potassium imbalance

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pathophysiology

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  • 1. Disorders of potassium metabolism Yu-Hong Jia, Ph.D Department of pathophysiology Dalian medical university
  • 2. Potassium function
    • Participates in many metabolic processes, e.g. regulation of protein and glycogen synthesis.
    • Maintain osmotic and acid-base balance between intra- and extra- cell.
    • Maintain resting membrane potential (RMP) of cellular membrane.
  • 3. . Normal potassium metabolism
  • 4. K + Na + ATPase K + H + K + channel 140-160 mmol/L 4.20.3mmol/L 50-200mmol/day K + ingestion Kidney colon skin (90%) insulin -adrenergic agonist ECF [K + ] K + : 50-55mmol/kg B.W toxin (Ba) acid-base state Pump-leak
  • 5. free filtration reabsorption (90% of filtered potassium) secretion or reabsorption (in normal diet, secretion is major) K + K + K + Proximal tubule &Henles 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. factors affecting renal secretion of K +
    • the activity of Na + -K + -ATPase in principle cells;
    • luminal membrane permeability to K +
    • the activity of Na + -K + -ATPase
    • luminal membrane permeability to potassium
    • K + concentration gradient between interstitial fluid and tubular cell ->K + counterflow into the interstitial fluid
    • urinary flow rate-> rapidly remove the K + secrected by tubular cells-> the K + concentration in tubular lunmen->K + concentration gradient across luminal membrane-> K + secretion
    • Increased H + concentration inhibits Na + -K + -ATPase in principle cells -> K + secretion, on the contrary, H + concentration->K + secretion
    • aldosterone ADS
    • Extracellular K + concentration
    • Urinary flow rate
    • Acid-base state
    K + secretion K + secretion K + secretion
  • 8. K + Na + ATPase K + H + K + channel 140-160 mmol/L 4.20.3mmol/L 50-200mmol K + ingestion Kidney colon skin (90%) insulin -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. . Disorders of potassium metabolism
  • 10. Classification of Disorders of potassium metabolism:
    • Hypokalemia
      • Serum potassium concentration 5.5mmol/L
    • 1. Etiology and pathogenesei
    • (1). Potassium intake
    • (2). Potassium shift from intracellular to extracellular fluid
    • (3). potassium excretion
    hypokalemia, hyperkalemia Potassium deficit Hypokalemia, normal serum potassium
  • 11. Hypokalemia: etiology and pathogenesis (3). K + excretion
    • Unable to eat, i.e. coma, digestive tract obstruction
    • Fasting, i.e. after operation of digestive tract
    (1). K + intake (2). K+ shift from ECF to ICF
    • Use of some drug, i.e. insulin, -adrenergic agonist
    • Toxin poisoning, i.e. barium
    • Alkalosis
    • Familial hypokalemic periodic paralysis
    • Via kidney
    • Via gastrointestinal tract
    • Via skin
  • 12. Familial hypokalemic periodic paralysis
    • A rare inherited disorder with autosomal dominant trait.
    • Characteristic feature: recurrent episodes of muscle weakness accompanied with hypokalemia, automatically relieved without treatment.
    • Mechanism: related with mutation of genes coding for skeletal muscle L-type calcium channel, sodium channel subuint, or potassium channel accessory subunit.
  • 13. Excessive renal loss of potassium
    • Use of certain diuretic agents i.e. acetazolamide and furosemide.
    • Primary and secondary aldosteronism
    • Alkalosis
    • Renal tubular acidosis
    • Magnesium deficit
    K + H + alkalosis Urinary flow rate ECF volume-> secondary ADS increase
  • 14. Renal tubular acidosis (RTA)
    • Acidosis caused by renal tubular dysfunction.
      • Type RTA: distal renal tubular acidosis, caused by reduced H + secretion in the distal nephron
      • Type RTA: proximal renal tubular acidosis, caused by impaired reabsorption of HCO 3 - in the proximal tubule.
  • 15. Hypokalemia: etiology and pathogenesis (3). K + excretion
    • Unable to eat, i.e. coma, digestive tract obstruction
    • Fasting, i.e. after operation of digestive tract
    (1). K + intake (2). K+ shift from ECF to ICF
    • Use of some drug, i.e. insulin, -adrenergic agonist
    • Toxin poisoning, i.e. barium
    • Alkalosis
    • Familial hypokalemic periodic paralysis
    • Via kidney
    • Via gastrointestinal tract
    • Via skin
    Use of certain diuretic agents, Primary and secondary aldosteronism Alkalosis, Renal tubular acidosis, Magnesium deficit
  • 16. Excessive gastrointestinal loss of K + vomit, diarrhea, gastric suction
    • Direct K + loss through gastrointestinal juice
    • Gastrointestinal juice loss-> extracellular fluid volume decrease-> ADS secretion increase-> renal excretion of K + increase
    • vomiting-> gastric acid (HCl) loss -> alkalosis is resulted in ->K + shift into cells via H + -K + exchange and increased renal excretion of K +
  • 17. Hypokalemia: etiology and pathogenesis (3). K + excretion
    • Unable to eat, i.e. coma, digestive tract obstruction
    • Fasting, i.e. after operation of digestive tract
    (1). K + intake (2). K+ shift from ECF to ICF
    • Use of some drug, i.e. insulin, -adrenergic agonist
    • Toxin poisoning, i.e. barium
    • Alkalosis
    • Familial hypokalemic periodic paralysis
    • Via kidney
    • Via gastrointestinal tract
    • Via skin
    Use of certain diuretic agents, Primary and secondary aldosteronism Alkalosis, Renal tubular acidosis, Magnesium deficit Vomit, dirrhea, gastric suction Heavy sweat in hot environment
  • 18. Hyperkalemia: etiology and pathogenesis (3). K + excretion
    • Rapid intravenous infusion of KCl or potassium salt of penicillin
    (1). K + intake (2). K+ shift from ICF to ECF
    • Deficiency of insulin, i.e. diabetes mellitus
    • -adrenergic antagonist
    • acidosis
    • Cell injury, i.e. trauma, hemolysis
    • Familial hyperkalemic periodic paralysis
    • Glomerular filtration rate decrease, i.e. oliguric stage of renal failure
    • Renal tubular secretion of K + decrease
      • ADS, i.e. adrenal cortical insufficiency ( Addison disease)
      • acidosis
  • 19. Familial hyperkalem