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m2 CA2 > Approach to Bone Pain > Flashcards

Approach to Bone Pain Flashcards

1
Q

Common causes of bone pain?

A

Trauma, Tumour, Infection

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2
Q

What are insufficiency/fragility fractures?

A

Fractures by normal physiological stress applied on abnormal (weakened) bones
@spine, tib/fib, pelvis
predisposing factors: osteoporosis, corticosteroid therapy, post-irradiation

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3
Q

What is stress fracture?

A

Fracture resulting from abnormal stress on normal bone

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4
Q

What are the imaging findings on a stress fracture?

A

Linear sclerosis on radiograph
Focal periosteal reaction (new bone formation)

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5
Q

Types of fractures

A
  1. Hairline
  2. Linear
  3. Oblique Non-displaced
  4. Oblique Displaced
  5. Spiral
  6. Comminuted (broken at 3 or more sites)
  7. Segmental
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6
Q

Stages of Fracture Healing

A
  1. Hematoma forms between 2 ends of bone, creating fibrin mesh, which seals fracture site. Periosteum is stripped from bone surface.
  2. Traumatic inflammation: Migration of inflammatory cells and macrophages
  3. Demolition: Macrophage invades and phagocytose the hematoma and tissue debris
  4. Granulation tissue: neovascularization and fibroblasts from surrounding cells
  5. Callus formation (soft bone) occurs over weeks: Periosteal reaction - haphazard osteoid formation producing a woven bone
    -> external callus: bridges fracture site outside bone
    -> internal callus: bridges fracture in medullary cavity
    => callus is well established (by 3rd week) but still woven bone (mechanically weak)
  6. Remodelling occurs over months: Organised osteoclastic and osteoblastic activity replacing woven bone with compact lamellar bone
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7
Q

Principles of NORMAL fracture healing

A
  • Close apposition of fractured bone ends
  • Immobilisation
  • Adequate healing capacity
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8
Q

Causes of delayed and impaired fracture healing

A
  1. Poor apposition of fractured bone ends
  2. Poor blood supply
  3. Poor general nutritional status
  4. Foreign bodies or non-viable tissue
  5. Infection
  6. Conditions that suppress healing: Corticosteroids, immunosuppression, immunodeficiency
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9
Q

Complications of fracture

A
  1. Problems related to union of bones:
    - delayed union
    - mal-union (union with angulation)
    - fibrous union (fibrous scar -> false joint)
    - non-union
  2. Infection (osteomyelitis, septic arthritis)
  3. Thrombosis and embolism
  4. Soft tissue injury
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10
Q

What is osteoporosis?

A

A condition where the bones are weakened to a point that they can break easily.

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11
Q

Treatment for osteoporosis

A
  1. Lifestyle and diet
    - exercise
    - calcium
    - vitamin D
  2. Antiresorptive Agents
    - Bisphosphonates
    - Denosumab
    - Oestrogens
    - Calcitonin
  3. Anabolic Agents
    - Romosozumab
    - Parathyroid hormone therapies
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12
Q

How do bisphosphonates work?

A

Slow bone loss by increasing osteoclast cell death
- [ORAL] Risedronate, Alendronate (take on empty stomach with 240ml plain water, wait 30 mins before taking food)
- [IV] Zoledronic acid

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13
Q

Significant adverse effects of bisphosphonates & contraindications

A

Atypical femoral fractures
Hypocalcaemia
Severe bone, joint, muscle pain
Osteonecrosis of jaw

contraindications: pts with hypocalcaemia, pregnant

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14
Q

How does denosumab work?

A

Human monoclonal antibody against RANKL
Prevents development of osteoclasts
- subcutaneous injection every 6 months
- co-administer with calcium and vitamin D

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15
Q

Adverse effects of denosumab & contraindications

A

Bone, joint, muscle pain
GI effects
(atypical femur fractures, osteonecrosis of jaw uncommon)

Do NOT discontinue as may cause increased risk of spinal column fractures when discontinued

contraindications: pts with hypocalcaemia, pregnant

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16
Q

How does oestrogen work?

A

Oestrogen can help maintain bone density
- oestrogen therapy used for bone health in younger women or women whose other menopausal symptoms also requires treatment
- Raloxifene:
– selective oestrogen receptor modulator
– mixed oestrogen receptor agonism and antagonism
– mimics effects of oestrogen on bone density in postmenopausal women
– reduces risk of breast cancer
– increases risk of blood clots and hot flashes

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17
Q

Adverse effects of oestrogen therapy

A

increases risk of breast cancer and blood clots which can cause stroke

18
Q

How does calcitonin work?

A

Calcitonin is a peptide hormone secreted by parafollicular cells of the thyroid gland

Calcitonin reduces blood calcium levels, opposing effects of parathyroid hormone

Inhibits osteoclastic bone resorption

IV, SC, IM injection or nasal spray

19
Q

Adverse effects and contraindications of calcitonin

A

Red streaks on skin
Injection site reaction (redness, warmth)

contraindications: hypocalcaemia, hypersensitivity

20
Q

How does Romosozumab work?

A

Humanised mouse monoclonal antibody against sclerostin
Removes sclerostin inhibition of the canonical Wnt signalling pathway that regulates bone growth
-> increases bone formation and decreases bone resorption

  • SC injection once monthly for 12 months
21
Q

Adverse effects and contraindications of romosozumab

A

MI, increased risk of CV death, stroke

contraindications: hypersensitivity, hypocalcaemia, history of MI or stroke

22
Q

How do parathyroid hormone therapies work?

A

Teriparatide
Stimulates new bone formation and increase bone strength
- once daily SC injection (max treatment 24 months)

23
Q

Adverse effects and contraindications of parathyroid hormone therapies

A

Calciphylaxis, hypercalcaemia

contraindication: hypersensitivity, pre-existing hypercalcaemia, renal impairment, pregnancy

24
Q

Primary vs Secondary bone tumours

A

Primary bone tumours
- uncommon
Metastasis
- common

25
Q

What are some Benign Primary Tumours?

A
  1. Exostosis/Osteochondroma
  2. Enchondroma
  3. Simple Bone Cyst
  4. Osteoid osteoma
26
Q

What is osteochondroma/exostosis?

A
  • most common benign bone tumour that arises near end of long bone
  • benign cartilage-capped tumour that is attached to the underlying skeleton by a bony stalk
  • usually solitary
27
Q

What is enchondroma?

A
  • benign cartilaginous tumour that arises from diaphyseal medullary cavity
  • painless swelling
  • usually occurs at small bones eg phalanges of hands

imaging features:
- stippled, flocculent calcifications
- bulbous expansion

histological features:
- mature hyaline cartilage
- no cytological atypia
- no permeation of bone trabeculae or marrow invasion
- no invasion of soft tissue

28
Q

What is simple bone cyst?

A
  • occurs in metaphysis
  • occurs in young child
  • benign, fluid containing lesion
  • cyst-like structure with fibrous wall
  • amorphous pink material with a cementum-like appearance
29
Q

What is osteoid osteoma/osteoblastoma?

A
  • benign bone forming tumour characterised by extensive reaction and pain disproportionate to size
  • more common in young males

radiographic appearance:
- oval lytic lesion located within cortical bone
- sclerosis may obscure underlying lytic nidus on radiograph
- +/- central sclerotic focus within nidus

CT imaging:
- calcified nidus
- reactive periosteal/cortical thickening

histological appearance:
- anastomosing woven bone trabeculae rimmed by abundant osteoblasts
- loose and vascular intratrabecular spaces
- no malignant features (ie. atypia, malignant osteoid, invasion)

30
Q

What are some of the malignant primary bone tumours?

A
  1. Ewing’s sarcoma (occurs in very young pts in the paediatrics age group)
  2. Osteosarcoma (occurs in teenagers to young adults)
  3. Chondrosarcoma (occurs in elderly patients)

Look at patient’s age!

31
Q

What are the features of osteosarcoma?

A

KEY features:
- BONE FORMING tumour
- Malignant histological features:
-> malignant tumour cells (ie. pleomorphic, cytological atypia, hyperchromatic nuclei)
-> malignant lace-like pattern of osteoid
-> invasive growth pattern
-> tumour necrosis
- Metastasise to lungs

other features:
- occurs in teenagers to young adults
- can be a sclerotic lesion
- classic sunburst periosteal reaction (seen in radiograph)
- occurs at metaphysis of long bones
- arises from the medullary cavity and extends to cortex
- fleshy appearance with necrosis and haemorrhage

32
Q

What are the features of chondrosarcoma?

A
  • malignant bone tumour that produces cartilaginous matrix
  • cytological atypia
  • permeation of bone trabeculae
  • locally aggressive tumour that invades surrounding bone and soft tissue
  • large lobulated tumour, pearly white or light blue, with focal calcification
33
Q

Difference between enchondroma and chondrosarcoma

A

Enchondroma:
- mature hyaline cartilage
- no cytological atypia
- no permeation of bone trabeculae
- no soft tissue or marrow invasion

Chondrosarcoma:
- malignant tumour that produces cartilaginous matrix
- cytological atypia
- permeation of trabeculae
- soft tissue and marrow invasion

34
Q

What are the features of Ewing’s Sarcoma?

A
  • permeative destruction
  • saucerisation defect
  • onion skin periosteal reaction

due to translocation t(11,22)(q24;q12)

35
Q

What modalities can be used in secondary bone tumour/metastasis?

A
  • MRI
  • Bone scan
  • Plain film
36
Q

What is Osteomyelitis?

A

Infection of bone that involves bone cortex, medulla and periosteum
- main causative agents:
staph aureus
e. coli
streptococci
h. influenzae
salmonella
mycobacterial tuberculosis
- infection through:
1. direct implantation (open wound)
2. bloodborne spread (lung TB to bone)
3. weakened immunity or vascular insufficiency
4. extension from contiguous site

37
Q

likely location of osteomyelitis with age?

A

children: long bone (upper and lower limbs)
adult: feet, vertebral spine, femur

38
Q

what is the progression of osteomyelitis?

A
  1. Bacterial infects and proliferates producing bone microabscesses
  2. Infection and inflammation spread within shaft of bone, Haversian system and periosteum
  3. If infection extends to joint or synovium -> septic arthritis
  4. Inflammation impairs blood supply to bone causing bone ischaemia and necrosis
  5. Inflammatory exudate lifts periosteum away from the bone cortex
  6. Rupture of the periosteum leads to an abscess in the surrounding soft tissue and the eventual formation of a draining sinus in chronic osteomyelitis
  7. The lifting of the periosteum by inflammatory exudate forms a layer of woven bone called involucrum
  8. The involucrum often surrounds the underlying dead infected bone
39
Q

What is chronic osteomyelitis?

A
  • acute osteomyelitis may persist and progress to chronic osteomyelitis
  • due to weakened immunity
  • potential complications of chronic OM:
    pathological fracture and deformity
    secondary amyloidosis
    sepsis or distant sites of infection
    malignant transformation
40
Q

What is tuberculous osteomyelitis?

A
  • type of chronic osteomyelitis caused by mycobacterium
  • spread to bone from lung via blood borne route or lymphatic drainage

KEY histological features:
- chronic inflammation with epithelioid granulomas and necrosis

41
Q

What is spinal tuberculous osteomyelitis?

A
  • affects vertebral spine
  • can cause:
    compression fractures
    severe deformities
    neurological deficits due to cord and nerve compression
42
Q

What is spondylodiscitis?

A
  • infection of intervertebral disc and adjacent vertebrae

m2 CA2 (22 decks)

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