Sodium

1. Clinical Biochemistry
SIMS-305
Dr. Ali Raza
Senior Lecturer
Centre for Human Genetics and Molecular Medicine (CHGMM),
Sindh Institute of Medical Sciences (SIMS), SIUT.
1

2. Group. II: SODIUM

3. SODIUM
• Chief Electrolyte
• Large conc. in extracellular fluid (ECF)
• Mainly associated with Chloride as
• NaCl
• NaHCO3
 Absorption of Sodium:
• Sodium Pump (Na+-K+ ATPase)
• Situated in plasma membrane of
Intestinal
Renal cells

4. SODIUM PUMP (Na+-K+ ATPase)
• Na-pump is an enzyme,
• Requires Mg++ and ATP
• Uses the energy (ATP) to transport
three Na+ outside
two K+ inside the cell membrane

5. SODIUM PUMP
• Intracellular Na+ conc. is 10 mM
• Extracellular Na+ conc. is 150 mM
• Na-pump maintain both magnitudes and direction of
transmembrane concentration gradients of those ions

6. Forms of Sodium Pump
 Na+-K+ ATPase exists in two forms:
• E1
• E2

7. Sodium Pump Mechanism
E1 form E2 form E form
Three sodium ions and two K ions are transported across cell
membrane

8. Sodium Pump Mechanism
The E1 form:
• Presents its ion binding and phosphate binding sites on the
cytoplasmic surface of the membrane.
• Three sodium ions from cytoplasm bind with the ion binding
sites of E1.
• This leads to the phosphorylation of aspartate residue of E1
with the help of ATP and Mg++.
• Results in conformational change and E1 becomes E2.

9. Sodium Pump Mechanism
E2 exposes
• Ion binding and phosphate binding sites, lowers the
affinity of the ATPase for Na+ and releases it into the ECF.
• K+ ions from ECF bind to the respective ion binding site,
lowers the affinity of E2 for phosphate.
• This dephosphorylation changes the conformation of E2 to
E1 again and lowers its affinity for K+ ions.
• This leads to release of the K+ ions from ATPase into the
cell.

10. Sodium Pump Mechanism

11. Sodium - FUNCTIONS
Fluid balance
 Blood viscosity
Acid-base balance
Role in resting membrane potential
 Role in Action Potential
 Neuromuscular excitability

12. Sodium - FUNCTIONS
Fluid balance:
• maintains osmotic pressure of extracellular fluids (ECF)
• helps in retaining water in ECF.
 Neuromuscular excitability:
• Na+ is also involved in neuromuscular irritability
Acid-base balance: Na+-H+ exchange in renal tubule to
acidify urine.
 Maintenance of viscosity of blood:
• Salts of Na with globulins are soluble
• Na+ and K+ maintaining the degree of hydration of the
plasma proteins.

13. Sodium- FUNCTIONS
 Role in resting membrane potential:
• Plasma membrane has a poor Na+ permeability and passive
Na+ inflow through it.
• Na-pump keeps Na+ conc. far higher outside than inside.
separation of charges of the membrane, Polarisation
Role in Action Potential:
• A local depolarisation of nerve or muscle fibre is observed
in stimulation.
• This rapidly increases its permeability to Na+ causing
considerable transmembrane influx of Na+ down its inward
conc. gradient.

14. Sodium - CLINICAL ASPECT
Clinical conditions are of two major types
I. Hypernatraemia
II. Hyponatraemia

15. CLINICAL ASPECT
Hypernatraemia :
• infers that the extracellular sodium is excessive
relative to water.
• A high plasma sodium conc. does not necessarily
mean that the total body sodium content is
increased
• Decrease in body water
• Increase in body sodium

16. Specific conditions in which hypernatraemia occurs
 Simple Dehydration
 Diabetes Insipidus
 Osmotic Loading
 Excess Sodium

17. Hypernatraemia
Simple dehydration:
• Result of excessive sweating with inadequate
or no water replacement.
Diabetes Insipidus:
• Condition characterized by large amounts of dilute
urine and increased thirst.
• Water loss due to lack of antidiuretic hormone (ADH)
• kidney cells are unable to respond to the hormone.

18. Hypernatraemia
Osmotic loading:
• Due to large excretory quantities of very soluble
substances (glucose, urea,)
• Osmotic effect of these substances on the urine causes
excretion of large amounts of water.
• Relatively little sodium is excreted. So the plasma level rises.
• ill patients on high protein diet, urea is formed which is
then excreted in very large amounts along with large
volumes of water.

19. Hypernatraemia
Excess sodium
• 0.9 % NaCl is administered intravenously –154mEq/L.
• Excessive use of isotonic saline particularly in
children leads to hypernatraemia.
• Administration of NaHCO3 in treatment of acidosis
may cause Hypernatraemia

20. II. Hyponatraemia
 Diuretic medication
 Excessive sweating
 Kidney diseases
 Congestive heart failure
 Gastrointestinal loss

21. Diuretic medication:
• Many diuretic medications act by promoting excretion of
Na by kidney.
• To lower the total body sodium and extracellular water
• E.g: this objective is desired, viz. congestive heart failure,
chronic kidney disease and hypertension.
• Reduced total body sodium is achieved but extracellular
volume reaches critical dimension
• there is a counter effort to retain water which then dilutes
the sodium and hyponatraemia results.

22. II. Hyponatraemia
 Excessive sweating:
• Loss of fluids of high Na+ and Cl–
(like sweating)
• but replaced by salt deficient fluids
• water by mouth
• Glucose solution by IV.

23. Kidney diseases:
• Kidneys, glomerulus is the one in which blood is
filtered and Na is reabsorbed by the renal tubules.
• Due to kidney dysfunction, Na+ is not reabsorbed and
is thus excreted in the urine.
• There is also a progressive failure to excrete water.

24. Congestive heart failure:
• Hyponatraemia is common in
heart failure for two reasons:
a) Diuretics administration
b) Congestive heart failure : cause low Na+ conc.
• It is because the low cardiac output is sensed
incorrectly by the brain as low blood volume,
• Calling increased secretion of ADH.

25.  Gastrointestinal loss
• Diarrhoea:
• Result in reduced sodium/chloride levels
in plasma and extracellular fluid.