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Endocrinology > Endocrine Control of Calcium Metabolism > Flashcards

Endocrine Control of Calcium Metabolism Flashcards

1
Q

State some roles of calcium in the body.

A

Control of neuromuscular excitability (hypocalcaemia leads to hyperexcitability because Ca2+ normally blocks the Na+ channels)

Muscle Contraction

Strength in bone

Blood clotting

Intracellular second messenger

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2
Q

Where is calcium mainly stored?

A

Bone - 99% is stored as hydroxyapatite crystals in bone.

COMPLEX HYDRATED CALCIUM SALT

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3
Q

How is calcium present in the blood? What is the main component?

A

Unbound ionised calcium - 50%

Bound to plasma proteins - 45%

Tiny bit as soluble salts

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4
Q

What is the usual daily intake of calcium?

A

1000 mg/day

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5
Q

What is the concentration of unbound ionised calcium in the blood?

A

1.25 mM

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6
Q

What two hormones raise plasma calcium concentration?

A

Parathyroid Hormone

Calcitriol (1,25-dihydroxycholecalciferol)

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7
Q

What hormone decreases plasma calcium concentration?

A

Calcitonin

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8
Q

Where is parathyroid hormone produced?

A

Parathyroid Glands (four of them) - produced in the follicular cells

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9
Q

Where is calcitonin produced?

A

Parafollicular cells in the thyroid gland

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10
Q

Describe the effects of parathyroid hormone on the kidneys.

A
  1. Increases calcium reabsorption
  2. Increases phosphate excretion
  3. Stimulates 1 alpha hydroxylase activity
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11
Q

Describe the effects of PTH on bone.

A

Inhibits osteoblast acitivity

Stimulates osteoclasts ( via OAFs, osteoclast activating factors). PTH stimulates osteoclasts to break down bone matrix to release Ca+2.

Example of OAF = RANKL

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12
Q

Describe the effects of PTH on the small intestines.

A

PTH increases the activity of 1 alpha hydroxylase (in the kidneys), which is involved in the production of calcitriol, which increases calcium and phosphate absorption in the small intestine.

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13
Q

How does PTH increase calcium release from bone?

A

PTH has a direct effect in inhibiting osteoblasts. PTH makes the osteoblasts produce osteoclast activating factors (such as RANKL) that bind to receptors on osteoclasts and stimulates the break down of bone matrix to release calcium.

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14
Q

What can stimulate PTH release?

A
  1. Low plasma calcium concentration
  2. Catecholamines (by binding to beta receptors)
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15
Q

Describe the negative feedback loops on PTH.

A

Increased plasma calcium concentration has a negative feedback effect on PTH

Calcitriol also has a negative feedback effect

Catecholamies stimulate PTH release from PTG

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16
Q

What is the precursor of calcitriol?

A

Cholecalciferol

17
Q

Where does cholecalciferol come from?

A

Diet Sun Light (UV converts 7-dehydrocholesterol to cholecalciferol)

NOTE: cholecalciferol is VITAMIN D3

18
Q

Describe the reactions that have to take place to convert the precursor to calcitriol.

A
  1. 7-Dehydrocholesterol converted into cholecalciferol via UV light
  2. Cholecalciferol (inactive) travels to the liver where 25-hydroxylase converts it to 25-hydroxycalciferol, which is then stored in the liver.
    1. It then moves to the kidneys where 1 alpha hydroxylase (stimulated by PTH) converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (calcitriol)
19
Q

Describe the effects of calcitriol.

A

SMALL INTESTINE: Increased calcium and phosphate reabsorption

BONES: Increase osteoblast activity

KIDNEYS: Increase Calcium reabsorption and Phosphate excretion

20
Q

How does calcitriol and PTH decrease phosphate reabsorption in the kidney? Draw a diagram to represent this

A

They block the sodium/phosphate cotransporter Calcitriol does this via the action of FGF23 (fibroblast growth factor 23)

21
Q

Describe the effects of calcitonin.

A

BONES: Inhibits osteoclast activity

KIDNEYS: Increase sodium excretion and hence increase urinary excretion of phosphate and calcium.

22
Q

State a physiological benefit of calcitonin.

A

During pregnancy women need a higher plasma calcium concentration (e.g. for milk), calcitonin protects the bone from break down.

23
Q

State three causes of hypocalcaemia.

A

Hypoparathyroidism Pseudohypoparathyroidism Vitamin D Deficiency

24
Q

What two signs are used to demonstrate hypocalcaemia?

A

Trousseau’s Sign: Slight pressure on arm causes hand to spasm

Chvostek’s Sign: the twitching of the facial muscles in response to tapping over the area of the facial nerve

25
Q

What does vitamin D deficiency cause in children and adults and what are the clinical features ?

A

Children - rickets, bowing of bones

Adults - osteomalacia, fractures

Why? decreased calcifictaion of bone matrix

26
Q

State three causes of hypercalcaemia.

A

Primary hyperparathyroidism Tertiary hyperparathyroidism Vitamin D Toxicosis

27
Q

Describe the differences between primary, secondary and tertiary hyperparathyroidism.

A

Primary - caused by parathyroid adenoma producing huge amounts of PTH

Secondary - caused by other reasons e.g. renal excretion of Ca2+ ions leading to compensatory increase in release of PTH (this causes low Ca2+ because it is being lost from the kidneys)

Tertiary - initial chronic low plasma calcium concentration - parathyroid gland is massively stimulated for a long time and so PTH production becomes autonomous and stops responding to negative feedback (leads to hypercalcaemia)

PRIMARY AND TERTIARY ASSOCIATED WITH HYPERCALCAEMIA

28
Q

State some consequences of parathyroid hormone excess.

A
  1. Kidney stones (calcium deposits)
  2. Increased risk of fracture
  3. Nephrocalcinosis
  4. Duodenal ulcers
  5. Bone lesions
29
Q

What is a distinctive clinical feature of primary hyperparathyroidism?

A

Clubbing of the fingers

periosteal bone erosion in terminal phalanges

30
Q

What are the symptoms of pseudohypoparathryroidism(also called Allbright Heriditary Osteodystrophy)?

A
  1. Facial appearance (short stature, round face)
  2. low IQ
  3. subcutaneous calcification and shortening of metacarpals
  4. other endocrine disorders (eg hypothyroidism, hypogonadism)
31
Q

What causes pseudohypoparathryroidism(also called Allbright Heriditary Osteodystrophy)?

A

-Targert organ resistance to PTH ( several Underlying Causes) - Due to defective G protein - cAMP isn’t increased intracellularly in response to PTH receptor activation

32
Q

Describe briefly how calcium sensing receptors work

A

G protein coupled receptor Ligand ( Ca+2) binds to receptor causing a conformational change

33
Q

How is PTH and Calcitonin synthesised and what is its mechanism of action?

A
  • PTH initially synthesised as protein pre-proPTH whilst calcitriol is synthesisd as pre-procalcitonin
  • PTH polypeptide had 84 AAs Calcitonin 32 AA

BOTH

  • Binds to transmembrane G protein linked receptors
  • Activation of adenyl cyclase, but also probably PLC as second messenger systems
34
Q

What is the overall effect of PTH ?

A

Increase blood Ca+2

35
Q

Name an example of OAFs

A

RANKL

36
Q

How do you differentiate between hypoparathyroidism, pseudo-hypoparathyroidism and vitamin d deficiency?

A
37
Q

What stimulates calcitonin release/

A
  1. Increased calcium plasma concentration
  2. Gastrin

Endocrinology (15 decks)

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