急性炎症课件

INFLAMMATIONINFLAMMATION1AcuteinflammationChronicinflammationRepairResolutionAbscessInjuryAcuteinflammationChronicinfl2“Inflame〞–tosetfire.Inflammationis“Adynamicresponseofvascularisedtissuetoinjury.〞Itisaprotectiveresponse.Itservestobringdefense&healingmechanismstothesiteofinjury.“Inflame〞–tosetfire.3WhatisInflammation?Areactionofalivingtissue&itsmicro-circulationtoapathogenicinsult.Adefensemechanismforsurvival.

WhatisInflammation?Areactio4Reactionoftissuestoinjury,characterizedclinically

by:heat,swelling,redness,pain,andlossoffunction.Pathologically

by:vasoconstrictionfollowedbyvasodilatation,stasis,hyperemia,accumulationofleukocytes,exudationoffluid,anddepositionoffibrin.Reactionoftissuestoinjury,5HowDoesItOccur?Thevascular&cellularresponsesofinflammationaremediatedbychemicalfactors(derivedfrombloodplasmaorsomecells)&triggeredbyinflammatorystimulus.Tissueinjuryordeath--->ReleasemediatorsHowDoesItOccur?Thevascular6EtiologiesMicrobialinfections:bacterial,viral,fungal,etc.Physicalagents:burns,trauma--likecuts,radiationChemicals:drugs,toxins,orcausticsubstanceslikebatteryacid.Immunologicreactions:rheumatoidarthritis.EtiologiesMicrobialinfections7CardinalSignsofInflammationRedness:Hyperaemia.Warm:Hyperaemia.Pain:Nerve,Chemical mediators.Swelling:ExudationLossofFunction:PainCardinalSignsofInflammation8急性炎症课件9TimecourseAcuteinflammation:Lessthan48hoursChronicinflammation:Greaterthan48hours(weeks,months,years)CelltypeAcuteinflammation:NeutrophilsChronicinflammation:Mononuclearcells(Macrophages,Lymphocytes,Plasmacells).Timecourse10

Pathogenesis:Threemainprocessesoccuratthesiteofinflammation,duetothereleaseofchemicalmediators:Increasedbloodflow(rednessandwarmth).Increasedvascularpermeability(swelling,pain&lossoffunction).LeukocyticInfiltration.

Pathogenesis:Threemainpro11MechanismofInflammationVasodilatationExudation-EdemaEmigrationofcellsChemotaxisMechanismofInflammationVas12Themajorlocalmanifestationsofacuteinflammation,comparedtonormal.Vasculardilationandincreasedbloodflow(causingerythemaandwarmth).Extravasationanddepositionofplasmafluidandproteins(edema).leukocyteemigrationandaccumulationinthesiteofinjury.Themajorlocalmanifestations13Changesinvascularflow(hemodynamicchanges)SlowingofthecirculationoutpouringofalbuminrichfluidintotheextravasculartissuesresultsintheconcentrationofRBCsinsmallvesselsandincreasedviscosityofblood.

LeukocytemarginationNeutrophibecomeorientedattheperipheryofvesselsandstarttostick.Changesinvascularflow(hemo14TimescaleVariableminordamage----15-30minutesseveredamage----afewminutesTimescaleVariable15Lymphaticsininflammation:Lymphaticsareresponsiblefordrainingedema.Edema:Anexcessoffluidintheinterstitialtissueorserouscavities;eitheratransudateoranexudateLymphaticsininflammation:Lym16Transudate:Anultrafiltrateofbloodplasmapermeabilityofendotheliumisusuallynormal.lowproteincontent(mostlyalbumin)Transudate:17Exudate:Afiltrateofbloodplasmamixedwithinflammatorycellsandcellulardebris.permeabilityofendotheliumisusuallyalteredhighproteincontent.Exudate:18Pus:Apurulentexudate:aninflammatoryexudaterichinleukocytes(mostlyneutrophils)andparenchymalcelldebris.Pus:19LeukocyteexudationDividedinto4stepsMargination,rolling,andadhesiontoendotheliumDiapedesis(trans-migrationacrosstheendothelium)Migrationtowardachemotacticstimulifromthesourceoftissueinjury.PhagocytosisLeukocyteexudationDividedint20急性炎症课件21急性炎症课件22Phagocytosis3distinctstepsRecognitionandattachmentEngulfmentKillingordegradationPhagocytosis3distinctsteps23急性炎症课件24Defectsinleukocytefunction:Marginationandadhesionsteroids,leukocyteadhesiondeficiencyEmigrationtowardachemotacticstimulusdrugschemotaxisinhibitorsPhagocytosisChronicgranulomatousdisease(CGD)Defectsinleukocytefunction:25InflammationOutcomeAcuteInflammationResolutionChronicInflammationAbscessSinusFistulaFibrosis/ScarUlcerInjuryFungusVirusCancersT.B.etc.InflammationOutcomeAcuteInfl26ChemicalMediators:Chemicalsubstancessynthesisedorreleasedandmediatethechangesininflammation.Histamine

bymastcells-vasodilatation.Prostaglandins

–Causepain&fever.Bradykinin

-Causespain.ChemicalMediators:Chemicalsu27MorphologictypesofacuteinflammationExudativeorcatarrhalInflammation:excessfluid.TBlung.Fibrinous–pneumonia–fibrinMembranous(fibrino-necrotic)inflammationSuppuration/Purulent–Bacterial-neutrophilsMorphologictypesofacuteinf28Serous–excessclearfluid–Heart,lungAllergicinflammationHaemorrhagic–b.v.damage-anthrax.Necrotisinginflammation.Serous–excessclearfluid–29Acuteinflammationhasoneoffouroutcomes:AbscessformationProgressiontochronicinflammationResolution--tissuegoesbacktonormalRepair--healingbyscarringorfibrosisAcuteinflammationhasoneof30Abscessformation:"Alocalizedcollectionofpus(suppurativeinflammation)appearinginanacuteorchronicinfection,andassociatedwithtissuedestruction,andswelling.Abscessformation:"Alocalized31Site:skin,subcutaneoustissue,internalorganslikebrain,lung,liver,kidney,…….Pathogenesis:thenecrotictissueissurroundedbypyogenicmembrane,whichisformedbyfibrinandhelpinlocalizetheinfection.Site:skin,subcutaneoustissu32Carbuncle-Itis