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Musculoskeletal/Rheum > Acquired Bone Diseases > Flashcards

Acquired Bone Diseases Flashcards

1
Q

What is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue leading to enhanced bone fragility and a consequent increase in fracture risk?

A

Osteoporosis

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2
Q

What type of physical activity best stimulates bone remodeling?

A

Resistance exercises (load magnitude influences bone density more than the number of load cycles)

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3
Q

How are menopause and osteoporosis connected?

A

Decreased estrogen appears to increase secretion of inflammatory cytokines such as TNF-alpha, IL-1 and IL-6, which stimulate osteoclast recruitment and activity by increasing the levels of RANKL, diminishing the expression of OPG, decreasing osteoclast proliferation and preventing osteoclast apoptosis.

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4
Q

What is the histological hallmark of osteoporosis?

A

bone that is histologically normal, but decreased in quantity

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5
Q

At what DEXA scan score can you diagnose osteoporosis?

A

T-score of −2.5 or lower

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6
Q

How do biphosphates treat osteoporosis?

A

decrease bone resorption by retarding dissolution of hydroxyapatite crystals, decrease osteoclast formation, increase osteoclast apoptosis and module crosstalk from osteoblasts

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7
Q

What are adverse effects of biphosphates?

A

osteonecrosis of the jaw and atypical subtrochanteric femoral fractures

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8
Q

What are the adverse effects of estrogen receptor modulators (raloxifene and basedoxifene)?

A

venous thromboembolism and stroke

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9
Q

What are adverse effects of estrogen replacement?

A

myocardial infarction and cerebral infarction as a complication of atherosclerosis (due to thrombosis); promotion of carcinomas

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10
Q

What drug is a human monoclonal antibody that inhibits RANKL?

A

Denosumab

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11
Q

How does denosumab work?

A

inhibits the RANKL to inhibit osteoclast formation, function, and survival

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12
Q

Administration of PTH in women will help reduce the risk of what fractures?

A

vertebral fractures (but NOT hip fractures)

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13
Q

What is cathepsin K?

A

lysosomal cysteine protease with high collagenase activity expressed predominantly in osteoclasts

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14
Q

What drug is directed against cathepsin K?

A

odanacatib

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15
Q

What affect does odanacatib have on osteoclasts?

A

suppress osteoclast function without impairing osteoclast viability and thus maintain bone formation by preserving the osteoclast-osteoblast crosstalk

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16
Q

What is a simple, complete fracture?

A

full thickness

not displaced

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17
Q

What is a simple, incomplete fracture?

A

NOT full thickness

NOT displaced

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18
Q

What is a closed fracture?

A

fracture with intact overlying skin

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19
Q

What is an open fracture?

A

fracture with broken skin over broken bone

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20
Q

What is a compound fracture?

A

displacement with penetration of the skin surface, a broken bone compounded by a break in the overlying skin

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21
Q

What is a comminuted fracture?

A

complex fracture, with multiple fragments of bone

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22
Q

What is a stress fracture?

A

slowly developing fracture that follows a period of increased physical activity in which the bone is subjected to repetitive loads

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23
Q

What is a “greenstick” fracture?

A

fracture of a long bone extends only partially through the shaft, is common in infants when bones are soft and heals rapidly

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24
Q

What is a “pathologic” fracture?

A

fracture due to intrinsic disease of the bone, from a force that would not have broken a normal bone

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25
Q

What is the role of the hematoma in fracture healing?

A

seals off the fracture site, provides a fibrin mesh, and creates a framework for the influx of inflammatory cells and ingrowth of fibroblasts and new capillaries

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26
Q

What is the funciton of the procallus?

A

provides some anchorage between the ends of the fractured bones, but not structural rigidity sufficient for weight bearing

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27
Q

How long does it take the soft tissue callus to become the bony callus?

A

two weeks

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28
Q

When does the bony callus reach its maximal girth?

A

end of the 2nd or third week

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29
Q

How does the bony callus form?

A

Cartilage is formed along the fracture line and undergoes endochondral ossification, forming a contiguous network of bone with newly deposited bone trabeculae in the medulla and beneath the periosteum

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30
Q

What is the name of the pathological form of bone healing, which occurs when the ends of fractured bones are not closely enough aligned with each other to form callus and to continue the remodeling process to make a perfectly healed bone?

A

Fibrous nonunion

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31
Q

What happens with fibrous nonunion?

A

Fibrous replacement of tissue between the two ends that undergoes cystic degeneration and the bone becomes lined by synovial like cells that create a false joint

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32
Q

What is the most important cause of delayed, distorted or aborted bone fracture healing?

A

Infection (especially common in open fractures)

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33
Q

Most cases of bone infarcts are due to what?

A

fractures or corticosteroid therapy

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34
Q

Medullary infarcts involve what part of bone?

A

trabecular bone and marrow, usually sparing cortex because it has collateral blood flow

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35
Q

What part of bone is involved with subchondral infarcts?

A

triangular or wedge-shaped segment of tissue that has the subchondral bone plate as its base undergoes necrosis.

36
Q

Why is overlying cartilage not affected by subchondral infarcts?

A

it can get nutrients from synovial fluid

37
Q

What is creeping substitution?

A

In the healing response, osteoclasts resorb necrotic trabeculae. Trabeculae that remain act as scaffolding for the deposition of new bone.

38
Q

What type of bone infarct undergoes creeping substitution?

A

medullary infarcts (too slow for subchondral infarcts)

39
Q

What surgery is highly related to osteonecrosis complications?

A

joint replacement

40
Q

Where is spongy bone most commonly infarcted?

A

near the convex surfaces of joints

41
Q

Why is infarction and necrosis of a bone shaft more difficult?

A

it has collateral circulation

42
Q

Osteonecrosis of what location is a complication of sickle cell disease or glucocorticoid use?

A

femoral head (called avascular necrosis)

43
Q

Why are adverse skeletal events the most common glucocorticoid-related complication associated with successful litigation?

A

Patients are rarely warned about the common skeletal side effects of steroid therapy (fractures in up to 50% of chronic users and osteonecrosis in up to 40%)

44
Q

What is the major cause of osteomyelitis?

A

pyogenic bacterial infection (ex. staph aureus)

45
Q

What is osteomyelitis?

A

inflammation of bone and marrow

46
Q

How do infectious organisms reach the bone in osteomyelitis?

A

(1) hematogenous spread
(2) extension from a contiguous site
(3) direct implantation

47
Q

What type of osteomyelitis occurs in children? Where?

A

osteomyelitis is hematogenous and develops in long bones, typically in the metaphysis

48
Q

Why does osteomyelitis occur in adults?

A

occurs as a complication of open fractures, surgical procedures or diabetic infections of the feet

49
Q

Waht are risk factors for osteomyelitis?

A

presence of foreign material from orthopedic surgery, peripheral vascular disease, sickle cell disease and congenital phagocyte function defects

50
Q

How does staph aureus bind to bone?

A

express cell wall proteins that bind to bone matrix components such as collagen, which facilitates adherence of the bacteria to bone

51
Q

Where does osteomyelitic occur in adults? Why is this different from children?

A

epiphyses and subchondral regions (because growth plate is closed and the metaphyseal blood vessels reunite with epiphyseal counterparts)

52
Q

What occurs in the acute phase of osteomyelitis?

A

bacteria proliferate and induce a neutrophilic inflammatory reaction.

53
Q

How long does it take bone cells and marrow to become necrotic in osteomyelitis?

A

Necrosis of bone cells and marrow ensues within the first 48 hours after bacterial proliferation

54
Q

What complication of osteomyelitis may be seen in children due to their loosely attached periosteum?

A

Subperiosteal abscesses may form that can dissect for long distances along the bone surface

55
Q

What is dead bone called?

A

a sequestrum

56
Q

What occurrence in osteomyelitis leads to a soft tissue abscess which can channel to the skin as a draining sinus?

A

rupture of the periosteum

57
Q

What complication of osteomyelitis is seen in infants due to epiphyseal infection spreading along the articular surface or along tendons into a joint?

A

septic or suppurative arthritis

58
Q

During the healing process of osteomyelitis, what is the term for the newly deposited bone that forms a “shell of living tissue” around the necrotic bone?

A

involucrum

59
Q

What is a small intraosseous abscess that frequently involves the cortex and is walled off by reactive bone?

A

Brodie abscess

60
Q

What morphological variant of osteomyelitis typically develops in the jaw and is associated with extensive new bone formation that obscures much of the underlying osseous structure?

A

Sclerosing osteomyleitis of Garré

61
Q

What type of infection is produced by the organisms that cause osteomyelitis? What are the major cell types in the infection?

A

continuously suppurative infection with a predominance of neutrophils throughout the time course

62
Q

What is the characteristic radiologic finding of osteomyelitis?

A

lytic focus of bone destruction surrounded by a zone of sclerosis

63
Q

How do you treat osteomyelitis?

A

antibiotics and surgical drainage is usually curative

64
Q

Mycobacterial osteomyelitis is a rare complication of what disease?

A

Tuberculosis

65
Q

What part of the body is typically involved with mycobacterial osteomyelitis?

A

spine (40%)

66
Q

What is another name for Tb spondylitis?

A

Pott Disease

67
Q

What are the complications of Pott Disease?

A

permanent compression fractures that produce scoliosis or kyphosis and neurologic deficits secondary to spinal cord and nerve compression

68
Q

What is the most common mutation in Paget Disease of Bone?

A

mutations in the SQSTM1 gene

69
Q

What do the mutations in the SQSTM1 gene do?

A

increase the activity of NF-kB, which increases osteoclast activity

70
Q

What is Paget Disease of bone?

A

a disorder of unbalanced and excessive osteoclast and osteoblast function leading to increased bone turnover and increased, but disordered and structurally unsound bone mass

71
Q

What mutations can be seen in some juvenile cases of Paget Disease of Bone?

A

Activating mutations in RANK and inactivating mutations in OPG

72
Q

What may also (other than genetics) play a role in Paget Disease of Bone?

A

Chronic infection of osteoclast precursors by measles or other RNA viruses

73
Q

What are the three phases of Paget Disease of Bone?

A

(1) an initial osteolytic stage, (2) a mixed osteoclastic-osteoblastic stage, which ends with a predominance of osteoblastic activity and evolves ultimately into (3) a final burned-out quiescent osteosclerotic stage

74
Q

What causes osteomalacia and rickets?

A

vitamin D deficiency or its abnormal metabolism

75
Q

What is the fundamental defect in osteomalacia/rickets?

A

impairment of mineralization and a resultant accumulation of unmineralized matrix

76
Q

What is the difference between Rickets and Osteomalacia?

A

Rickets refers to the disorder in children, in whom it interferes with the deposition of bone in the growth plates. Adults get osteomalacia which predisposes them to fractures.

77
Q

What does PTH do to bone?

A

activates osteoclasts, increasing bone resorption and calcium mobilization

78
Q

Does PTH directly act on osteoclasts?

A

NO- mediates these effects indirectly by increased RANKL expression on osteoblasts

79
Q

What does PTH do to the kidney/gut?

A

increased resorption of calcium by the renal tubules, increased urinary excretion of phosphates and increased synthesis of active vitamin D by the kidneys, which in turn enhances calcium absorption from the gut

80
Q

What diseases can occur due to symptomatic, untreated primary hyperparathyroidism?

A

osteoporosis, brown tumors and osteitis fibrosa cystica

81
Q

Where is osteoporosis due to hyperparathyroidism most generalized?

A

phalanges, vertebrae and proximal femur

82
Q

What is it called when osteoclasts tunnel into and dissect centrally along the length of the trabeculae, creating the appearance of railroad tracks?

A

dissecting osteitis (occurs in hyperparathyroidism)

83
Q

What happens to the marrow space in dissecting osteitis?

A

replaced by fibrovascular tissue

84
Q

What occurs as a result of microfractures and secondary hemorrhages associated with dissecting osteitis?

A

brown tumor

85
Q

What is osteitis fibrosa cystica?

A

combination of increased bone cell activity, peritrabecular fibrosis, and cystic brown tumors

86
Q

What is the bone disease due to secondary hyperparathyroidism in patients with renal failure?

A

Renal osteodystrophy

87
Q

Why does osteodystrophy occur in chronic renal failure?

A

inadequate synthesis of active vitamin D, which ultimately affects gastrointestinal calcium absorption

Musculoskeletal/Rheum (12 decks)

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