Sharma DSA: Clinical MSK radiology Flashcards

1
Q

Osteoporosis

A

-decreased cortical thickening

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2
Q

Osteopetrosis

A

-diffuse, dense bone

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3
Q

Osteitis deformans (paget disease of bone)

A

-thickening of calvarium

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4
Q

Osteonecrosis (avascular necrosis)

A
  • X ray: irregular lucencies with adjacent sclerosis

- MRI: dark serpinginous necrotic bone

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5
Q

Ankylosing spondylititis spondylititis

A

-Bamboo spine

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6
Q

Giant cell tumor

A

-Soap bubble appearance

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7
Q

Osteochondroma

A

-exotosis of bone

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8
Q

Osteosarcoma

A
  • “sunburst pattern”

- Codman triangle around metaphysis of long bones

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9
Q

Ewing sarcoma

A

-Onion skin around diaphysis of long bone

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10
Q

Type 1 vs Type 2 osteoporosis

A
  • 1: post menopausal

- 2: >70 yrs old

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11
Q

What is the cell dysfunction in osteoporosis and osteopetrosis?

A
  • porosis: blasts are the problem

- Petrosis: clasts are the problem

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12
Q

What enzyme mutation impairs the ability of osteoclasts to generate acidic environment?

A

-Carbonic Anhydrase

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13
Q

What gets filled in osteopetrosis?

A
  • the bone marrow spaces

- this can lead to pancytopenia, extramedullary hematopoiesis

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14
Q

Pathology of Osteitis deformans (paget disease of bone)

A
  • increased bone resorption (osteoclasts), followed by exuberant new bone formation
  • the new bone is abnormal and woven with disorganized collagen
  • The increased bone formation results in bone enlargement and deformity because of poor
  • increased risk of developing osteogenic sarcoma
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15
Q

What is the marker for Paget disease of bone?

A
  • normal Ca2+ phosphorous levels
  • Serum alkaline phosphate elevated
  • Urine hydroxyproline increased
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16
Q

What does the skull look like in paget disease?

A
  • diploic thickening of inner and outer calvarium
  • cotton wool appearance: mixed lytic and sclerotic lesions
  • Frontal bone enlargement, with the appearance of the skull falling over the facial bones
17
Q

What kind of pattern will we see with paget disease?

A

-mosaic pattern

18
Q

Osteonecrosis (avascular necrosis)

A
  • infarction of bone
  • most common site is the femoral head (medial circumflex femoral artery)
  • painful
19
Q

Radiology for osteonecrosis

A
  • crescent sign
  • double line on T2W1
  • rim sign form osteochondral fragmentation
20
Q

Ankylosing spondylitis

A
  • Arthritis w/o rheumatoid factor
  • HLA-27
  • spine and SI joints
  • bamboo spine
  • atlantoaxial subluxation
21
Q

Giant Cell Tumor (osteoclastoma)

A
  • 20-40 y/o
  • locally aggressive benign tumor
  • at the knee
  • arise in epiphysis but may extend into metaphysis
22
Q

Radiology of giant cell tumor (osteoclastoma)

A
  • Soap bubble appearance
  • multinucleated giant cells
  • narrow zone of transition
  • overlying cortex: thinned, expanded or deficient
23
Q

Clinical course

A
  • typically treated with curretage
  • but 40% to 60% have local recurrence
  • adjuvant therapy with RANKL inhibitors like denosumab has been recently added to the regimen
24
Q

Osteochondroma

A
  • males <25
  • develop only in bones of endochonral origin and arise from the metaphysis near the growth plate of long tubular bones especially around the knee
  • occasionally, they develop around from bones of the pelvis, scapula, and ribs
  • slow growing, impinge on nerves
25
Q

radiology of osteochondroma

A

-cartilage capped tumor that is attached to the underlying skeleton by a bony stalke

26
Q

What is the best imaging modality to assess cartilage thickness and thus malignant transformation of osteochondroma?

A

-MRI

27
Q

Osteosarcoma

A
  • bimodal distribution
  • in kids: around the knee
  • in adults: they will have conditions that predispose to osteosarcoma… most commonly in the pelvic area
28
Q

Radiology for osteosarcoma

A
  • Codman triangle because cortex lifted by tumor

- sunburst appearance of bone (sharpey’s fibers

29
Q

What is the method of choice for tumor staging in osteosarcoma?

A

-MRI

30
Q

Where does osteosarcoma like to met to?

A

-the lungs!

31
Q

Ewing Sarcoma

A
  • malignant tumor characterized by primitive round cells without obvious differentiation
  • t(11,22) causing fusion of EWS-GLI 1
  • white boys <15
  • diaphysis of long bones
32
Q

How does Ewing sarcoma present?

A
  • painful enlarging masses, and the site of infection is warm, tender, and swollen
  • some affected individuals have systemic findings that mimic infection, including fever, elevated ESR, anemia, and leukocytosis
33
Q

Radiology of Ewing sarcoma

A
  • destructive lytic tumor… moth-eaten appearance

- periosteal rxn produces layers of reactive bone deposited in an onion-skin fashion

34
Q

Clinical course of ewing sarcoma

A
  • extremely aggressive with early mets, but responsive to chemo
  • amount of chemo-induced necrosis is an important prognostic finding