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Calcium, parathyroid & MEN flashcards

16 high-yield MRCP Part 1 cards from the Intellect Medicos Endocrinology & Diabetes 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 are the typical calcium, phosphate and PTH results in primary hyperparathyroidism?

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   High calcium, low phosphate, and a raised or inappropriately normal PTH.

   Why? About 85% are due to a single parathyroid adenoma. Familial hypocalciuric hypercalcaemia is the key differential.

2. According to NICE, which features in primary hyperparathyroidism warrant referral for parathyroidectomy?

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   Symptoms of hypercalcaemia, end-organ disease (renal stones, fragility fractures, osteoporosis), or adjusted calcium ≥2.85 mmol/L.

   Why? Parathyroidectomy is the only curative treatment.

3. Which imaging is used to localise a parathyroid adenoma before surgery?

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   Neck ultrasound first, with a sestamibi (Tc-99m MIBI) scan as the usual second modality.

   Why? Localisation allows a focused, minimally invasive parathyroidectomy. Imaging is for surgical planning, not for diagnosis, which is biochemical.

4. What is the mechanism of action of cinacalcet?

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   A calcimimetic — it increases the sensitivity of the parathyroid calcium-sensing receptor, lowering PTH.

   Why? NICE: consider it in primary hyperparathyroidism if surgery is unsuitable, declined or unsuccessful and adjusted calcium is ≥2.85 mmol/L with symptoms or ≥3.0 mmol/L. It is also used for secondary hyperparathyroidism on dialysis.

5. In primary hyperparathyroidism, what is the NICE position on bisphosphonates?

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   Use them to reduce fracture risk, but NOT to treat the chronic hypercalcaemia.

   Why? Bisphosphonates do not correct the underlying PTH excess.

6. What is the first step in treating acute severe hypercalcaemia (e.g. Ca²⁺ >3.5 mmol/L)?

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   IV rehydration with 0.9% sodium chloride.

   Why? Patients are volume depleted from polyuria and vomiting; saline also increases renal calcium excretion.

7. After rehydration, what is the drug of choice for hypercalcaemia of malignancy?

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   An IV bisphosphonate (e.g. zoledronic acid or pamidronate).

   Why? They inhibit osteoclast bone resorption; calcium falls over 2–4 days and the effect lasts about 2 weeks.

8. Hypercalcaemia from which causes responds to glucocorticoids?

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   Sarcoidosis, myeloma and vitamin D excess.

   Why? In sarcoidosis, activated macrophages make calcitriol (1α-hydroxylase activity), increasing gut calcium absorption; steroids suppress this.

9. Name two drugs that can cause hypercalcaemia.

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   Thiazide diuretics and lithium (also vitamin D).

   Why? Thiazides reduce renal calcium excretion; lithium raises the PTH set point.

10. What urine test distinguishes familial hypocalciuric hypercalcaemia (FHH) from primary hyperparathyroidism?

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    Calcium:creatinine clearance ratio — below 0.01 in FHH.

    Why? FHH is an autosomal dominant inactivating mutation of the calcium-sensing receptor (CaSR); mild lifelong hypercalcaemia with low urinary calcium and normal or mildly raised PTH.

11. What are the calcium, phosphate and PTH results in secondary hyperparathyroidism due to CKD?

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    Low or normal calcium, high phosphate and high PTH (with low vitamin D).

    Why? Treat with phosphate control (diet ± binders) and activated vitamin D (e.g. alfacalcidol).

12. In a long-term dialysis patient, calcium becomes HIGH with a very high PTH. What has developed, and what is the definitive treatment?

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    Tertiary hyperparathyroidism; parathyroidectomy (cinacalcet if not fit for surgery).

    Why? Prolonged stimulation makes the parathyroids secrete PTH autonomously.

13. A woman with short 4th and 5th metacarpals, short stature and round face has low calcium, high phosphate and HIGH PTH. What is the diagnosis?

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    Pseudohypoparathyroidism.

    Why? End-organ resistance to PTH from a mutation in the G-protein alpha subunit (GNAS). Treat with calcium and vitamin D.

14. What is the commonest feature of MEN type 1, and which gene is affected?

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    Primary hyperparathyroidism (about 90%); MEN1 (menin) gene.

    Why? MEN1 = the 3 Ps: parathyroid, pancreatic (e.g. gastrinoma, insulinoma) and pituitary tumours. Autosomal dominant. MEN 4 is the same pattern caused by CDKN1B.

15. Which MEN syndrome features a marfanoid habitus and mucosal neuromas?

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    MEN 2B (RET mutation).

    Why? MEN 2B also has medullary thyroid carcinoma and phaeochromocytoma but NOT hyperparathyroidism. MEN 2A: medullary carcinoma, phaeochromocytoma and parathyroid hyperplasia.

16. Which gene is mutated in autoimmune polyendocrine syndrome type 1, and what are its three main features?

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    AIRE (autosomal recessive); hypoparathyroidism, chronic mucocutaneous candidiasis and Addison's disease.

    Why? Type 2 (polygenic, HLA-DR3/DR4) is Addison's with type 1 diabetes and/or autoimmune thyroid disease.