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MMB > MMB [046]a Postmenopausal Osteoporosis > Flashcards

MMB [046]a Postmenopausal Osteoporosis Flashcards

1
Q

What is osteoporosis ?

A

• A medical condition in which the bones become brittle and fragile from loss of tissue, typically as a result of hormonal changes, or deficiency of calcium or vitamin D

• The fragility and weakness of bone make it subject to fracture

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2
Q

Causes of osteoporosis ?

A

typically as a result of hormonal changes, or deficiency of calcium or vitamin D

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3
Q

•….(hormone) plays an important role in the growth and maturation of bone as well as in the regulation of bone turnover in adult bone.

•…..(hormone) deficiency leads to increased osteoclast formation and enhanced bone resorption

A

Estrogen

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4
Q

List interventions and medications used in : Prevention and Treatment of osteoporosis

A

• Hormone replacement therapy (HRT)

• Bisphosphonates

• Tibolone

• Selective Estrogen Receptor Modulators

• Strontium ranelate

• Calcium and vitamin

• others

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5
Q

Mechanism of action of : Hormone Replacement Therapy ?

A

• The major physiological effect of estrogen is to inhibit bone resorption.

  • Direct action
  • enhancing apoptosis
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6
Q

• With estrogen deficiency, there is large increase in bone resorption caused by:

A
  • increased osteoclast (OC) numbers (due to enhanced OC formation and reduced OC apoptosis).

-increased OC activity.

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7
Q

Risks of Hormone Replacement Therapy ?

A

• breast cancer
-inconclusive for E + P
-no increase with E alone

• stroke
-dose
-no increase if HRT initiated below age 60 years

• venous thrombo-embolism
-dose / route
-transient increase seen with oral HRT
-no increase with transdermal HRT

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8
Q

Comment on the breast cancer risk of HRT medication

A

• inconclusive for E + P

• no increase with E alone

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9
Q

Comment on the risk of stroke associated with HRT medication

A

• dose dependent

• no increase if HRT initiated below age 60 years

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10
Q

Comment on the risk of venous thrombo-embolism associated with HRT medication

A

• dose / route dependent

• transient increase seen with oral HRT

• no increase with transdermal HRT

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11
Q

Explain Bisphosphonates Mechanism of action

A

• The bisphosphonates inhibit the resorption of bone by osteoclasts and may have an effect on osteoblasts.

• They are structurally similar to pyrophosphate, a normal product of human metabolism. This structure gives the drugs a high affinity for bone and they probably remain in bone for many years.

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12
Q

Why does bisphosphonates have a high affinity for bone and they probably remain in bone for many years ?

A

• They are structurally similar to pyrophosphate, a normal product of human metabolism. This structure gives the drugs a high affinity for bone and they probably remain in bone for many years.

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13
Q

risks of Bisphosphonates ?

A

• gastro-intestinal side-effects

• atrial fibrillation
-more severe with IV bisphosphonates

• osteonecrosis of the jaw
- more common with IV bisphosphonates
-follows dental extractions only

• inflammatory eye disease
- only with IV bisphosphonates

• oesophageal cancer
-only with oral bisphosphonates
-taken for >3 years

• femoral stress fractures
-long term bisphosphonates

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14
Q

Comment on risk of atrial fibrillation associated with Bisphosphonates

A

more severe with IV bisphosphonates

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15
Q

Comment on risk of jaw osteonecrosis associated with Bisphosphonates

A

• more common with IV bisphosphonates

• follows dental extractions only

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16
Q

Comment on risk of inflammatory eye disease associated with Bisphosphonates

A

• only with IV bisphosphonates

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17
Q

Comment on risk of oesophageal cancer associated with Bisphosphonates

A

• only with oral bisphosphonates

• taken for >3 years

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18
Q

Comment on risk of femoral stress fractures associated with Bisphosphonates

A

• long term bisphosphonates

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19
Q

What’s Tibolone ?
In 4 points

A

• Tibolone is a synthetic hormone drug that possesses oestrogenic, progestogenic and weak androgenic properties

• Tibolone itself has no biological activity; its effects are the results of the activity of its metabolites on various tissues.

• Tibolone is effective in preventing bone loss, without stimulating the endometrium.

• The tissue-selective effects of tibolone are the result of metabolism, enzyme regulation and receptor activation that vary in different tissues.

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20
Q

•…..(synthetic hormone HRT) itself has no biological activity; its effects are the results of the activity of its metabolites on various tissues.

A

Tibolone

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21
Q

•….(synthetic hormone HRT) is effective in preventing bone loss, without stimulating the endometrium.

A

Tibolone

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22
Q

How does The tissue-selective effects of Tibolone acquire ?

A

• The tissue-selective effects of tibolone are the result of metabolism, enzyme regulation and receptor activation that vary in different tissues.

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23
Q

Tibolone risks ?

A

• breast cancer
- reduced risk in normal women
- increased risk in breast cancer survivors

• stroke
-apparent increased risk

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24
Q

Comment on breast cancer risk associated with Tibolone

A

• reduced risk in normal women

• increased risk in breast cancer survivors

25
Q

Comment on stroke risk associated with Tibolone

A

• apparent increased risk

26
Q

What are SERMs ?

A

Selective Estrogen Receptor Modulators

27
Q

Give a famous example of SERMS

A

Raloxifene

28
Q

What is Raloxifene ?

A

• Raloxifene is an oral selective estrogen receptor modulator (SERM).

29
Q

Raloxifene mechanism of action ?

A

• The biological actions of raloxifene are largely mediated through binding to estrogen receptors. This binding results in activation of estrogenic pathways in some tissues (agonism) and blockade of estrogenic pathways in others (antagonism).

• It has estrogenic actions on bone and anti-estrogenic actions on the uterus and breast.

30
Q

Action of Raloxifene on bone ?

A

It has estrogenic actions on bone

31
Q

Action of Raloxifene on the uterus and breast ?

A

It has anti-estrogenic actions on the uterus and breast.

32
Q

What is Strontium Ranelate ?

A

• A strontium (II) salt of ranelic acid, is a medication for osteoporosis.

33
Q

In vitro means ?

A

Outside of the natural environment

34
Q

In vitro effect of Strontium ranelate ?

A

• Strontium ranelate is known to increase in vitro osteoblast differentiation from progenitors, as well as osteoblast activity and survival

35
Q

Strontium Ranelate effect on bone ?

A

• Concerning bone-antiresorbing mechanisms, strontium ranelate decreases osteoclast differentiation and activity, while increasing their apoptosis.

36
Q

Comment on Strontium Ranelate’s effect on knee osteoarthritis

A

• It can slow the course of osteoarthritis of the knee.

37
Q

….(drug) is promoted as a dual action bone agent (DABA).

A

Strontium Ranelate

38
Q

What’s Teriparatide ?

A

• Is the recombinant form of parathyroid hormone.

39
Q

…… are the main minerals necessary for bone health.

A

Calcium and phosphate

40
Q

…..(hormone) is naturally produced by the body and is the key regulator of calcium and phosphate metabolism in the bone and kidney.

A

PTH

41
Q

Teriparatide mechanism of action ?

A

• Is the recombinant form of parathyroid hormone.

• Teriparatide binds to the same receptors as natural PTH and mimics the favorable effects of PTH on bone health.

42
Q

Teriparatide risks ?

A

• bankruptcy! Haha 🤣
-£5,000 for 18 month course

• hypersensitivity reactions

• hypercalcaemia

• hypercortisolism

• ? increased osteosarcoma risk (animals)

43
Q

Newest treatment approaches to osteoporosis ?

A

• target signalling systems to bone cells

• target cellular action of bone cells

44
Q
A
45
Q

What is Denosumab ?

A

Denosumab Is a human IgG2 monoclonal antibody, with affinity and specificity for human RANKL( receptor activator of nuclear factor kappa –B ligand)

46
Q

Denosumab mechanism of action ?

A

• a human IgG2 monoclonal antibody , with affinity and specificity for human RANKL ( receptor activator of nuclear factor kappa –B ligand) ; which is a soluble protein essential for the formation, function, and survival of osteoclasts, the cells responsible for bone resorption.

• Denosumb prevents RANKL from activating its receptor RANK , on the surface of osteoclasts and their precursors.

47
Q

What’s Cathepsin K ?

A

• it inhibits the cysteine protease cathepsin K (CatK), abundantly expressed in osteoclasts, which is responsible for the degradation of bone matrix proteins.

48
Q

What are human cysteine cathepsins ?

A

• The human cysteine cathepsins are a family of very close cousins of which there are 11 lysosomal cysteine proteases or cathepsins.

These proteins are synthesized, stored in lysosomes, and then are secreted to the external environment into the protective space under the osteoclast, where they will do their proteolytic activity.

49
Q

Examples of Cathepsin K Inhibitors ?

A

• odanacatib (Merck)
-50 mg weekly
-phase 3

• ONO-5334 (Ono)
-300 mg daily
-phase 2

• MIV-711 (Medivir)
-pre-clinical

50
Q

Cathepsin K Inhibitors in phase 3 clinical trials ?

A

• odanacatib (Merck)

51
Q

Cathepsin K Inhibitors in phase 2 clinical trials ?

A

• ONO-5334 (Ono)

52
Q

Cathepsin K Inhibitors in pre-clinical trials ?

A

• MIV-711 (Medivir)

53
Q

….(drug) Has similar reduction properties to bone resorption markers like bisphosphonates

A

Cathepsin K Inhibitors

54
Q

….(drug) has lesser reduction in bone formation markers than bisphosphonates

A

Cathepsin K Inhibitors

55
Q

….(drug group) is characterized with rapid offset of action after stopping therapy

A

Cathepsin K Inhibitors

56
Q

….(drug) has skin adverse events when combined with balicatib

A

Cathepsin K Inhibitors

57
Q

What’s Sclerostin ?

A

• Sclerostin is an osteocyte secreted protein, negatively regulates osteoblasts and inhibits bone formation.

58
Q

Mechanism of action for : Sclerostin Antibody AMG 785 ?

A

• Sclerostin is an osteocyte secreted protein, negatively regulates osteoblasts and inhibits bone formation.

• Sclerostin monoclonal antibody (AMG 785) inhibits sclerostin osteolytic effect.

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