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Pathophys > Bones Patho > Flashcards

Bones Patho Flashcards

1
Q

What are the differences bt cortical and trabecular bone

A

Cortical bone

  • hard outer layer
  • compact bone tissue= high density
  • Porosity 5-30%
  • 80% of the total bone mass

Trabecular bone

  • Allows room for blood vessels and marrow
  • 20% of bone mass(10x surface area of compact bone)= low density
  • Porosity of 30-90%
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2
Q

what are haversian and volkmann’s canals

A

haversian- interconnecting, longitudinal channels in bone tissue through which blood vessels, nerve fibers, and lymphatics pass.

volkmann’s- they run for the most part transversely, perforating the lamellae of the haversian system, and connect the canals of that system.

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3
Q

where are Haversian and osteons located

A

cortical bone

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4
Q

what is trabecular bone AKA

A

cancellous or spongy bone

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5
Q

does changes in the rate of bone turnover occur more in cortical or trabecular bone

A

trabecular

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6
Q

do all bones contain both cancellous & cortical elements

A

yes, but proportions can differ

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7
Q

where do long bones like the femur have the most bone turnover

A

much more at the end bc the shaft is mainly cortical bone whereas the ends are thin cortex with coarse cancellous bone prominent

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8
Q

what are 5 functions of the skeletal system

A 
Mineral homeostasis
Houses hematopoietic elements
Mechanical support for movement
Protects Viscera
Determines body size and shape
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9
Q

what is the epiphysis, metaphysis, and diaphysis

A

Epi-extends from subarticular bone plate to base of growth plate
Meta-coarse cancellous bone from growth plate to diaphysis
Dia- body or shaft of the long bone

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10
Q

what zone of a long bone is most important in hematogenous infection, tumors, and skel malformations

A

metaphysis bc more cancellous bone

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11
Q

what are osteoprogenitor cells

A

precursors to osteoblasts

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12
Q

what are osteocytes

A

ostoeblasts surronded by organic matrix. They are important regulators of bone mass and have mechanotransduction function

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13
Q

what is bone tissue regulated by

A

Transcription factors
Cytokines
Growth factors

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14
Q

what is hydroxapatite

A

a complex phosphate of calcium that occurs as a mineral and is the chief structural element of bone
-Ca, phosphate, and OH-

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15
Q

what is osteocalcin

A

a protein component of bone

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16
Q

what is osteopontin

A

a protein component of bone

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17
Q

what are the layers of bone

A

circumferential lamellae- run parallel to the surface of the bone
concentric lamellae- bony plate that surrounds haversian canals
interstitial lamellae-Any of the layers of bone between adjacent Havers.

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18
Q

what is the role of B-catenin

A

anchors osteoblasts to bone

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19
Q

what are osteoclasts derived from

A

machrophages

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20
Q

what is BMP

A

Bone morphogenic proteins

  • functions by activating osteoblasts
  • used in meds to cause spinal fusion
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21
Q

what can occur with long term use of drugs that inc BMP

A

overgrowth and tumors

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22
Q

what is LRP 5/6

A

LDL receptor related proteins 5 and 6

-surface receptors on osteoblasts that function by activating osteoblasts

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23
Q

how long after a fx should you begin to see healing on Xray

A

4th week otherwise not healing correctly

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24
Q

osteoblasts have receptors that bind what

A

PTH, estrogen, Vit D, Leptin

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25
Q

what senses tension on a bone and what pathway makes the bone resist the tension (mechanotransduction)

A

osteocytes sense tension on bones and signal osteoblasts to build and prevent osteoporosis/fxs

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26
Q

what is the diff in woven and lamellar bone

A

woven is less strong and should only be found in new bone (healing fx, embryonic bone). It is always abn in adults

Lamellar bone is regualr-parallels alignment of collagen into sheets

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27
Q

what is osteocalcin

A

marker for osteoclast activity

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28
Q

when will you see density changes in a bone scan? what can be used to earlier monitor osteoporosis meds

A

bone density scans will take 2 yrs before changes are seen. osteocalcin can be checked earlier

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29
Q

what is a osteoid

A

bone matrix not yet mineralized; takes approx 12 days (mineralization lag time)

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30
Q

what must bind to activate osteoclasts

A

RANK ligand (on osteoblast) binds to RANK-R (on osteoclast precursor)= differentation(activation) of osteoclast

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31
Q

what blocks the RANK-RANK ligand interaction

A

osteoprotegrin cells (drugs can target this to prevent osteoporosis)

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32
Q

what is involved in osteoclast differentiation regulation

A

M-CSF (monocyte colony stimulation factor), IL-1, TNF (ODP)

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33
Q

how many nuclei are contained in mature osteoclasts

A

6-12

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34
Q

what is estorgens effect on RANK ligand activation

A

estrogen inc osteoprotegrin and dec RANK lignad activation= dec osteoclast activation

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35
Q

what are Howship lacunae

A

small depressions in bone where osteoclasts are found

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36
Q

what is the relationship bt osteoclasts and pH

A

Osteoclasts generate an acidic environment

Acid digests organic components

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37
Q

what are the 3 essentials for osteoclastogenesis

A

1) TNF related receptor RANK
2) RANK ligand
3) M-CSF (monocyte colony stim factor)

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38
Q

what is NF-kappabeta

A

RANK +RANKL activates NF-kappabeta

Signaling increasing oteoclastogenesis

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39
Q

what is the functional unit of bone? how does it change with aging

A

Composed of osteocytes, osteoblasts, and osteoclasts
Control bone formation and resorption
Early in live: bone formation dominates
Later in life: remodeling occurs

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40
Q

what % of the skeleton gets remodeled/yr

A

10% (but less with age)

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41
Q

when is typical peak bone mass

A

early adulthood

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42
Q

does bone resorption and formation occur at the same location

A

No, they occur on separate surfaces

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43
Q

what is the definition of osteoporosis? how does it affect cortical and trabecular bone

A

porous bones and reduced bone mass from dec thickness of cortex and reduction in number and size of trabeculae of cancellous bone

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44
Q

what are the diff types of osteoporosis

A

1) Type 1 (postmenopausal)=disrupted connections bt trabeculae from inc osteoclast activity
2) Type 2 (senile)= reduced trabecular and cortical` thickness from loss of osteoblast activity
3) Secondary form endocrine, neoplastic(MM), GI, Drugs

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45
Q

what is the BMD criteria for osteopenia and osteoporosis

A

Osteopenia-BMD 1-2.5 SD below the mean for young adults (Tscore=-1 to -2.5)
osteoporosis- BMD more than 2.5 SD below young adult mean (Tscore<-2.5)

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46
Q

how is the osteoporosis T score diff from the Z score

A

T score is developed from 30 yr female

Z score- age and gender is matched

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47
Q

where is the most common location for osteoporosis

A

Spine: because of the abundance of cancellous bone in the spine, osteoporotic changes are most conspicuous
Can lead to kyphosis (dowager’s hump)

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48
Q

what are the DEXA recommendations

A

Who should get a DEXA, (NOF 2013)
• Woman age 65 or older
• Man age 70 or older
• If you break a bone after age 50
• Woman of menopausal age with risk factors
• Postmenopausal woman under age 65 with risk factors
• Man age 50-69 with risk factors

Other
• An x-ray showing bone loss
• Back pain with possible break in spine
• Height loss of ½ inch or more within one year
• Total height loss of 1 ½ inches from your original height

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49
Q

what age related bone loss causes osteoporosis

A

0.5%-0.7%/yr

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50
Q

how does age affect vit D levels

A

As one ages there is a decrease in renal 1 alpha-hydroxylase and less conversion of vitamin D to its active form

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51
Q

what are calcium and vit D intake recommendations

A

Calcium
Adults under age 50: 1000mg
Adults 50 and over: 1200mg

Vit D
Adults under age 50: 400-800IU
Adults 50 and over: 800-1000IU

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52
Q

what type of vit D has the longer half life

A

D3: cholecalciferol

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53
Q

how are cytokines involved in type 1 osteoporosis

A

Cytokines stimulate osteoclast recruitment by increasing RANKL while diminishing expression of OPG.

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54
Q

what is the pathophys of type 1 osteoporosis

A

dec estorgen and inc IL-1, IL-6, TNF= inc expression of RANK ligand= inc osteoclast activity

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55
Q

what is the pathophys of type 2 osteoporosis

A

1) dec replicative activity of osteoprogenitor cells 2)dec sythetic activity of osteoblasts
3) dec biologic activity of matrix bound growth factors
4) reduced physical activity

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56
Q

what is raloxifene

A

estrogen R modulator primarily used for Breast Ca but can be used for osteoporosis

57
Q

what are Alendronate, Risedronate, Ibandronate, and Zoledronic acid

A

bisphosphonates used to inhib osteoclasts by affecting proton pump

58
Q

what is forteo

A

PTH analog- if given in intermittent exposure it actually stimulates osteoblasts

59
Q

what is the risks associated with forteo

A

bone Ca so only give for 2yrs

60
Q

what is denosumab

A

antibody to RANKL

61
Q

what are the risks with bisphosphonates

A

the effects of bisphosphonates stay in the bone for 5yrs= inc risk for atypical fx

62
Q

what endocrine conditions may cause osteoporosis

A

1) corticosteriods(cushings) =inhib osteoblasts and Ca absorption
2) hyperparathyroidism= osteoclast recruitment
3) hyperthyroidism= inc osteoclast activity
4) hypogonadism

63
Q

how does alcoholism cause osteoporosis

A

inhib osteoblasts

64
Q

what is pagets dz

A

Disease of bone remodeling with numerous osteoclasts and large active osteoblasts
Osteoclast mediated bone resorption followed by new bone formation(either solitary or multiple sites) and collagen arranged in woven pattern

Disorganized mosaic pattern bone with increased vascularity and fibrosis

65
Q

what is thought to cause pagets dz

A

thought to be viral- paramyxovirus, canine distemper
but also genetic autosomal dom pattern with incomplete penetrance
-mutation in SQSTM1 gene which enhances RANK signaling=inc osteoclast activity
-RANKL and RANK/OPG mutations also found

66
Q

what are the 3 phases of pagets dz

A

1)Initial osteolytic stage= lysis of cortex

2)Mixed osteoclastic-osteoblastic stage
Ends with predominance of osteoblastic activity and evolves into the next stage
Cortex thickened & accentuation of cancellous bone

3)Burnt-out quiescent osteosclerotic stage=little cellular activity leaving disorganized bones

67
Q

what stage of pagets is considered the “hot” resorptive stage

A

1st (osteolytic) stage when osteoblast isotope take up occurs

68
Q

what is the net effect seen with pagets dz

A

gain in bone mass with newly formed bone disordered and architecturally unsound.

69
Q

what Xray effects occur with advanced pagets

A

thinner cortex earlier on but, with time, Affected portion is enlarged, sclerotic, and exhibits irregular thickening of both the cortical and cancellous bone.

  • tibia often bows out.
  • Axial skeleton and femur involved in 80% of cases
  • Craniofacial enlargement
  • Lysis in frontal and parietal bones:
  • Spontaneous fractures (usually transverse)
70
Q

what lab changes are expected with pagets

A

Alk Phos high, increase urinary hydroxyproline

[Ca2+] normal unless immobilized

71
Q

besides fxs what other complications can result from Pagets

A
  • Deafness (involvement of ossicles)
  • Nerve entrapment (impingement of CN8 at foramen
  • Spinal stenosis
  • Osteogenic sarcoma: 0.7-0.9%
  • Hypercalcemia (rare)
  • Skull can become heavy and collapse over C1 vertebra resulting in: compression of brain and spinal cord
72
Q

what is platybasia

A

flattening of the base of skull from pagets, impinges foramen magnum= compression of medulla and cord

73
Q

what is pagetic steal

A

lightheadedness due to shunting of blood from brain to bone

74
Q

what is pagets treatment

A

target osteoclasts- bisphosphonates, clacitonin, mithramycin

75
Q

what is the net effect of PTH

A

1) PTH stimulates osteoblasts causing them to synthesize and secrete RANKL=RANKL binds to RANK in osteoclasts= Large amounts of PTH and continued RANKL prevents osteoclast apoptosis= Increase serum [Ca2+]
2) PTH= inc PO4 extretion and inc Ca reabsorption in kidney

76
Q

what is the relationship bt PTH and vit D

A

PTH= inc hydroxylation of vit D in kidney= activation of vit D= inc Ca absorption in intestines, inc bone resorption, dec renal Ca excretion, and inc phosphate excretion

77
Q

what is primary hyperparathyroidism? what typically causes it?

A

PTH raised inappropriately relative to [Ca2+]

may be Autonomous hyperplasia or tumor (Usually adenoma (85%))

78
Q

what is secondary hyperparathyroidism? what typically casues it

A

Prolonged states of hypocalcemia resulting in compensatory hypersecretion of PTH
-usually from kidney failure=bones only source of Ca

79
Q

why does renal dz lead to weak bones

A

1) dec active vit D

2) dec regulation of Ca and phosphorus= inc excretion of Ca and dec excretion of phosphorus

80
Q

what causes familial hyperparathyroidism

A

mutaions in Calcium sensing-R (CASR) gene

81
Q

is cortical or cancellous bone affected more in hyperparathyroid

A

cortical= thinned cortex

82
Q

what is osteitis fibrosa cystica

A

the anatomic changes known from excess PTH
1)Dissecting osteitis:osteon hallowed out by osteoclasts

2) Osteitis fibrosa: trabecular bone reabsorbed and marrow replaced with fibrosis
3) Osteitis fibrosa Cystica: brown tumor (fibrosis with bleeding)

83
Q

Xrays from osteitis fibrosa cystica can look like multiple myeloma with punch lesions. what test differentiates the 2

A

MM has benz proteins in the urine

84
Q

what is dysotoses

A

A disorder in the development of bone
-Failure of a bone to develop:Congenital absence of a bone: phalanx, rib, clavicle

  • Formation of extra bones: supernumerary digit (polydactyl)
  • Fusion of two adjacent digits (syndactyly)
85
Q

what occurs with a mutation to the homeobox gene (HOXD13)

A

Extra digit between third and fourth fingers and syndactyly

86
Q

what occurs with loss of function mutations in RUNX2

A

RUNX2 Normally produces transcription factors important in osteoblastogenesis

Mutation results in cleidocranial dysplasia

  • Patent fontanelles
  • Delayed closure of cranial sutures
  • Wormian bones: extra sutures
  • Delayed eruption of secondary teeth
  • Primitive clavicles
  • Shortened height
87
Q

what does mutation in the FGF receptor 3(chr 4) cause

A

Normally FGF3 inhibits cartilage proliferation

Mutations in FGFR3 cause constitutive activation and therefore suppresses growth=achondroplasia/dwarfism

88
Q

how is FGFR3 mutation in dwarfism passed

A

autosomal dom on chr4 but 80% spontaneous mutation(mainly on paternal allele)

89
Q

what are the manifestations of achondroplasia

A

Shortened proximal extremities

Trunk of relative normal length

Enlarged head with bulging forehead

Depression of the root of the nose.

Skeletal abnormalities usually not associated with changes in longevity, intelligence, or reproductive status

90
Q

what is thanatophoria

A

the most common lethal form of dwarfism

91
Q

what is the pathophys of thanatophoria

A

“gain of function” of FGFR3

Gene product gains a new and abnormal function

92
Q

what are the manifestations of thanatophoria

A

Micromelic shortening of limbs

Frontal bossing

Macrocephaly

Small chest cavity=resp insufficiency

Bell shaped abdomen

93
Q

what is type 1 collagen dz known as

A

Osteogeness imperfecta

-Most common inherited disorder of connective tissue

94
Q

what does type 1 collagen dz affect

A

Principally affects bone

Other Type 1 collagen tissue also affected: joints, eyes, ears, skin, and teeth

95
Q

where are the 4 types of collagen located

A

type 1= bONE
type 2= carTWOlage
type 3= thREEticulum
type 4= basement membrane

96
Q

what are common s/sx of osteogeness imperfecta (type 1 collagen dz)

A

“Brittle” bone disease, too LITTLE bone, BLUE sclera

97
Q

what is the pathogenesis of oseogeness imperfecta

A

point mutation affecting glycine residue in genes which code for the alpha-1 and alpha-2 chains of COLLAGEN 1

98
Q

what is the inheritance pattern of oseogeness imperfecta

A

autosomal dominant

99
Q

what are the diff osteogeness imperfecta types

A

Type 1: Autosomal dominant-decrease synthesis of alpha-1 chain

  • Compatible with survival: Normal life span
  • Childhood fractures which decrease in puberty
  • Blue sclera, hearing loss(fusion of ossicles), dental imperfections (misshapen, bluish)
Type 2:  Autosomal dominant or recessive-alpha 1 and 2
perinatal lethal (multiple intrauterine fractures)
Type 3:  Autosomal dominant 75%, recessive 25%-alpha 2
progressive, deforming 
Type 4:  Autosomal dominant – short alpha 2 chain
compatible with survival
100
Q

mucopolysaccharidosis is a dz of what

A

a defect in folding and degradation of macromolecules, specifically a lysosome storage dz that dec enzymes that degrade
DERMATAN SULFATE
HEPARAN SUFLATE
KERATAN SULFATE

101
Q

what anatomical changes result from mucopolysaccharidosis

A

Chiefly CARTILAGE disorders: short, chest wall, malformed bones
Undegraded GAGs accumulate in connective tissue, neurons, and hepatocytes.

102
Q

what is osteopetrosis AKA

A

marble bone dz

103
Q

what are the diff types of osteopetrosis(marble bone dz)

A

1)Autosomal Dominant: One type is due to CARBONIC ANHYDRASE deficiency= Carbonic Anhydrase is necessary for osteoclasts to generate protons from CO2 and water.
Relatively benign, some anemia

2)Autosomal Recessive: Usually affects the proton pump in osteoclasts
Severe, death due to anemia, cranial nerve entrapment, hydrocephalus and infection. Also see extramedullary hematopoiesis

104
Q

why can anemia result from dec osteoclast activity

A

dec osteoclast= inc bone thickness= dec marrow fxn= anemia

105
Q

what is chacteristic of the “marble” bones

A
  • “MARBLE” bone, brittle, sclerosis (break like a piece of chalk) from dec osteoclast resorption
  • Diffusely DENSE bone with Erlenmeyer Flask deformity of distal humerus.
106
Q

why is osteopetrosis treated with bone marrow transplant

A

osteoclasts are derrived from monocytes

107
Q

what is the similarities and difference bt ricketts and osteomalacia

A

both are vit D deficiency/dysfunction but ricketts is in children, whereas, osteomalacia is in adults

108
Q

what is renal osteodystrophy

A

any bone disorder due to chronic renal disease

109
Q

what are ricketts and osteomalacia predisposed to

A

fractures and pseudofractures(look like fx but only dec in Ca/vit D

110
Q

what are the skeletal changes from chronic renal dz

A

Increased osteoclastic bone resorption

Delayed matrix mineralization (osteomalacia)

Osteosclerosis (fibrotic tissue replaced bone)

Growth retardation

Osteoporosis.

111
Q

what are the 3 major types of renal osteodystrophy

A

High turnover osteodystrophy= Increased bone resorption and bone formation

Low turnover or aplastic disease= Adynamic bone (little osteoclastic and osteoblastic activity

Osteomalacia (mixed type of the two above)

112
Q

what is the pathogenesis of renal osteodystrophy

A

Chronic renal failure causes phosphate retention and hyperphosphatemia

  • Hyperphosphatemia induces secondary hyperparathyroidism
  • Hypocalcemia due to decrease levels of vitamin D
  • PTH markedly increases
  • Induction of osteoclast activity
  • Metabolic acidosis associated with renal failure stimulates bone resorption and release of calcium from bone matrix
113
Q

what are the 3 phases of fractures

A

1)HEMATOMA: Rupture of blood vessels creates a hematoma which fills the fracture gap
Degranulated platelets and migrating inflammatory cells release PDGF, TGF-beta, FGF and interleukins which activate the osteoprogenitor cells in the periosteum, and medullary cavity.
2)SOFT CALLUS (“PRO”-CALLUS), ~1 week
Provides anchorage but no structural rigidity
3)HARD CALLUS (BONY CALLUS), several weeks
Maximum girth at end of second or third week
Woven bone then laminar bone

114
Q

what are complications of fxs

A

PSEUDARTHROSIS:false joint at site of fx

INFECTION (especially OPEN [communicating] fractures)

Malunion: doesn’t heal in correct alignment

Nonunion: doesn’t heal at all

115
Q

what is CEFAZOLIN (ANCEF)

A

cephalosporin given prophylactically before ortho surg

116
Q

what is osteonecrosis AKA

A

AVASCULAR necrosis or ASEPTIC necrosis

117
Q

what can cause osteonecrosis

A

Ischemia

  • Trauma
  • Steroids
  • Thrombus/Embolism
  • Vessel injury, e.g., radiation
  • INCREASED intra-osseous pressure=vascular compression
  • Venous hypertension too
118
Q

what are the 2 types of infarcts that cause osteonecrosis

A

Medullary infarcts involve cancellous bone and marrow

Subchondral infarcts cause triangular segment of tissue undergoes necrosis
Overlying articular cartilage remains viable as it receives nutrition from synovia fluid

119
Q

why is the cortex not affected in medullary infarcts

A

-Cortex is not affected because of its collateral blood flow

120
Q

how do medullary and subchondral infarcts present

A

Medullary- Present clinically silent except for large ones occurring in Gaucher disease, dysbarism, and sickle cell anemia
subchondral-Present with pain that is initially associated only with activity but becomes progressively more constant as secondary changes occur

121
Q

what is gaucher dz

A

autoimmune dz causing vasculitis

122
Q

what is the progression of medullary and subchondral infarcts

A

medullary-Remain stable over time

subchondral-Often collapse and predispose to severe, secondary osteoarthritis
More than 10% of joint replacements performed are for treatment of complications of osteonecrosis.

123
Q

what is the most common bacteria that causes osteomyelitis

A

Staph

124
Q

what type of pt is more likely to get osteomyelitis from E. coli, Pseudomonas, and Kleb

A

GI infections and IVDA

125
Q

what type of pt is more likely to get osteomyelitis from mixed infections

A

surgical procedures or open fxs

126
Q

what type of pt is more likely to get osteomyelitis from H flu and strep B

A

neonates

127
Q

what type of pt is more likely to get osteomyelitis from salmonella

A

sickle cell dz

128
Q

what is vertebral osteomyelitis associated with

A 
Septicemia
Bacterial arthritis
Pathologic fracture
Squamous cell carcinoma,
Amyloidosis
129
Q

where is the most common site for hematogenous cause of osteomyelitis

A

metaphyseal area d/t inc blood supply.

130
Q

If a otherwise healthy child gets osteomyelitis, what is the likely cause

A

Hematogenous spread (dental, dermal cut)

131
Q

what is involucrum?

A

(New bone)
A layer of new bone growth outside existing bone seen in pyogenic osteomyelitis (a sheath around the necrotic sequestrum)

132
Q

what is sequestrum

A

(dead bone)
a piece of dead bone that has become separated during the process of necrosis from normal/sound bone (fragment of necrotic bone embedded in the pus)

133
Q

what should be considered if arthritic changes occur at an early age

A

may be caused by involucrum

134
Q

what are potential complications of osteomyelitis

A

Subperiosteal abscess

Draining sinus: cloaca

Joint involvement

SEQUESTRUM (dead bone)-

INVOLUCRUM (new bone)-

135
Q

what is cloaca

A

the hole formed in the bone during the formation of a draining sinus

136
Q

what is POTTS dz

A

TB of the spine

137
Q

what does congenital osteomyelitis result from

A

syphilis

138
Q

what causes “sabre” shin

A

tertiary syphilis

Pathophys (15 decks)

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