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(msk) children's orthopaedics Flashcards

1
Q

define physis

A

cartilaginous disc separating the epiphysis from the metaphysis

is responsible for interstitial bone growth of long bones

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2
Q

where are the physes found in children’s long bones?

A

two physes for each long bone: at the proximal and distal end

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3
Q

why are physes important?

A

site of interstitial bone growth needed for bone lengthening as children grow

(reserve, proliferative, hypertrophic and calcification zones)

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4
Q

differentiate between epiphysis, metaphysis, diaphysis and physis

A

epiphysis = wide end of long bones containing spongy, cancellous bone

diaphysis = tubular shaft of bone from distal to proximal end

metaphysis = region that connects the epiphysis to the diaphysis

physis = cartilagenous growth plate between epiphysis and metaphysis where interstitial bone growth for bone lengthening takes place

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5
Q

what are the two types of bone development?

A

intramembranous ossification

endochondral ossification

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6
Q

what type of bones is intramembranous ossification important for?

A

flat bones (e.g. clavicle, cranial bones)

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7
Q

what type of bones is endochondral ossification important for?

A

long bones

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8
Q

what is the main difference between endochondral and intramembranous ossification?

A

intramembranous = mesenchymal cells to bone

endochondral = mesenchymal cells to CARTILAGE to bone

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9
Q

describe the process of intramembranous ossification

A

mesenchymal cells differentiate into osteogenic cells and then osteoblasts = ossification centre forms

osteoblasts secrete osteoid and become trapped in the matrix as calcification occurs

when trapped, osteoblasts become osteocytes and bone formation occurs

in the central regions, the trabecular matrix develops forming spongy bone

blood vessels condense here and supply this region to form spongy red bone marrow

cortical bone develops superficial to the cancellous bone

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10
Q

how does spongy bone develop in intramembranous ossification?

A

trabecular matrix develops and blood vessels condense and supply this region
= spongy, cancellous bone

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11
Q

how does cortical bone develop in intramembranous ossification?

A

osteoblasts secrete osteoid and become trapped in the matrix as osteocytes during calcification, forming cortical bone

(occurs superficial to spongy bone formation)

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12
Q

what is the ossification centre in intramembranous ossification?

A

when osteoblasts, recently differentiated from mesenchymal cells, accumulate in a region prior to osteoid secretion

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13
Q

describe the process of endochondral ossification

A

1) mesenchymal cell differentiation
2) hyaline cartilage model with a lateral bony collar forms
3) interstitional and appositional growth of cartilage model
4) central matrix of cartilage model begins to CALCIFY as blood vessels condense to supply this region = forming the primary ossification centre + perichondrium converted into periosteum
5) spongy bone forms a the centre and extends proximally and distally - cartilage/chondrocytes develop
6) osteoclastic activity in the centre breaks down some bone and cartilage to form the medullary cavity
7) secondary ossification centres develop with its own blood vessel and calcification at the epiphyseal proximal and distal end – calcification of the matrix
8) some cartilage remains = articular cartilage, physis

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14
Q

describe the process of endochondral ossification

A

hyaline cartilage model with a lateral body collar forms

interstitional and appositional growth of cartilage model

central matrix of cartilage model begins to calcify as blood vessels condense to supply this region forming the primary ossification centre

spongy bone forms at the centre and extends proximally and distally

osteoclastic activity in the centre breaks down some bone and cartilage to form the medullary cavity

by birth, at the proximal and distal epiphyseal regions, blood vessels form and calcification occurs = secondary ossification centres

secondary centres = bone development in epiphyseal regions

but remnants = articular hyaline cartilage and epiphyseal growth plates (of initial hyaline cartilage model)

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15
Q

what is endochondral ossification divided into?

A

primary endochondral ossification

secondary endochondral ossification

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16
Q

what is primary and secondary endochondral ossification?

A

primary

  • pre-natal
  • involved formation of primary ossification centres & subsequent central bone growth

secondary

  • post-natal, adolescent
  • involves the development of epiphyseal secondary ossification centres
  • long bone lengthening at epiphyseal growth plates
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17
Q

what are primary ossification centres?

A

sites of pre-natal endochondral ossification in the central part of the bone

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18
Q

what are secondary ossification centres?

A

sites of post-natal endochondral ossification in the epiphyseal part of the bone

= interstitial bone lengthening occurs

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19
Q

where do primary ossification centres form in endochondral ossification?

A

in the central (diaphyseal) portion of the hyaline cartilage model

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20
Q

where and when do secondary ossification centres form in endochondral ossification?

A

when = post-natally, adolescent years

where = epiphyseal portion of long bone

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21
Q

why does osteoclast activity occur in endochondral ossification?

A

medullary cavity formation

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22
Q

why is the articular cartilage and epiphyseal growth plate important in endochondral ossification?

A

the only remnants of the initial hyaline cartilage model

  • articular cartilage = joint articulation
  • growth plate = sites of interstitial bone growth and lengthening
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23
Q

what happens at the physeal (epiphyseal growth) plate?

A

interstital bone growth

= chondrocytes proliferate, mature, hypertrophy and then form a calcified matrix to add to the ossified bone of the diaphyseal edges

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24
Q

differentiate between the epiphyseal and the diaphyseal side in interstitial bone growth

A

epiphyseal side – hyaline cartilage active and dividing to form hyaline cartilage matrix

diaphyseal side – cartilage calcifies and cell death and then replaced by bone

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25
what are four ways in which children's bones differ primarily from adult bones?
physis remodelling potential elasticity speed of healing
26
why are children's bones more elastic than adult bones?
increased density of Haversian canals within children's bones to meet the increased metabolic demand
27
explain how the increased elasticity of children's bones helps with bone growth
increased elasticity = increased density of Haversian canals = more dense blood supply = increased bone growth
28
why do children have more Haversian canals in their bones?
to increase the vascular supply to the bone as children's bones are more metabolically active
29
what is the main consequence of the increased elasticity of children's bones?
increased plastic deformity of the bones | i.e. likely to bend before they break
30
what is a Buckle fracture?
where only one side of the bone buckles/crumples but the other side of the bone is unaffected (due to longitudinal force through bone cortex) i.e. torus fracture
31
what is a Greenstick fracture?
when bone bends to the extent that one side breaks and the other side remains intact (breaking twigs = the tough bark on one side will break but the bark on the other side remains intact)
32
what are Haversian canals?
microscopic tubes within cortical bone osteons housing the neurovascular supply to the bone
33
what is physeal growth?
(interstitial) bone growth at the epiphyseal growth plates at various sites at varying rates
34
which factors determine when growth at epiphyseal plates ceases?
puberty, menarche, parental height, genetic factors
35
in girls, when does physeal growth cease?
15-16
36
in boys, when does physeal growth cease?
18-19
37
what are two possible consequences of traumatic injuries to the physes?
1) growth arrest | 2) deformity
38
how are physeal injuries categorised?
based on the Salter-Harris scale
39
how can physeal injury lead to growth arrest?
when the entirety of the physeal plate is injured, interstitial bone growth is significantly impaired = growth arrest
40
how can physeal injury lead to deformity?
when a portion of the physeal plate is injured, interstitial bone growth continues in the intact region but stops in the injured region = deformity
41
what three factors do the speed of healing and remodelling potential depend on?
1) location of injury 2) age of patient 3) GROWTH level at the site of injury
42
which group of patients heal most quickly?
young children | greatest growth = fastest healing
43
which region of the upper limb heals most quickly and why?
shoulders and wrist regions | areas of greatest growth = fastest healing
44
which region of the lower limb heals most quickly and why?
around the knee (distal femur, proximal tibia) | areas of greatest growth = fastest healing
45
why is the rate of healing accelerated in children?
children's bones have very rapid growth rates greatest, rapid growth rates = fastest healing + remodelling potential
46
how is healing linked to growth rate?
the more rapid the growth rate in a region, the faster the healing and the more the remodelling potential of the area
47
list four paediatric congenital orthopaedic conditions
developmental dysplasia of the hip (DDH) club foot achondroplasia osteogenesis imperfects
48
what is developmental dysplasia of the hip?
disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
49
what does normal hip development require?
concentric reduction + balanced forces through the hip = hip needs to sit in acetabulum so they can exert forces on each other to produce a normal hip joint
50
what happens if the hip develops outside the acetabulum?
if hip develops outside the socket, lack of force and pressure exertion on the acetabulum = impaired acetabular development
51
what are the three types of DDH?
1) dysplasia 2) subluxation 3) dislocation
52
what is dysplasia in DDH?
hip lies in acetabulum BUT not centrally placed
53
what is subluxation in DDH?
hip lies in acetabulum but loosely pops in and out of socket due to shallow acetabulum
54
what is dislocation in DDH?
hip never been inside acetabulum, develops outside acetabulum very shallow
55
what are the risk factors for DDH?
female firstborn breech family history oligohydramnios Native America/Laplanders (nature of swaddling the baby)
56
how is DDH diagnosed?
in the baby check (screening in the UK) shows: - reduced range of motion - Barlow, Ortolani and Galeazzi tests show DDH
57
what are the findings in a baby check of a patient with DDH?
reduced RoM Barlow, Ortolani, Galeazzi tests shows DDH
58
what is the primary method of investigation for DDH?
ultrasound (up till 4 months) | for 4+ months = usually X-ray
59
how is DDH treated?
reducible hip and <6 months = Pavlik harness harness fails/6-18 months = surgical intervention (MUA, closed reduction, Spica cast)
60
in patients where a Pavlik harness fails, how is DDH treated?
surgical intervention (MUA, closed reduction, Spica cast)
61
why is ultrasound the preferred method of investigation for DDH?
shows hip positioning AND acetabular dysplasia/angles
62
what is clubfoot?
congenital bilateral deformity of the foot occurs in utero
63
what are the risk factors for clubfoot?
male (Hawaiian) family history genetics = PITX1 gene
64
what is CAVE deformity in clubfoot?
deformity seen in clubfoot due to excessive muscle contracture Cavus = high arch; intrinsic foot muscles, FDL, FHL Adductus = tibialis anterior + posterior Varus = tight tendinoachilles, tibilaise anterior + posterior Equinous = tight tendinoachilles
65
what causes the CAVE deformity in clubfoot?
muscle contracture
66
how is clubfoot treated?
1) Ponseti method = series of casts to correct deformity (gold standard) 2) operative treatments - soft tissue release - foot orthosis brace 3) further operative intervention - soft tissue release - tendon transfers
67
what is the gold standard treatment for clubfoot?
Ponseti method = series of casts to correct deformity
68
what operative interventions are offered for clubfoot?
soft tissue release foot orthotic braces (maybe even tendon transfers)
69
what is the most common skeletal dysplasia?
achondroplasia
70
what kind of genetic abnormality is achondroplasia?
autosomal dominant
71
how does achondroplasia manifest?
rhizomelic dwarfism - humerus < forearm - femur < tibia (normal trunk + normal cognitive development BUT significant spinal issues)
72
why does achondroplasia cause rhizomelic dwarfism?
achondroplasia = inhibition of chondrocyte proliferation in the proliferative zone of the epiphyseal growth plates = impaired secondary endochondral ossification = impaired interstitial bone growth = rhizomelic dwarfism
73
what is the normal adult height for patients with achondroplasia?
approx 125cm
74
what is osteogenesis imperfecta?
brittle bone disease due to impaired collagen production autosomal dominant or recessive
75
what happens to type I collagen in osteogenesis imperfecta?
1) quantitative problem = reduce synthesis of type I collage 2) qualitative problem = abnormal type I collagen produced = both result in decreased osteoid secretion SO brittle bones
76
what are the orthopaedic manifestations of osteogenesis imperfecta?
fragility fractures short stature scoliosis (spinal manifestation)
77
what are the non-orthopaedic manifestations of osteogenesis imperfecta?
cardiac problems blue scelera dentinogenesis imperfecta (soft, brown teeth) hypermetabolism (via PTH pathway) Wormian skull (impaired fusion of skull sutures)
78
what does a fracture pattern indicate?
the way the energy is dissapated through the bone
79
children's bones are more elastic - what is the implication of this?
more scope for plastic deformity = more likely to be deformed than be fractured unless force of injury very high
80
name some common fracture patterns
``` simple transverse oblique spiral comminuted avulsion greenstick buckle/torus ```
81
what is an oblique fracture?
the break has a curved or sloped pattern
82
what is a transverse fracture?
the broken piece of bone is at a right angle to the bone’s axis
83
what is a spiral fracture?
the bone is broken with a twisting motion
84
what is a comminuted fracture?
the bone breaks into several pieces
85
what is an avulsion fracture?
when a fragment of bone is separated from the main mass
86
what is the difference between open and closed fractures?
open = broken the skin (compound fracture) closed = under the skin (simple fracture)
87
how do you describe where in the bone the fracture has occurred?
proximal 1/3 middle 1/3 (diaphysis) distal 1/3
88
if in children, there is a fracture of the proximal or distal 1/3, why does the approach change?
in the proximal and distal 1/3s of children's long bones = secondary ossification centres AND epiphyseal growth plates = must assess extent of damage to these
89
define intra-articular and extra-articular fractures
intra-articular = fractures that extend into the joint extra-articular = fractures that do not extend into the joint
90
which is the preferred form of healing at intra-articular fractures?
primary (intramembranous) bone healing
91
which is the preferred form of healing at extra-articular fractures?
secondary (endochondral) bone healing
92
why is primary bone healing preferred for intra-articular fractures?
lack of callus formation prevents inflammation in the joint = reduces the risk of post-traumatic arthritis
93
what are the ways in which a bone can be displaced?
displaced angulated rotated shortened
94
which type of displacement is best tolerated by children's bones?
in the angle of function | i.e. displaced, angulated, shortened but NOT rotated
95
which type of displacement is tolerated least/not at all by children's bones?
rotated fractures not tolerated very well despite the huge remodelling potential of children's bones
96
how are physeal injuries classified?
Salter-Harris classification
97
injuries to which part of the bone are most dangerous in children's bones?
physis
98
explain Salter-Harris classification
type I-V risk of growth arrest increases with classification based on SALT 1) physeal (Separation) 2) fracture traverses physis and exits metaphysis (Above) 3) fracture traverses physis and exits epiphysis (Lower) 4) fracture passes (Through) epiphysis, physis, metaphysis 5) crush injury to physis
99
describe type I physeal injuries
physeal separation (S)
100
describe type II physeal injuries
fracture goes through physis and metaphysis (above)
101
describe type III physeal injuries
fracture goes through physis and epiphysis (lower)
102
describe type IV physeal injuries
fracture goes through epiphysis, physis and metaphysis (all)
103
describe type V physeal injuries
crush injury to physis
104
how does the risk of growth arrest change with physeal classification?
risk of growth arrest increases from type 1 -5
105
which type of physeal injuries are most common?
type II physeal injuries = above the physis i.e. physis + metaphysis
106
why is type V physeal injury the most dangerous for children?
crush injury to the complete physis = can significantly impair/inhibit secondary endochondral ossification = impaired interstitial bone growth = stunted long bone growth
107
which two factors affect growth arrest in physeal injury?
location of injury timing of injury
108
how does timing affect growth arrest in physeal injury?
older bone - closer to physeal closure = small amount of growth potential left to affect = reduced growth arrest younger bone - physis very active = greater amount of growth potential affected = more growth arrest
109
how does location affect growth arrest in physeal injury?
whole physeal injury = limb length discrepancy whole physeal injury = angular deformity
110
why is there an angular deformity in partial physeal injury?
non-affected side keeps growing
111
what are the two ways in which growth arrest can be treated?
1) minimise limb length discrepancy | 2) minimise angular deformity
112
how can limb length discrepancy be minimised in growth arrest?
shorten the long side (cross-nails to prematurely fuse physes) lengthen the short side (limb-lengthening device)
113
how can angular deformity be minimised in growth arrest?
stop growth on unaffected side reform bone (surgical intervention, osteotomy)
114
what are two ways growth arrest can manifest?
limb length discrepancy angular deformity
115
what are the four Rs of paediatric fracture management?
resuscitate, reduce, restrict/, rehabilitate
116
when reducing the fractures, what must you also do?
assess neurovascular status (!!!!!) = reduce secondary injury to soft tissue and neurovascular structures
117
what is open reduction?
realignment of the fracture under direct visualisation | e.g. mini-incision, full exposure
118
what is closed reduction?
realigning a fracture but without making an incision | e.g. traction, manipulation
119
give examples of closed reduction in paediatrics
1) applying a plaster (A&E or MUA in theatre) | 2) Gallows traction = skin traction applied to the femur to hold the long bones
120
why do we restrict/hold fractures?
provides stability for the fracture to heal
121
fracture holding can be fixation with metal or closed - which one is preferred in children and why?
remodeling and huge healing potential means that operative fixation (open holding) often can be avoided = so tend to use plasters and splints to hold
122
when may operative intervention/fixation be required to hold a fracture in children?
1) when the physis is compromised and there is an increased risk of growth arrest 2) fracture is beyond tolerance of remodelling
123
what must happen in children if metal is used to fixate and hold the reduced fracture?
metalwork must be removed at a later date
124
how does rehabilitation occur in children's fractures?
use, move, strengthen, weight bear | physio not usually required
125
what are the main differentials for a limping child?
1) septic arthritis (!!!!) transient synovitis perthes SUFE
126
what is septic arthritis?
presence of infection in intraarticular space - necrotic effect of proteases - pressure effect on the chondrocytes and cartilage due to oedema in the closed space = irreversible, long-term damage in the joint
127
how is septic arthritis treated?
surgical washout of the joint to clear the infection
128
how is septic arthritis classified?
``` Kocher's classification - non-weight-bearing - ESR > 40 - WBC > 12,000 - temperature > 38 (fever) = NEWT ``` = more of the above features present, the more likely the diagnosis of septic arthritis is
129
what are the key features of a septic arthritis history?
duration other recent illness associated joint pain & symptoms
130
what in the history indicates septic arthritis in the child?
child was previously well BUT now, off food/drink cannot move leg/hip fever = classic indicators of a septic arthritis kid
131
what is the most likely diagnosis if not septic arthritis?
transient synovitis | diagnosis of exclusion
132
what is transient synovitis?
inflammation of the joint in response to a systemic illness = associated muscle pain
133
how is transient synovitis treated?
supportive management | = fluids, antibiotics, observations
134
what is Perthes disease and who does it affect the most?
idiopathic necrosis of the proximal femoral epiphysis - males > females - ages 4-8
135
what must be excluded before diagnosing Perthes disease?
septic arthritis
136
how is Perthes differentiated from septic arthritis?
Perthes - more chronic: goes on for longer - cannot see the temperature + inflammatory markers seen in septic arthritis
137
what is the investigation of choice for Perthes disease?
plain film radiograph
138
how is Perthes disease treated?
supportive treatment referral to specialist for continuous observation and management
139
what is SUFE?
slipped upper femoral epiphysis = when the proximal epiphysis slips in relation to the metaphysis
140
which group is affected most by SUFE?
obese adolescent male | 12-13 year olds during rapid growth
141
what are the risk factors for SUFE?
family history endocrine underlying disorder (hypothyroidism, hypopituitarism) overweight male
142
what must be excluded before diagnosing SUFE?
septic arthritis
143
what are the classifications of SUFE?
acute chronic acute on chronic (history of limping in past but worse suddenly)
144
how is SUFE treated?
operative internal fixation 1) to prevent further slippage 2) to minimise long term growth problems and reduce risk of growth arrest (as physis can be affected)
145
how is SUFE differentiated from septic arthritis?
SUFE - not as acute as septic arthritis - cannot see the temperature + inflammatory markers seen in septic arthritis
146
what is the main differential for a limping child?
SEPTIC ARTHRITIS (!) = must be excluded before moving onto anything esle
147
how are paediatric fractures described?
``` P = pattern P = pieces (simple/fragmented) A = anatomy (where?) I = intra/extraarticular D = displacement, angulated, rotated, shortened S = Salter-Harris ```

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