children's orthopaedics Flashcards

1
Q

how are flat bone developed -just name

A

intramembranous mesenchymal cells-> bone

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2
Q

how are long bone developed- just name

A

endochondral mesenchymal -> cartilage -> bone

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3
Q

steps of intramembranous ossification

A
  1. condensation of mesenchymal cells-> differentiate into osteoblasts and form ossification centre
  2. secreted osteoid traps osteoblast which becomes osteocytes
  3. trabecular matrix and periosteum form
  4. compact bone develops superficial to cancellous bone. Blood vessels condense into red bone marrow
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4
Q

what is primary ossification centres of long bone formation- and when does it occur

A

pre-natal bone growth through endochondral ossification from central part of bone

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5
Q

what is secondary ossification centres of long bone formation

A

post-natal after primary ossification centre.

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6
Q

steps of endochondral primary ossification

A
  1. mesenchymal differentiation at primary ossification centre (POC) (in middle of bone diaphysis)
  2. cartilage model of future bony skeleton forms
  3. capillaries penetrate cartilage
    a)calcification at POC form spongy bone
    b)perichondrium transforms into periosteum
  4. cartilage and chondrocytes continue to grow at bone ends
  5. secondary ossification centre develops
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7
Q

secondary endochondral ossification steps

A

Long bone lengthening at physis

Epiphyseal side – hyaline cartilage divide, forming hyaline cartilage matrix

Diaphyseal side – Cartilage calcifies+ dies. Then replaced by bone

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8
Q

difference between children’s and adults skeleton

A

elasticity
physis
healing speed
remodelling

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9
Q

3 issues with elasticity

A

Plastic deformity
– Bone deformity persists after force removed.- no cortices fractured

Buckle fracture
– One side of the bone bends, raising a little buckle, without breaking the other side of the bone.

Greenstick
One cortex fractures but does not break the other side

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10
Q

cause of increased elasticity

A

Increased density of haversian canals

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11
Q

age of girl and boy when growth stops and physis closes

A

Girls 15-16
Boys 18-19

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12
Q

what can physeal injuries lead to

A

growth arrest and deformity

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13
Q

what is developmental dysplasia of the hip

A

head of the neonatal femur is unstable to the acetabulum

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14
Q

risk factor of DDH

A

female
first born
breech

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15
Q

DDH:
Examination and investigation

A

baby check

US-0-4month
x-ray-after 4 months

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16
Q

DDH treatment

A

pavlik harness 6months

if failed/6-18months:
MUA+ closed reduction and spica

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17
Q

proper name for clubfoot and cause

A

congenital talipes equinovarus

deformity from muscle contracture

18
Q

gene cause and commonest ethnicity to have club foot (congenital talipes equinovarus)

A

PITX1 gene
Hawaiians

19
Q

symptoms of clubfoot

A

CAVE
Cavus –high arch
Adductus of foot: Tight tib post and ant
Varus: Tight tendoachillies,
Equinous(toe pointing down): tight tendoachilles

20
Q

clubfoot treatment

A

ponseti method- series of casts to correct deformity

21
Q

what is achondroplasia

A

G380 mutation ofFGFR3 gene

inhibition of chondrocyte proliferation in physis

defect in endochondral bone formation

22
Q

signs of achondroplasia

A

Rhizomelic dwarfism

Humerus shorter than forearm
Femur shorter than tibia
Normal trunk
Adult height of approx. 125cm

23
Q

osteogenesis imperfecta (brittle bone disease)
cause

A

decrease T1 collagen
-less secretion/abnormal collagen production

leading to insufficient osteoid production

24
Q

effects of osteogenesis imperfecta on bone and non-ortho symptoms

A

Bones
Fragility fractures, Short stature, Scoliosis

Non-orthopaedic
Blue Sclera, brown soft teeth
Hypermetabolism

25
Q

paediatric fractures checklist

A

PAID
pattern
anatomy
intra/extra-articular
Displacement

salter-harris

26
Q

5 types of pattern in PAID

A

transverse
oblique
spiral
comminuted
avulsion

green stick
plastic deformity
buckle fracture

27
Q

anatomy in PAID

A

Ie. name of bone, proximal third, middle third or distal third

28
Q

intra/extra-articular of PAID–what kind of bone healing is preferred and why

A

Primary bone heading
-preferred in intra-articular fracture as minimise risk of post traumatic arthritis

secondary bone healing
-healing by callus

29
Q

4 types of displacement in PAID

A

displaced
angulated
shortened
rotated

30
Q

salter Harris classification for physeal injuries

A
  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
31
Q

growth arrest risk in relation to salter harris and most common type

A

risk increases from 1 to 5

type2 = most common

32
Q

growth arrest of whole physis vs partial

A

Whole physis – limb length difference

Partial – angulation as the non affected side keeps growing

33
Q

growth arrest treatment

A

limb length correction
a) shorten long side
b) lengthen short side

angular deformity
a)stop growth of unaffected side
b) reform bone (osteotomy)

34
Q

reduce- example of closed reduction

A

gallows traction - holding skin- long bone of lower limb can be reduced

35
Q

preferred restrict method

A

external -splints/plaster are preferred over internal

as kids have a great healing potential

36
Q

septic arthritis treatment

A

surgical washout of the joint to clear the infection

37
Q

septic arthritis- kocher’s classification

A

non weight bearing
ESR 40+
WBC 12,000+
Temp 38+

38
Q

transient synovitis diagnosis and treatment

A
  1. exclude septic arthritis

Is a inflamed joint in response to a systemic illness

antibiotics

39
Q

perthes disease

A

Idiopathic necrosis of the proximal femoral epiphysis

Usually 4-8 years old boys.
doesn’t affect 10+

40
Q

SUFE- commonest in? Associated with?
Treatment?

A

Obese adolescent male
10+ (12-13 y.o)

associated with hypothyroidism/hypopituitarism

treat: operative fixation to prevent further slip and minimise LT growth issues