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Phase 1b - Musculoskeletal & Rheumatology > How to Manage Orthopaedic Conditions > Flashcards

How to Manage Orthopaedic Conditions Flashcards

1
Q

What are the 3 causes of bone disorders?

A
  • Trauma
  • Stress
  • Pathological
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2
Q

What are the two categories of mechanisms of bone fractures other than trauma?

A
  • Abnormal stresses on normal bones
  • Normal stresses on abnormal bones
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3
Q

How does abnormal stress on a normal bone cause a bone fracture (5 steps)?

A
  1. Overuse
  2. Stress exerted on bone > Bone’s capacity to remodel
  3. Bone weakenning
  4. Stress fracture
  5. Risk of complete fracture
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4
Q

What are the activity related causes of abnormal stress on normal bone that cause bone fracture (3)?

A
  • Athletes
  • Occupational
  • Military
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5
Q

What are the pathological causes of normal stress on abnormal bones fractures (5)?

A
  • Osteopenia / Osteoporosis
  • Vitamin D deficiency / Calcium deficiency
  • Osteogenesis Imperfecta
  • Pagets disease
  • Malignancy
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6
Q

What is the pathophysiology of osteopenia / osteoporosis?

A
  • Osteoclast activity > Osteoblast activity → Disrupted microarchitecture
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7
Q

What are the causes of osteopenia / osteoporosis (3)?

A
  • Secondary osteoporosis:
    • Hypogonadism
    • Glucocorticoid excess
    • Alcoholism
  • Associated with fragility fracture (hip / spine / wrist)
  • Low energy trauma (fracture)
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8
Q

What T score on a DEXA scan diagnoses osteoporosis?

A
  • > -2.5
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9
Q

What is the gender epidemiology of osteopenia / osteoporosis?

A
  • Female:Male 4:1
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10
Q

What is the pathophysiology of Rickets / Osteomalacia?

A
  1. Vitamin D facilitates calcium, magnesium & phosphate absorption
  2. Inadequate calcium or phosphate leeds to defect in osteoid matrix mineralisation
  3. Osteomalacia / Rickets
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11
Q

What is the cause of Rickets / Osteomalacia?

A
  • Vitamin D or calcium deficiency in children (Rickets) or adults (osteomalacia)
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12
Q

What are the effects of Rickets / Osteomalacia?

A
  • In rickets (paeds), the epiphyseal growth plates can become distorted under weight of the body
  • In osteomalacia (adults), increased risk of fracture
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13
Q

What is the physiology of osteogenesis imperfecta?

A
  • There is a reduction in type I collagen secretion
    • ​Collagen is an extracellular matrix protein secreted by fibroblast & osteoblasts
    • Collagen provides mechanical strength and rigidity to bone
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14
Q

What is the causes of osteogenesis imperfecta?

A
  • Autosomal recessive (20%) / dominant (80%) condition
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15
Q

What are the effects of osteogenesis imperfecta (3)?

A
  • ​Increased fragility of bones
  • Increased bone deformities
  • Increased blue sclera
  • Affect hearing
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16
Q

What is osteogenesis imperfecta often mistaken as in children?

A
  • Can be mistaken as NAD in children – diagnosis is important medicolegally
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17
Q

Outline the pathophysiology of Paget’s disease (7 steps).

A
  • Increased osteoclastic activity
    • Mixed osteoclastic - osteoblastic activity
      • Excessive bone break down & disorganised remodelling
        • Deformity, pain, fracture or arthriti
      • Osteoblastic activity
        • Deformity, pain, fracture or arthritis
        • Malignant degeneration
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18
Q

What kind of fracture pattern is this?

A

Transverse

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19
Q

What kind of fracture pattern is this?

A

Oblique

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20
Q

What kind of fracture pattern is this?

A

Spiral

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21
Q

What kind of fracture pattern is this?

A

Comminuted

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22
Q

What is an impacted fracture?

A
  • One fracture is driven into the other as a result of compression
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23
Q

What is a greenstick fracture?

A
  • Partial fracture in which one side of the bone is broken
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24
Q

What is an open fracture?

A
  • A fracture in which at least one end of the bone penetrates the skin - presenting a potential risk of infection
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25
Q

What is a closed fracture?

A
  • A fracture in which the skin remains intact
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26
Q

What kind of displacement is this?

A

Translation

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27
Q

What kind of displacement is this?

A

Angulation

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28
Q

What kind of displacement is this?

A

Rotation

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29
Q

What kind of displacement is this?

A

Impication

30
Q

What non-union fracture?

A
  • Failure of bone healing within an expected time frame
31
Q

What is atrophic healing complications?

A
  • Healing completely ceased with no X-rays changes
32
Q

What is hypertrophic healing complications?

A
  • Excessive movement can facilitate hard callus formation
    • ​Secondary bone healing in response to sustained stimuli on the bone
33
Q

What is pseudoarthrosis?

A
  • A joint fibrocartilage capsule is formed due to a non-union fracture, the two fragments of bone of a fracture have not united
34
Q

What is malunion?

A
  • Bone healing occurs but outside of the normal parameters of alignment
35
Q

What factors affet tissue healing (6)?

A
  • Mechanical envirnoment:
    • Movement
    • Forces
  • Biological environment:
    • Blood supply
    • Immune function
    • Infection
    • Nutrition
36
Q

What is hard callus?

A
  • Weaker in comparison to normal bone however has better capability to withstand external forces and equates to the stage of clinical union
37
Q

What is the pre-requisite for fracture healing (3)?

A
  • Minimal fracture gap
  • No movement if direct (primary) bone healing or minimal movement if indirect (secondary) bone healing
  • Consider patients physiological state - nutrients, growth factors, age, diabetic, smoker
38
Q

What happens during the remodelling phase?

A
  1. During remodelling, the healed fracture and surrounding callus responds to activity, external forces, functional demands and growth
  2. The external callus is no longer needed and is therefore removed through osteoclast activity, and fracture site is smoothed & sculpted
  3. Epiphyses realign and residual angulation corrected
39
Q

What is secondary bone healing? What are the 4 steps?

A
  • Fast process resulting in callus formation (fibrocartilage)
    • Haematoma → Soft callus → Hard callus → Remodelling (Endochondral ossification)
  1. Step I (Week 1): Bleeding/haematoma
    • ​​Prostaglandin/cytokine released; growth factors increase local blood flow → Periosteal supply dominates
  2. Step II (Week 2-4): Granulation (Connective/fibrotic) tissue deposited
    • ​​Soft callus formation (Type-II collagen → Cartilage; fibroblasts woven blood (immature bone))
  3. Step III (1-4 months): Fracture is bridged with soft callus
    • ​​Hard callus formation succeeds (Laying down of osteoid → Type I collagen) facilitated by increased osteoblast activity
  4. Step IV (4-12 months): Bone is remodelled through endochondral ossification, lamellar bone in its place
    • ​​Callus responds to activity, external forces and the functional demands exerted onto the bone.
      • Balance of osteoclast and osteoblast activity to remodel bone (removal of excess)
40
Q

What happens during the reparative phase?

A
  • Soft callus formation (Type II collagen - cartilage)
  • Convert to hard callus (Type I collagen - bone)
41
Q

What is soft callus?

A
  • Plastic, easily deformed or bend, if the fracture is not adequately supported
42
Q

What is primary bone healing?

A
  • Intermembranous healing is associated with absolute stability
    • Osteoblasts move into fracture → In primary bone healing, the bone ends are in contact therefore the osteoblasts can traverse across and bone formation is accelerated, membrane forms
      • Membrane formation behaves as a conduit for osteoblasts to pass
    • Haversian remodelling occurs in circumstances that there is a little or no gap < 500mm
    • Slow process using a cutter cone concept
43
Q

What are the 3 phases of primary bone healing?

A
  • Inflammatory phase (Neutrophils , Macrophages) (Duration: Hours-Days)
  • Reparative phase (Fibroblasts, Osteoblasts, Chondroblasts) (Duration: Days-weeks)
  • Remodelling phase (Macrophages, Osteoclasts, Osteoblasts) (Duration: Months-years)
44
Q

What happens during the inflammatory phase?

A
  1. Haematoma formation
  2. Release of cytokines, growth factors & prostaglandins
  3. Fracture haematoma becomes organised & infiltrated by fibrovascular tissues → Forms matrix for bone formation & primary callus
45
Q

What is the Wolff’s Law?

A
  • States that bone grows and remodels in response to the forces that are exerted onto it
    • Placing stress in specific directions stimulate osteocyte activity
46
Q

How do you dignose a bone fracture (4 / 1)?

A
  • Hx / Clinical signs:
    • Pain (Nerves)
    • Swelling (Vessels)
    • Crepitus (Ligament)
    • Deformity (Tendons)
  • Imaging:
    • X-Rays (first line of management)
    • Bone scan
    • Radiograph
    • CT scan
    • MRI scan
47
Q

What methods are used to investigate a bone fracture (3)?

A
  • XRay (in most cases)
  • CT sometimes indicated
    • To make diagnosis
    • To assess pattern
  • MRI if unsure
48
Q

What is used when describing a fracture radiograph (4)?

A
  • Location:
    • Which bone and which part of bone?
  • Pieces:
    • Simple / Multifragmentary
  • Pattern:
    • Transverse / Oblique / Spiral
  • Displaced / Undisplaced:
    • Translated / Angulated
    • X / Y / Z plane
49
Q

What are the 4 steps to managing a bone fracture?

A
  • Resuscitate
    • ​Save the patients life, then worry about the fracture
  • Reduce
    • Bring the bone back together in an acceptable alignment
  • Rest / Hold
    • Hold the fracture in position to prevent distortion or movement
  • Rehabilitate
    • ​Get function back and avoid stiffness
50
Q

What are the possible ways to reduce a fracture (3C / 2O)?

A
  • Closed:
    • Manipulation
    • Skin traction
    • Skeletal traction
  • Open:
    • Mini-incision
    • Full explore
51
Q

What are the possible ways to rest a fracture (3C / 4IF / 2EF)?

A
  • Closed:
    • Plaster
    • Skin traction
    • Skeletal traction
  • Fixation:
    • Internal:
      • Intramedullary pins
      • Intramedullary nails
      • Extramedullary plate / screws
      • Extramedullary pins
    • External:
      • Monoplanar
      • Multiplanar
52
Q

What are the possible ways to rehabilitate a fracture (4)?

A
  • Use
  • Move
  • Strengthen
  • Weight bearing
53
Q

What are the possible systemic fracture complications (12)?

A
  • General:
    • Fat embolus
    • DVT
    • Infection​
  • Prolonged immobility:
    • UTI
    • Chest infection
    • Sores
  • Specific:
    • Neurovascular injury
    • Muscle / tendon injury
    • Non union / malunion
    • Local infection
    • Degenerative charge (intraarticular)
    • Reflex sympatheti dystrophy
54
Q

What is osteoarthritis?

A
  • A long term chronic disease characterised by the deterioration of cartilage in joints which results in bones rubbing together & creating stiffness, pain and impaired movement
55
Q

What is the pathophysiology of osteoarthritis?

A
  • Degenerative disease of chondral cartilage
  • Inflammation occurs late in disease
    • Inflammatory mediators include proteinases, which enhance the synthesis of proteinases & other catabolic factors to degrade the articular cartilage membrane
56
Q

What are the main risk factors of osteoarthritis (10)?

A
  • Age
  • Excess weight & obesity
  • Mechanical constraints (intense sport, some professions)
  • Heredity
  • Female
  • Osteonecrosis
  • Leg bone malalignment
  • Oestrogen deficiency
  • Metabolic syndrome
  • Advance hip osteoarthritis caused by spondylarthritis or rheumatoid arthritis
57
Q

What are the symptoms of osteoarthritis (3)?

A
  • Pain (exertional / rest / night)
  • Disability (walking distance / stairs / giving way)
  • Deformity
58
Q

How is osteoarthritis assessed (4)?

A
  • Look for scars from previous surgeries
  • Feel
  • Move
  • Special tests
    • ​Anterior drawer test
59
Q

What is the conservative management of osteoarthritis (5)?

A
  • Analgesics
  • Physiotherapy
  • Walking aids
  • Avoidance of exacerbating activity
  • Injections (Steroids / Viscosupplementation)
60
Q

What is the surgical management of osteoarthritis (6)?

A
  • Replace (knee / hip)
  • Realign (knee / big tow)
  • Excise (toes)
  • Fuse (big toe)
  • Synovectomy (rheumatoid)
  • Denervate (wrist)
61
Q

What is rheumatoid arthritis?

A
  • Chronic joint inflammation can result in joint damage
62
Q

Which autoantibodies are associated with rheumatoid arthritis (2)?

A
  • Rheumatoid factor
  • Anti-CCP
63
Q

What is the site of inflammation for rheumatoid arthritis?

A
  • Synovium
64
Q

What are the symptoms of osteomyelitis (4)?

A
  • Pain
  • Swelling
  • Discharge
  • Systemic symptoms:
    • Fever
    • Sweats with weight loss
65
Q

How is ostemyelitis diagnosed (3 / 4)?

A
  • Radiology:
    • Plain films
    • MRI scans: bone architecture / collection
    • CT if MRI unavailable
    • Bone scans: multifocal diseas
  • Bloods:
    • CRP
    • ESR
    • WCC
    • TB culture
66
Q

How is osteomyelitis managed (4)?

A
  • Antibiotics: IV for weeks
  • Surgical drainage: espescially bony collections
  • Chronic: antibiotic suppression / dressings
  • Amputation
67
Q

What are the symptoms of septic arthritis (3)?

A
  • Pain
  • Swelling
  • Systemic symptoms:
    • ​Fever
    • Sweating with weight loss
68
Q

What are the risk factors of septic arthritis (3)?

A
  • Immunosuppression
  • Pre-existing joint damage
  • IV drug use
69
Q

How is septic arthritis diagnosed (1 / Radiology 3 / Bloods 4)?

A
  • Joint aspirtaion
  • Radiology:
    • Plain films
    • MRI scans: bone architecture / collection
    • CT if MRI unavailable
    • Bone scans: multifocal diseas
  • Bloods:
    • CRP
    • ESR
    • WCC
    • TB culture
70
Q

How is septic arthritis managed (4)?

A
  • Surgery: joint washout & drainage
  • IV antibiotics
  • Immobilise joint in acute phase
  • Physiotherapy once over acute phase

Phase 1b - Musculoskeletal & Rheumatology (11 decks)

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