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Y3 Musculoskeletal pathology > Musculoskeletal Bone 3 > Flashcards

Musculoskeletal Bone 3 Flashcards

1
Q

Metabolic osteodystrophies are the result of …?

A

Disturbed bone growth, modelling or remodelling due to nutritional or hormonal imbalances

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2
Q

What are the 4 classifications of metabolic bone disorders?

A
  • Rickets
  • Osteomalacia
  • Fibrous osteodystrophy
  • Osteoporosis
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3
Q

What are the functions of calcitonin and parathyroid hormone?

A
  • Calcitonin inhibits the activity of osteoclasts
  • Parathyroid hormone inhibits the activity of osteoblasts and increases the activity of osteoclasts and RANK-L molecule leading to the reabsorption of bone
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4
Q

How does parathormone act at the kidney level?

A

Increases the reabsorption of calcium, inhibiting the reabsorption of phosphorus and increasing the synthesis of vitamin D

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5
Q

How does vitamin D work at the level of the GI system?

A

Increase the absorption of calcium and phosphorus from the gut which goes into the blood.

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6
Q

How does active vitamin D work at the level of the kidney?

A

Increases the absorption of phosphorus at kidney level and increases osteoclast activity so the net gain here is more calcium in blood

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7
Q

What is the function of active osteoblasts?

A

Cause a decrease of blood Ca as it is used in bone production, this decrease in Ca causes an increase in parathormone which consequently increases osteoclasts so there is a balance

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8
Q

What is the function of active osteoclasts?

A

Increase Ca in blood because it is taken from bone so there is another feedback mechanism to make sure there isn’t too much of it.
Ca increased in blood increases the activity of calcitonin which inhibits osteoclastic activity

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9
Q

What are the aetiological causes of osteoporosis?

A
  • Senility
  • Calcium deficiency (rare)
  • Starvation
  • Gastrointestinal parasitism
  • Inflammatory bowel disease
  • Corticosteroids
  • Disuse
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10
Q

Describe the pathophysiology of osteoporosis due to its different aetiological causes

A
  • Increased osteoclastic activity OC > OB
  • Starvation: reduced apposition of bone
  • Parasitism / IBD: due to malabsorption
  • Corticosteroid: collagen synthesis inhibition
  • Disuse: reduced weight bearing, increase OC activity
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11
Q

Describe the gross appearance of osteoporosis

A

Reduction in quantity of bone, the quality of which is normal.
Narrowed cortices, transverse reinforcement trabeculae and there is increased fragility

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12
Q

Describe the histological appearance of osteoporosis

A

Rare and smaller trabeculae. Normal calcification

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13
Q

How do parasites cause osteoporosis?

A
  • Parasites impair absorption of Ca and P from the GI tract.
  • The decrease in Ca in the blood leads to an increase in PTH, which stimulates an increase in osteoclast activity and an increase in vitamin D synthesis (this is not useful due to parasites blocking absorption).
  • Overall there is a net osteoclast activity over osteoblasts so your bone is going to grow
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14
Q

Which metabolic bone disorders have the same pathophysiology but are different in young and adult animals?

A

Rickets (young)

Osteomalacia (adults)

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15
Q

What is the aetiological cause of Rickets/Osteomalacia?

A

Commonly associated with Hypovitaminosis D and Hypophosphatemia

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16
Q

Describe the pathophysiology of Rickets/Osteomalacia?

A

Defective mineralisation at sites of bone growth (young animals) or at sites of bone remodelling (adults). Insufficient mineralization of newly formed osteoid

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17
Q

Describe the gross appearance of Rickets/Osteomalacia?

A

Gross lesions are most prominent at sites of rapid growth – metaphyseal/epiphyseal regions of long bones and costochondral junctions of ribs (rachitic rosary).
Disorganisation of trabeculae in the metaphysis (“Growth retardation lattice”) with extension of tongues of cartilage into the metaphysis

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18
Q

Describe the histological appearance of Rickets/Osteomalacia?

A

Failure of mineralisation of cartilage and osteoid, with persistence and disorganisation of hypertrophic chondrocytes at sites of endochondral ossification

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19
Q

Which two conditions can be associated with Rickets/Osteomalacia?

A

Fibrous osteodystrophy and osteoporosis

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20
Q

Describe how Hypovitaminosis D and Hypophosphatemia cause Rickets/Osteomalacia?

A
  • Vitamin D is not active because of low levels so phosphorus is not reabsorbed in the GI tract and there is inhibition of the reabsorption of phosphorus from the kidney
  • There is a decrease in Ca and P in the blood so they aren’t available for osteoid formation
  • The compensatory PTH mechanism is activated which leads to osteoclast activation and they reabsorb more bone
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21
Q

What are the 4 aetiological causes of fibrous dystrophy?

A
  • Primary PTH secreting tumour (Dog, Cat: rare): Primary Hyperparathyroidism
  • Renal failure (Dog, Cat: common): Secondary Renal Hyperparathyroidism
  • Low calcium/high Phosphorus diets (Horses): Nutritional hyperparathyroidism
  • PTH-like secreting tumour (Anal sac carcinoma) (Dog, Cat: rare): Pseudohyperparathyroidism
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22
Q

Describe the pathophysiology of fibrous osteodystrophy

A

SEVERE Increase in PTH (different mechanisms). Because there is so much PTH instead of osteoid formation collagen is produced

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23
Q

How does fibrous osteodystrophy appear grossly?

A

Bone enlargement, tooth loss, fractures, spongy appearance. Mandible is a classical location. Bones are soft

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24
Q

How does fibrous osteodystrophy appear histologically?

A

Excessive bone resorption (increased Ocl activity), accompanied by fibrous proliferation

  • Spicules of mineralised bone surrounded by fibrous tissue
  • Osteoclasts surround this mineralised bone
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25
Q

Describe the mechanism of primary hyperparathyroidism causing fibrous osteodystrophy

A
  • A lot of PTH is stimulating Ca reabsorption and is inhibiting P reabsorption
  • In the blood Ca increases and P decreases
  • PTH directly increases osteoclast activity via RANK-L
  • PTH also increases the activity of osteoblasts to produce collagen (normally osteoid)
  • Osteoclasts absorb the normal bone that is left
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26
Q

Describe the mechanism of secondary renal failure causing fibrous osteodystrophy

A
  • Normally phosphorus is cleared out of the blood by the glomerulus and is reabsorbed at a tubular level
  • If the kidney is failing the structure is compromised and not working, so phosphorus is not filtrated and it stays in circulation where the amount of it increases continually so PTH is also continually stimulated which in the same way as before leads to the stimulation of collagen production
27
Q

What are the 5 stages of fracture healing?

A
  • Haemorrhage
  • Haematoma
  • Proliferating collagen
  • Ossification (differentiation in osteoblasts) / Chondrification (in the centre if low oxygen)
  • Remodelling / Endochondral ossification
28
Q

What are the two classifications of how fractures occur?

A 
Physiological = e.g. you’ve been hit by a car because the strength applied to your bone is too much 
Pathological = your bone is not strong enough to sustain normal strength
29
Q

How are fractures classified?

A
  • Physiological vs pathological
  • Displaced vs displaced
  • Simple vs comminuted/complex
  • Articular vs epiphyseal vs diaphyseal
30
Q

What are 3 causes of pathological fracture healing?

A
  • Inadequate blood supply -> necrosis
  • Instability -> non-union -> Pseudarthrosis
  • Infection -> osteomyelitis
31
Q

Name the term used to describe inflammation of the following:

  1. Periosteum
  2. Bone
  3. Bone and bone marrow
  4. All bone structures
A
  1. Periosteitis
  2. Osteitis
  3. Osteomyelitis
  4. Panosteitis
32
Q

What are the causes of inflammation in bones?

A
  • Aseptic = tramatical
  • Bacterial = Actinomycosis, Tuberculosis, Brucellosis / yersiniosis / salmonellosis /(hematogenous spread)
  • Mycotic - rare Coccidiomycosis (Coccidioides immitis) [dog]
  • Viral e.g. distemper
33
Q

Where is the predilection site for bacterial osteomyelitis?

A

Capillary loops

34
Q

Which animals are most commonly affected by bacterial osteomyelitis?

A

++ Young animals (horse/ruminants)

35
Q

What are the aetiological causes of bacterial osteomyelitis in foals?

A 
E.coli
Streptococcus
Salmonella
Rhodococcus
Klebsiella
36
Q

What are the aetiological causes of bacterial osteomyelitis in calves?

A

Actinobacterium pyogenes

Salmonella

37
Q

What are the aetiological causes of bacterial osteomyelitis in dogs and cats?

A

Osteomyelitis tends to be secondary to penetrating injury, with Staph intermedius, Strep, Proteus and E. coli most commonly isolated

38
Q

Describe the pathogenesis of bacterial osteomyelitis

A

Inadequate passive immune transfer + bacterial septicemic infection: osteomyelitis

39
Q

How does bacterial osteomyelitis appear grossly?

A

Bone destruction and purulent material, bone fragility (also vertebrae)

40
Q

‘Lumpy jaw’ is a term used to describe which condition?

A

Mandibular osteomyelitis

41
Q

What is the aetiological cause of Mandibular osteomyelitis

A

Actinomyces bovis - affects cattle

42
Q

Describe the pathophysiology of Mandibular osteomyelitis

A

Oral injury, penetration of bacteria through mucosa close to the teeth, bone erosion, penetration inside the bone, pyogranulomatous osteomyelitis

43
Q

Describe the gross appearance of Mandibular osteomyelitis

A

Mandibular or maxillary swelling, gingival ulceration, displacement of teeth. Honeycomb appearance on cross section

44
Q

Describe the histological appearance of Mandibular osteomyelitis

A

Necrotic bone, purulent exudates and Splendore-Hoeppli figures

45
Q

Metaphyseal osteopathy is also known as?

A

Hypertrophic osteodystrophy

46
Q

Which spp/breed/age is affected by Metaphyseal osteopathy?

A

Dog, young growing, ++3-4 months, large breeds (Great Danes, GS, Weimaraner)

47
Q

What is the cause/pathophysiology of metaphyseal osteopathy?

A

Unknown

48
Q

Describe the gross appearance of Metaphyseal osteopathy?

A

Bilateral and symmetrical. Possibly swollen due to periosteal proliferation. ++ radius and ulna

49
Q

Describe the histological appearance of Metaphyseal osteopathy?

A

Persistence of calcified cartilage/primary spongiosa with thin trabeculae, disappearance of osteoblasts and suppurative inflammation and necrosis.

50
Q

What conditions/signs are associated with metaphyseal osteopathy?

A

Fever, anorexia, pain, lameness; fractures/infractions of lamellar bone

51
Q

Canine panosteitis is also known as?

A

Juvenile osteomyelitis

52
Q

Which breed/spp/age/gender is affected by Canine panosteitis?

A

Dogs, giant breeds, young 5-12 months. MALES +++

53
Q

What is the cause/pathophysiology of canine panosteitis?

A

Unknown

54
Q

Describe the gross appearance of canine panosteitis

A

None, mostly X Ray changes: radiodensity 10 days after clinical signs in medulla close to the nutritional foramen; one or more bones

55
Q

Describe the histological appearance of canine panosteitis

A

Expanding areas of fibrovascular tissue in the bone marrow cavity which are replaced by woven bone with resting and reversal lines; inflammation is low, but histiocytes and plasma cells possible

56
Q

Which sign is seen with canine panosteitis

A

Mild to severe lameness which can shift from one leg to another

57
Q

Name 3 benign neoplasms seen in bone

A
  • Osteoma
  • Ossifying fibroma
  • Fibrous dysplasia
58
Q

Name 2 malignant neoplasms seen in bone

A
  • Osteosarcoma

- Chondrosarcoma

59
Q

Name 2 common tumour-like lesions of bone

A
  • Aneurysmal bone cysts

- Exuberant fracture callus

60
Q

Describe the gross appearance of a chondrosarcoma

A

Nodular expansile lesions, mainly ribs and head

61
Q

Describe the histological appearance of a chondrosarcoma

A

Relatively well differentiated chondrocytes proliferating with abundant matrix. Mitoses rare

62
Q

Describe the gross appearance of an osteosarcoma

A

Destructive and/or osteoproliferative lesions. ++ weight bearing bones (++distal radius, proximal humerus, distal femur and distal tibia).

63
Q

Describe the histological appearance of an osteosarcoma

A

Moderately to poorly differentiated atypical osteoblasts (ranging from round to spindle) with high mitotic activity, associated with osteoid production

Y3 Musculoskeletal pathology (5 decks)

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