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SA Orthopaedics > Metabolic/nutritional bone disease > Flashcards

Metabolic/nutritional bone disease Flashcards

1
Q

What is the metabolic activity directed towards in normal bone?

A

Maintenance of ionic equilibria (esp. Ca and PO4)

Repair of damaged structures

Reaction to external stimuli

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2
Q

What is the shapem, structure, and behaviour of bone governed by?

A

Genetic determinants
Hormonal factors
Mechanical factors
Nutritional factors

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3
Q

Hormonal factors governing bone growth and behaviour

A

Pituitary (growth hormone)
Thyroid
Gonads (oestrogen)
Adrenal cortex (hyperadrenocorticism)

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4
Q

Effects of growth hormone on bone growth and behaviour

A

Excess: Gigantisism (acromegaly) (acquired), often a female cat that develops a wider head and large feet

Deficiency: Pituitary dwarfism (congenital)

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5
Q

Effects of thyroid hormone on bone behaviour and growth

A

Deficiency: failure of growth and variety of skeletal deformities

Excess: osteoporosis secondary to increased metabolic rate

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6
Q

Effect of oestrogen on bone growth and behaviour

A

Association between hypoestrogenism and osteoporosis in women
Oestrogen is a regulator of bone mass in mature skeleton
Mild osteoporosis occurs in spayed bitches but is not clinically significant

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7
Q

Effects of hyperadrenocorticism on bone growth and behaviour

A

Can lead to osteoporosis in dogs.

Glucocorticoids also reduce the rate at which bone is formed

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8
Q

Intramembranous osteogenesis

A

In all bones

mesenchyme -> matrix -> mineralised matrix -> bone

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9
Q

Endochondral ossification

A

In long bones

Mesenchyme -> chondroblasts -> chondrocytes -> mineralised scaffold -> bone

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10
Q

Woven (trabecular) bone

A

Haphazardly-arranged fibres

As bone growth occurs at the periosteum - trabecular bone formed first that then becomes compact

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11
Q

Lamellar (compact) bone

A

Haversian systems with concentric fibres

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12
Q

Endochondral ossification

A

Chondrocytes proliferate

Then they hypertrophy and lay down some mineral

Then die by apoptosis (and, unusually, swell as do so)

Osteoclasts remove some mineralised areas to allow vascularisation (capillary loops)

Primary trabeculae develop - later remodelled to secondary

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13
Q

Bone modelling

A

When bone formation and resorption occur on separate surfaces

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14
Q

Bone remodelling

A

The replacement of old tissue by new. Mainly occurs in the adult skeleton to maintain bone mass.

Bone formation and resorption at the same sites

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15
Q

5 stages of bone remodelling

A

Activation: pre-osteoclasts differentiate into mature active osteoclasts

Resorption: osteoclasts digest mineral matrix (old bone)

Reversal of signals: end of resorption

Formation: osteoblasts synthesize new bone matrix

Quiescence: osteoblasts become resting bone-lining cells on the newly formed bone surface

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16
Q

Osteodystrophy

A

A general term for dystrophic growth of bone

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17
Q

Ca/P ratio of bone mineral

A

1.67 and 1.5

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18
Q

Chief factors affecting osteodystrophies

A

Calcium, phosphorus, Vitamin D

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19
Q

Times at which osteodystrophies are more prevalent

A

Young and growing, pregnancy, lactation, egg production

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20
Q

Evidence of disturbance to endochondral ossification

A

Growth arrest line
Growth retardation lattice

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21
Q

Four main types of nutritional osteodystrophy

A

Osteoporosis
Osteomalacia
Rickets
Osteodystrophia fibrosa

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22
Q

Osteoporosis

A

Decreased amounts of bone (but normal composition)

23
Q

Osteomalacia

A

Decreased mineralisation of osteoid (softening of bone)

Usually due to failure of mineralisation of matrix

24
Q

Rickets

A

Decreased mineralisation of osteoid and cartilage

A disease of growing bones

25
Q

Osteodystrophia fibrosa

A

Osteoporosis or osteomalacia plus intertrabecular fibrosis (hyperparathyroidism)

26
Q

What bones does osteoporosis affect?

A

Vertebrae
Flat bones
Metaphysis of long bone

27
Q

Causes of osteoporosis

A

Malnutrition or simple starvation - often due to calcium deficit, combined with protein/calorie malnutrition

Disuse osteoporosis - following low muscular activity and reduced weight bearing

Senile osteoporosis - due to an increase in the numbers of dead osteocytes

Intestinal parasitism - due to malabsorption in the GI tract

Copper deficiency - due to deficiency of lysyl oxidase activity to cross link collagen and elastin

28
Q

Clinical presentation of osteomalacia

A

Slow onset
Shifting lameness
Susceptibility to fractures
Osteophagia may occur (scavenging)
Fertility of affeced animals often depressed
Hypophosphataemia and anaemia are common

29
Q

Causes of osteomalacia

A

Deficiency of phosphorus or vitamin D

Need prolonged vitamin D deficiency

30
Q

Pathology of osteomalacia

A

Excess deposition of matrix at stress points

Bones break easily, cortex is thin and spongy

Deformities occur

Tendons separate from their attachments

31
Q

Histology of osteomalacia

A

Active resorption of bone

Accumulation of excess unmineralised osteoid on trabecular surfaces

32
Q

Cause of rickets

A

Dietary insufficiency/imbalance

Calcium, vitamin D, and phosphorus

33
Q

What is the lesion in rickets?

A

Failure of mineralisation of (calcification) of bone and cartilage and failure of development of cartilaginous matrix, which then accumulates

Results in failure of vascularisation

Normal remodelling does not occur as the bone is protected from the action of osteoclasts by the unmineralised osteoid

34
Q

Clinical rickets

A

Bone cortex is soft - curvature/fractures
Distortion of ribs
At PM bones can be easily cut with a knife
Weakening of osteochondral junction
Irregular overgrowth of cartilage
Enlargement of joints
Normal alignment of teeth often disrupted

35
Q

Vitamin D refractory rickets

A

Signs of rickets can occur in the presence of a normal diet and the absence of uraemia (chronic renal failure)

plasma Calcitriol is found to be inappropriately low and there is loss of phosphorus in the urine and poor intestinal absorption.

Inherited X linked dominant condition

36
Q

Vitamin D dependent rickets

A

refractory to physiological dose of Vitamin D but responds to pharmacological doses

37
Q

Underlying metabolic changes in osteodystrophia fibrosa

A

Extensive osteoclastic resorption of bone and replacement with fibro-osseous tissue

38
Q

Causes of osteodystrophia fibrosa

A

Primary hyperparathyroidism due to hyperplasia or neoplasia

Secondary hyperparathyroidism much more common - nutritional or renal in aetiology

39
Q

Pathology of osteodystrophia fibrosa

A

Exatensive osteoclastic resorption of bone and replacement with fibro-osseous tissue

40
Q

Nutritional secondary hyperparathyroidism

A

Deficiency of Vitamin D/calcium and excess phosphorus

Seen in young fast growing animals

Commonly in puppies - poor bone density, increased fragility, epiphyseal cartilage not affected

41
Q

Renal secondary hyperparathyroidism

A

In animals with chronic renal failure

Plasma phosphorus increases, plasma calcium decreases

Stimulates release of PTH

Stimulates bone resoprtion

42
Q

Clinical signs of bone resorption

A

Loss of appetite, shifting lameness and anaemia.

The jaws swell, together with the maxilla and this swelling may spread to other bones of head - rubber jaw.

osteodystrophy is, in fact, generalised but it affects bones of skull most severely

43
Q

Histology of osteodystrophia fibrosa

A

Bone removed by osteoclasts

replaced by cellular connective tissue - becomes fibrillar with time

Articular cartilage may collapse - leads to DJD

44
Q

Toxic osteodystrophies

A

VItamin D poisoning
Vitamin A poisoning

45
Q

Vitamin D poisoning- lethal dose and toxic dose in dogs

A

88mg/kg

2-3mg/kg

46
Q

Acute vitamin D poisoning

A

Gastric and small intestinal haemorrhages and microscopically focal myocardial necrosis, plus mineralisation of multiple organs

47
Q

Chronic vitamin D toxicity

A

Mineralisation is more prominent, occuring on fibroeleastic tissue in many organs

Death usually due to renal failure

48
Q

Skeletal changes in vitamin D poisoning

A

Osteosclerosis or rarefaction of bone

49
Q

Types of lesions caused by vitamin A poisoning

A
  1. Cartilage damage
  2. Osteoporosis
  3. Exostoses
50
Q

Characterisation of vitamin A poisoning

A

Injury to growth cartilage
Osteoporosis
Deveolpment of exostoses or osteophytes

51
Q

Vitamin A toxicity

A

Most commonly seen in the cat - usually associated with a high liver diet

52
Q

Chronic vitamin A poisoning

A

Deforming cervical spondylosis
Periarticular osteophytes also develop about the proximal joints of forelimb

53
Q

Vitamin A deficiency

A

Abnormalities of modelling of membranous bones of skull

Volume of skull and spinal canal too small

Foraminae of spinal nerves too small and compress nerve (in cattle optic foramen affected - blindness, in puppies auditory foramen - deafness)

Osteoclasts are responsive to vitamin A and in its abscence there is inadequate resorption of endosteal bone - excessive deposition of periosteal bone secondary to reduced osteoclastic acitivity

SA Orthopaedics (13 decks)

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