Avascular Necrosis Flashcards

1
Q

What are the functions are structure of bones

A
  • Mechanical support/protection/movement. Mineral storage (calcium and phosphate) and haematopoiesis.
  • The shaft is the diaphysis, ends are the epiphysis, The metaphysis is the transitional area between the two.
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2
Q

Describe features of cortical bone

A
  • It is strong, compact bone organised in Haversian system/osteons. It has a slow turn over rate.
    An osteon consists of osteocytes surrounded by lacuna and canaliculi which allow for communication
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3
Q

Describe features of cancellous bone

A

This is the spongey/trabecular bone which can be found in the metaphysis and epiphysis of long bones and centrally in cuboid bones. Has a higher turnover rate but is less dense

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4
Q

What are the different bone cells

A
  • Osteogenic cells (stem cells)
  • Osteoblast (forms bone matrix. Can turn into osteocytes, apoptosis, bone lining cell)
  • Osteocyte (maintains bone tissue)
  • Osteoclast (Has abundant mitochondria and lysosomes which reabsorb bone)
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5
Q

Describe features of inorganic and organic bone matrix?

A
  • Inorganic: Abundant calcium phosphate. Responsible for compressive strength
  • Organic: Abundant type 1 collage. It’s responsible for tensile strength
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6
Q

What is the bone growth plate called?

A

Physis - it allows for remodelling after fracture. If the physeal blood supply is damaged it will lead to growth arrest

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7
Q

What are the two methods of fracture healthing?

A

Indirect healing (secondary) this is where a callus forms. Direct healing (primary) occurs with surgical repair

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8
Q

Describe the process of indirect fracture healing

A
  1. Fracture haematoma and inflammation. Occurs 6-8 hours after injury with removal of dead tissue/bone cells.
  2. Fibrocartilage callus
  3. Bony callus - Osteoblasts make woven bone
  4. Bone remodelling - osteoblasts/clasts remodel woven bone into compact bone
    Throughout the process a degree of movement is desirable to promote differentiation
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9
Q

Explain the formation of a fibrocartilage callus in fracture healing

A
  • New capillaries organise haematoma into granulation tissue called a procallus.
  • Fibroblasts and osteogenic cells invade the procallus and make collagen fibres to connect ends of broken bone together. Chondrocytes begin to produce fibrocartilage.
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10
Q

Describe the process of direct fracture healing

A
  • This occurs in a surgical situation which relies in absolute fracture stability.
  • There is no callus formation and instead cutting cones cross fracture site with osteoclast reabsorption and osteoblastic formation.
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11
Q

What is the blood supply of bone?

A
  • Endosteal arteries supply the inner 2/3rds of bone under high pressure.
  • Periosteal arteries supply outer 1/3rd of bone by low pressure
  • Metaphyseal-epiphyseal vessels supply the ends of long bones
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12
Q

What is the blood supply of the femoral neck?

A
  • Medial and lateral circumflex arteries of the profunda femoris form the extracapsular arterial ring. This sends ascending cervical vessels up the femoral neck and gives of epiphyseal branches
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13
Q

What fractures are the most prone to causing avascular necrosis?

A
  • Proximal pole of scaphoid fracture,
  • Talar neck fracture,
  • Intracapsular hip fractures,
  • Surgical neck of humerus
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14
Q

What can prevent fracture healing?

A
  • Increasing age,
  • Diabetes,
  • Anaemia,
  • Malnutrition,
  • Peripheral vascular disease,
  • Hypothyroidism,
  • Smoking,
  • Alcohol
  • Medications: NSAIDs, steroids and bisphosphonates
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15
Q

How can NSAIDs and bisphosphonates impact fracture healing?

A
  • NSAIDs can reduce local vascularity at the fracture site.
  • Bisphosphonates inhibit osteoclast activity which prevents bone remodelling.
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16
Q

Describe features of avascular necrosis/osteonecrosis

A
  • Bone infarction caused by interruption of blood supply. This can result in infarction of subchondral bone (bone right under joint surface) or collapse of joint surface.
17
Q

What are the risk factors for osteonecrosis/avascular necrosis?

A
  1. Alcohol abuse.
  2. Steroids/sickle cell diseases,
  3. Idiopathic
  4. Trauma
  5. Gout,
  6. Rheumatoid,
  7. Infection/inflammatory arthritis,
  8. Pancreatitis/pregnancy.
  9. SLE/Smoking
  10. Chronic renal failure
  11. Hyperlipidaemia
    AS IT GRIPS Collapse Happens
18
Q

What is the pathophysiology of avascular necrosis

A
  • Interruption of blood flow which could be due to extra/intraosseous (intra - sickle cell clot) or increased extravascular pressure.
  • In the early stages necrosis involves medullary bone first.
  • In later stages the sub-chondral bone weakens and collapses. The joint surface becomes irregular which causes further damage
19
Q

Explain the presentation of avascular necrosis

A
  • Asymptomatic,
  • Pain (night and rest)
  • necrosis of femur causes groin pain which worsens with weight bearing and motion. Limitation with internal rotation and abduction
  • Pain on joint movement,
  • Limp and restricted movement
  • Often bilateral
20
Q

What are the X ray changes seen with avascular necrosis?

A
  • Density changes,
  • Collapse of femoral head,
  • Joint space narrowing and degenerative changes
21
Q

What is the treatment for avascular necrosis?

A

In early stages aim for reperfusion and healing of infarcted region with core decompression, vascularised bone graft.
In later stages a total joint replacement is required.