《低钾血症》.pptVIP

低钾血症 一、钾的生理 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 二、引起低钾血症的原因 Insufficient potassium intake: Deficient dietary intake Transcellular shift of K (no depletion): 三、低钾血症的诊断思路 Barium poisoning 抑制钾在集合管管腔侧的传导 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 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 * * 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 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 1、Factors that modify transcellular K+ distribution（钾的肾外调节） Catecholamine ?-adrenergic/ ?-adrenergic Pancreatic hormone Insulin/Glucagon Acid-base status Blood PH( Acidosis/alkalosis ) Plasma HCO3- ( Low/high ) Modifying factors Alkalosis Glucagon Acidosis a-adrenergic Insulin b-adrenergic CELL K+ Potassium Homeostasis Renal Handling of K+ in PCT K+ (Paracellular route) K+ Cl- X- Reabsorption of Sodium Chloride — Lessons from the Chloride Channels, NEJM,2004,350(13):1282 Renal Handling of K+ in TAL CaSR 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 Hypokala