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MNI (bones and joints path) > L17- Metabolic Bone Disorders > Flashcards

L17- Metabolic Bone Disorders Flashcards

1
Q

describe the modeling and remodeling of bones of normal skeleton in different stages of life

A

1) childhood / adolescence: skeletal growth, osteoblastic activity&raquo_space; osteoclastic activity
2) 20s-30s: *Peak Bone Mass, 5-10% skeletal turnover per year; bone deposition = bone resorption
3) >late 30s: progressive bone loss (slow); bone loss > bone deposition

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2
Q

(1) is the tightly regulated unit that regulates bone remodeling. (2) is the key regulatory part of (1).

A

1- basic multicellular unit = coordinated activity of osteoblasts and osteoclasts

2- osteoblasts

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3
Q

osteoblasts in bone remodeling:

  • (1) stimulate osteoblasts
  • osteoblasts will then have (2) effects on other cells
A

1:

  • osteocytes
  • blood borne factors: PTH, Ca, PO4-, ect

2:

  • stimulates osteoclast development (differentiation)
  • activates osteoclasts
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4
Q

(1) will upregulate (2) expression in osteoblasts. (2) binds to (3) on osteoclasts in order to produce (4) effect. (5) is able to inhibit (2) via (6).

A

1- PTH, vitD, some malignancies
2- RANKL (receptor activator of NF-κB ligand)
3- RANK (TNF family)
4- activate osteoclasts and its precursors
5- OPG (osteoprotegrin- TNF family)
6- binds RANKL to prevent RANKL-RANK interaction

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5
Q

Regulation of Osteoclasts:

  • (1) from blood will activate (2) in bone
  • (2) has paracrine mechanisms to have (3) effect on osteoclasts
  • (4) in general will inc osteoclasts
  • (5) blocks or checks stimulation of osteoclasts
A

1- PTH, vitD3, IL-11
2- osteoblasts
3- inc activation, proliferation, fusion, differentiation, survival

4- M-CSF (macrophage colony stimulating factor)
5- OPG (osteoprotegrin)- binds RANKL

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6
Q

Osteoporosis:

  • (1) definition leading to inc risk of (2) mainly in (3) people
  • (localized/diffuse)
  • (primary/secondary) disease
A

1- diminished bone mass
2- fractures
3- elderly
4- both (one bone –> few bones –> bones on one side –> all bones)
5- both (primary- aging, secondary requires additional factors)

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7
Q

describe the effects aging has on bones and how it may lead to osteoporosis

A
  • dec activity of matrix-bound growth factors
  • dec replication from osteoprogenitor cells
  • dec synthetic activity of osteoblasts

-reduced physical activity

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8
Q

______ osteoporosis results from aging

A

senile

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9
Q

Post-menopausal Osteoporosis:

  • (1) years of progression
  • decreased levels of (2) in serum
  • (3) are the three effects from decreased (2)
A

1- ~10yrs post-menopause
2- estrogen

3:

i) inc CSF, IL-6 via osteoblasts–> inc osteoclast differentiation
ii) inc local CKs via osteoblasts –> inc osteoclast activation
iii) inc IL-1, TNF via peripheral blood monocyte –> inc (i) and (ii)

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10
Q

decreased estrogen levels will increase ______ levels which will stimulate osteoclast differentiation

A

CSF, IL-6

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11
Q

decreased estrogen levels will increase ______ levels which will stimulate osteoclast activation

A

local CKs

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12
Q

decreased estrogen levels will increase ______ levels from peripheral blood monocytes (include effects)

A

IL-1, TNF –> activates osteoblasts –> osteoclast proliferation/differentiation + activation

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13
Q

describe the effect of osteoporosis on vertebral bodies

A
  • inc risk of compression fractures –> scoliosis

- characterized by loss of horizontal trabeculae and thickened vertical trabeculae

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14
Q

list the general causes of secondary osteoporosis (hint- 5)

A
  • endocrine
  • neoplasia
  • GI
  • drugs

-immobilization (lack of physical activity)

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15
Q

what endocrine changes can cause OP

A

**hyperparathyroidism

  • hyperthyroidism
  • DM
  • Addison’s disease (no adrenals)
  • pituitary tumors (via hormone secretion)
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16
Q

what neoplasia can cause OP

A
  • carcinomatosis
  • multiple myeloma
  • paraneoplastic disease
17
Q

what GI changes can cause OP

A
  • malnutrition
  • malabsorption
  • **vitD, vitC deficiencies
  • hepatic insufficiency
18
Q

what drugs can cause OP

A
  • chemotherapy
  • corticosteroids
  • alcohol
19
Q

describe all the effects on bone from increased osteoclastic activity via hyperparathyroidism

A
  • osteoporosis
  • osteoclastic tunneling
  • cystic spaces
  • Giant cell tumor-like mass
  • neovascularization, hemorrhage

Brown tumor b/c of dried blood

20
Q

Paget’s Disease:

  • (1) definition
  • (2) affected age group
  • (males/females) are more affected
  • (4) most affected race
A

1- acquired disorder of bone remodeling, unknown cause
2- >40 y/o, incidence inc after 55 y/o
3- equally affected
4- whites

21
Q

Paget’s Disease:

  • (1) definition
  • (2) affected age group
  • (males/females) are more affected
  • (4) most affected race
A

1- acquired disorder of bone remodeling, unknown cause –> monoostotic (one bone) or polyostotic
2- >40 y/o, incidence inc after 55 y/o
3- equally affected
4- whites

22
Q

list the risk factors for Paget’s disease

A

Genetics- 15% have FHx, more prevalent in whites

Environmental- most likely viral infection (RSV) => trigger unregulated osteoclastic activity

23
Q

Paget’s Disease:

  • (1) brief pathogenesis
  • (2) list stages
A

1- unregulated osteoclastic activity –> inc resorption –> stimulated inc osteoblastic activity –> abnormal bone deposition

2:

i) osteolytic stage
ii) mixed lytic and blastic stage
iii) osteosclerotic (burnt-out) stage / end stage (inc bone mass)

24
Q

describe the osteolytic stage of Paget’s

A
  • unregulated osteoclastic activity
  • patchy, florid (red) bone
  • multinucleated osteoclasts, >100 nuclei
  • lytic lesions
25
Q

describe the mixed lytic and blastic stage of Paget’s

A
  • patchy areas of alternating osteoclastic and osteoblastic activity => remodeling, fibrosis, osteoid formation
  • thick and thin bony trabeculae
26
Q

describe the osteosclerotic stage of Paget’s

A

Burnt-out osteoclasts = end stage

  • irregular bone deposition
  • inc vascularity –> warmth
  • Histology: mosaic pattern with irregular cement lines
27
Q

describe the highlights of Paget’s disease histology

A

mosaic pattern of bone with dense sclerosis and haphazard / wavy cement lines (irregular bone formation)

28
Q

Paget’s disease clinical features

A

i) commonly asymptomatic
ii) generalized bone pain
iii) bone pain, warmth, tenderness, arthritis
iv) fractures with trivial trauma, localized bone deformities

  • inc skull/head size
  • CN-VIII compression via foramina –> deafness
29
Q

describe the diagnosis of Paget’s disease

A

X-Ray: results depend on stage (hypodense, mixed, hyperdense + thickening of layers)

  • inc ALP
  • inc urinary hydroxyproline
30
Q

Paget’s disease:

  • (1) sites in monoostotic form
  • (2) sites in polyostotic form
A

1- skull, tibia, femur, vertebra, humerus

2- pelvis, vertebra, skull

Note- 80% involve axial bone or femur

31
Q

Paget’s disease:

  • (1) common complications, bone
  • (2) rare complications
A

1:

  • deformities –> pain via nerve compression
  • fractures/microfractures –> pain
  • degenerative joint disease –> pain

2:

  • high output CHF (osteoblastic phase)
  • Tumors- sarcoma (5-10%, lethal), giant cell tumor, extra-osseous hematopoiesis
32
Q

(1) are the secondary changes to bone as a result of chronic renal insufficiency or (2).

A

1- renal osteodystrophy

2- secondary to changes from dialysis

33
Q

list the many mechanisms of renal osteodystophy (hint- 5)

A
  • CRF –> hyperphosphatemia –> hypocalcemia –> secondary inc PTH
  • renal tubular acidosis / low pH –> demineralization of matrix => osteomalacia (vitD deficiency)
  • dec production of secretory factors
  • Hypocalcemia: i) dec vitD metabolism via phosphate inhibition (kidney); ii) vitD malabsorption

-Dialysis –> Fe, Al (in dialysate) accumulates in bone –> prevents further bone deposition

34
Q

list the clinical features of renal osteodystrophy

A

-inc PTH –> inc osteoclastic activity –> inc resorption –> ***inc risk of fractures

  • dec matrix mineralization –> osteomalacia
  • osteoporosis –> inc risk of fractures
  • growth retardation
35
Q

list the risk factors / etiology of Vitamin D Deficiency

A
  • inadequate synthesis (lack of sun)
  • dec absorption (malnutrition, malabsorption)
  • end-organ resistance (inherited abnormal receptor)
  • phosphate depletion
36
Q

Vitamin D deficiency in children = ______ + clinical presentation and appearance of growth plate

A

Rickett’s- weak, misshapen long bones in growing skeleton

Growth plate: irregular hypertrophy of chondrocytes + poorly calcified osteoid

37
Q

Vitamin D deficiency in adults = ______ + clinical features

A

Osteomalacia- mature bone –> soft bones –> fractures, osteoporosis

38
Q

how does vitamin D deficiency affect bone health

A
  • dec calcium absorption, resorption, reabsorption
  • -> abnormal mineralization = undermineralized matrix
  • -> persistent hyaline cartilage
  • -> fractures, skeletal deformity
39
Q

describe the pathogenesis of scurvy and its affects on bone

A

i) vitC deficency
ii) failed cross-linking of collagen
iii) fragile capillaries and venules –> subperiosteal hemorrhages
iv) defective osteoid synthesis –> microfractures
v) bony deformities

MNI (bones and joints path) (10 decks)

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