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Med School > Fracture > Flashcards

Fracture Flashcards

1
Q

What comprises the organic (osteoid) part of bone?

A
  • 90% type I collagen
  • 10 % non collagenous proteins
    - Osteocalcin (Ca binding protein)
    - Osteopontin (glycoprotein)
    - Proteoglycans
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2
Q

What comprises the inorganic part of bone?

A
  • Hydroxyapatite (Ca(PO)OH)
  • Carbonate, citrate, sodium, magnesium
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3
Q

What comprises the axial skeleton? What is the rest of the skeleton referred to as?

A
  • Skull, ribcage, and vertebral column
  • Appendicular skeleton
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4
Q

What are the two types of bone and different names for them?

A
  • Cortical, dense, compact
  • Trabecular, spongy cancellous
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5
Q

Gross structure of a long bone?

A
  • The epiphysis is the rounded end of a long bone, covered in articular cartilage. Between the epiphysis and diaphysis (the long midsection of the long bone) lies the metaphysis, including the epiphyseal plate (growth plate - sometimes also called the physis).
  • The metaphysis and diaphysis have porous bone
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6
Q

Structure of periosteum?

A
  • Outer fibrous lining, anchored to bone by Sharpey fibres
  • 2 layers:
    Outer –> fibroblasts, type I collagen, nerves, BVs
    Inner –> periosteal cells (osteoprogenitor and bone lining cells)
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7
Q

Structure of endosteum?

A
  • Inner cellular lining of compact and spongy bone
  • One layer –> endosteal cells (osteoprogenitor and bone lining cells)
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8
Q

What are osteoblast precursors?

A
  • osteoprogenitor cells
  • mesenchymal cells
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9
Q

What are osteoclast precursors?

A
  • Myeloid/ hematopoietic progenitor cells (granulocyte/ monocyte progenitors)
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10
Q

Role of osteoblasts

A
  • Lay down and mineralize matrix
  • Secrete type I collagen, glycoproteins, proteoglycans, alkaline phosphatase (calcification)
  • Bone surface lining cells in quiescent adult bone
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11
Q

Role/ location of osteoclasts

A
  • Resorb bone tissue, release minerals and growth factors
  • Occupy Howship’s lacuna
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12
Q

Role/ location of osteocytes

A
  • Calcium regulation, maintain bone tissue, communication
  • Live blasts that are embedded in the bone matrix in lacuna
  • Have processes on canaliculi to communicate via gap junctions (transducing stress signals)
  • If mechanical stress will secrete matrix, can also degrade it for calcium homeostasis
  • Secrete sclerostin (inhibits bone formation)
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13
Q

How do osteoblast/clast progenitors develop and regulate each other>

A
  • Osteoclast precursor expresses RANK and will become an inactive osteoclast if it binds RANK-L (from stromal cells or activated T cells)
  • Osteoblasts release OPG which binds and inhibits RANK-L (inhibits osteoclast formation)
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14
Q

Describe intramembranous bone formation. Which bones develop this way?

A
  • richly vascularized mesenchymal tissue (no cartilage model)
  • flat bones of the skull/face/mandible/clavicle
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15
Q

Describe endochondral bone formation. Which bones develop this way?

A
  • Cartilage model acts as a precursor for bone
  • Mesenchymal cells differentiate into chondrocytes which make cartilage –> bony collar forms around cartilage –> hypertrophic chondrocytes secrete alkaline phosphatase –> chondrocytes die and matrix breaks down leading to the marrow cavity –> bvs grow through the thin bone collar –> osteoprogenitor cells contact bone spicules and become osteoblasts (PRIMARY OSSIFICATION CENTER - first site where bone forms in diaphysis) –> bvs grow through epiphyses (SECONDARY OSS CENTERS) –> epiphyseal cartilage forms between the epiphysis and diaphysis (GROWTH PLATE)
  • Axial bones that bear weight
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16
Q

What happens when max bone growth is reached?

A
  • Cartilage proliferation in the epiphyseal plate stops, deposition will occur until no more cartilage left –> epiphyseal closure
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17
Q

What are the different names for bone growth (length vs width)? How do they work?

A

Length –> Interstitial, endochondral ossification at epiphysis
Width –> Appositional, periosteal growth at diaphysis (blasts work outer and clasts work inner)

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18
Q

Differences between immature (woven) and mature (compact) bone?

A

Immature –> no organized lamellae, more cells per unit area, less mineralization
Mature –> each Osteon has a Haversian canal (BV and nerve supply), concentric lamellae, canaliculi, interstitial lamellae, Volkmann canals (horizontal)

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19
Q

Bone modelling vs remodelling

A

Modelling - how bone gets its shape, appositional and interstitial growth
Remodelling - adapting to function and injury (Haversian remodelling) i.e tissue renewal, changes in physical activity, fracture repair, malunion, surgical realignment

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20
Q

What is an osteon? How does it develop?

A
  • rings of concentric lamellae with a Haversian canal (blasts and capillary) in the middle
  • rings develop inwards during transformation from trabecular to compact bone
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21
Q

Difference of trabecular bone from cortical.

A
  • Also lamellar but doesn’t contain osteons
  • Trabeculae are surrounded by marrow
22
Q

How does bone shape modelling occur?

A
  • metaphysical inwaisting
  • influenced by soft tissue (tendons/ joint capsule)
23
Q

BMU

A
  • Bone metabolizing unit
  • contains blasts/ cytes/ clasts
  • consists of osteons in cortical, trabeculae in cancellous
  • Clasts cut a hole and blasts narrow it (Haversian remodelling)
24
Q

Phases of Bone remodelling?

A
  1. Activation –> clast recruitment (3-7d)
  2. Resorption –> clast tunneling (2-4w)
  3. Reversal –> time between resorption and deposition
  4. Formation –> blasts lay down and mineralize (4-6m)
25
Q

Wolff’s Law

A
  • bone will adapt to the loads it is placed under (more loading = stronger bone)
26
Q

What stimulates and inhibits remodelling?

A

(+) –> growth, thyroid and parathyroid hormones, vit D
(-) –> calcitonin, cortisone, calcium

27
Q

Stages of Fracture Healing

A
  1. Inflammation –> hematoma, necrotic tissues resorbed (few weeks)
    - granulation tissue forms, blasts proliferate, progenitor cells
  2. Repair –> soft callus replaced by endochondral ossified hard callus (weeks to months)
    - still too soft to weight bear, amount of callus is proportional to motion at the fracture
  3. Remodelling –> bone reshapes (continues for years)
    - woven bone replaced by cortical via Haversian remodelling
28
Q

How does metaphysical (cancellous) bone heal?

A

Internal callus (similar mechanisms and stages as cortical bone)

29
Q

Ways to fixate a femur fracture? What ages?

A
  • 0-3m –> Pavlik Harness
  • 3-36m –> Spica cast, traction
  • 2-10y –> flexible nails
  • 11-16y –> plates, trochanteric intramedullary nails (will still get callus) –> increases healing rate by causing inflammation, increases anatomy and function
  • Mature –> adult IM nail
  • Joints in general do not tolerate immobility
30
Q

Primary Bone Healing

A
  • rigidly fixed fractures, direct osteonal healing, some gap healing if under 1mm, 20% direct contact btwn fragment ends
31
Q

How do you classify physeal fractures?

A

salter-harris classification (refer to images)

32
Q

How long does a metaphysical fracture take to heal? When can you expect normal bone strength? What factors may lengthen or shorten this?

A
  • 6-8 weeks, normal strength around 1 year
  • double it if elderly/ cortical bone/ open fracture (lower union rates)/ smoker/ non-compliant
  • halve it for children
33
Q

Role of bone morphogenic proteins (BMP)
TGF-B
IGF-11
Platelet-derived GF

A

–> bone healing and formation
–> induces mesenchymal cells to make type II collagen
–> stimulates type I collagen, bone formation, cartilage matrix synthesis
–> attracts inflammatory cells to fracture

34
Q

How do TH/PTH, cortisone, and GH affect bones?

A

TH/PTH –> increases callus, affects remodelling
Cortisone –> anti-inflammatory thus decreasing callus
GH –> increases callus volume

35
Q

What are some causes of non-union?

A

instability, locking plates, decreased vascularization, infection, nicotine (vasoconstriction), NSAIDs, steroids

36
Q

What can cause avascular necrosis of the femoral head?

A
  • disruption of the medial branch of the circumflex ring
37
Q

What are child abuse red flags?

A
  • fracture in pre-ambulatory/ non-verbal child
  • no hx of injury/ not plausible
  • spiral fracture
  • rib fracture, corner fractures
  • multiple injuries with different stages of healing
  • delay in care seeking
  • TEN4FACESP (when bruising is suspicious) –> trunk, ears, neck, under 4 years, frenulum, angle of jaw, cheeks, eyelids, sclera, patterned
38
Q

Important tests if child abuse suspected

A
  • head CT/MRI
  • check retina within 24 hours
  • LFT/ amylase/lipase to assess for liver or pancreatic injury
39
Q

What do you do if you suspect child abuse?

A
  • legal duty to report (welfare worker/ MCFD)
  • SCAN (suspected child abuse and neglect clinics) or CPSU (child protection service unit)
  • DO NOT interview or probe the child, just report
40
Q

What constitutes Physical/ Emotional/ Sexual abuse and neglect?

A

Physical –> child under 2 and over 12, unreasonable force, incapable of learning, bodily injury, head, degrading, use of an object

Emotional –> violence in a relationship, development of anxiety/depression/agression/withdrawal in a child

Sexual –> exposure to sexual material, exploitation involves manipulation in exchange for something

Neglect –> failure to provide basic needs (food, shelter, supervision, healthcare)

41
Q

Risk factors for abuse?

A
  • premature, disease, disabled, SUD, young or single parents, poverty, domestic violence, criminal behaviour
42
Q

Different types of fractures?

A

Open (Compound) –> bone comes through the skin
Transverse –> horizontal line, all the way through
Oblique fractures –> what it sounds like, all the way through
Impacted (Comminuted) –> bone shatters into more than 2 pieces
Spiral –> bone breaks in a spiral fashion
Greenstick –> only one side, not all the way through

43
Q

Most common cause of clavicle fracture? Where does it normally break?

A
  • fall on shoulder, then direct trauma or FOOSH
44
Q

What does a bony callus on x-ray indicate?

A

The fracture is at least 2 weeks old

45
Q

What type of bone issue cannot be compensated for naturally?

A
  • rotational malalignments
  • angular deformities can be corrected to a certain degree
46
Q

What are causes of pathological bone fracture?

A
  • osteoporosis, hyperparathyroidism, Cushing’s, Paget’s, osteogenesis imperfecta, osteosarcoma, multiple myeloma, metastatic breast and prostate cancer
47
Q

What are risk factors for osteoporosis?

A
  • female, smoking, menopause, old age, caucasian, dementia, estrogen deficiency, genetics, decreased calcium and vitamin D, low weight, inadequate physical activity
48
Q

Paget’s
- mechanism
- common in
- diagnosis
- 3 different types
- signs and symptoms
- treatment
- indications for treatment

A
  • resorption and formation are decoupled, faster turnover
  • clasts increase in number and size, overactive blasts
  • increase in bone size but more brittle due to deformities
  • increases with age, more common in white males
  • diagnosed on x-ray (pelvis, femur, skull, tibia)
  1. Lytic (clasts)
  2. Mixed (blasts lay down disorganized bone)
  3. Sclerotic (no clast or blast activity)
  • increased urinary excretion of hydroxyproline (increased breakdown) and increased serum alkaline phosphatase (rapid rebuilding)
  • osteoarthritis, fracture, bone pain and deformity, spinal stenosis or CN palsy, malignancy: osteosarcoma (though rare)
  • bisphosphonates (zoldronate) or calcitonin IV
  • before ortho surgery, hypercalcemia/calciuria, pain, fractures, radiculopathy, serum alkaline phosphatase or hydroxyproline 2x above normal
49
Q

Tests for Bone Pain?
What would increased Ca/PO4/ALP suggest?

A
  • CBC, electrolytes, Ca, PO4, ALP, urine
  • DRE (could be metastatic prostate cancer)
  • would suggest active resorption of bone
50
Q

Bone Metastases
Treatment?

A
  • bone metastases are more common than primary neoplasms
  • 75% are prostate (esp. lumbar vertebrae), breast, lung, kidney
  • lytic lesions are the most common
  • Tx –> systemic chemo, radiation, bisphosphonates, denosumab, surgery
51
Q

Different bone lesion types?

A

Lytic –> tumor releases things that increase RANK-L and thus clasts

Sclerotic –> tumor releases things that increase blasts

52
Q

Leg discrepancy treatments?

A

1-2cm –> usually well-tolerated
2-8cm –> epiphysiodesis of longer leg (ablation of physis)
8-10cm –> distraction osteogenesis (stretching bone)

Med School (21 decks)

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