《病理学》第二章 细胞适应、细胞损伤和细胞死亡（英文）-教学课件（非AI生成）.ppt

ChapterII

Cellularadaptation,cellinjury,andcelldeath1

Knowledgeofetiologyremainsthebackbone:DiseasediagnosesUnderstandingthenatureofdiseasesTreatmentofdiseases.Etiology2

Whilemuchstillneedstobeuncoveredtolinkabnormalgenesandtheexpressionofdisease,gonearethetimewhenthemechanismsofmostdiseaseswereunknown?orobscure?ormysterious?3

Oneetiologicagent—onediseaseSeveraletiologicagents—onediseaseOneetiologicagent—severaldiseasesBASICRULESOFETIOLOGY4

CausesofcellinjuryanddiseaseOxygendeprivation(hypoxia,ischemia)NutritionalimbalancesPhysicalagentsChemicalagentsanddrugsInfectiousagentsImmunologicreactionsGeneticderangements5

HypoxiaIschemia(lossofbloodsupply)Inadequateoxygenation(cardiorespiratoryfailure)Decreaseofoxygen-carryingcapacityoftheblood(anemiaorCOpoisoning)6

HypoxiainjuryLossofoxidativephosphorylationandATPgenerationbymitochondria.ResultinginaerobicglycolysisbydecreasedATP(withincreaseinAMP)Depletedglycogen.ReducedintracellularpH:Lacticacidandinorganicphosphate.MitochondrialdamageClumpingofnuclearchromatin.7

8

PhysicalagentsTraumaHeatColdRadiation(UV)Electricshock9

ChemicalagentsanddrugsEndogenousproducts:ureaExogenousagents:Therapeuticdrugs:hormonesNon-therapeuticagents:leadoralcohol10

MechanismofchemicalinjuryDirectly:MercuryofmercuricchloridebindstoSHgroupsofcellmembraneproteins,causingincreasedpermeabilityandinhibitionofATPase-dependenttransport.11

Indirectly:Byconversiontoreactivetoxicmetaboliteswhichinturncausecellinjuryeitherbydirectcovalentbindingtomembraneproteinandlipid,ormorecommonlybytheformationoffreeradicals.Mechanismofchemicalinjury12

CCl4inSERoflivercell(P-450)–CCl3.–lipidperoxidationandautocatalyticreactions–swellingandbreakdownofER,dissociationofribosome,anddecreasedhepaticproteinsynthesis(lossoflip