1. Potassium, Calcium, Phosphate & Magnesium Balance
Dr.Mohammed Sharique Ahmed
Assistant proff. Physiology
Al Maarefa College

2. Potassium balance 98% of K+ is in ICF & 2% in ECF
ICF = 150 m Eq/L & in ECF = 4.5 mEq/L
Balance intake = out put
Maintance of K balance is important in normal functioning of excitable tissue

3. Potassium balance
For maintenance of balance body has to face two challenges
Distribution of K+ across cell membrane (internal K+ balance)
To adjust the out put of potassium in accordance with input -Renal mechanism that allow this variability (external K+ balance)

4. Internal Potassium Balance
Effect of hormones drugs & pathologic states
Insulin :
stimulates K+ uptake by the cell
It increase the activity of Na+-K+ ATPase
In type I D.M insulin hyperkalemia

5. Internal potassium balance (continued)
Acid base abnormalities:
ICF has considerable buffering capacity for H+
H+- K+ exchange
Alkalosis hypokalemia
Acidosis hyperkalemia
acid base disturbances often associated with K+ disturbances with the exception of
Respiratory acidosis & alkalosis
Acidosis caused by organic acids (lactic acid,ketoacids)

6. Internal potassium balance (continued)
Adrenergic agonist & antagonist:
Β2 agonist (albuterol) causes K+ shift inside the cell by increasing the activity of Na+-K+ ATPase
α – agonist causes K+ shift outside the cell
Osmolarity:
Increase osmolarity of ECF causes K+ to shift out of the cell
Mechanism involves water flow across the membrane

7. Internal potassium balance (continued)
Cell lysis :
Causes hyper kalemia
E.g. burn, rhabdomyolysis, chemotherapy
Exercise :
Exercise cause shift of K+ out of cell
( usually reverse during subsequent rest)
Those person who are treated β 2 agonist
Those with impaired renal functions

8. Internal potassium balance (continued)

9. External potassium balance
Excretion = intake
Normally urinary excretion = intake – (small amount excreted via GIT or sweat)
Dietary intake is variable , 50 – 150 mEq/day

10. Potassium handling by naphron

11. Potassium handling by nephron(continued)
Filtration :
Freely filtered across glomerular capillaries
Proximal convoluted tubule :
Reabsorbs 67% of the filtered load

12. Potassium handling by nephron(continued)

13. Potassium handling by nephron(continued)
Distal tubule & collecting ducts :
Responsible for adjustment of K+ excretion by either re absorption or secretion as dictated by need
α -Intercalated cells : absorption of potassium if person is on low K+ diet
Principle cells : if person on normal or high K+ diet potassium is excreted by principle cells
The magnitude of potassium excretion is variable depending on diet & several other factors for eg.aldosterone,acid base status ,flow rate etc

15. Factors affecting K+secretion
Magnitude of K+ secretion is determined by the size of electrochemical gradient across luminal membrane
Diet:
High K+ diet concentration inside thus principle cells increases electrochemical gradient across membrane

16. Factors affecting K+secretion(continued)
Aldosterone :
Aldosterone Na+ re absorption by principle cell by inducing synthesis of luminal membrane Na+ channels & basolateral membrane Na+- K+ channel
more Na+ is pumped out of the cell simultaneously more K+ pumped into the cell
Thus increasing the electrochemical gradient for K+ across the luminal membrane that leads to increase K+ secretion

17. Relationship between Na+ absorption & K+ secretion
High Na+ diet:
more Na+ will be delivered to principle cells ,more Na+ is available for Na+- K+ ATPase than more K+ is pumped into the cell which increases the driving force for K+ secretion
Diuretics :
loop & thiazide diuretics inhibit Na+ re absorption in part of tubule earlier to principle cells, so increases Na+ delivery to principle cells , more Na+ is reabsorbed & more K+ is excreted

18. Factors affecting K+secretion(continued)
Acid base disturbances :
The exchange of H+ & K+ ion across membrane underlies these effect
Alkalosis H+ in ECF H+ leaves & K+ enters the cell intracellular K+ contn driving force for K+
Acidosis H+ in ECF H+ enters & K+ leaves the cell intracellular K+ contn driving force forK+

19. Factors affecting K+secretion(continued)
Diuretics :
Loop diuretics & thiazide diuretics causes hypokalemia
By decreasing the sodium re absorption in upstream to the site of K+ secretion ,make more Na+ available for the principle cells ,so more Na+ will be given out & more K+ will be taken in by Na+ - K+ ATPase
Increase flow rate luminal K+ contn diluted driving force for K+ secretion

20. Loop diuretics: also contribute to hypokalemia by inhibiting Na+ - K+ -2cl co transport & thus K+ re absorption in thick ascending limb
K+ sparing diuretics: inhibits all of the action of aldosterone on principle cells & therefore inhibits K+ secretion
Luminal anions : such non re absorbable anions increase elcronegativity of lumen ,thereby increasing the electrochemical driving force for K+

21. CALCIUM BALANCE 99% of body’s calcium is in bone & 1% in ECF &ICF
Plasma concentration 5 mEq/L (10mg/dl)

23. Calcium Handling By Nephron
Filtration :
40% of plasma bound protein cannot be filtered ,only 60% get filtered
To calculate filtered load for Ca2+ correction is made

24. Calcium Handling By Nephron(continued)
Proximal convoluted tubule:
Ca2+ re absorption is tightly coupled to that of Na+
Thick ascending limb of loop of Henle:
Here also re absorption is tightly coupled to that of Na+ re absorption
Lumen positive potential diff generated by Na-K-2Cl co transporter drives re absorption of Ca2+
Loop diuretics also dec Ca2+ re absorption along with Na+

25. Calcium Handling By Nephron(continued)
Distal convoluted tubule :
Site of regulation of Ca2+ re absorption
Not coupled with Na+ reabsorption as in earlier segments
In the DCT ,PTH , Ca2+ reabsorption via basolateral receptor activation of adenyl cyclase & generation of cyclic AMP
Thiazide diuretics increases Ca2+ re absorption useful in T/t of idiopathic hypercalciurea

26. Phosphate Balance Constituent of bone & urinary buffer for H+
85% in bone & 15% in ICF & in ECF<0.5%
In ICF it is component of nucleotides, ATP & metabolic intermediates
In ECF it is in inorganic form ,in plasma about 10% is plasma bound

28. Role of PTH in phosphate re absorption
PTH inhibits phosphate re absorption in proximal tubule by inhibiting Na phosphate co transport
As a result it causes phosphaturea
This action is critical because phosphate that have been resorbed from bone is excreted in urine that phosphate would have other wise complexed Ca2+

29. Magnessium
80% is filterable & 20% bound to plasma proteins

31. Thank you

32. References Human physiology by Lauralee Sherwood, seventh edition
Text book of physiology by Linda .s contanzo,third edition
Text book physiology by Guyton &Hall,11th edition