potassium homeostasis and its renal handling

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  • 1. Addis Ababa UniversityCollege of Health ScienceDepartment of Medical Physiology
    Presentation on Potassium Homeostasis and its Renal Handling
    By Girmay F
    10/8/2011
    1
  • 2. presentation out line
    1.Objectives
    2. Introduction
    3. Physiological roles of potassium
    4. Potassium homeostasis
    4.1 Hormonal control of K+ homeostasis
    4.2 Miscellaneous factors
    5.Renal handling of potassium
    5.1 K+ secretion by the principal cells
    5.2 regulation of K+ excretion
    6. Clinical correlations
    • Hyperkalemia
    • 3. Hypokalemia
    7. References
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    Potassium homeostasis and its renal handling
  • 4. 1.Objectives
    At the end of this presentation students will able to:-
    Mention the major physiological role of potassium.
    Explain the main mechanisms of potassium homeostasis.
    Elaborate renal handling of potassium.
    Identify factors that affect potassium excretion.
    List the homeostatic disturbance of potassium.
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  • 5. 2.Introduction
    The total body stores are approximately 50 to 55 meq/kg.
    The main intracellular cation.
    98% located ICF,150 meq/L.
    2% located ECF,4meq/L.
    90% readily exchangeable
    10% non exchangeable
    Amount ingested = up to 100meq/d = 2.5 gm/d
    92% urinary excretion
    8% GIT excretion
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    Potassium homeostasis and its renal handling
  • 6. Introduction ..cont’d
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    Potassium homeostasis and its renal handling
  • 7. 3.Physiological roles of potassium
    1.Roles of intracellular K+:
    Cellular volume maintenance
    Intracellular pH regulation
    Cell enzyme function
    DNA/protein synthesis
    Cell growth
    2.Roles of transcellular K+ ratio:
    • Resting cell membrane potential
    • 8. Neuromuscular excitability
    • 9. Cardiac pacemaker rhythmicity
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    Potassium homeostasis and its renal handling
  • 10. 4.Potassium homeostasis
    1.Internal balance ( ICF and ECF K+ distribution)
    2. External balance ( Renal excretion of K+)
    1.Internal balance
    Physiological and pathological conditions can influence this process.
    • Hormones like insulin , catecholamines ,aldosterone
    • 11. Acid base imbalance
    • 12. Changes in osmolarity
    • 13. Exercise
    • 14. Cell lysis
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    Potassium homeostasis and its renal handling
  • 15. 4.1 Hormonal control of K+ homeostasis
    Insulin and beta 2agonsists shifts K+ to the cell, by increase the activity of Na+,K+-ATPase, the 1Na+-1K+-2Cl- symporter, and the Na+-Cl- symporter.
    Aldosterone acting on uptake of K+ into cells and altering urinary K+ excretion.
    Stimulation of α-adrenoceptors releases K+ from cells, especially in the liver.
    insulin and epinephrine act within a few minutes, aldosterone requires about an hour to stimulate uptake of K+ into cells.
    10/8/2011
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    Potassium homeostasis and its renal handling
  • 16. 10/8/2011
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    Potassium homeostasis and its renal handling
  • 17. 10
    Hormonal control of K+ homeostasis
  • 18. 4.2 Miscellaneous factors …..
    1.Acid base imbalance
    Metabolic acidosis increases the plasma [K+].
    Metabolic alkalosis decreases the plasma [K+] .
    2.Plasma osmolarity
    • Hyperosmolarity associated with hyperkalemia .
    • 19. A fall in plasma osmolality has the opposite effect.
    3.Cell lysis
    • Crush injury,burns,tumor lysis syndrome, rhabdomyolysis associated with destruction of cells and release of K+ to ECF.
    4. Exercise
    vigorous exercise, plasma [K+] may increase by 2.0 mEq/L.
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    Potassium homeostasis and its renal handling
  • 20. …………Cont’d
    Physiological: Keep Plasma [K+] Constant
    Epinephrine
    Insulin
    Aldosterone
    Pathophysiological: Displace Plasma [K+] from Normal
    Acid-base balance
    Plasma osmolality
    Cell lysis
    Exercise
    Drugs That Induce Hyperkalemia
    Dietary K+ supplements
    ACE inhibitors
    K+-sparing diuretics
    Heparin
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    Potassium homeostasis and its renal handling
  • 21. 5.Renal handling of potassium
    The PCT reabsorbs about 67% of the filtered K+ under most conditions by K+-H+ exchanger and K+-Cl- symport.
    20% of the filtered K+ is reabsorbed by the TALH.
    The distal tubule and collecting duct are able to reabsorb or secrete K+.
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  • 22. ……….cont’d
    The rate of K+ reabsorption or secretion by the distal tubule and collecting duct depends on a variety of hormones and factors.
    Most of the daily variations in potassium excretion is caused by changes in potassium secretion in the distal and cortical collecting tubules.
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  • 23. ……………cont’d
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  • 24. 5.1 K+ SECRETION BY PRINCIPAL CELLS
    Secretion from blood into the tubule lumen is a two-step process:
    1.uptake of K+ from blood across the basolateral membrane by Na+,K+-ATPase and
    2. diffusion of K+ from the cell into tubular fluid via K+ channels.
    • Three major factors that control the rate of K+ secretion by the distal tubule and the collecting duct
    The activity of Na+,K+-ATPase .
    The driving force (electrochemical gradient) for movement of K+ across the apical membrane.
    The permeability of the apical membrane to K+ .
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  • 25. ……..cont’d
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  • 26. ………….Cont’d
    Intercalated cells reabsorb K+ via an H+,K+-ATPase transport mechanism located in the apical membrane .
    This transporter mediates uptake of K+ in exchange for H+. This phenomena only occur during low potassium dietary intake.
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  • 27. 5.2 REGULATION OF K+ SECRETION ..
    1.Dietary K+
    A diet high in K+ increases K+ secretion .a diet low in K+ decreases K+ secretions.
    2. Aldosterone
    Increases K+ secretion.
    Hyperaldosteronism increases K+ secretion and causes hypokalemia .
    Hypoaldestronism decreases K+ secretion and causes hyperkalemia
    MOA
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  • 28. …………….cont’d
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  • 29. …..cont’d
    3.Acid–Base
    Acidosis decreases K+ secretion.
    Alkalosis increases K+ secretion
    Metabolic acidosis may either inhibit or stimulate excretion of K+ .
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  • 30. ………….cont’d
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  • 31. ………….Cont’d
    4.Flow of Tubular Fluid
    A rise in the flow of tubular fluid (e.g., with diuretic treatment, ECF volume expansion) stimulates secretion of K+ within minutes.
    A fall (e.g., ECF volume contraction caused by hemorrhage, severe vomiting, or diarrhea) reduces secretion of K+ by the distal tubule and collecting duct.
    MOA
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  • 32. ………….Cont’d
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  • 33. 10/8/2011
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    ……………..Cont’d
  • 34. 6.Clinical correlations
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    1.Hyperkalemia
    plasma concentration of K+ > 5.5 mEq / L
    Causes
    a. Reduced excretion- acute renal failure
    -potassium –sparing diuretics.
    b. Increased intake or release .
    -potassium supplements
    - Rhabdomyolysis
    -Hemolytic sates
  • 35. ………………..cont’d
    c. Trans cellular shifts of potassium
    • Acidosis
    • 36. Beta blockers ,cell destruction
    • 37. Insulin deficiency
    • 38. Addison’s disease
    • 39. Cell lysis
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  • 40. 28
    ……………….cont’d
    Clinical manifestation
    Early – hyperactive muscles , paresthesia
    Late - Muscle weakness, flaccid paralysis
    Dysrhythmias
    Bradycardia , heart block, cardiac arrest
    Change in ECG pattern
    • Appearance of tall, thin T waves on the ECG.
    • 41. prolong the PR interval, depress the ST segment
    • 42. Lengthen the QRS interval of the ECG.
    • 43. As plasma [K+] approaches 10 mEq/L, the P wave disappears, the QRS interval broadens, the ECG appears as a sine wave, and the ventricles fibrillate .
  • 29
    ………..cont’d
    2.Hypokalemia
    Serum K+ < 3.5 mEq /L
    Causes
    In diabetic patient
    Insulin gets K+ into cell
    Ketoacidosis – H+ replaces K+, which is lost in urine
    β – adrenergic drugs or epinephrine
  • 44. 30
    ……………cont’d
    Decreased intake of K+
    Increased K+ loss
    Diuretics
    Metabolic alkalosis
    Trauma and stress
    Conn’s diseases
    Redistribution between ICF and ECF.
  • 45. 31
    ………….Cont’d
    Clinical manifestation
    Neuromuscular disorders
    Weakness, flaccid paralysis, respiratory arrest, constipation
    Dysrhythmias
    Cardiac arrest
    Prolongs the QT interval, inverts the T wave, and lowers the ST segment of the ECG.
  • 46. 7.References
    Berne and levy physiology, sixth edition Bruce M.Koeppen, Bruce A. Stanton
    Guyton and Hall Textbook of Medical Physiology, 12th Edition.
    Human physiology: The Basis of Medicine, 3rd Edition.
    Institutional websites
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  • 47. THANK YOU