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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
Bone disorders
``` Metastatic disease Hyperparathyroidism Osteomalacia/Rickets Osteoporosis Paget's disease ```
26
What happens to the spine of a patient with osteoporosis?
Increase in biconcavity of lower thoracic bodies
27
Osteoporosis symptoms
Propensity to fractures - spine or hip No abnormal routine biochemical tests Diagnosis relies on DEXA/Xray
28
Osteoporosis definition
Decreased bone mass with deranged bone micro architecture
29
Antiresorptive treatments
Bisphosphonates (most common) Oral/IV Alendronic acid/zoledronic acid Denosumab - RANKL monoclonal antibody Raloxifene
30
Anabolic treatment
Terparatide SC | Synthetic PTH
31
Efficacy of treatment for osteoporosis
50-70% reduction in vertebral fractures 25-35% reduction in hip fractures
32
How do bisphosphonates work
Mimic pyrophosphate structure Taken up by skeleton Ingested by osteoclasts
33
Bisphosphonates - problems
``` 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
Types of bone mets
Lytic Sclerotic/osteoblastic Usual sites of spread inc. spine, pelvis, femur, humerus, skull
35
Lytic bone mets
Destruction of normal bone (osteoclasts) Breast/lung Kidney/thyroid
36
Sclerotic/osteoblastic mets
Deposition of new bone Prostate Lymphoma Breast/lung (15-25%)
37
Bone mets - clinical presentation
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
Symptoms of mild hypercalcaemia
``` Polyuria, polydipsia Mood disturbance Anorexia Nausea Fatigue Fatigue Constipation ```
39
Symptoms of severe hypercalcaemia
``` Abdo pain Vomiting Coma Pancreatitis Dehydration Cardiac arrythmias ```
40
Causes of hypercalcaemia
Either non-PTH mediated or PTH-mediated Mainly malignancy and sporadic 1° hyperparathyroidism respectively
41
Parathyroid hormone
PTH Secreted by chief cells of parathyroid gland stimulated by high blood calcium
42
Primary hyperparathyroidism
Ca: high PTH: inappropriately high Low phosphate and high alk phos common Sporadic or familial
43
Secondary hyperparathyroidism
Ca: normal or low PTH: appropriately high Phosphate high if due to chronic kidney infection Causes: mainly CKD or vit D deficiency
44
Tertiary hyperparathyroidism
Ca: usually high PTH: inappropriately high Phosphate can high or low Causes: after prolonged secondary HPT, usually in CKD
45
Primary hyperparathyroidism - clinical presentation
Severe hypercalcaemia +/- symptomatic renal/skeletal disease
46
Primary hyperparathyroidism - who?
>45 | Women>M
47
Primary hyperparathyroidism - benign cancers
Adenomas (benign) - 85% of cases have single adenoma 5% have double Most encapsulated and consist of parathyroid chief cells
48
Primary hyperparathyroidism - malignant cancers
Parathyroid carcinoma 1-2% of all HPT Invasion seen in histology Usually aggressive with significant hypercalcaemia and possibility of distant mets
49
Primary hyperparathyroidism - hyperplasia
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
Primary hyperparathyroidism - which genetic syndromes?
MEN1 MEN2 Familial hyperparathyroidism
51
Primary hyperparathyroidism - ectopic adenomas
Rarely ectopic adenomas in mediastinum Some parathyroid adenomas found in thymus gland (due to embryological migration)
52
Primary hyperparathyroidism - classical clinical presentation
Hypercalcaemia Renal disease Bone disease Proximal muscle wasting
53
Primary hyperparathyroidism - investigations
Radiography - ectopic PT tissue in mediastinum
54
Primary hyperparathyroidism - indications for surgery
Symptomatic hypercalcaemia In asymptomatic patients: Ca>0.25mmol/l above normal. Renal stone disease Calculated creatinine clearnace (
55
Calcimimetics
Activates CaSR in PT gland - reducing PTH secretion
56
Paget's disease - what is it
rapid bone turnover and formation leading to abnormal bone remodelling
57
Paget's disease - who?
``` 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
Paget's disease - clinical presentation
``` 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
Paget's disease - managment
Labs Plain X-rays Nuclear medicine bone scan
60
Osteomalacia - pathogenesis
lack of mineralisation of bone due to vitamin D deficiency or lack of calcium and/or phosphate
61
Osteomalacia - adult form, childhood
Widened osteoid seams with lack of mineralisation Child - rickets - widened epiphyses & poor skeletal growth
62
Osteomalacia - main causes
Insufficient Ca absorption from intestine (lack of dietary Ca/vit D) Excessive renal phosphate excretion (rare genetic)
63
Osteomalacia - clinical features
Diffuse bone pains - symmetrical Muscle weakness Bone weakness High alk phos, low vit D, possibly low Ca and high PTH
64
Osteomalacia - who?
Ageing pop Nursing home residents Asian (hijab/burka wearing) Malabsorption
65
Pic on slide 71
is good summary

Clinical Pathology (65 decks)

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