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MSK 2 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Name some congenital bone disorders

A
  • Chondrodysplasias
  • Osteopetrosis
  • Osteogenesis imperfecta
  • Congenital hyperostosis
  • Osteochondromatosis
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2
Q

What is Chondrodysplasias and what types of animals does it affect?

A
  • Hereditary disorders of bone growth result of primary
    lesions in growth cartilage
  • Defect in bones having endochondral ossification (long
    bones) but not in bones with intramembranous
    ossification (flat bones)
  • Short-legged and normal-sized heads
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3
Q

What is Osteopetrosis?

A
  • Defect in bone resorption by osteoclasts
  • Although bone mineral density is increased, bones can
    be more fragile
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4
Q

What are the three main metabolic bone diseases?

A
  1. Osteoporosis
  2. Rickets/Osteomalacia
  3. Fibrous osteodystrophy
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5
Q

What is the pathology associated with Osteoporosis?

A

Reduced bone mass (normal bone quality, well mineralized)

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6
Q

What are some of the causes of Osteoporosis?

A
  • malnutrition
  • physical inactivity
  • dietary calcium deficiency
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7
Q

What are the consequences of Osteoporosis?

A
  • Brittle bones

- fractures

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8
Q

What is Rickets/Osteomalacia?

A

Failure of mineralization in growing skeleton (rickets) and adults (osteomalacia)

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9
Q

What are some of the causes of Rickets/Osteomalacia?

A
  • calcium/vitamin D deficiencies
  • phosphorus deficiency
  • chronic renal disease
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10
Q

What are the consequences of Rickets/Osteomalacia?

A
  • Bone deformities

- Thickening of growth plates and fractures

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11
Q

What is the pathology associated with Fibrous osteodystrophy?

A

Increased widespread osteoclastic resorption of bone and replacement by fibrous tissue

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12
Q

What are some of the causes of Fibrous osteodystrophy?

A
  • Primary hyperparathyroidism
  • Secondary hyperparathyroidism (renal or nutritional)
  • Pseudohyperparathyroidism (certain neoplasia)
  • Lack of UV in reptiles (the disease is usually referred as metabolic bone disease)
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13
Q

What are the consequences of Fibrous osteodystrophy?

A
  • Lameness,
  • fractures,
  • deformities
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14
Q

What are the typical causes of Hypervitaminosis D?

A
  • Ingestion of plants calcinogenic plants (e.g. Solanum
    sp. , Trisetum flavescens) (herbivores)
  • Feed overdoses (pigs and horses)
  • Ingestion of certain drugs (e.g. rodenticide)
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15
Q

What is the pathology associated with Hypervitaminosis D?

A
  • Produce hypercalcemia and/or hyperphosphatemia

and consequently metastatic mineralization

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16
Q

What are the typical sites of mineralization in Hypervitaminosis D?

A
  • vessels,
  • lung,
  • kidney
  • stomach
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17
Q

What is the cause of scurvy?

A
  • Vitamin C is required for collagen synthesis
  • Guinea pigs, some primates, and some bats cannot
    synthetize vitamin C
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18
Q

What are the consequences of scurvy?

A
  • Osteopenia: bone fragility, fractures
  • Metaphyseal, articular, muscular and subcutaneous
    haemorrhages
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19
Q

What is osteitis?

A

Inflammation of bone

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20
Q

What is Periostitis?

A

Inflammation of bone with involvement of periosteum

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21
Q

What is Osteomyelitis?

A

Inflammation of bone with bone marrow involvement

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22
Q

What are the routes of infection in inflammatory bone disease?

A
  1. Haematogenous
  2. Trauma
  3. Inflammation of adjacent tissues (e.g. periodontitis –
    maxilla/jaw, otitis – tympanic bulla)
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23
Q

What is the signalment of Metaphyseal osteopathy?

A
  • Young dogs (2-6 months)

- Usually large breeds

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24
Q

What is the presentation of Metaphyseal osteopathy?

A
  • Lameness, fever, swollen painful metaphyses in
    multiple long bones
  • Suppurative and fibrinous osteomyelitis of the
    trabecular bone of the metaphysis
  • Most cases resolve completely
  • Unknown aetiology
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25
Q

What is Hypertrophic Osteopathy and what is it associated with?

A
  • Dogs
  • Progressive, bilateral periosteal new bone formation in the diaphyses of distal limbs
  • Usually associated to intrathoracic neoplasms or
    inflammation
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26
Q

What is the signalment and presentation of Craniomandibular Osteopathy (“lion jaw”)?

A
  • Hereditary condition
  • West Highland white terrier (WHWT)
  • Thickening of mandibles, occipital and temporal bones
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27
Q

What is the cell of origin of osteosarcomas?

A

Osteoblast

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28
Q

What is the primary site of osteosarcomas?

A

Predominantly metaphyses of larger appendicular bones

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29
Q

What is the behaviour of osteosarcomas?

A

Highly malignant with early metastasis

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30
Q

What is sclerosis?

A
  • Localised area of increased bone opacity
  • Response of bone to wall-off ‘pathology’ e.g. infection,
    cyst
  • Response to increased or abnormal loading: Wolff’s
    Law
31
Q

What artefacts can appear on a radiograph that look like new bone?

A
  • Superimposition of structures (bone or soft tissue)
  • Adjacent bone loss – can see increased opacity on
    other bone due to this
  • Foreign material e.g. on coat
32
Q

What artefacts can appear on a radiograph that look like bone loss?

A
  • Gas, or defect in soft tissues
  • Mach lines – where 2 bones overlap (mimics hairline
    fractures) – increased opacity
33
Q

What is the appearance of an aggressive lesion on a radiograph?

A

rapid bony change = minimal time for bone to remodel

34
Q

What is the appearance of a non-aggressive lesion on a radiograph?

A

slow-growing, benign more chronic process – remodelling possible – organised looking change

35
Q

How can you assess whether a lesion is aggressive or non-aggressive on a radiograph?

A
  • Bone destruction (lysis)
  • Periosteal reaction
  • Lytic edge character
  • Cortical disruption
  • Transition from normal to abnormal bone
  • Rate of change (10-14 days)
36
Q

Give examples of Radiographic signs of degenerative joint disease?

A
  • Soft tissue swelling / joint effusion – certainly in the
    acute phase
  • Changes in subchondral bone opacity – may see
    sclerosis
  • Changes in joint space – difficult to assess unless
    animal is weight bearing
    • Initially widens due to effusion, then narrows due to
      cartilage erosion
  • Osteophyte formation – new bone
    • Form at chrondrosynovial junction, on non-weight-
      bearing surfaces
  • Joint mice or osteochondral fragments within the joint
    cavity
  • Joint subluxation (hip joint)
  • Cyst formation (rare)
37
Q

Where are the typical locations of osteophytes in the stifle?

A
  • Proximal/distal patella
  • proximal trochlear ridge (femur)
  • both femoral epicondyles
  • fabellae
  • proximal tibia
38
Q

Where are the typical locations of osteophytes in the elbow?

A
  • dorsal anconeal process (ulna)
  • cranial joint aspect
  • lateral epicondylar crest (humerus)
  • Medial epicondyle (humerus)
  • Medial coronoid process (ulna)
  • Trochlear notch (ulna)
39
Q

What is Metabolic Bone disease?

A
  • Generalised bone disease

- Usually a decrease in opacity = osteopenia

40
Q

What are the causes of metabolic bone disease in reptiles?

A
  • Inappropriate feeding and/or husbandry
  • Imbalance of Ca, P, or Vit D in body
    • Usually too low dietary Ca or Vit D or excess P
41
Q

What is the presentation of metabolic bone disease in reptiles?

A
  • Lethargy, reluctance to move
  • Osteopenia
  • Pathological fractures
42
Q

What is the signalment of Metaphyseal osteopathy?

A

Usually young, medium-large breed dogs

43
Q

What is the radiographic presentation of Metaphyseal osteopathy?

A
  • Localised lesion, but affects multiple long bones (esp
    R+U)
  • Early changes: radiolucent line adjacent to metaphyses
  • Later: periosteal new bone formation and sclerosis
44
Q

What is the presentation of Hypertrophic osteopathy?

A
  • Periosteal new bone formation
  • Soft tissue swelling
  • No joint involvement or bone destruction – just affects
    long bones
  • Metacarpal / metatarsal bones affected first, but then
    spreads to other bones
45
Q

What is Hypertrophic osteopathy secondary to?

A

Secondary to space-occupying lesion in thorax or abdomen (image thorax/abdomen)

46
Q

What is the radiographic presentation of Craniomandibular osteopathy?

A
  • Reactive periosteal new bone formation on mandible
    and ventral skull bones
  • Increased bone density
47
Q

What is the clinical presentation of Panosteitis?

A
  • Shifting lameness in young growing dogs esp. GSD
  • May be polyostotic
  • Affects fore legs more commonly than hind legs
  • Self-limiting - full recovery
48
Q

What is the radiographic presentation of Panosteitis?

A
  • Increased opacity of medullary canal – irregular, heterogenous
  • ‘Thumb prints’
  • Thickening of cortical bone
  • Often centered around nutrient foramina
49
Q

What is the clinical presentation of Immune-mediated polyarthritis?

A

Painful, stiff, depressed animal often with swollen joints and ligamentous laxity

50
Q

What is the radiographic presentation of Immune-mediated polyarthritis?

A
  • Bony changes in erosive form only
  • Multiple lytic lesions, around and ‘crossing’ joints
  • Affects all joints, but changes most common / initially seen in carpi and hocks
51
Q

What is the radiographic appearance of Bone cysts?

A
  • Usually oval/circular, and well marginated +/- sclerotic
    rim
  • Usually near joints
52
Q

What are the Predilection sites of bone cysts?

A

equine stifle and fetlock

53
Q

How do you Evaluate bones related to their radiographic (or Roentgen) signs?

A
  • Number
  • Location
  • Size
  • Shape
  • Margination
  • Radiopacity (including internal architecture)
54
Q

How can Aggressive versus non-aggressive bone lesions be assessed?

A
  • Bone destruction (lysis)
  • Periosteal reaction
  • Lytic edge character
  • Cortical disruption
  • Transition from normal to abnormal bone
  • Rate of change (10-14 days)
55
Q

What is a simple fracture?

A

only 1 fracture line i.e. bone split into 2 pieces

56
Q

What is a transverse fracture?

A
  • Fracture ≤ 30 degrees perpendicular to long axis of
    bone
  • Inter-digitating i.e. fracture surface irregular with spikes
    and depressions on both ends of fractured bone that
    “interdigitate” with each other
57
Q

What is an oblique fracture?

A

Fracture line > 30 perpendicular to long axis of bone

58
Q

What is a spiral fracture?

A
  • Spiral = oblique fracture

- curves / spirals around the bone

59
Q

What is a Comminuted fracture?

A
  • more than one fracture line that connect
  • may be multiple joining fractures
  • end result = 3 or more pieces of bone
60
Q

What is a Segmental fracture?

A
  • Special type of comminuted fracture
  • RARE
    • 2 or more fracture lines that do not connect
    • Each bone is a complete piece of cortex
    • Result = 3 or more pieces of bone
    • Wedge / Butterfly
61
Q

What is an avulsion fracture?

A
  • Apophyseal bone avulsed

- insertion point of tendon or ligament

62
Q

When do Physeal fractures usually occur?

A

Physeal fractures usually only happen in young (skeletally immature) animals

63
Q

What are the FIVE primary physiologic

forces acting on a normal bone?

A
  1. Axial Compression - Main force of weight-bearing
  2. Bending - compressive force eccentrically loading of bone
  3. Shear - sideways bone displacement
  4. Torsion - axial rotation / twisting
  5. Tension - only applies at point of insertion of ligaments
    (apophysis) NOT diaphyseal bone
64
Q

When does TENSION AVULSION – EXTERNAL occur?

A

occurs when ligaments or tendons apply

a distractive force

65
Q

Give examples of external tension avulsion (don’t worry about knowing all of them)?

A
  • gluteal muscles, greater trochanter
  • patella tendon on the tibial tuberosity
  • triceps, olecranon of ulna
  • common calcaneal tendon, calcaneous
66
Q

What is axial compression? How does it work on different fractures?

A
  • Produces a compressive force
  • Compression is good if fracture is
    transverse or fragment ends interdigitate
  • On an oblique fracture produces a shear
    force over-riding and collapse of fracture e.g. if oblique
    or comminuted
67
Q

Which forces are plates strong and weak to?

A

Strong: to tension (stretching)
Weak: To Bending

68
Q

Which fractures are unstable to all forces?

A

Comminuted or non-reconstructed

69
Q

What is strain theory?

A
  • Measurement of the strain (% movement) at the fracture
  • Strain is a measure of the distance moved by the fracture ends as the animal weight bears
  • Different healing tissue types can cope with different degrees of deformation
  • An indication of the degree of stability required of the implants
70
Q

What is strain reduced by?

A
  • increasing the distance between the fracture ends, i.e.
    big fracture
  • gap or resorbing some of the bone as occurs early in
    fracture
  • reducing movement = fracture repair and stabilising
  • reducing movement = as callus develops
71
Q

What is primary healing of bone?

A

Bone apposition & reduction = stability

ideally compression

72
Q

What is secondary healing of bone?

A
  • Bone not apposed reconstructed
  • Relative movement instability
  • Callus formation
73
Q

What force does axial compression cause in bone?

A

‘axial’ compression creates a bending

force within bone

74
Q

Which forces are plates weak to?

A

weak to bending

MSK 2 (4 decks)

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