Processes Flashcards

1
Q

Bone Turnover

A
  1. Activation (3 days)
  2. Resorption (30 days)
  3. Formation (90 days)
  4. Mineralisation (6 months)
  5. Maturation
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2
Q

Fracture Healing

A

ENDOCHONDRAL OSSIFICATION

  1. Haematome and Granulation Tissue
  2. Cartilaginous Callus
  3. Boney callus and cartilaginous remnants.
  4. Remodelling
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3
Q

Role of PG in cartilage

A
  1. Negative PGs stuck in matrix.
  2. Positive ions attracted to PGs.
  3. Increase concentration of ions in cartilage.
  4. Water enters to equalise concentration.
  5. Causes osmotic pressure.
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4
Q

How are nutrients delivered to cartilage.

A

Diffusion of small molecules through the synovial fluid.

Convective transport for large molecules.

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5
Q

Progression of OA - cartilage matrix alteration.

A
  1. Fibrillation of cartilage surface.
  2. Decrease in PG content.
  3. Increase in water content.
  4. Collagen II network damage.
  5. Blood vessels crossing tidemarks.
  6. Stiffening of subchondral bone.
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6
Q

Progression of OA - Response of chondrocytes.

A
  1. Chondrocytes detect damage.
  2. Proliferate and synthesis matrix.
  3. MMPs degrade matrix molecules.

The balance between 2 and 3 result in the stabilisation of matrix.

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7
Q

Progression of OA - Decline in chondrocyte response.

A
  1. Death of chondrocytes.
  2. Down regulation of cells to anabolic signals.
  3. Loss of cartilage.
  4. Subchondral bone thickening.
  5. Osteophyte bone formation at joint periphery.
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8
Q

Joint replacement wear

A
  1. debris leads to pseudosynovial membrane at interface between implant and bone.
  2. Infiltration of fibrocytes and macrophages.
  3. Activates osteocytes resorbing bone.
  4. Aseptic loosening.
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9
Q

Formation of menisci

A
  1. Mesenchymal cells originating from chondrogenic blastema.
  2. Cells arise from perichondrium and anlagen.
    Week 8: distinct structures in the knee.
    Week 8-16: Alignment of cells and beginning of EXM.
    As person mature number of cells decrease.
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10
Q

Disc Degeneration

A
  1. Increase fibre content of the nucleus.
  2. Decreased hydration of nucleus and annulus.
    - decrease PG content and charge density.
  3. Thickness of endplates become irregular.
  4. Focal defects occur.
  5. Alteration in distribution of collagen Type 1 and 2.
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11
Q

Annular Injury

A
  1. Rings softened, overstretched, torn.
  2. Normal viscoelasticity exceeded.
  3. Cannot stabilise/limit motion.
  4. Nucleus pulposus exerts pressure on the weak part.
  5. Buckling occurs.
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12
Q

Healing process of tendon/ligaments

A
  1. Inflammatory stage (3-7days)
    - infusion of blood to form a clot.
  2. Proliferation stage (2-3 weeks)
    - fibroblasts synthesis in collagen.
  3. Remodelling stage (< yr)
    - decrease in cell density.
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13
Q

Muscle contraction

A
  1. AP arrives at nerve ending resulting in an endplate potential
  2. Endgate potential propagated to the motor unit
  3. Rise in calcium ion levels
  4. Ca2+ binds to troponin
  5. Tropomyosin exposes a binding site on actin
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14
Q

Joint Development

A
  1. Mesenchymal condensation
  2. Joint Initiation
  3. Interzone Formation
  4. Morphogenesis
  5. Joint Maturation
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15
Q

Mechanism of gout

A
  1. High levels of urate in the blood.
  2. Tophi - deposition of urate crystals.
  3. Leukocytes seek out crystals and chondrocytes produce enzymes in response.
  4. Osteoblast-mediated bone resorption amplified.
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16
Q

Procedure of a spinal fusion

A
  1. Remove the intervertebral disc
  2. Insert an intervertebral cage if needed
  3. Insert bone graft to promote bridging
  4. Fix with screws, plates and/or rods
17
Q

Stages of Perthes Disease

A
  1. Necrosis
  2. Collapse
  3. Repair
  4. Remodelling