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Systemic Pathology (Spring 2015) > L4: Bone, Joint, and Muscle Path (Dark) > Flashcards

L4: Bone, Joint, and Muscle Path (Dark) Flashcards

1
Q

bone anatomy

A

osteon made up of osteocytes surrounding Haversian canal

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2
Q

chars. of intramembranous ossification

A
  • flat bones
  • no growth plates
  • susceptible to fibrous osteodystrophy
  • not affected by chondrodysplasia
  • ossification center begins in the fibrous CT membrane
  • osteoid is secreted into the fibrous membrane
  • forms woven bone and periosteum
  • final layer of compact bone
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3
Q

chars. of endochondral ossification

A
  • long bones (arms, legs, ribs)
  • requires growth plates
  • predominantly increases length (not width)
  • hyaline cartilage –> 1ary ossification center + periosteum –> 2ary ossification center –> medullary cavity –> compact bone, periosteum, spongy bone
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4
Q

physeal plate

A

where 2 ossification centers meet each other

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5
Q

zone of proliferation

A

chondrocytes proliferating

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6
Q

zone of hypertrophy

A

where chondrocytes get larger

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7
Q

growth plate fx requires:

A

angiogenesis

  • needs adequately mineralized collagen/cartilage
  • needs adequate blood vessel quality
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8
Q

what dz process affects columnar cartilage/provisional zone of calcification

A

Rickets

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9
Q

what dz process affects osteoid formation

A

Osteogenesis imperfecta

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10
Q

what dz process affects bone remodeling in compact bone

A

osteopetrosis

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11
Q

transverse fracture

A

straight across fracture

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12
Q

oblique fracture

A

fracture at an angle

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13
Q

zones across a growth plate**

A
  • resting
  • proliferating
  • hypertrophic
  • ossification
  • trabecular cone
  • if orderly developed cartilage gets disrupted, will have growth problems*
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14
Q

spiral fracture

A

looks oblique in 2 different views of the fracture

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15
Q

“greenstick” fracture

A
  • incomplete fracture
  • usually in younger dogs where you get fracture through one cortex but not another
  • usually not displaced
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16
Q

comminution

A

multiple fragments present in fracture

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17
Q

mnemonic for fracture classification

A

O (open v. closed)
L (location)
D (degree - complete or incomplete)

A (articular extension)
C (comminution/pattern)
I (intrinsic bone quality)
D (displacement, angulation, rotation)

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18
Q

stages of fracture healing

A

1) hematoma
2) fibrocartilagenous callus
3) bony callus
4) remodeling

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19
Q

Salter fracture

A
  • fracture through a growth plate
  • can induce growth deformities
  • classified by the fracture location
  • 5 main types (“SALTR”) - see slide 17**
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20
Q

Type 1 “Straight” Salter fracture

A

fracture straight through growth plate

-5%

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21
Q

Type 2 “Above” Salter fracture

A

starts above then travels through growth plate

-75%

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22
Q

Type 3 “Lower” Salter fracture

A

starts below then travels through growth plate

-10%

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23
Q

Type 4 “Through” Salter fracture

A

starts above and passes vertically through growth plate to end below growth plate
-10%

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24
Q

Type 5 “cRush” Salter fracture

A

growth plate compressed

-uncommon

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25
Q

Craniomandibular osteopathy

A
  • proliferation of bony tissue around jaw, mandible, and TMJ
  • primarily in Westies and Scotties
  • autosomal recessive
  • starts at 3-7mo, stops at 11-13mo
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26
Q

Osteogenesis imperfecta

A
  • defect in matrix synthesis (ie. type I collagen)
  • char. by excessive bone fragility –> fractures
  • usually short lifespan
  • without effective collagen synthesis, can’t get effective osteogenesis
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27
Q

Osteopetrosis

A
  • failure of bone remodeling
  • increased bone density
  • has “bone in bone” appearance
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28
Q

Chondrosyplasia

A
  • composed of multiple syndromes
  • achondroplasia (failure to generate cartilage)
  • disproportionate dwarfism
  • affects bones with growth plates the most
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29
Q

Osteoporosis

A
  • bone loss - resorption > formation
  • disuse, malnutrition, corticosteroids, etc.
  • susceptible to pathologic fracture
  • osteoclast activity exceeds osteoblast activity
  • a concern in older humans
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30
Q

osteopenia

A

decreased numbers of thin trebeculae

-usually progresses to osteoporosis

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31
Q

scurvy***

A
  • only in species lacking L-gulonolactone oxidase
  • lack of vit. C–> dec. lysine and proline hydroxylation in collagen –> impaired collagen synthesis –> weakened vessel walls and physeal cartilage deformity –> periarticular hemorrhage and osteochodrodysplasia
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32
Q

Fibrous osteodystrophy

A

Primary or secondary hyperparathyroidism:

  • primary: caused by functional parathyroid adenomas or parathyroid hyperplasia
  • secondary: Ca:P imbalance in feed (too much P or too little Ca), or kidney disease
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33
Q

Rickets

A
  • defect in endochondral ossification
  • only in young animals (b/c problem at growth plates)
  • def. in Vit. D or phosphorus
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34
Q

Hypertrophic osteopathy

A
  • due primarily to intrathoracic space occupying mass
  • periosteal proliferation
  • joints NOT involved**
  • etiology unclear
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35
Q

Hypertrophic OsteoDystrophy (metaphyseal osteopathy)

A
  • “Double physeal line”
  • young dogs
  • acute inflammation in the primary spongiosa
  • necrosis of osteoblasts
  • usually self-limiting
36
Q

Eosinophilic Panosteitis

A
  • happens around nutrient foramen

- patchy increased radiodensity in marrow cavity

37
Q

Legg-Perthes Disease

A
  • avascular necrosis of the femoral head
  • small breed dogs
  • occurs prior to physeal closure (4-11mo)
38
Q

Osteomyelitis***

A
  • SERIOUS condition
  • causes: sx, penetrating wound, fracture, hematogenous spread
  • tx difficult
  • can be acute or chronic
  • can be caused by many species of bacteria
  • commonly centered around physes because bacteria get caught in blood supply here**
  • main causes: Bordetella bronchiseptica and/or Pasteurella multocida**
39
Q

malignant tumor of lymphocytes

A

lymphosarcoma

40
Q

malignant tumor of macrophages

A

histiocytic sarcoma

41
Q

malignant tumor of endothelial cells

A

hemangioma

42
Q

benign tumor of fibroblasts

A

fibroma

43
Q

malignant tumor of fibroblasts

A

fibrosarcoma

44
Q

tumor of plasma cells

A

multiple myeloma

  • common in bones
  • can produce Bence-Jones protein in urine
45
Q

2 big things to remember about osteosarcoma

A
  • away from elbow, towards knee (except for horses, which can get it on mandible)
  • pathologic fractures very common
  • does NOT bridge joints
46
Q

benign tumor of osteocytes

A

osteoma

47
Q

malignant tumor of osteocytes

A

osteosarcoma

48
Q

benign tumor of chondrocytes

A

chondroma

49
Q

malignant tumor of chondrocytes

A

chondrosarcoma

50
Q

osteochondromatosis

A

a condition involving a proliferation of osteochondromas

  • benign
  • proliferation of growth plate cartilage
  • grow with skeleton
  • tend to see around ribs and costochondral jxs
  • don’t typically cause problems but if occurs in spinal cord can cause compressive damage
51
Q

multilobular tumor of bone

A

forms stripey pattern on flat bone

52
Q

2 ways synovium reacts to injury

A

1) hypertrophy (very common)
2) pannus (granulation tissue on articular surface)
- can damage underlying cartilage**
- can progress to ankylosis (pathologic fusion of joint)

53
Q

arthrodesis*

A

ELECTIVE fusion of the joint

54
Q

cartilage has poor blood supply and limited regenerative capacity

A

:)

55
Q

Fibrillation

A
  • forms vertical clefts in cartilage
  • dull, yellow-brown cartilage
  • can be reversible
56
Q

Eburnation

A

polishing of exposed subchondral (below the cartilage) bone

-bone effectively taking place of cartilage

57
Q

Osteophytosis

A

osteophytes form around unstable joint such as with arthritis

58
Q

“joint mice”

A

calcified bony piece of tissue that is free floating in the joint

59
Q

Inflammatory Arthritis

A

Caused by acute (penetrating wound, septicemia) or Chronic (immune-mediated, virus, untreated acute arthritis) arthritis
-pus in joint common CS

60
Q

Sharpei fever

A

immune-mediated inflammatory arthritis in Sharpeis.

  • cyclic high fever, inflammatory arthritis, then goes away
  • most develop amyloidosis from repeated arthrosis
61
Q

Osteoarthritis

A
  • DJD
  • decreased proteoglycan synthesis
  • inc. metalloenzyme synthesis degrades proteoglycans
  • typically an aging lesion
  • lesions: fibrillation, cartilage erosion, osteophytosis, eburnation, synovial hyperplasia
62
Q

Osteochondritis Dissecans (OCD)

A
  • osteochondrosis: area of damage to the cartilage; tends to be thicker and has problems in underlying blood supply
  • OCD when flap separates from underlying bone (joint mouse when brakes off)
  • more common in horse, dog, pig
  • usually in younger animals
63
Q

most common neoplasm of joints*

A

synovial cell sarcoma

-looks similar to osteosarc, but involves joint

64
Q

disc structure

A

outer annulus fibrosis

inner nucleus pulposus

65
Q

IVDD

A
  • annulus fibrosis cracks, tears, or can rupture
  • releases nucleus pulposus
  • Type I: sudden; more common in chondrodystrophic breeds
  • Type II: gradual (tends to be in larger dogs)
  • CS: ataxia, painful, placing and CP deficits, dec. motors
66
Q

Wobblers

A
  • stenosis (narrowing) of vertebral column
  • rule-out for IVDD
  • tends to be in younger animals
  • more common in horses, large breed dogs
  • tends to be dynamic (ie. gets worse or better with certain motion)
67
Q

Dural ossification

A
  • “ossifying pachymeningitis” - inflamm. of the dura mater
  • generally incidental
  • few have neuro signs
68
Q

Hip Dysplasia

A
  • degenerative, non-inflammatory
  • generally large-breed dogs
  • deformation of the joint: subluxation of the femoral head
  • osteophytes and fibrous CT form. to stabilize joint
  • genetic component
69
Q

Elbow Dysplasia

A
  • degenerative, non-inflamm.
  • usually large breeds (esp. GSD)
  • ununited anconeal process
  • fragmented medial coronoid process
  • OCD of elbow
70
Q

chars. of normal muscle

A
  • myofibers - single muscle cells
  • peripheral nuclei
  • striations
  • high blood supply
71
Q

2 fiber types

A 
Type I:
-slow twitch
-large number of mitochondria
-postural and sustained activity
Type II:
-fast twitch
-fewer mitochondria
-rapid activity
72
Q

2 distributions of muscle injuries***

A

focal, multifocal

73
Q

2 timelines of m. injuries***

A

monophasic (all m. stages in the same state of damage/repair)
polyphasic (ie. chronic toxin exposure)

74
Q

heart attack (or other vascular injury) would be classified as:***

A

focal, monophasic

75
Q

Responses to injury

A 
hypertrophy
atrophy
degeneration
necrosis - calcification
regeneration
fibrosis
76
Q

types of muscle damage

A 
circulation
myositis
congenital
extertional myopathies
nutritional myopathies
toxins
neoplasia
denervation
77
Q

m. damage: circulation

A

-if lot of weight put on muscle such as in Downer cattle or equine anesthesia, will compress blood vessels –> myonecrosis

78
Q

m. damage: myositis

A

Bacterial:
-typically clostridium
-abscesses
Parasitic:
-Toxoplasma, Trichinella (pigs), Sarcocystis (horses)
Autoimmune:
-systemic lupus erythematosus, polymyositis, purpura hemorrhagica, etc.

79
Q

Congenital Myopathies

A
  • malignant hyperthermia
  • muscular dystrophy
  • equine rhabdomyolysis
  • hyperkalemic periodic paralysis (HYPP)
  • fainting goats
  • “spayleg”
80
Q

chars. of Equine Rhabdomyolysis

A
  • congenital myopathy
  • sporadic
  • polysaccharide storage myopathy
  • recurrent exertional rhabdomylolysis (a breakdown of muscle tissue that releases a damaging protein into the blood)
81
Q

spayleg

A
  • congenital myopathy in pigs

- back leg muscles aren’t strong enough to support their weight so they sink down and splay out

82
Q

Exertional Myopathies

A
  • capture myopathy: usually lethal and stress has been identified as the single most determining factor, exacerbated by muscle exertion
  • disuse (ie. cast)
83
Q

Nutritional Myopathies

A
  • malnutrition –> atrophy

- vit. E/selenium deficiency –> white m. disease

84
Q

m. damage: toxins

A

Monensin

-horses more sensitive than cattle

85
Q

m. damage: neoplasia

A

Rhabdomyoma (benign)

Rhabdomyosarcoma (malignant)

86
Q

m. damage: denervation

A
  • brachial plexus avulsion –> will get severe m. atrophy, phantom itches
  • laryngeal hemiplegia

Systemic Pathology (Spring 2015) (10 decks)

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