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10. CP - Endocrine System and Disease > (51) Diseases of the bone and new markers > Flashcards

(51) Diseases of the bone and new markers Flashcards

1
Q

What is the purpose of bone?

A
  • structural support for the body
  • protection of vital organs
  • blood cell production (bone marrow)
  • storage bank for minerals (especially calcium)
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2
Q

What is cortical bone and trabecular bone?

A

Cortical bone = hard, outer layer

Trabecular bone = spongy, inner layer

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3
Q

What 2 types of cells are associated with bone?

A

Bone forming cells and bone reabsorbing cells (osteoblasts and osteoclasts)

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4
Q

What is the extracellular component of bone composed of?

A
  • organic matrix = mainly collagen

- inorganic components = hydroxyapatite and minerals (calcium and phosphate)

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5
Q

What is the name for bone before it has mineralised?

A

Osteoid

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6
Q

Bone matrix is mineralised by what? (to form mature bone tissue)

A

Hydroxyapatite (calcium-phosphate-hydroxide salt)

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7
Q

Briefly, what do osteoblasts do?

A

Produce and secrete bone matrix and help with mineralisation

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8
Q

Briefly, what do osteoclasts do?

A

Absorbs bone tissue during growth and healing

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9
Q

Describe some features of bone as a dynamic tissue

A
  • extracellular matrix
  • protein and mineral
  • mainly collagen
  • constant remodelling
  • highly vascular tissue
  • metabolically active
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10
Q

What does collagen do?

A

Provides tensile strength

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11
Q

What are osteoblasts?

A

Terminally differentiated products of mesenchymal stem cells that make osteoid

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12
Q

What is osteoid?

A

Non-mineralised organic matrix, consists of mainly type 1 collagen
- prerequisite for mineralisation

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13
Q

What do osteoblasts do?

A
  • make osteoid
  • communicate with other bone cells
  • make hormones eg. osteocalcin, matrix proteins and alkaline phosphatase
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14
Q

What is the name for osteoblasts that are buried/trapped within the matrix?

A

Osteocytes

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15
Q

Describe the appearance of osteoclasts

A

Large and multi-nucleated with a ruffled-resorption border

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16
Q

Where are osteoclasts found?

A

In bone pits (resorption bays)

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17
Q

What do osteoclasts do?

A
  • break down bone = critical for repair and maintenance of bone
  • produce enzymes that are secreted to break down extracellular matrix
  • help enhance blood calcium levels
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18
Q

Which enzymes do osteoclasts produce? (secreted to break down extracellular matrix)

A

Tartrate resistant acid phosphatase (TRAP) and Cathepsin K

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19
Q

Which hormones are osteoclasts regulated by?

A

PTH, calcitonin and IL-6

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20
Q

RANK ligand and osteoprotegrin do what?

A

Help with osteoclastic maturation and activity

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21
Q

What are osteocytes?

A

Trapped/buried osteoblasts

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22
Q

Describe the appearance of osteocytes

A

Star-shaped

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23
Q

How do osteocytes communicate with each other?

A

Via cytoplasmic extensions

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24
Q

What are the functions of osteocytes?

A
  • mechanosensory properties

- involved with regulating bone matrix turnover

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25
Q

Describe bone remodelling

A

Normal bone is in a constant state of turnover caused by resorption by osteoclasts and formation by osteoblasts

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26
Q

How often is the adult skeleton completely replaced?

A

Every 10 years

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27
Q

Simply, what is osteoporosis?

A

When there is more bone destruction than there is formation

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28
Q

What are the 4 main stages in the bone cycle?

A
  • resting
  • resorption
  • osteoid formation
  • mineralisation
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29
Q

How is bone mass measured?

A

Total mass of skeletal calcium in grams

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30
Q

How does bone mass change with age?

A

Increases from birth until a peak at around 30-40 where it then starts declining

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31
Q

Where is there a steeper decrease in bone mass in women at around the age of 50?

A

Due to menopause

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32
Q

Why is there a decrease in bone mass with increasing age? A

A

As there is increased bone resorption but decreased bone formation

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33
Q

What 4 things about bone might you want to investigate?

A
  • gross structure
  • bone mass (calcium)
  • cellular function/turnover
  • microstructure/cellular function
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34
Q

How is bone gross structure investigated?

A

X-ray

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35
Q

How is bone mass (calcium) investigated?

A

DEXA

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36
Q

How is bone cellular function/turnover investigated?

A

Biochemistry

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37
Q

How is bone microstructure/cellular function investigated?

A

Biopsy, qCT

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38
Q

What are the biochemical markers of bone formation?

A

Products of active OB:

  • alkaline phosphatase (TAP, BAP)
  • osteocalcin (OC)
  • procollagen type 1 prepeptides (P1NP)
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39
Q

What are the biochemical markers of bone resorption?

A

Degradation products of bone collagen:

  • hydroxyproline
  • pyridinium crosslinks
  • crosslinked telopeptides of type I collagen (NTX, CTX)

+ osteoclast enzymes

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40
Q

What are the osteoclast enzymes?

A
  • tartrate-resistant acid phosphatase (TRACP 5b)

- cathepsin K

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41
Q

When is alkaline phosphatase measured?

A

Measured by the lab in LFTs and bone profiles

Specific isoenzymes can be measured where there is diagnostic doubt

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42
Q

In health, what are the alkaline phosphatase levels?

A

50% liver

50% bone

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43
Q

What is bone alkaline phosphatase involved in?

A

Mineralisation

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44
Q

What is bone alkaline phosphatase released by?

A

Osteoblasts

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45
Q

Release of bone alkaline phosphatase is stimulated by increase bone remodelling in…

A
  • childhood/pubertal growth spurt
  • fractures
  • hyperparathyroidism (primary or secondary)
  • Paget’s disease of the bone
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46
Q

What is P1NP?

A

Procollagen type 1N propeptide

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47
Q

What is P1NP synthesised by?

A

Osteoblasts

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48
Q

P1NP is the precursor molecule of what?

A

Type 1 collagen

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49
Q

P1NP levels are affected by what?

A
  • increased with increased osteoblast activity
  • decreased by reduced osteoblast activity
  • serum concentrations not affected by food intake
  • has low diurnal and intraindividual variation
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50
Q

What are collagen cross-links (NTX, CTX)?

A

Cross-linking molecules which are released with bone resorption

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51
Q

What do collagen cross-links levels correlate with?

A

Correlate highly with bone resorption

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52
Q

When do collagen cross-links levels change?

A
  • increased in periods of high bone turnover (hyperthyroidism, adolescents, menopause)
  • decrease with anti-resorptive therapy
  • have diurnal variation
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53
Q

Collagen cross-links levels do not predict what?

A

Bone mineral density

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54
Q

Collagen cross-links (NTX, CTX) are increased in periods of high bone turnover. Give 3 examples of this

A
  • hyperthyroidism
  • adolescents
  • menopause
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55
Q

Collagen-related bone markers are based primarily on what?

A

On type 1 collagen, which is widely distributed in several tissues

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56
Q

Are changes in bone markers disease-specific?

A

Changes in bone markers are not disease specific, but reflect alterations in skeletal metabolism

Some markers are characterised by significant intra-individual variability

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57
Q

What are the uses of new bone markers?

A
  • evaluation of bone turnover and bone loss
  • evaluation of treatment effect
  • evaluation of compliance with medication
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58
Q

Bone markers can be used to evaluate treatment effect. Give and example

A

CTX used to monitor response to anti-resorptive therapy

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59
Q

Bone markers can be used to evaluate compliance with medication. Give 2 examples

A
  • P1NP used to monitor compliance with teriparatide

- CTX used to monitor compliance/response to anti-resorptive therapy

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60
Q

What is teriparatide?

A

A recombinant form of parathyroid hormone - an effective anabolic (bone growing) agent used in the treatment of some forms of osteoporosis

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61
Q

What do T scores mean?

A
  • 1 and above = normal born density
  • 1 to -2.5 = low bone mass (osteopenia)
  • 2.5 and below = osteoporosis
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62
Q

What is osteopenia?

A

When the protein and mineral content of bone tissue is reduced, but less severely than in osteoporosis

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63
Q

Which scan gives you T scores?

A

DEXA

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64
Q

What are the different types of bone disorders?

A
  • metastatic disease
  • hyperparathyroidism
  • osteomalacia/Rickets
  • osteoporosis
  • Paget’s disease
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65
Q

What is osteomalacia?

A

Softening of the bones, typically through a deficiency of vitamin D or calcium

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66
Q

Why is hyperparathyroidism?

A

An abnormally high concentration of parathyroid hormone in the blood, resulting in weakening of the bones through loss of calcium.

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67
Q

What is Paget’s disease of the bone?

A

Disrupts the normal cycle of bone renewal and repair, causing bones to become weakened and deformed

68
Q

What is osteoporosis?

A

The bones become brittle and fragile from loss of tissue, typically as a result of hormonal changes, or deficiency of calcium or vitamin D

69
Q

What might the spine of an osteoporosis patient show?

A

Increase in biconcavity of the lower thoracic bodies and in anterior compression of the mid-thoracic vertebral bodies

70
Q

What might the T scores of an osteoporosis patient be from a DXA scan?

A

T = -3.3 spine

T = -4.2 hip

71
Q

What might the blood tests of an osteoporosis patient show?

A

Unremarkable apart from vitamin D deficiency

72
Q

How might something to do with hormones cause osteoporosis?

A

Early menopause (before age 45)

73
Q

Generalised loss of bone in osteoporosis gives propensity to what?

A

Fractures of the hip and spine, even from simple falls

74
Q

What abnormalities are seen in routine biochemical tests in osteoporosis?

A

None - perhaps because they are too insensitive

75
Q

Diagnosis of osteoporosis relies on what?

A

DEXA/X-ray

76
Q

There is an increasing use of what in osteoporosis management?

A

Bone markers

77
Q

What is the actual definition of osteoporosis?

A

A systemic skeletal disease characterised by LOW BONE MASS and MICROARCHITECTURAL DETERIORATION of bone tissue, with consequent increase in bone fragility and susceptibility to fracture (FAILURE OF STRUCTURAL INTEGRITY)

78
Q

Where are the common sites of fracture in osteoporosis?

A
  • spine
  • neck of femur
  • wrist
79
Q

What is the definition of a fragility fracture?

A

A fracture caused by injury that would be insufficient to fracture a normal bone/ occurs as a result of minimal trauma, such as a fall from standing height or less, or no identifiable trauma

80
Q

What should be suspected in any person with history of fragility fracture?

A

Low bone mass

81
Q

What signs should prompt investigation for vertebral fractures?

A
  • unexplained loss of height
  • kyphosis
  • severe back pain
82
Q

What is the FRAX calculation tool?

A 
Fracture risk assessment - calculates 10 year probability of fracture. Takes into account:
- previous fracture
- smoking 
- glucocorticoids
- rheumatoid arthritis
- osteoporosis 
- alcohol
- femoral neck BMD 
etc
83
Q

What are some endocrine secondary causes of osteoporosis?

A
  • early menopause
  • amennorrhoea
  • hypogonadism
  • Cushings
  • diabetes
  • hyperparathyroidism
  • hyperthyroidism
    etc
84
Q

What are some GI secondary causes of osteoporosis?

A
  • coeliac disease
  • IBD
  • chronic liver disease
  • malabsorption
85
Q

What are some rheumatological secondary causes of osteoporosis?

A
  • rheumatoid arthritis

- other inflammatory arthropathies

86
Q

What are some haematological secondary causes of osteoporosis?

A
  • myeloma
  • haemaglobinopathies
  • systemic mastocytosis
87
Q

What are some respiratory secondary causes of osteoporosis?

A
  • COPD

- cystic fibrosis

88
Q

What are some drugs that can cause secondary osteoporosis?

A
  • steroids
  • heparin
  • ciclosporin
  • anti-convulsants
89
Q

What are the investigations done into secondary causes of osteoporosis?

A
  • calcium and bone profile
  • U&Es (estimated GFR)
  • TFTs
  • FBC
  • vitamin D
  • PTH
  • plasma viscosity (+/- myeloma screen)
  • coeliac screen
  • lateral X-ray T5-L5
  • testosterone, SHGB, LH, FSH, LFTs (male)
  • LH, FSH, estradiol, prolactin (female)
90
Q

What are some antiresorptive treatments?

A
  • bisphosphonates (oral/IV) - (alendronic acid/zoledronic acid)
91
Q

What are some anabolic treatments?

A
  • terparatide (subcut)

- synthetic PTH (parathyroid hormone)

92
Q

What is denosumab?

A

Used in preventing fractures and other cancer related bone problems in adults with cancer that has spread to the bone
- monoclonal antibody to RANK ligand

93
Q

What is raloxifene?

A

An oral selective estrogen receptor modulator (SERM) that has oestrogenic actions on bone

94
Q

Which mineral is also used in bone treatment?

95
Q

Describe the efficacy of bone treatments

A
  • 50-70% reduction in vertebral fractures

- 25-35% reduction in hip fractures

96
Q

Describe the mechanism of action of bisphosphonates

A
  • mimic pyrophosphate structure
  • ingested by osteoclasts
  • bisphosphonate released from osteoclast during bone resorption
  • impairs osteoclasts’ ability to form ruffled border etc.
  • inhibit osteoclast formation, migration, osteolytic activity and promote apoptosis
97
Q

Describe some problems with the use of bisphosphonates

A
  • poor absorption
  • difficult to take
  • can cause oesophageal/upper GI problems
  • flu-like side effects
  • osteonecrosis of the jaw
  • atypical femur fractures
98
Q

Describe 2 types of bone metastases

A
  • lytic

- sclerotic/osteoblastic

99
Q

What are lytic bone metastases?

A

Destruction of normal bone (osteoclasts)

100
Q

What are sclerotic/osteoblastic bone metastases?

A

Deposition of new bone

101
Q

Which cancers causes lytic bone metastases?

A
  • breast/lung

- kidney/thyroid

102
Q

Which cancers cause sclerotic bone metastases?

A
  • prostate
  • lymphoma
  • breast/lung (15-25%)
103
Q

Where are the usual sites of bone metastases?

A
  • spine
  • pelvis
  • femur
  • humerus
  • skull
104
Q

Describe 5 groups of presenting symptoms of bone mets

A
  • pain
  • broken bones
  • numbness, paralysis, trouble urinating
  • loss of appetite, nausea, thirst, confusion, fatigue
  • anaemia
105
Q

Describe the pain that occurs in born mets

A
  • often worse at night
  • gets better with movement initially
  • usually becomes constant
106
Q

Which bones get commonly broken in bone mets

A
  • femur
  • humerus
  • vertebral column

Pathological fractures

107
Q

Why do you get numbness, paralysis and trouble urinating in bone mets?

A

Spinal cord compression from bone metastases

108
Q

Why do you get loss of appetite, nausea, thirst, confusion and fatigue in bone mets?

A

Symptoms of hypercalcaemia

109
Q

Why do you get anaemia in bone mets?

A

Disruption of bone marrow

110
Q

What do the parathyroid glands do?

A

Control the body’s calcium levels - produce parathyroid hormone (PTH)

111
Q

What are the mild symptoms of hypercalcaemia?

A
  • polyuria, polydipsia
  • mood disturbance
  • anorexia
  • nausea
  • fatigue
  • constipation
112
Q

What are the severe symptoms of hypercalcaemia?

A
  • abdominal pain
  • vomiting
  • coma
  • pancreatitis
  • dehydration
  • cardiac arrhythmias
113
Q

What are the non-PTH mediated causes of hypercalcaemia?

A
  • malignancy
  • vitamin D intoxication
  • chronic granulomatous disorders eg. sarcoidosis
  • medications eg. thiazide diuretics, teriparatide
  • immobilisation
  • other endocrine conditions eg. hyperthyroidism, acromegaly
114
Q

What are the PTH-mediated causes of hypercalcaemia?

A
  • sporadic primary hyperparathyroidism

- familial (MEN1 and 2A, familial hypocalciuric hypercalcaemia, familial isolated hyperparathyroidism)

115
Q

Where are the parathyroid glands?

A

2 on each side of the thyroid gland, at the back

116
Q

What is parathyroid hormone (PTH) secreted by?

A

Chief cell of parathyroid gland

117
Q

What type of molecule is PTH?

A

Polypeptide containing 84 amino acids

118
Q

What stimulates the parathyroid gland to release PTH?

A
  • low levels of blood calcium
  • decreased serum magnesium
  • increased vitamin D
119
Q

What 3 main things does PTH do?

A
  • increases decomposition of bone, releasing calcium
  • increases absorption of calcium from food by intestines
  • increases reabsorption of calcium from urine by kidneys

These all increase levels of blood calcium

120
Q

What effect does increasing levels of calcium have on the parathyroid gland?

A

Negative feedback back to the parathyroid gland so less PTH produced

121
Q

What are the 3 different types of hyperparathyroidism (HPT)?

A
  • primary
  • secondary
  • tertiary
122
Q

What are the calcium levels in hyperparathyroidism?

A

primary = high

secondary = normal or low

tertiary = high

123
Q

What are the PTH levels in hyperparathyroidism?

A

primary = inappropriately high

secondary = appropriately high

tertiary = inappropriately high

124
Q

What are the phosphate levels in HPT?

A

primary = low phosphate and high alkaline phosphate

secondary = high phosphate if due to chronic kidney disease

tertiary = phosphate can be high or low

125
Q

What are the causes of primary HPT?

A

Sporadic or familial

126
Q

What are the causes of secondary hyperthyroidism?

A

Mainly CKD or vitamin D deficiency

127
Q

What are the causes of tertiary HPT?

A

After prolonged secondary HPT, usually in CKD

128
Q

What is tertiary hyperthyroidism?

A

A state of excessive secretion of parathyroid hormone (PTH) after a long period of secondary hyperparathyroidism and resulting in a high blood calcium level

129
Q

What is secondary hyperparathyroidism?

A

Excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels) and associated hyperplasia of the gland

130
Q

How does primary hyperparathyroidism present?

A

Used to present with severe hypercalcaemia and/or symptomatic renal and skeletal disease

Now presentation is much earlier and is usually asymptomatic

131
Q

Majority of cases of PHPT present at what age?

132
Q

Which gender is more affected by PHPT?

A

Women are 2x as likely to be affected compared to men

133
Q

What blood test results suggest PHTP?

A

Inappropriately elevated PTH in the presence of high calcium

134
Q

What accounts for 90% of cases of primary HPT?

A

Benign adenomas

85% = single adenoma
5% = double parathyroid adenomas
135
Q

Describe typical parathyroid adenomas

A

Most adenomas are encapsulated and consist of parathyroid chief cells

136
Q

What accounts for 1-2% of PHPT?

A

Parathyroid carcinomas (malignant)

137
Q

Describe the features of PHPT caused by carcinoma

A
  • features of invasion on histology

- usually aggressive disease, with significant hypercalcaemia, and possibility of distant metastases

138
Q

What account for 6-10% of cases of primary HPT?

A

Glandular hyperplasia

139
Q

Describe the features of glandular hyperplasia causing primary HPT

A
  • all 4 glands enlarged
  • lower glands usually larger than upper ones
  • usually composed of chief cells
140
Q

Is glandular hyperplasia causing primary HPT sporadic or familial?

A

Can occur sporadically or part of genetic syndromes (MEN1, MEN2A or familial hyperparathyroidism)

141
Q

How is glandular hyperplasia causing primary HPT treated?

A
  • medical or surgical therapy

- if surgery, 3.5 glands often removed

142
Q

Describe the features of ectopic adenomas causing primary HPT?

A
  • rarely ectopic adenomas in mediastinum
  • some parathyroid adenomas found in thymus gland
  • parathyroid cells which migrated during embryogenesis
143
Q

What are the classical clinical manifestations of PHPT?

A
  • symptoms related to hypercalcaemia (as described)
  • renal disease (nephrolithiasis, chronic kidney disease)
  • bone disease (osteoporosis, osteitis, fibrosa cystica)
  • proximal muscle wasting
144
Q

What drug is used in imaging to identify parathyroid adenomas in primary HPT?

A

Tc 99 sestamibi

  • can also identify ectopic parathyroid tissue in mediastinum for example
145
Q

What are the indications for surgery in PHPT?

A
  • symptomatic hypercalcaemia
  • in asymptomatic patients with:
  • calcium over 0.25mmol/L above normal
  • renal stone disease
  • creatinine clearance less than 60ml/min
  • age under 50 yeas
  • osteoporosis at any site or history of fragility fracture
146
Q

Why are calcimimetics (cinacalcet) used in HPT?

A

Activates CaSR (calcium sensing receptor) in the parathyroid gland, therefore leading to reduced PTH secretion

147
Q

What are calcimimetics used for in HPT?

A

Used to normalise calcium in symptomatic patients, or those who are not fit for or unwilling to have surgery

  • does not seem to alter bone disease
  • no data on renal outcomes or QoL
148
Q

What are the limitations of calcimimetics?

A

GI side effects, particularly nausea

149
Q

What happens in Paget’s disease of bone?

A
  • rapid bone turnover and formation
  • leading to abnormal bone remodelling

Can be polyostotic or monostotic

150
Q

Who does Paget’s disease of bone occur in?

A

Mainly over 50 years old, higher prevalence in men

151
Q

Does Paget’s disease generally come with family history?

A

FH in 10-15% of cases

Probably genetic and environmental triggers

152
Q

There are elevated levels of what in Paget’s disease of bone?

A

Elevated alkaline phosphatase - reflecting increased bone turnover

153
Q

What are the clinical features of Paget’s disease of bone?

A
  • bone pain
  • bone deformity
  • fractures
  • arthritis
  • cranial nerve defects if skull affected = hearing and vision loss
  • risk of osteosarcoma
154
Q

Which bones does Paget’s disease most commonly affect?

A
  • pelvis
  • femur
  • lower lumbar vertebrae
155
Q

What are the investigations into Paget’s disease?

A
  • lab assessment
  • plain X-rays
  • nuclear medicine bone scan
156
Q

What happens in osteomalacia?

A

Lack of mineralisation of bone due to vitamin D deficiency or lack of calcium and/or phosphate

157
Q

What are the differences between the adult and child forms of osteomalacia?

A

adult form = widened osteoid seams with lack of mineralisation

classic childhood rickets = widened epiphyses and poor skeletal growth

158
Q

What is an osteoid seam? (these are widened in osteomalacia)

A

On the surface of a bone, the narrow region of newly formed organic matrix not yet mineralised

159
Q

What are the main causes of osteomalacia?

A
  • insufficient calcium absorption from intestine (due to lack of dietary calcium or vit D deficiency/resistance)
  • excessive renal phosphatase excretion (rare genetic forms eg. hereditary hypophosphataemic rickets)
160
Q

What are the clinical features of osteomalacia?

A
  • diffuse bone pains, usually symmetrical
  • muscle weakness
  • bone weakness
161
Q

What are the levels of alkaline phosphatase, calcium etc that you would find in osteomalacia?

A
  • high alkaline phosphatase
  • low vitamin D
  • possibly low calcium
  • high PTH (secondary hyperparathyroidism)
162
Q

Which of the adult population are more at risk of osteomalacia?

A
  • nursing home residents/elderly
  • asian population (Hijab/Burka wearing)
  • malabsorption
163
Q

Summarise the biochemistry of hyperparathyroidism

A

Alkaline phosphatase = increased

Calcium = increased

Phosphate = decreased

PTH = increased

164
Q

Summarise the biochemistry of osteomalacia

A

Alkaline phosphatase = increased

Calcium = (low)

Phosphate = low

PTH = (high)

165
Q

Summarise the biochemistry of osteoporosis

A

Alkaline phosphatase = nil

Calcium = nil

Phosphate = nil

PTH = nil

166
Q

Summarise the biochemistry of Paget’s

A

Alkaline phosphatase = high

Calcium = nil

Phosphate = nil

PTH = nil

167
Q

Summarise the biochemistry of bone mets

A

Alkaline phosphatase = high

Calcium = (high)

Phosphate = nil

PTH = (low)

10. CP - Endocrine System and Disease (5 decks)

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