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Medicine phase 2 limbs and back > week 1 - bone and the skeleton > Flashcards

week 1 - bone and the skeleton Flashcards

1
Q

describe osteoblasts

A

involved in bone formation

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

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2
Q

describe osteocytes

A

dormant

sensitive to stimuli and communicate to osteoblasts

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3
Q

describe osteoclasts

A

involved in 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

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5
Q

six steps of bone remodelling

A 
activation 
resorption 
osteoblast recruitment 
osteoid formation
mineralization
quiescence
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6
Q

two types of bone growth

A

endochondral ossification - longitudinal

subperiosteal apposition - width

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7
Q

rate of bone remodelling depends on…

A

growth
hormones and growth / biochemical factors
mechanical stress

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8
Q

RANKL/RANK/OPG pathway

A

osteoblasts produce RANKL which binds to RANK on osteoclasts and activates them
OPG inhibits RANKL
absence of OPG causes long bone fragility fractures

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9
Q

composition of bone

A

inorganic - calcium hydroxyapatite

organic - type 1 collagen, proteoglycans, osteocalcin, cytokines/IL

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10
Q

result of loss of mineralization

A

osteomalacia / rickets

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11
Q

result of low bone mass

A

osteoporosis, osteogenesis imperfecta

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12
Q

disease resulting from high bone mass

A

osteopetrosis

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13
Q

disease resulting from high bone turnover

A

pagets, hyperparathyroidism, thyrotoxicosis

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14
Q

disease resulting from low bone turnover

A

adynamic disease, hypophosphatasia

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15
Q

describe osteoporosis

A

reduced total bone mass
adequate mineralisation of present osteoid
relatively increased bone resorption

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16
Q

menopausal osteoporosis

A

reduced bone mineral mass

estrogen deficiency

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17
Q

corticosteroid induced osteoporosis

A

steroids increase osteoclastic activity, decrease osteoblastic activity, impair collagen formation and cause increased bone turnover and poor bone formation and healing
corticosteroids increase bone resorption rate and depth and can block osteoblast action

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18
Q

relationship between PTH and ionised Ca

A

increases while the other decreases

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19
Q

causes of low Ca and high PTH

A

secondary hyperparathyroidism causes:
renal impairment
vitamin D deficiency

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20
Q

causes of low Ca and low PTH (hypoparathyroidism)

A 
destruction of parathyroid glands
idiopathic/autoimmune 
surgical removal 
radiotherapy
severe magnesium deficiency
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21
Q

causes of high Ca and high PTH

A

adenoma - in parathyroid glands - uncontrolled PTH causes increased calcium
hyperplasia also causes

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22
Q

causes of high Ca and low PTH

A 
malignancy 
excess intake
granulomatous disorders
sarcoid
medications
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23
Q

primary hyperparathyroidism

A

unregulated PTH secretion
hypercalcaemia
markedly increased bone turnover
may retain bone mass

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24
Q

clinical features

A

boney cavities
kidney stones
abdominal pain, vomiting
depression

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25
Q

signs of hyperparathyroidism on an x-ray

A

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

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26
Q

describe pagets disease

A

rapid bone turnover
bone resorption and formation are increased
disorganised structure
reduced bone strength
risk of fracture
linked to osteosarcoma tumour suppressor gene

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27
Q

describe osteopetrosis

A

failure of osteoclastic and chondroclastic resorption
failure of remodelling
genetic disorder

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28
Q

describe fluorosis

A

abnormal matrix mineralization

fluoride replaces calcium in the matrix

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29
Q

describe osteogenesis imperfecta

A

genetic
collagen one deficiency
low muscle tone

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30
Q

space age bone disease

A

reduced numbers of osteoblasts
minimal mechanical stress on bone
normal osteoclast numbers

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31
Q

types of calcium in serum

A

free (unbound) - 47%
bound to albumin - 47%
complexed - 6%

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32
Q

organs involved in calcium homeostasis

A

kidney, gut, bone, parathyroid glands

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33
Q

describe calcium homeostasis

A

absorbed mainly in duodenum and jejunum - Ca goes into blood
reabsorbed in kidney
resorption in bone

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34
Q

role of PTH in calcium homeostasis

A

stimulates renal tubular calcium reabsorption
promotes bone resorption
stimulates formation of calcitriol in kidney which enhances calcium absorption fom gut

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35
Q

calcitriol role in calcium homeostasis

A

role in promoting calcium and phosphate absorption from gut

increase bone resorption = calcium released

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36
Q

two pathways of calcium absorption

A

a cell mediated active transport pathway - controlled b calcitriol
passive diffusion - depends on luminal Ca concentration and is unaffected by calcitriol

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37
Q

where in the kidney is calcium reabsorbed

A

65% in proximal tubule
20% in thick ascending loop of henle
15% in distal convoluted tubule
last two are increased by effects of PTH

38
Q

where is PTH produced

A

parathyroid glands

39
Q

describe the secretion of PTH

A

regulated by free calcium and is sensed by calcium sensing receptors
as calcium levels fall, PTH rises

40
Q

what are calcium sensing receptors

A

g-coupled receptors on parathyroid cells and renal tubules

41
Q

major role of vitamin D

A

maintaining serum calcium within normal limits

42
Q

what does calcitriol do when dietary calcium is inadequate

A

calcitriol will increase bone resorption via vitamin D receptors on osteoblasts

43
Q

relationship between PTH and calcitriol

A

calcium sensing receptor detects fall in ionised calcium
this increases PTH production which is a major stimulus for calcitriol production
PTH production is suppressed directly and indirectly by increasing iCa

44
Q

hypocalcaemia causes

A

not enough PTH which could be due to:
neck surgery, autoimmune destruction of parathyroid glands or magnesium deficiency
could be due to a lack of vitamin D - malabsorption, little exposure to sunlight or renal disease (kidneys fail to make active form)

45
Q

hypercalcaemia causes

A

inappropriate production of too much PTH due to adenoma of parathyroid gland
inappropriate dosage of vitamin D
malignancy - lung cancer, breast cancer, multiple myeloma

46
Q

role of phosphate in the body

A

critical in skeletal development, bone mineralisation

47
Q

where is phosphate found

A

85% is in the mineralised matrix of bone
rest is mostly intracellular and bound to lipids and proteins - cell membranes, nucleic acids, enzyme cofactors, glycolytic intermediates and ATP
1% in extracellular fluids

48
Q

main hormones in phosphate homeostasis

A

PTH
fibroblast growth factor 23 (FGF 23)
calcitriol

49
Q

role of PTH and FGF23 in phosphate homeostasis

A

they inhibit the reabsorption of phosphate by acting on the renal tubule

50
Q

response to an increase in serum phosphate

A

PTH and FGF23 production increases - they then act on renal tubule to increase secretion of phosphate by reducing its reabsorption

51
Q

two types of bone

A

cortical bone and trabecular bone

52
Q

functions of osteoblasts

A

deposition of collagen and noncollagenous proteins
transport of mineral salts
secretes: cytokines/growth factors, enzymes and proteins

53
Q

some of the factors that stimulate osteoblast expression of RANK ligand

A

PTH, vitamin D, glucocorticoids, interleukins, TNF-alpha

54
Q

OPG function

A

it is a decoy receptor that prevents RANKL binding to RANK

inhibits osteoclast formation, function and survival

55
Q

what is sclerostin

A

a protein secreted by osteocytes

it inhibits Wnt signalling in cells

56
Q

fracture healing process

A

osteocytes near crack undergo apoptosis
lining cells pull away from bone matrix and form a canopy which merges with the blood vessels
stromal cells are released from sclerostin inhibition and/or exposed to other factors eg. IL-1 and they generate pre-osteoblasts - SCs also secrete M-CSF to help generate pre-osteoclasts
pre-osteoblasts proliferate and secrete other factors - also start to express RANKL
pre-osteoclasts to mature osteoclasts
osteoclasts bind to bone matrix with integrins and secrete acid and cathepsin K to resorb bone
bone-derived GFs IGF and TGF-beta are released
osteoclast undergos apoptosis - regulated by estrogen
pre-osteoblasts mature and secrete OPG instead of RANKL - OBs also secrete osteoid and mineralise it to fill the cavity
some OBs turn into osteocytes, some into lining cells and the rest undergo apoptosis
meanwhile osteoclasts have been re-establishing a network with each other and the lining cells
new matrix will accumulate mineral and increase in density for about 3 years

57
Q

how do long bones change as we age to an adult

A

increased length and diameter

58
Q

how does the spine change as we age to an adult

A

increased size and trabecular thickness

59
Q

factors affecting peak bone mass

A 
gender
calcium intake
growth hormone IGF axis 
steroid metabolism 
alcohol
gonadal status 
physical activity 
smoking
60
Q

effects of estrogen on bone acquisition

A

little effect on proliferating chondrocytes

major effect on terminally differentiating chondrocytes and mineralising bone

61
Q

function of estrogen on bone remodelling

A

decreased estrogen leads to increased RANKL

62
Q

risk factors for osteoporotic fractures

A 
age >65
vertebral compression fracture
malabsorption syndrome
primary hyperparathyroidism
hypogonadism
early menopause
rheumatoid arthritis 
smoker
low dietary calcium intake
63
Q

determinants of fracture risk

A

bone strength

extraskeletal conditions - propensity to fall and fall conditions

64
Q

lifestyle changes for prevention of osteoporosis and fractures

A 
adequate intake of dietary calcium
regular muscle strengthening exercise
stop smoking 
drink alcohol at safe levels 
minimise risk of falls 
wear a hip protector
65
Q

treatment of calcium and vitamin d reduces risk of what type of fracture

A

non vertebral fracture

66
Q

effects of hormone replacement treatment

A

prevents bone mineral density decreasing as much with age

effective on vertebral and non-vertebral fractures

67
Q

effects of selective estrogen receptor moderator

A

act on estrogen receptors

effective for vertebral fractures

68
Q

effect of bisphosphonates

A

increases bone mineral density
reduces fracture risk
effective on vertebral fractures and most biophosphonates are effective on non-vertebral fractures

69
Q

effects of teriparatide

A

stimulates bone formation

effective on vertebral and non-vertebral fractures

70
Q

effects of denosumab

A

binds to RANKL and inhibits osteoclast formation, function and survival
effective on all fractures

71
Q

effects of romosozumab

A

monoclonal antibody that binds and inhibits sclerostin

increases formation, decreases resorption

72
Q

formation of vitamin d

A

formed from 7 dehydrocholesterol - converted by a photolysis reaction and then isomerisation to cholecalciferol in the skin
transported to liver

73
Q

active form of vitamin d

A

calcitriol

1.25-dihydroxycholecalciferol

74
Q

principle actions of vit d

A

binds to vit d receptor becoming a transcription factor that modulates gene expression of transport proteins which are involved in calcium absorption in the intestine

maintains skeletal calcium balance by promoting intestinal calcium absorption, increases osteoclast numbers causing bone resorption, maintains calcium homeostasis via PTH for bone formation

75
Q

disease from vit d deficiency

A

rickets/osteomalacia

76
Q

osteomalacia

A

characterised by impaired mineralisation of bone leading to an accumulation of unmineralised bone matrix (osteoid)

77
Q

rickets

A

newly formed bone of the growth plate does not mineralise causing growth plate to become thick, wide and irregular

78
Q

clinical features of osteomalacia

A

initially asymptomatic
bone pain and tenderness
proximal muscle weakness without atrophy

79
Q

causes of vitamin d deficiency

A 
lack of sunlight
bizarre diets
partial gastrectomy 
small bowel malabsorption
pancreatic disease
chronic renal failure
anticonvulsants
80
Q

diagnosing osteomalacia

A

imaging
isotope bone scan
serum biochemistry
bone biopsy

81
Q

vitamin d can be used to treat..

A

osteomalacia and vitamin d deficiency

82
Q

causes of rickets

A 
vitamin d dependent rickets
hypophosphataemia disorders
fanconi syndrome
renal tubulopathies
hypophosphatasia 
fat malabsorption
83
Q

types of vitamin d dependent rickets

A

1A - vitamin d hydroxylation-deficient rickets
1B - vitamin d hydroxylation-deficient rickets
2A - vitamin d-dependent rickets
2B - vitamin d-dependent rickets with normal vitamin d receptor

84
Q

describe type 1A and 2A vitamin d dependent rickets

A

1A - mutation in the CYP27B1 gene - hydroxylation at alpha 1
2A - with/without alopecia - caused by a defect in the vitamin d receptor gene
most common types of vit d dependent rickets

85
Q

how does FGF23 regulate phosphate homeostasis

A

blocks phosphate reabsorption and causes excess phosphate loss

86
Q

FGF23 production

A

formed in osteocytes

under control of locally bone derived factors that are important for bone mineralisation

87
Q

describe tumoral calcinosis

A

defective FGF23 or GALNT3 (enzyme required for normal o-glycosylation of FGF23)
increased calcitriol and phosphate
ectopic calcification to remove excess phosphate

88
Q

AD hypophosphatemic rickets

A

FGF23 resistance to proteolysis

low calcitriol levels

89
Q

x-linked hypophosphataemic rickets

A

manifesting during late infancy at onset of walking
bowing long bones, widening metaphyses and rachitic rosary - short stature
low phosphate and low calcitriol and increase in FGF23
mutation in PHEX protein

90
Q

AR hypophosphataemic rickets

A

affects dentin matrix protein 1 (DMP 1)
involved in osteoblast maturation
exported to extracellular matrix regulating hydroxyapatite
DMP1 inhibits FGF23 expression
leads to bone, cartilage and dentin defects - severe hypophosphataemia and secondary unregulated FGF23

91
Q

hereditary hypophosphataemic rickets with hypercalcuria

A

defect of NPT2 phosphate transporter in proximal tubule
hypophosphataemia secondary to defects in proximal tubular phosphate transporter
rickets and short stature

92
Q

rickets treatments

A

additional phosphate
adequate 1.25 diOH vitamin d
avoid calciuria and elevated PTH

Medicine phase 2 limbs and back (6 decks)

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