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D & T exam 2 > Bones 1 > Flashcards

Bones 1 Flashcards

1
Q

what are the 3 types of cell in bone ? how many nuclei? basic multicellular unit

A

osteoclasts ( multiple_
osteoblasts (single nucleus)
osteocytes

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2
Q

RANKL located on what cell

A

osteoblasts and marrow stroma cells

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3
Q

RANK is located on what cell? role?

A

osteoclast precursor

- allow OC generation and survival

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4
Q

explain the M-CSF pathway

A
  1. M-CSF secreted by OB

2. M-CSF binds to OC: generation and survival

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5
Q

explain the WNT/Beta-catenin pathway

A
  1. WNT from marrow stromal cell
  2. LRP5 and LRP6 OB receptor bind WNT protein
  3. OB secretes OPG ( blocks RANK)
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6
Q

bone compositition

A

calcium hydroxyapatite

organic matrix with type I collagen

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7
Q

what are the two types of bone? where are they found

A

woven bone: random collagen
lammellar bone: ordered collagen
compact bone
spongy bone

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8
Q

name two bone enzymes

A

osteopontin

alkaline phosphatase

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9
Q

role of osteopontin ( osteocalcin)

A

levels parallel osteblast activity

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10
Q

alkaline phosphatase comes from what organ

A

osteoblasts

liver and placenta

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11
Q

woven bone?
how fast does it grow?
forces?

A

rapid bone growth
resists forces in all directions
pathologic in adults

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12
Q

lamellar bone replaces what

A

woven bone

stronger than woven bone

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13
Q

what process forms bone?

A

intramembranous ossification

  • direct from mesenchyme
  • appositional growth
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14
Q

location of epiphysis

A

distal to growth plate

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15
Q

location of metaphysis

A

beneath growth plate

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16
Q

location of diaphysis

A

center

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17
Q

Dysostosis

A

local problems in migration of mesenchyme and their condensation

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18
Q

dysplasia

A

global defect in regulation of skeletal organogenesis

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19
Q

Cleidocarnial dysplasia

  • inherited
  • defect protein
A

autosomal dominant

-RUNX2 (CBFA1)

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20
Q

clincial presentation for Cleidocranial dysplasia

A

short
abnormal clavicle
supernumery theeth
wormian bone ( extra sutural bone)

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21
Q

what goes wrong in achondroplasia

A
  • growth plate defect from paracrine cell defect

- reduced chondrocyte proliferation in growth plate

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22
Q

achondroplasia is a defect in what gene? what does it cause

A

FGFR3 point mutation

-inhibits cartilage growth

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23
Q

how is achondroplasia passed on to generations

A

paternal allele

autosomal dominant

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24
Q

what growth is still present for achondroplasia? what does this cause

A

appositional and intramembranous bone formation

-thick cortical bone

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25
Q

clinically what does achondroplasia look like

A 
short proximal limbs
normal turnk 
enlarged head 
depression of root nose 
normal reproductive and intelligence
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26
Q

what is the most common lethal dwarfism

A

Thanatophoric dwarfism

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27
Q

thanatrophoric dwarfism is a mutation in what

A

FGFR3

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28
Q

clinical presentation of thanatophoric dwarfism

A

cloverleaf leaf

bell-shaped abdomen

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29
Q

LRP5 is a receptor that activates what

A

WNT/beta-catenin in OB

- produces OPG (Blocks RANKL)

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30
Q

what disease has an inactive LRP5

A

osteoporosis pseudoglioma syndrome

  • skeletal fragility
  • loss of vision
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31
Q

Marble bone disease

A

osteopetrosis

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32
Q

what goes wrong in osteopetrosis

A

reduced osteoclast bone resorption
- cannot acidify pit
- defect in RANKL
LRP5 gain of function

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33
Q

in osteopetrosis bone deposition replaces what

A

medullary cavity

- no room for hematopoiesis

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34
Q

what does osteopetrosis look like on X-ray

A

Erlenmeyer flask

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35
Q

how is osteopetrosis passed down

A

autosomal dominant

36
Q

brittle bone disease

A

osteogenisis imperfecta

37
Q

Osteogensis imperfecta what goes wrong

A

type 1 collagen disease
- mutation of alpha 1 and 2 chains
extreme skeletal fragility

38
Q

what is the most common type of autosomal dominant bone disease

A

osteogenisis imperfecta

39
Q

clinical features of Autosomal dominant osteogensis imperfecta

A

blue sclera
hearing loss
dentin defect

40
Q

Type 2, 9, 10, 11 collagen disease has a defect in what?

A

hyaline cartilage

-

41
Q

Mucopolysaccharidoses is a defect in what

A

enzymes degrading dermatan sulfate, heparan sulfate, keratan sulfate

  • abnormal hyaline cartilage
  • malformed bone
42
Q

what is osteoporosis

A

increase bone porosity

decrease mall

43
Q

primary osteoporosis

A

senile, postmenopausal

44
Q

secondary osteoporosis

A

drugs, diabetes,

45
Q

compare osteoporosis and osteopenia

A

osteopenia: decrease bone mass
osteoporosis: osteopenia to point of risk of fracture

46
Q

senile osteoporosis what happens to the osteoblasts? cortex?

A

reduce metabolism

cortex is thinned

47
Q

when is skeletal mass peak for senile osteoporosis

A

young adult

48
Q

in postmenopausal osteoporosis what happens when estrogen is decreaed

A

increase inflammatory cytokines
increase RANKL
decrease OPG
OC>OB

49
Q

rickets

A

child vitamin D deficiency

50
Q

osteomalacia

A

adult vitamin D deficiency

51
Q

renal osterodystrophy

A

chronic renal disease

  • increase or decreased OC/OB activity
  • decrease Vitamin D conversion
52
Q

what happens to OC and OB in hyperparathyroidsim

A

more OC

53
Q

what does the X-ray look like for hyperparathyroidsim

A

bone loss radial aspect of middle phalange of index and middle finger
-osteopenia

54
Q

Paget disease involve what bone

A

axial skeleton

proximal femur

55
Q

what are the 3 stages of paget disease

A

osteolytic stage
mixed stage
osteosclerotic stage

56
Q

osteolytic stage

A

loss of bone mass

57
Q

mixed stage

A

osteolytic and osteoblastic

58
Q

osteosclerotic stage

A

jigsaw puzzle-like cement lines of lamellar bones

59
Q

paget disease has an increase in what enzyme? what values stay the same

A

alkaline phosphatase

normal Ca and PO4

60
Q

Paget disease: pain overgrowth can lead to

A

cranial nerve palsy

heavy skull

61
Q

what happens to the skin in Paget disease

A

warm skin over affected bone with hypervasculatiry

-high-output cardiac failure

62
Q

treatment for Paget disease

A

Calitonin and biphosphonates

63
Q

bony callus

A

woven bone

-overtime can bear weight

64
Q

Soft tissue callus

A

easily disrupted
hematoma fibrin
osteoprogentor cells activated

65
Q

peak bone mass

A

early adulthood

66
Q

how can a genetic factor cause osteoprosis

A

vit D receptor polymorphism

67
Q

is an X-ray and serum levels of calcium, phosphorous, alkaline phosphate helpful in diagnosing osteoporosis

A

NO

68
Q

osteitis fibrosa cystica

A

severe form of parathyroidsm

69
Q

pseudoarthrosis

A

non union

70
Q

osteonecrosis

A

infarction of bone marrow

71
Q

most common cause of osteonecrosis

A

corticosteroid

72
Q

in osteonecrosis what is dead bone/fat replaced by

A

Ca soaps

73
Q

name 5 things that can cause avascular necrosis

A 
corticosteroid
pregnancy
infection
dysbarism 
sickle cell disease
74
Q

subchondral infarct what doe sit look like

A

wedge-shaped subchondral bone

75
Q

osteomyelitis

A

inflammation almost always from infection

76
Q

how does bacteria reach bone

A

hematogenous
direct
implantation

77
Q

X-ray for osteomyelitis

A

lytic bone lesion with surrounding sclerosis

78
Q

most common bacteria in pyogenic osteomyelitis

A

s. aureus

79
Q

most common bacteria in pyogenic osteomyelitis for infants

A

group B

H. influencza

80
Q

where does pyogenic osteomyeltissi occur in bone in neonate
children
adult

A

neonate: metaphysis/epophysis
children: metaphysis
adult: epiphysis and subchondral bone

81
Q

sequestrum

A

dead piece of bone

82
Q

brodie abscess

A

small intraosseous abscess often in cortex walled off by reactive boone

83
Q

involucrum

A

reactive surrounding bone

84
Q

process of pyogenic osteomyelitis

A

sequestrum
chronic inflammation : brodie abcxess
involucrum

85
Q

congential syphilis

A

at enchondral ossification centers and periosteum

86
Q

acquired syphilis of bone? what type of bone and clinical presentsion

A

bone in tertiary phase

saddle nose, saber shin ( tibia)

D & T exam 2 (27 decks)

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