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Hannah's Locomotor > Drugs Used to Treat Disorders of Bone > Flashcards

Drugs Used to Treat Disorders of Bone Flashcards

1
Q

List 5 disorders of bone metabolism and give an example of when each might arise

A

Hypocalcaemia (e.g. vitamin D deficiency)
Hypercalcaemia (e.g. some malignancies)
Hypophosphataemia (e.g. nutritional deficiency states)
Hyperphosphataemia (e.g. renal failure)
Osteoporosis (associated with ageing, post-menopause, corticosteroid use)

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2
Q

What is the relationship between bone and tetracycline use?

A

Tetracycline is incorporated into bone and may remain there for the life of the animal
It is used as a growth marker in mice

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3
Q

What % of trabecular bone is remodelled in adults every year? What % of cortical bone is remodelled? What is the relevance of this to pathology?

A

25%
3%
Disorders affecting bone metabolism preferentially affect trabecular bone; sites with predominantly trabecular bone are at risk of fracture (e.g. femoral neck, vertebral bodies)

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4
Q

How do osteoblasts regulate osteoclast activity?

A

Osteoblasts are stimulated by calcitriol, PTH and cytokines including IL-6 to express OPGL/RANKL
RANKL interacts with RANK on osteoclasts to stimulate the differentiation and activation of precursor cells (via the release of M-CSF)
Osteoblasts also release OPG which binds to OPGL to dampen osteoclast maturation

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5
Q

What does OPG stand for?

A

Osteoprotegerin

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6
Q

What is the effect of PTH on bone remodelling?

A

Increased osteoblast activity

Increased osteoclast activity

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7
Q

What is the effect of oestrogen on bone remodelling?

A

Decreased osteoclast activity

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8
Q

What is the effect of glucocorticoids on bone remodelling?

A

Increased osteoclast activity
Decreased osteoblast activity
Suppresses IGF and TGF-B (role in promoting osteoblast activity and bone formation)

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9
Q

What is the role of calcitonin in bone remodelling?

A

Decreased activity of osteoclasts

Decreased serum Ca2+

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10
Q

What is the effect of embedded cytokines (including BMP-2) on bone remodelling, when they are released?

A

Increased osteoblast activity

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11
Q

How does calcitriol increase plasma Ca2+?

A

Increased intestinal absorption
Decreased renal excretion
Increased osteoclast activity

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12
Q

How does PTH increase plasma Ca2+?

A

Increased calcitriol synthesis
Acts on osteoclasts and osteoblasts to liberate Ca2+ from bone
Decreased renal Ca2+ excretion

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13
Q

Define osteoporosis

A

Reduction in bone mass more than 2.5 SDs below the norm for healthy 30 year old women

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14
Q

Define osteopaenia

A

Reduction in bone mass 1-2.5 SDs below the norm for healthy 30 year old women

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15
Q

When is peak bone density attained?

A

20s-30s

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16
Q

Describe the pathophysiology of osteoporosis

A

Increased production of cytokines results in activation of osteoclasts
The life span of osteoclasts increases whilst the lifespan of osteoblasts decreases
These factors combine to produce deeper, larger resorption cavities in bone
Shorter lifespan of osteocytes due to increased apoptosis causes microdamage to the bone
The microdamage and large resorption cavities in the bone produce more fragile bone which fractures easily

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17
Q

List 3 antiresorptive agents used to treat disorders of bone

A

Bisphosphonates
Selective oestrogen receptor modulators
RANKL inhibitors

18
Q

List 4 bone anabolic agents

A

PTH
Oral Ca2+
Oral vitamin D
Calcitonin

19
Q

Give an example of a bisphosphonate

A

Alendronate

20
Q

What are bisphosphonates?

A

Enzyme resistant analogues of pyrophosphate (P-O-P)

21
Q

How do bisphosphonates prevent bone resorption?

A

They are incorporated into the bone matrix and ingested by osteoclasts during bone maturation, causing apoptosis

22
Q

How often are bisphosphonates administered? Why?

A

Weekly; they accumulate at sites of bone mineralisation and remain there for long periods

23
Q

What are 4 possible adverse effects of bisphosphonates?

A

Oesophagitis
Oesophageal cancer (?)
Atypical fractures (?)
Osteonecrosis of the jaw (?)

24
Q

What is the role of oestrogen in bone metabolism?

A

Decreases osteoclast proliferation, differentiation and activation
Promotes osteoclast apoptosis
Increases life span of osteoblasts and osteocytes
Does not INCREASE bone mass but MAINTAINS mass and slows loss

25
Q

How is oestrogen administered to treat bone disorders?

A

With progesterone

26
Q

What are some of the risks of using oestrogen to treat bone disorders?

A

CVD

Breast cancer

27
Q

Give an example of a selective oestrogen receptor modulator

A

Raloxifene

28
Q

How does raloxifene work?

A

Agonist at oestrogen receptors in bone and CV tissue

Antagonist at oestrogen receptors in mammary tissue and uterus

29
Q

What has replaced HRT as the mainstay treatment for osteoporosis?

A

SERMs

30
Q

Give an example of a RANKL inhibitor

A

Denosumab

31
Q

What is denosumab?

A

A human monoclonal antibody which binds RANKL to inhibit its activity, thereby reducing osteoclastic activity

32
Q

Describe the paradoxical nature of PTH’s effect on bone

A

Once daily subcutaneous administration of PTH favours its role in bone anabolism (acute promotion of osteoblast development and activity)
Continuous or high exposure to PTH favours bone catabolism by promoting osteoclast activity

33
Q

What oral calcium salts are used as adjunctive therapy in osteoporosis?

A

Calcium gluconate

Calcium lactate

34
Q

What is one possible adverse effect of the use of calcium salts for adjunctive therapy in osteoporosis?

A

GI disturbances

35
Q

What other chemical element is prescribed orally as an adjunctive therapy in osteoporosis?

A

Strontium (close to Ca2+ in the periodic table, also absorbed into bone)

36
Q

What is oral vitamin D used to treat?

A 
Deficiency states (e.g. rickets, osteomalacia)
Endocrine dysfunction (hypoparathyroidism)
Chronic renal disease (calcitriol cannot be produced in the kidney)
37
Q

What are the available forms of oral vitamin D?

A 
Vitamin D2 (converted to D3 in the liver)
Calcitriol (biologically active D3)
38
Q

What forms of calcitonin are available for prescription?

A

Natural (porcine) calcitonin

Synthetic (salcatonin)

39
Q

How is calcitonin administered?

A

SC or IM injection

40
Q

When is calcitonin used?

A

In hypercalcaemia associated with malignancy

With other agents in osteoporosis

41
Q

What are the 3 mechanisms by which malignancy may produce a hypercalcaemia?

A

Osteolytic metastases (most commonly from breast cancer) with local release of cytokines (including osteoclast activating factors)
Tumour secretion of parathyroid hormone-related peptide (PTHrP)
Tumour production of calcitriol

Hannah's Locomotor (10 decks)

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