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MSK and Soft Tissue > Osteoporosis > Flashcards

Osteoporosis Flashcards

1
Q

What is osteoporosis?

A

A condition characterised by decreased bone mass and micro architectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture

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2
Q

BMD changes to classify as osteoporosis?

A

BMD >2.5 SDs below the peak bone mass for you adults

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3
Q

What is osteopenia as per BMD?

A

BMD with T score between -1.0 and -2.5 SD below mean

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4
Q

What is primary osteoporosis?

A

Type 1: most common in post-menopausal women due to decline in oestrogen, worsens with age
Type 2: occurs after age 75, seen in females and males at 2:1 ratio; possibly due to Zn deficiency

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5
Q

Causes of secondary osteoporosis?

A
  • GIT: malabsorption, CLD, gastrectomy
  • Bone marrow disorders: MM, lymphoma, leukemia
  • Endocrine: Cushing’s syndrome, hyperparathyroidism, hyperthyroidism, premature menopause, diabetes
  • Malignancy: secondary to chemo, myeloma
  • Drugs
  • Other: RA, SLE, AnkSpond, renal disease, poor nutrition, immobilisation
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6
Q

What are the drugs precipitating osteoporosis?

A
  • Corticosteroid therapy
  • Phenytoin
  • Chronic heparin therapy
  • Androgen deprivation therapy
  • Aromatase inhibitors
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7
Q

CFx of osteoporosis?

A

Often asymptomatic:

  • Height loss due to vert #
  • Fractures: most common in hip, vertebrae, humerus and wrist
  • Pain (esp backache) ass/w #
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8
Q

Xray features of osteoporotic vertebral fractures?

A
  • Vertebral compression and crush #
  • Wedge fractures
  • Codfishing sign = weakening of subchondral plates and expansion of intervertebral discs
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9
Q

What are the indications for BMD testing in adults 50+?

A 
-All age 65+
Those with clinical RFx for #:
-fragility # after age 40
-prolonged steroid use
-other high risk medications
-parental hip fracture
-vert# or osteopenia identified on XR
-current smoking
-high alcohol intake
-low body weight
-RA
-Other disorders with strong association
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10
Q

What is the treatment for osteoporosis?

A 
LIFESTYLE: diet ++ calcium and Vit D; exercise (esp weight bearing); stop smoking, reduce caffeine
DRUG:
-Bisphosphonates (1st line)
-RANKL inhibitors
-Parathyroid hormone (teriparatide)
-DABA (strontium)
-Calcitonin (2nd line)
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11
Q

What is the function of bisphosphonates?

A

Inhibit osteoclast formation/binding

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12
Q

What are the bisphosphonates?

A

Alendronate, risendronate, zoledronic acid

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13
Q

What are the RANKL inhibitors? Function?

A

Denosumab; binds RANKL inhibiting osteoclast formation, activity and survival.

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14
Q

Osteoporosis treatment to consider selective to post menopausal women?

A
  • SERM

- HRT (oestrogen + progesterone)

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15
Q

What are the SERMS? (name and function)

A

e.g. raloxifene.

Agonist effect on bone, antagonist on breast, uterus.

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16
Q

DXA Z score?

A

The number of SDs above or below the mean for the patients age, sex and ethnicity

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17
Q

DXA T score?

A

The number of SDs above or below the mean for a healthy 30y adult of the same sex and ethnicity as the patient

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18
Q

Vit D target?

A

> 50 nmol/L

19
Q

What is P1NP?

A

Bone formation marker; cleared by liver endothelial cells

20
Q

What is CTX?

A

Bone resorption marker; cleaved during bone resorption. Cleared by kidneys.

21
Q

What are the goals of osteoporosis therapy?

A
  • Fracture risk reduction
  • Reduction in mortality by avoiding hip fractures
  • Improved quality of life; preserved mobility and independence
22
Q

Function of teriparatide?

A

Intermittent PTH stimulates osteoblasts

23
Q

What is strontium? How does it work?

A

Dual action bone agent; both activates osteoblasts and inhibits osteoclasts. Chemically similar to calcium and can be incorporated into bone.

24
Q

CIx to strontium?

A 
-Increased risk of MI
therefore Cix = 
-IHD / PVD / CVD
-HT
Other relative contraindications include other significant RFx for CV events
25
Q

When is teriparatide reimbursed by PBS?

A

-SEVERE OP (T

26
Q

What are the possible underlying aetiologies of fractures in the setting of chronic kidney disease?

A
  1. Osteoporosis
  2. Osteomalacia
  3. Hyperparathyroidism
  4. Adynamic bone disease
  5. Post transplantation (steroid, calcineurin inhibitors)
27
Q

How are bisphosphonates excreted?

A

Renally

28
Q

How should bisosphonate therapy be altered in CKD?

A

Dose reduction as renally excreted; reduce from fortnightly to monthly (i.e. by 50%)

29
Q

Most likely cause of fractures in setting of CKD?

A

Stage 1-3 CKD:

-# most likely osteoporotic rather than due to CKD-MBD

30
Q

Frequency of bisphosphoate therapy?

A

Weekly alendronate

Weekly/monthly risendronate

31
Q

Frequency of denosumab therapy?

A

6monthly injection

32
Q

What is osteonecrosis of the jaw?

A

Exposed necrotic bone >8 weeks

33
Q

RFx for ONJ?

A
  • IV / prolonged bisphosonate

- Steroid / smoker / poor oral hygiene

34
Q

Rate of ONJ for oral bisphonates?

A

Rate of 1 in 100 000 patient years of exposure

35
Q

When can drug holiday be considered from osteoporosis treatment?

A

If BMD increases to >T - 2.5 at femoral neck after 3-5y, a drug holiday can be considered but only if the pt monitored for any subsequent bone loss.

36
Q

What is renal osteodystrophy?

A

Changes to mineral metabolism and bone structure secondary to chronic kidney disease

37
Q

What are the bone diseases of renal osteodystrophy?

A

Renal osteodystrophy represents a mix of:

  1. Osteomalacia
  2. Adynamic bone disease
  3. Osteitis fibrosa cystica
  4. Mixed uremic osteodystrophy
38
Q

What is adynamic bone disease?

A

Low bone turnover due to excessive suppression of parathyroid gland

39
Q

What is osteitis fibrosa cystica?

A

Increased bone turnover due to secondary hyperparathyroidism

40
Q

What is mixed uremic osteodystrophy?

A

Bone high and low bone turnover, characterised by marrow fibrosis and increased osteoid

41
Q

Pathophysiology of renal osteodystrophy?

A

Combination of hyperphosphatemia (inhibits 1,25 Vit D synthesis) and loss of renal mass (reduced 1a hydroxylase)

42
Q

Clinical features of renal osteodystrophy?

A
  • Soft tissue calcifications (necrotic lesions if vessels involved)
  • Osteodystrophy (generalised bone pain and fractures)
  • Pruritus
  • Neuromuscular irritability and tetany may occur
  • Radiologic features
43
Q

Ix in renal osteodystrophy?

A

-CMP (corrected Ca2+)
-PTH
-ALP
-Imaging (XR, BMD)
+/- bone biopsy

44
Q

Treatment of renal osteodystrophy?

A

PREVENTION!

  • Maintenance of normal serum Ca2+ and PO4(3-) by restricting phosphate intake to 1g OD
  • Ca2+ supplements
  • Phosphate binding agents
  • Vit D supplementation

MSK and Soft Tissue (33 decks)

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