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Endocrinology Y2 > Endocrine and Metabolic Bone Disorders > Flashcards

Endocrine and Metabolic Bone Disorders Flashcards

1
Q

Role of osteoblasts?

A

bone formation, make bone, help deposit calcium

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2
Q

Role of osteoclasts?

A

dissolve bone and liberate calcium

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3
Q

Where is RANKL found

A

osteoblast surface

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4
Q
  • RANKL binds to X to stimulate YYYY
A

X - RANK receptors

YYYY - osteoclast formation and activity

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5
Q
  • Osteoblasts express receptors for X and Y
A

PTH and CALCITRIOL

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6
Q

Where are RANK receptors found

A

Osteoclast precursors

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7
Q

2 types of bone?

A

Cortical bone: hard bone on the outside

Trabecular bone: spongy, “trabecular” bone on the inside.

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8
Q

What is cortical bone

A

hard bone on the outside

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9
Q

What is Trabecular bone

A

spongy, “trabecular” bone on the inside.

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10
Q

What is spongy bone on the inside known as

A

Trabecular bone

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11
Q

What is hard bone on the outside known as

A

cortical bone

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12
Q

newly formed bone matrix is called …

A

osteoid

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13
Q

Osteoid is …

A

newly formed bone matrix

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14
Q

Vit D deficiency in children causes?

A

RICKETS

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15
Q

What part of the bone does a Vit D deficiency affect in children

A

 Affects cartilage of epiphyseal growth plates and bone

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16
Q

Vit D deficiency in adults causes?

A

OSTEOMALACIA

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17
Q

What part of the bone does a Vit D deficiency affect in adults

A

after epiphyseal close, affects bone

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18
Q

Affects of rickets? (3)

A

Skeletal abnormalities and pain, growth retardation, increased fracture risk

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19
Q

Affects of osteomalacia? (3)

A

Skeletal pain, increased fracture risk, proximal myopathy

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20
Q

What is a looser zone

A

areas that have lost the mineralisation of the bone due to vit D deficiency

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21
Q

What is PRIMARY HYPERPARATHYROIDISM

A

A parathyroid adenoma leads to a busy parathyroid gland meaning serum PTH goes up - autonomous PTH secretion

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22
Q

What is secondary HYPERPARATHYROIDISM

A

a physiologically appropriate high PTH level and a low/normal calcium (because of e.g. renal failure, vitamin D deficiency)

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23
Q

What is tertiary HYPERPARATHYROIDISM

A

Chronically low plasma calcium which can happen because of renal failure, the overworked parathyroid glands can become autonomous without a cancer being involved

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24
Q

How does decreased renal function lead to vascular calcification (3 steps)

A

lower renal function, so less calcitriol, so more PTH and so more phosphate absorbed in the intestines and so increased serum phosphate which contributes to vascular calcification

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25
Q

How does decreased renal function lead to osteitis fibres cystica (like 8/9 steps)

A

decrease in renal function will lead to a decrease in the production of calcitriol (because of a lack of 1alpha hydroxylase)
decreased calcitriol leads to decrease in calcium absorption from the intestines leading to hypocalcaemia
hypocalcaemia will stimulate PTH release
PTH will break down bone matrix
breaking down of bone matrix will lead to osteoporosis
Due to the hypocalcaemia you get a decrease in bone mineralisation
combination of the increased bone resorption and decreased bone mineralisation will lead to osteitis fibrosa cystica a

26
Q

Osteitis fibrosa cystica appears on X rays as ….

A

Brown tumours

27
Q

TREATMENT OF OSTEITIS FIBROSA CYSTICA (3)

A
  1. Treat HYPERPHOSPHATAEMIA with low phosphate diet, and phosphate binders which reduce GI phosphate absorption
  2. ALPHACALCIDOL (i.e. calcitriol analogues)
  3. PARATHYROIDECTOMY in tertiary hyperparathyroidism indicated by hypercalcaemia and/or hyperparathyroid bone disease
28
Q

Osteoporosis is characterised by: (3)

A
  • Loss of bony trabeculae
  • Reduced bone mass
  • ## Weaker bone (predisposed to fractures after minimal trauma)
29
Q

Osteoporosis is more common in… because…

A

More common in post-menopausal women (loss of oestrogen’s positive effect on bone)

30
Q

OSTEOPOROSIS is defined as :

A

Bone mineral density (BMD)  2.5 SDs below the average value for young healthy adults

31
Q

Bone mineral density predicts…

A

BMD predicts fracture risk

32
Q

What measures Bone mineral density

A

Dual Energy X-ray Absorptiometry (DEXA)

33
Q

Dual Energy X-ray Absorptiometry (DEXA) measures …

A
  • Mineral (calcium) content of bone measured

More mineral = greater bone density

34
Q

Difference between osteomalacia and osteoporosis?

A

OSTEOMALACIA:

  • Vit D deficiency (adults) causing inadequately mineralised bone
  • Serum biochemistry abnormal (low 25(OH) vit D, low Ca2+, high PTH (secondary hyperparathyroidism)

OSTEOPOROSIS:

  • Bone reabsorption exceeds formation
  • Decreased bone mass
  • Serum biochemistry normal
  • Diagnosis via DEXA scan
35
Q

Similarities between osteomalacia and osteoporosis?

A

BOTH PREDISPOSE TO FRACTURE

Both have weak bones

36
Q

PREDISPOSING CONDITIONS FOR OSTEOPOROSIS: (5)

A

Postmenopausal oestrogen deficiency

  • Age-related deficiency in bone homeostasis e.g. osteoblast senescence
  • Hypogonadism in young men/women
  • Endocrine conditions
  • Iatrogenic
37
Q

What are the iatrogenic causes of Osteoporosis (2)

A

Prolonged use of glucocorticoids

Heparin

38
Q

What are the Endocrine causes of Osteoporosis (3)

A

Cushing’s
Hyperthyroidism
Primary hyperparathyroidism

39
Q

TREATMENT OPTIONS FOR OSTEOPOROSIS: (4)

A
  1. Oestrogen/Selective Oestrogen Receptor Modulators (SERMS)
  2. Bisphosphonates
  3. Denosumab
  4. Teriparatide
40
Q

Use of E limited due to concerns over … (2)

A

breast cancer and venous thromboembolism

41
Q

SERMS used in osteoporosis?

A

TAMOXIFEN and RALOXIFENE

42
Q

Of TAMOXIFEN and RALOXIFENE, which is the better SERM

A

Raloxifene as it has Oestrogenic activity in bone, but anti-oestrogenic at breast and uterus

whereas tamoxifen is oestrogenic in uterus (endometrial proliferation)

43
Q

How do BISPHOSPHONATES work (3)

A

Bind avidly to hydroxyapatite and ingested by osteoclasts- impair ability of osteoclasts to reabsorb bone
 Decrease osteoclast progenitor development and recruitment
 Promote osteoclast apoptosis

44
Q

First line treatment for osteoporosis?

A

Bisphosphonates

45
Q

What are bisphosphonates used for and what do they do (4)

A

Osteoporosis (1st line)
Malignancy Associated hypercalcaemia, reduce bone pain from metastases
Paget’s disease- reduce bony pain
Severe hypercalcaemic emergency- I.V. initially (rehydrate first)

46
Q

RoA and absorption of busphosphonates? 1/2 life?

A
  • Orally active but poorly absorbed; take on an empty stomach as food reduces drug absorption
  • Accumulates at site of bone mineralisation and remains part of bone until it’s resorbed (months/years)
47
Q

Unwanted effects of bisphosphonates?

A

Oesophagitis
Osteonecrosis of the jaw-
Atypical fractures

48
Q

What is DENOSUMAB

A
  • Human monoclonal antibody
49
Q

What does DENOSUMAB do

A
  • Binds RANKL, inhibiting osteoclast formation and activity

- Hence, inhibits osteoclast-mediated bone resorption

50
Q

2nd line treatment for osteoporosis?

A

Denosumab

51
Q

What does TERIPARATIDE do

A
  • Increases bone formation and resorption, but formation outweighs resorption
52
Q

Whats teriparatide

A
  • Recombinant PTH fragment- amino-terminal 34 amino acids of native PTH
53
Q

Big con of teriparatide?

A
  • Expensive
54
Q

What is PAGET’S DISEASE (OF BONE) and whats it caused by

A

 Accelerated, localised but disorganised bone remodelling

 Excessive bone resorption (osteoclastic overactivity) followed by a compensatory increase in bone formation (osteoblasts)

55
Q

PAGET’S DISEASE (OF BONE) effect on bone?

A

BONE FRAILTY, HYPERTROPHY AND DEFORMITY

56
Q

PAGET’S DISEASE (OF BONE) is characterised by…

A

by abnormal, large osteoclasts- excessive in number

57
Q

Where do you woven bone

A

Pagets disease

58
Q

CLINICAL FEATURES of Pagets disease? (8)

A
  • Skull, thoracolumbar spine, pelvis, femur and tibia most commonly affected
  • Arthritis
  • Fracture
  • Pain
  • Bone deformity
  • Increased vascularity (warmth over affected bone)
  • Deafness (cochlear involvement)
  • Radiculopathy (pinched nerve)- due to nerve compression
59
Q

Pagets disease plasma levels of:
Ca
Alkaline phosphatase

A

Ca - normal

Alkaline phosphatase - increase

60
Q

Treatment for Pagets disease? (2)

A
  1. BISPHOSPHONATES- reduce bony pain and decrease activity

2. Simple analgesia

Endocrinology Y2 (18 decks)

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