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Disorders of potassium metabolism Yu-Hong Jia, Ph.D Department of pathophysiology Dalian medical university
Potassium function ,[object Object],[object Object],[object Object]
Ⅰ . Normal potassium metabolism
K + Na + ATPase K + H + K +  channel 140-160 mmol/L 4.2±0.3mmol/L 50-200mmol/day  K +  ingestion Kidney colon skin (90%) insulin β-adrenergic agonist ECF [K + ] K + : 50-55mmol/kg B.W toxin (Ba) acid-base state Pump-leak
①  free filtration   ②  reabsorption (90% of  filtered potassium) ③ secretion or reabsorption (in normal diet, secretion is major) K + K + K + Proximal tubule &Henle’s loop Distal tubule & Collecting duct
Three elements for achieving potassium secretion: 1. Na + -K + -ATPase on basolateral membrane 2. Permeability of luminal membrane to K+ 3. Electrochemical gradient from blood to tubular lumen ATPase Na + K + K +  channel K + Principal cell Basolateral  membrane luminal membrane peritubular interstitial  tubular lumen K +
factors affecting renal secretion of K + ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],↑ ↑ ↑ K +  secretion ↑ K +  secretion ↑ K +  secretion
K + Na + ATPase K + H + K +  channel 140-160 mmol/L 4.2±0.3mmol/L 50-200mmol K +  ingestion Kidney colon skin (90%) insulin β-adrenergic agonist ECF [K + ] 50-55mmol/kg B.W ADS ECF K +  concentration Urinary flow rate acid-base state toxin drug acid-base state
Ⅱ . Disorders of potassium metabolism
Classification of Disorders of potassium metabolism: ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],hypokalemia,  hyperkalemia Potassium deficit Hypokalemia, normal serum potassium
Hypokalemia: etiology and pathogenesis (3). ↑K +  excretion ,[object Object],[object Object],(1). ↓K +  intake (2). ↑K+ shift from ECF to ICF ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Familial hypokalemic periodic paralysis ,[object Object],[object Object],[object Object]
Excessive renal loss of potassium ,[object Object],[object Object],[object Object],[object Object],[object Object],K + H + alkalosis ↑ Urinary flow rate ↓ ECF volume-> secondary ADS increase
Renal tubular acidosis (RTA) ,[object Object],[object Object],[object Object]
Hypokalemia: etiology and pathogenesis (3). ↑K +  excretion ,[object Object],[object Object],(1). ↓K +  intake (2). ↑K+ shift from ECF to ICF ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Use of certain diuretic agents, Primary and secondary aldosteronism Alkalosis, Renal tubular acidosis, Magnesium deficit
Excessive gastrointestinal loss of K +  — vomit, diarrhea, gastric suction ,[object Object],[object Object],[object Object]
Hypokalemia: etiology and pathogenesis (3). ↑K +  excretion ,[object Object],[object Object],(1). ↓K +  intake (2). ↑K+ shift from ECF to ICF ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Use of certain diuretic agents, Primary and secondary aldosteronism Alkalosis, Renal tubular acidosis, Magnesium deficit Vomit, dirrhea, gastric suction Heavy sweat in hot environment
Hyperkalemia: etiology and pathogenesis (3).  ↓ K +  excretion ,[object Object],(1).  ↑ K +  intake (2). ↑K+ shift from ICF to ECF ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Familial hyperkalemia periodic paralysis ,[object Object],[object Object]
2. Alterations of metabolism and function ,[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],Electrical gradient Chemical gradient K + 140-160mmmol/L 4.2±0.3mmol/L Resting membrane potential (RMP) Excitable cell ,[object Object],[object Object],- - - - - + + + + + Na + ATPase RMP ≈ ﹣ 59.5lg Intracellular K +  concentration extracellular K +  concentration
[object Object],is a wave of depolarization and repolarization that moves across a cell membrane ,[object Object],The critical value of depolarization that can provoke action potential.
 
hypokalemia ,[object Object],[object Object],[object Object],[object Object],[object Object],hyperkalemia
Irritability (excitability) ,[object Object],[object Object],[object Object],[object Object],[object Object],↑ -> ↓ ↓ ↓ hyperkalemia ↓ ↑ ↑ hypokalemia irritability Difference (between RMP and threshold potential) RMP (negtive value) Neuromuscular cell
hypokalemia ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],hyperkalemia
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],↑ -> ↓ ↓ ↓ hyperkalemia ↑ ↓ ↓ hypokalemia irritability Difference (between RMP and threshold potential) RMP (negtive value) heart
[object Object],[object Object],[object Object],[object Object],↓ ↓ ↓ hyperkalemia ↓ ↓ ↓ hypokalemia conductivity Difference (between RMP and threshold potential) RMP (negtive value) heart
[object Object],[object Object],↓ ↓ hyperkalemia ↑ ↑ hypokalemia contractility Ca 2+  inward flow heart
[object Object],[object Object],[object Object],[object Object],↓ ↓ ↑ hyperkalemia ↑ ↑ ↓ hypokalemia automaticity Net inward current Membrane Permeability to K + heart
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Comparation between action potential and normal electrocardiogram ,[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],ventricles repolarize phase 3 accelerate Peaking of T wave ventricles repolarize phase 3 prolong ventricles repolarize phase 2 inward calcium current accelerate Depressed S-T segment Flattened T wave
hypokalemia ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],hyperkalemia ↓[K + ] ECF H + -K +  exchange ↓[H + ] ECF ↑[H + ] ICF ↑Renal excretion of H +   aciduria K +  shift out of cells H +  shift into cells alkalosis (Paradoxical aciduria) ↑[K + ] ECF H + -K +  exchange ↑[H + ] ECF ↓[H + ] ICF ↓Renal excretion of H +   Alkaline urine K +  shift into cells H +  shift out of cells acidosis (Paradoxical alkaline urine)
hypokalemia ,[object Object],[object Object],[object Object]
 
 

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Potassium Imbalance

  • 1. Disorders of potassium metabolism Yu-Hong Jia, Ph.D Department of pathophysiology Dalian medical university
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  • 3. Ⅰ . Normal potassium metabolism
  • 4. K + Na + ATPase K + H + K + channel 140-160 mmol/L 4.2±0.3mmol/L 50-200mmol/day K + ingestion Kidney colon skin (90%) insulin β-adrenergic agonist ECF [K + ] K + : 50-55mmol/kg B.W toxin (Ba) acid-base state Pump-leak
  • 5. ① free filtration ② reabsorption (90% of filtered potassium) ③ secretion or reabsorption (in normal diet, secretion is major) K + K + K + Proximal tubule &Henle’s loop Distal tubule & Collecting duct
  • 6. Three elements for achieving potassium secretion: 1. Na + -K + -ATPase on basolateral membrane 2. Permeability of luminal membrane to K+ 3. Electrochemical gradient from blood to tubular lumen ATPase Na + K + K + channel K + Principal cell Basolateral membrane luminal membrane peritubular interstitial tubular lumen K +
  • 7.
  • 8. K + Na + ATPase K + H + K + channel 140-160 mmol/L 4.2±0.3mmol/L 50-200mmol K + ingestion Kidney colon skin (90%) insulin β-adrenergic agonist ECF [K + ] 50-55mmol/kg B.W ADS ECF K + concentration Urinary flow rate acid-base state toxin drug acid-base state
  • 9. Ⅱ . Disorders of potassium metabolism
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