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Sodium, potassium & calcium flashcards

17 high-yield MRCP Part 1 cards from the Intellect Medicos Nephrology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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1. What is the first investigation to classify hyponatraemia?

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   Serum (plasma) osmolality.

   Why? Normal osmolality suggests pseudohyponatraemia (high lipids or protein); high osmolality suggests hyperglycaemia or mannitol. Only hypotonic hyponatraemia is then assessed by volume status and urine sodium.

2. A hypovolaemic patient with hyponatraemia has a urine sodium above 20 mmol/L. Name two likely causes.

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   Renal salt loss — e.g. diuretics (thiazides), mineralocorticoid deficiency (Addison's), salt-losing nephropathy, cerebral salt wasting.

   Why? Extra-renal losses (vomiting, diarrhoea) give a urine sodium below 10–20 mmol/L because the kidney retains sodium.

3. What is the first-line treatment of chronic euvolaemic hyponatraemia (e.g. SIADH) without severe symptoms?

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   Fluid restriction (about 500–1000 mL/day).

   Why? Treat the cause. Tolvaptan (V2 antagonist) or other measures are second-line under specialist supervision.

4. What is the initial treatment of severely symptomatic hyponatraemia (e.g. seizures, reduced consciousness)?

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   150 mL of 3% hypertonic saline IV over 20 minutes, repeated (up to twice more) until sodium has risen by about 5 mmol/L.

   Why? A 5 mmol/L rise is usually enough to reduce cerebral oedema. Then stop hypertonic saline and limit the rise to 10 mmol/L in the first 24 hours.

5. What is the maximum safe rise in serum sodium when correcting chronic hyponatraemia?

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   No more than 10 mmol/L in the first 24 hours, then no more than 8 mmol/L in each further 24 hours (about 18 mmol/L over 48 hours).

   Why? Faster correction risks osmotic demyelination: brain cells that adapted by losing osmolytes shrink rapidly when sodium rises. Aim lower in high-risk patients (alcohol excess, malnutrition, hypokalaemia, liver disease).

6. What is the classic MRI appearance of central pontine myelinolysis (osmotic demyelination)?

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   Symmetrical T2 hyperintensity in the central pons — a 'trident-shaped' lesion.

   Why? It presents days after over-rapid correction with dysarthria, dysphagia, quadriparesis or locked-in syndrome. Risk is higher with alcohol excess, malnutrition, cirrhosis and hypokalaemia.

7. A patient has K+ 6.9 mmol/L with broad QRS complexes. What is the FIRST drug to give, and what does it do?

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   IV calcium — 30 mL of 10% calcium gluconate over 10 minutes (or 10 mL of 10% calcium chloride over 5 minutes); it stabilises the cardiac membrane.

   Why? Calcium does not lower potassium; it buys time while insulin–glucose shifts potassium into cells. UKKA prefers calcium chloride in cardiac arrest or peri-arrest and gluconate otherwise. Repeat if ECG changes persist.

8. What is the standard insulin–glucose regimen for severe hyperkalaemia in the UK, and its main risk?

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   10 units soluble insulin with 25 g glucose IV over 15 minutes; main risk is hypoglycaemia (often delayed).

   Why? Insulin drives potassium into cells via Na+/K+-ATPase. If pre-treatment glucose is below 7 mmol/L, follow with 10% glucose at 50 mL/h for 5 hours; monitor capillary glucose for 6 hours.

9. What dose of nebulised salbutamol is used as an adjunct in hyperkalaemia?

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   10–20 mg nebulised (consider only 10 mg in ischaemic heart disease).

   Why? Beta-2 agonists shift potassium into cells. It is an adjunct to insulin–glucose, never monotherapy; up to 40% of dialysis patients do not respond, and non-selective beta-blockers may block the effect.

10. Name an oral potassium binder used to remove potassium in moderate–severe hyperkalaemia.

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    Sodium zirconium cyclosilicate (or patiromer).

    Why? SZC exchanges sodium and hydrogen for potassium in the gut; patiromer exchanges calcium. UKKA no longer recommends calcium resonium for acute or chronic hyperkalaemia. NICE TA1148 (2026) also allows SZC for persistent K+ ≥5.5 mmol/L in CKD 3b–5 or heart failure so RAAS inhibitors can be optimised.

11. What are the first two steps in treating severe hypercalcaemia?

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    IV fluid rehydration with 0.9% saline, then an IV bisphosphonate (e.g. zoledronic acid or pamidronate).

    Why? Hypercalcaemia causes polyuria and dehydration, which worsen it. Bisphosphonates take 2–4 days to work; calcitonin acts faster but briefly.

12. Familial hypocalciuric hypercalcaemia is caused by mutation of which gene, with what inheritance?

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    The calcium-sensing receptor gene (CASR); autosomal dominant.

    Why? The parathyroid 'sees' calcium as low, so PTH is normal or mildly raised and urinary calcium is LOW (calcium:creatinine clearance ratio <0.01). Parathyroidectomy does not help.

13. What is the classic triad of milk–alkali syndrome?

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    Hypercalcaemia, metabolic alkalosis and renal impairment.

    Why? It follows excess intake of calcium with absorbable alkali (e.g. calcium carbonate antacids).

14. Which sign of hypocalcaemia is more specific: Trousseau's or Chvostek's?

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    Trousseau's sign (carpopedal spasm with BP cuff inflation).

    Why? Chvostek's sign (facial twitch on tapping the facial nerve) occurs in some normocalcaemic people. Hypocalcaemia also prolongs the QT interval.

15. Hypocalcaemia is not correcting despite IV calcium. Which electrolyte should be checked and corrected?

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    Magnesium.

    Why? Hypomagnesaemia impairs PTH secretion and causes PTH resistance, so calcium will not correct until magnesium is replaced.

16. What is the emergency treatment of severe symptomatic hypocalcaemia (tetany, seizures)?

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    IV 10% calcium gluconate (e.g. 10 mL over 10 minutes) with cardiac monitoring, then an infusion if needed.

    Why? Rapid injection can cause arrhythmias, so give slowly with ECG monitoring. Oral calcium and vitamin D are used for milder or chronic cases.

17. Name three causes of hypokalaemia WITH hypertension.

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    Any three of: primary hyperaldosteronism (Conn's), Cushing's syndrome, Liddle syndrome, liquorice excess, 11β-hydroxylase deficiency, glucocorticoid-remediable aldosteronism.

    Why? Mineralocorticoid excess (real or apparent) causes sodium retention and potassium loss. Without hypertension think diuretics, GI loss, RTA types 1–2, Bartter and Gitelman.