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Case 14 > Normal Bone Health + Disease > Flashcards

Normal Bone Health + Disease Flashcards

1
Q

What is the difference between cortical and trabecular bone?

A
  • Cortical = higher density

- Trabecular = spongy + more metabolically active

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2
Q

What is the composition of bone?

A

Inorganic hydroxyapatite = Ca + phosphate + organic compounds (collagen)

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3
Q

What is articular cartilage?

A
  • @ bone joint surfaces
  • Water, collagen, proteoglycans
  • Chondrocytes
  • Provides smooth lubricated surface for articulation + resist compressive forces
  • Mainly type 2 collagen and no BV’s
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4
Q

What is the metabolic function of bone?

A

Ca homeostasis in ECF

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5
Q

What does hypocalcaemia lead to?

A
  • Nerve and muscle cells hyperactive

- Tetany (muscle spasms)

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6
Q

What does hypercalcaemia lead to?

A
  • Depressed NS function

- Deposition of excess Ca and phosphate (kidney stones)

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7
Q

What is the balance of Ca in bones under control of?

A
  1. PTH
  2. Vitamin D
    Ingested or converted from 7-dehydrocholesterol to cholecalciferol
    Undergoes hydrogenation in Liver > 25-Vit D > Kidney > 1,25-Vit D
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8
Q

When is PTH released and what effect does it have?

A
  • Secreted when low Ca
  • Kidney - stimulates hydroxylation in kidneys, increases resorption of Ca in kidney, promotes urinary excretion PO4
  • Bone - osteoclasts stimulation
  • Overall increases Ca and reduces PO4
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9
Q

When is calcitonin and what effect does it have?

A
  • Secreted when high Ca
  • Bone - osteoclast inhibition
  • Overall decreases Ca2+
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10
Q

What is primary hyperthyroidism?

A
  • Enlargement of one or more of the PTH glands
  • PTH hyper secretion - elevated blood Ca levels
  • Adenoma (benign)
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11
Q

What are the symptoms of hypercalcaemia?

A
  • Bones
  • Stones
  • Groans (abdominal)
  • Moans (psychiatric)
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12
Q

What is hypoparathyroidism?

A
  • Complication of thyroid surgery

= Reduced Ca level = muscle spasms + tetany, paraesthesia around mouth/feet

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13
Q

What is bone remodelling controlled by?

A
  • Transcription factors

- Cells signalling pathways

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14
Q

Summarise bone remodelling

A
  1. Resorption - osteoclast apoptosis + removal
  2. Reversal - osteoblast recruitment + differentiation + activation
  3. Formation - matrix synthesis + mineralization
  4. Quiescence - osteoclast recruitment + diff + activation
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15
Q

Summarise bone healing

A
  1. Inflam - hematomas, increase capillary perm = inflammation mediators
  2. Repair - haematoma replaces with fibrous tissue + cartilage = soft callus = replaces with hard > callus ossifies
  3. Remodelling
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16
Q

What is the main difference between primary and secondary bone healing?

A
  • Primary - fracture fixed with surgery, no callus

- Secondary - heals with callus

17
Q

Define osteoporosis

A

Disease characterised by low bone mass an micro-architectural deterioration of bone tissue = enhances bone fragility + increase in fracture risk

18
Q

What causes osteoporosis?

A
  • Osteoclast > osteoblast
  • Some trabecular bone completely lost = loss of connectivity between adjacent bones
  • Remodelling rates higher in trabecular bone than cortical
19
Q

What are the risk factors for osteoporosis?

A 
Age
Gender
Genetic
Lifestyle
Low BMI
Physical inactivity
Low oestrogen in women (post menopause)
20
Q

What are the main fractures seen in osteoporosis?

A

Hip, vertebral + colles

21
Q

How is osteoporosis diagnosed?

A

Measurement of BMD using DEXA

Fracture risk increases with any decrease in BMD

22
Q

How is osteoporosis managed?

A
  • Exercise
  • Ca (+/- vit D supplements)
  • Smoking cessation
  • Reduced EtOH
  • Falls prevention
  • Hip protectors
23
Q

How is osteoporosis treated?

A
  1. Bisphosphonates
    e.g. Aldendronate, ibrandronate, risedronate, zoledronate
    Reduce bone breakdown by inhibiting osteoclasts
  2. PTH analogues
    e.g. Teriparatide
    Increase bone formation
24
Q

What is osteomalacia/rickets?

A
  • Normal bone vol but lower mineral component
  • Vit D deficiency
  • Secondary cause of osteoporosis= less bone but normal matrix:mineral
  • Low Ca = soft bone
  • Rickets in children (B4 growth plates close)
25
Q

What medications cause vitamin D deficiency?

A

Phenytoin, Rifampicin

26
Q

How is osteomalacia/rickets treated?

A

Vit D

Oral calcitriol

27
Q

What is Pagets disease?

A

Disordered bone metabolism
- osteoclast overactivity
- compensatory osteoblast activity
= woven mosaic bone

28
Q

What are the symptoms of pagets disease?

A

Bone pain
High CO
Compression effects

29
Q

How is pagets disease diagnosed?

A

X ray
Blood tests - increased ALP, normal Ca, Fit D, PTH, Phosphate
Urinary hydroxyproline increased
Isotope bone scan = increased uptake

30
Q

How is pagets disease treated?

A

Bisphosphonates - Risedronate, Zolendronate

31
Q

Which cancers may metastasise to bone?

A

Breast, kidney, thyroid, prostate, lung

32
Q

Where are common sites for bone mets?

A

Vertebrae, pelvis, proximal femur/humerus, ribs, skull

May be lytic (destructive) or sclerotic (abnormal bone formation) or mixture

33
Q

What is the presentation of bone metastases?

A

Pain
Pathological fracture
Spinal cord compression
Elevated ALP + Ca

Case 14 (9 decks)

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