内科学 急性肾衰竭顾勇精.ppt
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1、内科学内科学 急性肾衰竭顾勇急性肾衰竭顾勇第1页,本讲稿共39页ARFD1.Definition and conceptD2.Pathogenesis D3.Pathology and pathophysiologyD4.Acute tubular necrosisD5.Special type of ARFD6.Handling of ARF第2页,本讲稿共39页Definition of ARFDSyndromeDQuick decline of GFR A series of clinical manifestationDAccumulation of nitrogen-containi
2、ng tastes第3页,本讲稿共39页Incidence of ARFDCommon hospitalization:5%DICU:30%Hou SH et al.Am J Med.1983;74:243第4页,本讲稿共39页Features of ARFDKidney:complete restoration of functionDHigh incidence of complicationDHigh morbidity&mortalityDOther organs damage第5页,本讲稿共39页Classification of ARFDPrerenal:Hypoperfusion
3、,functionality:55%-60%DRenal:35%-40%DPostrenal:urinary tract:5%第6页,本讲稿共39页Causes of prerenal ARFDLow volume:bleeding,lost from G-I,kidney,skin,third spaceDLow cardiac output:myocardium,valve,DSystemic vasodilatation:medicine,infection,allergy,liver failureDRenal arterial systole:shock,medicine,liver
4、 failure第7页,本讲稿共39页Renal ARFDRenal great vesselsDGlomeruleDAcute tubular necrosis:ischemia/poisoning DTubules and interstitium第8页,本讲稿共39页Postrenal ARF Position:DUreterDbladder neckDAnterior urethraCause:Stone,coagulated blood,Crystal,edema,deligationTumor,fibrosis,stenosis,prostate gland etc.第9页,本讲稿
5、共39页ATNDPathologyDPathophysiologyDCourse of diseaseDDiagnosis and differential diagnosisDComplication第10页,本讲稿共39页Decline of GFR in ARFDAbnormal renal hemodynamicsDTubular impairment:obstruction,back flow第11页,本讲稿共39页Factors involved in renal hemodynamicsDEndothelin:increasing receptor blockingDEDNO:d
6、ecreasingDOthers:Platelet Activating Factor(PAF)AdenosineDMedulla edemaDTubuloglomerular feedback:TGF第12页,本讲稿共39页Tubular impairmentDObstruction:lCaducous epithelial cells and components lCastDBack flow:Impaired integrity of epithelial cellsAccording to histology:tubular cells fall off and necrosis,c
7、ast第13页,本讲稿共39页Metabolic change after tubular cell damageDDecreased ATPDCellular swellingDIncreased intracellular calciumDIntracellular acidosisDActivation of phosphatidaseDActivation of proteaseDOxidative stress第14页,本讲稿共39页Consequence of damaged tubular cellslIntactlSublethallDeath:Apoptosis/necros
8、isDDepend on:different site,toxin concentration,time第15页,本讲稿共39页Necrosis Apoptosis in ARFDNecrosis:lcellular swelling,chondriosome changelDestroy membranous IntegritylRelease protein lysaselperipheral cell damage/inflammationDApoptosis:lActive energy consumption processlcell nucleus shrinkagesmall D
9、NA fragment lcell membrane:blebbing but integrity lapoptotic body phagocytosislNo peripheral cell damage and inflammation.Depend on severity of impairment第16页,本讲稿共39页Repair,Regeneration and Recovery DRecovery of Sublethal cellsDScavenge necrotic cells and intracavitary castsDRegeneration of epitheli
10、al cells:replace necrotic and caducous cellsDTubular epithelial cells integrity and function restoration第17页,本讲稿共39页Course of ATNDInitiation:no parenchyma impairmentDMaintenance:parenchyma impairment:1-2 weeks,may be 11 monthsDRecovery第18页,本讲稿共39页Diagnosis and differential diagnosis of ATNDDiagnosis
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