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BRS Bioregulatory Systems > Regulation Of Calcium And Phosphate > Flashcards

Regulation Of Calcium And Phosphate Flashcards

1
Q

What is calcium and how much is recommended adult intake?

A

Most abundant metal in body

Recommended adult intake is 1000 mg/day

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2
Q

Calcium distribution in body

A
  • 99% in skeleton and teeth as calcium hydroxyapatite crystals
  • 1% intracellular
  • 0.1% extracellular which is tightly regulated
    • 2.5 mmol/L in plasma, where 45% is biologically active unbound ionised Ca2+ and 55% is bound Ca2+ (45% bound to plasma proteins like albumin and 55% to anions like bicarbonate, phosphate, lactate)
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3
Q

What 3 hormones are responsible for regulating serum calcium and phosphate?

A
  • Parathyroid hormone (PTH) secreted by parathyroid glands
  • Metabolite of Vitamin D3 (Calcitriol)
  • Calcitonin secreted by thyroid parafollicular cells → can reduce calcium conc acutely but no -ve effect if parafollicular cells removed e.g. in thyroidectomy - so isn’t a main player in calcium regulation
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4
Q

What are 2 types and sources of Vitamin D?

A
  • Vitamin D2 (ergocalciferol) from diet e.g. oily fish
  • Vitamin D3 (cholecalciferol) synthesised in skin when exposed to sunlight
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5
Q

How is vitamin D3 made and both D2 and D3 metabolised?

A

In skin when exposed to sunlight, 7-dehydrocholesterol → pre-vitamin D3 → vitamin D

Vitamin D becomes activated after undergoing both hydroxylation steps (1st hydroxylation by 25-hydroxylase in the liver, 2nd hydroxylation by 1-alpha-hydroxylase in the kidney)

1,25(OH)2 cholecalciferol is aka calcitriol - the active form of vitamin D, produced by the 2nd hydroxylation

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6
Q

What does the 1st hydroxylation step produce

A

25-OH cholecalciferol

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7
Q

What is serum 25-OH cholecalciferol a good indicator of?

A

Body vitamin D status, as calcitriol is difficult to measure in blood

25-OH cholecalciferol is biologically inactive

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8
Q

How does calcitriol regulate its own synthesis?

A

It decreases transcription of 1-alpha-hydroxylase - negative feedback

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9
Q

What are the(3) effects of calcitriol?

A
  • Bone- increases Ca2+ reabsorption from bone, by binding to calcitriol receptors on osteoblasts which release Osteoclast activating factors (OAFs) which switch on osteoclasts. (for VSAQ purposes: increases osteoclast activity)
  • Kidney- increases Ca2+ and phosphate reabsorption by kidney from urine
  • Increases calcium and phosphate reabsorption from gut
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10
Q

How does calcitriol action on bone depend on serum calcium?

A

Low serum calcium - Calcitriol increase reabsorption from bone (osteoclasts > osteoblasts)

Normal serum calcium - Calcitriol works to increase bone formation (osteoblast > osteoclast)

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11
Q

What is the rate limiting step for active Vitamin D synthesis?

A

1-alpha-hydroxylase converting 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol

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12
Q

What secretes PTH?

A
  • Chief cells in parathyroid glands
  • Secreted as a large precursor (pre-pro-PTH) & cleaved into PTH
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13
Q

What detects the changes in circulating calcium concentration?

A

G-protein coupled calcium sensing receptors on chief cells

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14
Q

How is PTH secretion related to calcium levels?

A

If serum calcium conc. high, PTH secretion inhibited

If serum calcium is low, more PTH secreted

  • High ECF Ca2+ conc means more Ca2+ binds to receptors on parathyroid cells so PTH secretion inhibited
  • Low ECF Ca2+ conc means less Ca2+ binding to receptors on parathyroid cells so PTH secreted
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15
Q

What are the (3) effects of PTH on the kidney?

A
  • Increase Ca2+ reabsorption from kidney from urine
  • increases expression of 1-alpha-hydroxylase → this increases calcitriol synthesis
  • decreases renal phosphate reabsorption (Overall the effects on phosphate is neutral- it causes loss through kidney and gain through gut)
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16
Q

Explain the affect of PTH on bone and how it does this.

A
  • Increases reabsorption of calcium from bone (for VSAQ purposes: increases osteoclast activity)
  • PTH binds to PTH receptor on osteoblasts (cells that build bone)
  • Stimulates osteoblasts to make osteoclast activating factors (OAFs) e.g. RANKL (receptor activator of nuclear factor kappa-B ligand)
  • Osteoclasts (cells that consume bone) are switched on and dissolve bone, releasing calcium
17
Q

What are the effects of PTH on the gut

A

Gut- through increase in calcitriol synthesis, there is increase in Ca2+ and phosphate absorption from gut (so PTH doesn’t directly affect gut)

18
Q

How is PTH regulated (2 ways)?

A
  • PTH causes increase in plasma Ca2+ which has negative feedback as it binds to Ca2+ receptors on the chief cells and decreases PTH secretion
  • PTH also increases calcitriol synthesis by increasing action of 1-alpha-hydroxylase → chief cells also have calcitriol receptors and there’s negative feedback again as high calcitriol levels cause decrease in PTH secretion
19
Q

Which cells secrete calcitonin?

A

Parafollicular cells of the thyroid gland

20
Q
  • What effect does calcitonin have on serum calcium?
A

Reduces serum calcium

21
Q

Outline the actions of calcitonin on the bone and kidney

A

Reduces osteoclast activity

Increases Ca2+ excretion through urine (by preventing renal reabsorption of calcium)

Overall affect → Reduced calcium levels

22
Q

How does phosphate reabsorption in kidneys happen?

A
  • Phosphate reabsorbed via sodium-phosphate transporter (symporter) cells- this also therefore results in less sodium excretion in urine
  • Increased phosphate loss in urine would lower serum phosphate levels
23
Q

How does PTH work here affect phosphate

A
  • PTH inhibits renal phosphate reabsorption by inhibiting these transporters
  • In primary hyperparathyroidism, serum phosphate is low due to increased urine phosphate excretion
24
Q

What factor regulates serum phosphate?

A

FGF23

  • Fibroblast Growth Factor 23 is derived from bone
  • Also inhibits phosphate reabsorption in kidneys by inhibiting Na-PO4 transporters
  • Also inhibits calcitriol synthesis causing less phosphate absorption from gut from food
25
Q

What is hypercalcaemia?

A

High serum calcium

26
Q

How does it affect sodium influx?

A
  • There’s high extracellular calcium
  • Ca2+ blocks Na+ influx, so there’s LESS membrane excitability
27
Q

What are the signs and symptoms?

A
  • Stones, Abdominal moans and Psychic groans (mnemonic SAP)
  • 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 (pancreas inflammation)
  • Psychic groans- CNS effects e.g. fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L)
28
Q

What are causes of hypercalcaemia

A
  • Primary hyperparathyroidism- too much PTH- usually due to parathyroid gland adenoma
    • There is no negative feedback since there’s too much PTH so there’s high PTH and also high calcium
  • Malignancy- metastases in bone produce local factors that activate osteoclasts, increasing Ca2+ reabsorption from bone
  • Vitamin D excess (rare)
29
Q

What is hypocalcaemia?

A

Low serum calcium

30
Q

How does it affect sodium influx?

A
  • There’s low extracellular calcium so this enables greater Na+ influx as there’s less competition for Na+ to move across membrane
  • Means MORE membrane excitability
31
Q

What are clinical symptoms?

A
  • sensitises excitable tissues
  • Paraesthesia (tingling) of hands, mouth, feet, lips
  • Convulsions- fits
  • Arrhythmias- unusual heart rhythms
  • Tetany- contract muscles but can’t relax again
  • Mnemonic- CATs go numb
32
Q

Name and explain the 2 signs used to identify hypocalcaemia

A
  • Chvostek’s signTap facial nerve just below zygomatic archPositive response - twitching of facial muscles → Indicates neuromuscular irritability due to hypocalcaemia
  • Trousseau’s sign
  • Inflate a BP cuff for several minutes around patient’s arm
  • This induces carpopedal (fingers) spasm and muscles contract and can’t relax again (tetany)
  • Tetany in fingers
  • This is due to neuromuscular irritability due to hypocalcaemia
33
Q

2 main causes of hypocalcemia

A

Vitamin d deficiency
Low PTH levels

34
Q

Vitamin d deficiency

A

Malabsorption/dietary insufficiency

Inadequate sun exposure

Liver disease → reduced synthesis of 25-hydroxylase

Renal disease/disorder for the hydroxylation of 25-hydroxycholecalciferol into calcitriol

Vitamin D receptor defects

Causes rickets in children

In adults leads to osteomalacia

35
Q

Low pth levels hypoparathyroidism

A
  • Surgical- neck surgery could have damaged parathyroid glands
  • Auto-immune- one of the most common reasons
  • Magnesium deficiency- it’s needed to make PTH
  • Congenital (agenesis of parathyroid gland i.e. it doesn’t develop in embryo- rare)
36
Q

Which other ion is needed to make PTH?

BRS Bioregulatory Systems (54 decks)

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