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DEMS Unit 4 > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

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1
Q

Bone remodeling

A

remove older, weaker bone and replacing with newer, stronger bone

  • osteoclasts remove by creating resorption pit
  • osteoblasts secrete osteoid (bone specific collagen) to fill pits up
  • Ca adn Phosphate calcify
  • osteoblasts become encased into bone as osteocytes and can sense where sites of stress and can remodel there where bone needed
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2
Q

what controls bone resorption

A

Rank-L; made by osteoblasts

  • Binds to RANK on osteoclasts to stimulate resorption by osteoclasts
  • bone marrow secretes Osteoprogeterin (OPG) -decoy receptor for RANK-L–binds RANK-L to prevent stimulating osteoclasts
  • how much bone resorption depends on how much OPG compared to RANK-L
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3
Q

What controls bone formation

A

Wnt pathway

  • aka Frizzled/LRP-5/Beta catenin
  • stimulates osteoblasts to make new bone
  • Slcerostin = protein in bone inhibiting this pathway/preventing bone formation
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4
Q

Osteoporosis

A

Compromised Bone strength

- predisposes to increased risk for fragility fractures= fractures from no/minimal trauma–standing height or less

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5
Q

3 main types fragility fractures

A

Spine, hip, wrist

Fragility fractures = osteoporosis

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6
Q

Risk factors for fragility fractures

A

Age
Falls
Low bone mass
Previous fractures

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7
Q

Osteopenia

A

T score -1 SD below mean

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8
Q

Osteoporosis definition

A

T score - 2.5 or fragility fracture

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9
Q

Risk factors for low bone mass

A
  • Non modifiable: age, race, gender, fam hx, early menopause
  • Modifiable: low Ca intake, Low vit D intake, estrogen deficiency, sedentary, cigarette, excess EtOH, excess caffeine, medications (steroids, thyroid hormone excess)
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10
Q

does low bone mass mean osteoporosis

A

NO–large differential

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11
Q

meds putting at risk for low bone mass

A

glucocorticoids, thyroid hormone, anticonvulsants, thiolidinediones, PPIs, SSRIs, SGL-2

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12
Q

Prevention/Treat Osteoporosis

A

Ca: 1000-1500 mg/day (Ca and PO4)
1000 Vit D
Exercise
Falls– prevent

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13
Q

pharmacologic idea behind treating osteoporosis

A

decrease bone reabsorption and increase formation

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14
Q

Osteomalacia and Rickets

A
  • O= adults
  • R = children
  • impaired bone mineralization resulting on soft, weak bones
  • Inadequate Ca x Phosphate product for bone mineralization
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15
Q

Phosphate Disorders

A
  • Acquired hypophosphatemia (poor oral intake, renal phosphate wasting–can be cause of meds damaging kidneys)
  • Congenital hypophosphatemic Ricket’s -95% cases of rickets (Vitamin D resistant Ricket’s– won’t respond to vit D) – have renal phosphate wasting and impaired 1,25 vit D formation
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16
Q

hypophosphatemic Rickets

A

vitamin D resistant

  • Renal phosphate wasting
  • Impaired 1,25 (OH)2 Vitamin D formation–further reduction in phosphate and Ca
  • have to give phosphate and vitamin
17
Q

vit D disorders

A
  • acquired deficiency
  • acquired 1,25 vit D def
  • Congenital 1 alpha hydroxylase def- vit D dependent Rickets type 2
  • Congenital vit D receptor def– vit D dependent Rickets type 2
18
Q

Osteomalacia

A
  • pain typically in long bones
  • deformities (soft, tend to bow)
  • fractures, pseudofractures (Milkman’s and looser’s lines)
19
Q

RIckets sxs

A

Proximal muscle weakness, short stature, deformities, pain

- Radiology shows bowing of long bones and flaring of ends of long bones and delayed calcification of epiphyses

20
Q

Paget’s Disease of Bone

A

idiopathic bone condition
- excessive/unregulated
bone resorption and formation
- biopsy shows thicker, disorganized, weaker, larger, highly vascular
- genetic predisposition and chronic paramyxovirus infection

21
Q

Evidence for Genetic Disorder

A
  • familial aggregation (1540%)
  • 18q Linkage– familial expansile osteolysis
  • mutation of osteoprotegerin gene = Juvenile Paget’s dz
    so excessive resorption
  • Mutation of sequestosome 1/P62 gene found in 40-80% Paget’s families
22
Q

Sequestosome I (SQSTM1/p62)

A
  • controls how osteoclasts develop, work, and undergo apoptosis
  • ubiquitin binding protein that forms ubiquitinated chains that function as protein scaffolds for IL-1 and TNF induced NF_kappaB activation, which regulates RANK signalling that controls osteoclast differentiation, activity, and survival
23
Q

STSTMI mutation

A

linked to Paget’s Disease

24
Q

Viral disorder link in Paget’s

A
  • Geographic variation
  • link to dog ownership
  • time trends related to measles
  • direct viral studies–show paramyxovirus-like inclusions in nuclei - cytoplasm of osteoclasts
25
Q

Unifying hypothesis of Paget’s DIsease

A

Development of Paget’s requires:
- genetic component enhances osteoclast formation/reactivity
- paramyxovirus infection (induces chagnes in osteoclast precursors)
-

26
Q

Paget’s SXS

A

Skeletal: Pain, deformity, fractures, osteoarthritis, hypervascularity, acetabular protrusion, osteogenic sarcoma

27
Q

Most common sites of Paget’s diseaes

A
  • can be monostotic or polyostotic
  • Pelvis
  • Skull
  • Vertebrae
  • Femur
  • Tibuia

Neuro: deafness, cranial nerve compression due to compression fo holes nerves travel through (bony), spinal cord compression (vascular)

CV: atherosclerosis, aortic stenosis, congestive heart failure (high output)–due to highly vascular bones

28
Q

Clinical course of Paget’s Disease of Bone

A
  • initially high osteoclast activity –elevated NTX/CTX, breakdown products of bone
  • Mixed: about 1- years later, then high osteoclastic and osteoblastic activity; get elevated NTX/CTS as well as Alk Phos from osteoblast activity
  • osteoblastic: finally like 20 years out, low resorption so low NTX/CTX,below level of formation. Alk phos tends to be high, but may be low after a while
29
Q

Paget’s Disease labs

A

remodeling markers elevated; xray features very specific, bone scan, bone biopsy–occasionally needed

30
Q

Osteolytic lesions on radiology

A

“blade of grass” sign in long bones; resorption front in flat borne
- osteosclerotic lesions near lytic areas
thickened, disordered trabeculae
thickened, expanded cortex
Expansion of bone size

31
Q

Bone scan in Paget’s Disease

A

Focal areas of Intense Uptake when in osteoblastic phase

32
Q

Histology on Paget’s

A
  • increased osteoclast numbers/nuclei (20-100 per cell)
  • increased osteoblasts in periphery
  • disorganized, mosaic, woven

DEMS Unit 4 (16 decks)

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