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.InflammationZhaoYueSection1.Introduction1.Definition:
1)Inflammation:
adefensivereactioninlivingtissuewithvascularsystemtoinjuriousstimuli.2)ReactionofBVsisthecentrallinklimitingandkillinginjuredfactoreliminatingandabsorbingnecrotictissue3)Theinflammatoryresponsesiscloselyintertwinedwiththeprocessofrepair4)Significance
(1)Beneficial:
withoutinflammationInfectionswouldgouncheckedinjuredorgansmightremainpermanentfesteringsoreswoundwouldneverheal
(2)Harmful:
hypersensitivereactionstodrugs,toxinsunderliecommonchronicdiseasesrheumatoidarthritis,atherosclerosis,andlungfibrosisfibrousrepairdisfiguringscarsorfibrousbandsthatcauseintestinalobstructionorlimitthemobilityofjoints.2.Causesofinflammation1.Biologicfactors:
bacteria,Virus,fungi,parasitesthemostcommon2.ChemicalfactorsExogenous:
drugs,acidEndogenous3.Physicalagents:
trauma,burn4.Allergicreaction:
GN,TBlupus3.Basicpathologicchanges1.AlterationDegeneration,necrosisoflocaltissueandcellslParenchymalCcellularswellingfattychangecoagulative,liquefactivenecrosislMesenchymalCmucoidchangeamyloidchangefibrinoidnecrosishyalinechange2.Exudation:
Ininflammatoryfoci,theescapeoffluid,proteins(fibrin),bloodcellsfromvascularwallintointerstitialtissue,bodycavitiesorsurfaceofthebodyandmucosa3.ProliferationParenchymal:
epithelium,hepatocyteMesenchymal:
fibroblast,EC,histocyte4.Clinicaltypes1)Acuteinflammation
(1)Relativelyshortduration,lastingforafewdaysorafewweeks
(2)Lesionsexudationoffluid,neutrophilsdegeneration,necrosis2)Chronicinflammation
(1)longerdurationforafewmonthsoryears
(2)LesionsProliferation:
BV,fibrosisLC,PC,Macrophageinfiltration病病例例六六病史:
病史:
男性,男性,4040岁,颈部患岁,颈部患“疖疖”,红、,红、肿、肿、热、痛,热、痛,1010天后局部红肿发展至手天后局部红肿发展至手掌大,体温掌大,体温3838,局部手术切开引流。
,局部手术切开引流。
当晚即恶寒、高热、头痛,次日体检发当晚即恶寒、高热、头痛,次日体检发现病人轻度黄疸,肝脾肿大,体温现病人轻度黄疸,肝脾肿大,体温3939,WBCWBC计数计数21.0G/L21.0G/L。
思考题:
思考题:
用所学的炎症知识,作出病理诊用所学的炎症知识,作出病理诊断并解释上述临床表现。
断并解释上述临床表现。
Section2.AcuteinflammationlTwomajormechanismsofhostdefense:
AntibodyLeukocyteslmajorcomponents:
1)Changesofhemodynamics2)FluidexudationFluidexudation3)LeukocyteLeukocyteextravasationextravasationandandphagocytosisphagocytosisagainstmicrobesI.Changesofhemodynamics1.Alterationinvascularflowandcaliber1)Transientvasoconstrictionofarterioles:
lastingforafewseconds.2)Vasodilationandincreasedbloodflow
(1)Arteriolardilationopeningofnewcapbedsincreasedbloodflowinflammatoryhyperemia
(2)Relatedtothefactorsof:
Bodyfluid:
chemicalmediatorNervous:
axonreflection3)Slowingofbloodflow:
increasedpermeabilityofthemicrovasculatureoutpouringoffluidintoextracellulartissuesconcentrationofRBCandincreasedviscosityofbloodstasisofbloodflowNormalbloodflowVasodilationincreasedbloodflowSlowingofbloodflowStasisofbloodflowExtravasation(fluidandleukocyte)2.IncreasedvascularpermeabilityIncreasedpermeabilitythemostimportantcauseresultinginexudationoffluidandproteinMechanismofIncreasedpermeability1)ECretractionFormationofendothelialgapsinvenuleslImmediatetransientresponse:
occursrapidlyafterexposuretothemediatorandisusuallyreversibleandshort-lived(15to30minutes)lmostcommonmechanismofvascularleakageandiselicitedby:
histamine,bradykinin,substanceP,leukotriene2)CytoskeletalreorganizationDelayedprolongedresponselinducedbycytokines(IL-1,TNF,IFN-),lincreasedpermeabilityafteradelayof4to6hourslastingformorethan24hourslinvolvesvenulesaswellascap.ltheendothelialcellsretractfromoneanother3)IncreasedtranscytosisacrosstheendothelialcytoplasmBytranscytoplasmicchannelVEGF,histamine,bradykinin,Increasingthenumberandthesizeofchannels4)DirectendothelialinjuryImmediatesustainedresponse:
severeburn,purulentBacteriaresultinECnecrosisanddetachmentleakagestartsimmediatelyafterinjurysustainedatahighlevelforseveralhoursuntildamagedBVthrombosedandrepaired5)Leukocyte-mediatedendothelialinjuryMild-to-moderatethermalinjury,toxin,x-radiatonincreasedleucocyteinfiltrationinvolvesvenulesaswellascap.LeukocyteadheretoECactivatedReleasingtoxicspeciesandproteolyticenzymes6)Highpermeabilityofnewcapsduringrepair,endothelialcellsproliferateandformnewbloodvesselsNewvesselssproutsremainleakyuntilECsdifferentiateandformintercellularjunctions.Certainfactorsthatcauseangiogenesis(VEGF)increasepermeabilityIncreaseddensityofreceptorforvasoactivemediatorsinthesurfaceofEClDiagrammaticrepresentationoffivemechanismsofincreasedvascularpermeabilityininflammationII.Fluidexudation1)Majorcauses:
Increasedvascularpermeabilityescapeofaprotein-richfluidintotheinterstitiumThelossofproteinreducesintravascularcolloidosmoticpressureincreasesthecolloidosmoticpressureoftheinterstitialfluidBloo
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