12 - Calcium Metabolism Flashcards

1
Q

How does PTH increase calcium release from bone?

A
  • PTH makes osteoblasts produce osteoclast activating factors (RANKL)
  • OAFs bind to receptors on osteoclasts
  • stimulates break down of bone matrix to release calcium
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2
Q

What are the functions of calcium?

A
  • neuromuscular excitability
  • muscle contraction
  • strength in bones
  • intracellular second messenger
  • intracellular co-enzyme
  • hormone/neurotransmitter stimulus-secretion coupling
  • blood coagulation (factor IV)
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3
Q

What are the causes of hypocalcaemia?

A
  • hypoparathyroidism
  • pseudohypoparathyroidism
  • vitamin d deficiency
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4
Q

What are the features of hypoparathyroidism?

A

INSUFFICIENT PTH

  • reduced calcium
  • reduced PTH
  • increased PO4
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5
Q

What are the features of pseudohypoparathyroidism?

A

RESISTANCE TO PTH

  • reduced calcium
  • increased PTH
  • reduced PO4
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6
Q

What are the features of vitamin D deficiency?

A
  • reduced calcium
  • increased PTH
  • reduced PO4
    RICKETS AND OSTEOMALACIA
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7
Q

What are the signs of hypocalcaemia?

A
  • Trousseau’s sign

- Chvostek’s sign

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8
Q

What are the causes of hypercalcaemia?

A
  • primary hyperparathyroidism
  • tertiary hyperparathyroidism
  • vitamin d toxicosis
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9
Q

What are the symptoms of hypercalcaemia?

A
  • painful bones
  • renal stones
  • abdominal groans
  • psychic moans
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10
Q

How is Ca2+ regulated?

A
  • increased by parathyroid hormone (PTH - secreted by parathyroid gland)
  • increased by 1,25(OH)2 vitamin D3 (calcitriol - produced by kidneys)
  • decreased by calcitonin (produced by parafollicular cells in thyroid)
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11
Q

How is PTH regulated?

A
  • stimulates enzyme leading to calcitriol synthesis
  • increased calcitriol synthesis leads to increased plasma calcium concentration
  • parathyroid cells respond to changes in plasma calcium concentration (have Ca2+ receptors)
  • Ca2+ receptors activated with fall in calcium concentration
  • calcitriol has negative feedback on PTH
  • β receptors on cells producing PTH stimulated by catecholamines to secrete PTH (positive feedback)
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12
Q

What are the actions of PTH on kidneys, bone, small intestine and blood?

A
  • kidneys: increases Ca2+ reabsorption, PO43- excretion and stimulates 1 α hydroxylase activity (increases calcitriol synthesis)
  • bone: increases Ca2+ mobilisation (osteoclasts stimulated, osteoblasts inhibited) and increases bone resorption
  • small intestine: increases Ca2+ and PO43- absorption
  • [Ca2+] in blood increases
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13
Q

What are the actions of calcitriol on the kidneys, small intestine and bone?

A
  • kidneys: increased Ca2+ and PO43- reabsorption
  • small intestine: increased Ca2+ and PO43- absorption
  • bone: increased osteoblast activity
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14
Q

How is calcitriol regulated?

A
  • cholecalciferol sourced from diet and sunlight (taken up by liver)
  • 25-hydroxylase converts cholecalciferol to 25-hydroxy-cholecalciferol (stored in liver)
  • 1 α hydroxylase converts 25-hydroxy-cholecalciferol to calcitriol (in kidneys)
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15
Q

How is calcitonin regulated?

A
  • stimulated by increase in plasma calcium conc.

- gastrin also stimulates production

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16
Q

What are the actions of calcitonin on the kidneys, urine and bone?

A
  • kidneys: increases Na2+ secretion
  • urine: increases Ca2+ and PO43- excretion
  • bone: inhibits osteoclast activity
17
Q

How is phosphate reabsorbion inhibited?

A
  • transporters for PO43- ions on apical membrane
  • PTH inhibits transporter
  • PO43- excreted in urine
  • calcitriol blocks phosphate transporter (FG23) and inhibits its reabsorption
18
Q

What are the different types of hyperparathyroidism?

A
  • primary
  • secondary
  • tertiary
19
Q

What is primary hyperparathyroidism?

A

tumour in parathyroid causes large increase in PTH secretion

20
Q

What are the features of secondary hyperparathyroidism?

A
  • low plasma calcium concentration from diseases (e.g. renal failure)
  • leads to loss of calcium in urine
  • stimulates PTH release
21
Q

What are the features of tertiary hyperparathyroidism?

A
  • initial chronic low plasma calcium ion concentration
  • parathyroid gland massively stimulated for long time
  • PTH becomes autonomous and stops responding to negative feedback