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Clinical pathology > Bone and new markers > Flashcards

Bone and new markers Flashcards

1
Q

Composition of bone

A
  • Cortical bone - hard outer layer makes up 80%
  • Trabecular/cancellous bone = Spongy inner layer 20%
  • Extracellular = organic matrix (collagen) + Inorganic components (calcium eg)
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2
Q

Osteoblasts

A
  • Create and repair new bone
  • Make osteoid - consisting of type 1 collagen
  • Make hormone - osteocalcin
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3
Q

Osteoclasts

A
  • Breakdown old bone
  • Releases calcium into the bloodstream
  • Found in bone pits
  • Produce enzymes such as TRAP and cathepsin K to dissolve bone
  • Responsive to hormones eg IL-6
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4
Q

Osteocytes

A
  • Buried osteoblasts
  • Communicate via cytoplasmic extensions
  • Mechanosensory properties
  • Co-ordinate regulation of bone turnover - osteocytes signal osteoclast where bone needs to be broke
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5
Q

Is Bone a a dynamic tissue?

A

Yes - Constant remodelling, highly vascular tissue, metabolically active.

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6
Q

Bone cycle

A
  • Resting bones with lining cells
  • Osteocytes signal that bone needs to be broke
  • Osteoclasts reabsorb area of bone and signal osteoblasts
  • Osteoblasts from osteoid to form hard bone
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7
Q

What affects the bone cycle

A
  • Loss of oestrogen = more loss of bone mass
  • With increasing age, the rate of bone resorption exceeds the rate
    of bone formation, hence there is a gradual decrease in bone mass
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8
Q

What is DEXA scanning

A
  • Bone mass (calcium) investigation - shine a little bit of radiation through bone for densitometry result.
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9
Q

Alkaline phosphate

A
  • Biochemical marker of bone formation
  • Elevated ALP from liver or bone problems
  • Bone specific ALP = involved in mineralisation, released by osteoblasts
  • Release stimulated by increased bone remodelling - due to puberty, hyperparathyroidism, Paget’s
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10
Q

P1NP - procollagen type 1N propeptides

A
  • Biochemical marker of bone formation
  • Synthesised by osteoblasts – pecursor molecule of type 1 collagen
  • Increased with increased osteoblast activity, decreased by reduced osteoblast activity
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11
Q

Collagen cross-links (NTX, CTX)

A
  • Biochemical marker for bone resorption
  • Cross-linking molecules released in bone resorption
  • Increased in periods of high bone turnover
  • sensitive to nutrition so needs to be done fasted in the morning
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12
Q

Osteoporosis

A
  • low bone mass and microarchitectural deterioration of bone tissue, increase in bone fragility and susceptibility to fracture.
  • diagnosis relies of DEXA/X-ray (less than -2.5)
  • Increased Kyphosis - changed centre of balance
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13
Q

What is a fragility fracture

A
  • A fracture that should not occur = suggestive of low bone mass
  • Common sites - Lumbar spine, wrist, neck of femur
  • FRAX calculation tool
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14
Q

Secondary causes of osteoporosis

A
  • Diabetes
  • Cushing’s
  • Prostate cancer
  • Hormone ablation from breast
  • Hyperparathyroidism
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15
Q

Treatment of osteoporosis

A
  • Antiresorptive treatments = work on osteoclasts (Raloxifene, denosumab)
  • Anabolic treatment on osteoblasts
  • First line is bisphosphonates - taken up by skeleton , ingested by osteoclasts and bisphosphonate kills osteoclast so potently antiresorptive.
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16
Q

Bone metastases

A

2 types:

  • Lytic = breast/lung, kidney/ thyroid
  • Sclerotic/osteoblastic = deposition of new bone
17
Q

Presenting symptoms of bone metastases

A
  • Bone pain, broken bone
  • Numbness due to spinal cord compression
  • Hypercalcaemia (especially lytic)
18
Q

Hypercalcaemia symptoms

A
  • Mild = polyuria, anorexia, nausea, constipation

- Severe = abdominal pain, vomiting, pancreatitis, cardiac arrhythmias, kidney stone

19
Q

Causes of hypercalcaemia

A
  • check PTH hormone (would expect it to be suppressed)
  • Malignancy – PTH low – 95% of hypercalcaemia case
  • Vitamin D intoxication
  • Sporadic primary hyperparathyroidism – PTH high – no negative feedback
20
Q

Parathyroid hormone

A
  • PTH secreted by chief cells
  • Low calcium detected by calcium sensing receptor which tells parathyroid gland to make X amount of PTH which then acts on bone, bowel and kidneys to restore blood calcium – negative feedback
21
Q

Primary hyperparathyroidism

A
  • Inappropriately elevated PTH in the presence of high calcium suggests PHPT
  • Symptoms of hypercalcaemia
22
Q

Causes of PHPT

A
  • Benign – single adenoma accounts for 85% of PHPT
  • Glandular hyperplasia – all 4 glands enlarged; 6-10%
  • Ectopic adenoma
  • Parathyroid carcinoma
23
Q

Treatment of PHPT

A
  • Surgery for symptomatic hypercalcaemia

- Calcimimetics - Cinacalcet suppresses calcium by reducing PTH secretions

24
Q

Paget’s disease

A
  • Cotton wool appearance in trabecular bone – thickened deformed cortical bone
  • increased bone breakdown (lytic areas)
  • Abnormal bone remodelling
  • Elevated ALP reflecting increased bone turnover
25
Q

Clinical features of Paget’s disease

A
  • Bone pain
  • Bone deformity
  • Fractures
  • Most commonly affects pelvis, femur and lower lumbar vertebrae
26
Q

Management of Paget’s

A
  • Investigations – X-rays (appearance), nuclear medicine bone scan (activity and extent of disease)
  • Treatment – bisphosphonates – reduce osteoclast function; monitor disease using TAP, BAP or P1NP
27
Q

Osteomalacia

A
  • Lack of mineralisation in bone
  • Adult form – widened osteoid seams with lack of mineralisation
  • Classic childhood rickets – widened epiphyses and poor skeletal growth
28
Q

Causes of Osteomalacia

A
  • Insufficient calcium absorption from intestines - due to lack of dietary calcium or vitamin D deficiency/ resistance
  • Excessive renal phosphate excretion – rare genetic forms e.g. hereditary hypophosphataemic rickets
29
Q

Clinical features of Osteomalacia

A
  • possibly low calcium and high PTH (secondary hyperparathyroidism)
  • Diffuse bone pains – symmetrical, muscle weakness, bone weakness
  • High ALP, low Vit D

Clinical pathology (69 decks)

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