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LCRS > Endocrinology 11 - Endocrine Control of Calcium Metabolism > Flashcards

Endocrinology 11 - Endocrine Control of Calcium Metabolism Flashcards

1
Q

List the roles of calcium in the body

A
  • Neuromuscular excitability
  • Muscle contraction
  • Strength in bones
  • Intracellular secondary messenger
  • Coenzyme
  • Involved in blood coagulation
  • Neurotransmitter release
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2
Q

How is most calcium found in the body?

A
  • In the form of salts
  • Mainly present in the bone as a hydrated salt (hydroxyapatite)
  • Some calcium is found as ionised calcium, bound to protein or bioactive
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3
Q

What percentage of calcium is bound and unbound in the blood?

A

50% unbound and ionised
45% bound to plasma proteins
5% diffusible salts

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4
Q

What hormones are involved in calcium ion regulation?

A
  • Parathyroid hormone
  • Calcitonin (decrease)
  • Calcitriol (vitamin D3)
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5
Q

Where is parathyroid hormone (PTH) secreted from?

A

Parathyroid glands

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6
Q

Where is calcitonin secreted from?

A

The parafollicular cells.

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7
Q

What type of receptor are calcium sensing receptors?

A

G protein coupled receptors

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8
Q

How is parathormone initially synthesised?

A

As pre-proPTH

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9
Q

What receptors do parathormone and calcitonin bind to?

A
  • Transmembrane G coupled receptors

- Activates adenyl cyclase and PLC

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10
Q

Describe the actions of parathyroid hormone.

A
  • Increases breakdown of bone (resorption) via activation of osteoclasts and inhibition of osteoblasts
  • Increases calcium in the blood by increasing absorption of the kidney and prodction of calcitrol (via 1-alpha hydroxylase)
  • Also increases excretion of phosphate from the kidneys
  • Increases calcium and phosphate absorption at the SI
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11
Q

Describe the process that occurs when PTH binds to receptors in bone

A
  • PTH binds to receptors on osteoblasts
  • Osteoblasts produce osteoclast activating factors
  • An example of this is RANKL
  • Osteoclasts then perform bone breakdown
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12
Q

Describe the regulation of PTH

A
  • PTH release is stimulated by decreased plasma calcium, catecholamines (dopamine, noradrenaline - bind to beta receptors)
  • PTH release is inhibited by negative feedback, when the plasma calcium increases and by calcitrol.
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13
Q

What are the actions of dihydroxycholecalciferol?

A
  • Calcitrol
  • Increases osteoblast activity in bone, and calcium absorption in the small intestine (for use in bones)
  • Increases phosphate absorption in the SI
  • Increases calcium and phosphate reabsorption in the kidney
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14
Q

What are the actions of fibroblast growth factor 23?

A
  • Production is stimulated by phosphate and calcitrol
  • It inhibits production of calcitrol (negative feedback)
  • It reduces phosphate levels in the blood, reducing expression of the sodium phosphate transporter in the kidney
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15
Q

What is calcitonin synthesised as?

A

Pre-procalcitonin

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16
Q

Which factors regulate calcitonin production?

A
  • Increases plasma calcium ion concentration increases calcitonin
  • The hormone gastrin stimulates calcitonin production, as well as production of stomach acid
  • Production decreases when the decreased plasma calcium ion conc occurs
17
Q

Describe the actions of calcitonin

A
  • Works to decrease plasma Ca2+, though it has a limited effect
  • Increases excretion of Ca2+ at the kidneys
  • Inhibits osteoclast activity
18
Q

List the three endocrine causes of hypocalcaemia.

A
  • Hypoparathyroidism
  • Pseudohypoparathyroidism
  • Vitamin D deficiency
19
Q

What are the two signs of hypocalcaemia?

A

Tetany can be seen by these signs:

  • Trousseaus sign (hand curling up)
  • Chvosteks sign (face twitching too much at a small stimulus)
20
Q

What is another name for pseudoypoparathyroidism?

A

Allbright hereditary osteodystrophy

21
Q

What is the cause of pseudohypoparathyroidism?

A
  • Target organ resistance to PTH

- Due to defective Gs protein, which increases cAMP in response to receptor activation

22
Q

What are the features of pseudohypoparathyroidism?

A
  • Short stature, round face
  • Low IQ
  • Subcutaneous calcification and bone abnormalities
  • Endocrine disorders
23
Q

What are the names for vitamin D deficiency in children and in adults?

A
  • Rickets in children

- Osteomalacia in adults

24
Q

What are the clinical features of vitamin D deficiency?

A
  • Bone matrix has decreased calcification, resulting in the bone softening
  • Bowing in children
  • Fractures in adults
25
Q

Describe levels of plasma Ca, PO4 and PTH in hypoparathyroidism.

A
  • Low calcium
  • Low PTH
  • High plasma PO4
26
Q

Describe levels of plasma Ca, PO4 and PTH in pseudohypoparathyroidism.

A
  • High PTH
  • High PO4
  • Low clacium
27
Q

Describe levels of plasma Ca, PO4 and PTH in vitamin D deficiency

A
  • High PTH
  • Low PO4
  • Low calcium
28
Q

What are the endocrine causes of hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Tertiary hyperparathyroidism
  • Vitamin D toxicosis
29
Q

What happens in primary hyperparathyroidism?

A
  • There is an ademona, casing excessive production of hormones
  • Production is not stopped by negative feedback
30
Q

What happens in secondary hyperparathyroidism?

A
  • There is low plasma calcium, for example due to renal failure
  • Therefore, the parathyroids overproduce PTH while levels of calcium are low or as they should be
31
Q

What happens in tertiary hyperparathyroidism?

A
  • There is initially chronic low plasma (secondary hyperparathyroidism), for example renal failure. The cause of low plasma is then treated.
  • The parathyroid glands become autonomous and no longer respond to feedback
32
Q

What does parathyroid hormone excess cause?

A
  • High calcium
  • Phosphate excretion
  • Polyurea
  • Kidney stones
  • High calcitonin
  • Gastric acid
  • Bone lesions or rarefaction (shortening)
  • Fractures
33
Q

Where is calcitriol produced?

A

Kidney

LCRS (24 decks)

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