最新病理學(xué)英文課件6

中國醫(yī)科大學(xué)病理學(xué)英文課件6中國醫(yī)科大學(xué)病理學(xué)英文課件61Section1.Introduction

1.Definition:

1)Inflammation:adefensivereactioninlivingtissuewithvascularsystemtoinjuriousstimuli.2)ReactionofBVsisthecentrallinklimitingandkillinginjuredfactoreliminatingandabsorbingnecrotictissue3)TheinflammatoryresponsesiscloselyintertwinedwiththeprocessofrepairSection1.Introduction

1.D2最新病理學(xué)英文課件63最新病理學(xué)英文課件64最新病理學(xué)英文課件65最新病理學(xué)英文課件66最新病理學(xué)英文課件67最新病理學(xué)英文課件68Section2.AcuteinflammationTwomajormechanismsofhostdefense:AntibodyLeukocytesmajorcomponents:1)Changesofhemodynamics

2)Fluidexudation3)LeukocyteextravasationandphagocytosisagainstmicrobesSection2.AcuteinflammationT9最新病理學(xué)英文課件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最新病理學(xué)英文課件636②Redcelldiapedesis:

apassiveprocess,determineinjuredextent③Thetypeofleukocytevarieswiththeageofinflammatorylesion:i)Acute:neutrophilspredominateduringthefirst6~24hs;arereplacedby

monocytein24~48hsii)Chronic:

LC,PC,monocyteLCPCNeutrophilsMC②Redcelldiapedesis:LCPCNeu37Basophil12-15μmEosinophil12-15μmNeutrophil12-15μmMonocyte14-20μmLmphocyte6-8μmRBC7.5μmBasophilEosinophilNeutroph38最新病理學(xué)英文課件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

結(jié)束語謝謝大家聆聽?。?！79

結(jié)束語謝謝大家聆聽?。。?9中國醫(yī)科大學(xué)病理學(xué)英文課件6中國醫(yī)科大學(xué)病理學(xué)英文課件680Section1.Introduction

1.Definition:

1)Inflammation:adefensivereactioninlivingtissuewithvascularsystemtoinjuriousstimuli.2)ReactionofBVsisthecentrallinklimitingandkillinginjuredfactoreliminatingandabsorbingnecrotictissue3)TheinflammatoryresponsesiscloselyintertwinedwiththeprocessofrepairSection1.Introduction

1.D81最新病理學(xué)英文課件682最新病理學(xué)英文課件683最新病理學(xué)英文課件684最新病理學(xué)英文課件685最新病理學(xué)英文課件686最新病理學(xué)英文課件687Section2.AcuteinflammationTwomajormechanismsofhostdefense:AntibodyLeukocytesmajorcomponents:1)Changesofhemodynamics

2)Fluidexudation3)LeukocyteextravasationandphagocytosisagainstmicrobesSection2.AcuteinflammationT88最新病理學(xué)英文課件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