Metabolic Disorders of bone Flashcards

1
Q

what are osteoblasts?

A

bone formation
at the end of the bone remodelling cycle they remain as resting osteocytes

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2
Q

what are osteocytes?

A

dormant; sensitive to stimuli and communicate to osteocytes

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3
Q

what are osteoclasts?

A

bone resorption
derived from monocyte precursors in marrow

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4
Q

what is bone remodelling?

A

coordinated osteoclastic resorption and osteoblastic proliferation
maintains skeletal structure

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5
Q

what is the annual rate of bone turnover?

A

cortical - 4%
trabecular - 25%

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6
Q

what are the six steps of the BMU as the basis of bone remodelling?

A
  1. activation: osteoclasts
  2. resorption : bone matrix
  3. osteoblast recruitment
  4. osteoid formation
  5. mineralisation
  6. quince
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7
Q

what is longitudinal bone growth?

A

endochondral ossification

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8
Q

what is bone growth by width?

A

subperiosteal

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9
Q

what happens at the same time as endosteal bone resorption?

A

medullary cavity expansion

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10
Q

what does bone growth depend on?

A

growth
hormones and growth/biochemical factors
mechanical stress

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11
Q

what happens during growth?

A

turnover is high, formation-> resorption -> net bone gain

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12
Q

what happens during adulthood?

A

turnover moderate , formation < resorption -> net bone loss

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13
Q

what is involved with regulating bone remodelling?

A

RANKL/RANK/OPG pathway

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14
Q

how is oestrogen involved in bone growth?

A

limits the expression of RANK ligand

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15
Q

how does OPG affect bone growth?

A

binds to RANK ligand

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16
Q

what can unopposed RANK ligand activity lead to?

A

long bone fragility fractures

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17
Q

what is the role of OPG in the regulation of bone mineral density?

A

normal levels - no BMD change
OPG absent - decreased BMD
OPG excess - increased BMD

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18
Q

what is the composition of bone?

A

inorganic 2/3rd
-calcium hydroxy apatite
organic 1/3rd
-type 1 collagen (tensile)
-peoteoglycans (compressile)
-osteocalcin (bone proteins)
-cytokines/IL

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19
Q

when is peak bone mass attained?

A

between 25-30

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20
Q

what ages is the consolidation stage in bone mass?

A

between 26-40

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21
Q

what normal bodily process in females causes age related bone mass loss?

A

menopause

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22
Q

how much does bone mass increase each year during puberty and onwards?

A

2-3% up to a peak of 30 years
remains steady until about age 35-40

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23
Q

what is the bone loss rate in women after menopause?

A

2-3% per year for next 8-10 years (mainly trabecular)

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24
Q

what are the determinants of bone density?

A

-calcium and phosphates
-parathyroid hormone (PTH)
-cholecaldiferol and calcitriol
-estrogen and other sex hormones
-calcitonin

25
Q

what are metabolic bone disorders?

A

abnormailities of formation (bone morphology)
metabolism of bone
(functions)

26
Q

what is the pathology of bone disorders?

A

loss of mineralisation - osteomalacia/rickets
low bone mass - osteoporosis, osteogenesis imperfecta
high bone mass - osteoporosis
high bone turnover - pagets, hyperthyroidism, thyrotoxicosis
low bone turnover - adynamic disease, hypophosphastasia

27
Q

what are some biomechanics tests for bone disorders?

A

-serum Ca/PO4 (rarely ionised calcium)
-alkaline phosphate (bone turnover)
-PTH
-vit D activity (measured by 25-HCC)
-specific endocrine test
-markers of bone turnover
-FGF-23

28
Q

what is osteoporosis?

A

reduced total bone mass
adequate mineralisation of present osteoid
many factors
oestrogen deficiency
relatively increased bone resorption

29
Q

what is menopausal osteoporosis?

A

reduced bone mineral mass
normal mineral to matrix ratio
estrogen deficiency

30
Q

what is corticosteroid induced osteoporosis?

A

increased osteoclast activity
decreased osteoblastic activity
impaired collagen formation
increased bone turnover and poor bone formation and healing
steroids increase bone resorption rate and depth similar to menopause. bone formation does not increase

31
Q

what happens when low calcium and high PTH?

A

(secondary hyperthyroidism)
renal impairment
vit D deficiency

32
Q

what happens when high calcium and High PTH?

A

primary hyperthyroidism (adenoma; hyperplasia)

33
Q

what happens when low calcium and low PTH?

A

(hyperthyroidism)
idiopathic/autoimmine
surgical removal (thyroid surgery)
radiotherapy
severe magnesium deficiency

34
Q

what happens when high calcium and low PTH?

A

malignancy
excess intake
granulomatous disorders
sarcoid
medications

35
Q

what is primary hyperthyroidism?

A

-unregulated PTH secretion
-hypercalcaemia (low phosphate)
-markedly increased bone turnover
-may retain bone mass, but in elderly or other risk factors, often osteoporosis

36
Q

how can hyperthyroidism be seen on x rays?

A

-subperiosteal bone resorption
-generalized decrease in bone density
-brown tumours
-chondrocalcinosis
knee, wrist and shoulder

37
Q

what is pagets disease?

A

-rapid bone turnover
-both bone resorption and formation increased
-disorganised structure
-reduced bone strength
-risk of fracture
-linked to osteosarcoma tumour suppressor gene
-increased rates of bone turnover with development of disorganised woven bone

38
Q

what is osteopetrosis?

A

failure of osteoclastic and chondroclastic resorption
failure of remodelling
genetic disorder

39
Q

what is fluorosis?

A

abnormal matrix mineralisation
fluoride replaces calcium in the matrix
endemic in india
iatrogenic flurosis

40
Q

what is osteogenesis imperfecta?

A

-genetic bone disorder
-defect/deficency collagen I
-various types
-recurrent childhood fractures
-deformities
-ligaments laxity, low muscle tone
-bluish sclerae

41
Q

what is space age bone disease?

A

astronauts can lose on average 1 to 2 percent of bone mass each month
-minimal mechanical stress on bone
-decreased osteoblasts

42
Q

what are biophosponates?

A

slow the rate the bone is broken dow in your body.

43
Q

what are some different types of biophospohonates?

A

-alendronic acid
-ibandronic acid
-risedronate
-zolendronic acid

44
Q

how should biophosponates be taken?

A

Always take bisphosphonates on an empty stomach with a full glass of water. Stand or sit upright for 30 minutes after taking them. You’ll also need to wait between 30 minutes and 2 hours before eating food or drinking any other fluids.

45
Q

what are the main side effects of biophosponates?

A

-irritation to the food pipe
-swallowing problems
-stomach pain
-osteonecrosis

46
Q

what is osteonecrosis?

A

the cells in the jaw bone die, which can lead to problems with healing. If you have a history of dental problems
rare but serious side effect of biophosponates

47
Q

what are selective oestrogen receptor modulators (SERMs)?

A

SERMs are medicines that have a similar effect on bone as the hormone oestrogen. They help to maintain bone density and reduce the risk of fracture, particularly of the spine

48
Q

what is an example of a SERM?

A

raloxifene

49
Q

what are the side effects associated with raloxifene?

A

hot flushes
leg cramps
increase of blood clots s

50
Q

what is teriparatide?

A

Parathyroid hormone is produced naturally in the body. It regulates the amount of calcium in bone.
used to stimulate cells that create new bone. You take them as an injection once a day. parathyroid hormone can increase bone density. However, it’s only used in a small number of people whose bone density is very low and when other treatments are not working.

51
Q

what are the common side effects associated with parathyroid hormone?

A

nausea, headaches, dizziness

52
Q

what are biological medicines?

A

They work by slowing down the rate at which your bones are broken down and speeding up the rate at which your cells build bone. They’re given by injection every month or every few months.

53
Q

what are some common biological medicines used for OP?

A

denosumab
romosozumab

54
Q

what are some common side effects for biologics?

A

muscle or joint pain, rashes, constipation and cold-like symptoms.

55
Q

what is hrt

A

HRT has also been shown to keep bones strong and reduce the risk of getting osteoporosis. If you already have osteoporosis it can strengthen your bones and reduce your risk of breaking a bone.

56
Q

what is vitamin D commonly synthesised as?

A

cholecalciferol

57
Q

where is cholecalciferol turned into calcifediol?

A

liver

58
Q

where is calcifediol tuned into calcitriol?

A

kidney