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LCRS Endocrinology > Endocrine bone disorders > Flashcards

Endocrine bone disorders Flashcards

1
Q

What is the most important product of vitamin D metabolism?

A

1,25 dihydroxycholecalciferol -calcitriol

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2
Q

What is the principal effect of calcitriol?

A

Stimulates intestinal absorption of calcium and phosphates (and magnesium)

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3
Q

What is the precursor of calcitriol?

A

25 hydroxycholecalciferol

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4
Q

What effect can 25 hydroxycholecalciferol have?

A

In high concentrations, it can have calcitriol effects

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5
Q

Why is the intestinal absorption of ions important?

A

Provides ions necessary for bone mineralisation

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6
Q

What other effects does calcitriol have?

A

Stimulates osteoclast formation from precursors in bone and their activity
Stimulates osteoblasts
Renal effects- increased calcium reabsorption and decreased phosphate reabsorption

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7
Q

What is the definition of vitamin D deficiency?

A

Lack of mineralisation in the bone

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8
Q

What does vitamin D deficiency result in?

A

Softening of bone
Bone deformities
Bone pain
Severe proximal myopathy

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9
Q

What is vitamin D deficiency referred to as in children?

A

Ricket’s

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10
Q

What is vitamin D deficiency referred to as in adults?

A

Osteomalacia

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11
Q

What are the causes of vitamin D deficiency?

A 
Diet
Lack of sunlight
Gastrointestinal malabsorptive states
Liver disease
Renal failure 
Receptor defects
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12
Q

How is vitamin D formed by UV light?

A

UV acts on 7-dehydrocholesterol in the skin to form cholecalciferol (vitamin D3)

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13
Q

What is the other source of vitamin D?

A

Diet- ergocalciferol (vitamin D2)

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14
Q

What happens to cholecalciferol once it is formed?

A

It gets converted to 25-hydroxycholecalciferol in the liver, then it goes to the kidneys where it is converted to the active and powerful 1,25 dihydroxycholecalciferol in the kidneys via the action of 1 alpha hydroxylase which is stimulated by PTH

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15
Q

How do you gage the amount of calcitriol in a patient?

A

25-hydroxycholecalciferol is measured as a gage of the amount of calcititrol because calcitriol is difficult to measure however this method is reliant on good renal function

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16
Q

If you were to diagnose vitamin D deficiency what would you look for?

A

Plasma 25-hydroxycholecalciferol would be low
Plasma calcium would be low
PTH= high
Plasma phosphate would be low

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17
Q

Why is PTH high?

A

Secondary hyperparathyroidism- plasma calcium is low so stimulates release of PTH, which will attempt to increase plasma calcium and could potentially mask hypocalcaemia

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18
Q

How does decreased renal function make bone disease worse?

A

Decrease in renal function =
Decrease production of calcitriol because 1alpha hydroxylase is required
Decreased phosphate excretion so plasma phosphate increases
Decreased calcitriol will cause decreased calcium absorption from the intestines leading to hypocalcaemia which will stimulate PTH
PTH will break down bone matrix to restore calcium and will lead to osteoporosis

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19
Q

What can vitamin D excess lead to?

A

Hypercalcaemia and hypercalciuria due to increased intestinal absorption of calcium (main effect of calcitriol)

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20
Q

What can vitamin D excess occur as a result of?

A

Excess treatment with active metabolites of vitamin D

Granulomatous disease- sarcoidosis, leprosy and tuberculosis

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21
Q

Why is granulomatous disease a cause of vitamin D excess?

A

Granulomatous tissue can convert 25 hydroxycholecalciferol to active metabolite 1,25- dihydroxycholecalciferol because granulomatous tissue have 1 alpha hydroxylase so this is ectopic calcitriol production

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22
Q

What is Paget’s disease?

A

Very active (increased), localised but disorganised bone metabolism - usually slowly progressive

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23
Q

What is Paget’s characterised by?

A

Abnormal large osteoclasts

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24
Q

What are the causes of Paget’s disease?

A

Significant genetic component

Evidence of viral origin

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25
Q

What percentage of over 60s are affected by Paget’s?

A

More than 10% (but majority will experience no symptoms)

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26
Q

What are the symptoms of Paget’s disease?

A

Increased vascularity
Increased osteoclast/osteoblast activity (osteoclast first)
Increased incidence of fractures
Bone pain

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27
Q

Which bones are most commonly affected by Paget’s disease?

A 
Pelvis
Femur
Spine
Skull 
Tibia
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28
Q

How do you diagnose Paget’s disease?

A 
Plasma calcium= normal
Plasma alkaline phosphate= usually high
Radiology demonstrating variable features including:
Loss of trabecular bone
Increased density
Deformity
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29
Q

What is the largest (65%) component of bone mass?

A

Inorganic mineral component

30
Q

What does the inorganic mineral component contain?

A

Calcium hydroxyapatite crystal

31
Q

What does the inorganic mineral component do?

A

Fills the space between the collagen fibres

32
Q

What makes up 95% of the organic component (osteoid)?

A

Collagen fibres

33
Q

What is the normal plasma calcium range?

A

2.2-2.6mmol/l

34
Q

What hormones increase plasma calcium?

A

Parathyroid hormone

Vitamin D

35
Q

What hormone decreases plasma calcium?

A

Calcitonin (not specifically important in humans)

36
Q

What are the effects of increased PTH in response to low calcium?

A

Mobilises calcium from bone to increase plasma calcium
Direct effect to increase reabsorption of calcium in the kidneys
Stimulates activation of vitamin D which leads to increase in calcium
Stimulates kidneys to make 1alpha hydroxylase

37
Q

What responds to the increase in calcium due to PTH?

A

Parathyroid gland- decreases PTH secretion

38
Q

What are the signs and symptoms of hypocalcaemia?

A 
Parasthesia
Arrhythmia
Convulsions
Tetany
(CATs go numb)
39
Q

What is parasthesia?

A

Abnormal sensation such as numbness or tingling without a cause

40
Q

Why do you experience muscle cramps and tetany with hypocalcaemia?

A

Hypocalcaemia senstises excitable tissues

41
Q

What signs are used to check for hypocalcaemia?

A

Chvostek’s signs

Trousseau’s sign

42
Q

What are Chvostek’s signs?

A

Tap the facial nerve just below the zygomatic arch

A positive response= twitching of the facial muscles indicates neuromuscular excitability

43
Q

What is Trousseau’s sign?

A

Inflation of the blood pressure cuff for several minutes induces carpopedal spasm due to neuromuscular excitability

44
Q

What are the causes of hypocalcaemia?

A 
Vitamin D deficiency
Hypoparathyroidism (Low PTH)
Surgical- neck
Autoimmune
PTH resistance
Renal failure
45
Q

What are the signs and symptoms of hypercalcaemia?

A

Stones and Polyuria- Nephrocalcinosis, renal colic and chronic renal failure
Abdominal moans- GI effects e.g. Anorexia, nausea, dyspepsia, constipation and pancreatitis
Psychic groans- CNS effects e.g. Fatigue, depression, impaired concentration, altered mentation and coma
(Stones, abdominal moans and psychic groans)

46
Q

What are the causes of hypercalcaemia?

A

Primary hyperparathyroidism (parathyroid adenoma)
Malignancy (Tumours/metastases)- bone metastases lead to increased calcium
Conditions with high bone turnover- Hyperthyroidism, Paget’s disease and vitamin D excess

47
Q

If you were diagnosing primary hyperparathyroidism, what would you expect to see?

A

Calcium- high

PTH- high (parathyroid adenoma doesn’t respond to negative feedback of calcium)

48
Q

If you were diagnosing hypercalcaemia of malignancy, what would you expect to see?

A

Calcium- high
PTH- low
Increased bone turnover due to bony metastases, calcium rises but negative feedback still in place so PTH is suppressed

49
Q

When treating a patient for vitamin D deficiency, what affects their treatment choice?

A

Renal function

50
Q

How would you treat someone with vitamin D deficiency with normal kidney function?

A

Give 25-hydroxy vitamin D
Patient can convert this to calcitriol via 1alpha hydroxylase
Supplements are ergocalciferol or cholecalciferol

51
Q

How would you treat someone with vitamin D deficiency with renal failure?

A

Don’t have 1alpha hydroxylase activity
So can’t activate 25-hydroxy vitamin preparations
Give alfacalcidol- 1,hydroxycholecalciferol

52
Q

What does RANK ligand (RANKL) do?

A

Important molecule that increases the activation of osteoclasts
Stimulates maturation of osteoclasts from osteoclast precursors which stimulates bone resorption

53
Q

What do osteoblasts do?

A

Synthesise osteoid and participate in mineralisation/calcification of osteoid

54
Q

What do osteoclasts do?

A

Release lysosomal enzymes which break down bone

55
Q

What is osteoporosis?

A

Condition of reduced bone mass and distortion of bone microarchitecture which predisposes to fracture after minimal trauma

56
Q

What is the clinical definition of osteoporosis?

A

Having a bone mineral density that is 2.5 standard deviations or more below the average value for young healthy adults

57
Q

How is bone mineral density measured?

A

Dual-energy X-ray absorptiometry

58
Q

What conditions predispose you to osteoporosis?

A

Post-menopausal oestrogen deficiency
Age-related deficiency in bone homeostasis
Hypogonadism in young men and women
Endocrine conditions- cushing’s, hyperthyroidism and primary hyperparathyroidism
Iatrogenic- prolonged use of glucocorticoids and heparin

59
Q

How can you treat osteoporosis?

A

Oestrogen/selective oestrogen receptor modulators (SERMs)
Bisphosphonates
Denusomab
Teriparatide

60
Q

Why is the use of oestrogen therapy limited?

A

Increased risk of breast cancer and venous thromboembolism

61
Q

What are the two types of selective oestrogen receptor modulators?

A

Tissue selective ER antagonists and agonists

62
Q

What is a common example of a tissue selective ER antagonist/anti-oestrogen?

A

Tamoxifen

63
Q

What do ER antagonists do?

A

Antagonise ERs in breast
Oestrogenic activity in the bone and endometrium
Use is limited because of effects on endometrium

64
Q

What is a common example of a tissue selective ER agonist?

A

Raloxifene

65
Q

What do ER agonists do?

A

Oestrogenic activity in bone

Anti-oestrogenic activity in breast and uterus

66
Q

How do bisphosphonates work?

A

Binds avidly to hydroxyapatite and is ingested by osteoclasts- it impairs osteoclasts ability to resorb bone, it also decreases maturation of osteoclasts from their precursors
Net result- reduced bone turnover

67
Q

What are bisphosphonates used for?

A

Osteoporosis
Malignancy
Paget’s disease
Severe hypercalcaemic emergency after saline

68
Q

What are the unwanted actions of bisphosphonates?

A

Oesophagitis
Flu-like symptoms
Osteonecrosis of the jaw
Atypical fractures

69
Q

What is denusomab?

A

A human monoclonal antibody

70
Q

How does denusomab work?

A

Binds to RANKL and inhibits osteoclast formation and activity so inhibits resorption (second line treatment to bisphosphonates)

71
Q

What is teriparatide?

A

Recombinant fragment of PTH

72
Q

What does teriparatide do?

A

Increases bone formation and resorption (formation more)
(Third line treatment)
Very expensive

LCRS Endocrinology (18 decks)

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