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diseases of the bone Flashcards

1
Q

what are the purposes of bone?

A

to protect the organs, to support the body, to aid movement, to store calcium and minerals and to produce blood cells from the bone marrow

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2
Q

what are the components of bone?

A

there is cortical bone, trabecular bone, cells, extracellular components

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3
Q

what is the cortical layer?

A

it is the hard outer layer of bone

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4
Q

what is the trabecular layer?

A

it is the spongy inner layer

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5
Q

what types of cells are found in bone?

A

bone forming cells, bone resorbing cells and bone coordinating cells

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6
Q

what is the extracellular component of bone?

A

there is organic matrix and inorganic part

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7
Q

what is the organic matrix?

A

it makes up 30% of the extracellular layer and is made of mainly collagen for osteoid and ground substance

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8
Q

what is the inorganic part of extracellular material?

A

it represents 70% of the extracellular part and is made of hydroxyapatite which is calcium and phosphate and minerals such as magnesium, sodium and potassium

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9
Q

what is the anatomy of the bone?

A

the outermost layer is the periosteum membrane covering the bone, and then inner is the endosteum. Within the cortical layer is the endosteum and this contains the yellow marrow.. Inside the yellow marrow is vessels and nerves. Within the spongy layer is the red marrow and this contains the trabeculae

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10
Q

what is an osteon?

A

it is a unit of the compact bone. It contains lamellae, canaliculi, haversian canals and lacunae containing osteocytes

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11
Q

what connects haversian canals in the outer hard bone?

A

volkmanns canals

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12
Q

what is the main role of osteoblast?

A

they create and repair new bone

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13
Q

what do osteoblasts do in order to complete their function?

A

they mineralise organic matrix, they communicate with other bone cells, they become osteocytes, they make hormones and they also make osteoid

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14
Q

what are the characteristics of collagen?

A

it makes up most of the oteoid/ECM and is for tensile strength. It is produced by osteoblasts

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15
Q

what is hydroxyapatite?

A

it is calcium phosphate hydroxide salt and is involved in mineralisation

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16
Q

what is the function of bone remodelling?

A

it is vascular, metabolically active and is for cellular processes

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17
Q

what is the function of osteoclasts?

A

they break down old bone

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18
Q

what are the components of osteoclasts?

A

there is RANKL and PTL and IL-6

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19
Q

what is RANKL?

A

it is a osteoprotegrin that is a decoy receptor which binds and thereby opposes the RANK ligand which is another cytokine that activates osteoclasts and causes bone resorption

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20
Q

what is PTL?

A

it is a calcitonin that is produced in humans by the parafollicular cells or C cells of the thyroid gland - it is involved in helping to regulate the calcium and phosphate in the blood that opposes the action of the PTH

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21
Q

what is IL-6?

A

it is an interleukin that is a proinflammatory cytokine and an antiinflammatory myokine encoded by the IL6 gene. In addition osteoblasts secrete IL6 to stimulate osteoclast formation

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22
Q

what is the remodelling process in normal bone in adults?

A

normal bone is in constant state of turnover caused by resorption by osteoclasts and formation by osteoblasts - the adult skeleton is replaced every ten years

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23
Q

what is the process of making osteocytes?

A

it is an osteoprogenitor cell making an osteoblast and then making an osteocyte

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24
Q

what is the cross sectional structure of bone?

A

the outer layer is the osteoblasts and osteoclasts within them. Within the bone is the lamella with osteocytes between each one, and a central canal with a nerve, lymphatic vessel, artery and vein within it

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25
Q

what is bone mass?

A

it is the total mass of skeletal calcium in grams

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26
Q

what happens to bone with ageing?

A

there is bone growth until the age of around 35 in females and males (more growth in males), an then there is decreasing bone mass with age and also in females bone loss due to menopause

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27
Q

what is osteoporosis?

A

it is when bone destruction > bone formation

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28
Q

what is the pathological process behind osteoporosis?

A

the osteoclast precursor makes osteoclasts and mononuclear cells in around three weeks for resorption but the osteoblast precursor makes osteoblasts in three months for formation and mineralisation

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29
Q

what is the bone cycle?

A

it is osteoclasts involved in resorption which takes weeks, osteoclast stimulation comes from RANK and RANKL and the release of calcium from the bone. There is then osteoclast inhibition which is by denosumab and OPG and formation from osteoblasts of the osteoid and reabsorption of calcium which takes months

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30
Q

what happens to the bone cycle with age?

A

bone formation decreases and resorption increases

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31
Q

what is the remodelling cycle?

A

there are three consecutive phases whereby there is resorption during which osteoclasts digest old bone, reversal when mononuclear cells appear on the bone surface and formation when osteoblasts lay down new bone until the resorbed bone is completely replaced

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32
Q

what does investigation of bone disease include?

A

gross structure, bone mass and calcium, cellular function and turnover and cellular function through microstructure

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33
Q

how can bone mass/calcium and gross structure be examined?

A

mass through DEXA

structure through Xray, MRI and CT

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34
Q

how are cellular function, turnover and microstructure looked at?

A 
function through biochemistry
biopsy and qCT for microstructure
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35
Q

how does bone formation occur?

A

through the products of active OBs

these are osteocalcin, procollagen type 1 propeptides and alkaline phosphatases TAP and BAP

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36
Q

how does bone resorption occur?

A

through degradation products of bone collagen and through osteoclast enzymes

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37
Q

what are the degradation products of bone collagen for bone resorption?

A

they are pyridinium crosslinks, hydroxyproline and crosslinked telopeptides of type 1 collagen which are NTX and CTX

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38
Q

what are the osteclast enzymes of bone resorption?

A

tartrate resistance acid phosphatase and cathepsin K

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39
Q

what are the characteristics of alkaline phosphatases?

A

they are identified in liver functions tests and bone profiles and in health found in the liver, bone and intestines. Specific isoenzymes can be measured when there is diagnostic doubt

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40
Q

what is bone alkaline phosphatase?

A

it is the phosphatase that is involved in mineralisation that is released by osteoblasts and the release is stimulated by increased bone remodelling such as in childhood or puberty, fractures, hyperparathyroidism (primary and secondary) and pagets disease of the bone

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41
Q

What is P1NP?

A

it is procollagen type 1N propeptide that is synthesised by osteoblasts and a precursor to type 1 collagen. It has low diurnal and intraindividual variation and the serum concentrations are not affected by food intake but increase when osteoblast activity does and vice versa

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42
Q

what are NTX and CTX?

A

they are collagen crosslinks and they are crosslinking molecules that are released and therefore correlate highly with bone resorption.

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43
Q

what are the characteristics of CCLs?

A

they have high diurnal variation, are increased in periods of high bone turnover, they do not predict bone mineral density and they are decreased by anti-resorptive therapy

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44
Q

what are bone markers?

A

they are collagen related markers that are primarily based on type I collagen which is widely distributed in several tissues

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45
Q

what is the use of bone markers?

A

they are not disease specific but reflect alterations in skeletal metabolism and some are characterised by significant intraindividual variability

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46
Q

what are the other specific uses of bone markers?

A

for the evaluation of bone turnover and bone loss, treatment effect and adherence with medication

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47
Q

what is CTX used for as a bone marker?

A

it is used to monitor the response or compliance with anti-resorptive therapy

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48
Q

what is P1NP used for?

A

it is used to monitor the compliance with terparatide

49
Q

what are the T categories of WHO and IOF?

A

-1 and above means that bone density is considered normal, -1 to -2.5 is osteopenia and -2.5 and below is osteporosis

50
Q

what is osteoporosis?

A

it is decreased bone mass and deranged bone micro architecture that results in the failure of structural integrity and is a system skeletal disease that is characterised by low bone mass and microarchitectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture

51
Q

what types of bone disorders are there?

A

metastatic disease, osteomalacia and porosis, hyperparathyroidism and pagets disease

52
Q

where are common fracture sites in osteoporosis?

A

spine and hip

neck of femur and wrist

53
Q

what are the common risk factors in bone loss?

A

ageing and glucocorticoids

54
Q

what is the diagnosis of osteoporosis based on?

A

there are no abnormalities in routine biochemical tests and therefore relies on DEXA and Xrays, and there is increasing use of bone markers in management

55
Q

what is the epidemiology of osteoporosis fragility fractures?

A

1 in 2 women and 1 in 5 men will sustain fragility fractures after the age of 50 years and there is a risk of another in the first 2 years after the first. The level of admissions of hip fractures is increasing and will be up to a 65% increase

56
Q

what are the costs of hip fractures?

A

accounts for 85000 unplanned admissions every year and costs 1.8 million bed days and £1.9bn in costs and then also social care costs

57
Q

what are the effects of hip fractures?

A

they result in isolation, loss of mobility and independence and depression and could be reduced by the correct assessment of those who suffer one

58
Q

what is a fragility fracture?

A

it is a fracture that is caused by injury that would be insufficient to fracture a normal bone or has no identifiable trauma or minimal

59
Q

what are the risk factors for fragility fractures?

A

age, sex, vertebral fracture (number and severity) previous fracture, alcohol, smoking, drugs, inflammatory conditions, malabsorption, falls, T1DM, family history and BMI but is independent of BMD

60
Q

what is the relationship between fractures and age?

A

osteoporotic fracture incidence correlates with progressive trabecular and cortical bone loss over time (high in vertebral early after loss and hip fracture occurs later)

61
Q

what are the main causes of secondary osteoporosis?

A

endocrine. gastrointestinal, rheumatological, haematological, respiratory, metabolic, drugs and other

62
Q

what are the endocrine causes of secondary osteoporosis?`

A

amernorrhoea in pre menopausal women, menopause, diabetes, hyperprolactinaemia, cushings, hormone ablation for breast or prostate cancer, hypogonadism, hyperthyroidism and hyperparathyroidism

63
Q

what are the GI causes of secondary osteoporosis?

A

coeliac disease, chronic liver disease, IBD, any causes of malabsorption

64
Q

what are rheumatological causes of secondary osteoporosis?

A

RA and other inflammaotry arthropathics

65
Q

what are the respiratory causes of secondary osteoporosis?

A

COPD and CF

66
Q

what are the haematological causes of secondary osteoporosis?

A

systemic mastocytosis, haemoglobinopathies and myeloma

67
Q

what are the metabolic and drug causes of secondary osteoporosis?

A

homocystinuria

glucocorticoids, heparin, ciclosporin, anti convulsants, aromatase inhibitors, androgen deprivation

68
Q

what are other causes of osteoporosis?

A

CKD and immobility

69
Q

what are the investigations for secondary causes of osteoporosis?

A

calcium and bone profile, LFTs, UandEs, FBCs, vitamin D, PTH, plasma viscosity, coeliac screen
in young men then a 9am fasting testosterone which include LH, SHBG, FSH and LFTs
in young amenorrhoeic women then FSH, LH oestradiolk and prolactin

70
Q

when would a later xray of T5-L5 be considered for osteoporosis?

A

when there is loss of height, back pain or kyphosis

71
Q

what are used for the treatment and prevention of osteoporotic fractures?

A

biphosphonates

72
Q

what is the course of biphosphonates?

A

they are ingested by osteoclasts and taken up by the skeleton - they mimic pyrophosphate structure

73
Q

what are the complications of biphosphonates?

A

nausea, vomiting, difficulty swallowing, osteonecrosis of the jaw, atypical femur fractures and heartburn

74
Q

what are the two classes of treatments for osteoporotic fractures?

A

anti-resorptive treatments and anabolic treatments

there are also sclerostin inhibitors such as romosozumab which are inbetween both classes

75
Q

what are antiresorptive treatments?

A

there are RANKL-inhibitors such as denosumab, there are bisphosphonates such as the oral therapy alendronate or IV zoledronate and SERMS such as raloxifene

76
Q

what are anabolic treatments?

A

PTH or pTHrP analogues such as teriparatide

77
Q

how do biphosphonates work?

A

they modulate the signalling from osteoblasts to clasts and are concentrated in newly mineralising bone under the clasts. There is local release during bone resorption that inhibits clast formation, migration and osteolytic activity and promotes apoptosis

78
Q

how does denosumab work?

A

it binds to and inhibits the RANK ligand, and prevents this from binding to RANK. It then inhibits osteoclast formation and osteoclast function and survival

79
Q

what are the types of bone metastases?

A

lytic and sclerotic

80
Q

what is lytic bone metastasis?

A

it is the destruction of normal bone by osteoclasts that results from breast, lung kidney and thyroid cancers

81
Q

what is sclerotic/osteoblastic metastasis?

A

it is the deposition of new bone from prostate, lymphoma, breast or lung cancer

82
Q

what are the usual sites of bone mets?

A

spine, femur, pelvis, skull and humerus

83
Q

what are the presenting symptoms of bone mets?

A

anaemia, pain, broken bones, numbness, paralysis, trouble urinating, loss of appetite, thirst, nausea, confusion and fatigue

84
Q

how does pain present in bone mets?

A

worse at night and initially better with movement, and usually becomes constant

85
Q

what are the broken bones known as?

A

pathological fractures that are commonly in the femur humerus and vertebrae

86
Q

why is there numbness etc?

A

spinal cord compression from mets

87
Q

why is there anaemia and loss of apetite etc?

A

there are symptoms of hypercalcaemia and disruption of bone marrow

88
Q

how is hypercalcaemia classified ?

A

mild and severe

89
Q

what is mild hypercalcaemia?

A

when there is nausea, fatigue, constipation, anorexia, mood disturbance, polyuria and polydipsia

90
Q

what is severe hypercalcaemia?

A

abdo pain, vomiting, coma, pancreatitisa, cardiac arrhythmia and dehydration

91
Q

what are the causes of hypercalcaemia?

A

they can be PTH or on PTH mediated

92
Q

what is PTH mediated hypercalcaemia?

A

when the PTH is supressed or low - this can be from malignancy, vit D intoxication, chronic granulomatous disorders such as sarcoidosis, medications such as diuretics, immobilisation or other endocrine disorders such as hyperthyroidism

93
Q

what are PTH mediated causes of hypercalcaemia?

A

PTH is high
primary hyperparathyroidism, familial (MEN2a and 2b, familial hypoacalciuric hypercalcaemia and familial isolated hyperparathyroidism)

94
Q

what is parathyroid hormone?

A

it is a polypeptide made of 84 amino acids and is secreted by chief cells of the parathyroid gland

95
Q

in a histology what is the anatomy of the parathyroid gland?

A

the white is the adipose tissue and there are chief cells within the oxyphil cells. There is a capsule around the outside

96
Q

what is primary hyperparathyroidism?

A

it is inappropriately elevated PTH with hypercalcaemia. However it is now usually presenting earlier in the course of disease and asymptomatically, and is twice as likely in women than men. It is usually in over 45 years olds.

97
Q

how does the parathyroid gland regulate the parathyroid hormones?

A

low levels of blood calcium and reduced Mg2+ stimulate the parathyroid gland to release PTH. This results in increased bone decomposition to release calcium, increased calcium absorption from food by the intestines and increased reabsorption by the kidneys from urine. This results in increased levels of calcium in the blood which then negatively feedback to the parathyroid gland and inhibits it

98
Q

what else feedback to the parathyroid gland to stimulate it?

A

decreased magnesium ions and increased vitamin D (1,25 dihydroxyvitamin D3)

99
Q

what senses calcium blood changes?

A

the CaSR on the gland - calcium sensing receptor

100
Q

briefly describe primary hyperparathyroidism?

A

calcium is usually elevated and HPT is inappropriately high. There is commonly low phosphates and high alkaline phosphatases and the causes are sporadic or familial

101
Q

briefly describe secondary HPT?

A

the calcium is normal or low and HPT is appropriately high. The phosphate is present if due to CKD and the causes are mainly CKD or vit D deficiency

102
Q

briefly describe tertiary HPT?

A

calcium is usually high and HPT inappropriately high. The phosphate can be high or low and the causes are after prolonged secondary HPT usually in CKD

103
Q

what sort of adenomas can cause HPT?

A

adenomas which are benign, glandular hyperplasia, ectopic adenomas or parathyroid carcinomas which are malignant

104
Q

what is the epidemiology of the adenoma causes of PHT?

A

benign adenomas are single and account for 85% of HTP, glandular hyperplasia accounts fro around 6-10% of HPT and carcinoma around 1-2%

105
Q

what is glandular hyperplasia?

A

when all four glands are enlarged and can occur sporadically or genetically, and are treated with medical or surgical therapy

106
Q

where are ectopic adenomas of the parathyroid found?

A

rarely in the mediastinum, but some are found in the thymus gland as parathyroid cells have migrated during embryogenesis

107
Q

what are the features of carcinoma of the parathyroids?

A

in histology they are invasive - it is an aggressive disease with significant hypercalcaemia and possibility of distant metsh

108
Q

what are the clinical manifestations of hyperparathyroidism?

A

proximal muscle wasting, bone disease such as osteoporosis and osteitis fibrosa cystica, renal disease such as nephreolithiasis and CKD and symptoms related to hypercalcaemia

109
Q

what is used in HPT imaging?

A

Tc99 sestamibi - wait for 15 minutes to 2 hours

CT SPECT Tc99 MIBI - ectopic tissue in thyroid tissue in mediastinum can be commonly picked up from 5 mins - 2 hours

110
Q

when is surgery used for HPT?

A

when there is symptomatic hypercalcaemia or there is asymptomatic in patients with PHPT that have renal stone disease, are less than 50 years, osteoporosis, fragility fractures,24 hour urine calcium above 10mmol/day creatinine clearance <60ml/min or calcium greater than 0.35mmol/L above normal

111
Q

what is the medical option for HPT?

A

calcimimetics such as cinacalcet. They will activate the CaSR in the parathyroid gland and therefore reduce the PTH secretion. This will normalise the calcium in symptomatic patients or those who are unfit or unwilling to have surgery

112
Q

what are the issues with calcimimetics?

A

there is no data on the outcomes on renal disease or quality of life and does not seem to alter bone disease

113
Q

what is pagets bone disease?

A

it is a disease of rapid bone turnover and formation that leads to abnormal bone remodelling. It is mainly in over 50s and higher prevalence in men. There are probable genetic and environmental factors and FHx in 10-15% of cases - it can be polyostotic or monostotic - there is elevated alkaline phosphatase that reflects the high turnover

114
Q

what are the clinical features of pagets bone disease?

A

bone pain and deformities and arthritis and fractures. There are cranial nerve defects if the skull is affected such as vision and hearing loss and risk of osteosarcoma. It most commonly affects the femur, lower lumbar vertebrae, pelvis

115
Q

what is osteomalacia?

A

it is lack of mineralisation in the bone and there is the adult form which is widened osteoid seams with lack of mineralisation, classic childhood rickets with widened epiphyses and poor skeletal growth

116
Q

what are the causes of osteomalacia?

A

can be from poor absorption of calcium in the intestine from lack of in diet or vitamin D resistance or deficiency or excessive renal phosphate excretion where there are rare genetic forms such as hereditary hypophosphataemia rickets

117
Q

what are the clinical features of osteomalacia?

A

diffuse bone pain that is usually symmetrical, muscle and bone weakness, low vitamin D and potentially calcium, high alkaline phosphate and PTH

118
Q

what adult population is at risk of osteomalacia?

A

nursing home residents and the elderly, malasorption patients and the asian population/those who wear hijabs or burkas

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