低钾血症学习.pptx

,#,单击此处编辑母版标题样式,会计学,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,1,低钾血症学习,PPT,第,1,页,/,共,20,页,K,+,Balance Diagram,Lungs,Intercellular,Intracellular,Kidneys,Lost in urine,Plasma,Normal Values:,Major Functions:,Mouth,Stomach,Small,Intestine,Large,Intestine,Lost in,Feces,Ingested,Lost in sweat,K,+,3.5-5.0,mEq/L,Maintains intracellular osmolarity,controls resting potential of nerve and muscle,exchanged for H,+,to correct pH,exchanged for Na,+,when distal tubules reabsorb Na,+,Passive diffusion,Active transport,Filtered into glomerulus,depending on blood pressure,and GFR,Secreted by,aldosterone-controlled,Na,+,/K,+,ATPase,in distal tubule,Na,+,/K,+,ATPase,activated by insulin,epinephrine;inhibited,by digitalis,beta blockers,Passive diffusion,K,+,/H,+,exchange,Repolarization,(,exercise,seizures),Reabsorbed in proximal tubule,and loop of Henle,K,+,/H,+,exchange,第,2,页,/,共,20,页,K,+,3.5-5.5,mEq/L,Total:60 mEq,K,+,channel,Na,+,K,+,K,+,Na,+,Na-K ATPase,Na-K ATPase,+,+,+,+,+,+,+,_,_,_,_,_,_,_,K,+,Distribution of potassium,K,+,150 mEq/L,Total:4000 mEq,第,3,页,/,共,20,页,1,、,Factors that modify transcellular K,+,distribution,（钾的肾外调节）,Modifying,factors,Acid-base status,Blood PH(,Acidosis/,alkalosis,),Plasma HCO,3,-,(,Low,/,high,),Pancreatic hormone,Insulin/,Glucagon,Catecholamine,-adrenergic/,-adrenergic,Alkalosis,Glucagon,Acidosis,a,-adrenergic,Insulin,b,-adrenergic,CELL K+,第,4,页,/,共,20,页,Potassium Homeostasis,第,5,页,/,共,20,页,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,第,6,页,/,共,20,页,Renal Handling of K,+,in PCT,K,+,(Paracellular route),K,+,Cl,-,X,-,第,7,页,/,共,20,页,Reabsorption of Sodium Chloride Lessons from the Chloride Channels,NEJM,2004,350(13):1282,Renal Handling of K,+,in,TAL,CaSR,第,8,页,/,共,20,页,K reabsorption by,H-K exchanger in intercalated cells,K secretion by,Na,-K exchanger in Principal cells,Renal Handling of K,+,in DCT and CT,第,9,页,/,共,20,页,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 excess,第,10,页,/,共,20,页,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,Liddles syndrome,antibiotics,carbonic anhydrase inhibitors),(3)Diuretics,(4),Magnesium depletion,第,11,页,/,共,20,页,三、低钾血症的诊断思路,第,12,页,/,共,20,页,Differential Diagnosis of Hypokalemia,Hypokalemia,Metabolic alkalosis,Hypertension,GI wasting,Y,N,Urine K,Urine Cl,Insufficent intake,Intracellular transition,RTA,N,High,Low,High,Plasma renin,Laxatives,Renal wasting,Diuretics,Bartter/Gitelman syn,Urine Ca/Cr,Diuretics,RAS,Renin secret,Cushing syn,Plasma Aldo,Hyperaldosteronism,Y,High,High,Normal,Low,Low,Congenital adrenal hyperplasia,Chronic liguorice ingestion,Apparent mineralocorticoid excess,Liddles syn,Carbenoxolone,High,Low,Bartters syn,Gitelmans syn,Insulin,-adrenergic,hyperthyroidism,Periodic Hypok-,alemic Paralysis,第,13,页,/,共,20,页,Barium poisoning,约50-55%在近端肾小管重吸收,Renal wasting,Intercellular,Reabsorbed in proximal tubule,Extra-renal losses:,depending on blood pressure,Lost in sweat,K+/H+exchange,Pancreatic hormone,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,、,CAH,Cushing,、,ACTH,分泌过多,第,14,页,/,共,20,页,Metabolic alkalosis,(1)Diarrhea,Barium poisoning,Transcellular shift of K(no depletion):,(1)Diarrhea,Secreted by,肾小管酸中毒、糖尿病酸中毒、乙酰唑胺,b-adrenergic,Insulin/Glucagon,Lost in urine,Na-K ATPase,Lost in urine,Maintains intracellular osmolarity,controls resting potential of nerve and muscle,exchanged for H+to correct pH,exchanged for Na+when distal tubules reabsorb Na+,原发性钾缺失时，肌肉的细胞内镁缺失而无低镁血症,b-adrenergic,-adrenergic/-adrenergic,Urine Ca/Cr,Thank you,！,第,15,页,/,共,20,页,Barium poisoning,抑制钾在集合管管腔侧的传导,第,16,页,/,共,20,页,Thyrotoxic 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,第,17,页,/,共,20,页,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,第,18,页,/,共,20,页,1,、,Factors that modify transcellular K,+,distribution,（钾的肾外调节）,Modifying,factors,Acid-base status,Blood PH(,Acidosis/,alkalosis,),Plasma HCO,3,-,(,Low,/,high,),Pancreatic hormone,Insulin/,Glucagon,Catecholamine,-adrenergic/,-adrenergic,Alkalosis,Glucagon,Acidosis,a,-adrenergic,Insulin,b,-adrenergic,CELL K+,第,19,页,/,共,20,页,Potassium Homeostasis,第,20,页,/,共,20,页,