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

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

25
What causes hypertrophic osteodystrophy? What is the pathogenesis? What are the clinical signs? What are the radiographic abnormalities?
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
What causes panostetitis? Describe the pathogenesis? What are the clinical signs and the radiographic abnormalities?
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
What are the different presentations of hip dysplasia in different species?
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
What causes Legg-calve Perthes disease? What is the pathogenesis? What are the clinical signs? What are the radiographic abnormalities?
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
What are medial and lateral angular limb deformities? What are the potential locations in a horse? What happens in canines?
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
What are the flexural deformities equine and bovine?
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