List: Causes of Hyper/Hypokalaemia

TL;DR

For MRCP Part 1, electrolyte disorders are tested repeatedly because they integrate renal physiology, endocrinology, pharmacology and emergency medicine. List: Causes of Hyper/Hypokalemia is a favourite revision topic, with exam questions often asking candidates to identify the most likely underlying mechanism rather than simply recalling potassium values. This guide provides the highest-yield causes, common examination traps, a short clinical case and practical revision tips.

Why this matters

Hyperkalaemia and hypokalaemia appear across multiple MRCP specialties:

• Nephrology

• Cardiology

• Endocrinology

• Emergency medicine

• Intensive care

• Clinical pharmacology

Candidates should rapidly distinguish:

• Reduced intake versus increased loss

• Renal versus extrarenal causes

• Transcellular shifts versus true potassium depletion

• Genuine hyperkalaemia versus pseudohyperkalaemia

Core sections

Potassium physiology in one minute

Approximately 98% of total body potassium is intracellular, with only around 2% present extracellularly.

Normal serum potassium:

3.5–5.0 mmol/L

Potassium homeostasis depends on:

• Renal excretion

• Aldosterone

• Insulin

• β2-adrenergic stimulation

• Acid-base balance

• Cellular integrity

Remember:

Serum potassium may be normal despite severe total body depletion.

The 10 highest-yield causes of hyperkalaemia

Cause	Mechanism	High-yield MRCP clue
Acute kidney injury	Reduced renal excretion	Rising creatinine
Chronic kidney disease	Reduced potassium clearance	Advanced CKD
ACE inhibitors/ARBs	Reduced aldosterone	Hypertension treatment
Potassium-sparing diuretics	Reduced potassium secretion	Spironolactone, eplerenone, amiloride
Addison's disease	Aldosterone deficiency	Hyperpigmentation, hypotension
Metabolic acidosis	Potassium shifts extracellularly	DKA, renal failure
Tissue breakdown	Potassium release	Rhabdomyolysis, burns, tumour lysis
Insulin deficiency	Reduced cellular uptake	Diabetic ketoacidosis
β-blockers	Reduced intracellular uptake	Non-selective agents
Excess potassium administration	Increased intake	IV potassium or supplements

The 10 highest-yield causes of hypokalaemia

Cause	Mechanism	High-yield MRCP clue
Loop diuretics	Renal potassium loss	Furosemide
Thiazide diuretics	Renal potassium loss	Hypertension
Vomiting	Secondary hyperaldosteronism	Metabolic alkalosis
Diarrhoea	Gastrointestinal loss	Metabolic acidosis
Hyperaldosteronism	Increased renal secretion	Resistant hypertension
Insulin therapy	Intracellular shift	DKA treatment
β2 agonists	Cellular uptake	Salbutamol
Hypomagnesaemia	Renal potassium wasting	Refractory hypokalaemia
Cushing syndrome	Mineralocorticoid effect	Hypertension
Poor dietary intake	Rare alone	Malnutrition, alcoholism

The five most tested subtopics

1. Drug-induced potassium disorders

The MRCP examination frequently tests medication side effects.

Hyperkalaemia drugs

• ACE inhibitors

• ARBs

• Spironolactone

• Eplerenone

• Amiloride

• Trimethoprim

• NSAIDs

• Heparin

• Tacrolimus

• Ciclosporin

Hypokalaemia drugs

• Furosemide

• Bumetanide

• Thiazides

• Corticosteroids

• Amphotericin B

• High-dose penicillins

• Salbutamol

• Theophylline

• Insulin

2. Acid-base disorders

Metabolic acidosis

Usually causes extracellular potassium movement.

Result:

Hyperkalaemia

Important exception:

Diarrhoea causes metabolic acidosis and hypokalaemia because potassium is lost in stool.

Metabolic alkalosis

Encourages intracellular potassium movement.

Result:

Hypokalaemia

Common causes include:

• Vomiting

• Diuretics

3. Endocrine disorders

Hyperkalaemia

Think:

• Addison's disease

• Hypoaldosteronism

Hypokalaemia

Think:

• Primary hyperaldosteronism (Conn syndrome)

• Cushing syndrome

• Apparent mineralocorticoid excess

4. Renal causes

Hyperkalaemia commonly results from:

• Acute kidney injury

• Chronic kidney disease

• Type IV renal tubular acidosis

Hypokalaemia commonly results from:

• Bartter syndrome

• Gitelman syndrome

• Renal tubular disorders

• Diuretic therapy

5. ECG findings

Every MRCP candidate should recognise these.

Hyperkalaemia

Progression:

• Tall peaked T waves

• PR prolongation

• Loss of P waves

• Broad QRS

• Sine-wave pattern

• Ventricular fibrillation or asystole

Hypokalaemia

Features include:

• Flat T waves

• ST depression

• Prominent U waves

• Prolonged QT (apparent)

• Ventricular arrhythmias

Practical study list

The following checklist covers the causes most commonly appearing in MRCP questions.

1. Renal failure

2. ACE inhibitors

3. Potassium-sparing diuretics

4. Addison's disease

5. Tumour lysis syndrome

6. Rhabdomyolysis

7. Diuretics

8. Vomiting

9. Diarrhoea

10. Hyperaldosteronism

11. β2 agonists

12. Hypomagnesaemia

If you can explain why each causes potassium abnormalities, you are well prepared for most examination questions.

Practical examples / mini-cases

Mini-case

A 67-year-old man with diabetic nephropathy is started on ramipril. One week later his blood results show:

• Potassium: 6.2 mmol/L

• Creatinine: increased from baseline

ECG demonstrates peaked T waves.

Question

What is the most likely cause?

A. Excess dietary potassium

B. Addison's disease

C. ACE inhibitor therapy

D. Vomiting

E. Hyperthyroidism

Answer

C. ACE inhibitor therapy

Explanation

ACE inhibitors reduce aldosterone secretion, impairing renal potassium excretion. Patients with chronic kidney disease are particularly susceptible to clinically significant hyperkalaemia.

Practical study-tip checklist

✓ Learn potassium disorders by mechanism, not isolated diseases.

✓ Memorise common drug causes.

✓ Always associate endocrine disease with aldosterone abnormalities.

✓ Never forget hypomagnesaemia as a cause of refractory hypokalaemia.

✓ Revise ECG changes alongside biochemical abnormalities.

✓ Distinguish potassium redistribution from true potassium loss.

✓ Practise interpretation using timed single-best-answer questions.

For additional practice, use the MRCP Part 1 overview:

https://www.crackmedicine.com/mrcp-part-1/

Strengthen your revision with Free MRCP MCQs:

https://www.crackmedicine.com/qbank/

Watch clinician-led explanations in the MRCP lectures:

https://www.crackmedicine.com/lectures/

Common pitfalls (5 bullets)

• Confusing pseudohyperkalaemia with true hyperkalaemia. Haemolysed blood samples, marked thrombocytosis or severe leukocytosis can falsely elevate serum potassium.

• Assuming normal serum potassium excludes depletion. Significant total body potassium loss may exist despite a normal blood result.

• Forgetting hypomagnesaemia. Potassium replacement often fails until magnesium deficiency is corrected.

• Missing drug interactions. ACE inhibitors combined with spironolactone or renal impairment markedly increase hyperkalaemia risk.

• Ignoring ECG changes. Treatment urgency depends on both potassium concentration and cardiac manifestations.

FAQs

Why is hyperkalaemia dangerous?

Hyperkalaemia alters cardiac membrane excitability and may rapidly cause fatal arrhythmias. ECG abnormalities warrant urgent assessment and treatment.

Why does insulin lower serum potassium?

Insulin stimulates Na⁺/K⁺-ATPase activity, shifting potassium into cells. This effect is utilised therapeutically in severe hyperkalaemia.

Which drugs are most commonly tested in MRCP potassium questions?

ACE inhibitors, ARBs, spironolactone, amiloride, loop diuretics, thiazides, insulin and β2 agonists are among the highest-yield medications.

Why is hypomagnesaemia associated with hypokalaemia?

Magnesium deficiency increases renal potassium wasting. Potassium replacement alone is frequently ineffective until magnesium is corrected.

How should I revise potassium disorders for MRCP Part 1?

Organise causes into mechanisms—reduced excretion, increased loss, intracellular shifts and endocrine disorders—then reinforce learning with practice questions and ECG interpretation.

Ready to start?

Potassium disorders are among the highest-yield electrolyte topics in MRCP Part 1 and frequently integrate physiology with clinical reasoning. Build confidence by revising the underlying mechanisms rather than memorising isolated lists.

Continue your preparation with:

• MRCP Part 1 Overview: https://www.crackmedicine.com/mrcp-part-1/

• Free MRCP Question Bank: https://www.crackmedicine.com/qbank/

• MRCP Video Lectures: https://www.crackmedicine.com/lectures/

You may also find these related topics useful during revision:

• Drug Rashes: SJS vs TEN vs DRESS

• Phagocyte Defects: CGD & Chediak-Higashi

Sources

1. MRCP(UK). https://www.mrcpuk.org/

2. Kidney Disease: Improving Global Outcomes (KDIGO). https://kdigo.org/

3. National Institute for Health and Care Excellence (NICE). https://www.nice.org.uk/

4. European Society of Cardiology Guidelines. https://www.escardio.org/

5. British National Formulary (BNF). https://bnf.nice.org.uk/