Calcium Part II Flashcards

1
Q

List some symptoms of hypercalcaemia.

A
  • Polyuria/polydipsia
  • Constipation
  • Confusion, seizures, coma → NOTE: these tend to occur when calcium level >3 mmol/L

Bones, stones, abdominal groans, psychiatric moans

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2
Q

What test should you do in patients with hypercalcaemia?

A

PTH-→ suppressed= cancer or sarcoidosis/ vit D excess/ thyrotoxicosis

not suppressed= primary hyperparathyroidism or familial hypocalciuric hypercalcaemia

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3
Q

What are the main causes of primary hyperparathyroidism?

A
  • Parathyroid adenoma
  • Parathyroid hyperplasia (associated with MEN1)
  • Parathyroid carcinoma
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4
Q

Outline the serum biochemistry features of primary hyperparathyroidism.

A
  • High calcium
  • Inappropriately raised PTH (could be within normal range but this is still inappropriate in hypercalcaemia)
  • Low phosphate (phosphate trashing hormone)

affects W>M

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5
Q

Outline the pathophysiology of familial benign hypercalcaemia.

A

A mutation in the calcium-sensing receptor (CaSR) leads to a reduced threshold for PTH release (leads to mild hypercalcaemia)

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6
Q

Why don’t patients with familial benign hypercalcaemia get kidney stones?

A

PTH causes increased renal calcium absorption, thereby reducing urine calcium

Familial hypocalcuric hypercalcaemia

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7
Q

What are the three types of hypercalcaemia of malignancy?

A
  • Humoral hypercalcaemia of malignancy (e.g. small cell lung cancer) → high calcium caused by PTHrP release
  • Bone metastases (e.g. breast cancer) → high calcium caused by local bone osteolysis
  • Haematological malignancy (e.g. myeloma) → high calcium caused by cytokines
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8
Q

List some other non-PTH driven causes of hypercalcaemia.

A
  • Sarcoidosis (sarcoid tissue expresses 1 alpha hydroxylase)
  • Thyrotoxicosis (increases bone resorption)
  • Hypoadrenalism (reduced renal Ca2+ transport)
  • Thiazide diuretics (reduced renal Ca2+ transport)
  • Excess vitamin D (e.g. sun beds)
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9
Q

Outline the management of hypercalcaemia.

A
  • Fluids, fluid and more fluids! (0.9% normal saline, 1L over 1 hour)
  • Bisphosphonates but only if there is cancer (stops cancer from eating bone)
  • Treat the underlying cause.
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10
Q

Why shouldn’t bisphosphonates be given in patients with hypercalcaemia without cancer?

A

Calcium keeps falling as bone is indestructible

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11
Q

List some symptoms and signs of hypocalcaemia

A
  • Neuromuscular excitability (Chvostek’s sign, Trousseau’s sign)
  • Stridor (due to laryngeal spasm)
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12
Q

Mechanism underlying trousseau sign

A

increase in albumin in the area with inflated cuff= more calcium binds to albumin so ionised calcium falls further, increasing neuromuscular excitability as depolarisation occurs easier

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13
Q

Patient presenting with hypocalcaemia. What is best test to do next?

A

repeat and adjust for albumin then PTH

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14
Q

Recall some differentials for hypocalcaemia when the PTH is high

A

This is an appropriate response to low calcium - SECONDARY HYPERPARATHYROIDISM

Could be due to:

  1. Vit D deficiency (most common cause)
  2. CKD (as low renal alpha-1-hydroxylase)
  3. Pseudohypoparathyroidism (gene deficit –> PTH resistance)
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15
Q

Recall some differentials for hypocalcaemia when the PTH is low

A

This is an inappropriate response (low calcium should cause high PTH)

Could be due to:

  1. Surgical mishap during thyroidectomy
  2. Autoimmune hypoparathyroidism (rare)
  3. Di George syndrome (even rarer! Agenesis of parathyroids)
  4. Magnesium deficiency - can be caused by OMEPRAZOLE
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16
Q

Why is magnesium deficiency relevant to calcium?

A

mg needed for the enzyme needed to make PTH

17
Q

What is tertiary hyperparathyroidism?

A

begins with hypocalcaemia and high PTH

bones are osteopaenic

big parathyroid glands and taking oral calcium

when patient has kidney transplant, PTH can exert an effect and parathyroids are tumourous so they keep producing

18
Q

Rank diseases from high to low calcium

A
  1. Cancer
  2. primary hyperparathyroidism
  3. osteoporosis and pagets normal
  4. secondary hyperparathyroidism
19
Q

What is osteitis fibrosa

A

loss of cortical bone increasing fracture risk

occurs in long term untreated primary hyperparathyroidism

20
Q

What is renal osteodystrophy

A

no 1a-hydroxylase due to secondary hyperparathyroidism + retention of aluminium from dialysis but actually dialysis doesn’t affect