Fracture Flashcards
(52 cards)
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
2
Q
What comprises the inorganic part of bone?
A
- Hydroxyapatite (Ca(PO)OH)
- Carbonate, citrate, sodium, magnesium
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
4
Q
What are the two types of bone and different names for them?
A
- Cortical, dense, compact
- Trabecular, spongy cancellous
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
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)
7
Q
Structure of endosteum?
A
- Inner cellular lining of compact and spongy bone
- One layer –> endosteal cells (osteoprogenitor and bone lining cells)
8
Q
What are osteoblast precursors?
A
- osteoprogenitor cells
- mesenchymal cells
9
Q
What are osteoclast precursors?
A
- Myeloid/ hematopoietic progenitor cells (granulocyte/ monocyte progenitors)
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
11
Q
Role/ location of osteoclasts
A
- Resorb bone tissue, release minerals and growth factors
- Occupy Howship’s lacuna
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)
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)
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
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
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
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)
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)
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
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
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
- Activation –> clast recruitment (3-7d)
- Resorption –> clast tunneling (2-4w)
- Reversal –> time between resorption and deposition
- Formation –> blasts lay down and mineralize (4-6m)
25
Wolff's Law
- bone will adapt to the loads it is placed under (more loading = stronger bone)
26
What stimulates and inhibits remodelling?
(+) --> growth, thyroid and parathyroid hormones, vit D
(-) --> calcitonin, cortisone, calcium
27
Stages of Fracture Healing
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
How does metaphysical (cancellous) bone heal?
Internal callus (similar mechanisms and stages as cortical bone)
29
Ways to fixate a femur fracture? What ages?
- 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
Primary Bone Healing
- rigidly fixed fractures, direct osteonal healing, some gap healing if under 1mm, 20% direct contact btwn fragment ends
31
How do you classify physeal fractures?
salter-harris classification (refer to images)
32
How long does a metaphysical fracture take to heal? When can you expect normal bone strength? What factors may lengthen or shorten this?
- 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
Role of bone morphogenic proteins (BMP)
TGF-B
IGF-11
Platelet-derived GF
--> 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
How do TH/PTH, cortisone, and GH affect bones?
TH/PTH --> increases callus, affects remodelling
Cortisone --> anti-inflammatory thus decreasing callus
GH --> increases callus volume
35
What are some causes of non-union?
instability, locking plates, decreased vascularization, infection, nicotine (vasoconstriction), NSAIDs, steroids
36
What can cause avascular necrosis of the femoral head?
- disruption of the medial branch of the circumflex ring
37
What are child abuse red flags?
- 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
Important tests if child abuse suspected
- head CT/MRI
- check retina within 24 hours
- LFT/ amylase/lipase to assess for liver or pancreatic injury
39
What do you do if you suspect child abuse?
- 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
What constitutes Physical/ Emotional/ Sexual abuse and neglect?
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
Risk factors for abuse?
- premature, disease, disabled, SUD, young or single parents, poverty, domestic violence, criminal behaviour
42
Different types of fractures?
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
Most common cause of clavicle fracture? Where does it normally break?
- fall on shoulder, then direct trauma or FOOSH
44
What does a bony callus on x-ray indicate?
The fracture is at least 2 weeks old
45
What type of bone issue cannot be compensated for naturally?
- rotational malalignments
- angular deformities can be corrected to a certain degree
46
What are causes of pathological bone fracture?
- osteoporosis, hyperparathyroidism, Cushing's, Paget's, osteogenesis imperfecta, osteosarcoma, multiple myeloma, metastatic breast and prostate cancer
47
What are risk factors for osteoporosis?
- female, smoking, menopause, old age, caucasian, dementia, estrogen deficiency, genetics, decreased calcium and vitamin D, low weight, inadequate physical activity
48
Paget's
- mechanism
- common in
- diagnosis
- 3 different types
- signs and symptoms
- treatment
- indications for treatment
- 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
Tests for Bone Pain?
What would increased Ca/PO4/ALP suggest?
- CBC, electrolytes, Ca, PO4, ALP, urine
- DRE (could be metastatic prostate cancer)
- would suggest active resorption of bone
50
Bone Metastases
Treatment?
- 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
Different bone lesion types?
Lytic --> tumor releases things that increase RANK-L and thus clasts
Sclerotic --> tumor releases things that increase blasts
52
Leg discrepancy treatments?
1-2cm --> usually well-tolerated
2-8cm --> epiphysiodesis of longer leg (ablation of physis)
8-10cm --> distraction osteogenesis (stretching bone)
