MSK Pathology 1 Flashcards

1
Q

Bone interstitium.

A

Matrix:
- Type I collagen polymers.
- Provides support for cells.
Mineral osteoid:
- Hardness.
- Compressional resistance.

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2
Q
  1. Malformations…
    Vs…
  2. Deformities.
  3. Most vulnerable sites of malformations and deformities?
A
  1. Never normally formed in the first place.
    Primary structural defects due to localised errors in embryo development.
    E.g. due to teratogens, genetics, events in utero (e.g. extreme stress).
  2. Alterations in shape or structure that was previously normally formed.
    Can occur at any age.
    E.g. due to infections (CDV,BVDV, Schmallenberg), toxins, undernutrition.
  3. Growth plates.
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3
Q

Chondrodysplasia.

A

Disorders of bone growth due to primary defects in formation of cartilage.
Affects bones formed by endochondral ossification in cattle, dogs, sheep, cats and pigs.
Can be generalised or localised.
Aetiology:
- is often unknown.
- genetic defect (chondrogenesis).
– breed selection.
- secondary condition (lysosomal storage disease) – RARE!

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4
Q

Chondrodysplasia classification.

A

Generalised:
- affects whole skeleton (proportional dwarfism).
– hypopituitarism.
Localised:
- restricted to certain bones e.g. epiphyseal or metaphyseal cartilage.
- disproportionate dwarfism = normal sized head, short legs.
- e.g. brachycephalic dogs, dachshunds.

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5
Q

Angular limb deformities

A

FLs of fast-growing large breed dogs.
Partial or complete premature closure of the growth plates.
Distal ulnar physis is a common site.
- Ulna shorter than radius – radius bows dorsally.
–> causes carpus valgus, carpal laxity, carpal and elbow subluxation.

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6
Q

Physeal osteochondrosis.

A

Focal disturbance of endochondral ossification.
Likely vascular/genetic aetiology.
- Hypertrophic cartilage layer of growth plate.
- Hypertrophic chondrocytes remain viable.
Well-demarcated wedge of retained cartilage in the physis.
If growth plate involvement is extensive, can lead to fracture which can lead to angular limb deformities.

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7
Q

Ischaemic necrosis.

A

Septic:
- disrupts vascular supply to periosteum and/or trabecular bone.
Aseptic:
- trauma – vascular damage following fracture.
- infiltrating neoplasm.
- thromboembolism.
- avascular necrosis of femoral head.
– Legg-Calve-Perthes disease: Mini Poodle, westies, yorkies.
–> femoral head bone replaced by fibrous tissue.
–> femoral head collapse.
– femoral head fractures.

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8
Q

Metabolic diseases - Osteopenia / osteoporosis.

A

Localised or generalised decrease in bone density and/or mineralisation.
Cortical bone and trabeculae affected.
- thinner cortical bone than normal.
- medullary cavity enlarges.
– can become gelatinous as matrix lost.
- trabeculae more porous.

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9
Q

Mechanisms of osteopenia/osteoporosis.

A

Reduced bone matrix formation.
- generalised – protein and vit deficiencies and senile states.
- immobilisation/reduced physical activity.
- localised – poor irrigation (vascular origin).
Increased bone resorption
- fibrous osteodystrophy.
– primary hyperparathyroidism (rare) –> parathyroid neoplasia.
– secondary hyperparathyroidism.
–> nutritional: increased phosphorous, reduced calcium (increases PTH).
–> renal (chronic renal failure (common esp. in dogs).
–> excess glucocorticoids (reduces calcium absorption in GIT).
Deficient mineralisation - Rickets (growing)/osteomalacia (adults).
– vit D deficiency.
– phosphorus deficiency.
– imbalanced calcium : phosphorus ratio (high Ca, low P).
*Subsequent bone deformities
- Young animals: flared metaphyses, GPs large, growth cessation.
- Adult (modelling affected): pathological fractures, deformities.

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10
Q

Hypertrophic osteopathy.

A

Often associated with intrathoracic masses (hypertrophic pulmonary osteoarthropathy).
Dogs most affected.
Progressive, bilateral, periosteal new bone formation.
Secondary to a space-occupying lesion.
- intrathoracic tumours (paraneoplastic syndrome), inflammation.
Diaphysis and metaphysis of the distal limbs.
- abaxial aspect of 2nd and 5th metacarpals and/or metatarsals.
Current theory:
- reflex vasomotor changes mediated by the vagus nerve (mass puts pressure on vagus nerve) leads to increased blood flow to the extremities which leads to proliferation of connective tissue and periosteum.

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11
Q

Bone inflammation.

A

Septic:
- bacteria
- most common.
- can be life threatening.
- haematogenous.
– young farmed animals.
– vertebrae and metaphysis of long bones.
- direct intro – compound fracture/ surgery.
- direct extension – surrounding tissues e.g. tooth, joint.
Aseptic:
- vascular effects.

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12
Q

Periostitis.

A

Acute:
- simple (aseptic).
- septic – bacteria.
– form subperiosteal abscesses.
Chronic:
- fibrous – thickening in form of tightly adhering fibrous plate.
- ossifying – formation of new bone tissue.
– exostosis –> regular contour and surface masses.
– osteophytes –> irregular reliefs, spike and ridges.

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13
Q

Osteomyelitis.

A

Almost always of bacterial aetiology.
After open fractures or surgical interventions.
Haematogenous spread.
Acute:
- origin in the bone marrow itself or in the bone tissue.
– initial exudate purulent which compresses the bony tissue.
–> v painful.
Chronic:
- progressive osteolysis.
- subperiosteal neoformation.
- e.g. lumpy jaw – actinomyces bovis.

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14
Q
  1. Bone tumours originating in the cells of bone.
  2. Other primary neoplasms in the bone.
  3. Tumours in bone marrow.
A
  1. Osteosarcomas / osteomas.
    Chondromas / chondrosarcomas.
    Fibromas / fibrosarcomas.
  2. Liposarcomas.
    Giant cell tumours.
    Haemangiomas / haemangiosarcomas.
  3. Lymphoma / leukaemia.
    Plasma cell myelomas.
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15
Q

Osteosarcoma.

A

80% of long bone neoplasia in dogs.
Common in cats, rare in other spp.
Large and giant breeds - bones grow so quickly.
Associated with infarction, fractures and orthopaedic metallic implants.
Common sites:
- proximal humerus, distal radium, femur, distal ulna, proximal tibia, ribs, vertebrae.
Grows quickly, v invasive locally and painful.
Early haematogenous metastasis common.

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16
Q

Secondary tumours of bone.

A

Carcinomas more commonly than sarcomas.
- mammary gland.
- thyroid.
- prostate.
- ovary.
- lungs.
Common sites (dog):
- ribs, vertebrae and proximal long bones.
- often osteolytic.

17
Q

Arthropathy.

A

Disease affecting one or more joint structures.

18
Q

Response of joints to injury.

A

Common insults:
- trauma.
- joint instability.
- changes in lubrication.
- inflammation.
Response:
- inflammatory cells, death of chondrocytes, synovial lining cells.
– inflammatory cells and death of chondrocytes cause activation of matrix metalloproteinases (MMPs) and activate lysosomal enzymes and neutral proteases.
– Synovial lining cells also release lysosomal enzymes and neutral proteases.
–> this all causes degradation of the matrix of the joint surface.
Joint cartilage has no perichondrium so nutrition/oxygenation supply limited and so is regenerative ability.
Nutrition to joint cartilages ensured by pumping promoted by compression and decompression of cartilage during movement.
No innervation - only painful when subchondral bone or synovium involved.
Lose proteoglycan, which reduces joint lubrication, which disrupts collagen fibres, forming clefts (fibrillation), where chondrocytes attempt regeneration (clumping), get cartilage thinning, leading eburnation and bone exposure.
Chronically:
- hypertrophy of synovial villus.
- formation of fibrovascular tissue rich in macrophages originating from synovial membranes
– Pannus.
- extends over joint surfaces.
- releases fluids rich in proteases that degrade cartilage.

19
Q

Degenerative joint disease.

A

Disease where all 3 structures affected:
- periosteum:
– new bone growth and osteophyte formation.
- synovium:
– villous hypertrophy/hyperplasia, inflammation and pannus formation.
- cartilage:
– erosion and fibrillation.

20
Q

Arthritis.

A

Non-suppurative arthritis.
- e.g. viral, repetitive trauma.
- deposition of fibrin within synovium and articular cartilage.
– ideally resolves.
– but may persist:
–> lymphoplasmacytic synovitis (immune-mediated).
–> fibrous tissue +/- Pannus formation.
—> leads to further cartilage destruction, infection of subchondral bones and ankylosis (immobilisation).
Suppurative arthritis:
- bacterial.
- infiltration of joint by neutrophils.
– ideally resolves.
– but may persist.
–> release of lysosomal enzymes by neutrophils.
–> extension to periarticular structures.
—> leads to further cartilage destruction of cartilage, infection of subchondral bone, ankylosis.

21
Q

Routes of joint infection.

A

Haematogenous.
Spread from osteomyelitis.
Spread from soft tissue.
Diagnostic or therapeutic procedure.
Penetrating damage.

22
Q

Common pathogens causing arthritis.

A

Streptococcus.
Trueperella pyogenes.
Mycoplasma spp.
Escherichia coli.
Salmonella Dublin.

23
Q

Canine Immune Mediated Polyarthritis.

A

Cell-mediated response > rheumatoid factor (IgG) > immune complexes form in joints > activate innate immune defences > inflammation, leading to Pannus formation, synovitis, erosion of cartilage and fibrillation.

24
Q

Examples of developmental diseases of the joints.

A

Arthrogryposis - persistent flexure of the joint.
Hip dysplasia.
Osteochondrosis.
Cervical Vertebral Myelopathy (“Wobbler syndrome”) - dog, horse.
Patellar luxation/subluxation - dog, horse.
Atlanto-axial subluxation (miniature, toy dog breeds).

25
Q

Developmental disease - osteochondrosis.

A

Abnormalities in growth cartilage of joint.
Pigs, horses, poultry, large breed dogs.
Aetiology is multifactorial:
- vascular disruption.
- genetic.
- nutritional.
- trauma, biomechanical, anatomical factors.
Initial lesion usually unknown but involves failure of endochondral ossification.

26
Q

Osteochondrosis dissecans (OCD) process.

A

Vascular disturbance and wedge beneath cartilaginous surface.
Persistence of wedge forms a fissure, causing a fault line in the cartilage. Fissure grows and cartilage flap detached - ‘joint mouse’. Flap (dissecans) enters joint cavity.
Exposure of subchondral bone, cartilaginous edges, loose piece of cartilage floating in the joint.
Pain, discomfort, inflammation.

27
Q
A