中国医科大学病理学英文课件6.ppt
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中国医科大学病理学英文课件6.ppt
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Chapter4.Inflammation,ZhaoYue,Section1.Introduction1.Definition:
1)Inflammation:
adefensivereactioninlivingtissuewithvascularsystemtoinjuriousstimuli.2)ReactionofBVsisthecentrallinklimitingandkillinginjuredfactoreliminatingandabsorbingnecrotictissue3)Theinflammatoryresponsesiscloselyintertwinedwiththeprocessofrepair,4)Significance,
(1)Beneficial:
withoutinflammationInfectionswouldgouncheckedinjuredorgansmightremainpermanentfesteringsoreswoundwouldneverheal
(2)Harmful:
hypersensitivereactionstodrugs,toxinsunderliecommonchronicdiseasesrheumatoidarthritis,atherosclerosis,andlungfibrosisfibrousrepairdisfiguringscarsorfibrousbandsthatcauseintestinalobstructionorlimitthemobilityofjoints.,2.Causesofinflammation,1.Biologicfactors:
bacteria,Virus,fungi,parasitesthemostcommon2.ChemicalfactorsExogenous:
drugs,acidEndogenous3.Physicalagents:
trauma,burn4.Allergicreaction:
GN,TBlupus,3.Basicpathologicchanges,1.AlterationDegeneration,necrosisoflocaltissueandcellsParenchymalCcellularswellingfattychangecoagulative,liquefactivenecrosisMesenchymalCmucoidchangeamyloidchangefibrinoidnecrosishyalinechange,2.Exudation:
Ininflammatoryfoci,theescapeoffluid,proteins(fibrin),bloodcellsfromvascularwallintointerstitialtissue,bodycavitiesorsurfaceofthebodyandmucosa3.ProliferationParenchymal:
epithelium,hepatocyteMesenchymal:
fibroblast,EC,histocyte,4.Clinicaltypes,1)Acuteinflammation
(1)Relativelyshortduration,lastingforafewdaysorafewweeks
(2)Lesionsexudationoffluid,neutrophilsdegeneration,necrosis2)Chronicinflammation
(1)longerdurationforafewmonthsoryears
(2)LesionsProliferation:
BV,fibrosisLC,PC,Macrophageinfiltration,病例六,病史:
男性,40岁,颈部患“疖”,红、肿、热、痛,10天后局部红肿发展至手掌大,体温38,局部手术切开引流。
当晚即恶寒、高热、头痛,次日体检发现病人轻度黄疸,肝脾肿大,体温39,WBC计数21.0G/L。
思考题:
用所学的炎症知识,作出病理诊断并解释上述临床表现。
Section2.Acuteinflammation,Twomajormechanismsofhostdefense:
AntibodyLeukocytesmajorcomponents:
1)Changesofhemodynamics2)Fluidexudation3)Leukocyteextravasationandphagocytosis,againstmicrobes,I.Changesofhemodynamics,1.Alterationinvascularflowandcaliber1)Transientvasoconstrictionofarterioles:
lastingforafewseconds.2)Vasodilationandincreasedbloodflow
(1)Arteriolardilationopeningofnewcapbedsincreasedbloodflowinflammatoryhyperemia,
(2)Relatedtothefactorsof:
Bodyfluid:
chemicalmediatorNervous:
axonreflection3)Slowingofbloodflow:
increasedpermeabilityofthemicrovasculatureoutpouringoffluidintoextracellulartissuesconcentrationofRBCandincreasedviscosityofbloodstasisofbloodflow,Normalbloodflow,Vasodilationincreasedbloodflow,Slowingofbloodflow,Stasisofbloodflow,Extravasation(fluidandleukocyte),2.Increasedvascularpermeability,IncreasedpermeabilitythemostimportantcauseresultinginexudationoffluidandproteinMechanismofIncreasedpermeability1)ECretractionFormationofendothelialgapsinvenulesImmediatetransientresponse:
occursrapidlyafterexposuretothemediatorandisusuallyreversibleandshort-lived(15to30minutes)mostcommonmechanismofvascularleakageandiselicitedby:
histamine,bradykinin,substanceP,leukotriene,2)CytoskeletalreorganizationDelayedprolongedresponseinducedbycytokines(IL-1,TNF,IFN-),increasedpermeabilityafteradelayof4to6hourslastingformorethan24hoursinvolvesvenulesaswellascap.theendothelialcellsretractfromoneanother3)IncreasedtranscytosisacrosstheendothelialcytoplasmBytranscytoplasmicchannelVEGF,histamine,bradykinin,Increasingthenumberandthesizeofchannels,4)Directendothelialinjury,Immediatesustainedresponse:
severeburn,purulentBacteriaresultinECnecrosisanddetachmentleakagestartsimmediatelyafterinjurysustainedatahighlevelforseveralhoursuntildamagedBVthrombosedandrepaired,5)Leukocyte-mediatedendothelialinjury,Mild-to-moderatethermalinjury,toxin,x-radiatonincreasedleucocyteinfiltrationinvolvesvenulesaswellascap.LeukocyteadheretoECactivatedReleasingtoxicspeciesandproteolyticenzymes,6)Highpermeabilityofnewcapsduringrepair,endothelialcellsproliferateandformnewbloodvesselsNewvesselssproutsremainleakyuntilECsdifferentiateandformintercellularjunctions.Certainfactorsthatcauseangiogenesis(VEGF)increasepermeabilityIncreaseddensityofreceptorforvasoactivemediatorsinthesurfaceofEC,Diagrammaticrepresentationoffivemechanismsofincreasedvascularpermeabilityininflammation,II.Fluidexudation,1)Majorcauses:
Increasedvascularpermeabilityescapeofaprotein-richfluidintotheinterstitiumThelossofproteinreducesintravascularcolloidosmoticpressureincreasesthecolloidosmoticpressureoftheinterstitialfluid,Bloodpressureandplamacolloidosmoticforcesinnormalandinflammedmicrocirculation.,exudation:
Theescapeoffluid,proteins,andbloodcellsfromthevascularsystemintotheinterstitialtissueorbodycavities.Exudate:
aninflammatoryextravascularfluidthathasahighproteinconcentration,cellulardebris,andahighergravity.Itimpliessignificantalterationinthenormalpermeabilityofsmallbloodvesselsintheareaofinjury.Transudate:
afluidwithlowproteincontent(mostofwhichisalbumin)andalowergravity.Itisessentiallyanultrafiltrateofbloodplasmathatresultsfromosmoticorhydrostaticimbalanceacrossthevesselwall.,2)Distinguishbetweenexudateandtransudate,TransudateExudateVascularpermeabilityNormalIncreasedProteinconcentration30g/LProteintypeAlbuminKindsofproteinRivaltatestNegative(-)Positive(+)FibrinNoHaveSpecificgravity1.018Cellnumber1000106/LAutoagglutinationNoYesAppearanceClearCloudy,3)Functionsofexudate:
(1)Dilutelocaltoxinsreducetheinjurytotissue
(2)Bringinthenutritionalsubstanceforleukocytescarryoffthemetabolicproductsininflafoci(3)killthepathogen:
Ab,complement(4)Fibrinmesh:
limitthespreadingofpathogenicorganismslimittheremovingofM,III.Leukocyteextravasationandphagocytosis,1)Leukocyteextravasation:
leukocytepassthroughvascularwallintothesiteofinjury.Dividedintofollowingsteps:
MarginationandrollingAdhesionTransmigrationandchemotaxis,
(1)MarginationandrollingleukocyteincentralaxialcolumnBVdilation,speedofbloodflowmarginationrollingpavementingappearance,Leukocyticemigration,
(2)Adhesion:
a.Bybindingofcomplementaryadhesionmoleculesontheleukocyteandendothelialsurfacesb.Adhesionmolecules:
Theimmunoglobulinfamily:
I(V)CAM-1Integrinsselectins,c.Mechanismsofadhesiveprocess:
i)Redistributionofadhesionmoleculestothecellsurface:
Forexample:
P-selectinNormallypresentinW-PbodyofECHistaminethrombin,PAFRedistributedtothecellsurfaceBindingtothereceptorofleukocyte,ii)Inductionofadhesionmoleculessynthesis,Someinflammatorymediators,(IL-1,TNF)inducedthesynthesisandsurfaceexpressionofendothelialadhesionmoleculesForexample:
InnormalECNoexpressionofE-selectinIL-1TNFSynthesisandexpressE-selectin,iii)Increasedavidityofbinding,Forexample:
LFA-1Presentonneutrophils,monocyte,LCNotadheretoitsligandICAM-1onECowingtoleukocyteactivationLFA-1convertedfromastateoflow-affinitybindingtohighaffinitybindingtowardICAM-1,Regulationofendothelialandleukocyteadhesionmolecules.A,RedistributionofP-selectin.B,Cytokineactivationofendothelium.C,Increasedbindingavidityofintegrins,(3)Transmigrationandchemotaxis,Injuredvenulesorcaps,leukocytesinsertpseudopodsintojunctionbetweenECssqueezethroughinterendothelialjunctionssecretecollagenasedecomposetheBMescapeintointerstitialtissue,pseudopod,Adhensionandtransmigration,Redcelldiapedesis:
apassiveprocess,determineinjuredextentThetypeofleukocytevarieswiththeageofinflammatorylesion:
i)Acute:
neutrophilspredominateduringthefirst624hs;arereplacedbymonocytein2448hsii)Chronic:
LC,PC,monocyte,LC,PC,Neutrophils,MC,Basophil12-15m,Eosinophil12-15m,Neutrophil12-15m,Monocyte14-20m,Lmphocyte6-8m,RBC7.5m,Thetypeofemigratingleukocytevarieswiththetypesofstimulus:
i)Viralinfection:
LCfirstCtoarriveii)HypersensitivityreactionParasiteinfectioniii)Bacterialinfection:
neutrophils,Eosinophils,Chemotaxis:
afterextravasationleukocytesemigratetowardthechemicalmediatorsalongachemicalconcentrationgradient.Chemotacticagent:
Exogenous:
bacterialproductsEndogenous:
complements(C5a)leukotrieneB4(LTB4)cytokines:
chemokine,Chemotaxis,(4)TherolesofleukocytesAcriticalfunctionofinflammationistodeliverleukocytestothesiteofinjuryandtoactivatetheleukocytestoperformtheirnormalfunctionsinhostdefense.,Phagocytosis(ingestoffendingagents)Immunologicalfunction(killbacteriaandothermicrobes,andgetridofnecrotictissueandforeignsubstances)Leukocyteinducedtissueinjury,Phagocytosis:
Leukocyteemigratetoinflammatoryfocusengulfandkillordegradatethepathogenicorganismandtissuedebris.,a.Typesofphagocytes,Neutrophils:
1012umi)Azurophilicgranules:
NeutralproteinaseandacidichydrolaseDigestanddegradatedebris,deadbacteriaMyeloperoxidase,phospholipaseA2,lysozyme,andcationproteinkillthebacteria,ii)Specificgranules:
Lysozyme,lactoferrin,Alkaliphosphatase,phospholipaseA2Macrophage:
1224umi)SitedistributedinCT,liver(kupfferC)spleen,LN,lunginflammatoryfocus:
derivedfrombloodmonocyte,killbacteria,ii)Functions:
Phagocytosiseliminatethedeadbacteria,cells,debris,foreignbodiesthatcantbedigested,b.Processofphagocytosis:
Involvesthreesteps:
RecognitionandattachmentEngulfmentkillingordegradation,Recognitionandattachment:
i)Opsonins:
akindofproteininserumwhichenhancestheefficiencyofphagocytosisii)Opsonization:
microorganismcontactwiththeserumcontainedopsoninsandarecoatediii)MajoropsoninsFc
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