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Year 2 - BRS > 3.8 - Calcium dysregulation > Flashcards

3.8 - Calcium dysregulation Flashcards

1
Q

What two things increase serum calcium?

A
  • vitamin D - synthesised in skin or intake via diet
  • parathyroid hormone - secreted by parathyroid glands
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2
Q

What decreases serum calcium?

A
  • calcitonin - secreted by thyroid parafollicular cells
  • can reduce calcium acutely, but no negative effect if parafollicular cells removed e.g. thyroidectomy
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3
Q

How is vitamin D3 made?

A
  • UVB –> 7-dehydrocholesterol –> previtamin D3 –> vitamin D3 –> 25-hydroxylase –> 25(OH)cholecalciferol –> 1-alpha-hydroxylase –> 1,25(OH)2 cholecalciferol (calcitriol)
  • OR vitamin D2 from diet –> vitamin D3
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4
Q

What is a good indicator of body vitamin D status?

A

Serum 25-OH cholecalciferol (biologically inactive) as calcitriol is difficult to measure in blood

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5
Q

How does calcitriol regulate its own synthesis?

A

Decreases transcription of 1-alpha-hydroxylase (negative feedback)

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6
Q

What are the effects of calcitriol on bone?

A
  • low serum calcium = binds to calcitriol receptors on osteoblasts = release OAFs which switch on osteoclasts
  • normal serum calcium = increased osteoblast activity = increased bone formation
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7
Q

What are the effects of calcitriol on the kidney?

A

Increased calcium and phosphate reabsorption from urine

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8
Q

What are the effects of calcitriol on the gut?

A

Increased calcium and phosphate absorption from food/reabsorption from gut

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9
Q

What are the effects of PTH on bone?

A

Increases Ca2+ reabsorption from bone by switching on osteoclasts = increased serum calcium

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10
Q

What are the effects of PTH on the kidney?

A
  • increases Ca2+ reabsorption
  • increases PO4(3-) excretion (inhibits Na-PO4 cotransporter, increasing excretion)
  • increases 1-alpha-hydroxylase activity (increases calcitriol synthesis)
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11
Q

What are the effects of PTH on the gut?

A

Indirect - through increase in calcitriol synthesis, there is an increase in Ca2+ and PO4(3-) absorption

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12
Q

What is the overall effect of calcitriol and PTH?

A

Increase plasma calcium

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13
Q

How does FGF23 work to reduce serum phosphate?

A
  • fibroblast growth factor 23 is derived from bone
  • inhibits Na-PO4 co-transporter on PCT cells which is involved in reabsorption of phosphate (and sodium) from urine
  • also inhibits calcitriol synthesis causing less reabsorption from gut
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14
Q

How does PTH cause phosphate to be excreted?

A

PTH inhibits the sodium-phosphate cotransporters, meaning less phosphate is reabsorbed and more is excreted

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15
Q

What are the clinical symptoms of hypocalcaemia?

A
  • sensitises excitable tissues
  • mnemonic - CATs go numb
  • convulsions (fits)
  • arrhythmias
  • tetany - contract muscles but cannot relax again
  • paraesthesia - tingling (hands, mouth, feet, lips)
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16
Q

What is Chvosteks’ sign?

A
  • tap facial nerve below zygomatic arch
  • more membrane excitability = positive response = twitching of facial muscles
  • indicates neuromuscular irritability due to hypocalcaemia
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17
Q

What is Trousseau’s sign?

A
  • inflate BP cuff around arm
  • induces carpopedal spasm (tetany)
  • due to neuromuscular irritability due to hypocalcaemia
18
Q

What are two causes of hypocalcaemia?

A
  • low PTH levels (hypoparathyroidism)
  • low vitamin D levels
19
Q

What are causes of low PTH levels? (4)

A
  • surgical - neck surgery
  • autoimmune
  • magnesium deficiency
  • congenital (agenesis - rare)
20
Q

What are causes of low vitamin D levels?

A

Deficiency - poor diet/malabsorption, lack of UV light, impaired production (renal failure)

21
Q

What are the signs and symptoms of hypercalcaemia?

A
  • stones, abdominal moans, psychic groans
  • reduced neuronal excitability causes atonal muscles
  • stones - renal effects e.g. nephrocalcinosis (kidney stones, renal colic)
  • abdominal moans - GI effects e.g. anorexia, nausea, dyspepsia, constipation, pancreatitis
  • psychic groans - CNS effects e.g. fatigue, depression, impaired concentration, altered mentation, coma (>3 mmol/L)
22
Q

What are the causes of hypercalcaemia?

A
  • primary hyperparathyroidism - too much PTH (usually parathyroid gland adenoma) - no negative feedback = high PTH but high calcium
  • malignancy - cancer metastasised to bone produces local factors that activate osteoclasts, increasing Ca2+ reabsorption from bone
  • vitamin D excess (rare)
23
Q

What is the relationship between PTH and calcium?

A
  • if calcium falls, parathyroid glands sense this and release more PTH
  • if calcium is too high, there is negative feedback and parathyroid glands do not release PTH
24
Q

What happens in primary hyperparathyroidism?

A
  • parathyroid adenoma produces too much PTH
  • calcium increases, but no negative feedback to PTH due to autonomous PTH secretion from adenoma
25
What is the biochemistry of primary hyperparathyroidism?
- high calcium - low phosphate - increased renal phosphate excretion (inhibition of sodium-phosphate transporter in kidney) - high PTH (not suppressed by hypercalcaemia)
26
What is the treatment of primary hyperparathyroidism?
Parathyroidectomy
27
What are the risks of untreated primary hyperparathyroidism? (3)
- osteoporosis (due to osteoclasts constantly breaking down bone) - renal calculi (stones) - psychological impact of hypercalcaemia - mental function, mood
28
What happens in secondary hyperparathyroidism?
- normal physiological response to hypocalcaemia - calcium will be low/normal - PTH will be high (hyperparathyroidism) secondary to the low calcium - different from primary hyperparathyroidism where calcium is high
29
What are the causes of secondary hyperparathyroidism?
- most common cause is vitamin D deficiency due to diet, reduced sunlight - less common cause is due to renal failure - cannot make calcitriol
30
What is the general treatment for secondary hyperparathyroidism in people with and without kidney failure?
Vitamin D replacement
31
What is the treatment for secondary hyperparathyroidism in people with normal renal function?
- 25-hydroxy vitamin D - patient converts to 1,25(OH)2 vitamin D via 1-alpha-hydroxylase - can give ergocalciferol (25 hydroxy vitamin D2) or cholecalciferol (25 hydroxy vitamin D3)
32
What is the treatment for secondary hyperparathyroidism in people with renal failure?
- inadequate 1-alpha hydroxylation so cannot activate 25 hydroxy vitamin D - give alfacalcidol - 1-alpha hydroxycholecalciferol (active vitamin D)
33
What happens in tertiary hyperparathyroidism?
- rare - occurs in chronic renal failure - cannot make calcitriol = chronic vitamin D deficiency - parathyroid glands start secreting more PTH to make up for drop in calcitriol so calcium is not too low - parathyroid glands enlarge (hyperplasia of all 4 glands) to the point they cannot be switched off - autonomous PTH secretion happens causing hypercalcaemia
34
How is tertiary hyperparathyroidism treated?
Parathyroidectomy
35
How does tertiary hyperparathyroidism present as initially?
Secondary hyperparathyroidism - calcium falls and PTH rises (but over long period high PTH drive by enlarged PT glands increases calcium)
36
What is the diagnostic approach to hypercalcaemia?
- when looking at hypercalcaemia, always look at PTH - hypercalcaemia & suppressed PTH = hypercalcaemia of malignancy - hypercalcaemia & elevated PTH --> look at kidney function - normal kidney function = primary hyperparathyroidism - chronic renal failure = tertiary hyperparathyroidism - vitamin D deficiency --> low calcium, high PTH = secondary hyperparathyroidism
37
What happens in hypercalcaemia due to malignancy?
- high calcium - low / suppressed PTH
38
How do we differentiate between primary and tertiary hyperparathyroidism?
- primary if renal function is normal e.g. parathyroid adenoma - tertiary (all 4 glands hyperplastic) if chronic renal failure
39
How do you treat hypercalcaemia of malignancy?
Bisphosphonates - inhibit osteoclasts and stop them from absorbing bone = lowers calcium, less bony pain
40
When is hypercalcaemia of malignancy suspected?
- hypercalcaemia - suppressed PTH - previous history of cancer

Year 2 - BRS (84 decks)

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