Potassium

Question 1

What is the normal reference range (NR) for potassium and its primary role? (2)

Answer 1

Potassium is the main intracellular cation.

NR = 3.5–5.5 mmol/L.

Question 2

What does hypokalaemia always cause, and why? (2)

Answer 2

Always causes metabolic alkalosis.

Reason: H+ moves out of cells in exchange for K+.

Question 3

What categories can causes of hypokalaemia be split into? (4)

Answer 3

GI loss
Renal loss
Redistribution
Rare causes

Question 4

What are the GI causes of hypokalaemia? (3

Answer 4

Diarrhoea
Vomiting
Fistula

Question 5

What are the renal causes of hypokalaemia? (6)

Answer 5

Conn’s syndrome

Cushing’s syndrome

Loop diuretics

Thiazide diuretics

Osmotic diuresis

Bartter or Gitelman syndrome

Question 6

How does Cushing’s syndrome cause renal hypokalaemia? (1)

Answer 6

Ectopic ACTH stimulates mineralocorticoid receptors (MRs), leading to severe hypokalaemia.

Question 7

How do loop and thiazide diuretics cause hypokalaemia? (2)

Answer 7

Loop diuretics: Block the triple transporter in the ascending loop of Henle (Bartter syndrome mutation).

Thiazide diuretics: Block the Na+-Cl− transporter in the distal convoluted tubule (Gitelman syndrome mutation).

Question 8

What are the redistribution causes of hypokalaemia? (3)

Answer 8

Insulin
Alkalosis
Beta-agonists (e.g., Salbutamol)

Question 9

What are the rare causes of hypokalaemia? (2)

Answer 9

Renal tubular acidosis (RTA) Types 1 & 2

Hypomagnesaemia

Question 10

What is paradoxical aciduria in hypokalaemia? (1)

Answer 10

H+ is lost in urine as a physiological response where the kidney retains K+ in exchange for H+.

Question 11

How does hypokalaemia present clinically? (2)

Answer 11

Muscle weakness

Arrhythmias (e.g., ventricular fibrillation)

Question 12

What are the ECG changes in hypokalaemia? (3)

Answer 12

Flattened T waves

U waves

ST depression

Question 13

What is the management of hypokalaemia based on potassium levels? (2)

Answer 13

K+ 3–3.5 mmol/L:
Oral potassium chloride for 48 hours and recheck levels.

K+ <3 mmol/L:
IV potassium chloride.

Question 14

What are the types of renal tubular acidosis (RTA), and their key features?

Answer 14

Type 1 (distal RTA):
Most severe.
Distal failure of H+ excretion.
Associated with acidosis and hypokalaemia.

Type 2 (proximal RTA):
Milder.
Proximal failure to reabsorb HCO3−.
Associated with acidosis and hypokalaemia.

Type 4 RTA:
Aldosterone deficiency/resistance.
Associated with acidosis and hyperkalaemia.

Question 15

What happens in type 1 renal tubular acidosis?

Answer 15

Type 1 (distal RTA):

Most severe.
Distal failure of H+ excretion.
Associated with acidosis and hypokalaemia.

Question 16

What happens in type 2 renal tubular acidosis?

Answer 16

Type 2 (proximal RTA):

Milder.
Proximal failure to reabsorb HCO3−.
Associated with acidosis and hypokalaemia.

Question 17

What happens in type 4 renal tubular acidosis?

Answer 17

Type 4 RTA:

Aldosterone deficiency/resistance.
Associated with acidosis and hyperkalaemia.

Question 18

What are the 4 main causes of hyperkalaemia?

Answer 18

Renal impairment (CKD) – Main cause

Decreased renin – Type 4 renal tubular acidosis (RTA), NSAIDs

Drugs – ACE inhibitors (ACEis), ARBs, K+ sparing diuretics (e.g., Spironolactone)

K+ release from cells – Rhabdomyolysis, acidosis

Question 19

How does renal impairment (CKD) cause hyperkalaemia?

Answer 19

Reduced glomerular filtration rate (GFR) leads to decreased potassium excretion.

Question 20

What drugs can cause hyperkalaemia? (3)

Answer 20

ACE inhibitors (ACEis)

Angiotensin receptor blockers (ARBs)

Potassium-sparing diuretics (e.g., Spironolactone)

Question 21

How does rhabdomyolysis or acidosis cause hyperkalaemia?

Answer 21

Rhabdomyolysis releases intracellular K+ from damaged muscle cells.

Acidosis drives K+ out of cells in exchange for H+ ions.

Question 22

What are the key ECG changes seen in hyperkalaemia? (6)

Answer 22

Peaked/tented T waves
Bradycardia (progressing to asystole)
Prolonged PR interval
Flattened P waves
Widened QRS
Sine waves (indicate impending cardiac arrest)

Question 23

How is hyperkalaemia managed?

Answer 23

If K+ >6.5 mmol/L or ECG changes present:

1. IV 10mL 10% Calcium Gluconate – protects the myocardium by reducing excitability.
2. 10U Insulin + 50mL 50% Dextrose – drives K+ into cells.
3. Alternative: Nebulised Salbutamol (beta-agonist).

-> If K+ <6.5 mmol/L: Treat the underlying cause.

-> If K+ >7 mmol/L: Recheck the sample to ensure no haemolysis.

Question 24

How is hyperkalaemia managed when K+ is >6.5 mmol/L or ECG changes are present? (3 steps)

Answer 24

IV 10mL 10% Calcium Gluconate – Protects the myocardium by reducing excitability.

10U Insulin + 50mL 50% Dextrose – Drives potassium into cells.

Alternative: Nebulised Salbutamol (beta-agonist).

Question 25

What is the role of IV Calcium Gluconate in hyperkalaemia?

Answer 25

It protects the myocardium by stabilizing cardiac membranes and reducing excitability, preventing arrhythmias.

Question 26

How does insulin with dextrose help in hyperkalaemia?

Answer 26

Insulin promotes the uptake of potassium into cells, and dextrose prevents hypoglycaemia caused by insulin administration.

Question 27

How does nebulised salbutamol help in hyperkalaemia?

Answer 27

Salbutamol (a beta-agonist) drives potassium into cells via beta-adrenergic stimulation.