Ortho Introduction to Fractures Flashcards

(88 cards)

1
Q

Osteogenesis

A

Process of bone tissue formation
Embryos leads to bony skeleton
Occurs in the form of bone remodeling and bone repair

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2
Q

Endochondrial Ossification

A

Bone replaces a cartilage model

Long bone formation, physis, fracture callus

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3
Q

Intramembranous

A

Undifferentiated mesenchymal cells differentiate into osteoblasts which form bone
Flat bone formation

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4
Q

Appositional

A

Osteoblasts deposit new bone on existing bone

Periosteal bone enlargement (adds width)

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5
Q

Endochondrial Ossification

A
  1. Undifferentiated cells secrete cartilagenous matrix and differentiate into chondrocytes
  2. Matrix mineralizes and is invaded by vscalar buds
  3. Osteoprogenitor cells migrate in
  4. Osteoclasts resorb calcified cartilage
  5. Osteoblasts form bone
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6
Q

Osteoprogenator cells

A

Form mesenchymal stem cells

Lead to formation of osteoblasts, cartilage, fibrous tissue depending on fixation and oxygen tension

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7
Q

Osteoblasts

A

Mesenchymal stem cells
Receptors for PTH, Active Vitamin D, Glucocorticoids, Prostaglandins, Estrogen (stimulate bone growth)
Form bone by generating organic nonmineralized matrix

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8
Q

Osteocytes

A

Osteoblasts that have become surrounded in newly formed matrix
Canaliculi are long cytoplasmic process that connect neighboring osteocytes
Control extracellular calcium, phosphorous concentrations
Stimulated by calcitonin, inhibits PTH

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9
Q

Osteoclasts

A

Originate from macrophage lineage
Brush border membrane for increased surface area
Howship’s lacunae through resorption of bone surface
Inhibited by calcitonin

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10
Q

Zones of Physeal Growth

A
  1. Reserve zone-resting zone
  2. Proliferative zone
  3. Maturation/Hypertrophic zone
  4. Vascular invasion zone
  5. Provisional calcification
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11
Q

Collagen in Physis

A

Type II Collagen

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12
Q

Resting Zone

A

Small scattered chondrocytes

Store lipids, glycogen, proteoglycan for later growth and matrix production

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13
Q

Proliferative zone

A

Chondrocytes line up in direction of growth, proliferate and divide
Longitudinal growth occurs (columns of flattened dividing cells, top cell is the dividing mother
High O2 tension, proteoglycan

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14
Q

Zone of Maturation/Hypertrophy

A

chrondrocytes enlarge
large increase in cell volume
Increased cell height responsible for 44-59% of long bone growth
Differential growth due to differential cell size here
This is the weakest part of the physis, fractures occur here

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15
Q

Zone of Calcified Cartilage

A

Chondrocytes die and matrix starts to calcify

Calcification begins with the longitudinal septa

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16
Q

Apoptosis

A

Programmed cell death
Necessary for homeostasis
Terminally differentiated chondrocytes undergo apoptosis in the zone of calcification

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17
Q

Physeal Closure

A

Completely closed in skeletal maturity
Stops longitudinal bone growth
Decline in width of physis
Estrogen stops replicative sequence of chondrocytes (controls physis closure)

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18
Q

Intramembranous Ossification

A
  1. Occurs without a cartilage model
  2. Undifferentiated mesenchymal cells aggregate into layers or membranes
  3. Cells differentiate into osteoblasts depositing organic matrix
  4. Matrix mineralizes
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19
Q

Ossification Center

A

Location in tissues where ossification begins

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20
Q

Bipartate patella

A

Due to formation of 2 ossification centers

Fibrous tissue links 2 pieces together

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21
Q

Appositional Ossification

A

Primary bone healing

OSteoblasts align themselves on existing bone surfaces and lay down new bone

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22
Q

Fracture

A

Break in integrity of bone
Load force applied to the bone
Results in a decrease of the functional capability of the bone

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23
Q

Fracture Patterns

A

Determined by type and direction of force
Determined by physical characteristics of the bone
Determined by the speed of the force

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24
Q

Classifications of Fractures

A

Location in a bone
Diaphyses
Metaphysics
Epiphysis end of bone adjacent to jt.

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25
Orientation of Fractures
``` Transverse Oblique Spiral Comminuted Segmental Intra-articular ```
26
Displacement of Fractures
``` Non-displaced Displaced Angulated Bayonet Distracted ```
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Type I
Simple, transverse, short oblique with little communication
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Type II
Moderate fracture comminution
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Type III
Great degree of fracture comminution and instability
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Type III-A
Extensive soft tissue laceration, adequate bone coverage after debridement Free flaps are not necessary to cover bone Segmental fractures, such as gunshot injuries
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Type III-B
Extensive soft tissue injury with periosteal stripping and exposed bone after debridement Requires local or free flap to cover bone
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Type III-C
Same as B Extensive soft tissue injury with periosteal stripping and exposed bone after debridement Require local or free flap to cover bone
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Pediatric
Bone is more porous High proportion of articular cartilage Opens epiphyseal plates Periosteam much thicker (great blood supply) Higher osteoblastic activity Fractures can remodel Joint injuries and dislocations much less common (ligaments stronger than bone) Cartilagenous epiphyseal plate is weaker than joint capsulre or ligaments
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Why are hip fractures bad in kids?
Devastating due to AVN of femoral head
35
Tillaux Fracture
Occurs because of asymmetrical closure of distal tibia growth plate
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Triplane Fracture
Sagittal fracture line through epiphysis, transverse fracture line through physis, coronal fracture through metaphysis
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Types of Pediatric fractures
``` Plastic deformations Buckle Greenstick Complete Epiphyseal plate Apophyseal plate ```
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Salter Harris I
Widening of epiphyseal plate
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Salter Harris II
Fracture through plate and metaphysis
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Salter Harris III
Fracture through plate and epihysis
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Salter Harris IV
through plate, metaphysis and epiphysis
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Salter Harris V
Crushed epiphysis (compression fracture of growth plate leads to disturbances in growth)
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What are the orthopedic aspects of child abuse
Fractures in various stages of healing | Corner fractures can be noted at the corner of the metaphysis (jerked leg/arm)
44
Apophyseal Fractures
Fracture of a diaphysis that does not add length
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Modifying Factors of Fracture Healing
1. Bleeding 2. Resorption 3. Mesenchymal differentiation into osteo and fibro-progenitor cells 4. Callous formation
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Stages of Fracture Healing
1. Bleeding-->devascularizes and forms hematoma 2. Resorption-->osteoclasts and inflammatory response 3. Mesenchymal differentiation into osteo and fibro-progenitor cells 4. Callous formation
47
Bone Circulation
1. Nutrient artery system 2. Metaphyseal-epiphyseal system 3. Periosteal system
48
Stages of Fracture Healing
1. Hematoma and inflammatory response 2. Fracture hematoma maturation 3. Conversion of hypertrophic cartilage to bone 4. Bone remodeling
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Cells of early postfracture
Primaritive mesenchymal and osteoprogenitor cells facilitate production of the BMPs
50
Bone Growth Factors
BMP TGF-B IFG-II PDGF
51
Bone Morphogenic Protein
Stimulates growth Induces metaplasia of mesenchymal cells into osteoblasts Target for BMP is undifferentiated perivascular mesenchymal cell
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TGF-B
Induces mesenchymal cells to produce type II collagen and proteoglycans Induce osteoblasts to synthesize collagen Regulate cartilage and bone formation in fracture callus
53
Conversion of hypertrophic cartilage to bone
Undergo terminal differentiation, cartilage calcifies and new woven bone is formed Hard callus Woven bone is remodeled Mature bone eventually established and is not distinguishable from surrounding bone (week 17+)
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Cortical Bone Remodeling
Remodels by osteoclastic tunneling
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Cancellous bone Remodeling
Remodels by classic resorption followed by blasts laying down new bone
56
Wolff's Law
Bone remodels in response to mechanical stress
57
Piezoelectric Charge
``` Compression side (negative charge) activates blasts Tension side (positive charge) activates clasts ```
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Delayed Union
Fracture that has not healed in twice the normal healing time
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Nonunion
Fracture that has not healed in three times the normal healing time (6 months)
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Hypertrophic Nonunion
bone at fracture site form enormous amounts of bone with no healing (elephants foot)
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Malunion
Fracture that is united with unacceptable angulation, rotation or shortening
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Fracture Blisters
Occur in response to increased compartmental pressure | Caused by uneven extrinsic pressure
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Jones Fracture
Proximal fracture through 5th metatarsal | Rarely heals due to poor blood supply
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DVT and PE Increasing Risks
``` Locations of fracture Age of patient Body type Degree of Immobilization Compliance ```
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Signs and Symptoms of DVT and PE
``` Calf and thigh pain Edema distal to obstruction Homans sign Shortless of breath Decreased PO2 Chest pain Tachycardia Hypotension ```
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Fat Embolism
Fact without circulation Produce embolic phenomena With or without clinical sequelae
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Fat Embolism Syndrome
Fat in circulation associated with identifiable clinical pattern of symptoms and signs Risk high with femoral shaft fracture and concomitant head injury Multiple trauma with major visceral injuries and blood loss Hip/knee with intramedullary instrumentation
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Mechanical FES
1. Injury to adipose tissue 2. Rupture of veins within zone of injury 3. Mechanism that will cause passage of free fat into open end of vessels 4. Disrupted venules in marrow remain tethered open by osseous attachments
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Lehman Biochemical Theory
Plasma mediators mobilize fat from body stores into large droplets Degradation of embolized fat into free fatty acids
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FES Triad
Neurological abnormalities in 80% of FES pts Hypoxemia Petechia rash
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ARDS
Release of sytokines secondary to inflammation causes increase permeability of alveoli and capillary membranes causing pulmonary edema
72
Compartment Syndrome
Circulation and function of tissue in fibro-osseous space is compromised secondary to increased pressure in the space Increased pressure can result from bleeding, increase capillary permeability, decreased size of space (tight dressing)
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Signs and Symptoms of Compartment Syndrome
Pain, palor, parethesias and pulselessness
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Implants
``` Contractures Skin Coverage Loosening Infection Failure of implant ```
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Post-Traumatic Arthritis
``` Chronic pain Deformity Loss of motion Crepitance RSD (complex regional pain syndrome) ```
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Reflex Sympathetic Dystropy
RSD burning pain, increased skin sensitivity, changes in skin color/tecture/hair growth patterns, swelling and stiffness of affected joints, motor disability
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Type I RSD
Triggered by tissue injury
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Type II RSD
Triggered by nerve injury
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What are the causes of CRPS
Catecholamines released from sympathetic nerves acquire the capactiy to activate pain pathways frollowing a nerve or tissue injury
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Stages of CRPS
1. Acute-burning, swelling, pain 2. Dystrophic-thin shiny skin, loss of hair, contractures 3. Atrophic-loss of motion, loss of subcutaneous fat, osteoporosis, pathological fractures
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Avascular Necrosis
Disruption of blood supply to poorly vascularized bone leads to degeneration of the bone that is no longer vascularized Sites: femoral head, carpal navicular, talus, humeral head, metacarpal head
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Causes of AVN
Site, displacement, delay in immobilization, surgical approach, drug therapy, systemic disease, alcohol
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PAthological Fractures
Bone breaks in area weakened by another disease process Usually occurs with normal activity Treatment must address underlying disease process
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Bone Insufficiency Fractures
Fracture due to weakening of the bone from inadequate density (such as loss from osteoporosis)
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Causes of pathological fractures
Weakness of bones (altered metabolism of calcium, vitamin D, parathyroid hormones) Destruction of bone (infection, tumors, fibrous dysplasias)
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Subcapital Fracture of Hip
Fracture of the femoral neck This disrupts the blood supply to the head of the femur Disruption of calcium metabolism can cause bone to weaken, or an infection can cause bone resorption
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Stress Fracture
``` Fracture of bone that occurs secondary to repeated microtrauma Usually occur in weight bearing bones Seen in athletes See in atheletic wanabees Seen as an occupational disease Seen in military (march fracture) ```
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Pars Fracture
Weightlifting can cause it