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NP- Phase 3a Medicine > Paeds- MSK > Flashcards

Paeds- MSK Flashcards

1
Q

differential diagnosis of pain with no swelling in MSK

A
  • hypermobile joints syndrome
  • orthopaedics syndrome- e.g. Perthes
  • metabolic- hypothyroidism, lysosomal storage disease
  • tumour- benign/ malignant
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2
Q

differential diagnosis of pain with swelling in MSK

A
  • trauma
  • infection- septic/oesteomyelitis
  • rheumatic fever
  • JIA
  • vasculitis
  • CF
  • metabolic
  • malignancy
  • congenital
  • sarcoidosis
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3
Q

define JIA

A

Juvenile Idiopathic Arthritis

joint inflammation presenting in children <16 and persisting for at least 6 weeks with other causes excluded

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4
Q

how can JIA be classified?

A
  • Oligoarticular
  • polyarticular RF -ve
  • polyarticular RF +ve
  • systemic onset JIA
  • psoriatic
  • enthesitis related arthritis (ERA)
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5
Q

classification of JIA- describe:

oligoarticular JIA

A
  • most common
  • affects 1-4 joints during 1st 6 months
  • persistent and extended
  • 70% ANA positive
  • mostly affects ankles and knees
  • swelling, stiffness, reduced ROM, little pain
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6
Q

classification of JIA- describe:

Polyarticular RF -ve

A
  • 5+ joints during 1st 6 months
  • more common in females
  • peaks in toddlers and preadolescence
  • affects large and small joints
  • stiffness, little swelling
  • destructive arthritis
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7
Q

classification of JIA- describe:

Polyarticular RF +ve

A
  • 5+ joints during 1st 6 months with +ve RF seen on 2 occassions
  • symmetrical involvement of small joints
  • rheumatoid nodules
  • swelling and stiffness
  • systemic- fever, hepatosplenomegaly, serositis
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8
Q

classification of JIA- describe:

Systemic onset JIA

A
  • arthritis with >2 weeks daily fever + 1 of:
  • rash
  • lymph node enlargement
  • hepatosplenomegaly
  • serositis
  • MAS
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9
Q

classification of JIA- describe:

psoriatic JIA

A

arthritis and psoriasis

dactylitis, nail pitting, psoriasis

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10
Q

classification of JIA- describe:

enthesitis related arthritis

A
  • arthritis and enthesitis

- HLAB27, onse over 6, reiter syndrome

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11
Q

give some complications of JIA

A
  • chronic anterior uveitis
  • flexion contracture
  • growth failure
  • constitutional problems
  • osteoporosis
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12
Q

how is JIA diagnosed?

A
  • clinical !

FBC:

  • normocytic anaemia
  • ESR/ CRP raises
  • RF, HLAB27
  • raised platelets
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13
Q

how is JIA managed and treated?

A

manage:

  • refer to rheumatology
  • physio
  • hydrotherapy

treat:

  • NSAIDS
  • steroids- intra-articular
  • DMARD’s- methotrexate and sulfasalazine
  • biologics- tacilizumab, rituximab
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14
Q

what is juvenile SLE?

A

chronic, autoimmune disease affecting all organs

relapsing and remitting

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15
Q

describe the classification of SLE

A

SOAP BRAIN MD

Serositis
Oral ulcers
Arthritis
Photosensitivity

Blood (low- anaemia, leukopenia)
Renal 
ANA
Immunologic- (antibodies to DNA)
Neurologic (psych, seizures)

Malar rash
Discoid rash

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16
Q

what are the most common sites for osteomyelitis?

A

distal femur

proximal tibia

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17
Q

aetiology of osteomyelitis

A
  • staph aureus
  • group A beta heamolytic strep
  • haemophilus influenza
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18
Q

clinical signs in osteomyelitis

A
  • severe
  • immobile limb
  • red/warm/ tender over area
  • acute febrile illness
  • lethargy
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19
Q

investigations in osteomyelitis

A
  • XR- initially normal, then subperiosteal bone formation occurs after 7-10 days
  • MRI
  • blood cultures
  • FBC- raised infection markers
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20
Q

treatment of osteomyelitis

A

IV cefuroxime for at least 6 weeks

  • use co-amoxiclav or flucloxacillin if unsure
  • surgical drainage if unresponsive
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21
Q

if a child presents limping, what should be your first major concern?

A

septic arthritis

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22
Q

what organisms can cause septic arthritis?

A
  • staph aureus

- haemophilus influenza

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23
Q

how does septic arthritis present clinically?

A
  • erythematous, warm, acute tender joint
  • reduced ROM
  • febrile child
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24
Q

investigations and findings in a patient with septic arthritis

A
  • raised infection markers
  • blood cultures
  • USS of deep joints
  • aspiration of joint space with USS- definitive !!
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25
Q

how is septic arthritis managed?

A

long course Abx

wash out/ surgical drainage may be required

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26
Q

what is developmental dysplasia of the hip?

A

spectrum of severity ranging from mild acetabular dysplasia with a stable hip through to more severe forms of dysplasia with neonatal hip instability

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27
Q

risk factors for developmental dysplasia of the hip

A
  • female (6 times greater)
  • breech presentation
  • positive FH
  • firstborn child
  • oligohydramnios
28
Q

how does developmental dysplasia of the hip present clinically?

A
  • screening at 6-8 weeks

- signs of asymmetry

29
Q

describe the signs of asymmetry seen in developmental dysplasia of the hip

A
  • asymmetrical gluteal folds
  • limb length discrepancy
  • limitation and asymmetry of hip abduction
  • benign hip clicks
30
Q

what is the barlow test?

A

developmental dysplasia of the hip- attempts to dislocate an articulated femoral head posteriorly

31
Q

what is the Ortolani test?

A

attempts to relocate a dislocated femoral head- assessed in developmental dysplasia of the hip

32
Q

how is developmental dysplasia of the hip diagnosed ?

A
  • dynamic USS
33
Q

how is a patient with developmental dysplasia of the hip managed?

A
  • pavlik harness if younger than 4-5 months

- older= surgery

34
Q

what is transient synovitis of the hip?

A
  • irritable hip

- chief cause of hip pain in children aged 4-10

35
Q

how is transient synovitis of the hip diagnosed?

A

diagnosis of exclusion

36
Q

how is transient synovitis of the hip differentiated from septic arthritis?

A

septic arthritis:

WCC> 12

ESR> 40

37
Q

what findings would be seen clinically in a patient with transient synovitis of the hip?

A

pain on internal rotation of the hip

38
Q

how is transient synovitis of the hip managed?

A

self limiting- rest and analgesia

39
Q

what is Perthe’s disease?

A

temporarily disrupted blood flow to the femoral head causing avascular necrosis

bone remodelling occurs leading to abnormal ossification

40
Q

describe the epidemiology of perthes disease

A
  • 5-10

- males 4:1

41
Q

symptoms of Perthes disease

A
  • pain in hip/ groin
  • referred pain in thigh/ knee
  • pain worse on activity, relieved by rest
  • painful muscle spasms
  • limping
42
Q

how is a diagnosis of Perthe’s disease made?

A
  • limited abduction and internal rotation

- xray/ MRI= space widening

43
Q

give a later finding on XR/MRI in a patient with Perthes disease

A

decreased femoral head size w/ patchy density

44
Q

how is Perthe’s disease managed?

A
  • surgery
  • limit activity
  • physio
45
Q

describe the epidemiology of slipped upper femoral epiphysis (SUFE)

A
  • 10-16
  • male dominance
  • obesity is a major risk factor
46
Q

what is SUFE?

A

displacement of a growth plate with epiphysis slipping inferiorly and posteriorly

47
Q

when and how does SUFE present?

A
  • after a minor injury !
  • limping and hip pain
  • limited ROM
48
Q

how is SUFE managed?

A

fixation

49
Q

what is Achondroplasia?

A

reduced growth of cartilaginous bone

most common form of short-limb dwarfism

50
Q

describe the gene mutation seen in achondroplasia

A

G380R in fibroblast growth receptor 3 (FGFR3)

autosomal dominant !

51
Q

clinical presentation of achondroplasia

A
  • large skull, normal length trunk and short arms and legs
  • frontal bossing
  • lumbar lordosis
52
Q

what is osteogenesis imperfecta?

A

inherited condition causing fragility of bone

53
Q

aetiology of osteogenesis imperfecta

A
  • autosomal dominant (types 1 and 4)

- 90%- mutations in COL1A1 and COL1A2

54
Q

which types of ostoegensis imperfecta are more severe?

A

2 and 3

autosomal recessive

55
Q

clinical findings on X ray in osteogenesis imperfecta

A

low bone density

bowing of long bones

56
Q

how is a patient with osteogensis imperfecta managed?

A
  • physio and rehab
  • surgery if required
  • bisphosphonates- alendronate, zoledronate, pamidronate
57
Q

what is Rickets?

A

vitamin D deficiency

58
Q

how does Rickets present clinically?

A
  • metaphyseal expansions
  • bowing deformities
  • fractures
  • Harrison’s sulcus - indentation of softened lower ribcage where diaphragm attaches

Rackety rosary- palpable costochondral junctions

59
Q

causes of vitamin D deficiency

A
  • lack of exposure to sunlight
  • dark skin
  • lack of it in diet
  • malabsorption- coeliac, pancreatic insufficiency, CF
  • drugs- anticonvulsants (e.g. phenobarbital
  • impaired metabolic conversion- hepatic/ renal disease
60
Q

describe the biochemistry of a patient with Rickets

A
  • low phosphorus
  • serum calcium low
  • raised alkaline phosphatase
  • raised PTH
61
Q

what is Osgood Schlatter disease?

A

self-limiting disorder of the knee found during adolescence

osteochondiritis of the patella tendon insertion at the knee

62
Q

explain the pathophysiology behind Osgood Schlatter disease

A

Common in active adolescents, possibly caused by multiple small avulsion
fractures from contractions of the quadriceps muscles at their insertion
into the proximal tibial apophysis (ossification centre)

63
Q

how does Osgood Schlatter disease present clinically?

A
  • onset of pain and swelling below knee
  • relieved by rest
  • tenderness
64
Q

how is Osgood Schlatter disease diagnosed?

A

X-ray:
- irregular apophysis

  • seperation from tibial tuberosity
65
Q

presentation of a patient with osteogenesis imperfecta

A
  • BLUE/ GRAY SCLERA
  • fracture Hx
  • dental problems
  • short stature
  • hypermobility

NP- Phase 3a Medicine (22 decks)

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