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*Orthopaedic Surgery > Metabolic Bone Diseases: 2 > Flashcards

Metabolic Bone Diseases: 2 Flashcards

1
Q

Calcitonin

  1. Which drug names are these? 2
  2. FDA approved for?
  3. Reduction of vertebral fractures by about ___% in persons with prior vertebral fracture
  4. Has not been shown to reduce what?
A
  1. Miacalcin or Fortical
  2. FDA approved for the treatment of osteoporosis in women ≥5 years post menopause
  3. 30% in persons with prior vertebral fracture
  4. Has not been shown to reduce nonvertebral fractures
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2
Q

Calcitonin

  1. MOA?
  2. Dose?
  3. CI?
  4. SE? 3
A
  1. Antagonizes the effects of PTH
  2. 200 IU as a single daily nasal spray or subcutaneous injection
  3. Contraindicated with history of allergy to salmon
  4. Side effects
    - Rhinitis,
    - epistaxis,
    - allergic reactions
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3
Q

Hormone replacement therapy (HRT)

  1. When do we use this?
  2. What is this drug?
  3. How long is this therapy for?
A
  1. Only if failed other non-estrogen treatment options
  2. Prempro (estrogen/progesterone)
  3. 5 years of therapy
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4
Q

Risks with HRT therapy? 5

A
  1. ↑ risks of MI,
  2. CVA,
  3. invasive breast cancer,
  4. PE,
  5. DVT during 5 years of treatment

No MI risk if starting treatment within 10 years post menopause

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5
Q

Parathyroid hormone: Teriparatide (Forteo)

  1. How is this drug unique?
  2. When do we prescribe this?
    - Such as? 2
A
  1. Unique in that it stimulates bone formation
  2. For severe osteoporosis when other treatments have failed
    - continue to fracture 1 year after bisphosphonate therapy
    - Intolerant to bisphosphonate therapy
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6
Q

Parathyroid hormone: Teriparatide (Forteo)

  1. Efficacy?
  2. Dose?
  3. Max duration on this?
  4. Monitor for what?
A
  1. ↓ risk of vertebral fx by 65%, ↓ nonvertebral fx by 53%
  2. 20mcg subcutaneous injection daily
  3. Max duration of therapy is 24 months
  4. Monitor for alterations in serum calcium
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7
Q

Parathyroid hormone: Teriparatide (Forteo)
SE? 4

Should avoid administration in pt’s at risk for osteosarcoma such as? 5

A

Side effects:

  1. leg cramps,
  2. nausea,
  3. dizziness
  4. increased incidence of osteosarcoma in animal studies
  5. Paget’s disease,
  6. prior radiation therapy of the skeleton,
  7. bone mets,
  8. hypercalcemia,
  9. hx of skeletal malignancy
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8
Q

Denosumab (Prolia)

  1. What is this?
  2. MOA?
  3. Indicated for?
  4. Used in who?
A
  1. Monoclonal antibody
  2. Decreases bone absorption by inhibiting osteoclast activity
  3. Indicated for postmenopausal women and men at high risk of fracture
  4. Used in cancer patients (breast and prostate)
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9
Q

How to follow pt’s on Rx therapy for osteoporosis

4

A
  1. Monitor for side effects
  2. Monitor for recurrent fractures
  3. Yearly height measurement
  4. Serial DXA scans- Baseline and every 2 years
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10
Q

Ongoing monitoring for OP? 2

A
  1. If lose 2 cm or more in height (0.8 in) or more in a year need repeat vertebral imaging to evaluate for new or additional vertebral fractures
  2. DXA scan at initiation of treatment and every 2 years
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11
Q

Treatment for special populations

4

A
  1. Glucocorticoid induced
  2. Renal failure
  3. Androgen deficiency
  4. Malabsorption
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12
Q

What do we have to change in renal dialysis patients with op?

A

Calcitriol to enhance calcium absorption

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13
Q

Other Metabolic Bone Diseases

? 4

A
  1. Paget Disease of the bone
  2. Osteomalacia
  3. Rickets
  4. Renal osteodystrophy
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14
Q

Whats the second most common metabolic bone disease?

A

Paget disease (Osteitis deformans)

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15
Q

Paget disease (Osteitis deformans)

  1. Describe how the lesions may be patterned?
  2. Most commonly involves what?
  3. What are the rest of the areas that are also commonly involved (in order of frequency?) 4
A
  1. Lesions may be solitary or occur at various sites
  2. Most commonly involves the axial skeleton
    • Skull,
    • thoracolumbar spine,
    • pelvis,
    • long bones of the lower extremity (in order of frequency)
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16
Q

Paget’s is a disease of the osteoclast

  1. Increased rate of?
  2. Overgrowth where?
  3. What kind of disorder?
  4. Possible _____ etiology?
  5. Onset after what age?
  6. Gender?
  7. Associated with?
A
  1. Increased rate of bone remodeling
  2. Overgrowth of bone at single or multiple sites
  3. Genetic disorder
  4. Possible viral etiology
  5. Onset after age 55
  6. Men > women
  7. Associated with osteosarcoma
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17
Q

Symptoms of Paget’s disease

A
  1. Arthritis
  2. Pain
  3. Bone deformity
  4. Fractures
  5. Radiculopathy
  6. Chronic back pain
  7. Impaired functional status
  8. Hearing loss
  9. Headache
  10. Vertigo
  11. Tinnitus
  12. Asymptomatic
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18
Q

Metabolic complications of Paget’s disease

A
  1. Hypercalciuria

2. Increased incidence of kidney stones

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19
Q

Labs for Paget’s? 3

A
  1. ↑ Serum alkaline phosphatase
  2. Serum calcium should be normal unless fracture or immobilization
  3. Serum phosphorus should be normal
20
Q

Pagets

Imaging? 2

A

Xray

Bone scan

21
Q

Paget’s

  1. What will you see on X-ray? 3
  2. What will you see on bone scan? 2
A
    • Mixed lytic and sclerotic lesions
    • Long bone bowing
    • Bone thickening and enlargement
    • Increased bone remodeling and
    • blood flow

-More sensitive than x-ray early on

22
Q

Paget’s Dx? 5

A
  1. History and physical
  2. X-rays
  3. Elevated serum alkaline phosphatase
  4. Baseline bone scan needed
  5. Baseline serum calcium, 25-OH Vit D, phosphorus
23
Q

Paget’s Tx

  1. Goals? 2
  2. Tx? 2
A
  1. Goals:
    - decrease pain,
    - slow bone remodeling
  2. Supportive treatment
    - Vitamin D 800 IU, Calcium 1200 mg
    - Bisphosphonates
24
Q

Which biphosphanates for paget’s? 4

A
  1. Alendronate (Fosamax)(PO)
  2. Risedronate (Actonel) (PO)
  3. Pamidronate (IV)
  4. Zoledronic acid (IV)
25
Q

Osteomalacia

  1. PP?
  2. How is the consistency of the bone?
  3. Caused by disorders that result in? 3
A
  1. Decreased mineralization of newly formed bone
  2. Bone is soft but no loss of bone matrix
  3. Caused by disorders that result in
    - hypocalcemia,
    - hypophosphatemia,
    - or direct inhibition of the mineralization process
26
Q

2 main causes of osteomalacia

A
  1. Insufficient calcium absorption from the intestine

2. Phosphate deficiency

27
Q

Osteomalacia causes:
-Insufficient calcium absorption from the intestine? 3

-Phosphate deficiency? 2

A
  1. Lack of dietary calcium
  2. Vitamin D deficiency
  3. or resistance (chronic liver disease and kidney failure)
  4. Renal losses
  5. Decreased intestinal absorption
28
Q

Etiology of osteomalacia?

5

A

1 Malabsorption

  1. Gastric bypass surgery
  2. Celiac sprue
  3. Chronic hepatic disease
  4. Chronic kidney disease
29
Q

Symptoms of OM?

6

A
  1. Can be asymptomatic
  2. Bone pain and muscle weakness (94%)
  3. Bone tenderness (88%)
  4. Fracture (76%)
  5. Difficulty walking and waddling gait (24%)
  6. Muscle spasms, cramps, a positive Chvostek’s sign, tingling/numbness, or inability to ambulate(6-12%)
30
Q

Work up for osteomalacia

Initial Lab eval? 7

A
  1. Serum calcium
  2. Phosphate
  3. Alkaline phosphatase
  4. 25-hydroxyvitamin D (25-OHD)
  5. PTH
  6. Electrolytes
  7. BUN and creatinine
31
Q

Bone biopsy: OM

When may you need this?

A

May be needed if the diagnosis is in doubt or if the cause is unknown

32
Q

Labs vary depending on cause. Results for nutritional deficiency:

  • ↑ (2)
  • ↓ (3)
A

↑ Alkaline phosphatase (95-100%)
↑ PTH elevated (100%)

↓Serum calcium and phosphorus (27-38%)
↓ Urinary calcium (87%)
↓ 25-hydroxyvitamin D (calcidiol) (

33
Q

X-ray findings
for OM?
(most common 1)
5

A
  1. Most common finding : reduced bone density with thinning of the cortex
  2. Looser pseudofractures
  3. Fissures, or narrow radiolucent lines
  4. Loss of radiologic distinctness of the vertebral body trabeculae and
  5. concavity of the vertebral bodies (codfish vertebrae)
34
Q

Looser’s zones (fractures)

  1. What are these?
  2. Usually at what angle to the involved cortex?
  3. Associated most frequently with what? 2
  4. What type of fx are these?
  5. Describe the margins?
A
  1. Cortical infarctions
  2. wide transverse lucencies traversing bone usually at right angles to the involved cortex
  3. Associated most frequently with osteomalacia and rickets
  4. Pseudofractures and considered a type of insufficiency fracture
  5. Sclerotic irregular margins and are often symmetrical
35
Q

OM tx?

A
  1. Correct underlying cause

2. Vitamin D supplementation

36
Q

OM vit D management considerations? 4

A
  1. 50,000 IU Q week X 6-8 weeks
  2. Followed by 800 IU daily
  3. Check serum and urine calcium at 1 mo, 3 mo, then Q 6-12 mo
  4. Check serum 25-OH-Vit D at 3-4 mo post initiation of therapy
37
Q

OM

  1. Fx most commonly where? 2
  2. How is it different from OP?
  3. Why may the xray look like poor quality?
  4. What is a vitamin D metabolite and used for vitamin D replacement in renal and hepatic disease instead of Vit D2 or D3?
A
  1. Fractures most common in the
    - distal radius and
    - proximal femur
  2. Not a significant cause of hip fractures like osteoporosis
  3. Loss of mineralization may make the x-ray image look poor quality
  4. Calcitriol
38
Q

Rickets

  1. What is rickets?
  2. Rickets and osteomalacia usually occur together as long as what?
  3. After this?
A
  1. Deficient mineralization at the growth plate
  2. Rickets and osteomalacia usually occur together as long as the growth plates are open
  3. Only osteomalacia occurs after the growth plates have fused
39
Q

Cause

of rickets? 3

A
  1. Decreased calcium
  2. Decreased vitamin D
  3. Renal phosphate wasting
40
Q

Renal osteodystrophy

what is it?

A

Bone disease secondary to chronic kidney failure

41
Q

Types of bone disease secondary to renal failure

4

A
  1. Osteitis fibrosa
  2. Mixed uremic osteodystrophy
  3. Osteomalacia
  4. Adynamic bone
42
Q

Disorder of mineral and bone metabolism

5

A
  1. Calcium, phosphorus, vitamin D metabolism
    PTH
  2. Bone turnover
  3. Bone mineralization, volume, linear growth
  4. Bone strength
  5. Extraskeletal calcification also occurs
43
Q

Secondary hyperparathyroidism is a major contributor

  1. How?
  2. Decreased what? 2
  3. Increased what? 1
  4. Reduced expression of what? 3
A
  1. Phosphate retention
    • Decreased free ionized calcium
    • Decreased 1,25 dihydroxyvitamin D
  3. Increase fibroblast growth factor
  4. Reduced expression of
    - vitamin D receptors,
    - calcium sensing receptors,
    - fibroblast growth factor receptor
44
Q

Summary of secondary hyperparathyroidism in CKD

  1. Starts when?
  2. Calcitriol deficiency and hyperphosphatemia = what?
  3. Hypocalcemia causes an increase in what?
A
  1. Starts when GFR below 60 ml/min
  2. Calcitriol deficiency and hyperphosphatemia = hypocalcemia
  3. Hypocalcemia causes an increase in PTH
45
Q

Renal osteodystrophy: Define the following

  1. Osteitis fibrosis?
  2. Adynamic bone disease?
  3. Osteomalacia?
  4. Mixed uremic osteodystrophy?
A
  1. high turnover secondary to hyperparathyroidism
  2. low turnover, most common CKD related bone disease, due to suppression of the parathyroid glands
  3. low turnover with abn mineralization, not that common in CKD
  4. either high or low turnover and abnormal mineralization
46
Q

Renal osteodystrophy Summary

  1. Disorders chracterized by? 3
  2. Tx aimed at?
  3. Basis of treatment for secondary hyperparathyroidism in CKD? 3
A
  1. Disorders characterized by
    - bone turnover,
    - mineralization
    - volume
  2. Treatment is aimed at the underlying problem
  3. Basis of treatment for secondary hyperparathyroidism in CKD
    - Dietary restriction of phosphorus
    - Supplemental active form of vitamin D (calcitriol)
    - Phosphate binders

*Orthopaedic Surgery (28 decks)

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