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PAEDS - MSK / DERMATOLOGY Flashcards

1
Q

LIMP OVERVIEW
What is the main source of a limp?

A
  • Hip, then leg > knee > thigh > foot (least likely)
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2
Q

LIMP OVERVIEW
What are important differentials?

A

Intra-abdominal pathology like hernia, testicular torsion

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3
Q

LIMP OVERVIEW
What are some differentials for limp in a child 0–3y?

A
  • Trauma like # (accidental or NAI)
  • Infections (septic arthritis, osteomyelitis)
  • DDH (chronic)
  • Malignancy (Ewing’s, osteogenic sarcoma)
  • Neuromuscular disease (CP, Duchenne’s)
  • ANY CHILD <3Y WITH LIMP NEEDS URGENT ASSESSMENT*
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4
Q

LIMP OVERVIEW
What are some differentials for limp in a child 4–10y?

A
  • Trauma, infection, malignancy
  • Transient synovitis (acute)
  • Perthe’s disease (P for primary school, chronic)
  • Juvenile idiopathic arthritis (chronic)
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5
Q

LIMP OVERVIEW
What are some differentials for limp in a child >10y?

A
  • Trauma, infection, malignancy
  • Slipped upper femoral epiphysis (S for secondary school, acute/chronic)
  • JIA
  • Reactive arthritis
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6
Q

LIMP OVERVIEW
What are some general investigations for a child presenting with limp?

A
  • Full Hx + exam (top>toe)
  • General obs (HR, BP, temp)
  • FBC (WCC), CRP/ESR, blood cultures if septic
  • XR both AP + lateral for joint (+ joints above/below)
  • USS joint to look for thickening of capsule or effusion
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7
Q

DDH
What is developmental dysplasia of the hip (DDH)?

A
  • Abnormal relationship of femoral head to the acetabulum leading to aberrant development of hip causing instability
  • Spectrum of dysplasia (underdevelopment), subluxation (partial dislocation) or frank dislocation of the hip
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8
Q

DDH
What are some risk factors for DDH?
How would you manage them?

A
  • First degree FHx, breech at ≥36w or breech delivery ≥28w, multiple pregnancy
    – USS hip by 6w even if normal NIPE exam
  • Other = F>M 6:1, oligohydramnios
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9
Q

DDH
What is the clinical presentation of DDH?

A
  • Painless limp
  • Limited abduction (reduced ROM)
  • Leg length discrepancy
  • May have waddling or abnormal gait but otherwise well
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10
Q

DDH
What is the main investigation for DDH and what are you looking for?

A

NIPE at 72h + 6–8w

  • Leg length discrepancy
  • Restricted hip abduction of affected side
  • Barlow + ortolani tests
  • Clunking of hips on tests
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11
Q

DDH
What are you assessing for when you look at leg length discrepancy?

A

Galeazzi/Allis sign = difference in knee length when hips flexed + feet flat on bed

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12
Q

DDH
What are you assessing for when you look at barlow test?

A

Posterior hip dislocation (adduct hips + press down on knees)

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13
Q

DDH
What are you assessing for when you look at ortolani test?

A

Relocate a dislocated femoral head (abduct + push thigh anteriorly)

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14
Q

DDH
After the NIPE, what would be the investigation of choice if positive?
What other investigation might you perform?

A
  • USS by 2w of age
  • XR may be useful in older infants >3m
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15
Q

DDH
What is the management of DDH?

A
  • If <6m = Pavlik harness to hold femoral head in position (flexed + abducted) to allow the hip socket (acetabulum) to develop normal shape (remove after 6-8w)
  • Surgical reduction if harness fails or Dx >6m = hip spica cast to immobilise hip for prolonged period after surgery (risk of avascular necrosis + re-dislocation)
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16
Q

SEPTIC ARTHRITIS
What is septic arthritis?

A
  • Serious infection of the joint space as it can lead to bone destruction
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17
Q

SEPTIC ARTHRITIS
Who is it commonly seen in and how?

A
  • Most common <2y,
  • usually from haematogenous + soft tissue swelling
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18
Q

SEPTIC ARTHRITIS
What is the most common causative organism of septic arthritis?

A
  • Staphylococcus aureus
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19
Q

SEPTIC ARTHRITIS
What are common causes in…
i) infants?
ii) <4y?
iii) >4y?

A

i) GBS, S. aureus, coliforms
ii) S. aureus, pneumococcus, haemophilus
iii) S. aureus, gonococcus (adolescents)

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20
Q

SEPTIC ARTHRITIS
What is the clinical presentation of septic arthritis?

A
  • Usually single joint (knee or hip) + acute onset
  • Hot, red, swollen + painful joint (including at rest)
  • Refusal to weight bear
  • Stiffness + reduced ROM with pain if moved (hip may be held flexed)
  • Systemic = fever, lethargy, sepsis
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21
Q

SEPTIC ARTHRITIS
What are some investigations for septic arthritis?

A
  • FBC,
  • blood cultures,
  • CRP + ESR,
  • USS guided joint aspiration for MC&S
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22
Q

SEPTIC ARTHRITIS
what is the criteria for diagnosing septic arthritis?

A

Kocher’s modified criteria /5, ≥3 is likely
–Temp>38.5
– Raised CRP/ESR/WCC
– Non-weight bearing

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23
Q

SEPTIC ARTHRITIS
What is the management of septic arthritis?

A
  • IV empirical Abx (flucloxacillin) until sensitivities back
  • Arthroscopic lavage or surgical drainage if resolution does not occur rapidly or deep-seated joint (hip)
  • Immobilise joint initially but then mobilise to prevent deformity
  • Rest + analgesia
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24
Q

OSTEOMYELITIS
What is osteomyelitis?

A
  • Infection in the bone + bone marrow, often in the metaphysis of long bones
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25
Q

OSTEOMYELITIS
What are the two different types?

A
  • Acute = rapid presentation with acutely unwell child
  • Chronic = deep seated, slow growing infection + Sx
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26
Q

OSTEOMYELITIS
What causes osteomyelitis?

A

S. Aureus #1 or H. influenzae (directly via bone or haematogenous spreading)

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27
Q

OSTEOMYELITIS
What is the epidemiology?

A

M>F,
<10y

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28
Q

OSTEOMYELITIS
What are some risk factors?

A
  • Open #,
  • orthopaedic surgery,
  • sickle cell anaemia (Salmonella predominates),
  • immunocompromised (HIV),
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29
Q

OSTEOMYELITIS
What is the clinical presentation of osteomyelitis?

A
  • Acutely unwell child
  • Refusing to weight bear
  • Severe pain, swelling + tenderness
  • May have high fever (low grade if chronic)
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30
Q

OSTEOMYELITIS
What are some investigations for osteomyelitis?

A
  • FBC (Raised WCC), raised ESR/CRP, blood cultures, bone marrow aspiration MC&S
  • XR can be normal
  • MRI is best imaging to establish Dx
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31
Q

OSTEOMYELITIS
What is the management of osteomyelitis?

A
  • IV empirical Abx (flucloxacillin or clindamycin if allergy) until sensitivities back
  • Amoxicillin, cefotaxime or ceftriaxone if <4y + suspect H. influenzae
  • ?Surgical drainage or debridement of infected bone
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32
Q

PERTHE’S DISEASE
What is the pathophysiology of Perthe’s disease?

A
  • Disruption of blood flow to femoral head causing avascular necrosis of the bone
  • Affects the epiphysis of femur, which is bone distal to growth plate (physis)
  • Over time, revascularisation or neovascularisation + healing of the femoral head with remodelling of bone
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33
Q

PERTHE’S DISEASE
What are some risk factors for Perthe’s disease?

A
  • Social deprivation
  • LBW
  • Passive smoking
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34
Q

PERTHE’S DISEASE
What is the clinical presentation of Perthe’s disease?

A
  • 4-8y, mostly male, limp (no Hx of trauma)
  • Pain (often unilateral) in hip or groin (?knee referral) with restricted hip movements (internal + external rotation)
  • +ve Trendelenburg test (abductor dysfunction) = ‘sound side sags’
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35
Q

PERTHE’S DISEASE
What are the investigations for Perthe’s disease?

A
  • Blood tests all normal
  • XR of both hips (with frog views) is initial investigation + assesses healing
    – Flattening of femoral head
  • Technetium bone scan or MRI may be needed to confirm Dx if normal XR
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36
Q

PERTHE’S DISEASE
What are the complications of Perthe’s disease?

A
  • Premature fusion of the growth plates
  • Soft + deformed femoral head can lead to early hip OA
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37
Q

PERTHE’S DISEASE
What is the general management of Perthe’s disease?

A
  • Keep femoral head within acetabulum (cast, braces)
  • Physio to retain ROM in muscles + joints without excess stress on the bone
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38
Q

PERTHE’S DISEASE
What is the management of Perthe’s disease for…

i) <6y + less severe?
ii) older, severe or not healing?

A

i) Conservative + observe, bed rest, traction, crutches, analgesia (good prognosis)
ii) Surgery to improve alignment + function of the femoral head + hip

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39
Q

JIA
What is juvenile idiopathic arthritis (JIA)?

A
  • Autoimmune inflammation in joints > joint pain, swelling + stiffness
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40
Q

JIA
What is the criteria for a clinical diagnosis of JIA?

A
  • Onset before 16y with no underlying cause
  • Joint swelling/stiffness
  • > 6w in duration to exclude other causes (i.e. reactive)
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41
Q

JIA
What is the clinical presentation of JIA?

A
  • Joint pain, swelling + stiffness (particularly morning) = hallmarks
  • Limping/functional disability
  • Decreased ROM
  • Warmth + colour change
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42
Q

JIA
What are the 4 types of JIA?

A
  • Systemic JIA (Still’s disease)
  • Polyarticular JIA
  • Oligoarticular JIA
  • Enthesitis-related arthritis
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43
Q

JIA
How does systemic JIA (Still’s disease) present?

A
  • Subtle salmon-pink rash
  • High swinging fevers
  • Lymphadenopathy, weight loss, muscle pain, splenomegaly
  • Pleuritis, pericarditis + uveitis
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44
Q

JIA
What are the investigations for systemic JIA?

A
  • Antinuclear antibodies (ANA) + rheumatoid factor = NEGATIVE
  • Raised inflammatory markers = CRP/ESR, platelets + serum ferritin
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45
Q

JIA
What is the main complication of systemic JIA?

A
  • Macrophage activation syndrome = severe activation of immune system with massive inflammatory response
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46
Q

JIA
How does macrophage activation syndrome present?

A
  • Acutely unwell with DIC,
  • febrile,
  • anaemia,
  • thrombocytopenia,
  • bleeding,
  • non-blanching rash,
  • low ESR
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47
Q

JIA
What is the management of macrophage activation syndrome?

A

Life-threatening = supportive + steroids

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48
Q

JIA
What is polyarticular JIA?

A
  • ≥5 joints affected, equivalent of RA in adults
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49
Q

JIA
What are the features of polyarticular JIA?

A

Symmetrical, affects small joints (of hand + feet) as well as large joints (hips + knees)

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50
Q

JIA
How does polyarticular JIA present?

A

Mild systemic Sx = mild fever, anaemia + reduced growth

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51
Q

JIA
What is the immunology of polyarticular JIA?

A

If rheumatoid factor +ve = seropositive (tend to be older children)

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52
Q

JIA
What is oligoarticular JIA?

A

≤4 joints affected, often just monoarthritis

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53
Q

JIA
What is oligoarticular JIA classically associated with?

A

Anterior uveitis = ophthalmologist referral

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54
Q

JIA
what is the immunology of oligoarticular JIA?

A

ANA +ve but RF -ve

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55
Q

JIA
What is enthesitis-relataed arthritis?

A
  • Paeds version of seronegative spondyloarthropathies (ankylosing spondylitis, psoriatic/reactive arthritis, IBD-related arthritis)
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56
Q

JIA
What is the main feature?

A

Enthesitis = inflammation at the point a tendon or muscle inserts to bone

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57
Q

JIA
How might enthesitis-related arthritis present?

A
  • Sx of psoriasis (psoriatic plaques, nail pitting, dactylitis) or IBD
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58
Q

JIA
What is it associated with?

A
  • HLA-B27 gene
  • Prone to anterior uveitis = ophthalmology referral
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59
Q

JIA
What is reactive arthritis?

A
  • Arthritis that develops following an infection where the organism cannot be recovered from the joint
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60
Q

JIA
What causes reactive arthritis?

A

Post STI (chlamydia) in older children or Salmonella, Campylobacter

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61
Q

JIA
How does reactive arthritis present?

A
  • Reiter’s = can’t see (conjunctivitis), can’t pee (urethritis) and can’t climb a tree (arthritis)
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62
Q

JIA
What is the general management?

A

Sx (analgesia, NSAIDs, sometimes intra-articular steroids)

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63
Q

JIA
What are the XR features of JIA?

A

Same as RA (LESS) –

  • Loss of joint space
  • Erosions (causing joint deformity)
  • Soft tissue swelling
  • Soft bones (osteopenia)
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64
Q

JIA
What are some complications from JIA?

A
  • Chronic anterior uveitis > severe visual impairment
  • Flexion contractures of joints
  • Growth failure + constitutional problems like delayed puberty
  • Osteoporosis
65
Q

JIA
What is the non-medical management of JIA?

A
  • MDT approach = education, psychologist, physio, pain team, rheumatology
66
Q

JIA
What is the medical management of JIA?

A
  • NSAIDs for Sx relief during flares
  • Intra-articular steroids for oligoarthritis
  • Avoid systemic steroids if possible (osteoporosis, growth suppression)
    – IV methylprednisolone can be used if severe arthritis
  • DMARDs like methotrexate, rarely sulfasalazine for polyarthritis
  • Biologics if poor control like tocilizumab, adalimumab, etanercept
67
Q

TRANSIENT SYNOVITIS
What is transient synovitis?

A
  • ‘Irritable hip’ caused by transient inflammation of the joint synovial membrane
68
Q

TRANSIENT SYNOVITIS
What is it associated with?

A

Recent viral URTI,
small % will develop Perthe’s

69
Q

TRANSIENT SYNOVITIS
What is the clinical presentation of transient synovitis?

A
  • Limp + refusal to weight bear, 2–10y
  • Groin or hip pain (may be referred to knee)
  • Mild low-grade fever but otherwise systemically well
  • Limited internal rotation + pain on movement but comfortable at rest
70
Q

TRANSIENT SYNOVITIS
What are some investigations for transient synovitis?

A
  • # 1 = exclude septic arthritis so if suspect = cultures + joint aspiration
  • Normal WCC, slight increase in CRP
  • USS may show effusion but XR normal
71
Q

TRANSIENT SYNOVITIS
What is the management of transient synovitis?

A
  • Self-limiting with only simple analgesia + rest = rapid Sx improvement
  • Manage at home with safety netting + review to ensure no fever + Sx resolving
72
Q

SUFE/SCFE
What is slipped upper/capital femoral epiphysis? (SUFE/SCFE)?

A
  • Displacement of femoral head epiphysis postero-inferiorly along the growth plate (through zone of hypertrophy)
73
Q

SUFE/SCFE
What is SUFE/SCFE associated with?

A
  • Boys, >10y, obese + undergoing growth spurt
  • Metabolic endocrine abnormalities (hypothyroid)
74
Q

SUFE/SCFE
What is the clinical presentation of SUFE/SCFE?

A
  • May be Hx of minor trauma that triggers onset
  • Hip, groin, thigh or knee pain (disproportionate to severity of trauma)
  • Painful limp + may have antalgic gait
  • Very restricted internal rotation (+ abduction)
75
Q

SUFE/SCFE
What are the investigations for SUFE/SCFE?

A
  • XR initial Ix of choice (AP + frog-leg views)
  • Bloods (incl. inflammatory markers) normal
  • ?Technetium bone scan + MRI scan
76
Q

SUFE/SCFE
What is the management of SUFE/SCFE?

A
  • Surgery = internal fixation (pinning femoral head into position for prevention)
77
Q

OSGOOD SCHLATTERS
What is Osgood-Schlatters disease?
What is the epidemiology?

A
  • Inflammation at the tibial tuberosity where the patellar ligament inserts
  • 10–15y sporty males (football, basketball)
78
Q

OSGOOD SCHLATTERS
What is the clinical presentation of Osgood-Schlatters disease?

A
  • Visible or palpable hard + tender lump/swelling at tibial tuberosity
  • Pain in anterior aspect of knee, often unilateral
  • Exacerbated by physical activity, kneeling + extension of knee
79
Q

OSGOOD SCHLATTERS
What is the management of Osgood-Schlatters disease?

A
  • Reduce pain + inflammation = NSAIDs, ice, reduce exercise)
  • Stretching + physio once settled to strengthen joint + improve function
80
Q

GROWING PAINS
What are growing pains?

A

Diagnosis by exclusion –

  • Pain never present at start of day after waking but can awaken from sleep
  • Physical activities are not limited, no limp, settles with massage
  • Bilateral pain in lower limbs (shins/ankles) + not limited to joints
  • Can be worse after a day of vigorous activity + intermittent
81
Q

OSTEOPOROSIS
What is osteoporosis in paediatrics defined by?

A
  • ≥1 vertebral crush #
  • ≥2 long bone fractures by age 10 (≥3 by age 19)
  • Bone mineral density less than 2.5 standard deviations below the mean
82
Q

OSTEOPOROSIS
How would you investigate?

A
  • Bone mineral density less than 2.5 standard deviations below the mean
  • DEXA scan
83
Q

OSTEOPOROSIS
What are the causes of osteoporosis?

A
  • Inherited = osteogenesis imperfecta, haematological issues
  • Acquired:
    – Drug induced (Steroids)
    – Endocrinopathies (hypoparathyroidism)
    – Malabsorption
    – Immobilisation (disabilities)
    – Inflammatory disorders
84
Q

OSTEOGENESIS IMPERFECTA
What is osteogenesis imperfecta?

A
  • Autosomal dominant condition leading to brittle bones + prone to fractures
85
Q

OSTEOGENESIS IMPERFECTA
What is the pathophysiology?

A

Defects in type 1 collagen protein which is essential for the structure + function of bone, as well as skin, tendons + other connective tissues

86
Q

OSTEOGENESIS IMPERFECTA
What is the clinical presentation of osteogenesis imperfecta?

A
  • Bone fragility = recurrent + inappropriate #, joint + bone pain
  • Bone deformity (bowed legs, bent bones, scoliosis)
  • Impaired mobility due to poor muscle mass
  • Poor growth > short stature
  • Hypermobility as ligamentous laxity
87
Q

OSTEOGENESIS IMPERFECTA
What are some associations with osteogenesis imperfecta?

A
  • Conductive hearing loss (otosclerosis)
  • Blue/grey tinted sclera due to scleral thinness
  • Valvular prolapse, aortic dissection > aortic incompetence
  • Hernias
  • ‘Wormian bones’ = skull feels like bubble wrap (wiggly black lines on skull XR)
88
Q

OSTEOGENESIS IMPERFECTA
What are the investigations for osteogenesis imperfecta?

A
  • Clinical Dx with XR to diagnose fractures + bone deformities
  • DEXA scan to look at bone mineral density (osteoporosis)
  • 7 types under the sillence classification
89
Q

OSTEOGENESIS IMPERFECTA
In the Sillence classification, what is…

i) type 1?
ii) type 2?
iii) types 3–4?

A

i) Mildest form, common with blue sclera
ii) Lethal form, chest too small to allow breathing, lots of rib # + lungs do not function
iii) Normal sclera

90
Q

OSTEOGENESIS IMPERFECTA
What is the MDT management of osteogenesis imperfecta?

A
  • Physio + OT to maximise strength + function
  • Paeds for medical treatment + follow up
  • Orthopaedic surgeons to manage #
  • Pain team, specialist nurses for advice + support
91
Q

OSTEOGENESIS IMPERFECTA
What is the medical management of osteogenesis imperfecta?

A
  • Vitamin D supplementation to prevent deficiency
  • Bisphosphonates (IV pamidronate) to increase bone density + reduce #
92
Q

RICKETS
What is rickets?
What is it caused by?

A
  • Defective bone mineralisation > “soft” + deformed bones (paeds osteomalacia)
  • Vitamin D deficiency (recommended paeds intake 400IU = 10mg)
93
Q

RICKETS
What are some risk factors for rickets?

A
  • Darker skin (need more sunlight)
  • Lack of exposure to sun
  • Poor diet or malabsorption
  • CKD as kidneys metabolise vitamin D to active form
94
Q

RICKETS
What is the normal physiology of vitamin D?

A
  • Increases Ca2+ absorption at gut + reabsorption at kidneys + role in immunity
95
Q

RICKETS
What are some sources of vitamin D?

A

Sunlight, fortified cereals, eggs, oily fish

96
Q

RICKETS
What happens when there is inadequate vitamin D?

A
  • Lack of Ca2+ + phosphate in blood which are required for bone construction > defective bone mineralisation
  • Low Ca2+ causes secondary hypoparathyroidism as parathyroid gland tries to raise Ca2+ level by secreting parathyroid hormone
  • This leads to increased resorption of Ca2+ from the bones, worsening the issue
97
Q

RICKETS
What are the symptoms of rickets?

A
  • Bone pain, swelling + deformities
  • Muscle weakness + poor growth (gross motor delay)
  • Pathological or abnormal #
  • May have hypocalcaemic convulsions or carpopedal spasm
98
Q

RICKETS
What are some bone deformities seen in rickets?

A
  • Bowing of legs, knock knees
  • Harrison sulcus = indentation of softened lower ribcage at site of attachment of diaphragm
  • Rachitic rosary = ends of ribs expand at costochondral junctions causing lumps along chest
  • Craniotabes = soft skull with delayed closure of sutures + frontal bossing
  • Expansion of metaphyses (esp. wrist)
99
Q

RICKETS
What are some investigations for rickets?

A
  • Serum biochemistry
  • FBC + ferritin (Fe anaemia), inflammatory markers
  • Kidney, liver + TFTs, malabsorption screen (anti-TTG)
  • Autoimmune + rheumatoid tests
  • XR required to diagnose
100
Q

RICKETS
What would serum biochemistry show in rickets?

A
  • Low = calcium + phosphate
  • High = ALP + PTH
  • 25-hydroxyvitamin D levels deficient (<25nmol/L)
101
Q

RICKETS
What might an XR show in rickets?

A
  • Osteopenia (radiolucent bones)
  • Cupping
  • Fraying of metaphyses
  • Widened epiphyseal plate
102
Q

RICKETS
What is the management of rickets?

A

Prevention #1 –
- Breastfeeding women should take vitamin D supplement
- Dietary advice to increase calcium + vitamin D
- Children vitamin D deficient > ergocalciferol
Vitamin D + calcium supplementation for children with rickets + specialist input

103
Q

COMMON BIRTHMARKS
What is a salmon patch?

A
  • ‘Stork mark’
  • Most common vascular birthmark
  • Flat red or pink patches on baby’s eyelids, neck or forehead at birth
  • Fade completely in few months
104
Q

COMMON BIRTHMARKS
What is a cavernous haemangioma?

A
  • ‘Strawberry mark’
  • Raised marks on skin often red, F>M
  • Not present at birth, appear in first month, increase in size then shrink + disappear
  • Normally self-limiting, beware over eye + airway
105
Q

COMMON BIRTHMARKS
What is a capillary haemangioma?

A
  • ‘Port wine stain’ = permanent, often unilateral
  • Present at birth + grows with infant, treated with laser therapy
  • Seen in Sturge-Weber syndrome (neuro Sx)
106
Q

COMMON BIRTHMARKS
What is a naevi?

A
  • Mole, can be multiple present in Turner’s
107
Q

COMMON BIRTHMARKS
What is a slate grey naevi?
What are the differentials for slate grey naevi?

A
  • Mole, can be multiple present in Turner’s
  • ‘Mongolian blue spot’, disappear by 4, commonly lower back/buttocks, more common in non-Caucasian
  • Bruising + NAI so important to document
108
Q

COMMON BIRTHMARKS
What are café-au-lait spots?
What is the significance?

A
  • Flat, light brown patches on skin
  • > 5 = neurofibromatosis
109
Q

COMMON BIRTHMARKS
What are milia?

A

Milk spots (sebaceous plugs where sweat glands plugged by sebum), normal

110
Q

COMMON BIRTHMARKS
What are infantile urticaria?

A

Erythema toxicum neonatorum by histamine reaction = self-limiting red blotches with eosinophils on biopsy

111
Q

ECZEMA
What is eczema?

A
  • Chronic atopic condition caused by defects in normal continuity of skin barrier leaving tiny gaps for irritants, microbes + allergens to enter + trigger immune response
  • Leads to inflammation of the skin
112
Q

ECZEMA
What is the clinical presentation of eczema?

A
  • Infants = dry, red, itchy + sore patches of skin over face + trunk
  • Young children = extensor surfaces
  • Older children = mostly on flexor surfaces (creases), face + neck creases
113
Q

ECZEMA
What are some complications of eczema?

A
  • Opportunistic bacterial infection as skin breakdown leaves entry, particularly S. aureus
    – Presents as increased erythema, yellow crust, pustules
    – PO flucloxacillin or admit for IV if severe
  • Eczema herpeticum
114
Q

ECZEMA
What is the general management of eczema?

A
  • Avoid triggers (weather, stress, wash/cleaning products)
  • Maintenance = artificial skin barrier with emollients (E45), special soap substitutes
115
Q

ECZEMA
How should a flare of eczema be managed?

A
  • Thicker emollients (hydromol or epaderm)
  • Topical steroids (start with hydrocortisone > betnovate > dermovate)
  • Wet wraps = cover affected areas in thick emollient with wrap to keep moisture overnight
  • Severe = PO ciclosporin, corticosteroids
116
Q

ECZEMA
What are some side effects of using topical steroids?

A
  • Thinning of skin
  • Telangiectasia
  • Bruising
117
Q

PSORIASIS
What is the pathophysiology of psoriasis?

A
  • Chronic autoimmune condition where abnormal T-cell activation > hyperproliferation of keratinocytes + so psoriatic skin lesions
118
Q

PSORIASIS
What are the causes?

A
  • HLA-B13,
  • environmental triggers (alcohol, stress, group A strep)
119
Q

PSORIASIS
What are the different types of psoriasis?

A
  • Plaque
  • Guttate ‘rain-drop’
  • Erythrodermic + pustular
120
Q

PSORIASIS
How does plaque psoriasis present?

A
  • Well-demarcated, raised, silvery scaling lesions on extensor surfaces (elbows + knees)
  • Scalp involvement, most often at hair margin
121
Q

PSORIASIS
How does guttate psoriasis present?

A
  • Explosive eruption of very small circular plaques on trunk, often 2w after strep throat
  • Common in paeds, resolves in 3-4m
122
Q

PSORIASIS
How does erythrodermic + pustular present?

A
  • Most severe + life-threatening
  • Widespread inflammation of skin > extensive erythematous areas or pustules under areas of erythema
  • Systemic = pyrexia, malaise
  • Admit
123
Q

PSORIASIS
What is the clinical presentation of psoarisis?

A
  • Koebner phenomenon = new plaques of psoriasis at sites of skin trauma
  • Residual pigmentation of skin after lesions resolve
  • Auspitz sign = small points of bleeding when plaques scraped off
  • Nail changes (pitting + onycholysis)
124
Q

PSORIASIS
What are some associations of psoriasis?

A
  • 10–20% develop psoriatic arthritis
  • Increased risk of CVD, metabolic syndrome, VTE
125
Q

PSORIASIS
What is the management of psoriasis?

A
  • 1st line = topical steroids, topical vitamin d analogues (calcipotriol)
  • 2nd line = UV phototherapy
  • 3rd line = immunosuppression with methotrexate or biologics
126
Q

NAPPY RASH
What are the 2 main types of nappy rash?

A
  • Irritant dermatitis = friction between skin/nappy + contact with urine + faeces
  • Candida dermatitis = due to breakdown in skin + the warm, moist environment
127
Q

NAPPY RASH
How do you differentiate between irritant dermatitis and candida dermatitis?

A
  • Irritant = sore, red, inflamed skin but spares the skin creases
  • Candida = involves skin creases, satellite lesions (small similar lesions near edges of principle lesion) + may have oral thrush
128
Q

NAPPY RASH
What are some risk factors for developing nappy rash?

A
  • Delayed changing of nappies
  • Diarrhoea
  • Irritant soap products + vigorous cleaning
  • PO Abx predispose to Candida
129
Q

NAPPY RASH
What is the management of nappy rash?

A
  • Highly absorbent nappies
  • Maximise time not wearing + ensure dry before replacing nappy
  • Change nappy + clean skin ASAP
  • Water or gentle alcohol-free products to clean
  • Topical imidazole if candida
130
Q

STEVEN-JOHNSON
What is Steven-Johnson syndrome?
What versions are there?

A
  • Disproportional immune response causes epidermal necrosis > blistering + shedding of top layer of skin
  • SJS = <10% body surface, toxic epidermal necrolysis affects >10%
131
Q

STEVEN-JOHNSON
What are some potential causes of Steven-Johnson syndrome?

A
  • Meds = AEDs, Abx, allopurinol, NSAIDs
  • Infections = herpes simplex, mycoplasma pneumonia, CMV, HIV
132
Q

STEVEN-JOHNSON
What is the clinical presentation of Steven-Johnson syndrome?

A
  • Non-specific Sx of fever, cough, sore throat + itchy skin
  • Develop purple/red rash that spreads across skin, starts to blister
  • Few days later skin sheds leaving raw tissue underneath = PAINFUL
133
Q

STEVEN-JOHNSON
Where does it affect?

A
  • Non-specific Sx of fever, cough, sore throat + itchy skin
  • Develop purple/red rash that spreads across skin, starts to blister
  • Few days later skin sheds leaving raw tissue underneath = PAINFUL
  • Can involve lips + mucous membranes, urinary tract, lungs
  • Eyes can become inflamed + ulcerated
134
Q

STEVEN-JOHNSON
What are some complications of Steven-Johnson syndrome?

A
  • Secondary infection
  • Permanent skin damage due to skin involvement + scarring
  • Visual complications such as severe scarring or even blindness
135
Q

STEVEN-JOHNSON
What is the management of Steven-Johnson syndrome?

A
  • Admission as medical emergency, cease causative meds
  • Nutritional care, Abx, analgesia, ophthalmology input
  • Steroids, immunoglobulins + immunosuppressants by specialists
136
Q

DISCOID MENISCUS
what is it?

A
  • it is an abnormally shaped meniscus (usually lateral)
  • it usually presents in younger people
  • it is more prone to injury as it is more likely to get stuck/tear
137
Q

DISCOID MENISCUS
how does it present?

A
  • a visible or audible snap on terminal leg extension along with pain and swelling in the absence of trauma
138
Q

DISCOID MENISCUS
what are the investigations?

A
  • MRI - can show abnormal shape and any tears
  • clinical examination
139
Q

DISCOID MENISCUS
what is the management?

A
  • symptomatic = arthroscopic partial meniscectomy
  • asymptomatic = physiotherapy
140
Q

SCOLIOSIS
what is it?

A

it is lateral curvature in the frontal plane of the spine
- measured >10 degrees on x-ray

141
Q

SCOLIOSIS
what are the causes?

A
  • idiopathic = most common
  • congenital = usually from congenital structural defect of the spine e.g. spina bifida
  • secondary = neuromuscular imbalance (cerebral palsy, muscular dystrophy), disorders of bone or connective tissues
142
Q

SCOLIOSIS
what is the clinical presentation?

A
  • visible curve in spine
  • shoulders, waist or hips look uneven
  • one shoulder blade appears bigger
  • ribs stick out further on one side
  • low back pain
  • back stiffness
  • pain + numbness in legs
  • fatigue (due to muscle strain)
143
Q

SCOLIOSIS
what conditions can cause scoliosis?

A

cerebral palsy
muscular dystrophy
birth defects
infections
tumours
marfan syndrome
down syndrome

144
Q

SCOLIOSIS
what is the management?

A
  • braces
  • spinal fusion surgery
  • spine and rib-based growing operation
145
Q

TORTICOLLIS
what is it?

A
  • tilting of the head to one side caused by contraction of the neck muscles
146
Q

TORTICOLLIS
what are the different types?

A
  • congenital
  • acquired
147
Q

TORTICOLLIS
what are the causes of congenital torticollis?

A
  • congenital muscular torticollis (CMT) = usually noticed in 1st month after birth. It causes shortening + fibrosis of sternocleidomastoid (can have palpable mass)
  • malformed cervical spine
  • spina bifida
148
Q

TORTICOLLIS
what are the causes of acquired torticollis?

A
  • MSK = muscle spasm
  • infection = URTI, otitis media, dental infection, pharyngeal infection
  • atlantoaxial rotatory fixation
  • inflammation = juvenile idiopathic arthritis
  • neoplasm = CNS tumours
149
Q

TORTICOLLIS
how does it present?

A
  • awkward head posture for a prolonged time
150
Q

TORTICOLLIS
what are the investigations?

A

most of the time it is a clinical diagnosis
- cervical spine x-ray can be useful

151
Q

TORTICOLLIS
what is the management?

A

treat the cause
- muscle spasm = self resolve
- infection = antibiotics
- Congenital = physiotherapy

152
Q

OSGOOD SCHLATTERS
what is it?

A

it is an overuse injury that is common in skeletally immature athletic young people

it occurs secondary to repetitive activities such as jumping, sprinting etc.

153
Q

OSGOOD SCHLATTERS
when does it usually develop?

A

during the stage of bone maturation
10-12 in girls
12-14 in boys

154
Q

OSGOOD SCHLATTERS
what is the cause?

A

repeated traction over the tibial tubercle which results in microvascular tears, fractures and inflammation

155
Q

OSGOOD SCHLATTERS
what are the risk factors?

A
  • male gender
  • age - 12-15 in boys, 8-12 in girls
  • sudden skeletal growth
  • repetitive activities such as jumping and sprinting
156
Q

OSGOOD SCHLATTERS
what is the clinical examination?

A
  • anterior knee pain with or without swelling
  • pain aggravated by physical activity
157
Q

OSGOOD SCHLATTERS
what are the investigations?

A

clinical diagnosis

158
Q

OSGOOD SCHLATTERS
what is the management?

A
  • conservative treatment - RICE
  • surgical treatment in severe cases once the child has fully grown
  • physiotherapy

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