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Systemic Pathology > Bone, Joint and Muscle Pathology > Flashcards

Bone, Joint and Muscle Pathology Flashcards

1
Q

What bones are formed by intramembranous ossification?

A

Flat bones (these have no growth plates)

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2
Q

Describe intramembranous ossification

A
  • ossification center begins in the fibrous CT membrane
  • osteoid is secreted into the fibrous membrane
    • entrapped osteoblasts become osteocytes
  • form woven bone and periosteum
  • final layer of compact bone
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3
Q

What kinds of bones are formed via endochondral ossification?

A
  • long bones
    • requires growth plates
    • predominantly incr length
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4
Q

Describe endochondral ossification?

A
  • start with hyaline cartilage “model”
  • develops periosteum and primar ossification center in the middle of the bone
  • then dev. secondary ossification center at the ends
    • hyaline cartilage trapped b/t the two = growth plate
  • bone grows outwards from ossification centers
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5
Q

What are the zones that make up the growth plate?

A

Superficial

  • Resting zone
  • Proliferating zone
  • Hypertrophic zone
  • Ossification zone
  • Trabecular bone

Deep

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6
Q

What does growth plate function require?

A

requires:

  • angiogenesis
  • adequately mineralized collage/cartilage
  • adequate blood vessel quality
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7
Q

Where does achondroplasia affect in the growth plate?

A

the zone of resting cartilage

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8
Q

Where does rickets affect in the growth plate?

A
  • columnar cartilage in the provisional zone of calcification
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9
Q

What zone does osteogenesis imperfecta affect in the growth plate?

A

the zone of osteoid formation

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10
Q

Where in the growth plate does osteopetrosis affect?

A

the zone of bone remodeling in compact bone

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11
Q

Describe woven bone

A
  • polarized (remodeling lines are highlighted)
  • lines are going in many different directions
  • more osteocytes
  • more flexible
  • could be immature bone (not oriented to stress)
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12
Q

Describe laminar bone

A
  • more organized
  • mature bone - has been reoriented/reorganized to stress
  • fewer osteocytes
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13
Q

What is the mneumonic device you can use to remember descriptors for fractures?

A

OLD ACID

O: Open vs. closed

L: Location

D: Degree (complete vs. incomplete)

A: Articular extension

C: Comminution/Pattern

I: Intrinsic bone quality - pathologic fracture

D: Displacement, angulation, rotation

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14
Q

What are the four stages of fracture healing?

A
  1. Hematoma
  2. Fibrocartilagenous callus
  3. Bony callus
  4. Remodeling
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15
Q

What do you see histologically with bone necrosis?

A

empty lacunae (osteocytes have died off)

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16
Q

Why does bone necrosis occur with fractures?

A

loss of blood supply –> ischemia –> cell death

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17
Q

What stage of healing will the bone be in at days 7-10?

A

granulation tissue formation, with evident bone necrosis

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18
Q

What stage of healing will a fracture be at 3 weeks?

A

callus formation

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19
Q

What are Salter Harris fractures?

A

​fractures through a growth plate

  • can induce growth deformities
  • classified by fracture location
20
Q

What is the mneumonic used to remember Salter Harris fracture classifications?

A

SALTR

S: Straight - Type 1

A: Above (thru and above GP) - Type 2

L: Lower (thru and above GP) - Type 3

T: Through (passes through GP) - Type 4

R: cRush (causes most damage)

21
Q

Describe craniomandibular osteopathy

A
  • Craniomandibular osteopathy
    • ​also called ‘lion jaw’
    • primarily in Westies and Scotties
    • autosomal recessive
    • 3-7 mo, stops @ 11-13 mo
  • C/S: jaw pain, difficulty opening jaws
22
Q

Describe osteogenesis imperfecta

A
  • defect in matrix synthesis (e.g. type I collagen)
  • characterized by excessive bone fragility
    • ​fractures
23
Q

What is osteopetrosis?

A
  • failure of bone remodeling
  • increased bone density
24
Q

Describe chondrodysplasia

A
  • not just one syndrome
  • achondroplasia
  • disproportionate dwarfism
25
Q

Describe osteoporosis

A
  • bone loss – resorption > formation
  • d/t disuse, malnutrition, corticosteroids, etc
  • susceptible to fracture
26
Q

What is osteopenia?

A

decreased #s of thin trabeculae; go from osteopenia to osteoporosis

27
Q

Describe scurvy

A
  • only in species lacking L-gulonolactone oxidase (e.g. guinea pigs)
  • Pathogenesis:
    • lack of Vit C
    • weakened vessel walls and physeal cartilage deformity
    • periarticular hemorrhage and osteochondrodysplasia
28
Q

What are some caues of fibrous osteodystrophy?

A
  • Causes:
    • Primary hyperparathyroidism
      • functional parathyroid adenomas
      • parathyroid hyperplasia
    • Secondary hyperparathyroidism
      • Ca:P imbalance in feed
      • Kidney dz
29
Q

What is fibrillation?

A
  • Forms vertical clefts in cartilage
    • dull, yellow-brown cartilage
    • can be problematic b/c cartilage is avascular —> poor healing
30
Q

Define eburnation

A

Continued trauma over a bone that causes polishing of exposed subchondral bone

31
Q

Osteophytes are what?

A

Protuberant overgrowths of bone in attempts to stabilize an articular surface

32
Q

What is a joint mouse?

A

Fragment that breaks off of an articular surface

33
Q

What types of acute infections cause inflammatory arthritis?

A
  • Penetrating wounds
  • septicemia
34
Q

What types of chronic infections cause inflammatory arthritis?

A
  • Immune mediated
  • viral
  • Untreated acute arthritis
35
Q

Descreased viscosity of joint fluid is an indication of what disease process?

A

Arthritis (inflammatory or osteoarthritis)

36
Q

Describe osteoarthritis

A
  • Degenerative joint dz
  • typically an aging lesion
  • lesions:
    • fibrillation, cartilage erosion, osteophytosis, eburnation, synovial hyperplasia
  • Mechanical and biochemical aspects:
    • Decreased proteoglycan synthesis
    • Increased metalloenzyme synthesis — degrade proteoglycans
37
Q

Describe osteochondritis dessicans

A
38
Q

What is an example of joint neoplasm?

A
  • Synovial cell sarcoma
    • typically very aggressive, looks like osteosarcoma but doesn’t cross the joint
39
Q

Describe the structure of an intervertebral disc

A
  • Outer annulus fibrosis
  • inner nucleus pulposis
40
Q

Describe what occurs with degeneration of an IVD

A
  • Annulus fibrosis cracks, tears or can rupture
  • releases nucleus pulposus
  • Types:
    • I - sudden, more common in chrondrodysplastic breeds, most severe
    • II - gradual
41
Q

Describe dural ossification

A

Ossifying pachymeningitis; often incidental

42
Q

Describe hip dysplasia

A
  • Degenerative, non-inflammatory
  • generally large breed dogs
  • deformation of the joint
    • subluxation of femoral head if severe enough
43
Q

Describe elbow dysplasia

A
  • Degenerative, non-inflammatory
  • generally large breed- esp. GSD
  • Seen with:
    • ununited anconeal process
    • fragmented medial coronoid process
    • OCD of the elbow
44
Q

Describe Type I and Type II muscle fibers

A
  • Type I
    • slow twitch
    • large # of mitochondria
    • postural and sustained activity
  • Type II
    • fast twitch
    • fewer mitochondria
    • rapid activity
45
Q

What are some autoimmune causes of myositis?

A
  • Systemic lupus erythematosus
  • polymyositis
  • purpura hemorrhagica
46
Q

What are bacterial and parasitic causes of myositis?

A

Bacterial

  • mostly Clostridium (will cause emphysematous necrosis)
  • abscesses

Parasitic

  • Toxoplasma gondii
  • Trichinella spiralis
  • Sarcocystis spp.

Systemic Pathology (8 decks)

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