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Clinical Pathology > 51 - Diseases of the Bone and New Markers > Flashcards

51 - Diseases of the Bone and New Markers Flashcards

1
Q

Bone composition

A

Cortical - hard, outer layer
Trabecular bone - spony, inner layer
Cells - forming + resorbing
Extracellular - organic matrix of collagen + inorganic components

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2
Q

What inorganic components are there of bone?

A

Hydroxypatite

Minerals - Ca, phosphate

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3
Q

Bone is called what before mineralisation

A

Osteoid

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4
Q

What is the matrix mineralised by

A

Hydroxyapatite (calcium-phosphate-hydroxide salt)

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5
Q

What are osteoblasts?

A

Terminally differentiated products of mesenchymal stem cells which make osteoids

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6
Q

What are osteoids?

A

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

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7
Q

Functions of osteoblasts

A

Communicate with other bone cells
Make hormones (osteocalcin), matrix proteins and alkaline phosphatase
Prerequisite for mineralisation
Osteoblasts can be osteoclasts

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8
Q

What are osteoclasts?

A

Osteoblasts that are buried/trapped within the matrix

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9
Q

Osteoclasts appearance

A

Large, multinucleated
Ruffled-resorption border
Found in bone pits (resorption bays)

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10
Q

Osteoclast function

A

Break down bone
Produce enzymes which breakdown extracellularly matrix
Help enhance blood Ca levels
Regulated by hormones

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11
Q

Osteocytes

A 
Star shaped 
Trapped osteoblasts
Communicate via cytoplasmic extensions
Mechanosensory properties
Involved with regulating bone matrix turnover
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12
Q

Test for gross structure of bone

A

X ray

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13
Q

Test for bone mass

A

DEXA scan

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14
Q

Test for cellular function/turnover

A

Biochemistry

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15
Q

Test for microstructure/cellular function

A

Biopsy, qCT

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16
Q

Biomarkers for bone formation

A 
Alkaline phosphatase (TAP, BAP)
Osteocalcin
Procollagen type I (P1NP) - but loads of cells have type one collagen
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17
Q

Biomarkers for bone resorption

A

Hydroxyproline
Pyridinium crosslinks
Crosslinked telopeptides for of type I collagen

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18
Q

Osteoclast enzymes

A

Tartrate-resistant acid phosphatase

Cathepsin K

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19
Q

Alkaline phosphatase facts

A

Measured in LFTs and Bone profiles

50% liver and 50% bone
Specific isoenzymes can be measured if diagnostic doubt

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20
Q

What releases and stimulate alkaline phosphatase?

A

Osteoblasts

Childhood/pubertal growth spurts, fractures, hyperparathyroidism, Paget’s disease

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21
Q

P1NP - made where, describe activity

A

Osteoblasts make it - precursor for type one collagen
Low diurnal and intraindividual variation
[Serum] not affected by food intake
Increase with increased osteoblast activity
Decreased with reduced osteoblast activity

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22
Q

Collagen cross-links (NTX, CTX)

A

Cross-linking molecules which are released with bone resorption

Increased in periods of high bone turnover

Diurnal variation, do not predict bone mineral density, decrease with anti-resorptive therapy

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23
Q

Usefulness of bone markers

A

Collagen one - not specific but can detect changes in bones

Indication of bone turnover and/or loss

Evaluation of treatment effect (CTX)

Evaluation of medication compliances (P1NP)

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24
Q

DEXA gives what score

A

T-scores

  • 1 and above = normal
  • 1 and -2.5 = osteopenia
  • 2.5 and below = osteoporosis
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25
Q

Bone disorders

A 
Metastatic disease
Hyperparathyroidism
Osteomalacia/Rickets
Osteoporosis
Paget's disease
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26
Q

What happens to the spine of a patient with osteoporosis?

A

Increase in biconcavity of lower thoracic bodies

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27
Q

Osteoporosis symptoms

A

Propensity to fractures - spine or hip
No abnormal routine biochemical tests
Diagnosis relies on DEXA/Xray

28
Q

Osteoporosis definition

A

Decreased bone mass with deranged bone micro architecture

29
Q

Antiresorptive treatments

A

Bisphosphonates (most common)
Oral/IV
Alendronic acid/zoledronic acid

Denosumab - RANKL monoclonal antibody

Raloxifene

30
Q

Anabolic treatment

A

Terparatide SC

Synthetic PTH

31
Q

Efficacy of treatment for osteoporosis

A

50-70% reduction in vertebral fractures

25-35% reduction in hip fractures

32
Q

How do bisphosphonates work

A

Mimic pyrophosphate structure
Taken up by skeleton
Ingested by osteoclasts

33
Q

Bisphosphonates - problems

A 
Poor absorption
Difficult to take - sat up for hours
Can cause oesophageal/upper GI problems
Flu-like side effects
Osteonecrosis of jaw
Atypical femur fracture
34
Q

Types of bone mets

A

Lytic
Sclerotic/osteoblastic

Usual sites of spread inc. spine, pelvis, femur, humerus, skull

35
Q

Lytic bone mets

A

Destruction of normal bone (osteoclasts)
Breast/lung
Kidney/thyroid

36
Q

Sclerotic/osteoblastic mets

A

Deposition of new bone
Prostate
Lymphoma
Breast/lung (15-25%)

37
Q

Bone mets - clinical presentation

A

pain - worse and night and gets better with movement

Broken bones

Numbness, paralysis, trouble urinating

Loss of appetite, nausea, thirst, confusion, fatigue (from hypercalcaemia)

Anaemia from bone marrow disruption

38
Q

Symptoms of mild hypercalcaemia

A 
Polyuria, polydipsia
Mood disturbance
Anorexia
Nausea
Fatigue
Fatigue
Constipation
39
Q

Symptoms of severe hypercalcaemia

A 
Abdo pain
Vomiting
Coma
Pancreatitis
Dehydration
Cardiac arrythmias
40
Q

Causes of hypercalcaemia

A

Either non-PTH mediated or PTH-mediated

Mainly malignancy and sporadic 1° hyperparathyroidism respectively

41
Q

Parathyroid hormone

A

PTH
Secreted by chief cells of parathyroid gland
stimulated by high blood calcium

42
Q

Primary hyperparathyroidism

A

Ca: high
PTH: inappropriately high
Low phosphate and high alk phos common
Sporadic or familial

43
Q

Secondary hyperparathyroidism

A

Ca: normal or low
PTH: appropriately high
Phosphate high if due to chronic kidney infection
Causes: mainly CKD or vit D deficiency

44
Q

Tertiary hyperparathyroidism

A

Ca: usually high
PTH: inappropriately high
Phosphate can high or low
Causes: after prolonged secondary HPT, usually in CKD

45
Q

Primary hyperparathyroidism - clinical presentation

A

Severe hypercalcaemia +/- symptomatic renal/skeletal disease

46
Q

Primary hyperparathyroidism - who?

A

> 45

Women>M

47
Q

Primary hyperparathyroidism - benign cancers

A

Adenomas (benign) - 85% of cases have single adenoma
5% have double
Most encapsulated and consist of parathyroid chief cells

48
Q

Primary hyperparathyroidism - malignant cancers

A

Parathyroid carcinoma
1-2% of all HPT
Invasion seen in histology
Usually aggressive with significant hypercalcaemia and possibility of distant mets

49
Q

Primary hyperparathyroidism - hyperplasia

A

6-10% of HPT cases
All 4 glands enlarged

Can occur sporadically or part of genetic syndromes (MEN1, MEN2A or familial hyperparathyroidism)
Medial or surgical therapy e.g. 3.5 glands removed

50
Q

Primary hyperparathyroidism - which genetic syndromes?

A

MEN1
MEN2
Familial hyperparathyroidism

51
Q

Primary hyperparathyroidism - ectopic adenomas

A

Rarely ectopic adenomas in mediastinum

Some parathyroid adenomas found in thymus gland (due to embryological migration)

52
Q

Primary hyperparathyroidism - classical clinical presentation

A

Hypercalcaemia
Renal disease
Bone disease
Proximal muscle wasting

53
Q

Primary hyperparathyroidism - investigations

A

Radiography - ectopic PT tissue in mediastinum

54
Q

Primary hyperparathyroidism - indications for surgery

A

Symptomatic hypercalcaemia

In asymptomatic patients: Ca>0.25mmol/l above normal.
Renal stone disease
Calculated creatinine clearnace (

55
Q

Calcimimetics

A

Activates CaSR in PT gland - reducing PTH secretion

56
Q

Paget’s disease - what is it

A

rapid bone turnover and formation leading to abnormal bone remodelling

57
Q

Paget’s disease - who?

A 
Over 50
Higher prevalence in men
Genetic + enviro
FH in 10-15% of cases
Polyostotic or monostotic 
Elevated alk. phos. reflecting increased bone turnover
58
Q

Paget’s disease - clinical presentation

A 
Bone pain
Bone deformity
Fractures
Arthritis
Cranial nerve defects if skull affected
Risk of osteosarcoma
Most commonly affects pelvis, femur and lower lumbar vertebrae
59
Q

Paget’s disease - managment

A

Labs
Plain X-rays
Nuclear medicine bone scan

60
Q

Osteomalacia - pathogenesis

A

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

61
Q

Osteomalacia - adult form, childhood

A

Widened osteoid seams with lack of mineralisation

Child - rickets - widened epiphyses & poor skeletal growth

62
Q

Osteomalacia - main causes

A

Insufficient Ca absorption from intestine (lack of dietary Ca/vit D)

Excessive renal phosphate excretion (rare genetic)

63
Q

Osteomalacia - clinical features

A

Diffuse bone pains - symmetrical
Muscle weakness
Bone weakness
High alk phos, low vit D, possibly low Ca and high PTH

64
Q

Osteomalacia - who?

A

Ageing pop
Nursing home residents
Asian (hijab/burka wearing)
Malabsorption

65
Q

Pic on slide 71

A

is good summary

Clinical Pathology (65 decks)

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