metabolic bone dz Flashcards

(34 cards)

1
Q

RANK

A

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

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2
Q

OPG

A

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

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3
Q

Risk factors for fragility fractures of osteoporosis

A

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

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4
Q

How do vertebral fractures affect fracture risk

A

Increases risk by 5% of having another fracture

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5
Q

compare osteoporosis vs osteopenia

A

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

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6
Q

normal bone remodeling

A

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

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7
Q

Non-modifiable risk factors for low bone mass

A

Age, Race, Gender, Family History, Early Menopause

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8
Q

Modifiable risk factors for low bone mass

A

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

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9
Q

How is diagnosis of osteoporosis/osteopenia made

A

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

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10
Q

Who is treated for osteoporosis

A

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

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11
Q

Osteoporosis prevention and treatment

A
  1. Ca- 1000-1500mg/day. Supplement if dairy intake insufficient. 2. Vitamin D. 3. exercise- aerobic and resistance. 4. falls- assess and prevent
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12
Q

osteoporosis treatment

A
  1. anti-resorptive agents: bisphosphanates, denosumab, raloxifene, calcitonin, estrogens. 2. anabolic agents: teriparatide, romosozumab
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13
Q

Define osteomalacia

A

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

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14
Q

Causes of osteomalacia and rickets

A
  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)
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15
Q

clinical features of osteomalacia and rickets

A

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

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16
Q

Osteomalacia/rickets labs

A

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

17
Q

osteomalacia radiology

A

fractures, pseudofractures- milkmans fractures, loosers lines

18
Q

rickets radiology

A

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

19
Q

osteomalacia/rickets treatment

A
  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
Q

Define pagets

A

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

21
Q

Etiology of pagets disease

A

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

22
Q

Gene linked to Pagets disease

A

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

23
Q

Clues to the viral cause of pagets disease

A

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

24
Q

Pagets disease skeletal features

A

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