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Peadiatrics > Msk Disorders > Flashcards

Msk Disorders Flashcards

1
Q

How common is developmental dysplasia of the hip? What is included in DDH?

A

5/100

Dislocated hips - other acetabular dysplasia (where femoral head is in position but acetabulum is shallow)

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2
Q

Screening of DDH ? Manoeuvres called? Why are they unhelpful tests as the baby gets older?

A

Screened at birth and at 6 weeks
Barlow’s / ortolani’s
Contractures form

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3
Q

What are the warning signs (features) of DDH

A

Delayed walking
painless limp
Waddling gait

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4
Q

What two features are common in babies and do not represent DDH? How common?

A

Asymetrical skin creases -30% of all infants

Hip clicks - 10%

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5
Q

How is a diagnosis of DDH made?

A

uss is diagnostic
Femur may be shortened - Allis sign
O/e - limited abduction

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6
Q

What level of hip abduction should be achieved by children? Up to what age?

A

Supine children should be able to abduct a flexed hip fully until 2 years old

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7
Q

Why are X-Ray’s not useful for diagnosis of DDH

A

Femoral head doesn’t ossify until 4/12 (becomes useful then)

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8
Q

Management of DDH in

A
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9
Q

How often does a harness for DDH have to be worn? How often is it adjusted?

A

Constantly

Every 2 weeks

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10
Q

What happens if there is accelerated degenerative changes in DDH?

A

Open surgery

Often have total hip replacement in early adult life

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11
Q

What is (legg-calve-) perthes disease ? What happens? How long does it take?

A

Osteonecrosis of the skeletal head prior to skeletal maturity.
Idiopathic ischemia -> avascular necrosis at the upper femoral epiphysis with flattening and fragmentation of the femoral head.
Revascularisation & reossification occur and growth resumes (may not be normal)
3-4 years

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12
Q

Risk factors leg-calve-perthes disease?

A

Males 5:1

Family Hx

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13
Q

Features / presentation of leg clave perthes disease

A
  • insidious* onset of lump (+/- hip pain) between 3 and 12 years -> pain may be felt in hip, thigh or knee
  • Abduction and rotation are limited O/E*
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14
Q

Diagnosis of legg calve perthes

A

Hip X-ray - shows decreased height (flattening) and increased density of femoral head

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15
Q

Can you have more than one hip affected in LCP disease

A

Bilateral in 20%

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16
Q

Management in LCP disease if

A

Prognosis is good

Bracing with analgesia & mild activity restriction

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17
Q

Prognosis / Management of LCP in older children / more than 1/2 femoral head involved

A

Permanent deformity in 40% with early degenerative arthritis/
Several surgical options

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18
Q

What is transient synovitis often called

A

Irritable hip

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19
Q

Usual course of transient synovitis

A

Self limiting. Common esp in children 2-12yrs following viral URTI

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20
Q

Features of transient synovitis ? O/e?

A

Sudden onset hip pain (NON AT REST), limp and refusal to weight bare on affected side.
Limited abduction / rotation in otherwise well afebrile child

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21
Q

What is the key differential to transient synovitis ? When should this be queried ?

A

Septic arthritis

Febrile with pain at rest & refusal to even move affected joint

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22
Q

Why do you investigate transient synovitis ? What do you use to make a diagnosis?

A 
To exclude septic arthritis
Acute phase reactants - CRP, WBC, ESR (only *mildly raised*)
Blood cultures - should be *-ve*
X-ray hip - normal
Hip USS - may be small effusion
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23
Q

Management of transient synovitis

A

Supportive - bed rest and analgesia

Should resolve spontaneously in 2 weeks

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24
Q

What is slipped upper femoral epiphysis (SUFE)

A

Displacement of the epiphysis of the femoral head posterio-inferiorly

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25
Q

When does SUFE most commonly occur? In who?

A

10-15 (usually occurs around growth spirt / minor trauma)
Male (black / obese)
Delayed skeletal maturation & endocrine disorders
Family Hx

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26
Q

Presentation of SUFE ? O/e?

A

limp or with referred hip / knee pain

O/e - restricted abduction & internal rotation of hip

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27
Q

Diagnosis / treatment of SUFE

A

Hip X-ray (may require frog leg lateral view)

Surgical - usually pin fixation

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28
Q

2 common knee disorders (male / female)

A

Osgood - schlatter (physically active males)

Chondromalacia patellae - adolescent females

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29
Q

When should back pain be referred ?

A

Before adolescence - ?significant pathology

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30
Q

Causes of back pain in adolescence

A

Muscle spasm / soft tissue injury
Schearmann’s disease
Spondylolisthesis / spondylolisis
Tumours

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31
Q

Usual cause of muscle spasm / soft tissue injury

A

Sports

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32
Q

What is shearmanns disease ? Features?

A

Osteochonditis (avascular necrosis of ossification centre) of lower thoracic vertebrae)
Localised pain, tenderness, kyphosis

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33
Q

Usual location of spondylo- things ? What happens if there is anterior shift of the vertebral body?

A

L4/5

*lower back pain exacerbated by bending backwards (spondylisthesis)

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34
Q

What is scoliosis ? How many children affected?

A

Lateral deformity of the spine with rotational deformity

4%

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35
Q

How is scoliosis classified ? Egs?

A 
Vertebral abnormalities (eg. Ostegenesis imperfecta / hemivertebra)
Neuro muscular (eg. Polio / cerebral palsy)
Mischellaenous (eg. Idiopathic (most common) / dysmorphic syndromes)
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36
Q

What is hemivertebra

A

Lack of formation of one half of the vertebral body

37
Q

How can you demonstrate rotation in scoliosis

A

Child bends forwards - rib hump noted

38
Q

When does idiopathic scoliosis occur ? Who is it more common in ?

A

85% in adolescence

Females with FHx

39
Q

Management of various idiopathic scoliosis

A

Mild - none
Moderate - brace
Severe - surgery

40
Q

What is torticollis also called? Who is it usually in? What is the usual cause? Prognosis?

A

Wry neck - head turned persistently to one side
Common, self limiting in young children (often with URTI)
sternomastoid tumour
Usually resolves in 1 year

41
Q

What is osteomyelitis

A

Infection of the metaphysis of long bones - any bone can be affected

42
Q

When can osteomyelitis cause septic arthritis

A

When joint capsule is inserted distal to the epiphysis (eg. The hip)

43
Q

Usual cause of osteomyelitis

A

Haematogenous spread

Can occur directly from infected wound

44
Q

Usual pathogen in osteomyelitis ? Neonates?

A

Staph aureus (group B strep and E.coli in neonates)

45
Q

What disease has an increased risk of osteomyelitis and which types

A

Staphylococcal & salmonella osteomyelitis

In Sickle cell disease

46
Q

Features of osteomyelitis

A

Painful and immobile limb (pseudoparesis) in a febrile child
O/e - erythermatous, warm, swollen, and very tender

47
Q

How does osteomyelitis present in infants

A

More insidious, swelling and decreased limb movements

48
Q

Investigations in osteomyelitis

A

Acute phase reactants raised - CRP, ESR, WCC
Blood cultures - +ve in 50%
X-rays - takes 7-10 days

49
Q

What to do if +ve blood cultures in osteomyelitis

A

Joint aspiration for M, C & S

50
Q

What is seen on X-ray 7-10 days after infection? What can be done initially?

A

Subperiosteal elevations & localised decreased density.

Radionuclide scans can be used to elicit a likely site of infection (as there is increased uptake)

51
Q

Treatment of osteomyelitis

A

IV Abx until there is clinical recovery & acute phase reactants normalise followed by oral therapy for several weeks.
Surgical drainage if unresponsive to Abx

52
Q

Complications of osteomyelitis

A

Septic arthritis, growth disturbance & limb deformity (if epiphyseal plate infected)

53
Q

What is septic arthritis ? Vs OM more common?

A

Infection of the joint space

Yes it’s more common

54
Q

What can septic arthritis lead to ?

A

Disability and bone destruction

55
Q

Usual age for septic arthritis? Origin? How many joints? Usual cause?

A
56
Q

Features of septic arthritis

A

Painful joint -> limp, irritability, refusal to bear weight

Limb is held rigid (pseudoparesis) with tenderness and varying degrees of swelling / warmth

57
Q

Investigations for septic arthritis

A

Elevated acute phase reactants
Aspiration of joint for M, C & S
USS - can show effusions
X-rays - exclude trauma & other bony lesions

58
Q

Management of septic arthritis

A

Early and prolonged IV Abx

Surgical drainage - if recurrent or hip affected

59
Q

What is the most common childhood arthritis

A

Reactive

60
Q

What are the features of reactive arthritis

A

Transient joint swelling

61
Q

Usual cause of reactive arthritis ? Other causes?

A

Bacterial - salmonella, shigella, campylobacter, versilsia

Viral - rubella, parvovirus B19, influenza, herpes, cozsackie

62
Q

What is juvenile idiopathic arthritis

A

Children and adolescents with persistent joint swelling >6 weeks in the absence of infection or any other defined cause

63
Q

What are the types of JIA? What is the classification according to ?

A

Oligoarthrits 4, systemic (Still’s disease), psoriatic arthritis, enthesitis
RF/HLA B27

64
Q

Who gets affected by still’s disease ? Where does it affect? What are the other features ?

A

<5
hips, ankles, knees,

High fever, salmon pink rash, lymphadenopathy, myalgia, malaise
NO ARTHRITIS INITIALLY

65
Q

Seen on investigations for still’s disease?

A

Anaemia on FBC
Neutrophilia
Increased acute phase reactants

66
Q

Two types of polyarthrits and prognosis

A

RF -ve - good prognosis

RF +ve - Bad prognosis

67
Q

RF -ve polyarthrits joints affected ? Ages?

A

All ages and all joints
typically (not always) spares MCP joints
Cervical spine and TMJ’s may be involved

68
Q

Who is usually affected by RF +ve polyarthrits ? Which joints are affected? Other features?

A

Females >8
small joints of hands and feet (hip and knee also affected)
Early rheumatoid nodules in 10%, might be systemic vasculitis

69
Q

Who is usually affected by oligoarthrits ? Type of arthritis ? Affecting?

A

*Girls

70
Q

Investigations for oligoarthrits

A

Increased acute phase reactants

ANA (antinuclear antibodies) are almost always present

71
Q

Associations with oligoarthrits

A

1/3 will develop chronic iridocyclitis (uveitis)

72
Q

What happens if >4 joints are affected after 6/12 in oligoarthrits

A

Called ‘extended oligoarthrits ‘ - poor prognosis

73
Q

Management of JIA

A

MDT
1- Physiotherapy to optimise joint mobility, prevent deformity and increase muscle strength
2- medication -analgesia and reduced inflammation (NSAIDs), systemic steroids for severe disease / severe uveitis, methotrexate used early to reduce joint damage

74
Q

Egs of primary bone diseases

A

Achondroplasia, osteopetrosis, osteogenesis imperfecta

75
Q

What is the cause of achrondroplasia

A

Autosomal Dominant
Chromosome 4
*fibroblase growth factor gene (FGFR3)
(Half are new mutations)

76
Q

Clinical features of achondroplasia

A

Limbs - shortened (proximal>distal), bow legs (genu varum)
Neurological - hydrocephalus, delayed motor development, normal intelligence
Spine - short, lumbar lordosis, throacolumbar kyphosis
Ear - recurrent otitis media

77
Q

What is the other name for osteopetrosis ? What is it?

A

Marble bone disease

Hyper density of bones due to osteoclasts dysfunction - deficient carbonic anhydrase - bones are very brittle

78
Q

What is osteogenesis imperfecta often called ? What causes it? What are the characteristics?

A

Brittle bone disease
Group of disorders caused by mutations in type 1 collagen genes
fragile bones & frequent fractures

79
Q

What are the normal genes for mutation in osteogenesis imperfecta

A

COL1A1 / 1A2 genes in 90%

80
Q

Types of osteogenesis imperfecta

A

1- most common, autosomal dominant
2- lethal, usually multiple fractures before birth (often stillborn)
3- severe, progressively bone deformities, survival to adulthood rare
4 - moderate, bone fragility without other features of type 1

81
Q

How does type 1 osteogenesis imperfecta present ?

A

Recurrent fractures, blue tinged sclerae, sometimes hearing loss

82
Q

Management of osteogenesis imperfecta

A

BisPhosphonates - strengthens bone bit doesn’t areas underlying problem

83
Q

What is rickets

A

Failed mineralisation of growing bones

84
Q

What are the X-ray changes of rickets

A

Cupping of ends of bones
Splaying
Osteopenia

85
Q

What are the clinical findings in rickets

A

Bow legs, wide wristed with delayed motor development due to associated myopathy
Rickettic rosary

86
Q

What is rickettic rosary

A

Prominent knobs of bone at costochrondiral joints (ribs)

87
Q

Causes of rickets

A 
Vit d deficiency (nutritional, 1a-hydroxylase deficiency)
Phosphate deficiency (usually due to poor renal absorption 
Calcium deficiency
88
Q

What’s seen in bloods of rickets

A

Decreased - serum 25-OH vit D, phosphate

Increased - PTH, alkaline phosphatase

89
Q

Treatment of rickets

A

Vitamin D- calcitriol

Calcium in infants

Peadiatrics (14 decks)

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