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S3 Case 3 - Musculoskeletal > Pathophysiology of Osteoporosis > Flashcards

Pathophysiology of Osteoporosis Flashcards

1
Q

What are the determinants of bone strength?

A

Geometry + BMD

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2
Q

What regulates calcium?

A

Parathyroid hormone (PTH)
Calcitonin

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3
Q

How does PTH regulate calcium?

A

Increases calcium by stimulating osteoclasts, increasing intestinal absorption + decreases calcium excretion by kidneys

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4
Q

How does Calcitonin regulate calcium?

A

Decreases calcium by inhibiting osteoclast activity + increasing calcium excretion via kidneys

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5
Q

How does calcium regulation work overall?

A

Homeostasis remained by PTH + calcitonin
Rise in blood Ca = thyroid release calcitonin = stimulates Ca salt deposit in bone
Falling blood Ca = parathyroid gland release PTH = signals osteoclasts to degrade bone + release Ca into blood

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6
Q

What is osteoporosis?

A

Skeletal disorder where bone strength is compromised with an increased risk of fracture

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7
Q

What is osteomalacia + rickets?

A

Abnormal bone formation due to inadequate mineralisation

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8
Q

What are the causes of osteomalacia?

A

Severe, prolong VitD deficiency
Long term anticonvulsant therapy (eg. phenobarbital)

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9
Q

What is the pathophysiology of osteomalacia?

A

Normal bone resorption + formation
But body unable to fully mineralise newly formed osteoid tissue = decreased bone strength

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10
Q

What is the treatment of osteomalacia?

A

High dose of VitD

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11
Q

How does osteoporosis develop?

A

Osteoclast recruitment increased
Osteoblast-osteoclast coupling interrupted
= factors don’t adequately recruit osteoblasts
Lack of oestrogen = less bone stimulation + deposition = reduced later osteoblast recruitment

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12
Q

What does hormone dysregulation do to osteoporosis?

A

Accelerate it
= oestrogens + androgens help maintain bone mass

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12
Q

What happens in postmenopausal osteoporosis?

A

Increases proliferation + activation of osteoclasts
Prolongs survival of osteoclasts

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12
Q

What is type I osteoporosis?

A

Postmenopausal osteoporosis
= oestrogen deficiency

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13
Q

What is type II osteoporosis?

A

Senile osteoporosis
= bone loss due to increased bone turnover

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14
Q

How does long-term glucocorticoids cause osteoporosis?

A

Alteration in Ca absorption = secondary hyperparathyroidism
Inhibitory effect of sex hormone production
Inhibition of osteoblast function

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15
Q

How do anticoagulants (heparin) cause reversible osteoporosis?

A

Increased osteoclast activity
Decreased osteoblast activity
Antagonist effect on VitK

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16
Q

What other drugs may cause osteoporosis?

A

GnRH
Antiepileptics (eg. Phenytoin)
Loop diuretics (eg. Furosemide)

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17
Q

How is osteoporosis diagnosed?

A

BMD

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18
Q

What is the non-pharmacological treatment of osteoporosis?

A

Stop alcohol + smoking
Increase calcium in diet
Regular exercise
Avoid drugs that induce it

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19
Q

What are the pharmacological therapies for osteoporosis?

A

Bisphosphonates
Ca
VitD
Oestrogen
Oestrogen receptor modulators (SERM)

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20
Q

How much calcium should the average healthy adult receive?

A

1000mg

21
Q

How much calcium should someone over 65/osteoporosis/post-menopausal need?

A

1500mg

22
Q

How is total daily Ca achieved?

A

Diet + diet supplements

23
Q

What are the drug interactions for calcium?

A

Fe therapy impairs absorption
Tetracyclines 2hrs apart = avoid intestinal chelation

24
Q

What are the adverse effects of calcium?

A

Nausea
Constipation
Abdominal distension
Excess Ca = kidney stones

25
Q

What is given fir VitD?

A

Cholecalciferol

26
Q

How does Cholecalciferol work?

A

Improves Ca absorption in GI tract

27
Q

What are the adverse effects of Cholecalciferol?

A

Hypercalcemia (symptoms: anorexia, nausea + weakness)

28
Q

What are the drug interactions of Cholecalciferol?

A

Thiazide diuretics = increase risk of hypercalcemia

29
Q

What is the mechanism of action of Calcitonin?

A

Inhibits bone resorption by inhibiting osteoclast activity

30
Q

How is Calcitonin administrated?

A

Given by injection (SC/IM)

31
Q

What must patients do during the treatment of Calcitonin?

A

Ingest adequate Ca + VitD

32
Q

What are the adverse effects of Calcitonin?

A

Nausea + GI discomfort
Initial face flushing + dermatitis
Pruritis at site of injection

33
Q

What is the adverse effect of nasal Calcitonin?

A

Rhinitis

34
Q

What is the indication of Calcitonin?

A

2nd line treatment for osteoporotic patients who cannot tolerate other antiosteoporotic agents

35
Q

What is the indication of bisphosphonates?

A

1st line treatment for prevention of osteoporotic fractures

36
Q

How do bisphosphonates work?

A

Reduce bone absorption by inhibiting osteoclasts
By binding to hydroxyapatite on bone mineral surface
Taken up by osteoclast + modify activity
Induce apoptosis

37
Q

Where are bisphosphonates excreted from?

A

Kidneys
= not recommended for patients with impaired renal function

38
Q

What are the adverse effects of bisphosphonates?

A

Oesophagitis, gastritis + peptic ulcer
Mild fever
Aches following parentals

39
Q

What is the mechanism of action of oestrogen?

A

Supress bone resorption

40
Q

What are the adverse effects of oestrogen?

A

Increase incidence of breast + endometrial cancers
Increase risk of DVT + gall bladder disease

41
Q

What are the indications of SERMs?

A

Postmenopausal women at risk for osteoporosis who cannot take bisphosphonates
Post menopausal women at increased risk for breast cancer

42
Q

What is the indication of Teriparatide (recombinant PTH)?

A

Severe osteoporosis in men + postmenopausal women

43
Q

What is the mechanism of action of Teriparatide (recombinant PTH)?

A

Supplements production of parathyroid hormone
Regulates calcium-phosphate balance + stimulates new bone growth

44
Q

What is the administration of Teriparatide (recombinant PTH)?

A

Injected daily S/C
Use limited to 2-year duration

45
Q

What are the adverse effects of Teriparatide (recombinant PTH)?

A

Postural hypertension
Hypercalcemia
Associated with osteosarcoma

46
Q

What are the contraindications of Teriparatide (recombinant PTH)?

A

Untreated hyperthyroidism
Recurrent urolithiasis

47
Q

What is RANKL?

A

Mediator of osteoclast differentiation, activation + survival = primary mediator of bone resorption

48
Q

What is osteoprotegerin?

A

Alternative binding site for RANKL (decoy receptor), which cannot activate cellular signalling

49
Q

What is Denosumab?

A

Monoclonal Ab to RANKL

50
Q

What does Denosumab do?

A

Reduces osteoclast development = increases BMD
= reduces risk of fractures

51
Q

What is the mechanism of action of Denosumab?

A

RANKL to surface of pre-osteoclast
Activation of RANK by RANKL = maturation of osteoclast
Denosumab inhibits maturation by inhibiting RANKL
NO osteoclast = no bone resorption

S3 Case 3 - Musculoskeletal (14 decks)

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