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Patho Summer Test #1 > MSK 1B - Bone: Structure and Pathology > Flashcards

MSK 1B - Bone: Structure and Pathology Flashcards

1
Q

What are all connective tissues composed of?

A

Cells

Extracellular Matrix

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2
Q

What is the cellular component of connective tissue?

A

Fibroblasts

Osteocytes

Chondrocytes

Etc.

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3
Q

What is the extracellular matrix made out of?

A

Non-fibrous component –> ground substance (gel-like); -glyco-

Fibrous component –> collagen/elastin

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4
Q

What does collagen do?

A

Provide tensile strength

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5
Q

What does elastin do?

A

Provide elastic properties

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6
Q

What are the celluar components of bone?

A

Osteoblasts

Osteocytes

Osteoclasts

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7
Q

What do obsteoblasts do?

A

Form new bone

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8
Q

How do obsteoblasts form new bone?

A

Produce type 1 collagen

Produce osteoid (non-mineralized bone matrix)

Fascilitate mineralization (calcification) of osteoid to complete process

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9
Q

When can you call an osteoblast an osteocyte?

A

Once surrounding bone matrix (osteoid) is mineralized

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10
Q

Where are osteoblasts located?

A

Trabecular surfaces (cancellous/spongy surface)

Inner surface of Haversian’s canal

Inner surface of periosteum (active bone formation)

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11
Q

What is the name of the small cavity where osteocytes are located?

A

Lacunae

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12
Q

How much of the human skeleton is comprised of osteocytes?

A

90%

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13
Q

What is the function of osteocytes?

A

Directly stimulate remodeling process of bone

Assist by secreting enzymes to dissoolve surrounding mineralized bone to prepare for bone remodeling

Serve as sensory mechanism for mechanical stimulus to bone

Maintain homeostasis of the mineralized (calcified) bone

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14
Q

How do osteocytes maintain homeostasis of the mineralized (calcified bone)?

A

Recieve nutrients from capillaries that maintain mineral homeostasis

Syntehesize molecules to assist w/ bone calcification

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15
Q

Where are osteoclasts found?

A

Howship’s lacunae –> depression seen in microscopic view (areas of bone resorption)

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16
Q

What is the function of osteoclasts?

A

Resorption of bone –> Ca2+ into blood stream; resorption of low quality/surplus bone

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17
Q

How do osteoclasts break down bone?

A

Secrete acid/lytic enzymes to brekdown and dissolve surrounding bone

have microvilli projecting out from cell –> bone resobred @ base of microvilli

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18
Q

What happens to bone that is resorbed into osteoclasts?

A

Released into capillaries to allow elements to be recycled into new bone @ different site

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19
Q

What happens to osteoclasts after resportion is complete?

A

Degenerates

Becomes dormant until needed again

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20
Q

What are the matrix components of bone (8)?

A

Collagen fibers

Proteoglycans

Bone morphic proteins (BMP)

Glycoproteins

Osteocalcin

Bone albumin

Growth factors (cytokines)

Calcium Hydroxyapatite (HAP)

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21
Q

What are the function of glycoproteins?

A

Assist in collagen fiber formation

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22
Q

How much collagen in bone is type 1 collagen?

A

90%

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23
Q

What is the function of type 1 collagen?

A

Gives bone tensile strength

Gives bone weight bearing (compressive) strength

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24
Q

What synthesizes and secretes type 1 collagen?

A

Osteoblasts

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25
Q

What are proteoglycans?

A

Large polysaccharides attached to protein

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26
Q

Where are proteoglycans found?

A

Between collagen fibers of bone

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27
Q

What is the function of proteoglycans?

A

Assist type 1 collagen in resisting compressive strength of bone

Play role in calcification/fluid balance by attracting calcium via ion exchange

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28
Q

What is the function of bone morphic proteins (BMP)?

A

Promote formation of osteoblasts from stem cells

Promote osteogenesis in osteoblasts

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29
Q

What is the function of osteocalcin?

A

Promote osteoclast activity therefore promoting bone resorption

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30
Q

What is the function of bone albumin?

A

Attracts fluid and maintains fluid balance in bone

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31
Q

What is the function of growth factors (cytokines)?

A

Play role in differentiation, activation, growth and turnover of bone (and other tissues)

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32
Q

What does IGF-1 stimulate in bone?

A

Long growth

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33
Q

What is calcium hydroxyapatite (HAP)?

A

Insoluble crystal that deposits within the collagen fibers

**end stage of calcium crystalization for mineralization (calcification)

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34
Q

What is the function of calcium hydroxyapatite (HAP)?

A

Gives compressive strength to bone

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35
Q

What is the bone multicellular unit (BMU)?

A

Cluster of cells that breakdown an area of the bone surface, then fills it w/ new bone

**multiple BMU clusters are activated/inactivated @ any given point in time and in different locations on a bone

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36
Q

What is the stimuli for the bone multicellular unit (BMU)?

A

Mechanical stress

Trauma

Cytokines/hormones –> PTH, IGF, IL-1, IL-6, PGE, Calcitriol, TNF, NO

Can occur at random

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37
Q

What do pre-osteoblasts produce?

A

RANK-L

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38
Q

What does RANK-L do?

A

Signal pre-osteoclasts to mature into active osteoclasts

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39
Q

What inhibits pre-osteoclasts maturing into active osteoclasts?

A

Osteoprotogerin (OPG)

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40
Q

What does resorption of bone by osteoclasts form?

A

Small cavity

**goes on for 2 weeks and then osteoclasts undergo apoptosis

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41
Q

What inhibits the resorption of bone by osteoclasts?

A

Estrogen

Calcitonin

**after menopause there is a estrogen deficiency and you have prolonged resorption

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42
Q

What promotes resorption of bone by osteoclasts?

A

Acidosis

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43
Q

What are some of the hormones, proteins, and other substances that promote osteoblasts maturation/activity?

A

PTH

WNT

BMPs

IGF

FGF

PDGF

Calcitriol

Runx2

GST-RANK-Ligand

TGF-Beta

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44
Q

What do active osteoblasts secrete to form the osteoid?

A

Collagen

Other components of bone matrix

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45
Q

How does the osteoid mature?

A

Calcium is slowly crystallized in stages

**Calcium hydroxyapatite (HAP) is final crystallized form that binds to collagen fibers

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46
Q

What is bone remodeling dependent on?

A

Osteoblast activity coupled w/ osteoclast activity

47
Q

What is Wolff’s Law?

A

Mechanical stress leads to increased bone density

Removal of mechanical stress leads to bone loss

48
Q

What are the metabolic disorders of bone?

A

Osteoporosis

Osteomalcia

Paget’s Disease of Bone

49
Q

What are the 2 types of osteochondroses?

A

Osteonecrosis

Apophysitis

50
Q

What is osteopenia?

A

Low bone mineral density (BDM) but not severe enough to be considered osteoporotic

51
Q

What is the BMD value that is considered osteopenia?

A

Between -1 and -2.5

52
Q

What is osteoporosis?

A

Severe disease in bone mineral density

53
Q

What is the BMD value that is considered osteoporosis?

A

-2.5

54
Q

What is osteomalacia?

A

Softening of the bone

55
Q

What is osteopetrosis?

A

Increase in bone mineral density (too much)

56
Q

What happens to cause osteoporosis?

A

osteoclastic activity > osteoblastic activity

57
Q

What type of bone is usually affected by type1-postmenapausal primary osteoporosis?

A

Primarily cancellous bone

58
Q

What type of bone is usually affected by type2-age related primary osteoporosis?

A

Cancellous and cortical bone loss

**usually pts > 75

59
Q

What are the 3 phases of bone mass?

A

Growth phase - until growth plates close (90% of bone density)

Consolidation phase - bone density increases until peak bone mass is reached (10% of bone density)

Involution phase - gradual loss of bone density

60
Q

When is peak bone mass commonly reached?

A

30 yo

61
Q

After the peak bone mass is reached, what happens?

A

Short plateau of peak bone mass ~ 3 - 5 yrs followed by decrease in bone mass

62
Q

When does bone loss begin for women?

A

Age 35 - 40 yo

63
Q

Who rate of bone loss is higher, men or women?

A

Rate is equal (men start w/ higher amt so it takes them longer to reach osteoporotic levels)

64
Q

How much bone loss per year is considered normal age related bone loss?

A

0.5 - 1%

65
Q

When is the rate of bone loss in women accelerated?

A

After menopause d/t decrease in estrogen levels

66
Q

During the 1st decade after menopause what is the rate of bone loss?

A

Can increase to 3 - 5% per year

**15% of total bone mass may be lost during this time period

67
Q

What happens to the rate of bone loss after the 1st decade of menopause?

A

Rate of loss gradually slows

68
Q

What are some secondary causes of bone loss?

A

Pathology

Meds (corticosteroids)

Nutrition deficiencies

69
Q

What does the loss of estrogen after menopause cause?

A

Disruption of RANK-L and OPG homeostasis

**higher levels of RANK-L w/ reduced levels of OPG = increased osteoclastic activity

70
Q

What are the regions most affected during osteoporosis?

A

Cancellous (trabecular) bone:

Vertebrae

Metaphysic of long bone –> wrist/femur are common fracture sites

71
Q

What are some age related factors suggested to contribute to osteoporosis?

A

Decreased GH and IGF levels

Decreased androgens

Increased RANK-L and inhibited OPG

Lifestyle: poor nutrition and inactivity

72
Q

What are the risk factors for osteoporosis?

A

Hormonal status (post-menopausal women)

Physical Inactivity

Genetics (peak bone mass/loss varies between individuals)

Meds (long term corticosteroid use)

Tobacco (inhibits osteoblastic activity)

Alcohol (inhibits osteoblast activity)

Diet/nutrition

73
Q

What is the female triad of anorexia/bulemia that puts them at greater risk for osteoporosis?

A

Eating disorder

Amenorrhea

Osteoporosis

74
Q

For every decrease of 1 SD in bone mass density tests, will increase the risk of fracture by how much?

A

1.5 - 3 times

75
Q

What is a normal Bone mass density test value?

A

≤ 1 SD of the young adult mean

76
Q

What is a osteopenia bone mass density test value?

A

Between 1 and 2.5 SD below the young adult mean

77
Q

What is a osteoporosis bone mass density test value?

A

> 2.5 below the young adult mean

78
Q

What is the gold standard to do bone mass density tests?

A

DEXA or dual energy x-ray absorptiometry

**x-ray is a poor screening tool b/c it only detects significant bone loss

79
Q

What is osteomalacia?

A

Insufficient mineralization of bone

**not a loss, matrix doesn’t mineralize (calcify)

80
Q

What causes osteomalacia?

A

Poor nutrition (ie poor vitamin D intake)

Intestinal disease that impairs absorption

Renal disease

Medications

Tumors

81
Q

What will you see on x-ray in a patient w/ osteomalacia?

A

“Looser zones”

Milkman’s pseudofractures

Bowing of long bones

**oriented perpedicular to the long axis of the bone and don’t cross the entier bone

82
Q

What are rickets?

A

Childhood osteomalcia

83
Q

What is paget’s disease of bone?

A

Disease that results in bone deformation w/ associated complications

84
Q

What is the most common onset of paget’s disease of bone and who is affected more, men or women?

A

> 50 yo

M > F (8:1) ratio

85
Q

Pathologically what happens in paget’s disease of bone?

A

Excessive resorption is followed by excessive bone formation –> poor quality enlarged deformed bone

86
Q

What are the potential complications of paget’s disease of bone?

A

Fracture

Defority

Arthritis

Nerve Dysfunction (if compressed in skull)

Pain

87
Q

What is osteonecrosis (avascular necrosis - AVN)?

A

Death of bone d/t loss of blood supply

88
Q

What is the most common site for osteonecrosis?

A

Femoral head

89
Q

What are the early signs/symptoms of osteonecrosis (AVN)?

A

Often asymptomatic

  • *chronic = gradual onset of pain
  • *if fracture = acute onset of pain
90
Q

What are the common causes of osteonecrosis (AVN)?

A

Post-traumatic

Steroid use

Alcohol use

Idiopathic

91
Q

What is apophysitis?

A

a traction apophysitis of the secondary ossification center

92
Q

What are the different types of apophysitis?

A

Osgood-Schlatter disease

Olecronon apophysitis

Sever’s disease

93
Q

What happens w/ osgood-schlatter disease?

A

Patella tendon pulling on tibial tuberosity

94
Q

What happens w/ olecranon apophysitis?

A

Triceps tendon pulling on secondary ossification olecronon (see a lot w/ young athletes)

95
Q

What happens w/ sever’s disease?

A

Achille’s tendon pulling on the secondary ossification center of the calcaneous

96
Q

What is osteomyelitis?

A

Inflammation of bone caused by bacteria or other infectious agents (fungi, parasites, viruses

97
Q

What is acute osteomyelitis?

A

New episode of infection

98
Q

What is chronic osteomyelitis?

A

Inffective or delayed treatment w/ relapsing episodes

99
Q

What is exogenous osteomyelitis?

A

Trauma exposes bone to bacteria and other foreign substances

100
Q

What is hematogenous osteomyelitis?

A

Infection is spread to bone from pre-existing systemic infection

**MC = staph aureus

101
Q

Why is bone prone to osteomyelitis?

A

Physical arrangement of bone contains regions that immune defense mechanisms are unable to access

102
Q

What is the inflammation response to osteomyelitis?

A

Similar to other infections: –> impairs BV/lymph vessels in area

103
Q

What can the inflammation response to osteomyelitis cause in adults?

A

Can cause disruption of bone cortex

Potential for pathological fracture

104
Q

Pathologically what can happen in children w/ osteomyelitis?

A

Formation of:

Sequestrum (piece of dea bone)

Involucrum (layer of new bone)

105
Q

What happens in children w/ osteomyelitis that can cause sequestrum?

A

Inflammation can lift off periosteum from sub-periosteal abscess –> disrupts more of blood supply

106
Q

Why would a involucrum form in kids w/ osteomyelitis?

A

The lifting off of periostium increaes osteoblastic activity –> new bone growth

107
Q

Where is the most common place of osteomyelitis?

A

Adults = lumbar spine

Kids = metaphysis near growth plate in long bones (distal femur, proximal humerus, tibia, radium)

108
Q

What are the signs/symptoms of of osteomyelitis in adults?

A

Back pain

Low grade fever

109
Q

What are the signs/symptoms of osteomyelitis in children?

A

High fever

Local pain, redness, swelling

110
Q

Describe primary benign bone tumors

A

Well-differentiated

Slower growing

Surrounded by sclerotic rim (bones attempt to contain tumor)

Don’t tend to produce constant progressive bone pain

111
Q

What are examples of benign bone tumors?

A

Osteoid (osteoid osteoma or osteoblastoma)

Chondroid (enchondroma)

Fibrous (non-ossifying fibroma)

Mixed (osteochondroma)

112
Q

Describe primary malignant bone tumors

A

Agressive

Fast growing (can spread to other areas)

Bone can’t contain tumor

113
Q

What are some examples of malignant bone tumors?

A

things ending w/ sarcoma

114
Q

What are the patterns of bone destruction of primary bone tumors?

A

Geographic = well defined margins surrounding clear lytic area

Moth Eaten = less defined margins, surrounding lytic or partially lytic area

Permeative = poorly defined margins; abnormal lytic bone merged throughout bone

Patho Summer Test #1 (8 decks)

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