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Clinical Pathology > Theme 5: Bone and New Markers > Flashcards

Theme 5: Bone and New Markers Flashcards

1
Q

What is the purpose of bone?

A
  • structural support
  • protects vital organs
  • bank for calcium, phosphate etc
  • home for bone marrow
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2
Q

What is cortical bone?

A
  • the hard outer layer
  • a.ka compact bone
  • gives bone its smooth, white and solid appearance
  • accounts for 80% of total bone mass in adult skeleton
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3
Q

What is an osteon?

A

individual microscopic columns that together all make up cortical bone
functional unit of cortical bone

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4
Q

What is one osteon made up of?

A

multiple layers of osetoblasts and osteocytes around a central canal called the haversian canal

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5
Q

What connects individual osteons together?

A

Volkmann’s canals

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6
Q

What is the outer surface of cortical bone covered by?

A

periosteum

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7
Q

What is the inner surface of cortical bone covered by?

A

endosteum

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8
Q

What is the endosteum?

A

the boundary between the cortical bone and the inner trabecular bone

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9
Q

What is trabecular bone?

A
  • spongy inner layer
  • open cell porous network
  • thin formations of osteoblasts covered in endosteum create an irregular network of spaces
  • bone marrow and RBCs within these spaces
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10
Q

Where is bone marrow found?

A

trabecular bone

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11
Q

Which are the bone forming cells?

A

osteoblasts –> they create and repair new bone

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12
Q

Which are bone resorbing cells?

A

osteoclasts

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13
Q

Which are bone co ordinating cells?

A

osteocytes (which are trapped/buried osteoblasts)

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14
Q

what is the organic matrix of bone made up of?

A

mainly collagen (osteoid) and ground substance

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15
Q

What is the inorganic component of bone made up of?

A

hydroxyapatite (calcium and phosphate) and minerals (magnesium, sodium and potassium)

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16
Q

What are the 5 functions of osteoblasts?

A
  1. Make osteoid
  2. Mineralise organic matrix
  3. Communicates with other bone cells
  4. Makes hormones
  5. Become osteocytes
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17
Q

What do osteoclasts do?

A
  1. breakdown old bone
  2. produce enzymes such as TRAP to breakdown extracellular matrix
  3. Help enhance blood calcium levels
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18
Q

Which hormones regulate osteoclasts?

A

PTH, calcitonin and IL-6

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19
Q

What do osteocytes do?

A
  1. Give bone mechanosensory properties e.g how the bones know its being used
  2. Co-ordinate regulation of bone turnover - osteocytes tell the bones what to do and when to do it
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20
Q

Explain the bone cycle/ remodelling

A
  • normal bone is in constant state of turnover caused by resorption by osteoclasts and formation of osteoblasts
  • Osteoclasts reabsorb and break down bone
  • signals to osteoblasts
  • The nutrients are reabsorbed, and osteoblasts lay down new osteoid
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21
Q

What is the relationship between bone mass and age?

A
  • bone mass increases with age until peak at 30 in females and 45 in males
  • then bone mass decreases with age
  • with increasing age, osteoblastic activity falls and osteoclastic activity increases
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22
Q

Why do women loose bone mass more rapidly than men?

A

oestrogen helps maintain bone health so there is faster bone loss due to menopause

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23
Q

Which biochemical markers can we measure when looking at bone formation (i.e production of active osteoblasts) ?

A
  • alkaline phosphatase
  • osteocalcin
  • P1NP (procollagen type 1N propeptides)
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24
Q

Which biochemical markers can we measure when looking at bone resorption (i.e what is released when bone is broken down) ?

A
  • hydroxyproline
  • pyridinium crosslinks
  • cross linked telopeptides of type 1 collage (NTX, CTX)
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25
Q

Why is bone alkaline phosphatase useful to measure?

A
  • released by osteoblasts
  • release stimulated by increased bone remodelling/ when bone turnover changes
  • can show fractures, hyperparathyroidism, pagets disease and pubertal growth spurts
26
Q

What is P1NP and why do we measure it?

A
  • precursor molecule of type 1 collagen
  • synthesised by osteoblasts
  • increased with osteoblast activity
  • decreased by reduced osteoblast activity
27
Q

Why do we measure collagen cross links? (NTX, CTX)

A
  • Cross linking molecules which are released with bone resorption, correlate highly with bone resorption
  • increased in periods of high bone turnover - hyperthyroidism, adolescents and menopause
28
Q

What is DEXA imaging?

A
  • measures bone mass (bone density X-ray)

- measured in T-scores

29
Q

What is a T-score?

A

number of standard deviations away from the mean compared to a young healthy person of the same sex on a DEXA scan

  • 1 and above = normal bone density
  • 1 and -2.5 = low bone mass –> osteopenia
  • 2.5 and below –> osteoporosis
30
Q

What is osteoporosis?

A

a systemic skeletal disease characterised by LOW bone mass and deterioration of bone tissue, with consequent increase in bone fragility and susceptibility to fracture
-decrease bone mass –> failure of structural integrity

31
Q

What is a fragility fraction?

A
  • fracture that occurs as a result of minimal trauma, such as falling from a standing height or less, or no identifiable trauma
  • a fracture caused by injury that would be insufficient to fracture a healthy bone
32
Q

What are the common sites for fracture?

A
  • spine
  • neck of femur
  • wrist
33
Q

What are the risk factors for fracture?

A
  • age
  • sex - F>M
  • recent fragility fracture
  • smoking
  • alcohol
  • falls
  • drugs
  • inflammatory conditions
  • malabsorption
  • T1 DM
  • family history
  • BMI
34
Q

How can we predict the risk of a fracture for a patient with osteoporosis?

A

FRAX

35
Q

What are the secondary causes of osteoporosis?

A
  • early menopause
  • hyperthyroidism
  • cushings
  • any cause of malabsorption
  • RA
  • COPD
  • cystic fibrosis
  • glucocorticoids
  • immobility
  • CKD
36
Q

What are the different ways of investigating the secondary causes of osteoporosis?

A
  • calcium and bone profile
  • U&Es
  • TFTs
  • FBC
  • VitD
  • PTH
  • coeliac screen
  • FSH, LH, oestradiol, prolactin
37
Q

What is antiresorptive treatment?

A
  • for prevention of osteoporotic fractures
  • stops bone breakdown by acting on osteoclasts
  • commenest drugs are bisphosphonates
38
Q

What is anabolic treatment?

A

works on osteoblasts in preventing osteoporotic fractures

39
Q

What is the mechanism of action of bisphosphonates?

A
  • inhibit osteoclast formation, migration and osteolytic activity, promote apoptosis
  • modulate signalling from osteoclasts to osteoblasts
  • concentrated in newly mineralising bone and under osteoclasts
40
Q

What is denosumab?

A
  • a RANK ligant inhibitor (as RANK ligand causes osteoclasts to mature and develop)
  • highly effective injection
  • inhibits osteoclast formation, function and survival
  • increase in spine bone density
41
Q

Where can osteolytic bone mets occur?

A
  • breast/lung
  • kidney/thyroid
  • destroys normal bone (osteoclasts) –> can lead to hypercalcaemia
42
Q

Where can sclerotic/osteoblastic bone mets occur?

A
  • prostate
  • lymphoma
  • breat/lung
43
Q

Where are the usual sites of spread of bone metastases?

A 
spine
pelvis
femur
humerus 
skull
44
Q

What are the presenting features of bone mets?

A
  • Pain – often worse at nights and initially gets better with movement, usually becomes constant
  • Broken bones
  • Numbness, paralysis, trouble urinating – spinal cord compression from bone metastases
  • Loss of appetite, nausea, thirst, confusion, fatigue – symptoms of hypercalcaemia
  • Anaemia – disruption of bone marrow
45
Q

What are the symptoms of mild and severe hypercalcaemia

A

Mild:

  • polyuria, polydypsia
  • mood disturbance
  • anorexia
  • nausea, fatigue
  • constipation

Severe:

  • abdo pain
  • vomiting
  • coma
  • pancreatitis
  • dehydration
  • cardiac arrhythmias
46
Q

What is the next blood test you could do in anyone with a high calcium level?

A

parathyroid hormone - the predominant control for calcium levels

47
Q

How does PTH control calcium levels?

A

• When blood calcium becomes low, the calcium sensing receptors on parathyroid gland detect this and release parathyroid hormone
• This leads to restoration of calcium levels
• Once calcium has gone back to normal we have negative feedback mechanisms to reduce PTH levels
-Mg and VitD also affect PTH

48
Q

What are the non-PTH mediated causes of hypercalcaemia? (so PTH will be low)

A
  • malignancy
  • vitD intoxication
  • medications
  • immobilisation
  • endocrine disorders - hyperthyroidism, acromegaly, phaeochromocytoma
49
Q

What are the PTH mediated causes of hypercalcaemia? (so PTH will be high)

A

primary hyperparathyroidism

50
Q

What is primary hyperparathyroidism?

A
  • parathyroid glands malfunction and make too much PTH and don’t sense calcium properly so calcium raises as well
  • also will have low phosphate and high alk phos
51
Q

What is secondary hyperparathyroidism?

A
  • parathyroid working fine
  • low calcium is detected so we raise PTH
  • this is not a problem
  • causes are usually CKD or VitD deficiency
52
Q

What is the association between adenomas and PHPT?

A
  1. adenoma
    - single adenoma accounts for 85% of cases of PHPT
  2. Glandular hyperplasia
    - all 4 glands enlarged
  3. Ectopic adenomas
  4. Parathyroid carcinoma
53
Q

How would we treat patients with symptomatic hypercalcaemia?

A

surgery - removing parathyroid - is best option

54
Q

Which drugs can we use to treat PHPT?

A

Calcimimetics:

  • activate CaSR in the parathyroid gland
  • therefore leads to reduced PTH secretion
55
Q

What is Paget’s disease of bone?

A
  • rapid bone turnover and formation
  • leading to abnormal bone remodelling
  • mainly 50+ yo , M>F
  • polyostotic (affecting many bones) or monostotic (affecting one bone)
  • elevated alkaline phosphatase reflecting increased bone turnover
  • FH in 10-15% of cases
56
Q

What are the clinical features of Paget’s disease?

A
  • bone pain
  • bone deformation
  • fractures
  • arthritis
  • cranial nerve defects if skull affected - hearing and vision loss
  • risk of osteosarcoma
  • most commonly affects pelvis, femur and lower lumbar vertebrae
57
Q

What investigations of Pagets can we perform?

A

lab assessment
plain x-RAYS
Nuclear medicine bone scan

58
Q

What is the best treatment for Pagets?

A

bisphosphates - give bisphosphates to slow down bone turnover - same treatment as osteoporosis

59
Q

What is osteomalacia?

A
  • adult rickets

- lack of mineralisation of bone - not enough calcium, phosphate

60
Q

What is the difference between childhood rickets and osteomalacia in adults?

A

adult form - widened osteoid seams with lack of mineralisation
rickets - widened epiphyses and poor skeletal growth

61
Q

What are the causes of osteomalacia?

A
  1. Insufficient calcium absorption from intestine - due to lack of dietary calcium or vitD deficiency/resistance
  2. Excessive renal phosphate excretion
62
Q

What are the clinical features of osteomalacia?

A
  • diffuse bone pain - usually symmetrical
  • muscle weakness
  • bone weakness
  • high alk phos, low vitD, possibly low calcium and high PTH (secondary hyperparathyroidism)
  • malabsorption

Clinical Pathology (57 decks)

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