Orthopaedics: Intro and Developmental Diseases Flashcards

1
Q

What are the 5 functions of bones?

A

Skeletal support- movement

Protection

Haematopoiesis

Regulation of mineral haemostasis

Fat storage

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2
Q

What is trabecular and cortical bone?

A

Trabecular (cancellous) and woven bone-
Location- metaphysis, flat bones- dissipates load

Cortical bone-
dense bone or diaphysis, supports weight, protects organs, provides levers

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3
Q

Describe how bone develops?

A

Intramembranous ossification
Skull and scapula-
undifferentiated mesenchymal cells into osteoblasts
direct production of bone by osteoblasts

Endochondral ossification-
seen in long bones, formation and replacement of cartilage template by bone, increases length
Physis- key structures responsible for longitudinal bone growth

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4
Q

What is bone modelling?

When does it occur?

A

Ability of bone to change based on strain put on it in the developing animal
Osteoblasts from bone where there was none before, osteoclasts remove bone to alter shape- work together

Replacement of damaged bone

Fracture repair

Prevent accumulation of fatigue damage - microscopic damage

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5
Q

What is Wolff’s law

A

Primary regulator of bone remodelling

Adaptable- to life and excercise

Adaption-
Increase/Decrease- size/density

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6
Q

How does bone respond to load?

A

Bone is anisotropic- mechanical properties depend on- size and shape-
cortical thickness, mineralisation, magnitude, direction, rate

Forces- need to be stopped or bone wont recover-
compression, tension, bending, torsion, shearing

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7
Q

With load bones deform

What are the different types of bone deformation?

A

Elastic deformation-
with loading and unloading the bone deforms then returns to the original shape
stimulates modelling

Plastic deformation-
with loading and unloading the bone deforms and doesn’t return to original shape-
microcracks, cyclic fatigue, incomplete fractures

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8
Q

What are the practical implications of bone deformation?

A

Complete bone failure

Weakening of normal bone-
plastic deformation and repetitive loading = stress fractures
abnormal matrix- metabolic, neoplasia

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9
Q

What can cause the failure of a normal bone?

What are stress fractures and where do they commonly occur?

A

Single supra-physiological load- kick wound, hit by car
Internal truama-
Foot planted and body twists- stuck in hole

Stress fractures- fracture of weakened bone (cannot keep up)
racehorses- MCIII/MTIII condylar fracture, dorsal metacarpal disease

greyhounds- acetabulum, central tarsal bone

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10
Q

What is dorsal metacarpal disease?

A
  • Primary racing force on lateral side
  • Primary galloping side on medial side
  • Classical training give poor adaption to race- increased bone on medial side
  • Modified training gives better density and adaption to race
  • Grey hounds race anticlockwise- more weight on left- increased bone
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11
Q

What neoplasia can affect bones?

A

Osteosarcoma

Haemangiosarcoma

Multiple myeloma

Chondrosarcoma

Bacterial osteomyelitis

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12
Q

What causes metabolic bone disease?

A

Related to the metabolism of calcium and phosphorus
Controlled by:

vitamin D
PTH
Calcitonin
The mineral content of bone

PTH abnormality
Vit D deficiency
Paraneoplastic

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13
Q

What are developmental orthopaedic diseases?

A

Group of diseases

Cause musculoskeletal problems- various syndromes, age predisposition

Multifactorial

Disturbance in development- cartilage, bone

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14
Q

What are the different regions in a growth plate?

A

Resting cartilage

Proliferative cartilage

Hypertrophic cartilage

Calcifying cartilage

Secondary spongiosa

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15
Q

How can disturbances in endochondral ossification lead to developmental orthopaedic disease?

A

Physeal growth plate-
abnormal deposition of matrix, abnormal mineralisation, poor conversion to bone, retention of cartilage
Result- slow uneven growth

Articular-epiphyseal CC-
abnormal deposition of the matrix, abnormal mineralisation, retention of cartilage
Result- slow growth, uneven growth, cartilage flaps

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16
Q

What does slow, uneven growth from disturbances with endochondral ossification lead to?

ALD- angular limb deformities
FLD- flexural limb deformities
OCD- oestochondritis

Abnormal endochondral ossification- achondroplasia

Associated conditions-
Osteochondrosis- cartilage abnormalities
Osteochondrosis
Subchondral cystic lesions

A
17
Q

Describe the pathophysiology of osteochondritis dissecans?

What does it lead to?

What are the clinical signs?

A

Disruption of blood supply-
Affects the mineralisation of the subchondral bone
Alters biochem and biochemical properties of cartilage and subchondral bone
Affects the ability to adapt and withstand the force- shearing

Shear forces and weight baring-> separation at osteochondral junction -> cartilage flaps and fragmentation -> exposed subchondral bone-> irregular raised cartilage

Clinical signs- fluid swelling, radiography
DIRT- distal intermediate ridge tibia

18
Q

What is the aetiologies of osteochondrosis/dritis dissecans?

A

Rapid growth-
genetic potential, hormone, nutritional

Genetic predisposition

Nutrition-
excess energy and protein, imbalance of Ca:P- excess P
Imbalance of Cu:Zn- Cu collagen crosslinking

Hormone and GHF influence-
testosterone, GHF, hyperinsulinaemia

Trauma

In neck- WOBBLERS DISEASE

19
Q

What are the radiographic abnormalities of OCD?

A

Irregular subchonral bone

Osseous densities- mineralised cartilage, osteochondral fragments

Radiograph opposite- may underestimate damage

20
Q

How does developmental orthopaedic disease manifest in different species?

A

Equine-
Osteochondritis- OCD and subchondral bone cysts
Physitis
Angular limb deformities
Flexural deformities

Canine-
Osteochrondrosis- united anconeal process, fragmented medial coronoid process
Hypertrophic osteodystrophy
Legg calve perthes
Hip dysplasia

Bovine-
Oestoechrondrosis
Flexural deformities

Porcine-
Oesteochrondrosis

21
Q

What does developmental orthopaedic disease result in?

A

Abnormal endochondral ossification-
abnormal maturation of cartilage

Inappropriate relative growth-
bone vs soft tissue

22
Q

What is the aetiology of subchondral cyst-like lesions?

A

Abnormal endochondral ossification-
retention of cartilage core
collapse of cartilage

Trauma- articular cartilage and SC bone- pressure from SC bone

23
Q

What is physitis?

What are the clinical signs?

How does it progress?

A

Enlargement of the physis- inflammation, disrupted endochondral ossificatoin

Clinical signs-
lameness, stiff gait

Self-limiting

24
Q
A
25
Q

What causes hypertrophic osteodystrophy?

What is the pathogenesis?

What are the clinical signs?

What are the radiographic abnormalities?

A

Idiopathic

Pathogenesis- necrosis of the capillary loops of the cartilage of the metaphyseal physis, cuff of metaplastic cartilage and bone

Clinical signs- lameness, fever, lethargy, painful bone
primarily long bones, bilateral and symmetrical

Radiographic abnormalities-
Abnormal bone on the diaphyseal side of physis
Decreased radiodensity parallel to physis
Irregular widening of physis
Sub and extra-periosteal new bone

26
Q

What causes panostetitis?

Describe the pathogenesis?

What are the clinical signs and the radiographic abnormalities?

A

Idiopathic

Pathogenesis- fibrosis of bone tissue
increased osteoblastic and fibroblastic activity
Disorganised trabecular formation in SCB

Clinical signs-
acute lameness, shifting, lethargy, pain

Radiographic abnormalities
Increased opacity of medullary cavity
Indistinct trabecular pattern
Increased endosteal opacity

27
Q

What are the different presentations of hip dysplasia in different species?

A

Hip dysplasia in dogs-
genetic predisposition to laxity of the CF joint
abnormal anatomy of femoral head and acetabulum

Canine elbow dysplasia-
OCD, united anconeal process, fragmented coronoid process

Shetland shoulder syndrome-
Genetic abnormal humeral head and scapular glenoid

28
Q

What causes Legg-calve Perthes disease?

What is the pathogenesis?

What are the clinical signs?

What are the radiographic abnormalities?

A

Idiopathic

Pathogenesis-
Avascular necrosis of the femoral head
Bone remains mechanically stable initially
When SCB loses mechanical strength- collapse of articular surface

Clinical signs-
Acute onset lameness
Fracture/collapse of the femoral head

Radiographic abnormalities-
Osteolysis of the femoral head- SCB resorption
Collapsed and thickened femoral neck
Fracture

Treatment- surgical due to severity of arthritis, femoral head and neck extension

29
Q

What are medial and lateral angular limb deformities?

What are the potential locations in a horse?

What happens in canines?

A

Valgus- lateral deviation
Valrus- medial deviation

Equine potential locations-
Metaphyseal growth plate, epiphysis, cuboidal bones- carpus, tarsus, metaphysis

Canine-
Asynchronous growth of a pair of bones- shorter acts to create bowing
Radius and ulna > tibia and fibula
Differential growth between bones, after damage to one- trauma to growth plate

30
Q

What are the flexural deformities equine and bovine?

A

Pathogenesis
Disproportionate growth
Muscle-tendon unit vs bony skeleton
Bone functionally longer

Congenital- new born foals

Acquired- rapidly growing foals and yearlings, acute or chronic