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Semester 2 W1 Bone pain > Metabolic bone disease > Flashcards

Metabolic bone disease Flashcards

1
Q

What is osteopenia

A

When bone mass is 1-2.5 standard deviations below peak bone mass

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2
Q

What is osteoporosis

A

When bone mass is >2.5 SD below peak bone mass

Osteopenia that significantly increases risk of bone fracture

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3
Q

Name the two most common forms of primary osteoporosis

A

Senile osteoporosis and post-menopausal osteoporosis

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4
Q

What can cause secondary osteoporosis

A

Endocrine disorders, GI disorders, or drugs

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5
Q

Why is osteoporosis common in elderly

A

As osteoblasts age, they become less responsive to growth factors

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6
Q

WHy does inactivity (common in elderly) lead to osteoporosis

A

Mechanical factors stimulate bone remodelling

Load magnitude influences bone density. Resistance exercise better than repetitive endurance

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7
Q

How can dietary imput contribute to osteoporosis

A

Low calcium intake (common in adolescent girls) restricts peak bone mass

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8
Q

How does the menopause influence bone mass

A

Oestrogen deficiency contributes to osteoporosis due to high turnover

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9
Q

Is DVT more likely in patients with osteoporosis who suffer a fracture

A

yes, specifically dvt from legs

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10
Q

What is rickets

A

Osteomalacia in children as deposition of bone in growth plates is interfered with

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11
Q

What is osteomalacia

A

Bone formed during remodelling is undermineralised, predisposition to fractures. Unmineralised matrix accumulates

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12
Q

Which foods are vitamin D found in

A

Oily fish, beef liver, cheese, egg yolk

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13
Q

Why is vitamin D needed

A

To maintain Plasma calcium and phosphorous for metabolic functions, bone mineralisation, neruomusular function

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14
Q

What role does light play in vitamin D synthesis

A

Converts 7-Dehydro-cholesterol into cholecalciferol vit D3

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15
Q

What happens to Vit D3 once synthesised.

A

Binds to D-binding protein (DBP) and transported to the liver, converted by 25-hydroxylase to 25 hydroxy-vitamin D

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16
Q

What happens to 25-hydroxy-vitamin D when it circulates to the kidneys

A

Converted by alpha-1 hydroxylase to form 1-25 dihydroxy vitamin D (most active form)

17
Q

What regulates 1-25 dihydroxy vitamin D production

A

Hypocalcemia stimulates parathyroid hormone secretion, augmenting conversion by activating alpha 1 hydroxylase

Hypophospataemia directly activates alpha 1 hydroxylase

Increased levels of 1-25 dihydroxy vitamin D downregulates its synthesis inhibiting alpha 1 hydroxylase

18
Q

WHat does active vitamin D do in hypocalcaemic states

A

it, with PTH, increases resorption of calcium and phosphorous from bone supporting blood levels

19
Q

What does active vitamin D do in normal calcaemic states

A

Required for calcium deposition in epiphyseal cartilage and osteoid matrix

20
Q

How does vitamin D affect osteoblasts

A

Upregulates RANKL , activating RANK receptors on osteoclast precursors, developing. Also bone resorption

21
Q

How does Vitamin D affect mineralisation

A

Stimulates osteoclasts to form osteocalcin (calcium binding protein) promoting calcium deposition

22
Q

What causes vitamin D deficiency

A

Limited sunligt exposure or poor diet

Less commonly due to renal disorders or malabsorption

23
Q

What happens to calcium levels in Vit D deficiency

A

Hypocalcaemia, stimulating parathyroid to form PTH, activating renal alpha 1 hydroxylase, increasing active Vit D and calcium adsorption

Restored calcium levels, but phosphate excretion increases. mineralisation of bone impaired

24
Q

What two diseases does Vit D deficiency lead to

A

Rickets and osteomalacia

Bone loss and fractures in elderly

25
Q

What causes skeletal deformity in rickets

A

Excess umnineralised bone matric causing skeletal deformity.

This is due to inadequate calcification of epiphyseal cartilage, which overgrows into irregular masses. Osteoid matric deposits on catrilainous remnant, enlargement and lateral expansion of osteochondral junction

26
Q

Why is there abnormal overgrowth of capillaries and fibroblasts in rickets

A

Microfractures and stresses on poorly mineralised and formed, weak bone

27
Q

What is osteomalacia

A

Inadequate mineralisation of osteoid bone matrix, laid down by osteoblasts. Weak and vulnerable bone to fractures. Vertebral bodies and neck of femur especially

28
Q

Name some of the non-skeletal effects of vitamin D

A

Enhances immune cell differentiation and inflammation, inhibits tumour cell proliferations, and inhibits angiogenesis

29
Q

What is the main action of PTH

A

To increase serum calcium:

Activates osteoclasts from increased RANKL expression on osteoblasts

Increased resorption of calcium from renal tubules,

Increases syhtesis of active VIT D

30
Q

What causes primary hyperparathyroidism

A

benign (usually) tumour of parathyroid

31
Q

What causes secondary hyperparathyroidism

A

Underlying renal disease causing parathyroid glands to become hyperplastic

32
Q

What happens to cause tertiary hyperparathyroidism

A

Underlying renal disease causes hyperplasia of parathyroids, develops parathyoid adenoma with autonomous PTH secretion

33
Q

How can secondary hyperparathyroidism bone changes

A

Restoration of parathyroid hormone levels

34
Q

What does bones stones moans and groans mean in relation to parathyoid adenoma

A

Bones: Osteoporosis (PTH++), brown tumour of hyperparathyoidism, osteitis fibrosa cystica (cystic spaces)

Stones: Nephrolithiasis -Calcium oxalate stones, Nephrocalcinosis is the metastatic calcification of renal tubules

Moans - GIT disturbances include constipation, peptic ulcers, acute pancreatitis

CNS disturbances - Depression and seizures

35
Q

What is pagets disease characterised by

A

Increased but disordered and structurally unound bone

36
Q

Name some clinical features of pagets disease of bone

A

Lion face/skull leading to heavy head
Compression of the posterior fossa
Anterior bowinf of femurs and tibiae
Chalk stick fractures of legs

37
Q

What are the three phases of pagets disease

A

Osteolytic, mixed, and osteoslcerotic

38
Q

What is renal osteodystrophy

A

A spectrum of renal disease seen in patient with chronic renal disease, showing bone mineral deficiency

Semester 2 W1 Bone pain (6 decks)

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