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Sem 3 MSK > The Skeleton And Metabolism > Flashcards

The Skeleton And Metabolism Flashcards

1
Q

What are the 6 hormones that have skeletal effects?

A 
→ Estrogens
→ Androgens
→ Cortisol
→ PTH
→ Vitamin D 
→ Calcitonin
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2
Q

What is a hormone secreted from the skeleton?

A

→ FGF-23

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3
Q

What is the daily calcium intake?

A

→ 1000-1200

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4
Q

How is the calcium distributed in the body?

A

→ most is intracellular
→ the remaining 0.1% is in the plasma
→ half of the 0.1% is free calcium ions
→ the other half is protein bound

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5
Q

What is the only way to increase Ca2+?

A

→ Increase calcium absorption through the gut

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6
Q

What does bone turnover contribute to?

A

→ Homeostasis of serum calcium
→ phosphate
→ and PTH, vit D, calcitonin, FGF-23

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7
Q

What is PTH synthesized from?

A

→ Parathyroid chief cells

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8
Q

Where are the parathyroid glands located?

A

→ behind the thyroid

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9
Q

What is PTH secreted as?

A

→ 84 AA polypeptide

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10
Q

What is the role of PTH?

A

→ Defend against hypocalcaemia

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11
Q

What is the concentration of plasma Ca2+?

A

→ 2.2-2.6 mM

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12
Q

Where is free Calcium sensed?

A

→ by GPCR on chief cells

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13
Q

What is the stimulus for PTH release?

A

→ Low calcium

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14
Q

Where is calcitriol synthesized and in response to what?

A

→ in the skin

→ in response to UV

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15
Q

What is calcitriol?

A

→ Vitamin D

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16
Q

Describe calcitriol synthesis

A

→ 7dehydrocholesterol is in the skin
→ UV light turns it into cholecalcitriol (CCF)
→ 25 hydroxylase adds an OH group in the liver
→ it becomes 25 hydroxyCCG
→ 1a hydroxylase stimulated by PTH in the kidney adds another OH group
→ 1,25 dihydroxyCCF is formed or calcitriol

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17
Q

Where is the regulation site for calcitriol?

A

→ control of 1a hydroxylase in the kidney

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18
Q

What is calcitriol increased by?

A

→ PTH - upregulates 1a hydroxylase

→ Low phosphate

19
Q

What is the function of calcitriol?

A

→ Increase absorption of Ca and Pi from the GI tract

→ inhibits PTH

20
Q

What are the 4 actions of PTH?

A

→ Promotes release of Ca from bone
→ Increases Ca reabsorption
→ increases renal Pi excretion
→ upregulates 1a hydroxylase activity

21
Q

Describe how PTH works

A

→ hypocalcaemia stimulates PTH
→ PTH binds to osteoblasts and stimulates RANK ligand
→ RANK ligand binds to RANK receptors on osteoclasts
→ Bone breaks down and Ca2+ and phosphate are released into the blood

22
Q

Where are PTH receptors found?

A

→ osteoblasts

23
Q

How does PTH promote bone remodelling?

A

→ Activates osteoclasts via RANKL

→ promotes bone remodelling

24
Q

What does intermittent low dosage of PTH lead to?

A

→ favoring formation over reabsorption

25
Q

What does a persistent high concentration of PTH lead to?

A

→ excess resorption over formation

26
Q

Where is calcitonin secreted from?

A

→ C cells of the thyroid

27
Q

What stimulates calcitonin secretion?

A

→ high Ca2+

28
Q

What is the effect of calcitonin?

A

→ to lower Ca2+ by inhibiting osteoclasts

29
Q

What does calcitonin do in the kidney?

A

→ Decreases calcium and phosphate reabsorption

30
Q

What does calcitonin do in the bone?

A

→ Decreases bone resorption by inhibiting osteoclast activity

31
Q

What is used to treat Paget’s?

A

→ Synthetic calcitonin

32
Q

What is the lacunar-canalicular system for?

A

→ Communication between osteocytes

→ communication from osteocytes to surface cells and systemic circulation

33
Q

What is hypophosphatemic rickets?

A

→ Rare phosphate wasting conditions leading to bone mineralization defects

34
Q

What is the role of FGF-23?

A

→ to decrease phosphate

35
Q

What is FGF-23 expressed and secreted by?

A

→ osteocytes

36
Q

What is FGF-23 stimulated by?

A

→ Calcitriol and Pi

37
Q

What does FGF-23 do?

A

→ inhibits calcitriol synthesis

→ Increases renal Pi excretion (by reducing Na-Pi reabsorption from the proximal tubule)

38
Q

What are the clinical features of hypercalcaemia?

A

→ Depression, fatigue, anorexia, nausea vomiting
→ Abdominal pain
→ Renal calcification
→ Bone pain

39
Q

What are causes of hypercalcaemia in ambulatory patients?

A

→ Primary hyperparathyroidism

40
Q

What are causes of hypercalcaemia in hospitalised patients?

A

→ Malignancy

41
Q

What is primary hyperparathyroidism due to?

A

→ Benign adenoma in one or more PT glands

42
Q

How is primary hyperparathyroidism resolved?

A

→ removal of the affected gland

43
Q

What is hypercalcaemia of malignancy?

A

→ Tumor can secrete PTH related peptide

→ Binds and activates PTH receptor

Sem 3 MSK (4 decks)

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