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3a paeds > Paeds MSK > Flashcards

Paeds MSK Flashcards

1
Q

What is Osteogenesis imperfecta

A

Genetic condition (auto dom) that results in brittle bones that are prone to fractures

affect formation of collage

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2
Q

what type of collagen is affected in MC form of Osteogenesis imperfecta

A

type 1 collage

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3
Q

how does Osteogenesis imperfecta present

A
  • presents in childhood
  • fractures following minor trauma
  • blue sclera
  • deafness secondary to otosclerosis
  • dental imperfections are common
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4
Q

how is Osteogenesis imperfecta managed medically

A

Bisphosphates to increase bone density
Vitamin D supplementation to prevent deficiency

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5
Q

What do blood results for Osteogenesis imperfecta show

A

adjusted calcium, phosphate, parathyroid hormone and ALP results are usually normal in osteogenesis imperfecta

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6
Q

How is Osteogenesis imperfecta managed by MDT team

A

Physiotherapy and occupational therapy to maximise strength and function
Paediatricians for medial treatment and follow up
Orthopaedic surgeons to manage fractures
Specialist nurses for advice and support
Social workers for social and financial support

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7
Q

what is collagen

A

protein that is essential is maintaining the structure and function of bone, as well as skin, tendons and other connective tissues.

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8
Q

What is rickets

A

defective bone mineralisation causing “soft” and deformed bones

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9
Q

what causes rickets

A

deficiency in vitamin D or calcium

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10
Q

what are nutritional sources of Vit D

A

eggs, oily fish or fortified cereals

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11
Q

what are nutritional sources of calcium

A

diary
leafy greens
nuts

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12
Q

what is hereditary hypophosphataemic rickets

A

commonly x linked

genetic defects that result in low phosphate in the blood

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13
Q

what is Vitamin D

A

hormone (not technically a vitamin) created from cholesterol by the skin in response to UV radiation

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14
Q

what can lead to vitamin D deficiency.

A
  • Reduced sun exposure without vitamin D supplementation
  • Malabsorption disorders - IBD
  • CKD - kidney metabolize vit D to active form
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15
Q

Vit D is essential for absorption of what in intestine and kidneys

A

calcium and phosphate

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16
Q

what does low calcium and phosphate lead to

A

result in defective bone mineralisation

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17
Q

how does low calcium affect the parathyroid glad

A

causes a secondary hyperparathyroidism by secreting parathyroid hormone

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18
Q

what does parathyroid hormone stimulates

A

increased reabsorption of calcium from the bones

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19
Q

how does vit D def present

A

Rickets, osteomalacia

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20
Q

what are bone deformities associated with Rickets

A
  • Bowing of the legs, where the legs curve outwards
  • Knock knees, where the legs curve inwards
  • Rachitic rosary, where the ends of the ribs expand at the costochondral junctions, causing lumps along the chest
  • Craniotabes, which is a soft skull, with delayed closure of the sutures and frontal bossing
  • Delayed teeth with under-development of the enamel
  • kyphoscoliosis
  • Harrison’s sulcus
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21
Q

what investigation establishes a diagnosis of vit D def

A

Serum 25-hydroxyvitamin D less than 25 nmol/L

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22
Q

How does rickets present on XRay

A

osteopenia (more radiolucent bones).

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23
Q

what investigations can be ordered for rickets and what would they show

A

Serum calcium may be low
Serum phosphate may be low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high
Serum 25-hydroxyvitamin D

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24
Q

what addition investigations can be ordered to establish pathology in rickets

A

Full blood count and ferritin, for iron deficiency anaemia
Inflammatory markers such as ESR and CRP, for inflammatory conditions
Kidney function tests, for kidney disease
Liver function tests, for liver pathology
Thyroid function tests, for hypothyroidism
Malabsorption screen such as anti-TTG antibodies, for coeliac disease
Autoimmune and rheumatoid tests, for inflammatory autoimmune conditions

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25
Q

how is rickets managed

A

1st line = ergocalciferol -> vit D replacement

calcium lactate or calcium carbonat -> hypocalcaemia

ToUC
diet advice
sunlight exposure

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26
Q

what is the dose of ergocalciferol for children 6months to 12 years

A

6,000 IU per day for 8 – 12 weeks.

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27
Q

who si at higher risk of vit D def breastfed or formula babies

A

Breastfed babies

formula feed is fortified with vitamin D.

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28
Q

what is Transient synovitis

A

caused by temporary (transient) irritation and inflammation in the synovial membrane of the joint (synovitis).

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29
Q

what age is Transient synovitis common in

A

3 – 8 years

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30
Q

what is often associated with Transient synovitis

A

recent viral upper respiratory tract infection.

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31
Q

how does Transient synovitis present

A

within a few weeks of a viral illness

Limp
Refusal to weight bear
Groin or hip pain
Mild low grade temperature

otherwise well

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32
Q

how is Transient synovitis managed

A

symptomatic

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33
Q

what is Transient synovitis prognosis

A

significant improvement in symptoms after 24 – 48 hours.

Symptoms fully resolve within 1 – 2 weeks

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34
Q

when can a child with suggestive of transient synovitis be managed in primary care

A

if the limp is present for less than 48 hours and they are otherwise well

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35
Q

if children with Transient synovitis worsen what is management

A

followed up at 48 hours and 1 week to ensure symptoms are improving and then fully resolve

if not –> urgent assessment in secondary care

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36
Q

what is septic arthritis

A

infection inside a joint

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37
Q

what age is septic arthritis mc

A

under 4 years

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38
Q

how does septic arthritis present

A

Hot, red, swollen and painful joint
Refusing to weight bear
Stiffness and reduced range of motion
Systemic symptoms such as fever, lethargy and sepsis

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39
Q

what is kocher rules for septic arthritis

A
  • Fever higher than 38.6.
  • ESR > 40 millimeters per hour (mm/hour)
  • WCC > 12,000 cells/mm3
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40
Q

what is MC causative organisms of septic arthritis

A

Staphylococcus aureus

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41
Q

what are DDx for septic arthritis

A

Transient sinovitis
Perthes disease
Slipped upper femoral epiphysis
Juvenile idiopathic arthritis

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42
Q

How is septic arthritis investigated

A
  • joint aspiration: for culture.
  • raised WBC
  • raised inflammatory markers
  • blood cultures
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43
Q

what are other possible causative organisms of septic arthritis

A

Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)

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44
Q

how is septic arthritis managed

A

Empirical IV antibiotics
1st line = Flucloxacillin (often first-line)
Clindamycin (penicillin allergy)
Vancomycin (if MRSA is suspected)

Abx for 3-6 weeks
surgical drainage and washout of joint

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45
Q

what is Osteomyelitis

A

inflammation/infection of a bone and bone marrow, usually caused by bacterial infection.

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46
Q

what is Haematogenous osteomyelitis

A

when a pathogen is carried through the blood and seeded in the bone
MC most common form in children

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47
Q

where does Osteomyelitis typically occur

A

metaphysis of the long bones

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48
Q

what is MC causative organism of Osteomyelitis

A

staphylococcus aureus.

except in patients with sickle-cell anaemia where Salmonella species predominate

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49
Q

what is chronic Osteomyelitis

A

deep seated, slow growing infection with slowly developing symptoms.

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50
Q

what is acute Osteomyelitis

A

presents more quickly with an acutely unwell child

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51
Q

what are RF for Osteomyelitis

A

Open bone fracture
Orthopaedic surgery
Immunocompromised
Sickle cell anaemia
HIV
Tuberculosis

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52
Q

how does Osteomyelitis present

A

Refusing to use the limb or weight bear
Pain
Swelling
Tenderness
Fever

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53
Q

how is Osteomyelitis investigated

A

1st = XRay
GS = MRI
Blood test = raised CRP and ESR and WBC
Blood culture
BM aspiration and Bone Biopsy with histology and culture

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54
Q

how is Osteomyelitis managed

A

Surgical debridement of the infected bone and tissues

Antibiotic therapy = 6 weeks of flucloxacillin, possibly with rifampicin or fusidic acid added for the first 2 weeks

clindamycin if allergic

55
Q

How does Osteomyelitis present on XRay

A

Can be normal

  • Periosteal reaction (changes to the surface of the bone)
  • Localised osteopenia (thinning of the bone)
  • Destruction of areas of the bone
56
Q

what is Perthes Disease

A

disruption of blood flow to the femoral head, causing avascular necrosis of the bone

57
Q

where does Perthes Disease affect

A

the epiphysis of the femur, which is the bone distal to the growth plate (physis)

58
Q

what age does perthes disease mc occur in

A

4 – 8 years
5x more common in boys

59
Q

what are possible causes of perthes disease

A

genetics vascular anomalies

60
Q

what are 4 stages of perthes disease

A

Catterall staging

  • Stage 1 - Clinical and histological features only
  • Stage 2 - Sclerosis with or without cystic changes
  • Stage 3 Loss of structural integrity of the femoral head
  • Stage 4 Loss of acetabular integrity
61
Q

what is the main complication of perthes disease

A
  • osteoarthritis from deformed femoral head
  • premature fusion of the growth plates
62
Q

how does perthes disease present

A

slow onset
Pain in the hip or groin - 90% unilateral
Limp
Restricted hip movements
There may be referred pain to the knee

no history of trauma, if trauma think SUFE

63
Q

What is 1st line investigation for Perthes

A

XRay - can be normal

64
Q

what are other investigations for perthes disease

A

Technetium bone scan
MRI Scan
Blood test - usually normal

65
Q

what can be seen on MRI for perthes

A

avascular necrosis
joint effusion
marrow oedema

66
Q

what can be seen on XRay for perthes

A
  • early changes include widening of joint space
  • later changes include decreased femoral head size/flattening
67
Q

how is perthes managed

A

initial = conservative to maintain healthy position and alignment of joint, reduce damage and deformity

Bed rest
Traction
Crutches
Analgesia

Physiotherapy is used to retain the range of movement

Regular xrays are used to assess healing.

68
Q

what is the aim of sugery in perthes

A

aim is to improve the alignment and function of the femoral head and hip.

generally >6yrs

69
Q

what is Slipped upper femoral epiphysis

A

Displacement of the femoral head epiphysis postero-inferiorly

70
Q

what is mc age for SUFE

A

typically age group is 10-15 years
More common in obese children and boys

71
Q

what is RF for SUFE

A

obesity

72
Q

what are symptoms of SUFE

A

Hip, groin, thigh or knee pain
loss of internal rotation of the leg in flexion
Painful limp
bilateral 20% of cases

73
Q

what is the typical SUFE patient

A

adolescent, obese male
undergoing a growth spurt.
may be a history of minor trauma

74
Q

How does SUFE present on examination

A

limited movement of the hip

  • prefer to keep the hip in external rotation.
  • restricted internal rotation.
75
Q

What is the 1st line investigation for SUFE

A

XRay

AP and lateral (typically frog-leg) views are diagnostic

76
Q

what are other investigations that can used for SUFE diagnosis

A

Blood tests = normal –> used to exclude other causes of joint pain
Technetium bone scan
MRI scan
CT scan

77
Q

How is SUFE managed

A

Surgery

internal fixation: typically a single cannulated screw placed in the centre of the epiphysis

78
Q

What is Osgood-Schlatters Disease

A

inflammation of the patellar ligament at the tibial tuberosity

common cause of anterior knee pain

78
Q

what are complications of SUFE

A

osteoarthritis
avascular necrosis of the femoral head
chondrolysis
leg length discrepancy

79
Q

when does Osgood-Schlatters Disease typically occur

A

10 – 15 years

80
Q

what is the pathophysiology of Osgood-Schlatters Disease

A

microtrauma causing inflammation and subsequent avulsion fracture of the secondary ossification centre

81
Q

how does Osgood-Schlatters Disease present

A

Visible or palpable hard and tender lump at the tibial tuberosity
Pain in the anterior aspect of the knee
The pain is exacerbated by physical activity, kneeling and on extension of the knee

82
Q

how is osgood-schlatter disease investiagted

A

mostly clinical
Xray = elevation or fragmentation of the tibial tubercle

83
Q

how is Osgood-Schlatters Disease managed

A

Reduction in physical activity
Ice
NSAIDS (ibuprofen) for symptomatic relief

stretching and physiotherapy can be used to strengthen the joint

84
Q

what is a complication of Osgood-Schlatters Disease

A

full avulsion fracture, where the tibial tuberosity is separated from the rest of the tibia

85
Q

What is Developmental Dysplasia of the Hip

A

a structural abnormality in the hips caused by abnormal development of the fetal bones during pregnancy

leads to instability in the hips and a tendency or potential for subluxation or dislocation.

86
Q

What can untreated Developmental Dysplasia of the Hip lead to in adulthood

A
  • weakness
  • recurrent subluxation or dislocation
  • an abnormal gait
  • early degenerative changes.
87
Q

when is DDH usually picked up

A

newborn and infant physical examination (NIPE)

again at the six-week baby check

88
Q

What are RF for DHH

A
  • First degree family history
  • Breech presentation from 36 weeks onwards
  • Breech presentation at birth if 28 weeks onwards
  • Multiple pregnancy
  • female sex: 6 times greater risk
  • firstborn children
  • oligohydramnios
  • birth weight > 5 kg
89
Q

What is looked for in DDH newborn and infant physical examination (NIPE)

A

symmetry in the hips, leg length, skin folds and hip movements

90
Q

what findings may suggest DDH

A
  • Different leg lengths
  • Restriction in abduction (bilateral or one side)
  • Difference in the knee level when the hips are flexed
  • Clunking of the hips on special tests
91
Q

what two special tests are used to check for DDH

A

Ortolani test
Barlow test

92
Q

What is Barlow test

A

test for dislocatable hip

adduct the hip and bring the thigh towards the midline then apply posterior pressure on the knee

93
Q

what is Ortolani test

A

Flex the knees to 90°.
then abduct the legs by pushing the thighs outwards

should pop hip back in

94
Q

what is positive sign in Ortolani

A

distinctive ‘clunk’ which can be heard and felt as the femoral head relocates anteriorly into the acetabulum.

95
Q

what is investigation of choice in suspected DDH

A

ultrasound if <4.5 months

if > 4.5 months then x-ray

96
Q

How is DDH managed <6 months

A

<6 months = Pavlik harness

keeps the baby’s hips flexed and abducted.

97
Q

How is DDH managed >6 months

A

Surgery

After surgery a hip spica cast to immobilises the hip

98
Q

what is Juvenile idiopathic arthritis

A

condition affecting children and adolescents where autoimmune inflammation occurs in the joints

99
Q

when is JIA diagnosed

A

arthritis without any other cause, lasting more than 6 weeks in a patient under the age of 16.

100
Q

what are key features of JIA

A

joint pain and swelling:
usually medium sized joints e.g. knees, ankles, elbows
limp

101
Q

what are subtypes of Juvenile idiopathic arthritis

A

Systemic JIA
Polyarticular JIA
Oligoarticular JIA
Enthesitis related arthritis
Juvenile psoriatic arthritis

102
Q

what is Systemic JIA

A

systemic illness
idiopathic inflammatory

103
Q

what are features of Systemic JIA

A
  • pyrexia
  • salmon-pink rash
  • lymphadenopathy
  • arthritis
  • uveitis
  • anorexia and weight loss
104
Q

What should blood show for systemic JIA

A

Antinuclear antibodies and rheumatoid factors are typically negative

raised inflammatory markers, with raised CRP, ESR, platelets and serum ferritin.

105
Q

how does macrophage activation syndrome (MAS) present

A

acutely unwell child with disseminated intravascular coagulation (DIC), anaemia, thrombocytopenia, bleeding and a non-blanching rash.

106
Q

what is a key complication of systemic JIA

A

macrophage activation syndrome (MAS)

107
Q

what is a key investigation finding of macrophage activation syndrome (MAS)

A

low ESR

108
Q

what are infective DDx for fevers for more than 5 days

A

Kawasaki disease, Still’s disease, rheumatic fever and leukaemia.

109
Q

what is Polyarticular JIA

A

idiopathic inflammatory arthritis in 5 joints or more

tends to be symmetrical

small and large joints

110
Q

how are Polyarticular JIA and systemic JIa differentiated

A

Polyarticular = Systemic symptoms are mild

111
Q

what would bloods for rheumatoid factor show for Polyarticular JIA

A

Most children are negative for rheumatoid factor and are described as “seronegative”.

seropositive - older children and disease more similar to adults

112
Q

what is Oligoarticular JIA

A

aka Pauciarticular
60% of cases of JIA

It involves 4 joints or less
MC knee or ankle
not rlly associated with systemic symptoms

MC girls < 6yr

113
Q

what is a classic associated feature of Oligoarticular JIA

A

anterior uveitis

114
Q

how does Oligoarticular JIA present on bloods

A
  • Inflammatory makers will be normal or mildly elevated.
  • Antinuclear antibodies are often positive
  • Rheumatoid factor is usually negative.
115
Q

what is Enthesitis-Related Arthritis

A

male >6yrs

paediatric version of the seronegative spondyloarthropathy

Patients have inflammatory arthritis in the joints as well as enthesitis.

116
Q

what are seronegative spondyloarthropathy conditions

A
  • ankylosing spondylitis
  • psoriatic arthritis
  • reactive arthriti
  • inflammatory bowel disease-related arthritis.
117
Q

what is enthesis

A

point at which the tendon of a muscle inserts into a bone

118
Q

what can cause Enthesitis

A

can be caused by traumatic stress, such as through repetitive strain during sporting activities, or can be caused by an autoimmune inflammatory process.

119
Q

how can Enthesitis be investigated

A

MRI

120
Q

what gene is associated with enthesitis-related arthritis

A

HLA B27 gene

human leukocyte antige

121
Q

what associated conditions should a patient with enthesitis-related arthritis be checked for

A

psoriasis (psoriatic plaques and nail pitting)

inflammatory bowel disease (intermitted diarrhoea and rectal bleeding).

122
Q

how does enthesitis-related arthritis present on examination

A

tender to localised palpation of the entheses.

123
Q

where are entheses located in body

A

Interphalangeal joints in the hand
Wrist
Over the greater trochanter on the lateral aspect of the hip
Quadriceps insertion at the anterior superior iliac spine
Quadriceps and patella tendon insertion around the patella
Base of achilles, at the calcaneus
Metatarsal heads on the base of the foot

124
Q

what is Juvenile Psoriatic Arthritis

A

seronegative inflammatory arthritis associated with psoriasis

symmetrical polyarthritis affecting the small joints
or an asymmetrical arthritis affecting the large joints in the lower limb

125
Q

what are signs or symptoms of Juvenile Psoriatic Arthritis

A
  • Plaques of psoriasis on the skin
  • Pitting of the nails
  • Onycholysis, separation of the nail from the nail bed
  • Dactylitis, inflammation of the full finger
  • Enthesitis, inflammation of the entheses, which are the points of insertion of tendons into bone
126
Q

how is JIA managed

A
  • NSAIDs, such as ibuprofen
  • Steroids, either oral, intramuscular or intra-artricular in oligoarthritis
  • Disease modifying anti-rheumatic drugs (DMARDs)
  • Biologic therapy
127
Q

name Disease modifying anti-rheumatic drugs

A

methotrexate, sulfasalazine and leflunomide

128
Q

name Biologic therapy such as tumour necrosis factor inhibitors

A

etanercept, infliximab and adalimumab

129
Q

what is Torticollis

A

a painful neck.

130
Q

what causes Torticollis

A

minor local musculoskeletal irritation causing pain and spasms in neck muscles.

131
Q

what meniscus is affected in Discoid meniscus

A

lateral

132
Q

how does Discoid meniscus present

A

vague pain in the knee
“click” on the lateral side of the knee

133
Q

What are features of Growing pains

A

never present at the start of the day after the child has woken
no limp
no limitation of physical activity
systemically well
normal physical examination
motor milestones normal
symptoms are often intermittent and worse after a day of vigorous activity

3a paeds (12 decks)

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