Bone Disorders Flashcards

1
Q

what’s bone made of?

A

non-cellular mineralised matrix
- type 1 collagen = osteoid
- calcium phosphate
- protein and growth factors

  • osteoblasts
  • osteocytes
  • osteoclasts
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2
Q

why is mineralisation important?

A

to make the osteoid hard, makes bone stiff and strong

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3
Q

what is the function of bone?

A
  • physical integrity and support
  • protection for organs
  • attachment for muscles and tendons
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4
Q

what are the 3 main cellular elements of bone and their functions?

A

osteoblasts
- secrete collagen/osteoids
- mineralisation

osteocytes
- inactive osteoblasts
- trapped inside bone

osteoclasts
- stem from macrophages
- resorb bone

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5
Q

what is the difference between woven and lamellar bone?

A

woven bone = immature bone
- random osteoid
- rapid turnover
- remodelled to lamellar bone

lamellar bone
- parallel sheets
- normal healthy adult bone
- compact or trabecular/cancellous

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6
Q

which is stronger, woven or lamellar bone?

A

lamellar bone
- due to regular arrangement

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7
Q

the 2 types of bone

A

compact/cortical

trabecular/cancellous

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8
Q

describe cortical bone

A

hard outer shell
organised and regular
haversion system
surrounds cancellous bone

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9
Q

describe cancellous bone

A

spongy
marrow

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10
Q

describe the bone remodelling cycle

A
  1. activation
    - hormones or damage activate osteoblast
    - cytokines secreted
    - osteoclasts sticks to surface of bone
  2. resorption
    - osteoclasts secrete substance and resorb bone
    = pits on surface
    - apoptosis or migration of clasts
  3. reversal
    - monocytes clear debris
  4. formation
    - osteoblasts secrete matrix
    - mineralisation
    - some blast incorporate as osteocytes
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11
Q

what is osteoarthritis?

give aetiology.

A

progressive erosion of articular cartilage

aetiology
- primary - just happens
- secondary - pre-existing joint damage, metabolic disease, systemic disease

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12
Q

what is the pathogenesis of osteoarthritis?

A
  • erosion of articular cartilage
  • bone exposed
  • abnormal growth = osteophytes
  • cysts in the bone
  • narrow joint space
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13
Q

how does osteoarthritis clinically feature?

A

symptoms
- pain
- limited function

signs
- bony enlargements
- crepitus - crunch
- instability

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14
Q

how is osteoarthritis investigated and treated?

A

blood test
x-ray

physical
medications
surgery - joint replacement

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15
Q

what is rheumatoid arthritis

A

autoimmune condition with persistent inflammation

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16
Q

describe the pathogenesis of rheumatoid arthritis.

A
  • citrullination of arginine to citrulline
  • protein modification, becomes foreign
  • autoimmune response
  • T cells and cytokines
  • macrophages
  • fibroblasts
  • synovium proliferation and inflammation
  • synovitis
17
Q

how is rheumatoid arthritis investigated and managed?

A

blood tests
x-rays

no cure
medications - DMARDS
= disease modifying anti-rheumatic drugs

18
Q

what is padgets disease?

A

bone turnover is disordered
- more woven bone

19
Q

describe the pathogenesis of padgets disease.

A
  1. hot phase
    - osteoclast activity
  2. mixed phase
    - osteoblast and osteoclast activity
  3. cold phase
    - no activity
20
Q

how does padgets disease clinically present?

A

bone deformations
high fracture risk
bone pain
hypercementosis - cotton wool appearance
nerve compression - hydrocephalus

21
Q

how is pagets disease treated? also used for osteoporosis

A

bisphosphonates
- inhibit clasts resporption
= slow bone loss

22
Q

what is the biggest worry of using bisphosphonates?

A

the chance of developing BRONJ
- hinders bone healing

23
Q

what is osteomyelitis?

give aetiology.

A

inflammation of bone marrow

aetiology
- from infection
- staphlococcus aureus

24
Q

how does osteomyelitis clinically present?

A

fever
bone pain
tenderness

25
treatment for osteomyelitis?
immobilise antibiotics
26
what is osteonecrosis? - aetiology.
infarction of bone marrow aetiology = vascular insufficiency - alcohol - steroids - fractures
27
osteonecrosis is asceptic, wym?
not due to infection
28
describe the pathogenesis of osteonecrosis.
29
how does osteonecrosis clinically present? give management
joint pain collapse of articular bone - grafts - joint replacement
30
what is osteomalacia AKA rickets? give aetiology.
defective mineralisation of bone osteoid rickets = kids osteomalacia = adults aetiology - anything that interferes with bone mineralisation - vitamin D deficiency - blood calcium drops - renal failure
31
dental complications of rickets
hypophosphataemia - thin enamel - globular dentine - dental abscess more common hypoplasia missing teeth
32
osteogenesis imperfecta - definition - aetiology
brittle bone disease - type 1 collagen has gene mutation
33
describe the clinical features of osteogenesis imperfecta
increased fractures small discoloured teeth
34
achrondoplasia - definition - aetiology | frank from always sunny has achondroplasia
woven bone remodelled to lamellar bone = endochondral ossification - short limbs intramembral ossification - in the maxilla, skill and mandible aetiology - FGFR-3 mutation - impairs cartilage growth
35
define fracture
a loss of bone integrity and loss of the mechanical strength
36
how are fractures classified?
simple comminuted - fragments compound - out of the skin displaced - ends not aligned
37
describe the phases of fracture healing
1. inflammatory phase - haematoma forms - blood - lump of haemopoietic cells - macrophages, neutrophils, platelets activate cytokines - fibroblasts at site - granulation tissue - neovascularisation - fibrosis = callus formation - a scar within the site 2. reparative phase - primary callus - endochondral ossification converts soft cartilage to woven bone 3. remodelling phase - woven bone into cortical bone