfmentPhagosomephagolysosomePhagocytosisofaparticle(e.g.,bacterium)involvesattachmentandbindingofFcandC3btoreceptorsontheleukocytemembrane,engulfment,andfusionoflysosomeswithphagocyticvacuoles,followedbydestructionofingestedparticleswithinthephagolysosomes.ProcessofphagocytosisOpsoniz51③killingordegradation:i)Phagolysosome→releasemanyenzymesii)Killingisaccomplishedlargelybyoxygen-dependentmechanism③killingordegradation:52ThegenerationofreactiveoxygenintermediatesisduetotherapidactivationofNADPHoxidase,whichoxidizesNADPHand,intheprocess,reducesoxygentosuperoxideanion.Superoxideisthenconvertedintohydrogenperoxide(H2O2).TheH2O2generatedbytheNADPHoxidasesystemisgenerallynotabletoefficientlykillmicrobesbyitself.Theazurophilicgranulesofneutrophilscontaintheenzymemyeloperoxidase(MPO),which,inthepresenceofahalidesuchasCl-,convertsH2O2tohypochlorite(HOCl).TheH2O2-MPO-halidesystemisthemostefficientbactericidalsysteminneutrophils.Thegenerationofreactiveoxy53Oxygen-dependentmechanismOxygen-dependentmechanism54Oxygen-dependentmechanismProductionofmicrobicidalreactiveoxygenintermediateswithinphagocyticvesicles.Oxygen-dependentmechanismProd55iii)Oxygen-independentmechanismA.BactericidalpermeabilityincreasingproteinphospholipaseactivationphospholipiddegradationB.Lysozyme:hydrolyzesthecoatofBacteriaC.Cationicprotein(eosinophils):limitedbac.activitycytotoxictomanyparasites.iii)Oxygen-independentmechan56Immunologicalfunction:Bcell→PC→AbTcell→lymphokineNKC:dissolvecellinfectedbyvirusLeukocyte–inducedtissueinjury:Duringleukocyteactivation,phagocytosis,
lysosomalenzymesoxygen-derivedactivemetabolitesmediators(leukotriene,prostaglandin)→celltissueinjuryImmunologicalfunction:57(5)Defectinleukocytefunction(1)Acquired:AIDS
ThdestroyedandMφdysfunction(2)OthersDefectin
:leukocyteadhesion:recurrentbacterialinfectionsandimpairedwoundhealingphagolysosomefunction:neutropenia(decreasednumbersofneutrophils),defectivedegranulation,anddelayedmicrobialkilling
bonemarrowsuppression:leadingtoreducedproductionofleukocytesSevereinfection(5)Defectinleukocytefuncti58IV.InflammatorymediatorsThevascularandcellularreactionsofbothacuteandchronicinflammationaremediatedbychemicalfactorsthatarederivedfromplasmaproteinsorcellsandareproducedinresponsetooractivatedbytheinflammatorystimulus.Concept:AseriesofchemicalagentsproducedinresponsetooractivatedbytheinflammatorystimulusIV.InflammatorymediatorsT59Generalfeatures:①EndogenousIMoriginatedfromplasmaorcellsCell-derivedmediators:Sequestered
inintracellulargranulesthatneedtobesecretedSynthesizedinresponsetoastimulusGeneralfeatures:60Plasma-derivedmediators:
presentinprecursorformactivatedbyproteolyticcleavages②
Mostmediatorsperformtheirbiologicactivitybybindingtospecificreceptorsontargetcells.
SomehavedirectenzymaticactivitymediatedoxidativedamagePlasma-derivedmediators:61③Onechemicalmediatorcanstimulatethereleaseofothersmediatorsbytargetcellthemselves.
SecondarymediatorSimilarordifferenttotheinitialmediatorsAmplifyingoropposingactivities(counteractingtheinitialmediators)③Onechemicalmediatorcans62④Amediatorcanactononeorfewtargetcelltypes→differenteffectsdependoncellandtissuetypes.⑤Onceactivatedandreleasedfromcell,mostofthesemediatorsareshort-liveddecay,inactivated,scavenged,inhibited⑥Mostmediatorshavethepotentialtocauseharmfuleffects.④Amediatorcanactononeor631.
Mediatorsreleasedbycells1)Vasoactiveamines(1)Histamine:①Sites:Mastcellgranules(themajorsite)Basophilsandplatelets②Functionsdilationofarteriolesincreasepermeabilityofvenuleschemotaxistoeosinophils
1.Mediatorsreleasedbycells64③Stimulithatcausehistaminerelease:Physicalinjury:trauma,cold,heatImmunereaction:IgEmastcellFragmentsofcomplement:C3a,C5aHistamine-releasingprotein(leukocyte)Neuropeptides,substancePCytokines:IL-1,IL-8③Stimulithatcausehistamine65(2)5-HT(5-hydrooxytryptamine)orserotonin①Sites
PlateletsEnterochromaffincellsofintestine②Function:
increasesvascularpermeability③Stimulithatcause5-HTrelease:Collagen,thrombinAdenosinediphosphate(ADP)
Plateletactivatingfactor(PAF)(2)5-HT(5-hydrooxytryptamine66
2)Arachidonicacidmetabolites:(1)Prostaglandin(PG):Vasodilation;increasedpermeability;feverandpain(2)Leukotrienes(LT):ChemotacticagentofneutrophilsIntensevasoconstrictionandbronchospasmIncreasedvascularpermeability(3)Lipoxins(LX):anti-inflammationInhibitneutrophilchemotaxisandadhesionStimulatemonocyteadhesionStimulatevasodilation2)Arachidonicacidmetabolit67Generationofarachidonicacidmetabolitesandtheirrolesininflammation.Generationofarachidonicacid683).Cytokines:Types:CytokinesthatregulateLCfunction:IL-2,TGF-βCytokinesinvolvedinnaturalimmunity:TNF,IL-1Cytokinesthatactivatemacrophages:IFN-γ,IL-12Cytokinesthatstimulatehematopoiesis:IL-3,colony-stimulatingFChemokines:chemotacticactivityforleukocyte3).Cytokines:69③Majorcytokines:IL-1andTNFα,βECadherenttoleukocyteneutrophilschemotaxisstromareleaseofproteinaseFever,cachexia,anorexiaEnhance③Majorcytokines:IL-1andTN70Majoreffectsofinterleukin-1(IL-1)andtumornecrosisfactor(TNF)ininflammation.Majoreffectsofinterleukin-1714).Platelet-activatingfactor(PAF):①Sources
Platelet,basophils,Mastcell,neutrophilMonocyte,EC②Function:
ActivatesplateletVasodilation,increasedpermeabilityVasoconstrictionandbronchoconstrictionIncreaseleukocyteadhesion,chemotaxis4).Platelet-activatingfac725).lysosomalcomponentsNeutrophilsandmonocytescontainlysosomalgranulesvariousenzymesincreasedvascularpermeability,chemotaxis,tissuedamage5).lysosomalcomponentsNeutro736).Nitricoxide(NO)andoxyradical1)Nitricoxide(NO)①
SourcesEC(main),macrophagespecificneuronsinthebrain②Functions:Apotentvasodilator→SMrelaxationReducesptaggregationandadhesionInhibitsmastcell-inducedinflammationServesasanendogenousregulatorofleukocyterecuitment6).Nitricoxide(NO)andoxy74Functionsofnitricoxide(NO)inbloodvesselsandmacrophages.NOcausesvasodilation,andNOfreeradicalsaretoxictomicrobialandmammaliancells.NOS,nitricoxidesynthase.Functionsofnitricoxide(NO)752)Oxygen-derivedactivemetabolites①Releasedfromneutrophilsandmonocyte:Superoxideanion(O2-)Hydrogenperoxide(H2O2)Hydroxylradical(OH-)DependontheactivationoftheNADPHoxidativesystem2)Oxygen-derivedactivemetab76②Function:i)Lowlevels:increaseexpressionofchemokines(IL-8),cytokinesandendothelial,leukocyteadhesionmolecules→amplifytheinflaresponse→destroyphagocytosedmicrobesii)Athighlevel:releaseofthesepotentmediators→injurytoEC,RBCparenchymalC②Function:777).Nuropeptides:①Belongtoafamilyoftachykininincentralandperipheralnervoussystems,suchassubstancep(lung,intestine)②Functions:
IncreasedvascularPermeabilityTransmissionofpainsignalRegulationofbloodpressureStimulationofsecretionbyimmuneandendocrinecells7).Nuropeptides:①Belongto78
结束语谢谢大家聆听!!!79
结束语谢谢大家聆听!!!79中国医科大学病理学英文课件6中国医科大学病理学英文课件680Section1.Introduction
1.Definition:
1)Inflammation:adefensivereactioninlivingtissuewithvascularsystemtoinjuriousstimuli.2)ReactionofBVsisthecentrallinklimitingandkillinginjuredfactoreliminatingandabsorbingnecrotictissue3)TheinflammatoryresponsesiscloselyintertwinedwiththeprocessofrepairSection1.Introduction
1.D81最新病理学英文课件682最新病理学英文课件683最新病理学英文课件684最新病理学英文课件685最新病理学英文课件686最新病理学英文课件687Section2.AcuteinflammationTwomajormechanismsofhostdefense:AntibodyLeukocytesmajorcomponents:1)Changesofhemodynamics
2)Fluidexudation3)LeukocyteextravasationandphagocytosisagainstmicrobesSection2.AcuteinflammationT88最新病理学英文课件689I.Changesofhemodynamics1.Alterationinvascularflowandcaliber
1)Transientvasoconstrictionofarterioles:lastingforafewseconds.2)Vasodilationandincreasedbloodflow(1)ArteriolardilationopeningofnewcapbedsincreasedbloodflowinflammatoryhyperemiaI.Changesofhemodynamics1.A90(2)Relatedtothefactorsof:Bodyfluid:chemicalmediatorNervous:axonreflection3)Slowingofbloodflow:increasedpermeabilityofthemicrovasculatureoutpouringoffluidintoextracellulartissuesconcentrationofRBCandincreasedviscosityofbloodstasisofbloodflow(2)Relatedtothefactorso91NormalbloodflowVasodilationincreasedbloodflowSlowingofbloodflowStasisofbloodflowExtravasation(fluidandleukocyte)NormalbloodflowVasodila922.IncreasedvascularpermeabilityIncreasedpermeability→themostimportantcauseresultinginexudationoffluidandprotein
MechanismofIncreasedpermeability1)ECretraction
FormationofendothelialgapsinvenulesImmediatetransientresponse:occursrapidlyafterexposuretothemediatorandisusuallyreversibleandshort-lived(15to30minutes)mostcommonmechanismofvascularleakageandiselicitedby:histamine,bradykinin,substanceP,leukotriene2.Increasedvascularpermeabi932)CytoskeletalreorganizationDelayedprolongedresponseinducedbycytokines(IL-1,TNF,IFN-γ),increasedpermeabilityafteradelayof4to6hourslastingformorethan24hoursinvolvesvenulesaswellascap.theendothelialcellsretractfromoneanother3)IncreasedtranscytosisacrosstheendothelialcytoplasmBytranscytoplasmicchannelVEGF,histamine,bradykinin,Increasingthenumberandthesizeofchannels2)Cytoskeletalreorganization944)DirectendothelialinjuryImmediatesustainedresponse:
severeburn,purulentBacteriaresultinECnecrosisanddetachmentleakagestartsimmediatelyafterinjurysustainedatahighlevelforseveralhoursuntildamagedBVthrombosedandrepaired4)Directendothelialinjury955)Leukocyte-mediatedendothelialinjuryMild-to-moderatethermalinjury,toxin,x-radiatonincreasedleucocyteinfiltration
involvesvenulesaswellascap.LeukocyteadheretoECactivatedReleasingtoxicspeciesandproteolyticenzymes5)Leukocyte-mediatedendothel966)Highpermeabilityofnewcapsduringrepair,endothelialcellsproliferateandformnewbloodvessels①NewvesselssproutsremainleakyuntilECsdifferentiateandformintercellularjunctions.②Certainfactorsthatcauseangiogenesis(VEGF)increasepermeability③Increaseddensityofreceptorforvasoactive
mediatorsinthesurfaceofEC6)Highpermeabilityofnewca97DiagrammaticrepresentationoffivemechanismsofincreasedvascularpermeabilityininflammationDiagrammaticrepresentationof98II.Fluidexudation1)Majorcauses:①Increasedvascularpermeability→escapeofaprotein-richfluidintotheinterstitium②Thelossofprotein
reducesintravascularcolloidosmoticpressureincreasesthecolloidosmoticpressureoftheinterstitialfluidII.Fluidexudation1)Majorc99Bloodpressureandplamacolloidosmoticforcesinnormalandinflammedmicrocirculation.Bloodpressureandplamacollo100exudation:Theescapeoffluid,proteins,andbloodcellsfromthevascularsystemintotheinterstitialtissueorbodycavities.
Exudate:aninflammatoryextravascularfluidthathasahighproteinconcentration,cellulardebris,andahighergravity.Itimpliessignificantalterationinthenormalpermeabilityofsmallbloodvesselsintheareaofinjury.Transudate:afluidwithlowproteincontent(mostofwhichisalbumin)andalowergravity.Itisessentiallyanultrafiltrateofbloodplasmathatresultsfromosmoticorhydrostaticimbalanceacrossthevesselwall.exudation:Theescapeoffluid1012)Distinguishbetweenexudateandtransudate
Transuda
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