低钾血症

null低钾血症 低钾血症 一、钾的生理一、钾的生理null K+ Balance DiagramLungsIntercellularIntracellularKidneysLost in urinePlasma Normal Values: Major Functions:MouthStomachSmall IntestineLarge IntestineLost in FecesIngestedLost in sweatK+3.5-5.0 mEq/LMaintains intracellular osmolarity, controls resting potential of nerve and 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; inhibited by digitalis, beta blockersPassive diffusion K+/H+ exchangeRepolarization (exercise, seizures)Reabsorbed in proximal tubule and loop of HenleK+/H+ exchangenullK+ 3.5-5.5 mEq/L, Total: 60 mEqK+ channelNa+K+K+Na+Na-K ATPaseNa-K ATPase+++++++_ _ _ _ _ _ _ K+Distribution of potassium K+ 150 mEq/L, Total: 4000 mEq null1、Factors that modify transcellular K+ distribution（钾的肾外调节）AlkalosisGlucagonAcidosisa-adrenergicInsulinb-adrenergicCELL K+nullPotassium Homeostasis2、肾脏的调节2、肾脏的调节血钾在肾小球自由滤过 约50-55%在近端肾小管重吸收 约30-35%在髓袢重吸收 远端小管和集合管泌钾nullRenal Handling of K+ in PCTCl-X-nullReabsorption of Sodium Chloride — Lessons from the Chloride Channels, NEJM,2004,350(13):1282Renal Handling of K+ in TALnullK reabsorption by H-K exchanger in intercalated cellsK secretion by Na-K exchanger in Principal cellsRenal Handling of K+ in DCT and CT二、引起低钾血症的原因二、引起低钾血症的原因 Insufficient potassium intake: Deficient dietary intake Transcellular shift of K (no depletion): Hypokalaemic periodic paralysis Thyrotoxic periodic paralysis Barium poisoning Alkalosis Insulin excessnull Potassium depletion: Extra-renal losses: (1) Diarrhea (2) Rectal villous adenoma (3) Fistulas, Ureterosigmoidostomy (4) Laxative abuse Renal losses: (1) Excessive mineralocorticoids (primary& secondary aldosteronism, licorice，ingestion, glucocorticoid excess) (2) Renal tubular diseases (RTAs,leukaemia, Liddle’s syndrome,antibiotics, carbonic anhydrase inhibitors) (3) Diuretics (4) Magnesium depletion 三、低钾血症的诊断思路三、低钾血症的诊断思路nullDifferential Diagnosis of HypokalemiaHypokalemiaMetabolic alkalosisHypertensionGI wastingYNUrine KUrine ClNHighLowHighPlasma reninLaxativesRenal wastingDiureticsBartter/Gitelman synUrine Ca/CrCushing synPlasma AldoHyperaldosteronismYHighHighNormalLowLowHighLowBartter’s synGitelman’s synInsulin-adrenergichyperthyroidismPeriodic Hypok- alemic Paralysisnull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>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nullThank you！Barium poisoningBarium poisoning抑制钾在集合管管腔侧的传导Thyrotoxic periodic paralysisThyrotoxic periodic paralysis作用在细胞的Na－K-ATPase上，促进能量代谢和物质代谢 引起严重的恶心、呕吐，最终导致电解质紊乱低镁血症低镁血症40％的低镁血症患者伴有低钾血症 原发性钾缺失时，肌肉的细胞内镁缺失而无低镁血症