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NMSP Exam 2 > Bone Path > Flashcards

Bone Path Flashcards

1
Q

what are the components of the bone matrix?

A

osteoid
type 1 collagen
osteopontin
hydroxyapatite

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2
Q

woven bone

A

produced rapidly during fetal development and fracture repair

disorganized collagen structure

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3
Q

lamellar bone

A

slow production of stronger collagen structure

overtakes woven bone

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4
Q

osteoblasts

A

regulates mineralization

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5
Q

osteocytes

A

inactive osteoblasts

control calcium and phosphate levels

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6
Q

osteoclasts

A

multinucleated macrophages

bone resorption

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7
Q

what type of bones undergo endochondral ossification?

A

long bones

deposition of new bone at bottom of growth plates with longitudinal growth

bone growth

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8
Q

what type of bones undergo intramembranous ossification?

A

flat bones

deposition of new bone on the preexisting surface with appositional growth

bone remodeling

under control of hormones and growth factors

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9
Q

when is peak bone mass achieved?

A

in early adulthood after cessation of skeletal growth

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10
Q

when does bone resorption overtake bone formation?

A

fourth decade of life

decrease skeletal mass

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11
Q

what signaling pathways play a key role in homeostasis and remodeling of bones?

A

RANK, RANKL and OPG
WNT/B-catenin
M-CSF
Paracrine

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12
Q

what is the RANK?

A

receptor activator for NF-kB on osteoclast precursor

when stimulated by RANK-L, activates NF-kB for bone breakdown

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13
Q

where is RANK-L expressed?

A

osteoblasts and marrow stromal cells

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14
Q

what is OPG?

A

osteoprotegerin “decoy” receptor made by osteoblasts

can bind RANK-L and prevent interaction with RANK

bone building

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15
Q

what is the WNT/B-catenin pathway?

A

WNT proteins bind to LRP5 and LRP6 receptors on osteoblasts

trigger activation of B-catenin and OPG production

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16
Q

what inhibits the WNT pathway?

A

sclerostin produced by osteocytes

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17
Q

which factors stimulate bone growth?

A

estrogen
testosterone
vit D

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18
Q

what factors stimulate bone breakdown?

A

PTH
IL-1
glucocorticoids

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19
Q

what role does M-CSF play in bone homeostasis?

A

M-CSF receptor on osteoclast precursor stimulate tyrosine kinase cascade

results in generation of osteoclasts

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20
Q

describe the paracrine activity between osteoclasts and osteoblasts

A

breakdown of matrix by osteoclasts activates matrix proteins, GFs, cytokines and enzymes that activate osteoblasts

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21
Q

list the types of collagen and their location (boards only)

A 
1 - bones and scaring
2 - cartilage
3 - skin, vessels, and granulation tissue
4 - basement membrane
5 - ligaments and lungs
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22
Q

generally describe dysostosis disorders

A

abnormal migration and condensation of mesenchyme and differentiation in cartilage

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23
Q

what factors lead to dysostosis?

A

transcription factor defects: homeobox or cytokines

syndromic

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24
Q

what defects are classified as dysostosis?

A

aplasia
supernumerary digit
syndactyly
craniosynostosis

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25
Q

generally describe dysplasia disorders

A

global disorganization of bone and/or cartilage caused by mutations in genes controlling development or remodeling

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26
Q

what is brachydactyly and what protein mutation is associated with it?

A

short terminal phalanges of thumb and big toe

HOXD13

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27
Q

what is cleidocranial dysplasia?

A

AD RUNX2 mutation leading to:
delayed closure of cranial sutures - patent fontanelles
wormian bones - additional bones within sutures
delayed eruption of secondary teeth
primitive clavicle
short height

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28
Q

what is achondroplasia?

A

AD mutation causing FGFR3 GoF

abnormal cartilage growth resulting in:
short proximal extremities
normal trunk length
enlarged head
bulging forehead
depression root of the nose

*most common form of dwarfism

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29
Q

what is thanatophoric dysplasia?

A

lethal form of dwarfism

micromelic shortening of limbs
frontal bossing
macrocephaly
small chest cavity
bell-shaped abdomen
die soon after birth
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30
Q

what factors result in abnormal bone density?

A

LPR5 receptor defect - osteoporosis or osteopetrosis

RANK-L mutation

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31
Q

what is osteogenesis imperfecta?

*BOARDS

A

mutation in a1 and a2 chains of type 1 collagen

most common inherited disorder of connective tissue

4 subtypes

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32
Q

type 1 OI

A

AD inheritance

decreased synthesis of a1 chain + abnormal a1 or a2 chain

normal collagen structure but decreased amount

best prognosis!

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33
Q

what is the clinical presentation of type 1 OI?

A 
fractures before puberty
blue sclera
skeletal fragility
abnormal dentition
hearing impairment
joint laxity
triangular face
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34
Q

type 2 OI

A

AR or AD

abnormally short a1 chain + abnormal or insufficient a2 chain

lethal in utero or shortly after birth due to respiratory problems

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35
Q

OI treatment

A

surgical “rodding” of long bones

exercise, maintain healthy weight and nutrition

no smoking

no steroids

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36
Q

what differential dx is often seen with OI?

A

child abuse! types of fractures are similar to those in OI

fractures in multiple stages of healing
rib fractures
spiral fractures
no explanation of trauma

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37
Q

what is osteopetrosis?

A

marble bone disease/albers-schonberg disease

mutation in CLCN2 encoding proton pumps on osteoclasts resulting in carbonic anhydrase 2 deficiency

reduced bone resorption

acidification results in solubilized hydroxyapatite

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38
Q

what are the morphologic findings in osteopetrosis?

A

lack of medullary cavity
bulbous ends of long bones (Erlenmeyer flask)
neural foramina are small and compress nerves

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39
Q

describe the infantile form of osteopetrosis

A

SEVERE
AR
mediterranian or arab descent

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40
Q

what is the clinical presentation of infantile osteopetrosis?

A 
optic atrophy
deafness
facial paralysis
fractures
anemia
hydrocephaly
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41
Q

describe the adolescent form of osteopetrosis

A

MILD
AD
dx in adolescence or adulthood

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42
Q

what is the clinical presentation of adolescent osteopetrosis?

A

repeated fractures
mild cranial nerve deficits
anemia

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43
Q

describe mucopolysacchardoses

A

lysosomal storage diseases caused by a deficiency in acid hydrolase enzymes

mucopolysaccharides accumulate in chondrocytes causing structural defects in cartilage

44
Q

what is the clinical presentation of mucopolysaccharidoses?

A

short stature
chest wall abnormalities
malformed bones

45
Q

what is osteopenia?

A

decreased bone mass (1-2.5 SD below the mean)

precursor to osteoporosis

46
Q

what is osteoporosis?

A

osteopenia severe enough to increase risk of fracture

at least 2.5 SD below mean

47
Q

what fracture signifies osteoporosis?

A

atraumatic or vertebral compression fracture

48
Q

what factors contribute to osteoporosis?

A 
age
physical activity
genetics
nutrition
hormones
49
Q

describe how age contributes to osteoporosis

A

senile osteoporosis
decreased proliferative and biosynthetic potential
decreased cell response to growth factors

50
Q

describe how physical activity contributes to osteoporosis

A

mechanical forces stimulate bone remodeling
resistance exercises are best

decreased physical activity = decreased bone density

51
Q

what genetic factors contribute to osteoporosis?

A 
LRP5 
RANKL
OPG
RANK
HLA focus
estrogen receptor gene
vit D receptor gene
52
Q

describe how nutrition contributes to osteoporosis

A

insufficient calcium intake during the period of rapid growth restricts peak bone mass

*girls more affected than boys

53
Q

describe how hormones contribute to osteoporosis

A

post-menopausal estrogen deficiency results in decreased formation and resorption

also increases inflammatory cytokines which stimulate osteoclasts and increases RANKL

54
Q

what breast cancer treatment can increase bone loss?

A

Tamoxifen

55
Q

describe post-menopausal osteoporosis morphology

A

bone with an increased surface area
perforated thinned and lose interconnections
microfractures and vertebral collapse

56
Q

describe senile osteoporosis morphology

A

cortex thinned by subperiosteal and endosteal resorption

57
Q

who is predisposed to osteoporosis?

A

white women with light-colored hair and eyes

smokers

58
Q

how do you dx osteoporosis?

A

DEXA-scan - bone mineral density test

labs to r/o secondary causes

59
Q

what is the clinical presentation of osteoporosis?

A

thoracic and lumbar vertebral fractures
lumbar lordosis
kyphoscoliosis

60
Q

what is a possible complication of fractures in osteoporosis?

A

pneumonia

PE

61
Q

osteoporosis prevention

A

exercise
calcium
Vit D

62
Q

osteoporosis tx

A

bisphosphonates
hormone therapy
denosumab (anti-RANKL)

63
Q

what is Paget disease/osteitis deformans?

A

acquired disease of increased but disordered bone mass

either monostotic or polyostotic

64
Q

what is the most common form of Paget?

A

familial polyostotic

65
Q

what gene is associated with Paget?

A

SQSTM1

increased activity of NF-kB = increased osteoclast activity

66
Q

what is the morphological hallmark of Paget?

A

mosaic pattern of lamellar bone (sclerotic phase)

*jigsaw appearance with prominent cement lines

67
Q

describe the 3 phases of Paget

A
  1. lytic phase - large osteoclasts with 100 nuclei
  2. mixed phase - clasts + loss of blasts
  3. osteosclerotic phase - quiescent stage
68
Q

what is the clinical presentation of Paget?

A 
bowing of femurs and tibia
chalk-stick type fractures of long bones
spinal compression fractures
kyphosis
hypervascularity leading to CHF
69
Q

what would be seen in labs with Paget?

A

increased serum alk phos

normal calcium and phos

70
Q

Paget tx

A

calcitonin and bisphosphonates

71
Q

what is a possible outcome of bone transformation in Paget?

A

sarcomatous transformation into osteosarcoma or fibrosarcoma

72
Q

vit D deficiency in kids results in…

A

rickets

73
Q

vit D deficiency in adults results in…

A

osteomalacia

74
Q

what is the clinical presentation of rickets?

A 
frontal bossing
squared-off head
rachitic rosary of ribs 
pigeon breast deformity
lumbar lordosis
bowed legs
75
Q

how does hyperparathyroidism result in bone deformity?

A

PTH signals osteoclast activation to increase serum Ca

skeletal changes result from continued activation of PTH

76
Q

what 4 skeletal abnormalities are associated with untreated hyperparathyroidism?

A

osteoporosis
brown tumor
dissecting osteitis
von Recklinghausen disease

77
Q

what is dissecting osteitis?

A

clasts tunnel into and dissect centrally along the length of trabeculae creating the appearance of railroad tracks

78
Q

what is a brown tumor?

A

bone loss leads to microfractures

microfractures elicit influx of macrophages and fibrous tissue

creates a mass of reactive tissue

also called osteitis fibrosis cystica

79
Q

what is renal osteodystrophy?

A

skeletal changes associated with chronic renal disease

80
Q

what is the clinical presentation of renal osteodystrophy?

A

osteopenia/osteoporosis
osteomalacia
secondary hyperparathyroidism
growth retardation

81
Q

what are the 3 histologic subtypes of renal osteodystrophy?

A
  1. high turnover = resorption > formation
  2. low turnover = low activity overall
  3. mixed = areas with high and low turnover
82
Q

describe the pathogenesis of renal osteodystrophy

A

tubular dysfunction - hydroxyapatite dissolution
generalized renal failure - hyperphos, hypoCa
decreased production of secreted factors - low vit D

83
Q

what is known as the “silent crippler”?

A

renal osteodystrophy in kids

84
Q

describe the healing of bone fractures

A
  1. hematoma formation
  2. callus formation - woven bone + cartilage
  3. callus ossification - woven bone
  4. bone remodeling - lamellar bone
85
Q

what is osteonecrosis?

A

infarction of the bone and marrow secondary to vascular injury

most cases from fracture or corticosteroids

collateral flow preserves cortex

86
Q

describe subcondral infarcts

A

causes pain only with activity at first and then constant pain

collapse and may lead to secondary arthritis

triangular or wedge-shaped

87
Q

describe medullary infarcts

A

small, clinically silent infarcts that occur with Gaucher, dysbarism, and sickle cell anemia

involve trabecular bone and marrow

88
Q

what is “creeping substitution”?

A

after bone death, trabecular that remain intact serve as scaffolding for deposition of new bone

89
Q

what is osteomyelitis?

A

inflammation of the bone and marrow due to infection

usually a primary solitary focus but can be due to systemic infection

90
Q

describe pyogenic osteomyelitis

A

bacterial infection from hematogenous spread, extension from contiguous site or direct implantation

in kids due to mucosal injuries or minor skin infections

in adults due to open fractures, surgery, or diabetic infection

91
Q

what bacteria is the most common cause of osteomyelitis?

A

staph aureus

less common:
H. flu
Grp B strep

92
Q

if a culture comes back as mixed bacteria, what would you suspect as the cause of osteomyelitis?

A

surgery or open fracture

93
Q

sickle cell patients are predisposed to what bacterial infection?

A

salmonella

94
Q

what is sequestrum?

A

dead bone following subperiosteal abscess

becomes draining sinus

95
Q

what is involucrum?

A

newly deposited bone forms a shell of living tissue around the segment of dead bone

occurs in chronic osteomyeltitis

96
Q

what is a Brodie abscess?

A

chronic, small interosseous abscess that frequently involves the cortex and is walled off by reactive bone

97
Q

what is sclerosing osteomyelitis of Garre?

A

chronic jaw osteomyelitis associated with new bone formation that obscures the underlying osseous structure

98
Q

what is the clinical presentation of acute osteomyelitis?

A

malaise
fever/chills
leukocytosis
intense, throbbing pain over the affected region

99
Q

what will be seen on XR with acute osteomyelitis?

A

lytic focus of bone destruction surrounded by zone of sclerosis

100
Q

osteomyelitis tx

A

abx and surgical drainage

101
Q

what are some complications of chronic osteomyelitis?

A 
pathologic fracture
secondary amyloidosis
endocarditis
sepsis
SCC in draining sinus
sarcoma of infected bone
102
Q

what is mycobacterial osteomyelitis?

A

blood borne infection originating from a focus of active disease during early stages of infection

bone infection may persist for years before detected

histo: caseous necrosis and granulomas

103
Q

what is Pott disease?

A

tuberculous spondylitis

mycobacterial osteomyelitis of the spine

permanent compression fractures - scoliosis, kyphosis and neuro deficits

104
Q

what are complications associated with Pott disease?

A

tuberculous arthritis
sinus tract formation
psoas abscess
amyloidosis

105
Q

what skeletal abnormalities are associated with congenital syphilis?

A

saber shin - massive reactive periosteal bone deposition on medial and anterior surfaces of the tibia

106
Q

what skeletal abnormalities are associated with acquired syphilis?

A

saddle nose deformity

palate, skull and long bone deformities

NMSP Exam 2 (14 decks)

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