Download Potassium balance

Potassium, Calcium, Phosphate &
Magnesium Balance
Dr.Mohammed Sharique Ahmed
Assistant proff. Physiology
Al Maarefa College
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
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)
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
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)
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
Internal potassium balance
 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
(continued)
Internal potassium balance
(continued)
External potassium balance
 Excretion = intake
 Normally urinary excretion = intake – (small amount
excreted via GIT or sweat)
 Dietary intake is variable , 50 – 150 mEq/day
Potassium handling by naphron
Potassium handling by nephron(continued)
 Filtration :
 Freely filtered across glomerular capillaries
 Proximal convoluted tubule :
 Reabsorbs 67% of the filtered load
Potassium handling by nephron(continued)
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
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
principle cells increases
thus
electrochemical
gradient across
membrane
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
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
Factors affecting K+secretion
(continued)
 Acid base disturbances :
 The exchange of H+ & K+ ion across membrane
underlies these effect
 Alkalosis
cell
 Acidosis
cell
H+ in ECF
H+ leaves & K+ enters the
intracellular K+ contn
driving force for K+
H+ in ECF
H+ enters & K+ leaves the
intracellular K+ contn
driving force forK+
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
 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+
CALCIUM BALANCE
99% of body’s
calcium is in bone
& 1% in ECF &ICF
 Plasma
concentration 5
mEq/L (10mg/dl)

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
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+
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
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
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+
Magnessium

80% is filterable & 20% bound to plasma
proteins
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