SN7 SHORT NOTE 5M ★ High-yield

Describe the functions, regulation and disorders of sodium and potassium.

Biochemistry · 1st Professional — Pre-Clinical

Definition

Sodium and potassium are the chief cations of the extracellular and intracellular compartments respectively, and their gradient across the cell membrane underlies excitability, transport and cell volume.

Ion	Chief location	Serum level	Total body
Sodium	Extracellular	135–145 mEq/L	4000 mEq
Potassium	Intracellular (98%)	3.5–5.0 mEq/L	3500 mEq

The gradient is created by the Na+/K+-ATPase, pumping 3 Na+ out for 2 K+ in
Requirement — sodium about 5 g of salt per day; potassium 3–4 g

Functions

Sodium — determines extracellular volume and osmolality; nerve and muscle excitability; acid–base balance; drives secondary active transport of glucose and amino acids
Potassium — sets the resting membrane potential; essential for cardiac conduction, muscle contraction, protein and glycogen synthesis, and enzyme activity

Regulation

Hormone	Action
Aldosterone	↑ Na+ reabsorption and ↑ K+ excretion in the distal tubule
ADH (vasopressin)	Water reabsorption — controls sodium concentration, not total sodium
Atrial natriuretic peptide	↑ Sodium and water excretion
Insulin and β-agonists	Drive K+ into cells
Acidosis	Drives K+ out of cells → raises serum potassium

Disorders of Sodium

Hyponatraemia (< 135)	Hypernatraemia (> 145)
Causes — SIADH, diuretics, vomiting, diarrhoea, cardiac and hepatic failure, adrenal insufficiency, excess water	Causes — dehydration, diabetes insipidus, osmotic diuresis, inadequate water intake
Features — nausea, headache, confusion, seizures, coma (cerebral oedema)	Features — thirst, lethargy, irritability, weakness, seizures
Correct slowly — too rapid causes osmotic demyelination	Correct slowly — too rapid causes cerebral oedema

Disorders of Potassium

Hypokalaemia (< 3.5)	Hyperkalaemia (> 5.0)
Causes — vomiting, diarrhoea, diuretics, hyperaldosteronism, insulin therapy, alkalosis, refeeding	Causes — renal failure, potassium-sparing diuretics, ACE inhibitors, acidosis, haemolysis, rhabdomyolysis, Addison disease
Features — muscle weakness, cramps, ileus, arrhythmia, polyuria	Features — weakness, paraesthesiae, cardiac arrest
ECG — flattened T, prominent U wave, ST depression	ECG — tall peaked T, wide QRS, absent P, sine wave
Treatment — oral or intravenous potassium; correct magnesium	Treatment — calcium gluconate (protects the heart), insulin with glucose, salbutamol, bicarbonate, resins, dialysis

CLINICAL PEARL

Hyperkalaemia is the most immediately lethal electrolyte disturbance. Calcium gluconate is given first — it does not lower potassium at all, but stabilises the myocardium while the other measures take effect. Insulin with glucose acts within minutes by driving potassium into cells.

Applied Aspects

Pseudohyperkalaemia — from a haemolysed sample, a tight tourniquet, clenching the fist, or delay in analysis; always repeat before treating a surprising result
Refractory hypokalaemia is usually due to hypomagnesaemia — correct the magnesium first
Hyponatraemia in hyperglycaemia is dilutional — glucose draws water out of cells; correct the sodium by about 1.6 mEq/L for every 100 mg/dL of glucose above normal
Oral rehydration solution contains sodium, potassium, glucose and citrate — the glucose is essential, since SGLT-1 couples its absorption to sodium
In diabetic ketoacidosis, total body potassium is depleted despite a normal or high serum level; it falls sharply once insulin is started, and failure to replace it is a classic fatal error

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