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LCRS > Endocrinology 12 - Control of Calcium metabolism > Flashcards

Endocrinology 12 - Control of Calcium metabolism Flashcards

1
Q

What are the roles of calcium? (7)

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

What are the two main hormones that can increase calcium levels in the blood?

A
  1. PTH.

2. Calcitrol (steroid hormone, Vitamin D3).

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6
Q

What is the main hormone that can decrease calcium levels in the blood?

A
  1. Calcitonin - is not the main controlling influence of calcium ions.
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7
Q

Where is the source of PTH (Parathyroid hormone)?

A

The 4 parathyroid glands located in the thyroid.

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8
Q

Where is calcitonin made?

A

In the parafollicular cells found in between the follicles in the parathyroid.

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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? (6)

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 resorption of bone matrix and release of calcium from hydroxyapatite crystals.
  5. Inhibits Osteoblasts.
  6. Increases the absorption of Calcium and phosphate in the small intestine.
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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 reabsorption and decreases phosphate reabsorption in the kidneys.
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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 Liver has an enzyme (25-hyroxylase) converts cholecalciferol into 25-hydroxy-cholecalciferol and stored in liver.
  2. Kidneys produce enzyme (1-alpha-hydroxylase - stimulated by PTH) converts 25-hydroxy-cholecalcitriol into calcitriol.
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17
Q

How is phosphate reabsorption in the kidneys controlled?

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

How is calcitonin synthesized?

A

Synthesized as pre-procalcitonin.

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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. Hypoparathyroidism (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).
    BOTH ARE FORMS OF TETANY.
24
Q

What are causes of hypoparathyroidism? (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 (shortening of metacarpals).
  4. Endocrine disorders (hypothyroidism).
27
Q

What are the clinical features of vitamin D deficiency?

A
  1. Softening of the bone due to decreased calcification of the bone matrix - Bowling of the bones and fractures.
  2. Rickets in children.
  3. Osteomalacia in adults.
28
Q

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

A
  1. Hypothyroidism = 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
  1. A tumour in the parathyroid that causes increased amounts of PTH.
  2. The adenoma is not regulated by negative feedback from increased calcium levels.
31
Q

What is secondary hyperparathyroidism?

A
  1. Renal failure is a common cause.
  2. Loss of calcium in urine - stimulates parathyroid to release PTH.
  3. Increased PTH does its best to maintain the plasma Ca2+ level.
  4. No Hypercalcaemia.
32
Q

What is tertiary hyperparathyroidism?

A
  1. Initial chronic low calcium concentration.
  2. Hence the parathyroid is stimulated a lot for a long time.
  3. 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.

37
Q

What are hydroxyapatite crystals?

A

A complex hydrated calcium salt that is embedded in the bone matrix and acts as a reservoir.

38
Q

What is the total blood Ca2+ concentration?

A

2.5mM

39
Q

What is most of calcium in blood present as?

A
  1. Unbound and ionized - biologically active.

2. This needs to be controlled.

40
Q

What is the majority of the parathyroid made up of?

A

Majority made up of follicles but you get parafollicular cells in between.

41
Q

What are the two main sources of cholecalciferol?

A
  1. Diet - vit D2 from plants and vit D3 from meat/milk

2. UV light on skin breaks 7-dehydrocholesterol to cholecalciferol.

42
Q

What is cholecalciferol?

A
  1. It is Vitamin D3 - a steroid hormone than circulates around the body and is taken up by the liver.
  2. It is the precursor for calcitriol.
43
Q

What is a physiological benefit of calcitonin?

A
  1. During pregnancy - plasma Ca2+ levels raised as you need more Ca2+ (e.g. to produce milk).
  2. Calcitonin protects bone from being broken down to provide calcium.
44
Q

What are features of hypoparathyroidism?

A
  1. Abnormal 4th metacarpal.
45
Q

What happens to urinary excretion of cAMP if you give PTH to someone with surgical hypoparathyroidism, idiopathic hypoparathyroidism and pseudohypoparathyroidism?

A
  1. Surgical + Idiopathic = increase in cAMP excreted in urine as target cells are sensitive to PTH.
  2. Pseudohypoparathyroidism = no change as target resistance to PTH.
46
Q

Which types of hyperparathyroidism is associated with hypercalcaemia?

A

Primary and tertiary.

LCRS (22 decks)

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