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Met3b > Calcium disorders > Flashcards

Calcium disorders Flashcards

1
Q

Define hypercalcaemia.

A

calcium concentration >2.6 mmol/L (normal serum calcium = 2.2-2.6)

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2
Q

Distinguish between primary, secondary and tertiary hyperparathyroidism.

A
  1. Primary: one (or more) parathyroid gland produces excess PTH - may be asymptomatic
  2. Secondary: increased secretion of PTH in response to low calcium because of kidney, liver, or bowel disease
  3. Tertiary: autonomous secretion of PTH, usually because of CKD (long-standing 2° hyperparathyroidism can develop into 3°)
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3
Q

Describe the clinical features of acute hypercalcaemia.

A
  1. At levels <2.8 mmol/L:
    - polyuria + polydipsia
    - dyspepsia (calcium-regulated release of gastrin)
    - depression
    - mild cognitive impairment
  2. At levels <3.5 mmol/L:
    - all of the above, plus:
    - muscle weakness
    - constipation
    - anorexia + nausea
    - fatigue
  3. At levels >3.5 mmol/L:
    - all of the above, plus:
    - vomiting
    - dehydration
    - lethargy
    - cardiac arrhythmias (shortened QT interval)
    - coma
    - pancreatitis
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4
Q

What is the initial management of acute hypercalcaemia?

A
  • increase the circulating volume using normal saline, helping to increase the urinary output of calcium
  • loop diuretic (furosemide) - occasionally where there is fluid overloads, but it does not reduce serum calcium
  • IV bisphosphonates (pamidronate or zolendronic acid) after rehydrations (reduce bone turnover)
  • glucocorticoids when hypercalcaemia is due to vitamin D toxicity, sarcoidosis and lymphoma
  • gallium → for malignant hypercalcaemia not responsive to bisphosphonates
  • cinacalcet hydrochloride → calcimimetic agent that reduces parathyroid levels in secondary hyperparathyroidism
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5
Q

What are the potential causes of hypercalcaemia?

A
  1. PTH-mediated:
    - primary hyperparathyroidism → most common cause of hypercalcaemia (usually mild)
  2. Non-PTH-mediated:
    - Malignancy → most common cause of non-PTH-mediated hypercalcaemia
    - Granulomatous conditions: sarcoidosis and TB
    - Endocrine conditions: thyrotoxicosis, phaeochromocytoma and primary adrenal insufficiency
    - Drugs: thiazide diuretics, vitamin D and vitamin A supplements
    - Familial: familial hypocalciuric, hypercalcaemia
    - Other: prolonged immobilisation, calcium-alkali syndrome, AIDS
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6
Q

How can malignancy cause hypercalcaemia?

A

4 different mechanisms:

  1. Ectopic production of PTH-related peptide tumour cells
  2. Osteolytic hypercalcaemia
  3. Ectopic calcitriol (1,25-dihydroxyvitamin D)
  4. Ectopic PTH produced by tumour cells
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7
Q

In hyperparathyroidism, what result would you expect from the following investigations:

(a) Serum phosphate
(b) Serum alkaline phosphatase
(c) Urine calcium
(d) Urine phosphate
(e) PTH

A

(a) Serum phosphate: low
(b) Serum alkaline phosphatase: normal-high
(c) Urine calcium: high
(d) Urine phosphate: high
(e) PTH: high

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8
Q

In vitamin D excess, what result would you expect from the following investigations:

(a) Serum phosphate
(b) Serum alkaline phosphatase
(c) Urine calcium
(d) Urine phosphate
(e) PTH

A

(a) Serum phosphate: normal-high
(b) Serum alkaline phosphatase: low
(c) Urine calcium: high
(d) Urine phosphate: high
(e) PTH: low

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9
Q

In malignancy, what result would you expect from the following investigations:

(a) Serum phosphate
(b) Serum alkaline phosphatase
(c) Urine calcium
(d) Urine phosphate
(e) PTH

A

(a) Serum phosphate: often low
(b) Serum alkaline phosphatase: high (except in haematological malignancy)
(c) Urine calcium: variable
(d) Urine phosphate: high
(e) PTH: variable

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10
Q

In granulomatous disease, what result would you expect from the following investigations:

(a) Serum phosphate
(b) Serum alkaline phosphatase
(c) Urine calcium
(d) Urine phosphate
(e) PTH

A

(a) Serum phosphate: normal-high
(b) Serum alkaline phosphatase: normal-high
(c) Urine calcium: high
(d) Urine phosphate: normal
(e) PTH: low

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11
Q

In calcium alkali syndrome, what result would you expect from the following investigations:

(a) Serum phosphate
(b) Serum alkaline phosphatase
(c) Urine calcium
(d) Urine phosphate
(e) PTH

A

(a) Serum phosphate: normal-high
(b) Serum alkaline phosphatase: normal
(c) Urine calcium: normal
(d) Urine phosphate: normal
(e) PTH: low

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12
Q

In familial hypocalciuric hypercalcaemia, what result would you expect from the following investigations:

(a) Serum phosphate
(b) Serum alkaline phosphatase
(c) Urine calcium
(d) Urine phosphate
(e) PTH

A

(a) Serum phosphate: low-normal
(b) Serum alkaline phosphatase: normal
(c) Urine calcium: low (<200 mg/day)
(d) Urine phosphate: normal
(e) PTH: high

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13
Q

What can cause low PTH levels?

A
  • granulomatous disease
  • iatrogenic causes (e.g. renal dialysis)
  • adrenal insufficiency
  • thyrotoxicosis
  • vitamin D excess
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14
Q

What imaging techniques can be used to investigate the potential cause of hypercalcaemia?

A
  1. Plain x-rays: features indicative of bone abnormalities (demineralisation, bone cysts, pathological fractures, bony mets)
  2. USS, CT or IVP: abnormalities of the urogenital tract (calcification or stones)
  3. USS or technetium scan of parathyroid glands: if hypertrophy or adenoma is suspected
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15
Q

What are the symptoms of hypocalcaemia?

A
  • asymptomatic if mild (2.00-2.12 mmol/L)
  • neuromuscular irritability
  • paraesthesia (usually fingers, toes and around mouth)
  • tetany
  • carpopedal spasm
  • muscle cramps
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16
Q

What are the signs of hypocalcaemia?

A
  • Chvostek’s signs
  • Trousseau’s sign
  • Seizures
  • Prolonged QT interval which may progress to VF or heart block
  • Laryngospasm
  • Bronchospasm
17
Q

What is Chvostek’s sign?

A
  • AKA: Weiss’ sign, Schultze-Chvostek sign or facialis phenomenon
  • when the course of the facial nerve is tapped (as it passes in front of the ear, below the zygomatic arch), muscular spasm is provoked
  • seen as twitching of the face, nose or mouth
  • feature of latent tetany, hypocalcaemia or even normocalcaemia
18
Q

What is Trousseau’s sign?

A
  • occurs in hypocalcaemia and hypomanesaemia
  • results from enhanced neuromuscular excitability
  • inflat a BP cuff to a pressure above the patient’s SBP and maintain this pressure for several minutes
  • look for carpopedal spasm (flexion at the wrist, flexion at the MCP joints, extension of the interphalangeal joint and adduction of the thumbs and fingers)
  • patients may also experience paraesthesia of the fingers
19
Q

What are the signs of prolonged hypocalcaemia?

A
  • subcapsular cataract
  • papilloedema
  • abnormal teeth
  • ectopic calcification
  • dementia and confusion
20
Q

Describe the management of acute hypocalcaemia.

A

Treat where symptomatic, or at high risk of complications

  1. give 10ml (2.23 mmol) of calcium gluconate 10% by slow iV injection
    - repeat as necessary
  2. oral calcium preparation may need to be given as supplements to IV treatment of where IV access is difficult
  3. Monitor serum calcium concentrations regularly
  4. If low calcium persistent, give oral vitamin D
  5. If hypomagnesaemic, necessary to correct the magnesium level before the hypocalcaemia will resolve

Met3b (21 decks)

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