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1、低钾血症一、钾的生理K K+ +Balance Diagram Balance DiagramLungsIntercellularIntracellularKidneysLost in urinePlasmaNormal Values:Major Functions:MouthStomachSmall IntestineLarge IntestineLost in FecesIngestedLost in sweatK+3.5-5.0 mEq/LMaintains intracellular osmolarity, controls resting potential of nerve and
2、 muscle, exchanged for H+ to correct pH, exchanged for Na+ when distal tubules reabsorb Na+ Passive diffusionActive transportFiltered into glomerulus, depending on blood pressure and GFRSecreted by aldosterone- controlled Na+/K+ ATPase in distal tubuleNa+/K+ ATPase activated by insulin, epinephrine;
3、 inhibited by digitalis, beta blockersPassive diffusion K+/H+ exchangeRepolarization (exercise, seizures)Reabsorbed in proximal tubuleand loop of HenleK+/H+ exchangeK+ 3.5-5.5 mEq/L, Total: 60 , Total: 60 mEqmEqK+ channelNa+K+K+Na+Na-K ATPaseNa-K ATPase+ + +_ _ _ _ _ _ _ K+Distribution of Distributi
4、on of potassium potassium K+ 150 mEq/L, Total: 4000 Total: 4000 mEqmEq1 1、Factors that modify Factors that modify transcellulartranscellular K K+ +distributiondistribution（钾的肾外钾的肾外调节）调节）Modifying Modifying factorsfactorsAcid-base statusBlood PH( Acidosis/alkalosis )Plasma HCO3- ( Low/high ) Pancreat
5、ic hormoneInsulin/GlucagonCatecholamine-adrenergic/ -adrenergicAlkalosisAlkalosisGlucagonAcidosisa-adrenergicInsulinInsulinb b- -adrenergicadrenergicCELL K+Potassium Potassium HomeostasisHomeostasis2、肾脏的调节l血钾在肾小球自由滤过 l约50-55%在近端肾小管重吸收 l约30-35%在髓袢重吸收 l远端小管和集合管泌钾Renal Handling of KRenal Handling of K+
6、 +in in PCTPCTK+(Paracellular route)K+Cl-X-Reabsorption of Sodium Chloride Lessons from the Chloride Channels, NEJM,2004,350(13):1282Renal Handling of KRenal Handling of K+ +in in TALTALCaSRK reabsorption by H-K exchanger in intercalated cellsK secretion by Na-K exchanger in Principal cellsRenal Han
7、dling of KRenal Handling of K+ +in DCT and CT in DCT and CT二、引起低钾血症的原因 Insufficient potassium intake: Deficient dietary intakeTranscellular shift of K (no depletion): v Hypokalaemic periodic paralysis v Thyrotoxic periodic paralysis v Barium poisoning v Alkalosis v Insulin excess Potassium depletion
8、: vExtra-renal losses:(1) Diarrhea(2) Rectal villous adenoma(3) Fistulas, Ureterosigmoidostomy(4) Laxative abuse v Renal losses:(1) Excessive mineralocorticoids (primary& secondary aldosteronism, licorice，ingestion, glucocorticoid excess)(2) Renal tubular diseases (RTAs,leukaemia, Liddles syndrome,a
9、ntibiotics, carbonic anhydrase inhibitors)(3) Diuretics(4) Magnesium depletion三、低钾血症的诊断思路Differential Diagnosis of Differential Diagnosis of HypokalemiaHypokalemiaHypokalemiaMetabolic alkalosisHypertensionGI wastingYNUrine KUrine ClInsufficent intakeIntracellular transitionRTANHighLowHigh Plasma ren
10、in LaxativesRenal wasting Diuretics Bartter/Gitelman synUrine Ca/CrDiuretics RAS Renin secretCushing synPlasma AldoHyperaldosteronismYHighHighNormalLowLowCongenital adrenal hyperplasia Chronic liguorice ingestion Apparent mineralocorticoid excessLiddles syn CarbenoxoloneHighLowBartters synGitelmans
11、synInsulin-adrenergichyperthyroidismPeriodic Hypok- alemic Paralysis低血钾测尿钾尿钾正常高尿钾摄入少或吸收不良胃肠道丢失测PH碱中毒不定酸中毒测尿氯20mmol/L测血压正常高血压测Ald 高低低肾素高肾素低肾素正常或高肾素肾间质小管 疾病、低血镁 、锂盐肾小管酸中毒、 糖尿病酸中毒、 乙酰唑胺呕吐、腹泻、 高碳酸血症原醛利尿药、Batter或 Gitelman、低血 钾软病肾素瘤、肾 动脉狭窄、 恶性高血压Liddle、 CAHCushing、ACTH 分泌过多Thank you！Barium poisoningl抑制钾在集合管管腔侧的传导Thyrotoxic periodic paralysisl作用在细胞的NaK-ATPase上，促进 能量代谢和物质代谢 l引起严重的恶心、呕吐，最终导致电解 质紊乱低镁血症l40的低镁血症患者伴有低钾血症 l原发性钾缺失时，肌肉的细胞内镁缺失 而无低镁血症
