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Musculoskeletal Exam 1 > Orthopedic - Intro to Fractures > Flashcards

Orthopedic - Intro to Fractures Flashcards

1
Q

What is appositional growth?

A

Osteoblasts deposit new bone on existing bone. Such as in periosteal bone enlargement (width)

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2
Q

Process of Endochondral Ossification?

A

1) Undifferentiated cells secrete the cartilaginous matrix and differentiate into chondrocytes
2) Matrix mineralizes and is invaded by vascular buds
3) Osteoprogenitor cells migrate in
4) Osteoclasts resorb calcified cartilage
5) Osteoblasts form bone

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3
Q

What is a precursor cell for osteoblasts, cartilage, fibrous tissue.

A

Osteoprogenator cell

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4
Q

Where do osteoblasts originate from?
What do they have receptors for?
What does it produce?

A
  • Mesenchymal stem cells
  • PTH, Active Vit.D, Glucocorticoids, Prostaglandin, estrogen
  • Alkaline phosphatase
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5
Q

What concentrations do osteocytes control?
What are osteocytes stimulated by?
Where do they originate
What are the names of the canals created by osteoclasts?

A
  • extracellular calcium and phosphorus
  • Simulated by calcitonin (inhibited by) and inhibited by PTH
  • macrophage lineage
  • Howship’s lacunae
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6
Q

What are the zones of physeal growth?

A

Reserve zone (resting zone), proliferative zone, maturation/hypertrophic zone, vascular invasion zone.

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7
Q

What occurs in the resting zone and what occurs there?

A

scattered chondroctes

- stores lipid glycogen and proteoglycan for later growth and matrix production.

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8
Q

What occurs in the proliferating zone?

A
  • Chondrocytes stack and oriente in direction of proliferation and divide
  • Longitudinal growth occurs
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9
Q

What occurs in the zone of maturation/hypertrophy

A

Chondrocytes enlarge

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10
Q

What occurs in the zone of calcified cartilage?

A
  • Chondrocytes die and matrix starts to calcify, calcification begins.
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11
Q

What acts as a scaffold for osteoids creating bone?

A

remnants of cartilage

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12
Q

What mineral is responsible for branching, accretion and making bones harder?
- What is the predoninant mineral in bone?

A
  • calcium hydroxyapatite.

- Hydroxyapatite

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13
Q

What causes the physeal to close?

A

1) skeletal maturity
2) Stops longitudinal bone growth
3) Decline in width of physics
4) Primarily under control of estrogen in both sexes
5) Estrogen stops replicative sequence of condrocytes in both men and women

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14
Q

What two things are elevated in the proliferative zone.

A

High oxygen tension

High proteoglycan

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15
Q

In the hypertrophic zone what occurs here? What is elevated?

A

Differential growth due to differential cell size.

  • Increase in alkaline phosphatase
  • This is where fracture occur the most.
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16
Q

In intramembranous ossification what aggregates into layer? What do cells differentiate into? What mineralizes

A

Undifferentiated mesenchymal cells that soon mineralize through crystallization of calcium and differentiates into osteoblasts.

  • differentiate into osteoblast depositing organic matrix.
  • Matrix mineralizes
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17
Q

What is the area called where ossification begins?

A

-Ossification center

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18
Q

What is more than one ossification center in the patella called?

A

Bipartite patella (2), can also occur inthe tarsal narvicular bone.

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19
Q

What are fracture patterns determined by?

A

The type and direction of force.
By the physical characteristics of the bone
By the speed of the force

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20
Q

What is comminution?

A

high degree of velocity causing a break into smaller pieces.

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21
Q

Where the location of a fracture in a:
Epiphyseal fracture?
Metaphyseal fracture?
Diaphyseal fracture?

A
  • end of bone adjacent to joint
  • flaring at end of shaft of long bone
  • shaft of a long bone
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22
Q

What are orientation of fractures in:

  • Transverse?
  • Oblique?
  • Spiral?
  • Comminuted?
  • Segmental?
  • Intra-articular?
A
  • Transverse: perpendicular to long axis
  • Oblique: angulated fracture line
  • Spiral: mult-planar
  • Comminuted: more than 2 fragments
  • Segmental: separate segments
  • Intra-articular: enters into a joint
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23
Q 
What the classification of the displacement of fractures:
   Non-displaced?
     Displaced?
     Angulated?
     Bayonet?
     Distracted?
A 
Non-displaced: anatomic alignment
Displaced: not in usual alignment
Angulated:
Bayonet: longitudinal overlap of fragments
Distracted: gap between fragments
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24
Q

In fracture what is closed verse open fracture?

A

Closed- skin is intact

Open- hole in skin due to fracture

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25
Q

Differentiate the 3 Gustillo-Anderson Classification levels.

A

Type 3A - no significant vascular injury, extensive soft tissue laceration - adequate bone coverage
TypeIII-B: Not significant vascular injury, extensive soft tissue injury with exposed bone.
Type 3-C: same as B just with vascular injury

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26
Q 
What are the pediatric classification of fractures: 
    Plastic deformation?
    Buckle?
    Greenstick?
    Complete
A

Plastic deformation: bend
Buckle : only one cortex involved
Greenstick: crack of one cortex and buckle of the opposite
Complete: both sides break

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27
Q

What are the major differences between an adult and a pediatric skeleton?

A

In kids: Bone is more porous

  • Higher proportion of articular cartilage
  • Epiphyseal plates
  • Periosteum is much thicker
  • Higher osteoblastic activity
  • Joint injuries and dislocations much less common
  • Fractures can remodel
  • Cartilaginous epiphyseal plate is wekaer than joint capsule or ligaments
  • Potential for growth allows for marked remodeling of displaced fractures
  • Fractures around the hip in children devastating due to AVN of femoral head
  • Triplane and Tillaux ankle fractures are intra-articular and require anatomic reduction
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28
Q

Why does a tillaux fracture occur?

A

Because of asymmetrical closure of distal tibia growth plate. So does triplane fracture.

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29
Q

What is the most suspicious thing concerning child abuse in a musculoskeletal exam?

A

fractures in various stages of healing

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30
Q

What are the Slater Harris levels of Classification?

A 
S-H I: Widening of the epiphyseal plate
S-HII: Through plate and metaphysics
S-HIII: Through plate and epiphysis
S-HIV: Through both metaphysis and epiphysis
S-H V: Crushed epiphysis (worse)
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31
Q

What are the biological factors modifying fracture healing?

A
  • Vascularity
  • General nutrition
  • Hormonal
  • Co-morbid conditions
  • Nerve function
  • Age
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32
Q

What are the Mechanical factors modifying fracture healing?

A
  • Stability
  • Anatomic location
  • Bone loss
  • Comminution
  • Displacement
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33
Q

What are the stages of fracture healing?

A
  • Bleeding (devascularizes and forms hematoma)
  • Resorption (Osteoclasts and inflammatory response)
  • Mesenchymal differentiation into osteo and fibroprogenitor cells
  • Callous formation
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34
Q

When does blood flow peek in a fracture?

When does it return to normal?

A
  • Peaks at 2 weeks and returns to normal by 3-5 months
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35
Q

What are the three types of bone circulation?

A

1) Nutrient artery system- pierces the diaphysis and transverses the medullary canal.
2) Metaphyseal-epiphyseal system: periarticular vascular plexus
3) Periosteal system- supply the outer third of the diaphysis

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36
Q

What part of the long bone has the best blood supply and will repair the quickest?

A

The Metaphysis.

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37
Q

What are the stages of repair for bone?

A

1) Hematoma and inflammatory response
2) Fracture hematoma maturation
3) Conversion of hypertrophic cartilage to bone
4) Bone remodeling

38
Q

In the early post-fracture period primitive mesenchymal and osteoprogenitor cells facilitate production of what?

A

BMP’s (proteins that stimulate formationof new bone cells.

39
Q

What are 4 growth factors of bone?

A

Bone Morphogenic protein (BMP)
Transforming Growth Factor Beta (TGF-B)
Insulin Like Growth Factor II (IGF-II)
Platelet Derived Growth Factor (PDGF)

40
Q

BMP is osteoinductive, meaning that it induces metaplasia of what cells into what?
- What is the target cell for BMP?

A
  • mesenchymal cells into osteoblasts

- undifferentiated perivascular mesenchymal cell.

41
Q

What do transforming growth factor beta induce mesenchymal cells to form?

  • What does it induce osteoblasts to synthesize?
  • Where is TGF-B found and what does it regulate?
A
  • to produce type II collagen and proteoglycans
  • synthesize collagen
  • found in fracture hematomas and is believed to regulate cartilage and bone formation.
42
Q

What does fracture hematoma provide?

A

**- Provides progenitor cells and growth factors for mesenchymal cell differentiation.

43
Q

What stabilizes the fracture site?

A

Cartilage formation via chondrocytes

44
Q

Hypertrophic chondrocytes undergo terminal differentiation, cartilage calcifies, and what is formed?

A

new woven bone (weaker haphazard arrangement of collagen which eventually is replaced by mature bone)

45
Q

How is cortical bone remodeled?

How is cancellous bone remodeled?

A
  • osteoclastic tunneling

- clastic resorption followed by blasts laying down new bone

46
Q

What is wolff’s law?

A
  • Bone remodels in response to mechanical stress
47
Q

For piezoelectric charge which side/charge activates blasts and which activates clasts?

A
  • Compression side (-charge) activates blasts

- Tension side (+charge) activates clasts

48
Q

What is the initial histologic change observed in hypertrophic non-unions treated with plate stabilization?

A

Fibrocartilage mineralization

49
Q

What occurs with closed treatment “endochondral healing” with periosteal bridging?

A

Callus occurs

50
Q

What is the relationship between callus formation and the amount of immobilization of the fracture?

A

The amount of callus formation is indirectly proporational to the amount of immobilization of the fracture.

51
Q

Primary cortical healing occurs with what?

A
  • rigid immobilization and anatomic reduction
52
Q

What are the four types of inappropriate healing?

A

1) Delayed union - fracture that has not healed in twice the normal healing time
2) Nonunion - fracture that has not healed in three times the normal healing time
3) Atrophic nonunion - bone near the fracture becomes pointed with no apparent healing of fracture (due to blood supply)
4) Hypertrophic nonunion - Bone at fracture site form enormous amounts of bone with no healing
5) Malunion - Fracture that is united with unacceptable angulation, rotation, or shortening.

53
Q

What are the methods of fracture management?

A
  • Splinting
  • Casting
  • Braces (fracture braces hold arm in place)
  • Traction
  • Reductions
  • Internal fixation
  • External fixation:(pins into the outside of skin)
  • Bone grafting:(stimulate healing with another piece of bone)
  • Synthetic grafting
  • Electrical stimulation: (electrical current to stimulate bone to heal)
  • Nutritional supplements: (calcium and vit D)
  • Medications: stimulate bone and retain Ca.
54
Q

How do fracture blisters occur?

A
  • Occur in response to incased compartmental pressure, caused by uneven extrinsic pressure.
55
Q

What is a jones Fracture?

A
  • Fracture to the 5th metatarsal proximally. This type of fracture rarely heals.
56
Q

What is the worse systemic complication from a fracture?

What are some of the other complications

A
  • Thromoboembolis (DVT and PE)
  • Fat embolism syndrome, Acute respiratory distress syndrome, multiple organ failure, hemorrhagic shock, bleeding disorders (DIC), sepsis, gas gangrene
57
Q

What are some local complications of a fracture?

A

1) Vascular injury
2) Compartment Syndrome
3) Tendon and Soft Tissue injury

58
Q

What are factors increasing risk of a DVT and PE?

A

1) Location of fracture (long bones and extremities)
2) Age of patient (older)
3) Body type (heavier)
4) Degree of immobilization
5) Compliance

59
Q

What are some signs and symptoms of DVT/PE?

A
  • Calf and/or thigh pain
  • Edema distal to obstruction
  • Homans sign
  • Shortness of breath
  • Decreased PO2
  • Chest Pain
  • Tachycardia
  • Hypotension
60
Q

What is the difference between a fat embolism and a DVT?

A
  • Fat embolism crosses the BBB a DVT does not.
61
Q

Where does a microvascular occlusion occur in fat embolism syndrome?

A
  • Brain
  • Kidney
  • Lungs
  • Skin
  • Retina
62
Q

Contrast Fat embolism and Fat embolism syndrome?

A

Fat embolism: is fat within the circulation, which can produce embolic phenomena, with or without clinical sequelae
- Fat embolism syndrome: is fat in the circulation associated with an identifiable clinical pattern of symptoms and signs.

63
Q

What is the types of fractures see Fat embolism syndrome?
What types of orthopedic replacements is FES more commonly seen?
- What condition is FES reported in?

A
  • Risk of FES is especially high with femoral shaft fracture and concomitant head injury.
    Fatal in 10-15%
  • Hip/knee replacements
  • DMD
64
Q

What are some nontraumatic procedures that can increase the chance of getting FES?

A
  • Pancreatitis
  • DM
  • Osteomyelitis and panniculitis
  • Bone tumor lysis
  • Steroid therapy
  • Sickle cell ***
  • Alcoholic fatty liver
  • Lipid infusion
65
Q

How long will it take fat droplets in the circulation to eventually coalesce and embolus?

A
  • 85% occur within 48 hours of precipitating factor.
66
Q

What are 3 conditions that are needed for FES according to Gauss mechanical theory?

A

1) Injury to adipose tissue
2) Rupture of veins within zone of injury
3) Mechanism that will cause passage of free fat into open ends of vessels.
4) Disrupted venules in marrow remain tethered open by their osseous attachments.

67
Q

What is Lehman biochemical theory?

A
  • Plasma mediators mobilize fat from body stores.
  • Form large droplets
  • Degradation of embolized fat into free fatty acids (FFA)
  • Toxic
68
Q

How does FES cause a PE?

A
  • by blocking the capillaries in the lung
69
Q

What are the classic triad finding in FES?

A
  • Neurological abnormalities
  • Hypoxemia
  • Petechial rash
70
Q

Once over the BBB what histological sign will FES cause? What will it go out to effect?

A

micropetiache in the brain

- will progress within 48 hours to affect the patient’s attitude.

71
Q

What disorder is FES in the lungs indistinguishable to?

- What percentage of patients with FES acquire sever hypoxemia and require mechanical ventilation?

A
  • ARDS (occurs when fluid builds up in the tiny, elastic air sacs in your lungs.
  • 50%
72
Q

What is released in ARDS?

A
  • Cytokinins
73
Q

What is the last symptom of the triad to show up?

A
  • Petechial rash (from occlusion of dermal capillaries by fat globules, leads to extravasation of erythrocytes, resolves in 5-7 days, present in only 20-50%
74
Q

Where does the petechial rash appear?

A
  • Head, Neck, anterior thorax, subconjunctiva, axiallae
75
Q

What is compartment syndrome and where does it occur?

What are it’s causes

A
  • Circulation and function of tissue in a fibro-osseous space is compromised.
  • Secondary to increased pressure in the space (bleeding, increased capillary permeability, decreased size of space)
76
Q

What are common sites of compartment syndrome?

A
  • Elbow, calf, and forearm
77
Q

What is the treatment for compartment syndrome?

A

A Fasciotomy procedure- which cuts through the skin and fascia to release pressure.

78
Q

What are the signs and symptoms of compartment syndrome?

A
  • Pain
  • Palor: white looking
  • Paresthesias: numbness and tingling***
  • Pulselessness
79
Q

What disorders are associated with implants?

A
  • Contractures
  • Skin Coverage
  • Loosening
  • Infection
  • Failure of implant
80
Q

What results form Post traumatic arthritis (occuring within the joint)?

A
  • Chronic pain
  • Deformity
  • Loss of motion
  • Crepitance (crackles)
  • RSD (complex regional pain syndrome
81
Q

What is reflex sympathetic dystrophy (aka complex regional pain syndrome)

A
  • Disruption of the autonomic nervous system where skin can become swollen and red
    • ->Type 1: triggered by tissue injury
    • ->Type 2: Triggered by nerve injury
82
Q

What are some symptoms of complex regional pain syndrome?

A
  • “burning pain”
  • increased skin sensitivity
  • changes in skin color
  • Changes in skin texture (shiny, thin)
  • Changes in hair growth patterns
  • Swelling and stiffness of affected joints
  • Motor disability
83
Q

What causes CRPS?

A
  • Catecholamine (norepinepherine) released from sympathetic nerves acquire the capacity to activate pain pathways following a nerve or tissue injury. –> swollen extremitiy that they can’t fix
84
Q

What are the 3 stages of CRPS?

A
  • Acute: burning, swelling, pain
  • Dystrophic: thin shiny skin, loss of hair, contractures
  • Atrophic: loss of motion, loss of subcutaneous fat, osteoporosis, pathological fractures
85
Q

What is the treatment of CRPS?

A
  • Physical therapy
  • Psychotherapy
  • Sympathetic nerve block
  • Medications
  • Surgical sympathectomy
  • Spinal cord stimulators
  • Intrathecal drug pumps
86
Q

What are the most common sites of avascular necrosis?

A
  • Femoral head
  • Carpal Navicular
  • Talus
  • Humeral head
  • Metacarpal Head
87
Q

What type of hip dislocation might require a full replacement?

A

Posterior **

88
Q

What some key features of a pathologic fracture?

A
  • A bone breaks in an area weakened by another disease process (ex. osteoporosis)
  • Usually patient is aware of underlying disorder and fracture occurs with normal activity
  • Treatment must address underlying disease process**
89
Q

What are some causes of pathological fractures?

A
  • Weakness of bones (altered metabolism of calcium, Vit. D, parathyroid hormone)
  • Destruction of bone (infection, tumors, fibrous dysplasias)
90
Q

What is a stress fracture and how does it occur?

How does it present?

A
  • A fracture of bone that occurs secondary to repeated micotrauma and usually occurs in weight bearing bones.
  • Seen in athletes, military
  • Presents with a painful shin- not an obvious fracture
91
Q

Where is the most common place for a stress fracture?

A

in the metacarpal bone.

Musculoskeletal Exam 1 (11 decks)

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