biochemical disorders of bone Flashcards

1
Q

what is osteomalacia/ Rickett’s

A

lack of mineralisation of osteoid (immature bone) resulting in abnormally soft bone (ricketts in children)

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2
Q

what causes osteomalacia (5)

A

insufficient calcium absorption, insufficient Vit D absorption/ production, post-menopause, phosphate deficiency, long term-anticonvulsants

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3
Q

what causes insufficient calcium absorption (osteomalacia)

A

lack of diet, defective absorption in GI tract

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4
Q

what causes insufficient vit D absorption (osteomalacia)

A

lack of sunlight/ vit D from diet (GI causes) causing secondary hyperparathyroidism (most common cause)

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5
Q

how does post menopause causes osteomalacia

A

lack of oestrogen

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6
Q

what causes can cause phosphate deficiency (osteomalacia)

A

renal disease, alcohol abuse

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7
Q

what are the symptoms of osteomalacia (4)

A

bone pain (pelvis, spine, femur), deformity (bowed legs, square head, pigeon chest), easily fractures, hypocalcaemia (cramp, fatigue, seizures)

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8
Q

what investigations can be done for ostoemalacia

A

X ray, biochem: low ca, low Vit D, low phosphate, high ALP and PTH

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9
Q

how do you treat osteomalacia

A

vit D replacement (Ca and phosphate supplements)

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10
Q

what is osteoporosis

A

decreased bone mineral density leading to increased risk of fracture with little trauma

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11
Q

what is the bone density of osteoporosis vs osteopenia

A

osteoporosis bone density 2.5SD below mean, osteopenia is intermediate stage and 1-2.4 SD below mean

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12
Q

what causes osteoporosis (6)

A

idiopathic, hyperparathyroidism, steroids, post menopause (loss of oestrogen and increased osteoclasts), old age, genes

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13
Q

what is type 1 osteoporosis

A

post menopausal –> increased osteoclast activity

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14
Q

what are risk factors for osteoporosis

A

smoking, white, alcohol, post menopause, sedentary, bad diet, vit D deficiency

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15
Q

what is type 2 osteoporosis

A

in elderly with greater density decline than normal

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16
Q

where do fractures usually occur in type 2 osteoporosis

A

femoral neck and vertebra

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17
Q

what are secondary causes of type 2 osteoporosis

A

endocrine (cushings and hyperparathyroidism), GI (malnutrition), drugs and alcohol (corticosteroids)

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18
Q

how do you diagnose osteoporosis

A

DEXA bone scan (gold standard), serum Ca and phosphate

19
Q

what lifestyle measures can be used in osteoporosis management

A

exercise, increased Vit D in diet, sunlight

20
Q

outline osteoporosis treatment

A

non curative, just slow progress. bisposphates –> desunomab –> stromium ranelate –> hormone replacement therapy (post menopausal women) (zolendronic acid)

21
Q

what are bisphosphonates

A

reduce osteoclast activity eg alendronate

22
Q

what is desunomab

A

monoclonal antibody that reduces osteoclasts

23
Q

what is the use of zoledronic acid in osteoporosis

A

reduces fracture risk

24
Q

what is hyperparathyroidism

A

too much PTH resulting in decreased calcium and phosphate in the bone by increasing osteoclasts

25
Q

what stimulates PTH production

A

low serum Ca

26
Q

what hormone opposed PTH

A

calcitrol from thyroid increases Ca absorption to bone

27
Q

what are the symptoms of hyperparathyroidism

A

hypercalcaemia: bones, stones, abdo groans and psychic moans. (thirst, polyuria, N+V, depression, fractures)

28
Q

what causes primary hyperparathyroidism, what is the biochem, and how do you treat it

A

adenoma, hyperplasia of parathyroid. biochem: raised Ca, PTH and ALP, remove surgically

29
Q

what causes secondary hyperparathyroidism, what is the biochem, and how do you treat it

A

CKD or Vit D deficiency. biochem: high PTH, Ca low/normal, treat underlying cause

30
Q

what causes tertiary hyperparathyroidism, what is the biochem, and how do you treat it

A

overactivity from longterm secondary hyperparathyroidism. biochem: high Ca and PTH. parathyroidectomy

31
Q

hyperparathyroid management

A

treat underlying causes, bisphosphonates, cinacalct (ca mimic), HRT, parathyroidectomy (end stage)

32
Q

what is Pagets disease

A

altered bone remodelling –> increased osteoclastic activity and bone turnover

33
Q

what does Pagets lead to in the bone

A

cortical thickening, brittle bone, weakened and misshapen, soft tissue swelling

34
Q

what can cause Paget’s disease

A

old age, metabolic disease, genetics, virus eg paramyxovirus

35
Q

what are symptoms of Pagets

A

bone pain (pelvis, skull, spine, legs), arthritis and deformities, nerve compression, pathological fractures

36
Q

how do you treat Pagets

A

bisphosphonates, joint replacement, (calcitonin)

37
Q

what is avascular necrosis

A

bone infarction leading to necrosis of bone and bone marrow

38
Q

how can AVN cause OA

A

patchy slcerosis –> subchondral collapse –> OA

39
Q

what are common AVN sites

A

femoral head, humerus head, scaphoid

40
Q

what can cause AVN

A

alcohol or steroid abuse, thrombus, sickle cell anaemia, SLE, secondary to fractures

41
Q

how does alcohol and steroid abuse cause AVN

A

alters fat metabolism and promotes blood coagulation leading to compressed venous outflow

42
Q

how to investigate and treat AVN

A

MRI>X ray, drill holes to decompress bones, joint replacement

43
Q

which bone disease is qualitative

A

osteomalacia and rickett’s

44
Q

which bone disease is quantitative

A

osteoporosis