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Pathophysiology II Exam 2 Renal > MSK Module I > Flashcards

MSK Module I Flashcards

1
Q

Cortical bone (compact bone) makes up how much of the human skeleton?

A

80%

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2
Q

Does cortical bone (compact bone) have a slow or fast turnover rate?

A

Slow

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3
Q

What is the makeup of cortical bone (compact bone)?

A

Dense, tightly packed osteons w/ Haversian canal system

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4
Q

Cancellous bone (trabecular or spongy bone) makes up how much of the skeletal mass?

A

20%

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5
Q

Does cancellous bone (trabecular or spongy bone) have a high or low turnover rate?

A

Higher turnover compared to compact

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6
Q

Cancellous bone (trabecular or spongy bone) is less dense than cortical bone, but has what?

A

Large surface area

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7
Q

Because of cancellous bone (trabecular or spongy bone) having a large surface area, it is more susceptible to what?

A

Bone density loss

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8
Q

What is Wolff’s Law?

A

Mechanical stress/gravity stimulate bone remodeling
(mechanical stress increases bone density along “stress lines” or “gravity vectors”)

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9
Q

The density of the femoral neck varies due to what?

A

Mechanical stress lines

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10
Q

Areas not in the stress lines of the femoral neck may become susceptible to what?

A

Fracture

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11
Q

What is the periosteum?

A

Thin, double-layered, tough fibrous membrane that surrounds all bone except at ligament or tendon insertion sites

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12
Q

What is contained in the inner layer (cellular layer) of the periosteum?

A

-Sharpey’s fibers: anchor periosteum as well as tendons&ligaments to cortical bone
-Active and resting osteoblasts

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13
Q

What is contained in the outer layer (fibrous layer) of the periosteum?

A

-Capillaries and nerves

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14
Q

What is a periosteal reaction of the outer layer of the periosteum?

A

Fracture cortex or expanding tumor may disrupt periosteum and generate pain

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15
Q

Where is myeloid tissue located in bone marrow?

A

In the cavities between osseous component of bone (myelos=marrow)

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16
Q

What is the function of red (active) bone marrow?

A

Blood cell formation
-All RBCs, platelets, 60-70% of WBCs

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17
Q

What produces the other 20-30% of WBCs?

A

Lymphatic tissue of spleen, lymph nodes, thymus

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18
Q

Where is red (active) bone marrow located in adults?

A

Trabecular/Lymphatic tissue of spleen, lymph nodes, thymus bone of pelvic bones, vertebrae, cranium and mandible, sternum and ribs, proximal femur and humerus

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19
Q

What does the “yellow” of yellow (inactive) bone marrow represent?

A

Presence of fatty acids

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20
Q

Where is yellow (inactive) bone marrow located in adults?

A

Medullary cavity of long bones

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21
Q

What is a bone scan? What will it show?

A

Tracer injected/accumulates in areas of high cell metabolism/turnover

Scan will show normal areas of red bone marrow as well as abnormal areas of bone cellular metabolism
(tumor, infection, fracture/bine repair, arthritis, etc.)

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22
Q

What is apheresis?

A

Collection of stem cells by filtering blood for circulating blood cells (PBSC- peripheral blood stem cells)

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23
Q

What is a bone marrow harvest?

A

Collection of stem cells directly out of bone
*pelvis and sternum MC sites to harvest bone marrow

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24
Q

Stem cells can be filtered from blood in what structure after a baby is born?

A

Umbilical cord

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25
Q

Cellular components of bone?

A

Osteoblasts, Osteocytes, Osteoclasts, Osteoprogenitor cells

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26
Q

Extracellular components of bone?

A

Extracellular matrix: collagen, proteoglycans, ECM proteins, cytokines, GF, minerals, etc.

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27
Q

Osteoblasts originate from what?

A

Osteoprogenitor cells

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28
Q

Osteoblasts are located where in bone?

A

Along bone surfaces (trabecular, Harversian’s canal, inner surface of periosteum)

*also located deeper in bone and activated y fracture or trauma

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29
Q

Function of osteoblasts?

A

Secrete bone matrix which forms new bone during bone remodeling/repair: type I collagen, osteonectin, osteocalcin, OPG (osteoprotegerin), Alkaline phosphate

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30
Q

Elevated lab levels of alkaline phosphate indicate what?

A

Bone pathology

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31
Q

Osteoblasts also play a role in signaling what?

A

Osteoclast activity & function

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32
Q

Osteocytes are formed from what?

A

Osteoblasts

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33
Q

After osteoblast secretes bone matrix (osteoid), the matrix mineralizes and the osteoblast becomes what?

A

Osteocyte

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34
Q

Osteocytes located in a cavity are known as what?

A

Lacunae

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35
Q

Osteocytes make up how much of the cells in a mature human skeleton?

A

90%

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36
Q

Osteocytes have long cellular processes that communicate with with other bone cells through what?

A

Through the canaliculi

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37
Q

Do osteocytes have blood supply?

A

Yes, not “dead cells”
Blood supply via small capillaries

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38
Q

Osteocytes are very active in regulating what?

A

Mineralization homeostasis and bone remodeling

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39
Q

How do osteocytes maintain bone mineralization homeostasis?

A

By regulation of calcium & phosphorous concentrations

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40
Q

How do osteocytes regulate bone remodeling?

A

Detect physical stimuli & produce signals to regulate bone remodeling

Dissolve surrounding mineralized bone by secreted enzymes in prep for bone remodeling

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41
Q

If osteocytes are damaged, neighboring healthy osteocytes signal what?

A

RANKL production to stimulate bone remodeling

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42
Q

Stimuli of osteocyte regulation/remodeling?

A

Mechanical stress (positive or negative), hormones, drugs, cytokines, etc.

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43
Q

What cells are large, multinucleated, phagocytic cells that create resorptive pits (Howship’s lacunae)?

A

Osteoclasts

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44
Q

What are resorptive pits/Howship’s lacunae?

A

Microscopic depressions formed during bone modeling
*eventually get filled with new bone during remodeling

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45
Q

Function of osteoclasts?

A

Bone resorption, one of the initial steps of bone remodeling

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46
Q

How does bone resorption occur by osteoclasts?

A

Breaking down of mineralized bone and releasing calcium, phosphate, etc. that are resorbed into microvilli of osteoclast and secreted into plasma

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47
Q

What do osteoclasts secrete to break down/dissolve mineralized bone matrix?

A

Acid and lytic enzymes

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48
Q

Until they are needed again, osteoclasts undergo what?

A

Apoptosis or become dormant

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49
Q

According to NASA research, microgravity in space promotes what?

A

Osteoclast activity and bone density loss

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50
Q

Healthy bone is or is not constantly remodeling?

A

It is constantly remodeling

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51
Q

Healthy remodeling bone occurs in both ____ and ____ bone?

A

cortical and cancellous

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52
Q

Healthy remodeling of bone relies on what?

A

Balance between osteoclast and osteoblast activity

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53
Q

When does osteoporosis occur?

A

When osteoclast activity exceeds osteoblast activity

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54
Q

Activation of bone remodeling by hormones, drugs, physical stress, or trauma signaling the dormant osteoblasts to stimulate what?

A

Osteoclast maturation and activity

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55
Q

The resorption cavity follows what in compact bone?

A

Longitudinal axis of Haversian canals

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56
Q

The resorption cavity follows what in cancellous bone?

A

Surface of trebeculae

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57
Q

What is the reversal phase of bone remodeling?

A

Macrophages will clean up surface of the resorptive cavity to prep for laying down of new bone

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58
Q

What happens to osteoblasts in the formation phase of bone remodeling?

A

Mature and actively secrete bone matrix into the resorptive cavity

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59
Q

How is bone laid down in compact bone remodeling?

A

In concentric layers until a small canal is formed (Haversian canal)

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60
Q

How is bone formed in cancellous bone remodeling?

A

Trabeculae are broken down and new trabeculae are formed

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61
Q

What is the mineralization phase of bone remodeling?

A

New matrix mineralizes/ becomes new bone

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62
Q

What is the quiescence phase of bone remodeling?

A

Osteoblasts in the area of new bone formation are now at rest/dormant

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63
Q

Hormones, drugs, physical stress, or trauma signal resting osteoblasts to secrete what in order to stimulate osteoclast maturation/activity?

A

RANKL and M-CSF (cytokine)

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64
Q

When mature osteoblasts migrate to the cavity and secrete what?

A

-New bone matrix to fill cavity
-Osteoprotegerin (OPG) that inhibits osteoclast activity

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65
Q

What does OPG protect bone from?

A

Excess bone resorption by inhibition of osteoclast maturation/activity

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66
Q

Healthy bone remodeling and overall bone density relies on optimal _____ ratio?

A

OPG/RANKL

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67
Q

What does a high OPG/RANKL ratio promote?

A

Bone formation and increases bone density

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68
Q

What does a low OPG/RANKL ratio promote?

A

Bone resorption and decreases bone density

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69
Q

OPG/RANKL ratio is often used in research as a biomarker for what?

A

Bone mass/skeletal integrity

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70
Q

What can stimulate the release of RANKL?

A

PTH

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71
Q

Transient short-term PTH signaling on healthy bone will stimulate a short-term release in what?

A

Ca2+ from bone fluid

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72
Q

Sustained PTH signaling on healthy bone will stimulate what?

A

RANKL (stimulates osteoclast activity/bone resorption)

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73
Q

Do normal PTH levels create excess osteoclastic activity?

A

No, part of ongoing signaling which maintains a healthy bone density

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74
Q

Does excess PTH signaling disrupt bone density?

A

Yes, causes excess osteoclast activity leading to excessive bone resorption/loss of bone density

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75
Q

What can cause excess PTH secretion and may lead to osteoporosis?

A

Hyperparathyroidism

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76
Q

What can cause excess PTH and leads to osteolytic bone lesions?

A

Cancers

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77
Q

How can a total joint replacement recruit RANKL?

A

Periprosthetic osteolysis can loosen joint replacement hardware, microdebris from the loosened hardware stimulate PGE2 production and promote RANKL expression/increases osteoclast activity

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78
Q

What is the role of interleukin 6 (IL-6), IL-1 and other IL’s in a loosened total joint implant?

A

IL-1 stimulates RANKL
IL-6 promotes PGE2 synthesis which increases RANKL osteoclast activity

79
Q

What form of vitamin D stimulates RANKL?

A

1,25 dihydroxy vitamin D (active vitamin D)
***Although it stimulates RANKL, also inhibits osteoclasts, net result: promotion of bone formation

80
Q

What hormone promotes OPG release and inhibits RANKL release?

A

Estrogen, increases OPG/RANKL ratio –> protective effect on bone density

81
Q

What is directly related to post-menopausal estrogen loss?

A

Post-menopausal bone density loss

82
Q

What kind of exercise promotes OPG/inhibits RANKL, increases OPG/RANKL ratio, and has protective effect on bone?

A

Weight bearing/resistance exercise

83
Q

What inhibits OPG expression and promotes RANKL expression, decreases OPG/RANKL ratio, and promotes loss of bone density?

A

PTH (overall negative effect on bone density)

84
Q

Calcitonin interacts directly with which cells via cell-surface receptors?

A

Osteoclasts

85
Q

Effect of calcitonin on osteoclasts?

A

Inhibit bone resporption by decreasing # and activity of osteoclasts

86
Q

What is an initial fracture?

A

Disruption of periosteum and blood vessels in cortex/marrow
*causes fracture pain

87
Q

Characteristics of primary (direct) bone healing?

A

-Bone stabilization is very rigid
-No callus formation
-Longer time until stable

88
Q

Characteristics of secondary (indirect) bone healing?

A

-Bone stabilization is less rigid
-Callus formation
-Callus will provide quicker stability

89
Q

Three phases of secondary bone healing?

A

Inflammatory, reparative, remodeling

90
Q

How long does the inflammatory phase of secondary bone healing last?

A

days to 1-2 weeks

91
Q

Process of inflammatory phase of secondary bone healing?

A

increased blood flow to area after acute immune response to fracture–> hematoma forms –> osteoclast activity removes damaged bone –> GF promote initial fibroblast/osteoblast activity in area of damaged bone

92
Q

Imaging/x-ray of inflammatory phase of secondary bone healing?

A

Fracture line becomes more visible as necrotic tissue is removed from site

93
Q

How long does the reparative phase of secondary bone healing last?

A

up to several months

94
Q

Process of reparative phase of secondary bone healing?

A

Fibroblasts secrete fibrocollagenous matrix which forms a sioft fibrous callus at beginning –> osteoclasts secrete bony matrix which forms hard callus at end *considered immature bone that is stable but weaker than mature bone

95
Q

Imaging/x-ray of reparative phase of secondary bone healing?

A

Fracture line begins to disappear as hard callus forms

96
Q

How long does the remodeling phase of secondary bone healing last?

A

months to years

97
Q

Process of remodeling phase of secondary bone healing?

A

Immature bone gradually replaced by organized mature bone, bone returns to original shape

98
Q

Imaging/x-ray of remodeling phase of secondary bone healing?

A

Fracture line has disappeared and bone gradually remodels

99
Q

Whose fractures heal faster: children or adults?

A

Children

100
Q

Pathological fractures may or may not heal, and are a risk for what?

A

Complications

101
Q

What is gap healing in primary bone healing?

A

Rigid fixation w/ small gaps but NO movement or micro-movement at fracture site

102
Q

Phase 1 of gap healing in primary bone healing?

A

New bone laid down vertically to serve as initial stabilization, necrosis along fracture ends

103
Q

Phase 2 of gap healing in primary bone healing?

A

Longitudinal reconstruction of Haversian organization of bone–>osteoclasts create a cutting zone across fracture site –> capillary formation (angiogenesis) follows pathway of cutting zones–> capillaries deliver osteoblast precursors to area new bone is laid down

104
Q

What is contact healing in direct bone healing?

A

Rigid fixation with NO gaps and NO movement or micro-movement at fracture site

105
Q

What is the one phase of contact healing in direct bone healing?

A

Longitudinal reconstruction of Haversian organization of bone–>osteoclasts create a cutting zone across fracture site –> capillary formation (angiogenesis) follows pathway of cutting zones–> capillaries deliver osteoblast precursors to area new bone is laid down

**same as gap healing but skips phase 1

106
Q

Is determining when a fracture is healed an absolute science?

A

No

107
Q

Healing time of fractures vary with what?

A

Age and type of fracture

108
Q

Criteria for balancing between fracture healing vs. negative consequences of immobilization?

A

-Clinical judgement
-Radiographs (callus formation w/ disappearance of fx line, cortex outline restores)
-Anatomical location (different bones heal at different rates)

109
Q

Distal radial fractures take approximately how long to heal?

A

6-8 weeks

110
Q

Mid-diaphyseal fractures take approximately how long to heal?

A

3 months

111
Q

Fracture immobilization strategies?

A

Cast
Intramedullary rods/nails Pins,wires,screws
Compression plate
External fixator

112
Q

Which immobilization strategies allow for secondary bone healing with periostal callus formation?

A

Cast, Pins/wires/screws, Intramedullary rods/nails

113
Q

Which immobilization strategy allows for primary bone healing with NO periostal callus formation? Why do LE fxs need a longer period of non-weight bearing with primary healing?

A

Compression plate (primary healing is slower–>longer period of non-weight bearing NWB if lower extremity)

114
Q

Which type of bone healing will occur with a less rigid external fixator?

A

Secondary healing with callus formation

115
Q

Which type of bone healing will occur with a very rigid external fixator?

A

Primary healing with NO callus formation

116
Q

In addition to fracture itself there is also concern for damage to what in pediatric fractures?

A

Damage to growth plate, future growth impairment

117
Q

What % of pediatric fractures involve the growth plate?

A

15-30%

118
Q

What % of pediatric injuries that involve the growth plate have growth impairment of the bone?

A

estimated 1-10%

119
Q

Salter-Harris classification for pediatric fractures Type 1?

A

Disruption of the growth plate (distraction or slip injury)

*SCFE (slipped capital femoral epiphysis) is a type 1 Salter Harris injury

120
Q

Salter-Harris classification for pediatric fractures Type 2?

A

Fracture line through growth plate and metaphysis

121
Q

Salter-Harris classification for pediatric fractures Type 3?

A

Fracture line through growth plate and epiphysis

122
Q

Salter-Harris classification for pediatric fractures Type 4?

A

Fracture through metaphysis, growth plate, and epiphysis

123
Q

Salter-Harris classification for pediatric fractures Type 5?

A

Compression injury of the growth plate

124
Q

What is the classification of low bone mass (osteopenia)?

A

Low bone mineral density but not severe enough to be considered osteoporosis (BD between 1-2.5 SD below young adult men)

125
Q

What is the classification of osteoporosis?

A

Severe decrease in BMD
(BD < or = 2.5 SD of young adult men)

126
Q

What is the classification of osteomalacia?

A

Softening of the bone

127
Q

What is the classification of osteopetrosis?

A

Increased bone density

128
Q

What is primary osteoporosis?

A

Low BD unrelated to any underlying disease/condition

129
Q

What is secondary osteoporosis?

A

Low BD secondary to medication or disease/condition

130
Q

What is Type-1 primary osteoporosis? What kind of bone does it affect?

A

Post-menopausal, primarily affects cancellous bone

131
Q

What is Type-2 primary osteoporosis? What kind of bone does it affect?

A

Age-related (typical in >75 y/o), affects both cancellous and cortical bone

132
Q

What is peak bone mass?

A

From birth to 20’s the rate of bone formation occurs at faster rate than bone resorption, and bone mass will peak at 25-30 y/o

133
Q

Peak bone mass plateuas for how long?

A

~3.5 years

134
Q

Modifiable risk factors for low peak bone mass?

A

Smoking, alcohol, physical inactivity, poor nutrition

135
Q

The rate of bone loss is the same for men and women until what occurs?

A

Menopause

136
Q

Age-related bone loss in men and women starts at what age?

A

in the 30’s sometime after 3-5 yr plateau

137
Q

Normal age related bone loss rate for men and women before menopause?

A

0.5-1%/year

138
Q

Women reach osteoporotic levels faster than men due to what?

A

Menopause and men starting with a higher peak bone mass

139
Q

Rate of bone loss after menopause is most rapid when?

A

during the first decade post-menopause

140
Q

Rate of bone loss the first decade post-menopause?

A

increases up to 3-5%/year

141
Q

What % of bone mass is lost in the first decade post-menopause? What % of expected lifetime bone density loss does this amount account for?

A

After first decade 15% lost, accounts for 40-50% of lifetime density lost

142
Q

After the first decade post-menopause the rate of bone loss slows and returns to what rate?

A

“normal” age related loss of 1%/year

143
Q

Pathogenesis of post-menopausal osteoporosis?

A

Loss of estrogen–>reduces OPG–> decreases OPG/RANKL ratio–> favors osteoclast activity/promotes bone loss

144
Q

How does Raloxifine work for osteoporosis tx?

A

Stimulates OPG production

145
Q

How does Denosumab work for osteoporosis tx?

A

Inhibits RANKL

146
Q

How do Bisphosphates work for osteoporosis tx?

A

Inhibit bone resorption itself

147
Q

Pathogenesis of age-related osteoporosis?

A

Many factors contribute:
OPG/RANKL ratio gradually decreases
GH, IGF, androgens decrease with age
Lifestyle- inactivity w/ less mechanical stimulation, poor nutrition w/ little Vit. D/calcium, Tobacco inhibits OPG, Alcohol lowers OPG/RANKL ratio

148
Q

How does long term glucocorticoid use decrease bone mass?

A

Decrease OPG/RANKL ratio,
Inhibit OPG
Stimulate RANKL/osteoclasts

149
Q

The largest rate of bone loss occurs at what point of glucocorticoid use?

A

Initial 6 months of daily use, and then rate slows

150
Q

What is a significant concern in managing patients with osteoporosis?

A

Fracture risk

151
Q

Which bone is affected first by osteoporosis? What kind of fractures does this lead to?

A

Cancellous bone (vertebra, long bone metaphysis), lead to wrist, hip, and compression fxs

152
Q

Gold standard to measure bone density?

A

Dual energy x-ray absorptiometry (DEXA or DXA scan)
*this alone does not identify patients w/ highest fracture risk

153
Q

What is the online questionaire used to assess fracture risk (developed by Univeristy of SHeffield in association with the WHO)? What does it predict?

A

FRAX- Fracture Risk Assessment Tool, predicts 10-year likelihood of having a minimal trauma fracture

154
Q

What is osteomalacia?

A

Insufficient mineralization of bone (no bone loss occurs)

155
Q

Etiologies of osteomalacia?

A

-Poor Vit. D intake
-Intestinal dz impairing absorption
-Renal dz, meds, tumors

156
Q

What is Rickets?

A

Childhood osteomalacia

157
Q

Imaging/x-ray appearance of osteomalacia?

A

“Looser’s zones” or Milkman’s pseudofractures: lesions that resemble fxs but are actually poorly mineralized osteoid matrix oriented perpedicular/do not completely cross the full width

Deformed bowing of long bones

158
Q

What is Paget’s Disease of bone?

A

Severe bone deformation causing associated complications

159
Q

Onset of Paget’s disease? Prevalence in males/females?

A

> 50 y/o, M>F (ratio 8:1)

160
Q

Pathology of Paget’s disease?

A

Osteoblast/osteoclast signaling disrupted, causes rapid and abnormal bone remodeling leading to enlarged or deformed bone of poor quality
(disorganized collagen fibers, poor mineralization)

161
Q

Potential complications of Paget’s disease?

A

Fracture, deformity, arthritis, nerve dysfunction if compressed in skull, pain

162
Q

The term osteochondrosis refers to what?

A

bone growth disorders that involve ossification centers (osteonecrosis, apophysitis)

163
Q

Osteochrondrosis may result from what?

A

abnormal growth, injury, overuse of developing growth plate/surrounding ossification centers
*can be self limiting depending on age, severity, stress removal, etc.

164
Q

What is osteonecrosis?

A

Bone death due to loss of blood supply

165
Q

Clinical signs of osteonecrosis (avascular necrosis/AVN) ?

A

early: often no sx
chronic: gradual pain onset
Acute pain sx if fracture in area of necrosis

166
Q

Common sites of AVN/osteonecrosis?

A

Femoral head **MC
Scaphoid
Proximal humerus
Tibial plateau
Small bones of wrist/ankle

167
Q

Common causes of AVN/osteonecrosis?

A

post-traumatic, steroid use, alcohol use, idipopathic

168
Q

What is apophysitis?

A

Traction on secondary ossification center

169
Q

What is Osgood-Schlatter disease (Apophysitis)?

A

Patella ligament traction on tibial tuberosity

170
Q

What is Sinding-Larsen-Johansson disease (Apophysitis)?

A

Patella ligament traction on distal patella

171
Q

Apophysitis of the elbow is common in what population?

A

Young throwing athletes

172
Q

What is olecranon apophysitis?

A

Traction from triceps tendon

173
Q

What is medial epicondyle apophysitis?

A

Traction from common flexor tendon
*Little Leaguer’s Elbow

174
Q

What is Sever’s Disease (Apophysitis)?

A

Achilles tendon traction (pulling) on the secondary ossification center of the calcaneus

175
Q

What can cause osteomyelitis?

A

Microstructure of bone contains regions that make bone susceptible to infection if bacteria/foreign invaders gain access

176
Q

Adult inflammatory response to osteomyelitis?

A

Inflammation eventually disrupts bone cortex –> potential for pathological fracture

177
Q

Child inflammatory response to osteomyelitis?

A

Subperiosteal abscess: inflammation may lift off periosteum sequestrum (area of necrosis)
Involucrum formation: lifting off of periosteum causing increase in osteoblastic activity resulting in new bone growth

178
Q

Anatomical location of osteomyelitis in adults?

A

Lumbar spine

179
Q

Anatomical location of osteomyelitis in children?

A

Metaphysis near growth plate in long bones:
-distal femur
-proximal humerus
-tibia
-radius

180
Q

Signs/sx of osteomyelitis in adults?

A

Back pain w/ low grade fever

181
Q

Signs/sx of osteomyelitis in children?

A

High fever, local pain, redness, swelling

182
Q

Cells of benign primary bone tumors?

A

Well differentiated, look more like normal cells, tend to be slower growing

183
Q

Bone attempts to contain growth of benign primary bone tumors by forming what?

A

Sclerotic rim around the tumor

184
Q

In general, do benign primary bone tumors produce constant progressive bone pain?

A

No

185
Q

Examples of benign bone tumors?

A

Osteoid (osteoid osteoma, osteoblastoma)
Chronoid (enchondroma)
Fibrous (non-ossifying fibroma)
Mixed (osteochondroma)

186
Q

Radiographic characteristics of benign primary bone tumors that help provide helpful ddx info?

A

-Location of tumor (diaphysis, metaphysis, etc)
-Borders of tumor (benign: well defined small borders, malignant: ill-defined wide zone of transition)
-Morphology/matrix of tumor (recognizing patterns associated w/ cartilage, bone small round cell, giant cell, fibrogenic, vascular, chordoma helps assess tumor origin)

187
Q

What periosteal reaction refers to thickened callus formation caused by benign bone tumors that never occurs in malignant tumors?

A

Solid benign reaction

188
Q

What periosteal reaction refers to pushed out or lifted off of the bone appearance consistent with malignant bone tumors?

A

Onion skin (lamellated)

189
Q

What periosteal reaction refers to fast perpendicular growth that extends through the periosteum consistent with malignant bone tumors?

A

Spiculated (sunburst)

190
Q

What periosteal reaction refers to periosteum lifting from the bone consistent with malignant bone tumors?

A

Codman’s triangle

191
Q

What bone destruction pattern refers to well defined margins surrounding clear lytic area consistent with benign bone tumors?

A

Geographic pattern

192
Q

What bone destruction pattern refers to less defined margins surrounding lytic or partially lytic area consistent with malignant bone tumors?

A

Moth eaten pattern

193
Q

What bone destruction pattern refers to poorly defined margins with abnormal lytic bone merged throughout bone consistent with malignant bone tumors?

A

Permeative pattern

Pathophysiology II Exam 2 Renal (5 decks)

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