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VM742 BOD 3 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

osteoid

A

bone matrix of type I collagen & ground substance (proteoglycans)
produces scaffolding/strength of bone

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2
Q

tension on bone results in…

A

bone resorption

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3
Q

inactivity of bone results in…

A

bone resorption

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4
Q

mechanical load & compression on bone results in…

A

bone deposition

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5
Q

3 pathologies of infectious osteomyelitis

A

trauma
local extension from adjacent infected site (e.g. lumpy jaw)
hematogenous (septic)

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6
Q

why are young livestock at increased risk of septicemia –> physitis or osteomyelitis

A

decreased or failed passive transfer

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7
Q

Common aerobic etiologies for infectious osteomyelitis

A

Brucella
E. coli
Staph
Strep

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8
Q

Common anaerobic etiologies for infectious osteomyelitis

A

Salmonella (facultative)
Clostridium
Actinomyces

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9
Q

Common fungal etiologies for infectious osteomyelitis

A

Coccidioides immitis

Blastomyces dermatitidis

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10
Q

lameness or paresis, recumbency

fever

A

infectious osteomyelitis

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11
Q

Sequestrum & involucrum

A

trauma/hypoxia –> bone necrosis –> foreign body reaction, lytic/exudate pocket

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12
Q

2 pathologies of non-infectious osteomyelitis

A 
Panosteitis
Metaphyseal osteopathy (or hypertrophic osteodystrophy)
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13
Q

Signalment for panosteitis

A

young (5-18 mo) large breed male dogs

German shep, goldens

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14
Q

Recurrent shifting leg lameness (pain on palpation) - self limiting
anorexia, mild lethargy, +/- fever

A

Panosteitis

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15
Q

What lesions are caused by Panosteitis?

A

medullary fibrosis & ossification (looks enlarged on rads), vascular congestion/edema

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16
Q

Metaphyseal osteopathy (or hypertrophic osteodystrophy) causes what lesions

A
  • metaphyseal (NOT physeal) vascular & trabecular necrosis
  • suppurative inflammation
  • metaphyseal & periosteal bone proliferation
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17
Q

Signalment for HOD

A

younger (2-8 mo) large and giant breed dogs

Danes, Weimaraner’s, Boxers, German shep

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18
Q

Suspected causes of HOD

A

idiopathic
Diet - excess Ca, vitamins, calories, hypovitaminosis C
Genetic
Infectious - canine distemper vacc, E. coli sepsis

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19
Q

Severe, progressive lameness
lethargy, anorexia, fever
swollen painful metaphyses of distal radius, ulna, tibia

A

HOD

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20
Q

Pathognomonic sign of HOD

A

“double physis” on rad - reactive fare trying to stabilize metaphysis

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21
Q

What causes metabolic bone disease

A

calcium phosphorus imbalance

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22
Q

4 types of metabolic bone disease (all d/t Ca/P imbalance)

A

Osteoporosis
Osteomalacia
Rickets
Fibrous osteodystrophy

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23
Q

What is osteoporosis?

A
  • Not enough normal bone
  • decreased production of normal bone or excess bone removal
  • reversible
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24
Q

Causes of osteoporosis

A
  • physical inactivity, disuse atrophy
  • starvation (Ca deficiency = increased PTH)
  • decreased estrogen
  • glucocorticoids
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25
Q

Pathological fracture, bone deformities

Cortical thining, increased porosity of bone

A

oseoporosis

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26
Q

What is osteomalacia

A

defective mineralization of osteoid/cartilage - can lay down Ca & P on osteoid

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27
Q

What causes osteomalacia

A 
vit d deficiency (decreased Ca, P absorption)
Phosphorus deficiency (or Ca or both)
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28
Q

Pathological fractures, bone deformities
Extensive matrix of non-mineralized osteoid
cortical and trabecular thinning (soft bone)

A

osteomalacia

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29
Q

What is rickets

A

defective mineralization of osteoid specifically in the physis (how differs from osteomalacia)
happens in juveniles only

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30
Q

Causes of rickets

A 
Vit D (rarely hereditary) or P deficiency
Ca deficiency or excess (uncommon)
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31
Q

2 types of hereditary vit D deficiency

A

type I - enz deficiency (makes active form of vit D)

type II - vit D receptor defect

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32
Q

thick, wide irregular physes, metaphyseal flare, enlarged joints, valgus/varus deformities, rachitic rosary

A

rickets

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33
Q

Fibrous osteodystrophy

A

juveniles, rarely adults

High PTH –> excess Ca release from bone –> replacement fibrosis - soft spongy bones

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34
Q

Causes of fibrous osteodystrophy

A 
Primary hyperparathyroidism (rare)
Secondary " " (renal dz or nutritional issue)
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35
Q

How does renal dz cause secondary hyperparathyroidism (thus, fibrous osteodystrophy)

A

Decreased excretion of P = high P, low Ca = increased PTH secretion = more Ca mobilized from bone

36
Q

How does nutrition cause secondary hyperparathyroidism (thus, fibrous osteodystrophy)

A

high P, low Ca, low Vit D = increased PTH secretion = more Ca mobilized from bone
e.g. carn on meat diet, Pig/EQ on grain/bran diets, lack of UVB in reptiles

37
Q

lameness, pathological fracture
“rubber jaw” or twisted maxilla
swollen metaphyses (but physis normal) valgus/varus deformities

A

fibrous osteodystrophy

38
Q

Osteochondrodysplasia

A

abnormal endochondrial ossification –> defective cartilage development –> (disproportionate) dwarf stature or uncontrolled growth

39
Q

What causes osteochondrodysplasia

A

spontaneous or heritable of mutation FGFR3

40
Q

Osteopetrosis/Stone bone

A

osteoclast deficiency/dysfunc –> excess trabecular bone, failed osteoclastic remodeling –> cavity filled w/ cancellous bone, not spongy bone & marrow

41
Q

Causes of osteopetrosis

A

spontaneous congenital defect
hereditary - angus, paso fino
infectious: BVDV, FeLV, CDV

42
Q

lameness, neuro disease d/t flattened calvarium, tongue hangs out, pathological fracture & deformities, pancytopenia

A

osteopetrosis

43
Q

Osteogenesis imperfecta/Brittle bone dz

A

multiple genetic disorders –> failure to produce & cross link type I collagen, decreased osteonectin –> bone deformities
Calves, lambs, puppies

44
Q

bone fractures/deformities, tendon & ligament ruptures, weak enamel & sclera

A

osteogenesis imperfecta

45
Q

Hypertrophic osteopathy pathogenesis

A

Suspect vagal stimulation –> increased perfusion to periosteum –> blood pools –> peripheral hypoxia/reaction –> periosteal woven bone hypertrophy (just cortex)

46
Q

What is hypertrophic osteopathy comonly associated with?

A

Thoracic mass
Heartworm dz
Endocarditis
NEoplasia - urinary rhabdomyosarcoma, EQ ovarian tumors

47
Q

Swollen but firm (not edematous) limbs, lameness

A

Hypertrophic osteopathy

48
Q

Aseptic necrosis of the femoral head / Legg-Calve’-Perthes Dz pathogenesis

A

Loss of perfusion –> ischemic necrosis of femoral head –> subchondral bone collapse & fibrosis –> progressive hip joint pain

49
Q

Who gets Aseptic necrosis of the femoral head

A

young (4-12 mo) small terriers like yorkies, jack russels

50
Q

What is the most common primary bone tumor in domestics?

A

Osteosarcoma

51
Q

Osteosarcoma

A

malignant mesenchymal tumor of osteoblasts

produces osteoid

52
Q

Risk factors for osteosarcoma

A

Size – dogs >80 lb (St. Bernards, Danes, German shep)

Age – dogs > 7.5 yrs, cats >10/5 yrs

53
Q

Osteosarcoma locations

A

Dog - away from elbow, toward knee

Uncommonly cat anywhere, Rum/EQ flatbones of skull

54
Q

Osteosarcoma behavior

A

Osteolytic - destroys cortical bone, stimulates reactive woven bone & inflamm around site
Highly invasive but doesn’t cross joints/articular surfaces
often metastasizes to lungs early

55
Q

Chrondrosarcoma

A

malignant tumor of cartilage, usually affecting flat bones (nasal cavity), appendicular, joints, soft tissue

56
Q

Chrondrosarcoma behavior

A

osteolytic, invasive/space occupying

develops slower, metastasizes later (better for treatment)

57
Q

Fibrosarcoma

A

primary malignant tumor of fibroblasts
Often in periosteum/medulla of any flat/long bone
space occupying, lytic, destructive

58
Q

Osteoma

A

benign tumor of osteoblasts/cytes
Affects cortex, usually on flat bones, distal limbs
Rostral mandible in juv rum/EQ - eating issue

59
Q

Multilobular osteochondrosarcoma (MLO)

A

benign or malignant tumor of organized cartilage, bone and fibrocytes
space occupying - often calvarium/flat bones
see neuro dz or difficulty eating

60
Q

What is hyaline/articular cartilage composed of?

A

type II collagen
chrondrocytes
proteoglycans
water

61
Q

How does hyaline cartilage get it’s nutrition & oxygen supply?

A

subchondral bone

synovial fluid

62
Q

How does articular cartilage respond to injury?

A

poor healing capacity
superficial lesion = no healing, no progression
deep lesions = granulation, fibrocartilage
Fibrillation, eburnation

63
Q

Fibrillation

A

cartilage condenses/clumps, starts to fray

64
Q

Eburnation

A

subchondral bone exposed through cartilage

65
Q

How does synovium respond to injury?

A

inflammation
villous hyperplasia of synoviocytes
Pannus (fibroplasia over areas of eburnation)

66
Q

How does synovial fluid respond to injury?

A 
fluid volume increases
Viscosity changes (increased = fibrin, Ig presence, decreased = hyaluronic acid & proteoglucan loss)
67
Q

Periarticular lesions you may see with joint injury

A

Osteophytes
Enthesophytes
Joint mice

68
Q

What causes degenerative joint disease (thus, osteoarthritis)

A

chronic instability
abnormal/altered cartilage
abnormal/altered subchondral bone

69
Q

Mechanisms that cause infectious OA

A
  • direct inoculation of joint

- hematogenous/septic spread

70
Q

Causes of hematogenous spread –> OA

A

failure of passive transfer

Mycoplasma bovis or hyosynoviae, Strep, Staph, E.coli

71
Q

Immune-mediated polyarthritis (IMPA)

A

Type III hypersensitivity –> chronic joint inflamm, arthritis
Idiopathic, hereditary, secondary (SLE, rhematoid, neoplasia)

72
Q

Who is prone to IMPA

A

dogs - Akitas, beagles, boxers

73
Q

fever, lethargy, anorexia
joint swelling, shifting leg lameness, stilted painful gait
+/- back or neck pain

A

IMPA

74
Q

Osteochondrosis pathogenesis

A

Failed endochondrial ossification of the epiphysis –> unmineralized epiphyseal cartilage –> focal areas of abnormal thickening of cartilage

75
Q

What can osteochondrosis progress to?

A

Osteochondrosis dessicans
thick cartilage –> hypoxia –> necrosis & fragmentation of cartilage –> subchondral bone exposed, weakened –> subchondral cyst –> cavitating defect

76
Q

Risk factors for osteochondrosis

A

genetics - rapid growers
nutrition - high calories, Ca, protein, vitamins/minerals or low Cu
Management - mechanical stress, exercise etc.

77
Q

Who commonly gets osteochondrosis

A

pigs, chickens, large breed dogs, warmbloods, throughbreds

78
Q

Common sites of osteochondrosis

A

main appendicular joints: stifle, shoulder, fetlock, tarsus

79
Q

Lamenss, pain, decreased performance, decreased weight gain

A

osteochondrosis

80
Q

Who is especially prone to subchondral bone cysts & fractures

A

horses

81
Q

Synovial sarcoma

A

malignant neoplasm of synovial cells
large breed middle age dogs
often stifle or weight bearing appendicular joints
highly invasive into surrounding area (unlike osteosarcomas), many metastasize to lungs
amputate

82
Q

Periarticular histiocytic sarcoma

A

malignany neosplasm of synovial DC’s
large breed middle age dogs - bernese mountain dogs
invasive into soft tissue, osteolytic
majority matastasize & early

83
Q

Job of intervertebral disks

A

unite vertebrae
limit movement at intervertebral joint
distribute mechanical forces

84
Q

Job of nucleus pulposus

A

absorb shock, help w/ felxibility

85
Q

Job of annulus fibrosus

A

handles compression, equalizes load

86
Q

Job of intercaptial ligaments

A

stabilize ribs, vertebrae

Only exists between T2-T10, not cervical or lumbar regions (need more flexibility)

VM742 BOD 3 (3 decks)

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