MBBS viva · Endocrinology
Hypocalcaemia — calcium-PTH-vitamin D physiology, the magnesium trap and emergency management viva
A final-prof viva on the pathophysiology of hypocalcaemia (the membrane-stabiliser mechanism of tetany and the PTH-calcium-vitamin D axis), decoding a low-PTH/high-phosphate picture, defending the emergency IV calcium dose and the non-negotiable magnesium check, and the transition to chronic calcitriol. Examiner expects mechanism and dose-level detail, not labels.
clinicalVerification in progress
On this page
Study tools
Exam tags
NEET-PGINICETUSMLEPLAB
Write your answer
Saved on this device. No marking — you are the marker.
Interpretation
The examiner presents a blood gas / biochemistry panel showing a corrected calcium of 1.6 mmol/L, a high phosphate, a low PTH, and a QTc of 510 ms, and asks: "What is happening here, why is the patient tetanying, and how would you manage them?"
- Biochemistry: severe symptomatic hypocalcaemia in the setting of hypoparathyroidism (low PTH with high phosphate — PTH is normally phosphaturic, so without it phosphate rises). The prolonged QT flags an arrhythmia risk (torsades).[1]
- Clinical correlation: the classic picture is perioral and distal paraesthesia, carpopedal spasm and tetany, positive Chvostek and Trousseau signs, and in severe disease seizures, laryngeal stridor and arrhythmia — this is an emergency needing IV calcium.
- Always correct for albumin first (or use ionised calcium) so that pseudo-hypocalcaemia of hypoalbuminaemia is not over-treated, and always check magnesium — the most-missed driver of refractory disease.
Key points
The examiner will probe each of these; be ready to defend them at viva depth:
- Albumin correction reproduced verbatim — add 0.02 mmol/L calcium for every 1 g/L albumin below 40 g/L (0.8 mg/dL per 1 g/dL below 4.0). State why: about half of circulating calcium is albumin-bound, so low albumin falsely lowers total calcium without changing the (physiologically active) ionised fraction.[2]
- Why hypocalcaemia causes tetany — extracellular ionised calcium stabilises the resting nerve membrane (screens negative charges on the voltage-gated sodium channel). Low calcium lowers the activation threshold towards the resting potential, so nerves and muscles fire spontaneously: paraesthesia, tetany, carpopedal spasm, seizures. On the ECG it prolongs the QT (lengthens plateau phase 2), risking torsades — the opposite of hypercalcaemia which shortens the QT.[1]
- PTH-calcium-vitamin D axis — a fall in ionised calcium triggers PTH; PTH raises calcium via bone resorption, renal calcium reabsorption, and renal 1-alpha-hydroxylation of 25-OH-vitamin D to active 1,25-calcitriol (which increases gut absorption). Loss of PTH therefore also means loss of calcitriol production — which is why chronic hypoparathyroidism needs calcitriol, not native cholecalciferol alone.[1]
- PTH-phosphate decoder — low PTH + high phosphate = hypoparathyroidism; high PTH + low phosphate = vitamin D deficiency; high PTH + high phosphate = CKD. This is the pivotal first branch point after confirming the corrected calcium.[1][2]
- The magnesium trap — severe hypomagnesaemia (under about 0.4 to 0.5 mmol/L) causes refractory hypocalcaemia: magnesium is a cofactor for adenylate cyclase (PTH release) and is required for PTH action (PTH resistance). Until magnesium is corrected, calcium will not rise. Give IV magnesium sulphate 2 g over 10 to 20 minutes, then maintenance.
- Emergency therapy reproduced — IV calcium gluconate 10 percent, 10 to 20 mL (1 to 2 g) over 10 minutes, diluted in glucose, with continuous ECG monitoring, repeat as needed or start an infusion (100 mL of 10 percent calcium gluconate in 500 to 900 mL glucose over 12 to 24 h). Prefer calcium gluconate peripherally (calcium chloride is irritant, needs a central line, and extravasation necroses tissue).[1][2]
- Chronic therapy — oral calcium (1 to 2 g elemental/day) plus active vitamin D (calcitriol/alfacalcidol); target a low-normal calcium to avoid hypercalciuria (nephrocalcinosis, stones). Recombinant PTH(1-84) is reserved for refractory chronic hypoparathyroidism. Most post-surgical cases are transient (recover within weeks); 1 to 3 percent become permanent.
- High-yield associations — post-surgical (commonest), autoimmune (APS-1: hypoparathyroidism + Addison's + mucocutaneous candidiasis), DiGeorge (22q11.2), hungry bone syndrome after parathyroidectomy, basal ganglia calcification and cataracts in chronic disease, and a prolonged QT acutely.
References
- Pepe J, et al. Diagnosis and management of hypocalcemia. Endocrine 2020.[1]
- Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008.[2]
References2ShowHide
- [1]Pepe J, Colangelo L, Biamonte F, et al. Diagnosis and management of hypocalcemia. Endocrine, 2020.PMID 32367335
- [2]Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ, 2008.PMID 18535072