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Pathology > Bones / Joints > Flashcards

Bones / Joints Flashcards

1
Q

Developmental skeletal dysplasias

A

K9 chondrodysplastic dwarfism
Osteogenesis imperfecta
Osteochondrosis/osteochondritis dissecans

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2
Q

Types of Cartilage

A

Hyaline cartilage - shock absorber, template for endochondral ossification

Fibrocartilage - connections between connective tissue, tendon/ligament insertions

Elastic cartilage - flexible structures

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3
Q

Generalized chondrodysplasias

A

Congenital defects involving cartilage template and generalized (polyostotic) defect in ECO

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4
Q

Origin of chondrodyplasias

A

Defect in cartilage template required for EO

Spontaneous or heritable mutation

Defect in any part of skeleton from cartilage template

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5
Q

Disproportionate (chondrodysplastic) dwarfism

A

Breed standard in Bassett hound/corgis (autosomal dominant FGF4 mutation)

Lethal mutation in bulldog calves (Dexter, Holstein) (Col2A1 and aggrecan mutations) —> shortened malformed limbs

Secondary defects in cells or ECM (lysosomal storage) —> limb, spine, skull malformations (+other organs)

+/- early DJD (from malformation in shape of epiphysis —> joint instability / incongruency

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6
Q

K9 Chondrodysplasia

A

Chondrodysplastic phenotype (CDPA)

CFA18-FGF4 mutation (autosomal dominant)

Dysproportionate dwarfism - shortened, malformed limbs (standard in certain breeds)

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7
Q

K9 Chondrodystrophy

A

Chondrodystrophic phenotype (CDDY)

CFA12-FGF4 mutation (incomplete autosomal dominant)

Shortened, malformed limbs (additive effect), IVDD (premature degeneration —> IVD herniation —> neurologic signs)

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8
Q

Generalized osteodysplasias

A

Skeletal defects in which cartilage cells/matrix are ok
Bone cell/matrix affected (generalized deformities, monostotic or polyostotic malformations

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9
Q

Osteogenesis imperfecta

A

Osteopenic disease (puppies, calves, lambs, humans)
Decreased bone density, excessive bone fragility

Mutation in both Type I collagen synthesis (BOTH osteoblasts and odontoblasts affected = bone + teeth affected)

Thin, weak bone matrix —> increased fragility, thin dentin, joint laxity + “blue” sclera (thinning)

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10
Q

Focal chondrodysplasia

A

Developmental defects in ECO at focal, repeatable sites

Osteochondrosis + Osteochondritis dissecans

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11
Q

Osteochondrosis + osteochonritis dissecans

A

Heterogenous lesion(s) in GROWTH cartilage (dogs, horses, pigs, cattle, poultry); epiphyseal > metaphyseal

Focal defect in endochondral ossification

~50% of lesions bilaterally symmetrical

Secondary OA common

Common joints: stifle, shoulder, elbow (pig), hock

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12
Q

Etiopathogenesis of OC/OCD

A

Damage to vasculature within growth cartilage (cartilage canals)

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13
Q

Pathogenesis of OCD

A

Focal interruption of endochondral vascular invasion or ischemic necrosis —> ECO failure —> retained cartilage core —> pressure induced fissure —> OCD

Retention of growth cartilage at AEC or metaphyseal growth plate —> defect if large retainined and heals or fissure —> dissecting cartilage flap (OCD) —> secondary DJD

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14
Q

Factors affecting bone response to injury

A

Etiology/inciting cause
Point at which injury occurs (pre/post natal development, mature skeleton)

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15
Q

Osteodystrophy due to failure of normal growth/development

A

Nutritional, endocrine, metabolic imbalance
Both trabecular and compact bone

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16
Q

Osteodystrophy due to abnormality during remodeling of mature bone or in repair

A

Nutritional, endocrine, metabolic imbalance

trabecular&raquo_space; compact bone

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17
Q

Causes of osteodystrophy

A

Temporal imbalances:
Nutritional (protein, vitamins, minerals)
Endocrine/hormonal
Toxic origins (drugs)

GI/renal/hepatobiliary dysfunction
Affect all bone!

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18
Q

Important factors / hormones in bone control

A

Endocrine: PTH (parathyroid), Calcitonin (thyroid)

Kidneys: Ca/phosphate

Kidney/liver/skin/intestine: Vitamin D3

Local factors: RANKL

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19
Q

Bone modeling

A

Primary trabeculae removed/replaced with STRONGER/FEWER trabeculae WITHOUT cartilage template core —> less radioopaque

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20
Q

Function of bone remodeling

A

Maintain bone mass

Replace old bone / repair microfracture

Respond to metabolic/nutritional changes

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21
Q

Regulators of OCLs

A

RANKL (from osteoblasts —> OCL activation / diff)
PTH (indirect inc in OCL activation)
Calcitonin (dec bone resorption systemic)

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22
Q

Common metabolic osteodystrophies

A

Osteoporosis
Rickets/Osteomalacia
Fibrous osteodystrophies (Renal failure —> secondary hyperparathyroidism)

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23
Q

Osteopenia

A

Decreased bone density / mass

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24
Q

Osteoporosis

A

Clinical syndrome
Bone pain / pathologic fractures (due to osteopenia)

Bone shape is normal, but reduced trabecular&raquo_space; cortical bone (i.e. QUALITY is reduced)

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25
Q

Causes of osteoporosis

A

Protein calorie malnutrition
Calcium deficiency
Copper deficiency
Severe GI parasitism or IBD

Physical inactivity (disuse/immobilization)

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26
Q

Lesions of osteoporosis

A

Dec osteoblast activity

Dec trabecular bone —> dec compact bone —> dec bone density + inc porosity

Pathologic fractures and infractions (micro fractures) —> reduced bone length

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27
Q

Rickets and osteomalacia

A

Defective mineralization —> affect bone and growth cartilage

—> bone deformities (angular limb deformities, scoliosis, flared physes)
—> pathological fractures + subchondral collapse
—> bone pain

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28
Q

Rickets

A

soft/weak bones + growth plate cartilage

(Young, growing animals)

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29
Q

Osteomalacia

A

Softening of bones
In ADULT animals, cartilage not affected

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30
Q

Causes of rickets/osteomalacia

A

Nutritional deficiencies:
Vitamin D deficiency (typically with unconventional diet)
Phosphorous deficiency (herbivores with P deficiency diet)

Calcium deficiency NOT a cause (except in birds)

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31
Q

Phases of bone formation

A
  1. Osteoid formation
  2. Mineral deposition (lacking in rickets/osteomalacia)
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32
Q

Rickets / osteomalacia pathogenesis

A

Reduced mineralization in bone (or bone + growth plate - young) —> deposition of large soma of osteoid along endosteal bone surfaces + osteomalacia canals —> dec OCL resorption —> inability to bind / resort old bone; growth plate deformities (in young) (unmineralized growth cartilage —> dec primary trabeculae)

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33
Q

Lesions of rickets

A

Flared metaphyses and retained cartilage core at growth plate

Compact bone: bowed legs, catastrophic fractures
Trabecular bone: infractions

Bone surfaces lined by large seams of unmineralized osteoid (any site of remodeling, trabecular&raquo_space; cortical bone)

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34
Q

Lesions of osteomalacia

A

Bone surfaces lined by large seams of unmineralized osteoid (any site of remodeling, trabecular&raquo_space; cortical bone)

Weaked trabeculae: microfractures
Weakened compact bone: catastrophic fracture

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35
Q

Fibrous ostrodystrophy pathogenesis

A

Persistent + extreme inc PTH

Primary hyperparathyroidism —> inc OCL activity/bone resorption —> dec OB diff —> dec bone formation —> inc fibroblast diff —> fibrosis

Renal insufficiency or High P diet —> inc phosphate —> inc Ca precipitation —> secondary hyperparathyroidism —> inc PTH —> inc OCL —> bone resorption / replace with fibrous

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36
Q

Clinical fibrous osteodystrophy

A

K9: Rubber jaw
EQ: big head syndrome

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37
Q

Renal osteodystrophy can cause components of rickets/osteomalacia AND FOD due to …

A

Decreased Vitamin D3

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38
Q

Dynamic response of bone

A

Respond to:
Physiologic homeostatic process
Mechanical stress
Metabolic stress
Inflammatory stress

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39
Q

Osteoblasts

A

immature cells that “build bone”

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40
Q

Osteocytes

A

Mature cells that maintain bone

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41
Q

Osteoclasts

A

Macrophage like cells that resorb bone

42
Q

Woven bone

A

Immature bone

Temporary, high cellularity, poorly organized, rapid formation, poorly mineralized

Acts as a bandaid (weak)

43
Q

Lamellar bone

A

Mature bone

Low cellularity, organized, slow formation, STRONG, well-mineralized

44
Q

Sites of bone repair

A

Periosteum - outer surface of bones
Endosteum - lines inner surface of bone (interface between hematopoietic marrow and bone)

45
Q

Mechanisms of bone formation

A

Cutting cones - compact bone, “miners in tunnels”; slow and limited

Intramembranous ossification - FAST

Endochondral ossification - slow conversion

46
Q

Intramembranous ossification

A

Bone formed directly from mesenchyme WITHOUT cartilage template (fast)

Condensation of mesenchyme —> OB differentiation —> osteoid + HA —> ossification centers —> woven bone island —> remodeled to lamellar bone

47
Q

Reaction of joint to injury

A

Joint cartilage + soft tissue supports (tendon, ligament, menisci) have POOR REGENERATIVE RESPONSE + limited healing capacity

Final common pathway = degeneration

48
Q

Common etiologies of joint injury

A

Congenital instability/incongruence
Traumatic instability
Repetitive stress injury
Infection / inflammation

Common end-stage pathway = DJF

49
Q

Degenerative joint disease

A

Incorporates all anatomic components
Articular cartilage; subchondral bone; synovium; soft tissue structures (joint capsule, ligaments, menisci)

50
Q

End-points of DJD

A

Ankylosis (self fusion)
Arthrodesis (surgical fusion)
Arthroplasty (surgical reconstruction / replacement)

51
Q

Features of early cartilage degeneration

A

Gross: surface dullness/roughness, thinning (focal, regional, or diffuse)

Histo: PG loss with matrix contraction + clefts (less pink on histo); chondrocyte necrosis + loss

52
Q

Progressive cartilage degeneration

A

Gross: severe thinning + score lines, yellow discoloration

Histo: chondrocyte loss/dropout, chondrocyte clones

53
Q

Advanced cartilage degeneration

A

Gross: erosions—> full thickness ulcers —> subchondral bone hemorrhage —> hemarthrosis —> subchondral bone lysis —> collapse divots

Histo: matrix fraying/vertical fissures, erosions/ulcers, +/- fibrocartilage repair

54
Q

End-stage cartilage degeneration

A

Gross: full-thickness cartilage ulcers, subchonral bone hemorrhage

Histo: full thickness cartilage ulcer with horizotonal fissure; deep excavation/collapse of subchondral bone with subchondral hemorrhage

55
Q

Progressive lesions of DJD

A

“Adaptive” remodeling —> pathologic inc bone density from decrease in cartilage shock absorption —> excessive compressive forces —> sclerosis —> dec vascular access —> dec OCL remodeling —> bone failure —> catastrophic fractures

56
Q

Subchondral bone failure

A

Repetitive stress injury (overuse / obesity) —> subchondral failure + collapse —> catastrophic fractures

57
Q

Sequeale of subchondral bone failure

A

DJD characterized by

Subchondral “bone cysts” from synovial herniation
Eburnation (polishing of bone cartilage ulcers —> bone on bone contact)

58
Q

Osteophytosis

A

Progressive articular bone proliferation of DJD
Growth of osteophytes on bone

59
Q

Progressive lesions to synovium and joint capsule in DJD

A

Synovitis: (histo) increased layers and large cells in intima; increased vascularity, fibrosis, inflammation in subintima

Gross: hypertrophied (thickened), hyperemia (red) synovial membrane, effusions from intimal/subintimal changes

60
Q

Severe chronic lesions of synovium/joint capsule in DJD

A

Thickened synovium with subintimal neovascularization / fibrosis; superficial erosion; Proteinaceous exudate

Gross: super-thick synovial hypertrophy + hemosiderin from chronic hemorrage —> yellow-brown discoloration

61
Q

Canine hip dysplasia

A

Congenital joint laxity; large/giant breed dogs predisposed
Factors: genetics, obesity, excessive exercise

62
Q

Pathogenesis of canine hip dysplasia

A

Excessive joint laxity with instability —> chronic subluxation of coxofemoral joint —> secondary DJD with modeling of femoral head/acetabular cup + arthritis

63
Q

Fracture classifications

A

Traumatic vs pathologic

64
Q

Traumatic fracture

A

Normal bone broken by excessive force

65
Q

Pathologic fracture

A

Abnormal bone broken by Minaj trauma or during normal weight bearing forces

(Repetitive stress injury, congenital/metabolic bone disease), osteomyelitis, primary/metastatic neoplasia

66
Q

Fracture configurations

A

Closed vs open
Simple vs comminuted
Transverse vs Sagittal/parasagital
Avulsion
Articular

67
Q

Salter-Harris fractures

A

Involve growth plates (occur in young)
Type I, II, III, IV, V

68
Q

Type II Salter-Harris Fracture

A

Fracture extends across physis —> breaks out metaphysis

69
Q

Consequences if in growth plate fracture bone heals, but growth plate cartilage does not

A

Limb shortening or angular limb deformity

70
Q

Types of fracture healing

A

Direct (primary) healing —> rigid fracture stabilization
Indirect (secondary) healing —> biomechanical environment dictates how healing occurs, limited intervention (?)

71
Q

Stages of indirect bone healing

A

1 - Inflammation 0-7 d
2 - Repair
A - Soft callus 1-3 w. (Early callus - granulation tissue + woven bone + cartilage islands)
B - Bony callus 3-6 w
3 - Remodel > 8 w to yrs

72
Q

Response to a fracture

A

1 - tearing of periosteum + displacement of fracture ends —> trauma to adjacent soft tissue
2 - hemorrhage with hematoma + clot formation by fibrin polymerization
3 - Imparied blood flow —> necrosis of fracture ends + bone fragments
4 - release of cytokines + growth factors by platelets, macrophages in clot
5 - influx / proliferation of MSCs and granulation tissue formation
6 - OB differentiation, woven bone
7 - bridging callus —> soft callus —> hard callus

73
Q

Soft callus

A

Woven bone +/- cartilage with periosteal vessels forming within 1-3 w of fracture healing

Low O2 tension —> hyaline cartilage formation (radiolucent!) —> EO —> eventually radioopaque (hard callus)

74
Q

Primary fracture callus

A

Provides some stability to allow some degree of limb function until healing complete

75
Q

Complications of fracture healing

A

Mal-union / fibrous non-union
Inadequate blood supply
Infection (osteomyelitis, septic arthritis)

76
Q

Mal-union / fibrous non-union

A

Caused by poor or delayed healing
Permanent + painful

If articular —> early degenerative OA

77
Q

Impact of inadequate blood supply on fracture healing

A

Necrotic bone (sequestrum)
Poor healing / necrotic tissue —> substrate for infection

78
Q

Osteomyelitis / septic arthritis

A

Occurs at time of injury or delayed
Bacterial “squatters” in sequestrum / bone biofilms
Inhibits neovascularization / callus formation (delayed healing —> mal-union / fibrous non-union)

79
Q

Synovitis

A

Inflammation of synovial membrane and synovial fluid compartment

80
Q

Arthritis

A

Inflammation/degeneration of all components of joint (synovial membrane + joint capsule, cartilage, subchondral bone)

81
Q

Osteomyelitis

A

Inflammation of bone, including endosteum + medullary spaces

82
Q

Osteitis

A

Inflammation of cortex only

83
Q

Acute arthritis

A

Inflammatory cells + pro-inflammatory cytokines
- synovial hyperemia + edema
- reduced PG of synovial fluid + cartilage
- reduced synovial viscosity
- chondrocyte necrosis + loss of ECM

Orange, red, brown synovial fluid (if hemorrhage)
Increased turbidity (fibrin, neutrophils - if septic)

84
Q

Chronic arthritis

A

Cartilage lesions progressive thinning/erosions/ulcers
Stiffening of joint
Subchondral bone involvement
Reduced joint function + DJD

85
Q

Routes of joint infection

A

Septicemia (neonates > adults) : umbilicus, respiratory tract, GI

Direct penetration (more common in adults) - trauma, injection, surgery

Extension from local wound/septic epiphysitis

86
Q

Acute changes in synovium

A

Decreased viscosity (digestion of GAG + dilution by edema)
Turbid (fibrin / neutrophil)
Red/orange/brown discoloration
Hyperemic joint

87
Q

Chronic changes to synovium / joint

A

Suppurative —> lymphoplasmacytic inflammation
Synovial villus hypertrophy
Joint capsule fibrosis + Osteophytosis

88
Q

Acute changes to articular cartilage / subchondral bone

A

Yellowing + thinning cartilage surface
Fissures / collapse from ECM degeneration + chondrocyte necrosis

89
Q

Chronic changes to articular cartilage + subchondral bone

A

Focal or diffuse thinning, erosions, ulcers
Pannus formation “red velvet” surface
Subchondral bone sclerosis / disuse osteopenia

90
Q

Bacterial causes of infectious arthritis / osteomyelitis

A

G -: coliforms, Salmonella

G+: Strep, Staph, Actinomyces bovis, T pyogenes

Mycoplasma

91
Q

Fungal causes of infectious arthritis / osteomyelitis

A

Opportunistic fungi (Aspergillus, Candida)
Coccidiomycoides, Blastomyces

92
Q

Septic physitis/epiphysitis

A

In young growing animals - bacteria within vessels in ossification front of growth plates

Thrombosis / infarcts of intramedullary fat, marrow, bone —> sequestrum —> septic arthritis

93
Q

Sequestrum / sequestration

A

Necrotic bone islands —> will hypermineralize —> radioopaque; also resorption of surrounding bone (radiolucent rim)

94
Q

Occurrence of primary bone tumors in animals

A

Dogs > cats&raquo_space;> farm animals

95
Q

Most common primary bone tumors in SA

A

Osteosarcoma (appendicular > axial)
Chondrosarcoma (cartilage; flat bone predilection)

96
Q

Behavior of bone tumors

A

In dogs - most malignant
In cats - benign ~ malignant
In horses/cattle/other domestic - benign&raquo_space; malignant

97
Q

Osteosarcoma

A

80% of primary bone tumors in dogs
Large, giant breed dogs
75% appendicular skeleton; 2/3 in forelimbs, 1/3 hind

98
Q

K9 osteosarcoma

A

Malignant neoplasm of osteoblasts
Aggressive, invasive neoplasm
Frequent + RAPID metastasis (LN, lungs, bones)

Poor prognosis

Site of origin: central (most common), parosteal, periosteal, extraskeletal

Radiographic appearance: lyric to sclerotic, proliferative
Doesn’t directly cross joints! Pathologic fractures

99
Q

Diagnostic features of osteosarcoma

A

1 - osteolysis (destruction of bone architecture)
2 - osteoproliferation
3 - histology - neoplastic osteoblasts producing tumor osteoid (biopsy)

100
Q

Feline osteosarcoma

A

Malignant + locally in vases / aggressive
Slower metastasis + longer survival than in dogs

101
Q

Histiocytic sarcoma

A

Round cell neoplasm (interstitial dendritic cell or macrophage)
Locally invasive (joints) - often CROSSES joint!
Rottweiler (and black + tan) dogs
Stifle + elbow (elbow uncommon for OSA)

Hemophagocytic subtype —> anemia

Poor prognosis ~5.3 mo survival
Metastasis to liver, lung, lymph nodes

Pathology (21 decks)

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