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A TO REVISE - PHASE 3A > PAEDS MSK/DERMATOLOGY TO DO > Flashcards

PAEDS MSK/DERMATOLOGY TO DO Flashcards

1
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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2
Q

OSTEOMYELITIS
What causes osteomyelitis?

A

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

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3
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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4
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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5
Q

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

A
  • Social deprivation
  • LBW
  • Passive smoking
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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
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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14
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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15
Q

JIA
What is polyarticular JIA?

A
  • ≥5 joints affected, equivalent of RA in adults
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16
Q

JIA
What is oligoarticular JIA?

A

≤4 joints affected, often just monoarthritis

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17
Q

JIA
What is oligoarticular JIA classically associated with?

A

Anterior uveitis = ophthalmologist referral

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18
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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19
Q

JIA
How might enthesitis-related arthritis present?

A
  • Sx of psoriasis (psoriatic plaques, nail pitting, dactylitis) or IBD
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20
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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21
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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22
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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23
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
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24
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
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25
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)
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26
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
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27
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
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28
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
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29
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
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30
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)
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31
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
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32
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

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33
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)
34
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
35
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
36
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)
37
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
38
Q

RICKETS
What would serum biochemistry show in rickets?

A
  • Low = calcium + phosphate
  • High = ALP + PTH
  • 25-hydroxyvitamin D levels deficient (<25nmol/L)
39
Q

RICKETS
What might an XR show in rickets?

A
  • Osteopenia (radiolucent bones)
  • Cupping
  • Fraying of metaphyses
  • Widened epiphyseal plate
40
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

41
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
42
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
43
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)
44
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
45
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
46
Q

ECZEMA
What are some side effects of using topical steroids?

A
  • Thinning of skin
  • Telangiectasia
  • Bruising
47
Q

PSORIASIS
What is the pathophysiology of psoriasis?

A
  • Chronic autoimmune condition where abnormal T-cell activation > hyperproliferation of keratinocytes + so psoriatic skin lesions
48
Q

PSORIASIS
What are the different types of psoriasis?

A
  • Plaque
  • Guttate ‘rain-drop’
  • Erythrodermic + pustular
49
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
50
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
51
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
52
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)
53
Q

PSORIASIS
What are some associations of psoriasis?

A
  • 10–20% develop psoriatic arthritis
  • Increased risk of CVD, metabolic syndrome, VTE
54
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
55
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
56
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
57
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
58
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%
59
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
60
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
61
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
62
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
63
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)
64
Q

SCOLIOSIS
what conditions can cause scoliosis?

A

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

65
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
66
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
67
Q

TORTICOLLIS
what is the management?

A

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

68
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
69
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)

70
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

71
Q

OSTEOMYELITIS
What are some risk factors?

A
  • Open #,
  • orthopaedic surgery,
  • sickle cell anaemia (Salmonella predominates),
  • immunocompromised (HIV),
72
Q

JIA
What are the features of polyarticular JIA?

A

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

73
Q

JIA
How does polyarticular JIA present?

A

Mild systemic Sx = mild fever, anaemia + reduced growth

74
Q

JIA
What is the immunology of polyarticular JIA?

A

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

75
Q

JIA
what is the immunology of oligoarticular JIA?

A

ANA +ve but RF -ve

76
Q

JIA
What is it associated with?

A
  • HLA-B27 gene
  • Prone to anterior uveitis = ophthalmology referral
77
Q

JIA
What causes reactive arthritis?

A

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

78
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

79
Q

RICKETS
What are some sources of vitamin D?

A

Sunlight, fortified cereals, eggs, oily fish

80
Q

PSORIASIS
What are the causes?

A
  • HLA-B13,
  • environmental triggers (alcohol, stress, group A strep)
81
Q

JIA
How does macrophage activation syndrome present?

A
  • Acutely unwell with DIC,
  • febrile,
  • anaemia,
  • thrombocytopenia,
  • bleeding,
  • non-blanching rash,
  • low ESR
82
Q

JIA
What is the management of macrophage activation syndrome?

A

Life-threatening = supportive + steroids

A TO REVISE - PHASE 3A (16 decks)

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