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NMSP Exam II > Bones, Joints & Soft Tissues (Martin) > Flashcards

Bones, Joints & Soft Tissues (Martin) Flashcards

1
Q

What type of ossification occurs in long bones?

A

Endochondral ossification; cartilage mold; new bone deposits are deposited at the bottom of growth plates leading to longitudinal growth

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2
Q

What type of ossification occurs in flat bones?

A

Intramembranous ossification; mesenchyme directly ossified by osteoblast; NO CARTILAGE; appositional growth

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3
Q

Osteomalacia

A

weakened, soft bone

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4
Q

Osteitis deformans

A

deforming bone-itis

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5
Q

Osteodystophy

A

difficult/bad growing bone

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6
Q

What is the most common type of collagen in osteoid?

A

type I collagen

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7
Q
A

Woven bone; increased cells and disorganized; produced rapidly (fetal development and repair); haphazard arrangement with less structural integrity; abnormal in adults

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8
Q
A

Lamellar bone; parallel collagen and strong; slow production; adult bone

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9
Q

In which decade of life do you tend to have more resorption of bone than formation?

A

fourth decade; see a decrease in skeletal mass

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10
Q

RANKL and OPG are expressed and produced by which cells?

A

Osteoblasts

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11
Q

Explain the pathophysiology of RANK?

A

receptor on osteoclast that activates NF-kB which promotes their survival and increases bone breakdown

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12
Q

Osteoprogenitor cells (osteocytes) produce which protein that triggers activation and production of OPG?

A

WNT proteins; they bind LRP5 and LRP6 on osteoblasts activates B-catenin and produces OPG; favors bone deposition/formation

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13
Q

Sclerostin

A

produced by osteoclasts; inhibits WNT/B-catenin; suppressing bone formation

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14
Q

What three hormones are important in bone formation?

A

estrogen, testosterone and Vit. D

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15
Q

What is the role of estrogen, testosterone and Vit. D in bone physiology?

A

they all favor bone formation

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16
Q

The role of M-CSF in bone homeostasis and remodeling?

A

M-CSF receptor on osteoclast that stimulates tyrosine kinase cascade; crucial for osteoclast generation

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17
Q

Dysostosis

A

localized disruption of migration and condensation of mesenchyme and differentiation into cartilage anlage

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18
Q

Supernumerary digit

A

extra bones or digits

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19
Q

Syndactyly or craniosynostosis

A

abnormal fusion of bones

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20
Q

What homeobox protein mutation is commonly associated with short terminal phalanges and a big toe?

A

HOXD13 mutation; brachydactyly

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21
Q

Achondroplasia

A

dwarfism; AD FGFR3 GOF mutation; short proximal extremities with normal trunk length, enlarged head and bulging forehead; NO change in longevity, intelligence or reproductive status

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22
Q

Thanatophoric dysplasia

A

most common death form of dwarfism; FGFR3 GOF mut (more severe phenotype); small chest cavity (respiratory insufficiency); die at birth or soon after

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23
Q

Osteogenesis Imperfecta involves which type of collagen?

A

Type I

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24
Q

Brittle bone disease

A

Osteogenesis imperfecta; deficiency in type I collagen will see BITE signs and symptoms; type I normal lifespan; type 2 most severe (die in utero); type 3 severe (if survive utero) and type 4 is mild

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25
Q

Osteogenesis imperfecta

A

brittle bone disease; deficiency in type I collagen; BITE signs and symptoms; accordion-like shortening of limbs
type I - COL1A1 mut
type II COL1A1 or COL1A2 mut (most severe) - respiratory problems (undeveloped lungs)

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26
Q

Treatment for osteogenesis imperfecta?

A

Surgical “rodding” of long bones; exercise and good nutrition; no smoking or steroid use

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27
Q

Pathology in osteopetrosis

A

decrease in bone resorption due to deficient osteoclast function causing diffuse, symmetric skeletal sclerosis

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28
Q

What is the mutation in achondroplasia?

A

Gain of function FGFR3 mutation

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29
Q

Defect in type II osteogenesis imperfecta?

A

there is no triple helix of collagen type I; uniformly fatal in utero (multiple intrauterine fractures)

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30
Q

Defect in type I osteogenesis imperfecta?

A

the collagen structure is normal, there is just less of it; these patients have a normal lifespan with most fractures occurring BEFORE puberty

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31
Q

What are the two types of osteopetrosis?

A

“marble bone disease”
1. Alber-Schonberg disease
2. Carbonic Anhydrase 2 deficiency

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32
Q

Alber-Schonberg disease

A

an AD osteopetrosis “marble bone disease”; mut in CLCN7 which encodes for a proton-chloride exchanger in osteoclast; decreased bone resorption leading to diffuse symmetrical skeletal sclerosis

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33
Q

What is the mutation in Alber-Schonberg disease?

A

mut in CLCN7 which encodes for a proton-chloride exchanger in osteoclast; decreased bone resorption leading to diffuse symmetrical skeletal sclerosis; an AD osteopetrosis “marble bone disease”

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34
Q

What is the typical clinical prevention of a patient with osteopetrosis?

A

diffuse symmetrical skeletal sclerosis; bones lack a medullary cavity and can present as an Erlenmeyer flask on imaging

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35
Q

Carbonic Anhydrase 2 deficiency

A

an AR osteopetrosis “marble bone disease”; lack CA2 that is needed for osteoclastic activity and renal tubular cells (renal tubular acidosis); decreased bone resorption leading to diffuse symmetrical skeletal sclerosis

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36
Q

What is a symptom that is seen in Carbonic Anhydrase 2 deficiency and NOT in Alber-Schonberg disease?

A

renal tubular acidosis because renal tubular cells also depend on CA2; both are osteopetrosis disorders

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37
Q

Why do you see repeated infections in osteopetrosis?

A

the bones lack a medullary cavity; there is no hematopoiesis = no immune cells (leukopenia); will see extra medullary hematopoiesis involving the spleen (hepatosplenomegaly)

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38
Q
A

Erlenmeyer flask on imaging as seen in osteopetrosis

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39
Q

Osteoporosis

A

severe osteopenia (below 2.5 SD mean peak bone mass); most common forms are senile and postmenopausal

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40
Q

What are the two most common forms of osteoporosis?

A
  1. senile - age related with low turnover (decreased activity of osteoblasts)
  2. postmenopausal - estrogen deficiency (increased osteoclast activity)
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41
Q

What are the 5 factors affecting bone mass in osteoporosis?

A
  1. Age - senile, decreased proliferation (low turnover)
  2. decreased physical activity - immobility, paralysis, astronauts in zero gravity
  3. genetics - LRP5 gene defect (rare)
  4. insufficient ca2+ intake (adolescent girls)
  5. Hormonal - post menopausal (estrogen deficiency)
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42
Q

Tamoxifen

A

treatment for breast cancer that can increase bone loss (drug induced osteoporosis)

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43
Q

Senile osteoporosis

A

age related with low turnover (decreased activity of osteoblasts); cortex is thinned by subperiosteal and endosteal resorption

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44
Q

Post menopausal osteoporosis

A

estrogen deficiency (increased osteoclast activity); the trabeculae is thinned which increases the risk for micro fractures and vertebral collapse

45
Q
A

Osteoporotic vertebral body; loss of horizontal trabecular (post menopausal osteoporosis)

46
Q

How does osteoporosis affect the axial spine?

A

lumbar lordosis and kyphoscoliosis

47
Q

Risk factors for osteoporosis?

A

Caucasian, too much phosphorus in diet (sodas) and smoking

48
Q

How do you diagnosis osteoporosis?

A

using a bone mineral density test (DEXA-scan)

49
Q

(DEXA-scan)

A

bone mineral density test used to diagnose osteoporosis

50
Q

Pathophysiology of Rickets?

A

impairment of mineralization of bone due to a Vit. D deficiency in kids; interferes with deposition of bone in the growth plate

51
Q

Clinical presentation of Rickets?

A

frontal bossing, rachitic rosary of ribs, pigeon chest and bowed legs

52
Q

Untreated primary hyperparathyroidism leads to what 3 skeletal abnormalities?

A
  1. osteoporosis - dissecting osteitis “railroad tracks”
  2. Brown tumor - vascular, hemorrhage and hemosiderin deposition leading to cystic degeneration
  3. von Recklinghausen disease of bone - generalized osteitis fibrosis cystica
53
Q
A

“railroad tracks” appearance of trabecular seen in osteoporosis - dissecting osteitis caused by untreated hyperparathyroidism

54
Q
A

a brown tumor; vascular, hemorrhage and hemosiderin deposition leading to cystic degeneration caused by untreated hyperparathyroidism

55
Q

Paget Disease

A

aka Osteitis Deformans; an acquired bone disorder **axial skeleton and femur; can be associated with SQSTM1 gene mut that increases osteoclastic activity; “cotton wool” appearance; hallmark: mosaic pattern of lamellar bone - jigsaw-like appearance; bone growth compressed spinal and cranial nerves

56
Q

Sporadic cases of Paget Disease are associated with what mutation?

A

SQSTM1 gene mut that increases osteoclastic activity

57
Q

What bone disorder has a hallmark appearance of “mosaic pattern of lamellar bone”?

A

Paget Disease aka Osteitis Deformans; an acquired bone disorder

58
Q
A

“cotton wool” appearance on imaging; seen in Paget Disease aka Osteitis Deformans; an acquired bone disorder

59
Q

Labs and Treatment for Paget Disease?

A

increased alk phosphatase with NORMAL calcium AND phosphorus

TX: calcitonin and bisphosphonates

60
Q

Hypervascularity in Paget Disease can lead to what potential fatal complication?

A

high-output heart failure

61
Q
A

jigsaw puzzle-like pieces of lamellar bone seen in Paget Disease

62
Q

“Greenstick” fracture?

A

a fracture extending only partially through the bone, common in infants when bones are soft

63
Q

Stress fracture

A

slowly developing fracture that follows a period of increased physical activity (repetitive loads)

64
Q

Comminuted fracture

A

bone is fragmented

65
Q

Displaced fracture

A

ends of the bone at the fracture site are not aligned

66
Q

a simpe vs a compound fracture

A

simple - overlying skin is intact
compound - bones shows through overlying skin

67
Q

During the healing phase of bones; what changes would you observe at the end of the first week?

A

soft tissue callus or procallus; not structural rigidity for weight bearing

68
Q

During the healing phase of bones; what changes would you observe at the end of the second week?

A

soft callus transformed into bony callus

69
Q

Avascular necrosis (AVN)

A

infarction of the bone and marrow; most commonly caused by fractures or corticosteroids; the cortex is not usually involved due to collateral blood flow; subchondral infarcts are triangular or wedged shaped; can see “creeping substitution”

70
Q
A

wedge-shaped osteonecrosis; most commonly caused by fractures or corticosteroids

71
Q

What is the most common organism involved in pyogenic osteomyelitis?

A

staph aureus (80-90%)

72
Q

Sequestrum

A

dead bone following subperiosteal abscess; seen in acute osteomyelitis

73
Q

Involucrum

A

newly deposited bone that forms a shell of living tissue around devitalized bone; seen in chronic osteomyelitis

74
Q

Brodie abscess

A

small interosseous abscess that is walled off by reactive bone; seen in chronic osteomyelitis

75
Q

Pott’s disease

A

Tuberculous spondylitis involving the spine; can see loss of vertebral bodies on imaging; can cause permanent compression fractures leading to scoliosis or kyphosis

76
Q

Bone pathology that has clinical presentation of “saber shin” and/or “saddle nose”

A

skeletal syphilis

77
Q

What are the bone-forming tumors?

A

Osteoid osteoma - benign painful, worse at night, responds to NSAIDs, <2cm
Osteoid blastoma - benign, >2cm and does NOT respond to NSAIDs
Osteosarcoma - malignant painful enlarging mass

78
Q

Osteosarcoma

A

most common malignant tumor of bone; painful enlarging mass; check for prior radiation; 50% involves knee; x ray will show mixed lytic and blastic mass and “Codman triangle”

79
Q

X ray finding of a Codman triangle should make you suspect what bone pathology?

A

osteosarcoma; elevation of periosteum after bone breaks through cortex

80
Q

What is a major risk factor for osteosarcoma?

A

prior radiation

81
Q

70% of sporadic osteosarcoma cases involves a mutation to which gene?

A

RB gene mutation

82
Q

Osteosarcoma can lead to what other bone pathology?

A

chondroblastic osteosarcoma (if abundant cartilage is present)

83
Q

Osteosarcoma tends to spread to which organs?

A

lungs, bone and brain

84
Q
A

Codman triangle seen in osteosarcoma; elevation of periosteum after bone breaks through cortex

85
Q

What is the most common benign bone tumor?

A

ostechondroma; 85% are solitary and occur during early adulthood; a subtype - multiple hereditary exostosis which is AD can progress to a chondrosarcoma (malignant)

86
Q

What type of bone tumor can progress to a chondrosarcoma?

A

multiple hereditary exostosis which is AD and 3X more likely in men

87
Q

ostechondroma

A

benign bone tumor attached to skelton by a bony stalk capped by cartilage (bony mushroom appearance); can be painful if impinges on a nerve

88
Q
A

benign bone tumor attached to skelton by a bony stalk capped by cartilage (bony mushroom appearance); osteochondroma

89
Q
A

a well circumcised nodule of hyaline cartilage containing benign chondrocytes as seen in endochondroma (benign hyaline cartilage tumor)

90
Q

Chondrosarcoma

A

second most common malignant bone tumor; onset in 40s yrs; commonly involves the shoulders; painful enlarging mass and can spread hematogenously to the **lungs; on imaging - flocculent densities

91
Q

“flocculent densities” on imaging?

A

Chondrosarcoma - calcified matrix appears as foci of flocculent densities

92
Q
A

Chondrosarcoma - calcified matrix appears as foci of flocculent densities

93
Q
A

Chondrosarcoma - calcified matrix appears as foci of flocculent densities

94
Q

Ewing sarcoma family tumors (ESFT)

A

bone tumor of unknown origin; predilection for Whites; “small blue round cell tumor” that is painful and frequently tender, warm and swollen; has onion-skin appearance on x-ray; affects long bones *femur; balanced translocation of EWSR1 gene

95
Q

Ewing sarcoma family tumors (ESFT) typically affects which bones?

A

long bones *femur

96
Q

What is typical appearance on x-ray of someone with a Ewing sarcoma family tumors (ESFT)?

A

onion-skin appearance on x-ray

97
Q

Mutation involved with Ewing sarcoma family tumors (ESFT)?

A

balanced translocation of EWSR1 gene on chromosome 22; fusion of EWS-FL11

98
Q

What is an important prognostic finding in Ewing sarcoma family tumors (ESFT)?

A

the amount of chemotherapy-induced necrosis - the more necrosis, the better because it is indicative of sensitivity to the treatment

99
Q

What is the mutation in fibrous dysplasia?

A

somatic gain of function in GNAS1

100
Q

What is the inherited genetic susceptibility in Rheumatoid arthritis (RA)?

A

HLA-DR4

101
Q

hand deformities involved in Rheumatoid arthritis (RA)?

A

Boutonniere
Swan-neck
Ulnar deviation of fingers
radial deviation of wrist

102
Q

Rheumatoid nodules typically grows where?

A

on the extensor surfaces at pressure points (forearm, elbows, occiput and lumbosacral area)

103
Q

Characteristic of Rheumatoid nodules?

A

firm, nontender and round to oval; resemble necrotizing granulomas with a central zone of fibrinoid necrosis microscopically

104
Q

OA vs RA

A

OA - disease of cartilage, “wear and tear”, large joints, heberdens and Bouchard nodes, no systemic effects or morning stiffness and worse with activity and better with rest

RA - disease of synovium, autoimmune, inflammatory, swan-neck and ulnar deviation deformities, systemic effects and morning stiffness, worse with rest and better with activity

105
Q

Characteristics of OA?

A

disease of cartilage, “wear and tear”, large joints, heberdens and Bouchard nodes, no systemic effects or morning stiffness and worse with activity and better with rest

106
Q

Characteristics of RA?

A

disease of synovium, autoimmune, inflammatory, swan-neck and ulnar deviation deformities, systemic effects and morning stiffness, worse with rest and better with activity

107
Q

Gout

A

build up of crystallization of monosodium rate (MSU) due to hyperuricemia (>6.8 mg/dl); heavy alcohol consumption and obesity are risk factors

108
Q

Pseudogout

A

build up of calcium pyrophosphate crystals; chondrocalcinosis; AD ANKH mutation; crystals form chalky, white friable deposits; they are rhomboid and positively birefringent

109
Q

Liposarcoma

A

adipose malignancy; contain immature adipocytes = lipoblasts (irregular nuclei)

NMSP Exam II (12 decks)

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