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Respiratory/Musculoskeletal > P- Skeletal System > Flashcards

P- Skeletal System Flashcards

1
Q

What are the three bone groups of the skeleton?

A
  1. Axial- vertebrae, ribs, sternum
  2. Appendicular- limbs, scapula, pelvis
  3. Acral - hands and feet
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2
Q

What are the 4 regions of the bone?

A
  1. Diaphysis- midsection/shaft
  2. Metaphysis- area just under the physis
  3. Physis- growth plate
  4. Epiphysis - on the physis
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3
Q

What are the 2 different consistencies of bone? What is the majority of the body?

A

80% is compact (cortical, concentric, laminar pattern)

20% is trabecular (medullary, cancellous, spongy)

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4
Q

What are the cellular elements of bone?

What are the inorganic elements of bone?

A

Inorganic:

  1. type I collagen
  2. osteocaclin, osteonectin, proteoglycan
  3. hydroxyapatite- crystal lattice of calcium and phosphorus that solidifies the bony matrix

Cellular:

  1. Osteoblasts- synthesize type one cartilage and non-collagenous proteins of the bone matrix AND make an alkaline environment to lay down mineral
  2. Osteocytes- osteoblasts entombed in matrix that control Ca and Ph homeostasis
  3. Osteoclasts - bone resorption
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5
Q

What cell lineage do osteoblasts arise from?

What are their two major functions?

A

They arise from mesechymal stromal cells in the bone lining the medullary cavity.

  1. synthesis of type I collagen and non-collagenous protein of bone
  2. make the local environment alkaline so it is favorable to mineral deposition
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6
Q

What is the matrix secreted by osteoblasts called before it is mineralized? How long does it take to mineralize?
What happens if the mineralization is delayed?

A

Osteoid - takes 12 to 15 days for it to be mineralized by the deposition of hydroxyapatite.

If mineralization is delayed, a wide zone of osteoid is seen at sites of active bone formation (osteoid seam)

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7
Q

What ligands to osteoblasts change in response to?

A
  1. parathyroid hormones
  2. estrogen
  3. vitamin D
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8
Q

What is the morphology of osteocytes?

What are their 2 functions?

A

They are osteoblasts trapped in matrix. They have stellate shape and pseudopodia to communicate to each other and osteoblasts that line the bone surface.

  1. They control Ca and phosphorus homeostasis
  2. they respond to mechanical forces and microfractures to signal the osteoblasts to make more bone (remodeling/repair)
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9
Q

What cell lineage do osteoclasts arise from? What is their job?
What 4 signals differentiate them from precursors to active form?

A 
They arise from macrophage/monocyte lineage and are responsible for bone resorption.
They differentiate in response to:
1. RANKL (NfKb ligand) 
2. TNF 
3. IL-1
4. M-CSF
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10
Q

What is the 2 step process by which osteoclasts break down bone?
What is the excavation produced by osteoclasts called?

A
  1. dissolve the minerals by acidifying the extracellular space
  2. lysosomal proteases are released to digest the matrix proteins

The excavation is called “howship’s lacunae”

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11
Q

What is the difference between lamellar bone and woven bone?

A

Regular bone is lamellar- collagen is arranged in parallel and the small uniform osteocytes are scattered through the matrix.

Woven bone- forms rapidly in response to skeletal injury. It has osteocytes of various sizes and more numerous than lamellar bone. Collagen is in disarray

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12
Q

Where does woven bone exist in the adult skeleton?

A
  1. at sites of injury before it is replaced by lamellar bone

2. at tendonous insertions

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13
Q

What is the BMU?

A

Basic multicellular unit: osteoclasts break down old bone and osteoblasts replace it with new bone

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14
Q

What is the first step of remodeling? What is the currently accepted mechanism by which this occurs?
After this, how long does it take for osteoclasts to clear out a lacunae?
How long does it take for osteoblasts to replace it?

A

Activation- it is not well understood but current research suggest that osteocytes sense physical stress in the skeleton (mechanotransduction)

A new BMU starts every 10 seconds.
It takes 2-3 weeks for clasts to clear the old bone
It takes 3 months for blasts to build new bone

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15
Q

What is the major difference between remodeling and modelling of bone?

A

Remodeling- osteoblasts and osteoclasts communicate and are coupled to replace old bone with new (not adding or removing any total bone)

Modeling- leads to changes in the size and shape of bone (metaphysis must thin to width of diaphysis). Osteoblasts and clasts are still key, but they are UNCOUPLED.

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16
Q

Where are the 2 places where RANKL is?

What is the function of RANKL?

A
  1. on the surface of osteoblasts (upregulated by parathyroid, vitamin D and prostaglandin)
  2. produced by activated T cells involved with bone loss around joints affected by RA

RANKL binds to RANK receptor on osteoclast precursors causing them to mature

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17
Q

What is the secreted decoy receptor for RANKL ? What cell produces it?

A

Osteoprotegerin is secreted by osteoblasts and other cell types.
It competitively inhibits RANKr on osteoclasts from binding RANKL so the osteoclast precursor doesnt differentiate or mature.

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18
Q

What ratio controls the maturation and activity of osteoclasts?

A

RANK to osteoprotegerin

If there is decreased osteoprotegerin, more osteoclasts will activate and this can lead to dramatic loss of bone

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19
Q

Osteoblasts activate osteoclasts by upregulating RANKL.

How do osteoclasts activate osteoblasts?

A

They release anabolic cytokines like insulin-like growth factor (ILGF-1) and TGFb from digested bone

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20
Q

What are the 2 types of fracture? What is most common?

A
  1. trauma - most common

2. pathologic - fracture occuring in bone weakened by disease

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21
Q

A complete fracture disturbs what vessels?

What does this result in?

A

A complete fractures disturbs periosteal, cortical and medullary vessels resulting in local hemorrhage.
The hematoma is a source of kinin, PGs and inflammatory mediators (FGF, PDGF, and TGFb) which produce an inflammatory phase of bone repair.

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22
Q

How can you tell if a bone is necrotic?

A

Histiologically you will note an absence of osteocytes. This is a sign of necrotic bone.

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23
Q

What happens roughly one week after the fracture of bone?

A

Angioblasts and fibroblasts of the inflammatory response produce a procallus (soft, unstable)

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24
Q

What occurs in the reparative phase of the bone fracture?

A

Blood clot organizes and over several weeks:

  1. osteoclasts remove necrotic bone at the ischemic ends of the fracture
  2. chondroblasts and osteoblasts derived from progenitors in the periostium and medullary bone produce cartilage and woven bone to form a hard callus
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25
Q

What occurs during remodeling phase of fracture?

A

cartilage and woven bone are replaced by lamellar bone.

This takes months to years.

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26
Q

What are the 5 major causes of delayed bone healing after a fracture?

A
  1. poor nutrition
  2. infection
  3. instability at the fracture site
  4. poor bone quality (osteoporosis, osteogenesis imperfecta)
  5. remnants of necrotic bone aren’t cleared- osteoblasts cannot fill in the space because it is occupied
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27
Q

What is supperative (pyogenic) osteomyelitis? What are the 2 main ways this can occur?
What microorganism is associated with each pathway?

A

It is inflammation of the bone and bone marrow caused by infection.

  1. seeding of the microorganism after hematogenous spread– S. aureus
  2. infect as a direct extension - ex. diabetic ulcer, peridontal disease, fracture protrusion that allow infectious agents to enter the bone–polymicrobial
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28
Q

In hematogenous osteomyelitis, what determines where the bacteria will lodge in the bone?
Where does it typically go in neonates? Growing skeleton? Adult skeleton?

A

The vascular pattern at the physis.

  • Neonates- metaphyseal vessels extend to epiphysis so bacteria can lodge on either side
  • Growing skeleton the vessels cannot penetrate the growth plate so infection is in the metaphysis
  • Adults the vessels once again communicate with epiphysis so either side
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29
Q

How do patient with osteomyelitis present clinically? What do early radiographs show? Late radiographs?

A

They present with fever and pain at the site of infection. The overlying soft tissue is often erythematous and red.

Early radiographs:
mineralized bone has not been resorbed yet at the site of infection so there won’t be much to see.

Late radiographs (1 week later)
Lucency because RANKL > osteoprotegerin at the site of inflammation
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30
Q

What is necrotic bone from osteomyelitis called?

A

sequestrum

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31
Q

What happens when the exudate from osteomyelitis penetrates the cortex?

A

It elevates the periosteum, which activates periosteal osteoblasts to form a new sleeve of bone called the involucrum

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32
Q

What happens if the osteomyelitis lesion is neglected and it is able to break through the skin?

A

It will form a chronic draining tract (sinus) to the outside world.
Squamous cell carcinoma can develop in the tract.

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33
Q

Who is likely to develop granulamatous osteomyelitis? What bones are typically involved?
How does the infection get into the bone?

What is the disease called? What are the harmful sequelae?

A

1-3% of patients with TB get granulamatous osteomyelitis in the thoracolumbar/sacral vertebra.

The infection either enters the bone by hematogenous spread OR direct spread from the lungs/pulmonary lesions.

Pott’s disease.
Sequelae = compression of spinal nerves, scoliotic or kyphotic deformities

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34
Q

What is osteopetrosis?
What does it do to the density of the bone?
What are the extra-bone sequelae?

A

Osteoclast function is decreased and the people end up with too much bone–> sclerosis of the skeleton

Density of the bone is increased, but it will be brittle and easily fractured

  1. compression of cranial nerves
  2. extramedullary hematopoeisis/anemia
  3. hepatosplenomegaly
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35
Q

What are the 2 gene mutations associated with osteopetrosis?

Which can be cured with stem cell transplant?

A
  1. loss of carbonic anhydrase II - the osteoclast can’t locally acidify and thus are unable to break down the hydroxyapatite. CURE: stem cell transplant
  2. mutation in gene encoding RANKL- osteoclast poor osteopetrosis because the osteoclast precursors are unable to mature. Theorectic CURE: exogenous RANKL
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36
Q

A patient presents with blue sclera, poorly shaped teeth, hearing deficits and osteopenia. She has had multiple fractures and her bones are very brittle. What is the likely diagnosis? What is the genetic defect?

A

Osteogenesis Imperfecta- genetic disease where the synthesis of collagen type I is defective.
It can be in the a1 or a2 chain

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37
Q

If the multicellular unit is unbalanced __________ occurs. If the new bone formed by osteoblasts is not properly mineralized _________ occurs.

A
  1. osteoporosis

2. osteomalacia

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38
Q

What is osteomalacia?
What are people with this prone to?
What is seen histologically?

A

Softening of bone because of defective mineralization.
Bones are weak and prone to fracture with weight bearing.
Histologically you would see widened unmineralized osteoid seams lining the trabeculae.

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39
Q

What is osteomalacia called in children?

What are they prone to in addition to soft bones?

A

Rickets- they are prone to:

  1. conformation changes (bowing, bending)
  2. growth plates are overgrown and can fracture/bleed
  3. overgrowth of costrochondral junctions on the rib cage make “rachitic rosary”
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40
Q

Osteomalacia and rickets are most commonly secondary to a deficiency in what?

A

vitamin D

25hydroxyvitamin D is converted to 1,25 dihydroxyvitD in the kidney and is regulated by parathyroid hormone as well as serum Ca and phosphorus.

PTH stimulates vit D

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41
Q

Without vitamin D, what happens to dietary absorption of Ca and Phos? what does this lead to?

A

low vit. D leads to decreased absorption of ca and phos.

This means that they will not be able to mineralize the osteoid seam

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42
Q

When does the growing skeleton reach a peak bone mass? Which sex has higher bone mass? Which race has higher bone mass?

A

Peak in the 30s.
Men> women
Blacks> whites

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43
Q

What are the 2 main types of osteoporosis?

A

Type I - postmenopausal

Type II- senile

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44
Q

When does type I osteoporosis set in? What 2 things characterize it?
How much bone is lost/year?

A

It starts in the 5th decade of like with menopause and an abrupt loss of estrogen.

  1. increased osteoclast activity
  2. rapid bone loss

5-10% trabecular, 2% cortical

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45
Q

In type I osteoporosis, trabecular bone is lost more rapidly than cortical bone. What does this mean in terms of which bones get fractured?

A

People with type I are more likely to fracture vertebrae and proximal femur

46
Q

How does estrogen keep osteoclasts in check?

A
  1. upregulates FasL activating apoptosis of clasts

2. decreasing sensitivity of mature clasts to RANKL

47
Q

How does estrogen deficiency reduce the activity/life span of osteoblasts?

A

Estrogen withdraw increased production of IL7 and TNF which decreases activity of mature blasts

48
Q

When does senile osteoporosis begin in men and women? What is the characteristic of senile that differentiates it from post-menopausal?

A

It begins in the 30s and is characterized by decreased osteoblast activity. (postmenopausal is increased clast activity)

Lose 6-8% trabecula and 2-4% cortical A DECADE (so much slower decline than postmenopausal)

49
Q

What is secondary osteoporosis?

A

It is accelerated bone loss secondary to a pathology like:

  1. Cushing’s syndrome
  2. prolonged use of exogenous steroids
  3. immobilization
  4. periarticular osteoporosis (RA)- destruction of epiphyseal bone secondary to IL1 and TNFa released from the inflamed joint as well as from RANKL on the lymphocytes in the swollen synovium

by compromising blasts and decreasing ca absorption from the gut

50
Q

What is Paget Disease of bone?
What is the classic histological features?
How does the bone look grossly?

A

BMU is uncoupled resulting in regions where osteoclasts predominate and other areas where osteoblasts predominate.

Histologically it looks like a mosaic
Grossly it is sclerotic and deformed. There are no concentric lamella.

51
Q

What are the 5 major sequelae of Paget bone?

A
  1. pain caused by microfractures
  2. anterior bowing
  3. distortion of femoral heads –> secondary OA of the hips
  4. overgrowth of vertebrae compress spinal nerves
    5 osteosarcoma, chondrosarcoma
52
Q

What age and gender patient would you likely see degenerative joint disease?

A

OA is more common after age 50, and by age 70-80 roughly 85% of patients have it.
Women > men

53
Q

What joints are first affected by OA?

A
  1. DIPs- distorted by osteophytes (Heberden nodes)

2. knees, hips, vertebrae

54
Q

What is the etiological cause of OA?

A

Multifactorial:
-obesity increases stress on weight bearing joints causing bilateral degenerative joint disease of knees

  • previous injury to joints lead to distortion/poor distribution on weight bearing joints leading to degeneration
55
Q

What are the 2 main constituents of the extracellular cartilaginous matrix?
What maintains the integrity of the cartilaginous joint?

A
  1. type II collagen for tensile strength
  2. aggrecan - hydrated and resists compression

Integrity of the joint is maintained by remodeling

56
Q

What is thought to be the primary event leading to destruction of the cartilage in OA?

A

Degradation of aggrecan by ADAMTS 1, 4 and 5

57
Q

What sequence of events happens after the cartilaginous matrix of the joint breaks down in OA?

A
  1. FIBRILLATION– chondrocytes die and the articular surface becomes shaggy
  2. Cartilage thins and the underlying bone becomes sclerotic
  3. cracks form in the bone and synovial fluid leaks in forming a subchondral cyst
  4. all the cartilage is warn away the bone becomes EBURNATED
58
Q

Is OA symmetric or asymmetric?

How many joints are involved?

A

asymmetric and few joints are severely involved.

  • decreased mobility in the fingers, spine, joints
  • NO ankylosis (fusion/joint rigidity)
59
Q

How do joint symptoms differ from SLE and RA?

A

SLE- inflammation is not destructive to joints

RA- joints are destroyed and become ankylosed

60
Q

How does OA differ from RA in clinical presentation?

A

OA is not inflammatory, but RA is.

RA will present with fever and malaise in addition to the joint pain.

61
Q

In what decade of life does RA usually begin? Who is affected more, men or women?
What haplotype has been associated with RA?

A

3rd or 4th decade of life
Females are 3x more affected than males
HLA-DR4 haplotype is associated with RA

62
Q

How does RA differ from OA in terms of symmetry and whether it ankyloses?

A

RA is symmetrical and ankylosing

OA is asymmetric and does not anyklose

63
Q

What is the histology of a rheumatoid nodule?

A

central zone of fibrinoid necrosis surrounded by a rip of epitheloid macrophages, lymphocytes and plasma cells

64
Q

What is the purpose of the synovium? What does the intimal lining look like in a normal joint?
What does it look like in RA?

A

It provides nutrients to cartilage and produces lubricants for the joints.

Normal: intimal lining is composed of cells that resemble macrophages and fibroblast-like synoviocytes. Beneath this is aceuuluar tissue with sparse lymphocytes.

RA: intimal lining is hyperplastic (macrophages secrete pro-inflam cytokines and the fibroblast-like synoviocytes produce proteases, PGs and cytokines) and the synovium is infiltrated with CD4 T cells, B cells, macrophages, plasma cells.

65
Q

What is it called in RA when the synoviocytes invade the joint space?

A

Pannus- a sheet that covers the articular cartilage isolating it from metabolites in the synovial fluid

66
Q

What inflammatory mediators break down the cartilage matrix? What leads to the destruction of subarticular bone?

A

IL1 and TNFa released from the reactive synovium encourage breakdown of cartilage.
RANKL from the T cells in the synovium mature osteoclasts to destroy the subarticular bone

67
Q

What is an osteoma?
What age does it usually present?
What sex is more frequently affected?

A

It is a benign bone lesion that represents abnormal development (harmatomas)
It generally presents in middle aged people.
Women > Men

68
Q

What is the usual anatomic location of an osteoma?

How does the patient present?

A

exophytic masses on the bones of the skull

Usually presentation:

  1. facial asymmetry
  2. obstructed sinuses
  3. difficulty breathing, hearing
  4. headaches
  5. Gardner’s syndrome - osteoma, intestinal polyposis, fibromas in soft tissue, and sebaceous cysts of skin
69
Q

What is the gross pathology and microscopic pathology of an osteoma?

A

Gross: dense homogenous bone
Histiologically: dense sclerotic lamellar bone

70
Q

What is treatment for osteoma?

A

surgical removal of osteoma if symptomatic.

71
Q

A 50 year old woman presents with facial asymmetry, obstructed sinuses and difficulty breathing. On physical exam, you note she has intestinal polyposis, fibromas in soft tissue and sebaceous cysts in her skin.
What is the likely condition?

A

Gardner’s syndrome

72
Q

What is an osteoid osteoma? How does it differ from osteoblastoma grossly?

A

Osteiod osteoma is a benign tumor with well-demarcated central core surrounded by zone of reactive sclerotic bone.
OO 2cm

73
Q

What is the age range for osteoid osteomas?
Osteoblastomas?

What sex has a higher predilection for these benign tumors?

A

Osteoid osteomas affect 10-20.

Osteoblastomas affect 15-45

Men > women

74
Q

What bones are most affected by osteoid osteomas?

Osteoblastomas?

A

OO: cortex of long bones of the leg METAPHYSIS of femur/tibia

OB: axial skeleton/ vertebral column/transverse processes

75
Q

A 18 year old male presents with pain of increasing severity that worsen at night in his legs.
When he takes aspirin or NSAIDs it goes away. What is a resasonable diagnosis?

A

Osteoid osteoma

76
Q

A 23 year old male presents with pain of increasing severity in his vertebrae that is worse at night. He takes NSAIDs and aspirin and nothing improves. What is a likely diagnosis?

A

Osteoblastoma

77
Q

Why is pain associated with osteoid osteoma able to be treated with aspirin?

A

the lesion has a central core surrounded by reactive sclerotic bone.
The reactive core has PGE2 and prostacyclin which are implicated in the inflammation around the lesion.

78
Q

What is the gross and microscopic appearance of Osteoid osteoma and osteoblastoma?

A

Grossly:

  1. OO - less than 2cm central nidus (friable or sclerotic) with a distinct reactive sclerotic ring around it.
  2. OB- greater than 2cm nidus with surrounding cortex thinned

Microscopically:
Both - nidus is well demarcated with woven trabeculae and well differntiated osteoblasts

79
Q

What is osteosarcoma?

If it contains areas of chondroblastic or fibroblastic differentition what is it called?

A

It is a malignant tumor of bone where the malignant cells produce osteoid.
Chondroblastic osteosarcoma
Fibroblastic osteosarcoma.

OSTEO cannot be “trumped”

80
Q

What is the age range for osteosarcoma? What gender is more commonly affected?

A

It is bimodal:

  1. primary : 10 to 20 yrs
  2. secondary: >50
81
Q

What are some of the underlying bone abnormalities that can lead to osteosarcoma?

A
  1. Paget’s disease
  2. previous radiation
  3. metal surgical implants
82
Q

What are the common locations for primary osteosarcoma?

A

Metaphysis of distal femur, proximal tibia and humerus

“around the knees away from the elbow!”

83
Q

What are the common locations for secondary osteosarcoma?

A

femur, humerus, pelvis

NOT restricted to the metaphysis like primary osteosarcoma

84
Q

What is typical presentation of primary osteosarcoma?

What are long term effects?

A 
Presents with pain around the tumor lasting weeks/months
. 
Later effects:
1. joint pain and deformity
2. pathologic fracture 
3. metastasize to lung
85
Q

What does the blood work of osteosarcoma show?

A

Elevated serum alk phos due to increased cell turnover within and adjacent to the neoplasm

86
Q

What is a frequent radiographic finding for primary osteosarcoma?

A

The tumor has patchy areas of radiolucency and radiodensity reflecting variation in the amount of malignant bone produced.

If it destroys the cortical bone, it will elevate the periostium and stimulate more periosteal bone to get made. This presents as “Codman’s triangle”

87
Q

What is the gross pathology and microscopic findings of primary osteosarcoma?

What gene is frequently mutated in osteosarcomas?

A

Gross:

  1. heterogenous cut surface (ossified =white, hard and neoplasms = softer and chondriod)
  2. hemorrhage, necrosis

Microscopically:
1. neoplastic cells producing osteiod

Gene Mutation:
RB gene is mutated in 100% of osteosarcomas

88
Q

What is treatment for primary osteosarcoma?

A

Chemo AND surgery

89
Q

What age, sex and underlying conditions lead to secondary osteosarcoma?

A

Men older than 50 with underlying conditions like Paget’s bone disease, metal implants, prior radiation

90
Q

What does blood work of secondary osteosarcoma show?

A

Elevated alk phos due to high cell turnover

91
Q

Why is treatment of secondary osteosarcoma more difficult than primary?

A
  1. axial location (pelvis, hip, etc) are more complicated for surgical resection
  2. elderly cannot tolerate chemo well
92
Q

What is an osteochondroma?
What age does it affect?
Men or women?
What bones are most affected?

A

It is a benign tumor/harmatoma that arises in the growing skeleton from displaced growth plate cartilage that grows laterally at right angles to the axis.
10-30, M>F

It usually is on the metaphysis of long bones (near displaced growth plate)

93
Q

Describe the gross and microscopic pathology of osteochondroma.

A

Gross:

  1. stalk of well differentiated bone arising from the cortical surface
  2. covered by cap of well-differentiated cartilage

Microscopic:
1. cap is well differentiated cartilage that recapitulates the growth plate with endochondreal ossification

94
Q

What is the treatment for osteochondroma?

A

After sexual maturity is reached and the growth plate is closed, remove the tumor for cosmetic purposes or if they are on a nerve or interfere with motion

95
Q

What is endochondroma?
What age does it affect?
Men or women?
What bones are most frequently affected?

A

It is a benign tumor of hyaline cartilage that arises IN medullary cavities of long bones.
They can be painful and erode the cortex.

20-50 year old, men and women equally

Metaphysis and diaphysis of long bones, and in the hands and feet

96
Q

How do endochondromas look grossly? microscopically?

A

Gross:
well circumscribe lobules of cartilage
Micro:
well-differentiated hyaline cartilage

97
Q

What is the treatment for endochondroma?

A

No treatment- they are stable lesions

98
Q

What is a chondrosarcoma? What are the grades?
What age and gender are most frequently affected?
What bones are involved?

A

It is a malignant tumor of mesenchymal cells that produces cartilage.
It is graded 1-3 which determines the aggressiveness and likeliness to metastasize. 90% are grade 1 and 2 and are indolent/slow to metastasize. 10% are 3 and have high metastatic potential.

Men and women equally in the age 40-80.

Chondrosarcoma affects bones of shoulder, pelvis, proximal femur and ribs (CENTRAL)

99
Q

What is the most important feature in the differential diagnosis of benign vs. malignant cartilaginous neplasms?

A

Pain in chondrosarcoma

Asymptomatic in endochondroma

100
Q

What is the gross pathology and microscopic pathology of chondrosarcoma?

A

Gross:

  • tumor in the diaphysis filling the marrow cavity
  • translucent, hyaline, rubbery, nodular
  • low grade = thick cortex
  • high grade = thin cortex/bone destruction

Microscopic:
-cytologic atypia with mitotic figures and cellularity

101
Q

What is treatment for chondrosarcoma?

A

surgical resection with wide margins

102
Q

What is giant cell tumor of bone?
What age group is affected? Are males or females affected more?
What is the anatomic location of the tumors?

A

It is a locally aggressive neoplasms made of mononuclear cells AND osteoclast-like giant cells.
They destroy and do not produce anything!!!

This affects people 20-40 and females slightly more than males

It is the only tumor to be predominantly in the epiphysis of tubular long bones

103
Q

What is the effect of giant cell tumors on the bone?

A

They are lytic and produce a club like expansion at the end of the bone.
The tumor is soft friable and brown
The cortex is destroyed and replaced by narrow reactive bone
Necrosis and hemorrhage make”soap bubble” lesions on radiograph.

104
Q

What is the gross pathology of giant cell tumors?

Microscopic?

A

Gross:
1. heterogeneous surface with hemorrhage and necrosis

Microscopic:
mononuclear cells mixed with multinucleated giant cells

105
Q

What is treatment for giant cell tumors?

A

25% are locally aggressive and will recur after surgery.

Radiation therapy is NOT recommended

106
Q

What is Ewing sarcoma?
What age does it affect?
Men or women?
What bones?

A

It is a primary malignant round tumor of bone and soft tissue due to a chromosomal translocation.

It affects 10-20 year olds.
Men slightly more than women.

It arises in the medullary cavity (Diaphysis and metaphysis) of long bones

107
Q

What is the microscopic and gross appearance of Ewings sarcoma?

A

Gross:
Soft and tan grey in the diaphysis/metaphysis of long bone

Micro:
nests/sheets of round cells with NO production of cartilage or bone

108
Q

Which tumors of the bone affect primarily 10-30 age group?

A
  1. Osteoid osteoma
  2. Primary osteosarcoma
  3. osteochondroma
  4. Ewing tumor
109
Q

What tumors affect older people (40-80)?

A

chondrosarcoma

110
Q

Which 2 tumors do not make matrix?

A
  1. Ewing sarcoma

2. giant cell tumor

Respiratory/Musculoskeletal (36 decks)

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