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Tri 6 - Tumors > 11. Osteonecrosis > Flashcards

11. Osteonecrosis Flashcards

1
Q

Death of osseous cellular components and marrow

A

Osteonecrosis

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2
Q

mc location for trauma induced osteonecrosis?

A

intracapsular epiphyses

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3
Q

Osteonecrosis from Alcoholism mc affects the

A

femoral head

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4
Q

Osteonecrosis from Alcoholism possibly due to

A

fatty liver releasing fat

emboli, and increased marrow fat

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5
Q

most common theory for Osteonecrosis from Corticosteroids

A

fatty liver emboli

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6
Q

rapid removal from high pressure environment (diving) which forms nitrogen bubbles in blood vessels causing bone infarction

A

Caisson’s Disease

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7
Q

extensive epiphyseal and metaphyseal necrosis may occur bilaterally

A

Caisson’s Disease

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8
Q

mechanical infringement of marrow sinusoids by

lipid-laden histiocytes causing femoral head necrosis

A

Gaucher’s Disease

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9
Q

RA and SLE due to vasculitis of peripheral blood vessels

causes

A

vascular thromboses and tissue infarction

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10
Q

Corticosteroids increase incidence of

A

Osteonecrosis

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11
Q

sludging, thrombosis, and eventual infarction especially in epiphyses and metadiaphyseal regions

A

Sickle Cell Anemia:

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12
Q

how manuy rads are needed to produce osteonecrosis?

A

3000

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13
Q

how many rads in children are needed to affect epiphyseal

bone growth

A

300 - 400

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14
Q

very rarely causes bone infarcts due to fatty emboli

A

Pancreatitis

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15
Q

medullary and epiphyseal infarcts may occur in 30%

of pts with

A

gout

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16
Q

anatomically predisposed to osteonecrosis

A

Intraartcicular epiphyses

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17
Q

AVN usually takes how long to run its course?

A

2-8 yrs

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18
Q

obliteration of epiphyseal blood supply leading to
death of marrow cells and osteocytes, bone growth stops but the Adjacent articular cartilage continues to
grow

A

AVN: Avascular Phase

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19
Q

new vessels into necrotic bone causes deposition of new

bone onto necrotic bone, and resorption of dead bone, trabeculae thicken and bone density increases

A

AVN: Revascularization Phase

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20
Q

Avascular necrosis of the shoulder showing subchondral radiolucent line, aka

A

crescent sign

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21
Q

deformity occurs due to stress and forces applied during

A

revascularization and remodeling

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22
Q

“Mushroom” deformity

A

AVN femoral head

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23
Q

Infarcts heal with calcification

A

serpiginous configuration of healed infarcts

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24
Q

occurs at area of greatest mechanical stress of cortex indicating localized impaction fracture of weakened necrotic bone (step defect)

A

Collapse of Articular Cortex from Epiphyseal Infarction

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25
Q

thickened, irregular trabecular pattern causes increased bone density revascularization and repair phases

A

Mottled Trabecular Pattern:

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26
Q

very common in femoral capital epiphysis and subcortical in areas of greatest articular stress

A

Subchondral Cyst Formation

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27
Q

due to weakening of subchondral bone

A

Subchondral Fracture

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28
Q

separates articular cortex from underlying cancellous

bone (rim sign, crescent sign)

A

Subchondral Fracture

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29
Q

central high signal intensity surrounded by a serpentine, thin low signal margin

A

MRI of Metaphyseal - Diaphyseal Infarction

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30
Q

Bone scan of AVN: Initially a focal area of decreased activity appears, corresponding to the ________
Later increased activity corresponding to the phase of _________

A

local ischemia, hyperemia and osteoblastic repair

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31
Q

on MRI for AVN in 80% of patients

A

Double Line Sign

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32
Q

outer line of double line sign is the

A

low signal from sclerotic periphery

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33
Q

inner line of double line sign is the

A

high signal from edema (granulation tissue)

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34
Q

cortical infarction causes widening of small tubular bones of hands and feet

A

Sickle Cell Anemia

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35
Q

bilateral asymmetrical involvement (50% of cases) buttock, groin, thigh, knee pain gradual increase in pain and decreased ROM

A

Femoral head AVN

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36
Q

An orthopedic surgeon should perform what before Crescent sign appears

A

Core Decompression

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37
Q

Drill hole in bone a thin layer is removed which reduces pressure while increasing blood flow

A

Core Decompression:

38
Q

After a core decompression healthy bone is transplanted from one part of the body to the diseased area

A

Bone Grafting

39
Q

most sensitive and will demonstrate changes of AVN within 1 week after infarction

A

MRI

40
Q

at interface of viable and necrotic bone

A

Double Line Sign (MRI)

41
Q

arc like curvilinear radiolucency in subchondral aspect

of weight bearing cortex of femoral head that represents a pathologic subchondral fracture

A

Crescent (Rim Sign)

42
Q

Crescent (Rim Sign) is best seen on

A

Frog – Lateral view of hip

43
Q

can you determine source of AVN by radiograph?

A

NO

44
Q

Fractures that occur in the subchondral bone may be recognized by a

A

crescent lucent zone

45
Q

NEW NAME for Spontaneous Osteonecrosis of the Knee (SONK)

A

Subchondral Insufficiency Fracture

46
Q

Subchondral Insufficiency Fracture mc affects

A

medial femoral condyle of 60+ adults

47
Q

Subchondral Insufficiency Fracture usually progresses to collapse, fragmentation and loss of joint space suggesting

A

Charcot’s joint

48
Q

5 Stages Subchondral Insufficiency Fracture

A

Stage 1: Normal plain films, abnormal bone scan or MRI
Stage 2: Subtle flattening of femoral condyle
Stage 3: Area of radiolucency surrounding sclerotic area in subchondral bone
Stage 4: Radiolucency surrounded by a sclerotic halo
Stage 5: Secondary changes of DJD

49
Q

decreased medial tibiofemoral joint space subchondral cysts, sclerosis, osteophytes, chondrocalcinosis, and
varus deformity

A

Progressive DJD from Subchondral Insufficiency Fracture

50
Q

will permanently arrest growth at physis

A

1800-2600 Gy

51
Q

radiation changes in Adult Bone

A

3000 Gy = threshold for bone cell death

5000 Gy = definite bone cell death

52
Q

AVN of femoral capital epiphyses prior to

closure of growth plate (peaks 5-7 yo)

A

Legg-Calve-Perthes Disease

53
Q

Legg-Calve-Perthes Disease on Bone scan shows _______ uptake in femoral head

A

decreased

54
Q

increased medial joint space of hip

A

“Waldenstrom” Sign

55
Q

sclerosis indicates revascularization (cap entirely sclerotic)
widening and shortening of femoral neck

A

Snow Cap Appearance

56
Q

lucent defect at lateral epiphysis and adjacent metaphysis that indicates poorer prognosis

A

Gage’s Sign

57
Q

Snow Cap Appearance and Gage’s Sign

A

Legg-Calve-Perthes Disease

58
Q

overall enlargement of femoral head

A

Coxa Magna

59
Q

flattening of femoral head

A

Coxa Plana

60
Q

flattening of femoral head and increased transverse

dimension

A

Mushroom Deformity

61
Q

flattening of femoral head and increased transverse

dimension

A

Mushroom Deformity

62
Q

AVN of a metatarsal head (mc 2nd), females (13-18yo) with tenderness and pain over MT head

A

Freiberg’s Disease

63
Q

AVN of carpal lunate with radiating wrist pain, swelling, entrapment neuropathy and DJD

A

Kienbock’s Disease aka Lunate Malacia

64
Q

may cause mechanical stresses between lunate and

radius disabling vascular supply in up to 75% of cases

A

Negative ulnar variance

65
Q

advanced scapholunate collapse & chronic instability of wrist (Lunatotriquetral ligament may also be damaged)

A

SLAC lesion

66
Q

Sclerosis, irregularity and collapse of the lunate

A

Kienbock’s Disease

67
Q

common, painful, self limiting disorder involving patellar

tendon-tibial tubercle complex in adolescents

A

Osgood - Schlatter Disease aka Traction Apophysitis

68
Q

Do not confuse avulsed fragment with

A

multiple ossification centers of tibial tuberc

69
Q
  • overlying edema displaces soft tissue anteriorly
  • thickening of patellar ligament
  • poorly defined margins of patellar ligament due to edema
  • blurring of infrapatellar fat pad
  • distended infrapatellar bursa (MRI)
  • increased signal at site of insertion of patellar tendon
A

Soft Tissue Changes in Osgood - Schlatter

70
Q

traumatic growth arrest and growth plate fractures

(Schmorl’s nodes) during adolescent growth period that mc affects mid and lower TS

A

Scheuermann’s Disease

71
Q

adolescent disorder that may cause spinal pain, cosmetic deformity, and predispose pt to thoracic disc
herniation and premature DJD

A

Scheuermann’s Disease

72
Q

pain, fatigue, defective posture increased TS kyphosis

A

Scheuermann’s Disease (not AVN)

73
Q 
- irregular endplates
disc space narrowing and fibrosis
- increased TS kyphosis 
- multiple Schmorl’s nodes
- anterior vertebral body wedging (5 degrees
or more per vertebral body)
- Limbus bones
superimposed DJD
scoliosis
A

Scheuermann’s Disease

74
Q

Scheuermann’s Disease is thought to be due to a

A

growth abnormality of the vertebral body (anterior growth plage stops)

75
Q

small necrotic segment of subchondral bone (Joint Mouse) mc in knee with clicking, locking, pain, joint effusion

A

Osteochondritis Dissecans

76
Q

The Osteochondritis Dissecans Defect may contain

A

fibrous and fibrocartilaginous tissue

77
Q

Osteochondritis Dissecans is mc in lateral aspect of

A

medial femoral condyle

78
Q

MRI is helpful to assess Osteochondritis Dissecans lesion for

A

stability, detachment,

AVN, and loosening of fragment

79
Q

Affects medial (MC) and lateral aspects of dome of talus active pts 20-40 yo

A

Osteochondral Lesions of Talus

80
Q

fragment from medial posterior aspect of talus

due to

A

shearing force of distal tibia

81
Q

forceful inversion that compresses the lateral talar border against the adjacent fibula and creates a small, thin, wafer shaped fragment is difficult to
identify

A

Lateral Talar Osteochondritis Dissecans

82
Q

may involve any joint that is traumatized with a shearing-compressive force

A

Osteochondritis Dissecans

83
Q

disease involving capitellum of distal humerus that produced changes similar to those observed in Legg Calve Perthes disease.

A

Panner’s Disease / Osteochondrosis

84
Q

Panner’s should be distinguished from

A

osteochondritis

dissecans (which occurs in 13 + years)

85
Q

Panner’s is caused by an interference

A

in blood supply to growing epiphysis

86
Q

in patients under 20 years of age, capitellum is only supplied by

A

end arteries entering posteriorly

87
Q

AVN of navicular

A

Kohler’s disease

88
Q

Kohler’s Disease Treatment

A

soft longitundinal arch supporters, medial heel wedge, and limitation of strenuous activity

89
Q

delayed (usually two weeks) vertebral body collapse due to ischemia and non-union of the anterior vertebral body wedge fractures after major trauma

A

Kummel disease

90
Q

calcaneal Apophysitis from mechanical irritation

A

Sever’s Disease

91
Q

Painful inflammation of the calcaneal apophysis

A

Sever’s Disease

Tri 6 - Tumors (12 decks)

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