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Y1 Fwong LCRS Dulan > Endocrinology 12 - Control of Calcium metabolism > Flashcards

Endocrinology 12 - Control of Calcium metabolism Flashcards

1
Q

What are the roles of calcium?

A
  1. Neuromuscular excitability.
  2. Muscle contraction.
  3. Strength in bone.
  4. Intracellular second messenger.
  5. Intracellular co-enzyme.
  6. Hormone/neurotransmitter stumulus-secretion coupling.
  7. Blood coagulation (Factor IV).
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2
Q

How is calcium stored in the body?

A
  1. It is most present as calcium salts.
  2. Mainly found in bone (99%) as complex hydrated calcium salt.
  3. Present in blood as ionised calcium (Ca2+) and bound to plasma proteins. Only a small amount left as soluble salts.
  4. Only free unbound Ca2+ is bioactive.
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3
Q

How is calcium taken into the body?

A

Via the GI tract where the normal intake is 1000mg/24hr.

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4
Q

How is calcium lost from the body?

A
  1. Lost as faeces (850mg/24hr).
  2. Lost in urine (150mg/24hr).
  3. Cells lost every day will contain small amounts of calcium.
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5
Q

How can calcium levels in the blood be increased? (3)

A
  1. PTH.
  2. Calcitrol (steroid hormone, Vitamin D3).
  3. Breaking down hydroxyapatite crystals in the bone.
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6
Q

How can calcium levels in the blood be decreased?

A
  1. Calcitonin.
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7
Q

Where is the source of PTH?

A

The 4 parathyroid glands located in the thyroid.

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8
Q

Where is calcitonin made?

A

In the parafollicular cells.

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9
Q

What is PTH initially synthesised as?

A

It is initially synthesised as pre-proPTH.

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10
Q

What is the mechanism for PTH?

A

PTH binds to G-protein coupled receptors and leads to the activation of adenyl cyclase and PLC.

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11
Q

What are the actions of PTH? (5)

A
  1. Stimulates kidneys to excrete more phosphates.
  2. Increased calcium reabsorption in the kidneys.
  3. Stimulates synthesis of 1-alpha hydroxylase (which is involved in calcitriol synthesis).
  4. Stimulates Osteoclasts - causes reabsorption of bone matrix and release of calcium from hydroxyapatite crystals.
  5. Inhibits Osteoblasts.
  6. Stimulates an enzyme that synthesizes calcitriol.
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12
Q

What are the actions of Calcitriol?

A
  1. Increases absorption of calcium and phosphate in the small intestine.
  2. Minor effect on bone, stimulates osteoblasts (to store calcium).
  3. Increases calcium and phosphate reabsorption.
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13
Q

What is PTH mechanism in bone?

A
  1. Binds to receptors in osteoblasts not osteoclasts.
  2. Inhibits osteoblasts but causes osteoblasts to release Osteoclast Activating Factors (e.g. RANKL).
  3. Osteoclasts then activate and increase bone resorption.
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14
Q

What stimulates the release if PTH? (2)

A
  1. Decreased calcium levels in the blood (detected by calcium ion G-protein receptors in parathyroid gland cells).
  2. Catecholamines activate beta receptors on parathyroid gland cells.
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15
Q

How is PTH release decreased? (2)

A
  1. PTH has negative feedback on the parathyroid glands.

2. Vitamin D3 has negative feedback on the parathyroid glands.

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16
Q

How is calcitriol synthesized?

A
  1. The precursor is cholecalciferol.
  2. Cholecalciferol has two main sources - diet and UV light on skin breaks 7-dehydrocholesterol.
  3. Liver has an enzyme, 25-hyroxylase, converts cholecalciferol into 25-OH-D3 and stored in liver.
  4. Kidneys produce enzyme, 1-alpha-hydroxylase, converts 25-OH-D3 into calcitriol.
17
Q

How is phosphate reabsorption controlled?

A
  1. Apical membrane has phosphate ion transporters.
  2. PTH inhibits this transporter and phosphate not reabsorbed.
  3. Calcitriol stimulates release of FGF23 from osteocytes.
  4. FGF23 blocks phosphate transporter and phosphate not reabsorbed.
18
Q

How is calcitonin synthesized?

A

Synthesized as pre-procalcitonin.

19
Q

What is the mechanism for calcitonin?

A
  1. Binds to G-protein receptors.

2. Activates adenyl cyclase and PLC.

20
Q

How are calcitonin levels increased? (2)

A
  1. Increased calcium levels in the blood.

2. Gastrin.

21
Q

What are the actions of calcitonin?

A
  1. Inhibits Osteoclast activity.
  2. Increases the excretion of calcium, sodium and phosphate from the kidney to the urine.
    Very limiting effect.
22
Q

What are 3 endocrine causes for hypocalcaemia?

A
  1. Hypothyroidism (insufficient PTH).
  2. Pseudohypoparathyroidism (resistance to PTH).
  3. Vitamin D deficiency.
23
Q

What are 2 ways in which hypocalcaemia can be shown?

A
  1. Trousseau’s sign (pressure on arm and hand can go into contraction).
  2. Chvostek’s sign (tap facial nerve at the jaw and muscles contract).
24
Q

What are causes of hypothyroidism? (3)

A
  1. Idiopathic.
  2. Hypomagnesaemia (low magnesium).
  3. Suppression by raised plasma calcium concentration.
25
Q

What is Pseudohypoparathyroidism?

A
  1. Also known as Allbright Hereditary osteodystrophy.

2. Target organ resistance to PTH due to defective G-protein receptors.

26
Q

What are features of pseudoparathyroidism?

A
  1. Short stature and round face.
  2. Low IQ.
  3. Subcutaneous calcification and bone abnormalities.
  4. Endocrine disorders (hypothyroidism).
27
Q

What are the clinical features of vitamin D deficiency?

A

Softening of the bone due to decreased calcification of the bone matrix.

28
Q

How do you differentiate between hyperthyroidism, pseudoparathyroidism and vitamin D deficiency?

A
  1. Hyperthyroidism = Low PTH, Low Calcium and High Phosphate.
  2. Pseudoparathyroidism = High PTH, Low Calcium and High Phosphate.
  3. Vitamin D deficiency = High PTH, Low Calcium and Low Phosphate.
29
Q

What are 3 endocrine causes of hypercalcaemia?

A
  1. Primary Hyperparathyroidism.
  2. Tertiary Hyperparathyroidism.
  3. Vitamin D Toxicosis.
30
Q

What is primary hyperparathyroidism?

A

A tumour in the parathyroid that causes increased amounts of PTH. The adenoma is not regulated by negative feedback from increased calcium levels.

31
Q

What is secondary hyperparathyroidism?

A

Renal failure is a common cause. The target organ of PTH does not work properly and therefore even though PTH levels are high, calcium levels are not. Secondary does not cause hypercalcaemia.

32
Q

What is tertiary hyperparathyroidism?

A

Initial chronic low calcium concentration. Hence the parathyroid is stimulated a lot for a long time. Eventually PTH becomes autonomous and does not respond to negative feedback.

33
Q

What are parathormone excess effects on the kidneys? (6)

A
  1. Increased calcium reabsorption.
  2. Increased phosphate excretion.
  3. Polyuria.
  4. Renal stones.
  5. Nephrocalcinosis.
  6. Increased Vitamin D3 synthesis.
34
Q

What are the parathormone excess effects on the GI? (2)

A
  1. Increased gastric acid.

2. Duodenal ulcers.

35
Q

What are the parathormone excess effects on Bone? (3)

A
  1. Bone lesions.
  2. Bone rarefaction.
  3. Fractures.
36
Q

What is a feature of hyperparathyroidism?

A

Clubbing of fingers.

Y1 Fwong LCRS Dulan (22 decks)

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