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Year 2 LCRS Endocrinology > Metabolic bone disorders > Flashcards

Metabolic bone disorders Flashcards

1
Q

What are the two components of bone?

A
  1. Osteoid: unmineralised bone (organic component)
    • 35%
    • Mainly Type I collagen fibres
  2. Inorganic minergal component
    • 65%
    • Calcium hydroxyapatite crystals (that fill the space between the collagen fibres)
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2
Q

What is the function of the osteoblasts?

A

They built boneby synthesising collagen fibres and help in osteoid mineralisation

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3
Q

What is the function of osteoclasts?

A

They resorb bone and thereby free calcium and phosphate via the release of lysomal enzymes

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4
Q

How do osteoclasts get activated?

A

They differentiatiate in response to RANKL-Receptor stimmulation of surface

The RANKL is expressed on osteoblasts surfaces–> osteoclasts get activated by osteoblasts!

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5
Q

How to osteoblasts get activated?

A

Resond to PTH & calcitriol (1,25 (OH)2 vit D)

–> regulate bone formation and absorbtion

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6
Q

What is the cortical part of the bone?

A

The hard shell of the bone

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7
Q

What is the Trabecular part of bone?

A

spongy, inner part of bone

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8
Q

What is meant by the term “woven” bone

A

disorganised collagen fibrils, weaker

–> loss of lamellar sturcture

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9
Q

How do you call a bone that is weaker due to unoranised collagen fibres?

A

Woven bone

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10
Q

What is the normal structure of a bone called?

A

Lamellar pattern of bone :

collagen fibrils laid down in alternating orientations that makes it mechanically strong

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11
Q

What are the direct effects of Vitamine D deficiency on bone?

A

Inadequate mineralisation of newly formed bone matrix (osteoid)

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12
Q

How does Vitamin D deficiency present in children?

A

Rickets

  • skeletal abnormalities and pain, growth retardation, increased fracture risk
  • also affects cartilage and epiphysal growth
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13
Q

What does Vit D deficiency cause in adults?

A

OSTEOMALACIA

  • affects the bone (not the epiphysal)
  • skeletal pain, increased fracture risk, proxmyopathy

–> might lead to wabbeling gait and looser zones (in severe deficiency)

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14
Q

What is a looser zone in bone?

A

Fractures from inadequadly mineralised bone due to normal weight

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15
Q

Explain primary, secondary and tertiary Hyperparathyroidism

A
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16
Q

How does renal failure lead to vascular calcification?

A

Because there is reduced excretion of PO4 3-, therefore highter phosphate levels that form insoluble Calcium phosphate plaques

17
Q

What does renal failure in terms of bone health lead to?

A

It leads to

  1. more bone resorbtion (to kepp calcium levels because of VitD deficiency, no Ca2+ can be absorbed)
  2. Leading to osteitis fibrosa cystica –> hyperparathyroid bone disease
18
Q

What is osteitis fibrosa cystica?

A

Hyperparathyroid bone disease

leading to “Brown tumors”– >radiolucent bone lesions due to hight osteoclast activity stimmulated by high PTH to get Ca2+ up

rare now

19
Q

How do you treat osteitis fibrosa cystica?

A

Two main issues

  1. High Phosphate levels
    • low phosphate diet
    • Phosphate binders – reduce GI phosphate absorption
  2. Alphacalcitriol
    • to restore Vit D levels, decrease bone resorbiton due to low Ca2+
  3. Parathyroidectomy in 3. hyperparathyroidism
    • in hypercalcaemia + hyperparathyroid bone disease
20
Q

What exactly is osteoporosis?

A

Loss of bony trabeculae and reduced bone mass leading to weaker bone –> increase risk of fractures

21
Q

What is BMD?

What does it tell you?

A

BMD= Bone mineral density

Can be diagnostic of osteoporosis (T-score) if it is = 2.5 below average –>

22
Q

How is bone mineral density normally measured?

A

Via and DEXA (Dual Energy X-ray Absorptiometry ) of the femoral neck and lumbar spine

It measures the bone calcium content–> rthe more calcium, the higher the bone mineral density

23
Q

What are the factors that predispone you to osteoporosis?

A
  1. Post-menopausal hormone deficiency (oestrogen is protective)
  2. Age-related changes in bone homeostasis (osteoclast senescence)
  3. Hypogonadism in young women and in men
  4. Different endocrine conditons
  5. Latrogenic
    • heparin
    • prolonged glucosteriods
24
Q

What are latrogenic conditions?

A

Diseases that are caused by medical care

25
Q

Which endocrine disorders can cause Osteoporosis?

A

oCushing’s syndrome

oHyperthyroidism

oPrimary hyperparathyroidism

26
Q

What are the possible treatments for osteoporosis?

A
  1. •Oestrogen/Selective Oestrogen Receptor Modulators
  2. •Bisphosphonates
  3. •Denosumab (antibody)
  4. •Teriparatide
27
Q

Explain the use of oestrogen in osteoporosis

A
  1. Post menopausal
    • replace E2 to reduce bone resorbtion
    • also give progesterone if uterus is intact –> to cause period and prevent endometrial CA
  2. Main Risks are
    • Breast Cancer
    • Venous thromboembolism
28
Q

What is the MOA of Bisphosphonates?

A

They impair the osteoclasts and induce apoptosis –> redue bone reabsorbtion

Happens by Bind avidly to hydroxyapatite (that is digested by osteoclasts –> leads to disruption of intracellular enzymatic activity in osteoclast)

29
Q

What is the clinical use of bisphosphonates?

A

It is used in

  1. Osteoporosis –> reduce bone turnover
  2. Malgnancy
    • Associated hypercalcaemia
    • Reduce bone pain from metastases
  3. Paget’s disease – reduce bony pain
  4. After rehydration in severe hypercalcaemia emergency
30
Q

What are the main side effects of bisphospobates?

A

Unpleasent to take, need to take on empty stomach

  • Oesophagitis
    • may require switch from oral to iv preparatåion
  • Osteonecrosis of the jaw
    • greatest risk in cancer patients receiving iv bisphosphonates
  • Atypical fractures
    • may reflect over-suppression of bone remodelling in prolonged bisphosphonate use
31
Q

What is Denosumab?

When and how is it used?

A

It is a human antibody binding to RANKL

–> inhibits osteoclast activation –> reduces bone resporbtion

  • SC injection 6/12ly
  • 2nd line to bisphosphonates
32
Q

What is Teriparatide?

What and how is is used for?

A

•Recombinant PTH fragment

  • Increases bone formation and bone resorption, but formation outweighs resorption
  • 3rd line treatment for osteoporosis
  • Daily s.c. injection
  • £££
33
Q

What would be your fist, secound and third line treatment in OSteoporosis?

A
  1. Bisphosphonates
  2. Denosumab (RANKL antibody)
  3. Teriparatide (PTH fragement stimmulating bone formation)
34
Q

What is pagets disease of bone?

(Cause and consequence)

A

•Accelerated, localised but disorganised bone remodelling –> leading to WOVEN bone

MOA: Excessive bone resorption (osteoclastic overactivity) followed by a compensatory increase in bone formation (osteoblasts)

Leading to

  • hypertrophy with increased fragility and deformity
  • Characterised by abnormal, large osteoclasts – excessive in number
35
Q

What is the cause of pagets disease of bone?

A

It is not knonw

  • Genetic cause?
  • viral origin?
  • But most commonly seen in
    • Highest in UK, N America, Australia and NZ, Lowest in Asian and Scandinavia
    • No sex difference
    • appears over age of 50
36
Q

What are the clinical features of someone with pagets diseae?

A
  • Skull, thoracolumbar spine, pelvis, femur and tibia most commonly affected
  • Arthritis
  • Fracture
  • Pain
  • Bone deformity
  • Increased vascularity (warmth over affected bone)
  • Deafness – cochlear involvement
  • Radiculopathy – due to nerve compression
37
Q

How would you diagnose someonw with pagets disease of bone?

A

Normal Plasma Ca2+

Increased plasma alkaline phosphatase

Plain X-Rays:

  • Lytic lesions (early), thickened, enlarged, deformed bones (later)
  • Radionuclide bone scan demonstrates extent of skeletal involvement
38
Q

How would you treat pagets disease of bone?

A
  • Bisphosphonates – very helpful for reducing bony pain and disease activity
  • Simple analgesia

Year 2 LCRS Endocrinology (15 decks)

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