Approach to the patient with Calcium Disturbance

This is a bit of a tricky one so don't worry if you became stuck. The initial question stem is describing the clinical features of HYPOcalcaemia and the question itself is describing Trousseau's sign (a sign of hypocalcaemia). Trosseau's sign occurs in the absence of blood flow, in this context caused by the inflation of the blood pressure cuff, the hypocalcaemia and subsequent neuromuscular irritability will induce a spasm of the muscles of the hand and forearm. Calcium ions help to maintain the normal membrane potential by blocking sodium channels in the membrane. In low-calcium states, more sodium can enter the neurons, reducing the membrane potential and making it more susceptible to action potentials being triggered (source: Mechanism of Clinical Signs 3rd Ed., Ch 7 (Endocrinological Signs), by Dennis, Bowen and Cho - Clinical Key link.)

HYPOparathyroidism is caused by a relative or absolute deficiency of plasma parathyroid hormone. This leads to a low serum calcium level (less stimulation of calcitriol to cause calcium reabsorption) and elevated serum phosphate due to a reduction in phosphate excretion. Malabsorption and chronic renal failure will also cause hypocalcaemia, but will not have further blood test abnormalities. Hyperparathryoidism and sarcoidosis result in HYPERcalacaemia.

Vegetable oil is not a source of calcium but a great source of vitamin E. All of the others are good sources of calcium. This is a great resource to use: https://www.nhs.uk/conditions/vitamins-and-minerals/

This patient is presenting with the clinical features of acute onset of hypercalcaemia. Hypercalcaemia is deleterious to the function of excitable membranes leading to skeletal muscles and gastrointestinal smooth muscle fatigue. All of the answers are causes of hypercalcaemia however, given the history of renal cell carcinoma and the acute onset of symptoms this is more likely to be a hypercalcaemia of malignancy. Hypercalcaemia of malignancy is split into two types: Osteolytic hypercalcaemia and humeral hypercalcaemia. Humeral hypercalcaemia occurs as a result of tumour secretion of parathyroid hormone related peptide which leads to activation of oesteoclastic bone resorption and suppression of osteoblastic bone formation.

A short QT interval is seen in hypercalcaemia and results in an increased risk of cardiac arrest. Tented T waves are seen hyperkalaemia, long QT is seen in hypocalcaemia. ST segment elevation is seen in ischaemia. U waves are seen with delayed repolarisation.

Renal stones are a typical manifestation of hyperparathyroidism as the cause for hypercalcaemia. The other answer options will present with more generalised symptoms of hypercalcaemia.

Multiple myeloma is a disease associated with osteolytic bone disease, causing an increased release of calcium form the bone, thus leading to hypercalcaemia

According to Society of Endocrinology guidelines, in patients who are symptomatic or have an adjusted calcium concentration > 3mM, you should initially give 4-6 litres of 0.9 % saline over 24 hours. After rehydration, you can then give IV bisphosphonates (e.g. zoledronic acid).

Calcitonin is a second-line therapy and alendronic acid is an oral bisphosphonate used to treat post-menopause osteoporosis. If the patient had presented with signs of cauda equina or spinal cord compression from suspected spinal metastases, she would be confined to a bed until imaging is completed and reviewed.

Calcitonin inhibits the mobilisation of calcium from the bones and increases urinary excretion and so reduces calcium levels. Note that calcitonin is a second-line management of acute hypercalcaemia if the patient has not responded to IV fluid therapy and IV bisphosphonates (see Society of Endocrinology guidelines).

Tuberculosis causes hypercalcaemia due to a excessive extra-renal 1-alpha hydroxylase activity, this results in increased calcium reabsorption thus leading to hypercalcaemia (source).