CPM Flashcards

1
Q

How is osteoporosis diagnosed?

A

→Measurement of bone mineral density (BMD)

→Dual-energy X-ray absorptiometry (DEXA or DXA scan)

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2
Q

What are the stages of osteoporosis?

A

→osteopenia
→osteoporosis
→severe osteoporosis

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3
Q

What are the causes of osteoporosis?

A

→Hypogonadism – notably any cause of oestrogen deficiency

→Excess glucocorticoids – endogenous or exogenous- Cushing’s syndrome

→Hyperparathyroidism- excess resorption

→Hyperthyroidism

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4
Q

Why does oestrogen decreased after menopause?

A

→no more follicles

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5
Q

What are the treatments for osteoporosis?

A

→Bisphosphonates

→PTH analogues

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6
Q

How is osteoporosis treated in postmenopausal?

A

→HRT

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7
Q

How does Denosumab treat osteoporosis?

A

→human monoclonal antibody against RANK ligand

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8
Q

What is bisphophonate?

A

→inhibit function of osteoclasts: risedronate, alendronate- reduce rate of bone turnover

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9
Q

How does romosozumab treat osteoporosis?

A

→human monoclonal antibody against sclerostin

→Sclerostin inhibits Wnt signalling

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10
Q

What is osteomalacia?

A

→Loss of bone mineralization

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11
Q

What are symptoms of osteomalacia?

A

→Permanent deformities in bone growth (rickets)

→Diffuse aches and pains

→Chronic fatigue
Weak bones

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12
Q

What is elevated in osteomalacia?

A

→Elevated alkaline phosphatase- enzyme marker for bone turnover

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13
Q

What is a difference between osteoporosis and osteomalacia?

A

→osteoporosis is when there is loss of organic and mineralisation

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14
Q

What are the causes of osteomalacia?

A

→Vitamin D deficiency (most common), lack of Vit D supplements or sunlight exposure

→Mutations leading to errors in vitamin D metabolism (rare)

→Hypophosphataemia

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15
Q

In VitD deficiency, what are the levels of Ca, Pi, 25OHD3, 1,25OH, PTH?

A
→Ca- low
→Pi- low
→25 OH D3- low
→1, 25 OH D3- normal
→PTH- high
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16
Q

In renal disease, what are the levels of the hormones?

A
→Ca- low
→Pi- high
→25 OH D3- normal
→1, 25 OH D3- low
→PTH- very high
17
Q

In 1a hydroxylase mutation (Ricket’s type 1)?

A
→Ca- low
→Pi- low
→25 OH D3- normal
→1, 25 OH D3- normal
→PTH- high
18
Q

In 1a hydroxylase mutation (Ricket’s type 2)?

A
→Ca- low
→Pi- low
→25 OH D3- normal
→1, 25 OH D3- very high
→PTH- high
19
Q

What is VitD dependent rickets type 1?

A

→1α hydroxylase mutation1

20
Q

What is VitD dependent rickets type 2?

A

→Vit D receptor mutation

21
Q

What are the three disorders as a result of osteomalacia and hypophosphataemia?

A

→X-linked hypopho-phataemic rickets

→Autosomal dominant hypopho-phataemic rickets

→Oncogenic osteomalacia

22
Q

Which cells secrete FGF23?

A

→osteocytes

23
Q

Why does mutation in FGF23 cause excess phosphate excretion?

A

→Mutation changes proteolytic sequence so FGF-23 remains in circulation for longer

24
Q

What are the clinical manifestations of renal osteodystrophy?

A

→Impaired Pi excretion
→High plasma Pi
→Impaired Vit D activation
→Low plasma Ca because of less absorption
→PTH rises
→Excess bone resorption
→May be augmented by acidosis (impaired renal H+ excretion

25
Q

What does acidosis favour?

A

→bone mineralisation