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Endocrinology > Endocrine control of calcium metabolism > Flashcards

Endocrine control of calcium metabolism Flashcards

1
Q

What is the main form of calcium

A

Hydroxyapatite crystals in bone

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2
Q

In what forms are calcium present in the blood

A

50% unbound
45% bound to plasma proteins
5% diffusible salts (citrate, lactate)

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3
Q

What form of calcium is bioactive

A

free Ca2+

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4
Q

What are the roles 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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5
Q

What is the main route of calcium after intake

A

Intake -> GI tract -> blood -> kidneys

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6
Q

From the blood where may calcium travel

A

bone and other cells
kidney
Loss in hair, skin and nails

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7
Q

What is released when calcium levels are too low

A

Parathyroid hormone and calcitrol

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8
Q

Describe the calcium sensing receptor

A

G-protein coupled receptor that is activated by ligand binding (suppresses PTH)

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9
Q

Describe the process of PTH synthesis

A
  1. synthesised as pre-proPTH

2. cleavage to form PTH

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10
Q

Where is PTH synthesised

A

parathyroid glands

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11
Q

Where is calcitonin synthesised

A

parafollicular cells of the thyroid

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12
Q

How does PTH affect the kidneys

A

Increases calcium reabsoprtion
Increases phosphate excretion
Stimulate 1𝛼 hydroxylase activity to increase calcitrol synthesis

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13
Q

How does PTH affect the small intestine

A

Calcitrol synthesis in the liver stimulates increased calcium absorption
Increased phosphate absoprtion

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14
Q

How does PTH affect the bone

A

Stimulation of osteoclasts and inhibition of osteoblasts so an increase in bone resorption (decrease in bone mass)

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15
Q

Describe the process of PTH induced decreased bone resorption

A
  1. PTH binds to the PTH receptor on an osteoblast
  2. Osteoblasts release osteoclast activating factors (RANKL)
  3. Increased bone resorption
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16
Q

How is PTH regulated

A

Increased plasma calcium creates a negative feedback effect to reduce PTH levels from the parathyroid gland

17
Q

How is calcitriol synthesised

A
  1. UV light converts 7-dehydrocholesterol into cholecalciferol/ obtained from the diet
  2. Synthesis of 2,5-hydroxy-cholecalciferol in the liver (+2 OH groups)
  3. PTH stimulates 1𝛼 hydroxylase
  4. synthesis of 1,25-di-hydroxycholecalciferol in the kidney
18
Q

How does calcitriol affect the bone

A

Increased osteoblast activity

19
Q

How does calcitriol affect the kidneys

A

Increased calcium and phosphate reabsorption

20
Q

How does calcitriol affect the small intestine

A

Increased calcium and phosphate absorption

21
Q

How are circulating phosphate levels regulated

A

Fibroblast growth factor 23 once stimulated by high phosphate and vitamin D3 levels in the kidney

22
Q

How does FGF23 work

A

Inhibits the reabsorption of phosphate and sodium through the phosphate sodium cotransporter in the kidney (PTH does the same)

23
Q

What are the main effects of calcitonin

A

Increased urinary excretion of calcium, sodium and phosphate
Inhibition of osteoclast activity
Decrease calcium levels

24
Q

What are the three main causes of hypocalcaemia

A

Hypoparathyroidism
Pseudohypoparathyroidism
Vitamin D deficiency

25
Q

What are the signs of hypocalcaemia

A

Trousseau’s

Chvostek’s

26
Q

What are the features of hypoparathyroidism

A

low calcium, high phosphate, low PTH
Hypomagnesaemia
Suppression by raised calcium concentration

27
Q

What are the features of pseudohypoparathyroidsm

A

Target organ resistance to PTH (may be due to defective Gs protein)
low calcium, high phosphate, high PTH

28
Q

What are the clinical features of pseudohypoparathyroidism

A

Short stature
Round face
Low IQ
Subcutaneous calcification and one abnormalities
Endocrine disorders (hypothyroidism, hypogonadism)

29
Q

What can vitamin D deficiency cause

A

Ricketts in children

Osteomalacia in adults

30
Q

What are the clinical features of vitamin D deficiency

A

Decreased calcification of the bone matrix
Softening of the bone
Bowing of the bones
Fractures

31
Q

What are the features of vitamin D deficiency

A

Low calcium, low phosphate, high PTH

32
Q

What are some clinical features of hypercalcaemia

A 
Increased calcium reabsorption
Increase phosphate excretion
Polyuria
Renal stones
Nephrocalcinosis
Gastric acid release
Duodenal ulcers
Bone lesions
Bone rarefaction (reduction in density)
Fractures
33
Q

What is primary hyperparathyroidism

A

High levels of PTH are produced due to an adenoma growing in the glands, increasing the circulating calcium levels. -ve feedback system does not work

34
Q

What is secondary hyperparathyroidism

A

PTH levels remain high but calcium levels remain low, commonly due to kidney disease as it cannot reabsorb the calcium needed

35
Q

What is tertiary hyperparathyroidism

A

The parathyroid glands grow due to secondary parathyroidism and once this has been treated, the glands remain large and become autonomous, not responding effectively to feedback

36
Q

What is another cause of hypercalcaemia

A

Vitamin D toxicosis

Endocrinology (9 decks)

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