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Flashcards in metabolic bone dz Deck (34):
1

RANK

receptor on osteoclasts which facilitates bone resorption when RANK-L binds to it.

2

OPG

osteoprotegerin- a decoy RANK-L receptor which decreases bone resorption

3

Risk factors for fragility fractures of osteoporosis

Previous Fractures, Age (increases after 55), Falls, Low Bone Mass

4

How do vertebral fractures affect fracture risk

Increases risk by 5% of having another fracture

5

compare osteoporosis vs osteopenia

Osteopenia: Bone mineral density T score of -1 to -2.5 Osteoporosis: bone mideral density T score of < -2.5. Normal: BMD T score of >-1.0

6

normal bone remodeling

Resorption= formation, OC= OB, old bone = new bone. Bone mass remains stable

7

Non-modifiable risk factors for low bone mass

Age, Race, Gender, Family History, Early Menopause

8

Modifiable risk factors for low bone mass

Low Calcium Intake, Low Vitamin D Intake, Estrogen Deficiency, Sedentary Lifestyle, Cigarette Smoking, Excess Alcohol (> 2/day), Excess Caffeine (> 2/day), Medications

9

How is diagnosis of osteoporosis/osteopenia made

measure bone density at and base T score on lowest density site

10

Who is treated for osteoporosis

Anyone with a fragility fracture, vertebral fracture, hip fracture or T score 3% risk of hip fracture of >20% major OP fracture

11

Osteoporosis prevention and treatment

1. Ca- 1000-1500mg/day. Supplement if dairy intake insufficient. 2. Vitamin D. 3. exercise- aerobic and resistance. 4. falls- assess and prevent

12

osteoporosis treatment

1. anti-resorptive agents: bisphosphanates, denosumab, raloxifene, calcitonin, estrogens. 2. anabolic agents: teriparatide, romosozumab

13

Define osteomalacia

impaired bone mineralization due to inadequate Ca and Phosphate resulting in soft, weak bones. Called rickets in kids

14

Causes of osteomalacia and rickets

1. Vitamin D deficiencies- poor intake/sunlight, renal dz, hypoparathyroidism, congenital. 2. phosphate disorders- poor intak, renal phosphate wasting, congenital (Vitamin D resistant rickets- impaired Vit D formation or renal phosphate wasting)

15

clinical features of osteomalacia and rickets

osteomalacia: pain, deformities, fractures. Rickets: pain, deformities, muscle weakness, short stature

16

Osteomalacia/rickets labs

Decreased Ca, decreased phosphate, increased serum alkaline phosphatase, increased serum PTH, decreased urine Ca

17

osteomalacia radiology

fractures, pseudofractures- milkmans fractures, loosers lines

18

rickets radiology

Bowing of long bones, flaring ends of long bones, delayed epiphyseal calcification

19

osteomalacia/rickets treatment

1. Nutritional Vitamin D Deficiency- Vitamin D and Calcium. 2. Congenital 1 Alpha Hydroxylase Deficiency- Calcitriol and Calcium. 3. Congenital Vitamin D Receptor Deficiency- High Dose Vitamin D or Calcitriol and Calcium. 4. Congenital Hypophosphatemic Rickets- Calcitriol and Phosphate

20

Define pagets

An Idiopathic Bone Condition Characterized by Excessive/Unregulated Bone Resorption and Formation

21

Etiology of pagets disease

genetic component (enhances osteoclast formation/reactivity) plus chronic paramyxovirus infection (induces changes in osteoclast precursors)

22

Gene linked to Pagets disease

Sequestosome I/ p26- a ubiquitin binding protein that induces NF-kB activation and osteoclast differentiation/activity/survival.

23

Clues to the viral cause of pagets disease

it is associated with dog owners, specific locations (rare in africa/asia), osteoclasts show paramyxovirus-like inclusions in nuclei + cytoplasm.

24

Pagets disease skeletal features

pain, deformity, fractures, osteoarthritis, hypervascularity, acetabular protrusion, osteogenic sarcoma. Commonly involves pelvis, skull, vertebrae, femur and tibia

25

Pagets disease neurological clinical features

deafness (8th nerve, ossicles), cranial nerve compression (bony), spinal cord compression (vascular)

26

Pagets disease cardiovascular features

Atherosclerosis, Aortic Stenosis, Congestive Heart Failure
(High Output)Atherosclerosis, Aortic Stenosis, Congestive Heart Failure
(High Output)

27

pagets dz over time

high osteoclast activity > osteoclast and osteoblast activity equal > osteoblast activity higher

28

Pagets dz labs over time

elevated NTX/CTX (bone resorption marker) > elevated NTX/ CTX and elevated alkaline phosphatase (bone formation marker) > decreased NTX/ CTX and elevated or decreased alk phosph

29

Pagets disease diagnosis

1. elevated remodeling markers (NTX/ CTX, alk phos). 2. X ray features (very specific). 3. bone scan (very sensitive). 4. bone biopsy (occassionally needed)

30

Pagets radiology

1. Osteolytic Lesions- “Blade of Grass” Sign in Long Bones, Resorption Front in Flat Bones (~1 cm/yr). 2. Osteosclerotic Lesions near Lytic Areas. 3. Thickened, Disorganized Trabeculae. 4. Thickened, Expanded Cortex. 5. Expansion of Bone Size

31

Pagets bone scan

Focal areas of intense uptake

32

Pagets histology

Increased Osteoclast Numbers, Increased Osteoclast Nuclei (20-100 per cell),Increased Osteoblasts in Periphery, Disorganized Mosaic Woven Bone

33

When to treat Pagets disease

Pagetic Pain, Deformity or Fracture, Weight Bearing Bone Involvement, Extensive Skull Involvement, Neurological Complication, Impending Surgery on Pagetic Bone, Immobilization Hypercalcemia, Alkaline Phosphatase > 2 x Normal

34

Pagets disease treatment

1. anti-resorptive agents- bisphosphonates, calcitonin. 2. analgesics/NSAIDs. 3. corrective surgery