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DAQ1 - MBBS III S2 > Hypercalcaemia > Flashcards

Hypercalcaemia Flashcards

1
Q

Causes of hypercalcaemia

A

Mnemonic: Thinking CHIMPANZEES

Thinking - Thiazides, thyroid
C - Calcium supplementation
H - Hyperparathyroidism
I - Immobilisation/inherited (FHH)
M - Milk-alkali syndrome, medications (lithium)
P - Paraneoplastic PTHrP
A - Adrenal insufficiency
N - Neoplasm (multiple myeloma, breast, lung)
Z - Zollinger-Ellison syndrome
E - Excessive vitamin D
E - Excessive vitamin A
S - Sarcoidosis and granulomatous diseases

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2
Q

Acute management of severe hypercalcaemia (>3.5mg/dL)

A
  • IV fluids with 0.9% NaCl (monitor carefully and consider loop diuretics in renal insufficiency/CHF)
  • Bisphosponates
  • Calcitonin
  • Corticosteroids
  • RANKL inhibitors
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3
Q

Acute management of mild hypercalcaemia (2.5-3mg/dL)

A

No active or immediate management required. Identify and treat underlying cause.

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4
Q

Acute management of moderate hypercalcaemia (3-3.5mg/dL)

A

If asymptomatic or mild symptoms, treat as for mild (2.5-3mg/dL)
If severe or rapid progression of symptoms, treat as for severe (>3.5mg/dL)

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5
Q

Acute management of hypercalcaemic crisis or renal failure (>4.5mg/dL)

A

Haemodialysis; reserved for refractory life-threatening hypercalcaemia or if other therapies are contraindicated.

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6
Q

PTH-mediated causes of hypercalcaemia

A
  • Primary hyperparathyroidism
  • Tertiary hyperparathyroidism
  • Familial hypocalciuric hypercalcaemia
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7
Q

Non-PTH mediated causes of hypercalcaemia

A
  • Hypercalcaemia of malignancy
  • Granulomatous disorders (e.g. sarcoidosis)
  • Thyrotoxicosis
  • Immobilisation
  • Milk-alkali syndrome
  • Adrenal insufficiency
  • Thiazide diuretics
  • Excess vitamin D intake
  • Calcium supplementation
  • Lithium medications
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8
Q

Primary hyperparathyroidism is most commonly caused by:

A

Parathyroid adenoma or hyperplasia.

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9
Q

Primary hyperparathyroidism causes hypercalcaemia through which mechanism?

A

Excess PTH → increased production of 1,25-dihydroxyvitamin D via stimulation of 1-alpha-hydroxylase synthesis in the kidneys → hypercalcaemia

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10
Q

Tertiary hyperparathyroidism is caused by:

A

Renal failure

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11
Q

Tertiary hyperparathyroidism causes hypercalcaemia via which mechanism?

A

CKD → decreased conversion of calcidiol to calcitriol in kidney → decreased serum calcitriol concentrations → decreased Ca2+ absorption from small intestine → hypocalcaemia → triggers increased PTH release → persistent PTH elevation → reactive hypercalcaemia

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12
Q

Familial hypocalciuric hypercalcaemia mechanism

A

Autosomal dominant inactivating mutation in the CaSR gene → decreased sensitivity of Ca2+ sensing receptors in the parathyroid glands and kidneys; increased reabsorption of Ca2+ in the kidney → hypercalcaemia

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13
Q

What investigation results are consistent with a diagnosis of FHH?

A

Hypocalciuria, mild hypercalcaemia and normal or increased PTH levels.

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14
Q

Granulomatous disorders (e.g. sarcoidosis) cause hypercalcaemia through what mechanism?

A

Activation of mononuclear cells → increased hydroxylase activity → 1,25-dihydroxyvitamin D production outside the kidneys → increased intestinal absorption of calcium → hypercalcaemia

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15
Q

Thiazide diuretics cause hypercalcaemia by:

A

reducing renal calcium excretion.

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16
Q

Lithium medications cause hypercalcaemia by:

A

reducing renal calcium excretion and altering the PTH secretion set-point.

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17
Q

Thyrotoxicosis causes hypercalcaemia by:

A

Increased thyroid hormone levels → increased osteoclastic activity → increased bone resorption

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18
Q

Immobilisation results in hypercalcaemia by:

A

Lack of weight-bearing activities → osteoclast activation → bone demineralisation → hypercalcaemia

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19
Q

Milk-alkali syndrome is caused by:

A

consumption of large amounts of calcium carbonate (antacids)

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20
Q

What three features does milk-alkali syndrome present with?

A

Hypercalcaemia, metabolic alkalosis and AKI

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21
Q

The most common mechanism of hypercalcaemia of malignancy is:

A

paraneoplastic production of PTHrP

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21
Q

The most common mechanism of hypercalcaemia of malignancy is:

A

paraneoplastic production of PTHrP

22
Q

Multiple myeloma causes hypercalcaemia via:

A

osteolytic metastases which increase serum calcium levels due to local bone resorption

23
Q

What are the five common presenting signs of hypercalcaemia?

A

Nephrolithiasis (stones), arthralgias (bones), increased urinary frequency (thrones), abdominal pain/nausea/vomiting (groans), anxiety/depression/fatigue (psychiatric overtones)

24
Q

Hypercalcaemia causes acute pancreatitis via:

A

Ca2+ deposition in bile ducts blocking outflow of pancreatic secretions → increased intrapancreatic pressure → compression of pancreatic blood vessels–tissue ischaemia; activation of proteases–autodigestion of pancreatic tissue

25
Q

PTH effects bone by:

A

increasing bone resorption (induces RANKL expression in osteoblasts → binding of RANKL to RANK on osteoclasts → osteoclastic activation)

26
Q

PTH is produced by:

A

The chief cells of the parathyroid glands.

27
Q

Effect of PTH on the kidneys:

A

Increased urinary excretion of phosphate.

28
Q

The following blood picture fits which condition?

Hypercalcaemia
Hypophosphataemia
High ALP
High PTH

A

Primary hyperparathyroidism.

29
Q

The following blood picture fits which condition?

Hypercalcaemia
Hyperphosphataemia
High ALP
Very high PTH

A

Tertiary hyperparathyroidism

30
Q

PTH levels in hypercalcaemia of malignancy are usually:

A

suppressed unless concurrent primary hyperparathyroidism is present.

30
Q

PTH levels in hypercalcaemia of malignancy are usually:

A

suppressed unless concurrent primary hyperparathyroidism is present.

31
Q

An elevated serum PTHrP in combination with a suppressed serum PTH is suggestive of:

A

Hypercalcaemia of malignancy

32
Q

Phosphate levels in hypercalcaemia of malignancy are:

A

Low with hyperphosphaturia - PTHrP acts at the level of the kidney to reduce the renal phosphorus threshold.

33
Q

The following blood picture is consistent with which diagnosis?

Hypercalcaemia
Inappropriately normal or increased PTH
Hypocalciuria

A

Familial hypocalciuric hypercalcaemia (FHH)

34
Q

Which two causes of hypercalcaemia are associated with hypophosphataemia?

A

Primary hyperparathyroidism
PTHrP-mediated hypercalcaemia

35
Q

Increased levels of 1,25-dihydroxyvitamin can be caused by:

A

Lymphoma, granulomatous disease or calcitriol ingestion.

36
Q

Elevated 25-hydroxyvitamin D levels are due to:

A

vitamin D intoxication

37
Q

Patient’s who opt for non-surgical treatment of parathyroid adenoma should:

A
  • Avoid a high calcium intake
  • Limit vitamin D supplementation
  • Maintain a high water intake unless contraindicated
38
Q

Hypercalcaemia causes constipation by:

A

altering the charge balance across the cell membrane, decreasing contractility of GIT smooth muscle.

39
Q

Hypercalcaemia causes nephrolithiasis by:

A

the precipitation of Ca2+ with PO43- in the renal filtrate.

40
Q

Hypercalcaemia causes polyuria by:

A

Ca2+ directly inhibits the insertion of aquaporin channels in the collecting duct membrane → less water reabsorbed into renal vasculature → increased filtrate volume → polyuria

41
Q

Risk factors for primary hyperparathyroidism include:

A

Female sex, age > 60yo, positive FHx, current or historical lithium treatment, MEN1/2A/4 (autosomal dominant traits)

42
Q

MOA of bisphosphonates

A

Decrease bone resorption by inhibiting osteoclastic activity.

43
Q

Contraindications for bisphosphonates

A

Hypocalcaemia

43
Q

Contraindications for bisphosphonates

A

Hypocalcaemia

44
Q

Bisphosphonates adverse effects

A

Nausea, vomiting, hypocalcaemia, musculoskeletal pain

45
Q

MOA of calcitonin

A

Inhibits bone resorption and increases urinary excretion of calcium and phosphate

46
Q

Averse effects of calcitonin

A

Flushing, nausea, vomiting, dizziness, taste disturbance

47
Q

MOA of corticosteroids in the context of hypercalcaemia

A

Used for calcitriol-mediated hypercalcaemia. Inhibits 1-a-hydroxylase conversion of calcidiol into calcitrol, therefore lessening intestinal calcium absorption.

48
Q

Corticosteroid adverse effects

A

Short-term: fluid retention, hypertension, mood disturbances, weight gain.

Long-term: glaucoma, cataracts, hyperglycaemia, increased susceptibility to infections, osteoporosis, adrenal suppression, delayed wound healing, Cushingoid features.

49
Q

MOA of denosumab

A

Human monoclonal antibody that binds receptor activator of RANKL, preventing activation of RANK → decreased osteoclastic activity → reduced bone resorption

50
Q

Adverse effects of denosumab

A

Eczema, hypercholesterolaemia, musculoskeletal pain

51
Q

MOA of cinacalcet

A

Increases the sensitivity of calcium-sensing receptors on the parathyroid glands to extracellular calcium, thus reducing excretion of PTH and reducing serum calcium concentration.

DAQ1 - MBBS III S2 (5 decks)

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