Potassium disorders
Potassium Disorders
Preface: normal metabolism of potassium 1. normal serum potassium: 3.5-5.5mmol/L 2. distribution of potassium ICF: 98%(muscle: 75%) ECF: 20o 3. balance between intra-and extracellular k+ normal: 15 h 4. intake and loss of potassium intake: food: loss: urine: feces: sweat
Preface: normal metabolism of potassium 1. normal serum potassium: 3.5-5.5mmol/L 2. distribution of potassium ICF:98% (muscle:75%) ECF: 2% 3. balance between intra- and extracellular K+ normal: 15 h 4. intake and loss of potassium intake: food; loss: urine; feces; sweat
5. influencing facter of potassium homeostasis acidosis alkalosis porla serum insulin serum damage of cells IK+↑ADS IK↓ catabolism anabolism distal flow rate↓ distal flow rate t
5. influencing facter of potassium homeostasis acidosis alkalosis hypoxia serum insulin serum damage of cells [K+ ] ADS [K+ ] catabolism anabolism distal flow rate distal flow rate
I. Hypokalemia concept: serum potassium <3.5mmol/L 1. cause and pathogenesis ① intake I fast alkalosis injection of insulin 2 move into Barium poisoning cels hypokalemic periodic yI pe paralysis
I. Hypokalemia concept: serum potassium＜3.5mmol/L 1. cause and pathogenesis ① intake fast alkalosis injection of insulin ② move into Barium poisoning cells hypokalemic periodic paralysis
GI: vomiting; diarrhea; Gastrointestinal suction Skin: excessive sweats furosemide diuretic ③ losses diamox diuretic phase ofARF ren: pyelonephritis primary hyperaldosteronism lack of magnesium renal tubular acidosis
GI: vomiting; diarrhea; Gastrointestinal suction Skin: excessive sweats furosemide diuretic ③ losses diamox diuretic phase of ARF ren: pyelonephritis primary hyperaldosteronism lack of magnesium renal tubular acidosis
3. effect on bod 1) nerves and muscles excitability I my serums↓-30mv AP -60mv TP(Et) -90mv +二RP(Em) hyperpolarization
3. effect on body 1) nerves and muscles excitability 0 mv serum[K+ ] -30mv AP -60mv TP(Et) -90mv RP(Em) hyperpolarization
2) heart arrhythmia 0 mv serum+↓-30my 60mv 90mv depolarization
2) heart arrhythmia 0 mv serum[K+ ] -30mv -60mv -90mv depolarization
Excitability: [KlECF I-K permeability I- depolarization repolarization excitability ECGT wave↓ Conductivity: RP|-0 phase ofAP↓ conductivity I conductive block unidirectional block ECG P-R t
Excitability: [K+ ]ECF K+ permeability depolarization repolarization excitability ECG T wave Conductivity: RP 0 phase of AP conductivity conductive block unidirectional block ECG P-R
Autorhythmicity: T Contractility: acute; chronic I ③ Ren polyuria( sensitivity ofADH↓) 4 GI smooth muscles (hyperpolarization) 5 acid-base balance(metabolic alkalosis) 4. principles of treatment supply potassiun口服最好。原则:见尿补钾 血浓缩 anurla不排钾 补钾速度:10-20mmo/h 可能有酸中毒补钾浓度:20-40 mmolL
Autorhythmicity: Contractility: acute ; chronic ③ Ren polyuria (sensitivity of ADH ) ④ GI smooth muscles (hyperpolarization) ⑤ acid-base balance (metabolic alkalosis) 4. principles of treatment supply potassium 口服最好。原则：见尿补钾。 血浓缩 anuria 不排钾 补钾速度：10-20mmol/h 可能有酸中毒 补钾浓度：20-40mmol/L
病例8:患者,女性,22岁,因结核性腹膜炎和肠梗 阻进行手术,术后行持续胃肠减压7天,共抽吸液 体200ml。平均每天静脉补液(5%葡萄糖液) 2500m1。尿量2000m1。术后2周,患者精神不振 全身乏力,面无表情,嗜睡,食欲堿低·腱反射迟 钝 实验室检耷:血K+2.4mo1/L,血Na+140mmo1/L, 血C1103mol/I 辅助检查:ECG显示,Ⅱ、aⅦF、Ⅵ1、V5导联ST段 下降,aⅦF导联T波双向,V3有u波。 立即开始每日以KC1加入5%葡萄糖滴注,四天后 血K升至4.6mmol/L,上述表现恢复正常
病例8：患者，女性，22岁，因结核性腹膜炎和肠梗 阻进行手术，术后行持续胃肠减压7天，共抽吸液 体2200ml。平均每天静脉补液（5%葡萄糖液） 2500ml。尿量2000ml。术后2周，患者精神不振， 全身乏力，面无表情，嗜睡，食欲减低，腱反射迟 钝。 实验室检查：血K + 2.4mmol/L,血Na+140mmol/L， 血Cl- 103mmol/L。 辅助检查：ECG显示，Ⅱ、aVF、V1、V5导联ST段 下降，aVF导联T波双向，V3 有u波。 立即开始每日以KCl加入5%葡萄糖滴注，四天后 血K +升至 4.6mmol/L，上述表现恢复正常
