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Locomotor > Bone Pathology > Flashcards

Bone Pathology Flashcards

1
Q

What are the different ways to classify fractures?

A
  • by orientation of fracture line
  • open vs closed
  • comminuted (more than two pieces)
  • stress (repeated low force injury to a normal bone)
  • pathological (abnormal bone)
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2
Q

What are the 3 stages of fracture healing?

A
  1. Inflammatory phase
    - bleeding and haematoma formation
    - vascular granulation tissue
  2. Reparative phase
    - soft callus
    - hard callus (made of new woven bone)
  3. Remodelling phase
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3
Q

Describe the inflammatory phase of fracture healing

A

Haematoma formation

  • fibrin mesh creates a framework and the damaged matrix releases trapped growth factors and cytokines
  • stem cells are activated to start repair
  • granulation tissue formed
  • hours to days
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4
Q

Describe the first part of the reparative phase of fracture healing

A

Soft callus

  • cartilage formation (holds the fractured ends together but no structural rigidity)
  • periosteum repairs itself on the outside
  • days to weeks
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5
Q

Describe the second part of the reparative phase of fracture healing

A

Hard callus

  • osteoid formation and ossification
  • a thickened area of woven bone (rigid, but not as strong as it was)
  • weeks to months
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6
Q

Describe the remodelling phase of fracture healing

A

Woven bone –> lamellar bone, along lines of stress

  • result is complete reconstitution
  • takes months to years
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7
Q

What is the clinical management of a fracture?

A 
Goal = union 
How? 
- minimise the gap
- minimise the strain or movement 
- minimise any other factors that slow healing
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8
Q

What are some complications of fracture healing?

A
  • non-union
  • delayed union
  • mal-union
  • infection
  • osteonecrosis/AVN
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9
Q

What is osteoporosis?

A

Reduction in bone mass more than 2.5 SD below the norm for healthy 30yr old women

  • loss of both cells and matrix
  • loss of trabeculae and thinning of what remains

In women rapid decline in bone density following menopause

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10
Q

What is osteopaenia?

A

Reduction in bone mass 1-2.5 SD below the norm for healthy 30yr old women

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11
Q

What are the different classifications of osteomyelitis?

A
  • haematogenous
  • non-haematogenous (direct inoculation)
  • non-haematogenous (local invasion)
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12
Q

Describe the pathogenesis of haematogenous osteomyelitis

A
  • slow flow through looped capillaries and venous sinusoids
  • bacteria seed metaphyseal-epiphyseal junction
  • protected from the immune response
  • pressure from pus further limits blood supply
  • infection spreads to subperiosteal space, lifts the periosteum and invades the shaft
    • growth plate is a barrier to the infection
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13
Q

What are the most common microbiological causes of bone and joint infections?

A 
Staphlococcus aureus (95% and more) 
- then streptococcus pyogenes
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14
Q

What are the clinical features of bone and joint infections?

A

Fever, pain and tenderness, warmth, swelling

- history preceding trauma 1/3 cases

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15
Q

What are some differential diagnoses for bone and joint infections?

A
  • septic arthritis (often coexistent)
  • malignancy
  • cellulitis
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16
Q

What is the common treatment of bone and joint infections?

A

Flucloxacillin given IV for 3-5 days, then complete a 3 week course with oral antibiotics, provided uncomplicated and demonstrated response to Rx

17
Q

What are the signs and symptoms of osteoarthritis?

A
  • joint pain, worse at the end of the day
  • insidious onset with no systemic symptoms
  • reduced ROM, crepitus, osteophytes
18
Q

What are the risk factors for osteoarthritis?

A
  • age
  • obesity
  • previous injury/abnormality of joint
  • repeated heavy use of joint
  • genetics
19
Q

What is the pathophysiology of osteoarthritis?

A
  • damage stimulates chondrocyte hypertrophy, proliferation and enzyme/cytokine secretion
  • unravelling of cartilage matrix
  • thickening and microfractures in bone
  • shedding of cartilage “fibrillation”, erosions
20
Q

What is the morphology of osteoarthritis?

A
  • non-uniform loss of cartilage
  • subchondral thickening
  • osteophytes
21
Q

What are osteophytes?

A
  • cartilage growths that have become bone

- increases the joint stability

22
Q

What are the signs and symptoms of rheumatoid arthritis?

A
  • systemic symptoms (fever, weight loss, anaemia)
  • symmetric polyarthritis
  • morning stiffness
  • warm, swollen “rubbery” joints
  • rheumatoid nodules
  • eventual destruction and deformity of joints
23
Q

What are the risk factors for rheumatoid arthritis?

A
  • genetic
  • female gender
  • increased age
  • smoking
24
Q

What is the pathophysiology of rheumatoid arthritis?

A
  • self-reactive T-helper cells are activated
  • secrete cytokines (IL-1,6,17, TNF-alpha)
  • induce fibroblasts, macrophages, osteoclasts, B cells, T cells, plasma cells
  • “granulation tissue” like synovium, collagenases and MMPs, breakdown of cartilage and bone
25
Q

What is the morphology of rheumatoid arthritis?

A
  • mononuclear infiltrate in synovium with germinal centres
  • hyperplasia of synovium with villus formation, creates “pannus”
  • pannus invades and erodes cartilage
  • weakening and destruction of the ligaments
  • eventual fibrous and then bony union of the joints
26
Q

What are the signs and symptoms of gout?

A
  • acutely inflamed joint, seldom systemically unwell
  • tophi if chronic
  • spontaneous onset of excruciating pain, swelling, heat and redness
27
Q

What are the risk factors for gout?

A
  • males
  • increasing age
  • menopause
  • uric acid metabolism (increased intake or production, reduced excretion)
  • genetics and ethnicity
  • obesity, HTN, metabolic syndrome
28
Q

What is the pathophysiology of gout?

A

Metabolic disease

  • crystals activate inflammatory cells, synovial cells and complement
  • acute inflam cascade: “acute gout attack” –> IL-1, complement and chemotaxis, neutrophil lysis
  • can progress into chronic, disabling, “tophaceous” gout if untreated
29
Q

What is the morphology of gout?

A

Tophi

Locomotor (6 decks)

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