renal failure
DESCRIPTION
Renal failure. 患儿女, 11 月。因呕吐、腹泻伴发热 9 天,无尿 5 天入院。 9 天前无诱因出现腹泻,每天 3 ~ 4 次,伴频繁呕吐,非喷射状,量较多;同时发热,体温最高 41℃ 。给予口服抗生素治疗,三天后腹泻、呕吐次数减少,但体温仍在 38 ~ 39℃ 之间。近 5 天一直无尿。 体检: 呼吸 60 次 / 分,脉搏 120 次 / 分,血压 85/54mmHg 。 昏睡状态。双眼睑及球结膜水肿,睑结膜稍苍白,口唇干裂,咽充血,颈无抵抗;呼吸深大。 - PowerPoint PPT PresentationTRANSCRIPT
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Renal failure
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11959344138395 60/120/85/54mmHg 8.6mmol/L128mmol/L,100mmol/L, 1.98mmol/L2.33mmol/L, 37.12mmol/L,804.44mol/LpH7.17, PCO224.5mmHg, HCO3-8.6mmol/L, SBE -18.3mmol/LT
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1 IntroductionNormal function of the kidneyRenal insufficiencyCausesBasic manifestation of renal insufficiency
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Normal function of the kidneyRemove waste product from the bodyRegulate electrolyte and acid-base balance.1.ExcretionProduce reninEPO1,25(OH)2D3 and prostaglandinsInactivate gastrinPTH.2. Endocrine
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Renal insufficiencyDiseases Dysfunction of excretion and endocrine Symptomsand signs Edema, hypertension, oliguric, polyuria, hematuria, proteinuria, anemia, osteodystrophy.
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Causes:1 Primary renal diseasesPrimary glomerular diseases, Primary tubular diseases, Interstitial nephritis, et al.2 Secondary renal lesionCirculatory system diseases, immunity siseases, metabolic diseases, hematopathy, et al.
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Basic manifestation of renal insufficiency 1 Glomerular dysfunction2 Tubular dysfunction3 Endocrine dysfunction
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1 Glomerular dysfunctionGFRblood flownet filtration pressure Kf Glomerular permselectivity
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2 Tubular dysfunctionproximal tubuleRenal glycosuria, aminoaciduria, renal tubular acidosis, hypophosphatemialoop of HenleHypotonic or isotonic urine, polyuriadistal tubuleAcid-base and electrolyte disorders, polyuria
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3 Endocrine dysfunction ReninEndothelinsKKS disordersAA DisequilibriumEPO 1,25(OH)2D3
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2 Acute renal failure
DiseasesConceptionwater intoxication,azotemia, hyperkalemia, metabolic acidosis
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Section 1 Cause and Classification 1 causes Prerenal ~ Intrarenal ~ Postrenal ~2renallesion functional~ organic ~obstructive ~3urine volumeOliguric ~Nonoliguric ~*** Classification
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Causes 1 Prerenal factor renal blood flow Characteristicearly stage: functional~ late stage: organic ~(2) oliguria
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MechanismECFRBF GFRReabsorptionoliguriaImpaired homeostasis
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Causes (1) acute tubular necrosis,ATN 2/3 acute renal ischemiaacute renal poisoning hemoglobinuria, myoglobinuria (2) renal disease
Characteristic (1) parenchymal(2) oliguric ~nonoliguric ~2 intrarenal factor
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Differentiation between the two RFurine functionalRF organic RFspecific gravity> 1.020 < 1.015OP(mmol/L) > 700 < 250Na(mmol/L) < 20 > 40UrCr/SrCr > 40 < 20Sediment normalManicol test urine volume urine volume Necrosis epithelial cells,RBC,casts,albuminuria
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Causes Kidney stone, tumor, obstruction of necrosis tissueCharacteristic early stage: obstructive ~ late stage: organic ~ 3 Postrenal factor
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MechanismObstruction of the urinary tractBowmans capsule pressureNet filtration pressureGRFOliguria, anuria
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Section 2 Pathogenesis RBF1 Net filtration pressure BP < 60mmHg CO RBF BP (50-70mmHg) GFR (1/2 2/3) BP(40mmHg) GFR = 0Urinary obstruction intracapsular pressure
1 Glomerular factor
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2renal vessels constriction RBF sympathetic nerve Shock RAS prostaglandinkallikrein - kinin syetem ANP NO
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3 swelling endothelial cell ischemia Na+ - K+ - ATPase free radical endothelial cellular injury 4alteration of renal hemorheology fibrinogen Blood viscosity RBC PLT WBC
renal DIC
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Glomerular lesion filtration surface area Glomerular permselectivity GFR
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2 Tubular factortuble obstruction GFRpassive backflow GFR
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1 1 1 + ()
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(2) PLT GFR
2
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3AngADH GFR
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2 1 ATP ATP Na+ - K+ - ATPase Ca2+ - ATPase
Na+H2O Ca2+
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2(FR) (GSH) FR FR3GSH 4 Ca2+ A2
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5 ATP 6
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Section 3 Clinical Course and manifestation1 oliguria phasedaysweeks (1)features of urine urine volumeoliguria400ml/dor anuria100ml/d S.G.1.0101.020 Na+ tubular reabsorption dysfunction urine sediment:erythrocytes, casts, proteinuriaoliguric ARF
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(2) water toxication oliguriaCatabolism Transfuse fluidFluid retentionHypervolemic hyponatremiaCell edema
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(3) Hyperkalemia most serious Urinary excretion of K+Tissue destructionMetabolic acidosisTransfuse non-fresh blood, high K+ diethyponatremiaexchange of K+and Na+HyperkalemiaMovement of K+ from cells into ECF
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(4) Metabolic acidosis grogressive,difficult to correctGFR excretion of acid productionSecretion of HNH3 , reabsorption of HCO3Catabolism acid productionMetabolic acidosisHyperkalemia
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(5) Azotemia (NPN>40 mg/dl)Excretion of protein metaboliteProtein catabolism
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2 diuresis phase12W Mechanism
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manifestation polyuria>400 ml/dEarly stage Hyperkalemia, Azotemia , Metabolic acidosis Late stagedehydration, hypokalemia, hyponatremia, infection.3 recovery phase
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Nonoliguric ARFFeaures
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Section 4 Treatment Principle of ARF1. Treat the cause; 2. Rescue actively. .
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11959344138395 60/120/85/54mmHg 8.6mmol/L128mmol/L,100mmol/L, 1.98mmol/L2.33mmol/L, 37.12mmol/L,804.44mol/LpH7.17, PCO224.5mmHg, HCO3-8.6mmol/L, SBE -18.3mmol/LT
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Chronic Renal Failureetiological factors destruct nephronDysfunction of excretion and endocrine waste product , acid-base and electrolyte disorders dysfunction of endocrine Section 1 Conception
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Section 2 Causes of CRFRenal diseases chronic glomerulonephritis et alVascular disordersdiabetes mellitushypertensive diseasePeriarteritis nodosa, et alUrinary tract obstructionurinary calculusprostatic hyperplasia et al
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Section 3 Clinical Course of CRFcompensatory stage Renal insufficiency stage Renal failure stage Uremia stage
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GFRml/minBUN(mmol/L)Cr(umol/L)>50
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Section 4 PathogenesisIntact nephron hypothesisGlomerular hyperfiltration hypothesisTrade-off hypothesisTubulointerstitial injury
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Intact nephron hypothesis
causesProgressive reduction in the number of nephronsDestroy nephron persistentlyRenal compensation insufficiencyRenal failure
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Glomerular hyperfiltration hypothesisCompensatory glomerular hyperfiltration GlomerulosclerosisRenal failure
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Trade-off hypothesisGFR(P)()(PTH)()()
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() GFR PTH
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renal tubule -interstitial fibrosis
- Section 5 Changes of Function and Metabolism1 characteristics of urine volumenocturiapolyuria>2000ml/dor oliguria(
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1.035
1.020
1.012
1.008
1.002
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2 acid-base and electrolyte disorders (1)fluidpulmonary and cerebral edemaheart failuredehydration(2)NahyponatremiaHypernatremia(3) Khypokalemia or hyperkalemiaK+ diet emesisdiuretic(excrete K +)K+ oliguriaPotassium-sparing diureticacidosiscatabolism , hemolysisintake K +
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(4) Ca P P early stage : compensationPTH late stage: nephron bone dissolveCa P Vit D calcium phosphateToxic substance damage intestinal tract intake(5) Acidosis carbonic anhydrase NH3 H+ Absorption of intestine Ca
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3 azotemia (NPN>28.6mmol/L)BUN is not parallel to renal functionPlasma creatinine endogenous creatinine clearance rate ----CCR=Ucr VuPcr
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4 renal hypertension(1) Fluid and sodium retention(2) renin(3) kininPGE2
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5 hemorrhagic tendencyToxic substance inhibite the function of plateletPF3
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(1) EPO(2) bone marrow(3)bleeding(4) Erythrocyte life span(5)Fe and Folic acid deficiency6Al7 Renal anemia
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5 renal osteodystrophyD3
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(2)Vit D3 (4)Al (1)P Ca and secondary hyperparathyroidism(3) acidosisbone mineral lysisdecalcification, VitD3 absorption of intestine Ca
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GFR1,25(OH)2D3 PTH
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End-stage renal failureuremiaARFCRFToxinIntoxicationsymptom
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source 1. Metabolite 2. Ectogenesis toxin 3. Ectogenesis toxin metabolite 4. Normal activity materialUremia toxin
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common urea, guanidine, amines and phenolmiddle moleculesPTHAlUremia toxin
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change of function and metabolism
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Treatment principle
1treatment of the primary disease 2 dialysis therapy 3 renal transplantation
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35201 6104-52000ml/BP146/100mmHgHb40-70g/LRBC1.3-1.761012/L+RBCWBC5-7/HP32500-3500ml/1.01010 T37R20/P120/BP150/100mmHgRBC1.49 1012/LHb47g/LWBC9.6 109/L1.9mmol/L1.3mmol/L+RBC10-15/HpWBC0-2/Hp0-2/Hp2-3/LPX
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parenchymal