急性炎症课件.ppt

inflammation inflame tosetfire inflammationis adynamicresponseofvascularisedtissuetoinjury itisaprotectiveresponse itservestobringdefense healingmechanismstothesiteofinjury whatisinflammation areactionofalivingtissue itsmicro circulationtoapathogenicinsult adefensemechanismforsurvival reactionoftissuestoinjury characterizedclinicallyby heat swelling redness pain andlossoffunction pathologicallyby vasoconstrictionfollowedbyvasodilatation stasis hyperemia accumulationofleukocytes exudationoffluid anddepositionoffibrin howdoesitoccur thevascular cellularresponsesofinflammationaremediatedbychemicalfactors derivedfrombloodplasmaorsomecells triggeredbyinflammatorystimulus tissueinjuryordeath releasemediators etiologies microbialinfections bacterial viral fungal etc physicalagents burns trauma likecuts radiationchemicals drugs toxins orcausticsubstanceslikebatteryacid immunologicreactions rheumatoidarthritis cardinalsignsofinflammation redness hyperaemia warm hyperaemia pain nerve chemicalmediators swelling exudationlossoffunction pain timecourseacuteinflammation lessthan48hourschronicinflammation greaterthan48hours weeks months years celltypeacuteinflammation neutrophilschronicinflammation mononuclearcells macrophages lymphocytes plasmacells pathogenesis threemainprocessesoccuratthesiteofinflammation duetothereleaseofchemicalmediators increasedbloodflow rednessandwarmth increasedvascularpermeability swelling pain lossoffunction leukocyticinfiltration mechanismofinflammation vasodilatationexudation edemaemigrationofcellschemotaxis themajorlocalmanifestationsofacuteinflammation comparedtonormal vasculardilationandincreasedbloodflow causingerythemaandwarmth extravasationanddepositionofplasmafluidandproteins edema leukocyteemigrationandaccumulationinthesiteofinjury changesinvascularflow hemodynamicchanges slowingofthecirculationoutpouringofalbuminrichfluidintotheextravasculartissuesresultsintheconcentrationofrbcsinsmallvesselsandincreasedviscosityofblood leukocytemarginationneutrophibecomeorientedattheperipheryofvesselsandstarttostick timescale variableminordamage 15 30minutesseveredamage afewminutes lymphaticsininflammation lymphaticsareresponsiblefordrainingedema edema anexcessoffluidintheinterstitialtissueorserouscavities eitheratransudateoranexudate transudate anultrafiltrateofbloodplasmapermeabilityofendotheliumisusuallynormal lowproteincontent mostlyalbumin exudate afiltrateofbloodplasmamixedwithinflammatorycellsandcellulardebris permeabilityofendotheliumisusuallyalteredhighproteincontent pus apurulentexudate aninflammatoryexudaterichinleukocytes mostlyneutrophils andparenchymalcelldebris leukocyteexudation dividedinto4stepsmargination rolling andadhesiontoendotheliumdiapedesis trans migrationacrosstheendothelium migrationtowardachemotacticstimulifromthesourceoftissueinjury phagocytosis phagocytosis 3distinctstepsrecognitionandattachmentengulfmentkillingordegradation defectsinleukocytefunction marginationandadhesionsteroids leukocyteadhesiondeficiencyemigrationtowardachemotacticstimulusdrugschemotaxisinhibitorsphagocytosischronicgranulomatousdisease cgd inflammationoutcome fungusviruscancerst b etc chemicalmediators chemicalsubstancessynthesisedorreleasedandmediatethechangesininflammation histaminebymastcells vasodilatation prostaglandins causepain fever bradykinin causespain morphologictypesofacuteinflammation exudativeorcatarrhalinflammation excessfluid tblung fibrinous pneumonia fibrinmembranous fibrino necrotic inflammationsuppuration purulent bacterial neutrophils serous excessclearfluid heart lungallergicinflammationhaemorrhagic b v damage anthrax necrotisinginflammation acuteinflammationhasoneoffouroutcomes abscessformationprogressiontochronicinflammationresolution tissuegoesbacktonormalrepair healingbyscarringorfibrosis abscessformation alocalizedcollectionofpus suppurativeinflammation appearinginanacuteorchronicinfection andassociatedwithtissuedestruction andswelling site skin subcutaneoustissue internalorganslikebrain lung liver kidney pathogenesis thenecrotictissueissurroundedbypyogenicmembrane whichisformedbyfibrinandhelpinlocalizetheinfection carbuncle itisanextensiveformofabscessinwhichpusispresentinmultiplelociopenatthesurfacebysinuses occurinthebackoftheneckandthescalp furuncl