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Z Year 2 BRS MSK > Childrens Orthopaedics > Flashcards

Childrens Orthopaedics Flashcards

1
Q

What is the paediatric skeleton?

A

the paediatric skeleton and musculoskeletal system is NOT a miniaturised version of an adult

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2
Q

How many bones are in a child’s skeleton?

A
  • 270 bones

- a system that is in continuous change

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3
Q

What are the physis?

A
  • (growth plates) are the areas from which long bone growth occurs post-natally
  • Most long bones have 2 physis one proximally and one distally
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4
Q

What are the 2 types of bone development?

A
  1. Intramembranous

2. Endochondral

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5
Q

What is intramembranous bone development?

A
  • mesenchymal cells -> bone

- flat bones

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6
Q

What is endochondral bone development?

A
  • mesenchymal -> carilgae -> bone

- long bones

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7
Q

What is intramembranous ossification?

A
  1. Condensation of mesenchymal cells which differentiate into osteoblasts – Ossification centre forms
  2. Secreted osteoid traps osteoblasts which become osteocytes
  3. Trabecular matrix and periosteum form
  4. Compact bone develops superficial to cancellous bone
    - Crowded blood vessels condense into red bone marrow
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8
Q

When does intramembranous ossification happen?

A

-Development of Flat Bones -cranium and clavicle

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9
Q

Where does long bone formation happen?

A

the primary and secondary ossification centres

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10
Q

What are primary ossification centres?

A
  • sites of pre-natal bone growth through endochondral ossification from the central part of the bone
  • middle ofdiaphysis of the bone - prenatal
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11
Q

What are secondary ossification centres?

A

Occurs post-natal after the primary ossification centre and long bones often have several (the physis)

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12
Q

What happens to the tissue during endochondral ossifcation?

A

the tissue that will become bone is firstly formed from cartilage

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13
Q

What are the stages of endochrondral primary ossifcation?

A
  1. Mesenchymal Differentiation at the primary centre
  2. The cartilage model of the future bony skeleton forms
  3. Capillaries penetrate cartilage
  4. Calcification at the primary ossification centre – spongy bone forms
  5. Perichondrium transforms into periosteum
  6. Cartilage and chondrocytes continue to grow at ends of the bone
  7. Secondary ossification centres develop
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14
Q

What happens at secondary ossification centres?

A
  1. Post bone growth through Secondary ossification centres
    “The Physis’
  2. Long bone lengthening
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15
Q

Where does long bone lengthening happen?

A

at the physis (physeal plate)

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16
Q

What is the physis?

A
  • Zone of elongation in long bone

* Contains cartilage

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17
Q

What happens at the epiphyseal side?

A

hyaline cartilage active and dividing to form hyaline cartilage matrix

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18
Q

What happens at the disphyseal side?

A

Cartilage calcifies and dies and then replaced by bone

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19
Q

What can children bones do?

A

-Children’s bone can bend – more elastic than adult

•Increased density of haversian canals

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20
Q

What does this elasticity mean?

A
  • Plastic deformity
  • Buckle fracture
  • Greenstick
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21
Q

What is plastic deformity?

A

bends before breaks

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22
Q

What is buckle fracture?

A

Tarus like the column

23
Q

What is a greenstick fracture?

A
  • like the tree

- One cortex fractures but does not break the other side

24
Q

How does growth vary?

A
  • Growth occurs at varying rates at varying sites
  • Growth stops as the physis closes
  • Gradual Physeal closure, Puberty, Menarche, Parental height
25
Q

When does physis closure complete for girls?

A

15-16

26
Q

When does physis closure complete for boys?

A

18-19

27
Q

How are physeal injuries categorised?

A

by Salter-Harris

28
Q

What can physeal injuries lead to?

A

growth arrest

29
Q

What can growth arrest lead to?

A

deformity

30
Q

What is the speed of healing and remodelling potential dependent on?

A
  • The speed of healing and remodeling potential is dependent on the location and the age of the patient
  • Younger child heals more quickly
31
Q

Which physis grow more?

A
  • Physis at the knee grows more

* Physis at extreme of upper limb grows more

32
Q

What are some commin children’s congenital conditions?

A
  1. Developmental dysplasia of the hip
  2. Club foot
  3. Achondroplasia
  4. Osteogenesis imperfecta
33
Q

What is developmental dysplasia of the hip?

A
  1. Group of disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
  2. A ‘Packaging Disorder’ (IN UTERO)
  3. The normal development relies on the concentric reduction and balanced forces through the hip
34
Q

What is the spectrum with dysplasia?

A
  1. Spectrum with dysplasia – subluxation – dislocation
  2. Dysplasia 2: 100 Dislocation 2:1000
    - progressive
35
Q

What are the risk factors in developmental dysplasia of the hip?

A
  • Female 6:1
  • First born
  • Breech
  • FH
  • Oligohydramnios
  • Native American/Laplanders – swaddling of hip
  • Rare in African American/Asian
36
Q

What is the examination for developmental dysplasia of the hip?

A

-Usually picked up on baby check – screening in UK
1. RoM of hip
•Usually limitation in hip abduction
•Leg length (Galeazzi)
2. In those 3 months or older Barlow and Ortalani are non-sensitive

37
Q

What is the investigation for developmental dysplasia of the hip?

A
  1. Ultrasound – birth to 4 months
    •After 4 months X-ray
    •If prior to 6 weeks needs to be age adjusted
  2. Measures the acetabular dysplasia and the position of hip
38
Q

What is the treatment for developmental dysplasia of the hip if there is reducible hip and <6 months?

A

Pavlik harness 92% effective

39
Q

What is the treatment for developmental dysplasia of the hip if failed Pavlik Harness or 6-18 months?

A
  1. Secondary changes- capsule + soft tissue

2. MUA + Closed reduction and Spica

40
Q

What is congenital talipes equinovarus?

A
  • Congenital deformity of the foot (clubfoot)
    1. 1:1000
    2. Highest in Hawaiians
    3. M2:1F
    4. 50% are bilateral
41
Q

What are the causes of congenital talipes equinovarus?

A
  1. Genetic
  2. Approx. 5% likely of siblings
  3. Familial in 25%
  4. PITX1 gene
42
Q

What is the CAVE deformity due to muscle contracture?

A
  1. Cavus –high arch: tight intrinsic, FHL, FDL
  2. Adductus of foot: Tight tib post and ant
  3. Varus: Tight tendoachillies, tib post, tib ant
  4. Equinous: tight tendoachilles
43
Q

What is the treatment for clubfoot?

A

Ponseti Method

44
Q

What is the ponseti method?

A

Gold standard

  1. First a series of casts to correct deformity
  2. Many require operative treatment
    - Soft tissue releases
  3. Foot orthosis brace
  4. Some will require further operative intervention to correct final deformity
45
Q

What is achondroplasia?

A
  • The most common skeletal dysplasia

- Autosomal Dominant

46
Q

What is the cause of achondroplasia?

A
  1. G380 mutation ofFGFR3
  2. inhibition of chondrocyte proliferation in theproliferative zoneof thephysis
  3. results in defect in endochondral bone formation
47
Q

What are the symptoms of rhyzomelic dwarfism?

A
  1. Humerus shorter than forearm
  2. Femur shorter than tibia
  3. Normal trunk
  4. Adult height of approx. 125cm
    - Normal cognitive development
    - Significant spinal issues
48
Q

What is osteogenesis imperfecta?

A

Brittle bone disease

49
Q

What are the causes of osteogenesis imperfecta?

A

Hereditary – autosomal dominant or recessive

50
Q

Why is there decreased type 1 collage in osteogenesis imperfecta?

A

•Decreased secretion
•Production of abnormal collagen
-leads to Insufficient osteoid production

51
Q

What are the effects of osteogenesis imperfecta on the bones?

A
  • Fragility fractures
  • Short stature
  • Scoliosis
52
Q

What are the non-orthopeadic manifestations of osteogenesis imperfecta

A 
•Heart
•Blue Sclera
•Dentinogenesis imperfecta – brown soft teeth
•Wormian skull
-hypermetabolism
53
Q

How does a children’s skeleton differ to that of an adult?

A
  1. Elasticity
  2. Physis
  3. Speed of healing
  4. Remodelling

Z Year 2 BRS MSK (18 decks)

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