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Cardio > Seminar C Osteoporosis > Flashcards

Seminar C Osteoporosis Flashcards

1
Q

Trabecular bone action →

A
  1. Calcium reservoir

2. Site of haematopoiesis

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2
Q

Bone consists of

A

osteoid, a collagenous organic matrix, (organic phase) on which is deposited complex inorganic hydrated calcium salts known as hydroxyapatites (mineral phase)

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3
Q

Organic Phase

A

type 1 collagen and other non-collagenous proteins e.g.osteocalcin

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4
Q

Bone turnover mediated by

A

Cytokines (not completely sure)

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5
Q

Bone formation requires

A

osteoid synthesis and adequate calcium and phosphate for the laying down of hydroxyapatite

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6
Q

Osteoblasts secrete

A

Alkaline phosphatase - is essential to the process, probably acting by releasing phosphate from pyrophosphate.

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7
Q

Bone acts as important reservoir of

A

calcium, phosphate and, to a lesser extent, magnesium and sodium

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8
Q

Osteoblasts produce

A

Osteoid

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9
Q

Systemic Hormones bone control

A

PTH
Vitamin D
Oestrogen
Growth hormone

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10
Q

Local hormones bone control

A

Osteoclast regulatory e.g. OSF

Osteoblast regulatory e.g. Wnt signaling

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11
Q

Parathyroid Hormone → Secreted in response to

A

Plasma ionised Calcium

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12
Q

Parathyroid Hormone →PTH Function

A

Increase plasma calcium concentration and reduce plasma phosphate.

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13
Q

Parathyroid Hormone →PTH action on Kidneys

A

Increases the tubular reabsorption of calcium in the kidneys.

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14
Q

Parathyroid Hormone →PTH action on bone

A

Releases calcium into the ECF, and so increases the amount of calcium filtered by the glomeruli.

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15
Q

Calcitonin →

A

is a polypeptide hormone produced by C cells of the thyroid. Experimentally it can be shown to inhibit osteoclast activity, and therefore bone resorption, but it is not known if this has any physiological significance.

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16
Q

Calcium Sensing Receptors → Receptor Type

A

G protein coupled receptor

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17
Q

Calcium Sensing Receptors → Function

A

Regulates the secretion of parathyroid hormone and the reabsorption of urinary calcium and therefore plays an important role in extracellular calcium homeostasis.

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18
Q

Calcium Sensing Receptors → Clinical disorders associated with abnormalities of receptor

A
  • Familial benign hypocalciuric hypercalcaemia
  • Neonatal severe hyperparathyroidism
  • Autosomal dominant hypocalcaemia
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19
Q

Metabolic Bone Diseases

A
  1. Rickets and Osteomalacia
  2. Hypocalcaemia and Hypercalcaemia
  3. Paget’s disease
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20
Q

Rickets:

A

is defective mineralization of bones before epiphyseal closure in immature mammals due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium, potentially leading to fractures and deformity.

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21
Q

Osteomalacia:

A

is the softening of the bones caused by defective bone mineralization secondary to inadequate amounts of available phosphorus and calcium, or because of overactive resorption of calcium from the bone as a result of hyperparathyroidism (which causes hypercalcemia).

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22
Q

Common Cause →metabolic bone disease

A

Vitamin D deficiency
Impaired hydroxylation of Vitamin D
Vitamin D resistance

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23
Q

Vitamin D deficiency

A

Reduced sunlight exposure
Malabsorption
Dietary deficiency

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24
Q

Impaired hydroxylation of Vitamin D

A

Chronic renal failure (Most common)

Chronic liver failure

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25
Q

Vitamin D resistance

A 
Hypophosphataemic e.g. oncogenic osteomalacia
Sex linked hypophosphataemic rickets
Renal tubular disorders
Hypophosphatasia
Drugs (e.g. epileptics), toxins
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26
Q

Clinical presentation: of metabolic bone disease

A
  1. Bone pain
  2. Skeletal deformity
  3. Muscle weakness
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27
Q

Childhood onset (Rickets)

clinical picture

A
  • Widened and irregular epiphyses
  • Bowing of long bones (bow legs)
  • Rib deformities - the inward pull of the diaphragm produces a groove in the rib cage.
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28
Q

Adult onset - symptoms tend to be more vague metabolic bone disease

A
  • Bone pains
  • Proximal muscle weakness
  • Waddling gait
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29
Q

Symptomatic hypocalcaemia in severe cases causes

A
  • Convulsions
  • Tetany
  • Cardiac arrhythmias
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30
Q

Investigations:

A

Xrays

Bloods

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31
Q

Xrays show in osteomalacia

A

a. Looser’s zones in osteomalacia

b. Bowed legs and widened epiphyses in rickets)

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32
Q

Bloods → in metabolic bone disease show

A
  1. Corrected calcium lower end of normal or frank hypocalcaemia in severe cases
  2. Secondary hyperparathyroidism frequently develops to compensate for the low calcium
    - low serum phosphate, elevated PTH, elevated alkaline phosphatase
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33
Q

Treatment: of rickets

A

Dietary defiency Oral vitamin D (Cholecalciferol)
Malabsorption Paraentral vitamin D
Renal failure Alfacalcidol (1 alpha hydroxyl vitamin D)

34
Q

What causes rickets and Osteomalacia?

A

Inadequate activity of vitamin D.

This can be due to vitamin D deficiency, impaired hydroxylation of vitamin D, or resistance to vitamin D.

35
Q

What are the main clinical features?

A

The main symptoms are bone pain, skeletal deformity and muscle weakness.
Children with rickets may have bowed legs and rib deformities.

36
Q

What might you find on x-rays?

A

Loosers zones, widened and irregular epiphyses, bowed long bones.

37
Q

How do blood tests differ between osteomalacia and osteoporosis?

A

Blood tests are normal in osteoporosis.

In Osteomalacia corrected calcium is normal or low, and secondary hyperparathyroidism often develops.

38
Q

What is the general aim of treatment?

A

Replace the vitamin D.

39
Q

Definition osteoporosis

A

Osteoporosis is a bone disorder featuring progressive loss of bone tissue and bone mass leading to weakening of bone. In osteoporosis, the total mass of bone is reduced, but there are a few other abnormalities. It results from the progressive imbalance between bone resorption and bone formation that is a feature of normal ageing. Some degree of osteoporosis is inevitable in all elderly patients.
→ normally in trabecular bone

40
Q

Osteoporosis Characterised by

A

by low bone mass and micro-architectural deterioration of bone tissue, leading to enhanced bone fragility and an increase in fracture risk. Bone is normally mineralised but is deficient in quantity, quality and structural integrity.

41
Q

Bone remodelling →

process (6)

A
  1. Begins with recruitment of osteoclast precursors to the remodelling unit, where they differentiate into mature osteoclasts.
  2. Triggered by mechanical stimuli or release of chemotactic factors from micro fractures in damaged bone.
  3. During the phase of bone resorption, osteoclasts remove a specific amount of bone, and they then undergo programmed cell death (apoptosis) in the reversal phase.
  4. Bone formation follows on from the reversal phase, beginning with recruitment of osteoblast precursors to the remodeling site.
  5. These cells then differentiate into mature osteoblasts and start to form new bone matrix (osteoid), which subsequently becomes calcified to form mature bone.
  6. Some osteoblasts become buried in the newly formed bone matrix to form osteocytes, which interconnect with each other and with lining cells on the bone surface.
42
Q

Factors affecting peak bone mass →

A
  • Genetic factors strongly influence bone mass, accounting for 70-80% of its variance.
  • Sex hormone status
  • Nutrition
  • Physical activity
43
Q

Factors affecting Bone loss →

A

• In women, oestrogen deficiency is a major pathogenic factor in menopausal bone loss.
• In men, the relationship between age-related bone loss and declining testosterone levels is less well documented.
• In the elderly, vitamin D insufficiency and secondary hyperparathyroidism are common and contribute to age-related bone loss.
Other potential pathogenetic factors include declining levels of physical activity and intestinal calcium malabsorption.

44
Q

Factors affecting peak bone mass →

A
  • Genetic factors strongly influence bone mass, accounting for 70-80% of its variance.
  • Sex hormone status
  • Nutrition

Physical activity

45
Q

Risk Factors: Endogenous

osteoporosis

A
  • Advancing Age
  • Female
  • Caucasian or Asian race
  • Fam history
46
Q

Risk Factors: Exogenous

A
  • Hypogonadism (either sex)
  • Steroids
  • Low BMI
  • Previous or prevalent fragility fracture
47
Q

Risk Factors for sustaining a fracture →

A 
•	Low bone mass
•	Personal or family history of fracture
•	Risk factors for falls:
o	Confusion disorders
o	Medications e.g. anxiolytics, sedatives, antihypertensives
o	Neuromuscular disease
o	Alcohol
o	Environmental factors e.g. poor lighting, uneven floor
48
Q

DEXA

A
  • Bone mineral density is measured at the femur and the lumbar spine – given T and Z scores.
  • Minimal radiation
49
Q

Indication for requesting a DEXA scan

A

• Low trauma/fragility fracture
• Oral glucocorticoids for 3 months or more or repeated courses of high dose steroids.
• Suggestion of osteopepenia on X-ray
• Predisposing medical conditions e.g. malabsorption, hypogonadism, and thyroid disease.
• Family history of osteoporosis or related fractures (especially maternal hip fracture)
• Low lifetime exposure to oestrogens e.g.
o Premature menopause (less than 45 years)
o Prolonged secondary amenorrhoea
o Post hysterectomy and oophorectomy

50
Q

Z scores

A

• Gives an age-matched comparison of bone density

51
Q

T scores

A

Gives a score to relate current bone density to predicted peak bone mass
→Less than -2.5 = osteoporosis (treat)
→Between -1.0 and- 2.5 = osteopenia (treat if history of low trauma fracture, or if taking glucocorticoids)
→ Greater than -1.0 = normal

52
Q

Simple blood test effectiveness

for osteoporosis

A

• (Serum calcium, phosphate and alkaline phosphatase and urinary calcium0 are normal in primary osteoporosis.

53
Q

Biochemical screen useful for in osteoprosis

A
  • Renal or liver impairment

* Osteomalacia (raised alkaline phosphatase, low phosphate, raised level of parathyroid hormone and reduced vit D

54
Q

Other screens

A
  • Myeloma screen (plasma and urinary protein electrophoresis)
  • Screen for coeliac disease (antigliadin antibodies)
55
Q

Treatment → osteoporosis

A

Reduce risk of fracture

Diet →

Other Conservative measures →

Calcium and Vitamin D supplements →

56
Q

Reduce risk of fracture

A
  1. Stopping bone loss
  2. Reducing bone turnover
  3. Increasing bone mass and strength
  4. Reducing fall risk
57
Q

Diet →

A
  • Should include at least 1000mg of calcium daily (1500 mg post menopause)
  • 400-800 of Vitamin D
  • Calcium salts – decrease in bone turnover
58
Q

Other Conservative measures →

A

Pain Relief → combination of simple analgesics and use of TENS machine
Physio → improve mobility
Reducing fall risk →

59
Q

Calcium and Vitamin D supplements →

A

Adjunctive therapy

60
Q

Royal college of Physicians states that any patient over the age of 65 years beginning a course of glucocorticoid treatment for 3 months or over should

A

longer should be treated with a bisphosphonate ± calcium/vitamin D, without the need for a DEXA scan.

61
Q

Bisphosphonates: Action

A

Adhere to hydroxyapatite and inhibit osteoclasts thereby suppressing bone resorption.
Strong affinity for calcium phosphate and act exclusively in calcified tissues.

62
Q

Bisphosphonates: Most used example

A

Alendronate (weekly regimens)

Risedronate (weekly regimens)

63
Q

Bisphosphonates: Newer agent

A

Bisphosphonate ibandronate (monthly)

64
Q

Bisphosphonates: Intravenous options

A

Pamidronate
Ibandronate
Zoledronate (once a year)

65
Q

Bisphosphonates: In combination

A

Vitamin D and calcium supplements

66
Q

Bisphosphonates: Review of treatment

A

3-5 years reassement

67
Q

Bisphosphonates: Side Effects

A

Upper Gi problems – oesophagitis

Poor oral availability (take without meals just water)

68
Q

Raloxifene → Definition

A

Estrogen receptor modulators (SERMs) – exert estrogen-like effects on the skeleton, protect against breast cancer.

69
Q

Raloxifene → With menopause

A

Increases the severity of hot flushes

70
Q

Strontium → Effect

A

Stimulates osteoblasts activity and suppressing osteoclasts.

71
Q

Strontium → Problem with strontium

A

Incorporated into the skeleton, leading to an artefactual increase in bone mineral density which makes it difficult to monitor response to treatment by repeat DXA scanning

72
Q

Teriparatide → Definition

A

Recombinant parathyroid hormone (Teriparatide) for refractory osteoporosis

73
Q

Teriparatide → Dosage

A

Daily subcutaneous injection 8 month course

74
Q

Teriparatide → Confusing because

A

PTH stimulates osteoclasts, causing resorption of bone but evidence shows the daily pulses increases new bone formation.

75
Q

Teriparatide → NICE guidelines

A

Treatment option in patients with severe osteoporosis (multiple vertebral fractures and low BMD)

76
Q

Teriparatide →Evidence for treatment of

A

Back Pain

77
Q

Other Management Options →

Activated vitamin D

A

Calcitriol

Alfacalcidol

78
Q

Indication for activated Vitamin D

A

Young patients or women of childbearing age

79
Q

Calcitonin →Use for and contraindications

A

Analgesic effects in patients with acute calcitonin treatment difficult to tolerate due to nausea and vomiting.

80
Q

Vertebroplasty → Process

A

Percutaneous injection of bone cement directly into a fractured vertebral body

81
Q

Vertebroplasty →Use

A

Painful vertebral fractures

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