Metabolic bone disease Flashcards

(38 cards)

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
What causes skeletal deformity in rickets
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
Why is there abnormal overgrowth of capillaries and fibroblasts in rickets
Microfractures and stresses on poorly mineralised and formed, weak bone
27
What is osteomalacia
Inadequate mineralisation of osteoid bone matrix, laid down by osteoblasts. Weak and vulnerable bone to fractures. Vertebral bodies and neck of femur especially
28
Name some of the non-skeletal effects of vitamin D
Enhances immune cell differentiation and inflammation, inhibits tumour cell proliferations, and inhibits angiogenesis
29
What is the main action of PTH
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
What causes primary hyperparathyroidism
benign (usually) tumour of parathyroid
31
What causes secondary hyperparathyroidism
Underlying renal disease causing parathyroid glands to become hyperplastic
32
What happens to cause tertiary hyperparathyroidism
Underlying renal disease causes hyperplasia of parathyroids, develops parathyoid adenoma with autonomous PTH secretion
33
How can secondary hyperparathyroidism bone changes
Restoration of parathyroid hormone levels
34
What does bones stones moans and groans mean in relation to parathyoid adenoma
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
What is pagets disease characterised by
Increased but disordered and structurally unound bone
36
Name some clinical features of pagets disease of bone
Lion face/skull leading to heavy head Compression of the posterior fossa Anterior bowinf of femurs and tibiae Chalk stick fractures of legs
37
What are the three phases of pagets disease
Osteolytic, mixed, and osteoslcerotic
38
What is renal osteodystrophy
A spectrum of renal disease seen in patient with chronic renal disease, showing bone mineral deficiency