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Phase 3a Jemima > Paediatrics - orthopaedics, rheumatology and dermatology > Flashcards

Paediatrics - orthopaedics, rheumatology and dermatology Flashcards

1
Q

what is osteogenesis imperfecta

A

it is a genetic condition of type 1 collagen production, involving connective tissue and bones

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2
Q

what are the features of osteogenesis imperfecta

A

osteoporosis
fragile bones
blue sclera
dental fragility
hearing loss
ligamentous laxility
hypermobility of joints
short stature
easy bruising

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3
Q

what other conditions is osteogenesis imperfecta associated with

A

congenital cataracts

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4
Q

what are the four major clinical features which characterises osteogenesis imperfecta

A
  1. osteoporosis with abnormal bone fragility
  2. blue sclera
  3. dentinogenetic imperfecta
  4. hearing impairment
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5
Q

what is the pathophysiology of osteogenesis imperfecta

A

there is a disturbance in the synthesis of type 1 collagen, which is the predominant protein of the extracellular matrix of most tissue
in bone this defect results on osteoporosis which increases the tendency to fracture
type 1 collagen is also a major constituent of dentine, sclarae, ligaments, blood vessels and skin

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6
Q

what are the genetic abnormalities behind osteogenesis imperfecta

A

mutation in one of two genes that carry instructions for making type 1 collagen
mutations in the COL1A1 and COL1A2 genes are responsible for over 90% of cases

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7
Q

what are the three main types of osteogenesis imperfecta

A
  1. mild: type 1
  2. perinatal lethal: type 2
  3. progressive deforming: type 3
    types 4 and 5 are variable in severity and are uncommon
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8
Q

what are radiographic features that may be found in the head, neck and spine in someone with osteogenesis imperfecta

A

basilar invagination
wormian bones
kyphoscoliosis
vertebral compression fractures
codfish vertebrae
platyspondyly

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9
Q

what radiological features may be seen in the chest in someone with osteogenesis imperfecta

A

pectus excavatum or carinatum
accordion ribs

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10
Q

what are general radiological features seen in someone with osteogenesis imperfecta

A

severe osteoporosis
deformed gracile (overtubulated) bones
cortical thinning
hyperplastic callus formation
popcorn calcification
zebra stripe sign
formation of pseudo arthritis at sites of healing fractures

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11
Q

what features of osteogenesis imperfecta may be seen on antenatal scans

A

may show hypomobilisation of the fetal calvarium - decreased attenuation and abnormally increased visualisation of fetal brain
may show evidence of fractures
may be evidence of polyhydramnios

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12
Q

what might a CT show in someone with osteogenesis imperfecta

A

wormian bones
basilar invagination
osteosclerosis

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13
Q

what are features of osteogenesis imperfecta type 1

A

bones likely to break from mild to moderate trauma, most occurring before puberty
no change or only slightly changed stature with aging
loose joints and muscle weakness
blue, purple or gray tint to sclera
triangular face
curved spine with potential for compression of vertebrae
mild or no bone deformity
possible changes to strength and colour of teeth
possible hearing loss
normal collagen structure but less than the normal amount produced

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14
Q

what are features of osteogenesis imperfecta type 2

A

causes death at birth or shortly after because of the inability to breathe
numerous broken bones that develop before birth
severe bone deformities
very small stature
underdeveloped lungs
blue, purple or gray tint to sclera
improperly formed collagen

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15
Q

what are features of osteogenesis imperfecta type 3

A

most severe type among those who survive the neonatal period
easily broken bones with very little trauma over lifetime
moderate to severe bone deformity
small stature
blue, purple or gray tint to sclera
loose joints
poor muscle development in arms and legs
barrel shaped rib cage
triangular face
curved spine and compression/collapse of vertebrae
possible lung issues
often severe bone deformity
tooth fracture
possible hearing loss
improperly formed collagen

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16
Q

what is the treatment of osteogenesis imperfecta

A

dependent on the type
non lethal types
- surgical correction of deformities and prevention of fractures using rods
- bisphosphonates
- growth hormone therapy

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17
Q

what is rickets

A

rickets is a condition affecting children where there is defective bone mineralisation causing soft and deformed bones

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18
Q

what are causes of rickets

A

rickets is caused by a deficiency in vitamin D or calcium
rare form of rickets is caused by genetic defects that results in low blood phosphate

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19
Q

how is vitamin D obtained in the body

A

produces in response to sunlight
obtained through eating foods such as eggs, oily fish or fortified cereals or supplements

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20
Q

what is hereditary hypophosphataemic rickets

A

this is a rare form of rickets caused by an X linked dominant disorder, where there is low phosphate in the blood

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21
Q

what is the pathophysiology of rickets

A
  1. vitamin D is a hormone created by cholesterol in response to UV
  2. reduced sun without vitamin D supplementation leads to a deficiency
  3. malabsorption disorders can also cause vitamin D deficiency, and so can chronic kidney disease
  4. Vitamin D is essential for calcium and phosphate absorption as well as regulating bone turnover and promoting bone resorption to boost serum calcium
  5. inadequate vitamin D leads to a lack of calcium and phosphate in the blood, leading to defective bone mineralisation.
  6. low calcium also causes a secondary hyperparathyroidism
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22
Q

how does rickets present

A

lethargy
bone pain
swollen wrists
bone deformities
poor growth
dental problems
muscle weakness
pathological or abnormal fractures

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23
Q

what bone deformities can occur in rickets

A

Bowing of the legs - legs curve outward
knock knees - curve inwards
rachitic rosary - where the ends of the ribs expand and the costochondral junctions causing lumps along the chest
craniotabes - soft skull with delayed closure of the sutures and frontal bossing
delayed teeth - under-developed enamel

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24
Q

what investigations should be done in someone with suspected rickets

A

Serum 25-hydroxyvitamin D
W ray
serum calcium and phosphate
serum alkaline phosphatase
parathyroid hormone levels
FBC and ferritin
inflammatory markers
kidney function tests
liver function tests
thyroid function tests
malabsorption screen
autoimmune and rheumatoid tests

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25
Q

what level of serum 25-hydroxyvitamin D in the blood would establish a diagnosis of vitamin D deficiency

A

25 nmol/L or less

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26
Q

what is the management for children with rickets

A

children with vitamin D deficiency can be treated with vitamin D (ergocalciferol) with doses depending on the age
- dose for children between 6 months and 12 years is 6,000 IU per day for 8-12 weeks
children with features of rickets should be referred and treated with vitamin D and calcium. can also have surgery

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27
Q

how can you prevent rickets from occurring

A

breastfed babies are at higher risk of vitamin D deficiency than formula fed babies
breastfeeding women and all children should take vitamin D supplementation
NICE recommends 400 IU (10mg) supplement per day

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28
Q

what is transient synovitis

A

a temporary irritation and inflammation in the synovial membrane of a joint

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29
Q

what is transient synovitis often associated with

A

a recent viral upper respiratory tract infection

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30
Q

how does transient synovitis present

A

occurs within a few weeks of viral illness
hip presents in flexion, abduction and external rotation
limp
refusal to weight bear
groin or hip pain
limited range of movement: most commonly hip abduction
mild low grade fever
normal obs and should be systemically well

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31
Q

how is transient synovitis diagnosed

A

need to rule out septic arthritis
- bed side observations
- bloods: full screen + culture
- imaging: X-ray, USS

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32
Q

what is the management of transient synovitis

A

normally a self limiting disorder and so management is symptomatic with simple analgesia to help the discomfort
- children 3-9 may be managed in primary care if the limp is present for less than 48hrs and they are otherwise well - SAFTEY NET
- follow up at 48hrs and 1 weeks to ensure symptoms are improving and resolve

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33
Q

what percentage of patients may have recurrence of transient synovitis

A

20%

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34
Q

what is septic arteritis

A

this is infection within a joint

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35
Q

what age does septic arthritis most commonly happen in

A

in children under the age of 4

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36
Q

how does septic arthritis present

A

affects one joint - knee or hip mc
rapid onset of:
hot, red, swollen and painful joint
refusing to weight bear
stiffness and reduction in the range of movement
systemic symptoms such as fever, lethargy and sepsis

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37
Q

what are the causative organisms of septic arthritis

A

staphylococcus aureus is most common
neisseria gonorrhoea
group A strep (pyogenes)
haemophilus influenza
e. coli

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38
Q

what are differential diagnosis for septic arthritis

A

transient synovitis
perthes disease
slipped upper femoral epiphysis
juvenile idiopathic arthritis

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39
Q

how is septic arthritis diagnosed

A

Bloods: full screen + cultures
imaging: X-ray, ultrasound
joint aspiration and culture

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40
Q

how is septic arthritis treated

A

Empirical antibiotics IV given until sensitivities are known, choice of which depends on local guidelines (normally ceftriaxone and vancomycin)
antibiotics are given for 30-6 weeks
patients may require surgical drainage and washout to clear the joint of infection

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41
Q

what is osteomyelitis

A

it is an infection in the bone and bone marrow which typically occurs in the metaphysis of the long bones

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42
Q

how might infection be introduced to the bone in osteomyelitis

A

directly - open fracture
travelled through the blood after entering through another route such as skin or gums

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43
Q

what are risk factors for developing oseomyelitis

A

more common in boys
more common in children under 10
open bone fracture
orthopaedic surgery
immunocompromised
sickle cell anaemia
HIV
tuberculosis

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44
Q

how does osteomyelitis present

A

acutely with an unwell child/chronically with subtly features
refusing to use the limb or weight bear
pain
swelling
tenderness
may be afebrile or have a low grade fever

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45
Q

what investigations should be done for osteomyelitis

A

X ray is first line imaging, MRI is the best
bloods: inflammatory markers and wbc
blood culture
bone marrow aspiration/biopsy with histology and culture

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46
Q

how is osteomyelitis managed

A

extensive and prolonged antibiotic therapy - flucloxacillin, clindamycin if penicillin allergy, vancomycin if staph. aureus suspected
surgical drainage and debridement of infected bone

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47
Q

what is Perthes disease

A

involves the disruption of blood flow to the femoral head causing avascular necrosis of the bone, affecting the epiphysis of the femur

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48
Q

what is the most common ages Perthes disease affects

A

children aged 4-12 mostly between the ages of 5-8 and most commonly in boys

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49
Q

what are the causes of Perthes disease

A

idiopathic - theory suggests that repeated mechanical stress to the epiphysis may interrupt the blood supply

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50
Q

what is the presentation of Perthes disease

A

slow onset of:
pain in the hip or groin
limp
restricted hip movements and stiffness with loss of internal rotation and abduction
may be referred pain to the knee
muscle spasms
leg length discrepancy (late finding)

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51
Q

what investigations are done for Perthes disease

A

initial investigation - X ray
bloods: inflammatory markers
technetium bone scan
MRI scan

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52
Q

what is the main complication of Perthes disease

A

soft and deformed femoral head which leads to early hip osteoarthritis

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53
Q

how may patients with Perthes disease will need a total hip replacement

A

around 5% of patients

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54
Q

what is the management of Perthes disease

A

initial management in younger and less severe disease is conservative
help maintain a healthy position and alignment in the joint and reduce the risk of damage or deformity to the femoral head with: bed rest, traction, crutches, analgesia
physiotherapy
regular X rays
surgery to help with alignment and function

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55
Q

what are the radiographic findings in Perthes disease

A

asymmetrical femoral epiphyseal size
increased density of femoral head epiphysis
radiolucency
coxa plana: femoral head widening and flattening
coxa magna: proximal femoral neck deformity
sagging rope sign: thin sclerotic line running across the femoral neck
crescent sign is a specific finding in late stage disease and represents a subchondral fracture

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56
Q

what might increase the likelihood for surgery in perthes disease

A

age over 8 years old
more than 50% of the femoral head is damaged
nonsurgical management has been unsuccessful

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57
Q

what are the complications of Perthes disease

A

osteoarthritis
general join stiffness and immobility
premature physeal arrest, degenerative arthritis
acetabular dysplasia
unequal, shortened limb length

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58
Q

what is discoid menisci

A

A discoid meniscus is thicker than normal, and often oval or disc-shaped. It is more prone to injury than a normally shaped meniscus.

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59
Q

what is the clinical presentation of discoid menisci

A

frequently asymptomatic but discoid menisci are prone to cystic degeneration with subsequent tearing
if this happens it presents as: pain, locking or a clunk sensations
stiffness or swelling
pain
feeling as if the knee is giving way
inability to fully extend the knee

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60
Q

what is the pathophysiology of discoid menisci

A

there is decreased collagen fibres and loss of normal collagen orientation which predisposes them to intradiscal/meniscal mucoid degeneration

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61
Q

what are the different classifications of discoid menisci

A

complete vs incomplete
stable vs unstable

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62
Q

what is the difference between complete and incomplete discoid menisci

A

80% coverage of the tibial plateau is often used as the cut off between incomplete and complete

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63
Q

what is the difference between stable and unstable discoid menisci

A

stable: normal peripheral attachments with an intact posterior meniscofemoral ligament
unstable: lack or tear of a posterior meniscocapsular ligaments with an attachment only from the meniscofemoral ligament of Wrisberg

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64
Q

what are radiographic features of discoid menisci

A

plain radiograph: widening of the lateral joint space and cupping of the lateral tibial plateau
MRI: meniscal body width of 15mm or more is typically considered diagnostic (coronal)

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65
Q

what is the treatment of discoid menisci

A

conservative management
may need meniscal repair with partial or total resection

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66
Q

what are complications of discoid menisci

A

meniscal tears
intrasubstance mucoid degeneration
early bony degenerative change

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67
Q

what is the meniscus

A

it acts as a shock absorber between the femur and the tibia. it protects the thin articular cartilage that covers the ends of the bones and helps the knee to easily bend and straighten

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68
Q

what is incomplete discoid meniscus

A

the meniscus is slightly thicker and wider than normal

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69
Q

what is complete discoid meniscus

A

when the meniscus completely covers the tibia

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70
Q

what is hypermobile Wrisberg discoid meniscus

A

this occurs when the ligaments that attach the meniscus to the femur and tibia are not there. Without these ligaments even a fairly normal shaped meniscus can move around the joint and cause pain, as well as licking and popping of the knee

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71
Q

why is the discoid meniscus more proneto injury

A

due to the thick, abnormal shape f a discoid meniscus makes it more likely to get stuck in the knee or to tear

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72
Q

why is meniscus difficult to heal

A

because the meniscus lacks a strong blood supple and the nutrients that are essential to healing cant reach the injured tissue

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73
Q

what is the cause of discoid meniscus

A

it is a congenital defect that is present from birth

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74
Q

what is the surgical treatment for discoid meniscus

A

knee arthroscopy is the most common - few small incisions and meniscus is cut and reshaped

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75
Q

what is slipped upper femoral epiphysis

A

it is where the head of the femur is displaced (slips) along the growth plate

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76
Q

when is slipped upper femoral epiphysis most common

A

it is most common around the ages of 8-15
most common in boys around 12
rarer in girls, and presents around 11
it is more common in obese children

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77
Q

how does Slipped Upper Femoral Epiphysis present

A

typical presentation is an adolescent , obese male undergoing a growth spurt. There may be history of minor trauma
pain is disproportionate to the severity of the trauma
hip, groin, thigh or knee pain
restricted range of movement in the hip
painful limp

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78
Q

what will examination show for Slipped Upper Femoral Epiphysis

A

the patient will prefer to keep the hip in external rotation
they will have limited movement of the hip, particularly restricted internal rotation

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79
Q

how do you diagnose Slipped Upper Femoral Epiphysis

A

initial investigation is Xray
bloods: normal
technetium bone scan
Ct and MRI

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80
Q

how is Slipped Upper Femoral Epiphysis managed

A

surgery is required to return the femoral head to the correct position and fix it in place to prevent it slipping further

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81
Q

what is Osgood-Schlatter disease

A

inflammation at the tibial tuberosity where the patella ligament inserts and is common cause of anterior knee pain in adolescents

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82
Q

when does Osgood-Schlatter disease typically present

A

at around 10-15 years
more common in males

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83
Q

what is the pathophysiology of Osgood-Schlatter disease

A

the patella tendon inserts into the tibial tuberosity which is at the epiphyseal plate. stress from running, jumping and other movements at the same time as growth can result in inflammation on the tibial epiphysial plate.
there are multiple small avulsion fractures where the patella ligament pulls away pieces if the bone.
this leads to growth of the tibial tuberosity causing a visible lump below the knee
initially this is tender due to inflammation but as the bone heals it becomes hard and non tender

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84
Q

how does Osgood-Schlatter disease present

A

gradual onset of symptoms
visible or palpable hard and tender lump at the tibial tuberosity
pain in the anterior aspect of the knee
pain exacerbated by physical activity, kneeling and on knee extension

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85
Q

how is Osgood-Schlatter disease managed

A

reducing pain and inflammation
- reduction of physical activity
- ice
- NSAIDs for symptomatic relief
once symptoms settle, stretching and physiotherapy can be used to strengthen the joint and improve function

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86
Q

what is the prognosis of Osgood-Schlatter disease

A

symptoms should fully resolve over time
patient is usually left with a hard bony lump on their knee

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87
Q

what is a rare complication of Osgood-Schlatter disease

A

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

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88
Q

how do you treat a full avulsion fracture

A

this usually requires a surgical intervention

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89
Q

what is developmental dysplasia of the hip

A

it is a disorder of abnormal development resulting in dysplasia and potential subluxation or dislocation of the hip secondary to capsular laxity and mechanical factors

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90
Q

when does developmental dysplasia of the hip occur

A

most common abnormality in newborn infants.

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91
Q

which hip is most commonly affected in developmental dysplasia of the hip

A

due to the nature of how the baby sits in the womb the left hip is more commonly affected

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92
Q

what are risk factors of developmental dysplasia of the hip

A

family history of DDH
breeched baby
female sex
fixed root deformity
torticollis

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93
Q

what are clinical features of developmental dysplasia of the hip

A

leg length discrepancy
limitations in hip abduction on one side
significant bilateral restriction in abduction
in children older than 1 a Trendelenburg gait and toe walking may also be seen
asymmetrical buttock creases
hip locking/clicking
pain

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94
Q

what tests are used to screen babies for hip dysplasia

A

Ortolani and Barlow tests

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95
Q

what is the Barlow test

A

performed by adducting the hip (bringing the thigh towards the midline) whilst applying light pressure on the knee with your thumb, directing the force posteriorly.

If the hip is unstable, the femoral head will slip over the posterior rim of the acetabulum, producing a palpable sensation of subluxation or dislocation.

If the hip is dislocatable the test is considered positive.

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96
Q

what is the Ortolani test

A

Ortolani test is done with the baby on their back with the hips and knees flexed. Palms are placed on the baby’s knees with thumbs on the inner thigh and four fingers on the outer thigh. Gentle pressure is used to abduct the hips and apply pressure behind the legs with the fingers to see if the hips will dislocate anteriorly.

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97
Q

how is Developmental dysplasia of the hip diagnosed

A

when it is suspected an ultrasound of the hips will be investigation of choice and establish the diagnosis
all children with risk factors or examination findings should have an ultrasound
Xray can also be used in older infants (greater than 4-6 months)

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98
Q

what is the management of Developmental dysplasia of the hip

A

under 6 months: Pavlik harness
6-8 months or failure of Pavlik harness: closed reduction and spica casting
greater than 18 months (or failure of closed reduction): operative management (open reduction and hip reconstruction)

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99
Q

what is a Pavlik harness

A

it is used in Developmental dysplasia of the hip when the baby is under 6 months. it is fitted and kept on permanently and adjusted for growth. it holds the femoral head in the correct position to allow the acetabulum to develop a normal shape. The harness keeps the babies hips flexed and abducted

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100
Q

what are complications of Developmental dysplasia of the hip

A

recurrence
transient femoral nerve palsy with excessive flexion during Pavlik bracing
avascular necrosis due to retrograde femoral head blood flow (mc affected is the median circumflex femoral artery)

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101
Q

what is juvenile idiopathic arthritis

A

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

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102
Q

when is JIA diagnosed

A

when the arthritis is without any other cause
when it lasts more than 6 weeks
when it is in a patient under 16

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103
Q

what are the different subtypes of JIA

A

five key ones:
systemic JIA
polyarticular JIA
oligoarticular JIA
enthesitis related arthritis
juvenile psoriatic arthritis

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104
Q

what is systemic JIA

A

this is a systemic illness that can occur throughout childhood
it is an idiopathic inflammatory condition

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105
Q

what are the typical features of systemic JIA

A

subtle salmon pink rash
high swinging fevers
enlarged lymph nodes
weight loss
joint inflammation and pain
splenomegaly
muscle pain
pleuritis and pericarditis

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106
Q

will antinuclear antibodies and rheumatoid factor be positive or negative in systemic JIA

A

usually negative
however there will be raised inflammatory markers with raised CRP, ESR, platelets and ferritin

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107
Q

what is a key complication of systemic JIA

A

macrophage activation syndrome

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108
Q

what is macrophage activation syndrome

A

it is where there is a severe activation of the immune system with a massive inflammatory response

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109
Q

how does macrophage activation syndrome present

A

It presents with an acutely unwell child with disseminated intravascular coagulation (DIC), anaemia, thrombocytopenia, bleeding and a non-blanching rash. It is life threatening

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110
Q

what is a key investigation finding in macrophage activation syndrome

A

low ESR

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111
Q

what is polyarticular JIA

A

it involves idiopathic inflammatory arthritis in 5 joints or more

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112
Q

what are the features of polyarticular JIA

A

it tends to be symmetrical
can affect small joints of the hands and feet as well as larger ones
minimal systemic symptoms but there can be mild fever, anaemia and reduced growth

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113
Q

what disease is polyarticular JIA the same as in adults

A

rheumatoid arthritis

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114
Q

are children with polyarticular JIA rheumatoid factor positive or negative

A

most are negative - seronegative
if rheumatoid factor is positive they tend to be older children and adolescents and the disease pattern is much more similar to rheumatoid arthritis in adults

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115
Q

what is oligoarticular JIA

A

it involves 4 joints or less, usually affecting only a single joint

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116
Q

which joints does oligoarticular JIA commonly affect

A

the larger joints
- often the knee or ankle

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117
Q

who does oligoarticular JIA most commonly occur in

A

in girls under the age of 6

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118
Q

what is a classic feature that is associated with oligoarticular JIA

A

anterior uveitis

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119
Q

what are the features of oligoarticular JIA

A

4 or less joints affected
associated with anterior uveitis
patients tend to have no systemic symptoms
antinuclear antibodies are often positive, rheumatoid factor is usually negative

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120
Q

what is enthesitis related arthritis

A

this is thought of as a paediatric version of seronegative spondyloarthropathy
it is inflammation of the point where a tendon of a muscle inserts into a bone. Patients have inflammatory arthritis in the joints as well as enthesitis

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121
Q

what can enthesitis be caused by

A

traumatic stress such as repetitive strain during sport
autoimmune inflammatory process

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122
Q

what can help to diagnose enthesitis

A

an MRI scan (cant differentiate between what it is due to)

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123
Q

what gene do the majority of patients with enthesitis related arthritis have

A

HLA - b27

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124
Q

when assessing a patient with enthesitis related arthritis what else should you be considering

A

signs and symptoms of psoriasis
signs and symptoms of IBD
signs and symptoms of anterior uveitis

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125
Q

what are features of enthesitis related arthritis

A

patients will have tenderness to localised palpation of the entheses
may have signs of psoriasis, IBD or anterior uveitis

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126
Q

what key areas are worth palpating in patients with enthesitis related arthritis

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

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127
Q

what is juvenile psoriatic arthritis

A

this is a seronegative inflammatory arthritis when associated with psoriasis

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128
Q

what are signs associated with juvenile psoriatic arthritis

A

plaques of psoriasis on the skin
pitting of the nails
onycholysis - separation of the nail from nail bed
dactylitis - inflammation of full finger
enthesitis - inflammation of the entheses

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129
Q

how is juvenile idiopathic arthritis managed

A

MDT approach
NSAIDs such as ibuprofen
steroids either oral, IM or intra articular in oligoarthritis
DMARDs such as methotrexate, sulfasalazine and leflunomide
biologic therapy such as TNF inhibitors etanercept, infliximab and adalimumab

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130
Q

what is scoliosis

A

it is an abnormal side to side curve of your spine - can range from mild to severe

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131
Q

what are the different names for idiopathic scoliosis dependent on when it is diagnosed

A

infantile - younger than 3
juvenile - age 4-10
adolescent - 11-18
adult - any time after 18

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131
Q

what are the three types of scoliosis

A

idiopathic - most common
congenital - when vertebrae dont form as they should during development
neuromuscular - abnormalities in the muscles and nerves that support the spine causes this, usually occurs alongside neurological or muscular conditions like injury, cerebral palsy, spina bifida or muscular dystrophy

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132
Q

how common is scoliosis

A

affects an estimated 2% of people around the world

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133
Q

what are symptoms of scoliosis

A

back pain
difficulty standing upright
core muscle weakness
leg pain, numbness or weakness

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134
Q

what are the signs of scoliosis

A

uneven shoulders
shoulder blades that stick out
head that doesnt centre around the pelvis
uneven waist
elevated hip
constant leading to one side
uneven leg length
changes in skin appearance or texture (dimples, hair patches, discolouration)

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135
Q

what part of the spine does scoliosis affect

A

adolescents - most occur in the thoracic spine
adults - mainly lumbar or the lower spine

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136
Q

what can cause scoliosis

A

vertebrae malformation during development
genetic mutation
spinal injury
tumour
muscle/nerve condition

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137
Q

what are risk factors for developing scoliosis

A

biological family history of scoliosis
underlying nerve/muscle condition

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138
Q

what are complications of scoliosis

A

long lasting pain
physical deformity
organ damage
nerve damage
arthritis
spinal fluid leakage
difficulty breathing

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139
Q

how is scoliosis diagnosed

A

scoliosis screening - remove shirt and stand up straight and bend forward.
physical examination
X-rays (from front and side)
CT/MRI

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140
Q

how is scoliosis measured

A

measure the curve of the spine in degrees
no scoliosis diagnosis: less than 10 degrees
Mild: between 10-24 degrees
moderate: between 25-39 degrees
severe: more than 40 degrees

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141
Q

how is scoliosis treated

A

dependent on type and severity
- conservative: regular monitoring, analgesia, exercise/physio, back brace
- surgery: stabilise spine and relieve pressure on nerves

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142
Q

what surgery is done to correct scoliosis

A

spinal fusion: fuse vertebrae to stabilise spine, and use metal braces to hold spine in place
expandable rod: insertion of an expandable rod along vertebrae to support a child’s growing spine

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143
Q

what is torticollis

A

it is when the babies neck muscles cause their head to turn and rotate to one side due to a short, tight sternocleidomastoid muscle

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144
Q

what are the two types of torticollis

A

congenital - mc
acquired

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145
Q

when does acquired torticollis usually occur

A

in the first four to six months of a babies life

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146
Q

what are the symptoms of torticollis

A

babies head tilts to one side and the chin tilts to the other
limited movement of the babies head and neck
one shoulder will be higher than the other
swollen neck muscles
small pea sized limp in one of the babies neck muscles
uneven facial features

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147
Q

what additional symptoms may be present in acquired torticollis

A

severe neck pain
head tremors
headache

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148
Q

what causes torticollis

A

it is due to shortening of the sternocleidomastoid muscle.
It is unsure why it shortens but may be due to positioning in the womb, abnormal development, haemotoma, fibrosis or Klippel-Feil syndrome

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149
Q

what is Klippel-feil syndrome

A

a rare birth defect that causes the vertebrae in the neck to fuse

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150
Q

what causes acquired torticollis

A

because of swelling around the throat. This swelling causes the tissues surrounding the upper spine to loosen, allowing vertebrae to move out of the normal position.
this causes neck muscles to spasm and causing the head to tilt to one side
can also be due to GORD, vision problems, reaction to medications, scar tissue, cervical spondylarthritis, sandifer syndrome, grisel syndrome

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151
Q

what is Sandifer syndrome

A

rare condition which combines GORD with neck spasms

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152
Q

what is Grisels syndrome

A

rare complication of head and neck infections or ENT surgeries

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153
Q

how is torticollis diagnosed

A

physical examination
neck X ray
head and neck CT/MRI

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154
Q

what is the management of torticollis

A

stretching exercised and position changes can help congenital torticollis
may need surgery to lengthen SCM muscle
in acquired need to focus on the underlying cause: antibiotics, botox injections, heat therapy, massage, neck braces/collars, physical therapy

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155
Q

what are growth plates

A

they are found in the bones of children, but not adults. they are the area at the ends of long bones that allow the bones to grow in length

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156
Q

what are growth plates made from

A

hyaline cartilage

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157
Q

what is the difference between bones of children compared to adults

A
  1. children have growth plates
  2. children have more cancellous bone which is spongy and highly vascular making them more flexible but less strong
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158
Q

what are the differences in fractures in children compared to adults

A
  1. the younger the child the faster and better the healing of fractures
  2. when bones break in children they are much more likely to break clean in two
  3. children are more likely to get greenstick fractures where one side of the bone breaks while the other stays intact
  4. children are more likely to have a buckle fracture
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159
Q

what are types of fracture

A

Buckle
transverse
oblique
spiral
segmental
salter-harris (growth plate fracture)
comminuted
greenstick

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160
Q

what are issues with fractures in the growth plate

A

they can cause issues with growth of the bone

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161
Q

what classification is sued to grade growth plate fractures

A

the Salter harris classification
- the higher the grade the more likely it will affect growth

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162
Q

what are the different types of growth plate fractures

A

SALTR pneumonic
type 1: Straight across
type 2: Above
type 3: BeLow
type 4: Through
type 5: CRush

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163
Q

what are the principles of managing a fracture in children

A

think safeguarding - is it a reasonable fracture?
mechanical alignment via closed reduction via manipulation of the joint, or open reduction via surgery
then provide stability with fixing the bone

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164
Q

what are ways a bone can be fixed in place post fracture

A

external casts
K wires
intramedullary wires
intramedullary nails
screws
plate and screws

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165
Q

how do you manage pain in a child with a fracture

A

WHO have a pain ladder for children with two steps
1. paracetamol or ibuprofen
2. morphine

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166
Q

how may hip pain present in children

A

limp
refusal to weight bare
refusal to use affected leg
inability to walk
pain
swollen or tender joint

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167
Q

what are causes of joint pain in children 0-4 years old

A

septic arthritis
developmental dysplasia of the hip
transient arthritis

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168
Q

what are causes of joint pain in children 5-10 years old

A

septic arthritis
transient arthritis
perthes disease

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169
Q

what are causes of joint pain in children 10-16 years old

A

septic arthritis
slipped upper femoral epiphysis
juvenile idiopathic arthritis

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170
Q

what are red flags for hip pain in children

A

Child under 3 years
Fever
Waking at night with pain
Weight loss
Anorexia
Night sweats
Fatigue
Persistent pain
Stiffness in the morning
Swollen or red joint

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171
Q

when would you urgently refer a limping child

A

Child under 3 years
Child older than 9 with a restricted or painful hip
Not able to weight bear
Evidence of neurovascular compromise
Severe pain or agitation
Red flags for serious pathology
Suspicion of abuse

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172
Q

how do you manage a child with a limp/hip pain

A

bloods: inflammatory markers, anaemia
C-rays
ultrasound
joint aspiration
MRI

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173
Q

what is Talipes

A

it is a fixed abnormal ankle position that presents at birth

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174
Q

what is talipes equinovarus

A

this is when the ankle is in plantar flexion and supination

175
Q

what is talipes calcaneovalgus

A

this is when the ankle is in dorsiflexion and pronated

176
Q

what is the ponseti method

A

this is a way of treated talipes without surgery where the foot is manipulated towards a normal position and a cast is applied to hold it in position.
this is repeated over and over until the foot is in the correct position
at some point an achilles tenotomy is perfroed to release tension in the achilles tendon
after treatment with casts, a brace is used to hold the feet in correct position when not walking until the child is around 4

177
Q

what is positional talipes

A

this is a common condition where the resting position of the ankle is in plantar flexion and supination, however it is not fixed and there is no structural boney issue in the ankle
- muscles are slightly tight but bones unaffected
- foot can be moved into a normal position
- physiotherapist provide exercises to help move foot back into a normal position

178
Q

what is achondroplasia

A

it is the most common cause of disproportionate short stature (dwarfism)
- type of skeletal dysplasia

179
Q

what is the cause of achondroplasia

A

the achondroplasia gene (fibroblast growth factor receptor 3) is on chromosome 4, and achondroplasia results from either a sporadic mutation or inheritance of an abnormal copy
- causes abnormal function of the epiphyseal plates and restricts bone growth

180
Q

what is the inheritance pattern of achondroplasia

A

autosomal dominant

181
Q

what are features of achondroplasia

A

disproportionate short stature - average height is around 4ft
short digits
bow legs
disproportionate skull
foramen magnum stenosis

182
Q

what bones are affected in achondroplasia

A

limbs are more affected, with the femur and humerus being affected more than the bones in the forearm and lower leg
spine is less affected and patients have a normal trunk

183
Q

how does achondroplasia affect the skull

A

there is disproportionate skull as different areas of the skull grow by different methods
1. skull base grows and fuses via endochondral ossification and is affected, leading to a flattened mid face, nasal bridge, and foramen magnum stenosis
2. cranial vault grows and fuses via membranous ossification and is unaffected leading to a normal sized vault and frontal bossing

184
Q

what other conditions is achondroplasia associated with

A

recurrent otitis media
kyphoscoliosis
spinal stenosis
obstructive sleep apnoea
obesity
foramen magnum stenosis can lead to cervical cord compression and hydrocephalus

185
Q

what is the management of achondroplasia

A

no cure - MDT approach
pediatricians
specialist nurses
physiotherapists
occupational therapists
dieticians
orthopaedic surgeons - leg length durgery can add height but requires extensive surgery and recovery
ENT surgeons
genetics

186
Q

what surgery is done to help people with achondroplasia

A

leg lengthening surgery
- involves cutting the bone and separating the two parts creating a gap between them. Over a long time bone will form between the two parts, creating a longer bone

187
Q

what is Ehlers danlos syndrome

A

group of genetic conditions involving defects in collagen, causing hypermobility in the joints and abnormalities in the connective tissue of the skin, bones, blood vessels and organs

188
Q

what are the types of ehlers-danlos syndrome

A

Hypermobile
classical
vascular
kyphoscoliotic

189
Q

what are the key features hypermobile ehlers-danlos syndrome

A

it is the most common and least severe type
joint hypermobility
soft and stretchy skin
inherited in an autosomal dominant pattern

190
Q

what are features of classical ehlers danlos syndrome

A

very stretchy skin that feels smooth and velvety
severe joint hypermobility
joint pain
abnormal wound healing
lumps often develop over pressure points
prone to hernias, prolapses
prone to mitral regurgitation and aortic root dilation
inheritance is autosomal dominant

191
Q

what are features of vascular ehlers-danlos syndrome

A

most severe and dangerous
blood vessels particularly fragile and prone to rupture
patients have thin translucent skin
gastrointestinal perforation and spontaneous pneumothorax
patients monitored for vascular abnormalities
autosomal dominant inheritance pattern

192
Q

what are features of Kyphoscoliotic ehlers danlos syndrome

A

it is characterised initially by poor muscle tone as a neonate and infant, followed by kyphoscoliosis as they grow
significant hypermobility
joint dislocation is common
inheritance is autosomal dominant

193
Q

how does Ehlers-Danlos syndrome present

A

joint hypermobility and pain
joint dislocations
soft and stretchy skin
easy bruising
poor wound healing
bleeding
chronic pain and fatigue
headaches
POTS/autonomic dysfunction
GORD
abdominal pain and IBS
menorrhagia and dysmenorrhoea
premature rupture of membranes in pregnancy
urinary incontinence
pelvic organ prolapse
temporomandibular joint dysfunction

194
Q

what is the Beighton score

A

assess hypermobility and supports the diagnosis
one point is scored for each side of the body with a maximum score of 9

195
Q

what is the Beighton score testing in patients

A
  1. if they can place their palms flat on the floor with their legs straight (scores only 1)
  2. hyperextended elbows
  3. hyperextended knees
  4. ability to bend their thumb to touch their forearm
  5. hyperextended their little finger past 90 degrees
196
Q

how is Ehlers-Danlos syndrome managed

A

no cure - manage symptoms
regular follow up
physiotherapy to strengthen and stabilise joints
occupational therapy
moderating activity

197
Q

what is Henoch-schonlein purpura

A

it is an IgA vasculitis that presents with a purpuric rash affecting the lower limbs and buttocks in children

198
Q

what parts of the body does Henoch-scholein purpura affect

A

the skin, kidneys and gastrointestinal tract

199
Q

what is Henoch-schonlein purpura most commonly triggered by

A

upper airway infection or gastroenteritis

200
Q

what are the classical features of Henoch-schonlein purpura

A

purpura
joint pain
abdominal pain
renal involvement

201
Q

what causes the rash in Henoch-schonlein purpura

A

inflammation and leaking of blood from small blood vessels under the skin forming purpura

202
Q

where does the purpura typically present first in Henoch-schonlein purpura

A

start on the legs and spread to the buttocks
they can also affect the trunk and arms

203
Q

what joints are typically affected in Henoch-schonlein purpura

A

arthralgia/arthritis typically affect the knees and ankles in Henoch-schonlein purpura

204
Q

what can happen to GI system in Henoch-schonlein purpura

A

abdominal pain
gastrointestinal haemorrhage
intussusception
bowel infarction

205
Q

how does Henoch-schonlein purpura affect the kidneys

A

via IgA nephritis which can lead to microscopic or macroscopic haematuria and proteinuria

206
Q

how is Henoch-schonlein purpura diagnosed

A

exclude other causes of non-blanching rash
FBC and blood film
renal profile
serum albumin
CRP
blood cultures
urine dipstick
urine protein: creatinine ratio
blood pressure

207
Q

what is the diagnostic criteria for Henoch-schonlein purpura

A

palpable purpura + at least one of:
diffuse abdominal pain
arthritis or arthralgia
IgA deposits on histology
proteinuria or haematuria

208
Q

how is Henoch-schonlein purpura managed

A

supportive with simple analgesia, rest and hydration
steroids is debatable
monitored closely via urine dip and blood pressure

209
Q

what is the prognosis of Henoch-schonlein purpura

A

abdo pain usually settles within a few days
patients without kidney involvement can recover within 4-6 weeks
1/3 of patients will have recurrence within 6 months

210
Q

what are the three phases of kawasaki disease

A

Acute phase: unwell with fever, rash and lymphadenopathy
subacute: desquamation and arthralgia occur and risk of aneurysms
convalescent stage: remaining symptoms settle, blood tests return to normal, aneurysms may regress (lasts 2-4 weeks)

211
Q

what is rheumatic fever

A

it is an autoimmune condition triggered by streptococcus bacteria
it causes antibodies created to fight streptococcus bacteria to target tissues in the body

212
Q

what is the pathophysiology of rheumatic fever

A

caused by group A beta haemolytic streptococcus (pyogenes) which typically causes tonsillitis
antibodies created to fight this infection not only target the bacteria, but also match antigens on cells in the body resulting in a type 2 hypersensitivity reaction where the immune system attacks its own cells

213
Q

what type of hypersensitivity reaction is rheumatic fever

A

type 2 hypersensitivity

214
Q

when does rheumatic fever present after initial streptococcus infection

A

2-4 weeks after the initial infection

215
Q

how does rheumatic fever present

A

fever
joint pain
rash
shortness of breath
chorea
nodules

216
Q

what joint involvement can you get in rheumatic fever

A

migratory arthritis affecting the large joints, with hot swollen painful joints.
- different joints become inflamed and improve at different times

217
Q

what heart involvement can you get in rheumatic fever

A

carditis, inflammation throughout the heart, with pericarditis, myocarditis and endocarditis
- tachycardia or bradycardia
- murmurs (typically through mitral valve disease)
- pericardial rub on auscultation
- heart failure

218
Q

what skin involvement can you get with rheumatic fever

A

subcutaneous nodules - firm painless nodules over extensor surfaces of joints
erythema marginatum rash - pink rings of varying sizes affecting the torso and proximal limbs

219
Q

what nervous system involvement can you get in rheumatic fever

A

chorea - uncontrolled irregular rapid movements of the limbs

220
Q

how is rheumatic fever diagnosed

A

throat swab for culture
ASO antibody titres
ECHO, ECG and chest Xray
diagnosis is made using the jones criteria

221
Q

how do antistreptococcal antibody titres change though infection

A

they indicate recent infection and can support a diagnosis of rheumatic fever.
they rise over 2-4 weeks after initial infection. they peak around 3-6 weeks and then gradually fall over 3-12 months

222
Q

what is the jones criteria for diagnosing rheumatic fever

A

evidence of recent streptococcal infection plus:
two major criteria OR
one major plus two minor criteria

223
Q

what are the major criteria in the Jones criteria for rheumatic fever

A

joint arthritis
organ inflammation, such as carditis
nodules
erythema marginatum rash
sydenham chorea

224
Q

what are the minor criteria in the jones criteria for diagnosing rheumatic fever

A

fever
ECG changes (prolonged PR interval) without carditis
arthralgia without arthritis
raised inflammatory markers

225
Q

how is rheumatic fever managed

A

treatment of infections with antibiotics helps prevent rheumatic fever - Phenoxymethylpenicillin (V) for 10 days
patients with rheumatic fever - MDT
- NSAIDS
- Aspirin and steroids to treat carditis
- prophylactic antibiotics to prevent further infections and recurrence of rheumatic fever
- monitoring and management of complications

226
Q

what are the complications of rheumatic fever

A

recurrence
valvular heart disease (mitral stenosis)
chronic heart failure

227
Q

what is eczema

A

chronic atopic condition caused by defects in the normal continuity of the skin barrier leading to inflammation in the skin

227
Q

when does eczema usually present

A

presents in infancy with dry, itchy and sore patches of skin over the flexor surfaces and on the face and neck

228
Q

what is the pathophysiology of eczema

A

eczema is caused by defects in the barrier that the skin provides.
Gaps in the skin barrier provide and entrance for irritants, microbes and allergens that create an immune response, resulting in inflammation and the associated symptoms

229
Q

what are different types of eczema

A

atopic dermatitis
contact dermatitis
dyshidrotic eczema
neurodermatitis
nummular eczema
seborrheic dermatitis

230
Q

what are symptoms of eczema

A

dry skin
itchy skin
skin rash
bumps on your skin
thick, leathery patches of skin
flaky, scaly or crusty skin
swelling

231
Q

where are common places eczema presents

A

hands
neck
elbows
ankles
knees
feet
face, especially cheeks
in and around the ears
lips

232
Q

what is the management of eczema

A

maintenance and management of flairs

233
Q

what is done for maintenance in eczema treatment

A

create an artificial barrier over the skin - done using emollients that are thick and greasy
patients should avoid activities that can break down the skin barrier - bathing in hot water, scratching or scrubbing their skin, using soaps and body washes that remove natural oils

234
Q

how are flairs treated in eczema

A

thicker emollients, topical steroids, wet wraps (covering affected areas in a thick emollient and applying a wrap to keep moisture in)
treating complications such as bacterial or viral infections

235
Q

what specialist treatments are used in severe eczema

A

zinc impregnated bandages
topical tacrolimus
phototherapy
systemic immunosuppressants such as oral corticosteroids, methotrexate and azathioprine

236
Q

what are examples of thin emollient creams

A

E45
diprobase cream
oilatum cream
aveeno cream
cetraben cream
epaderm cream

237
Q

what are examples of thick, greasy emollient creams used in eczema

A

50:50 ointment (5% liquid paraffin)
hydromol ointment
diprobase ointment
cetraben ointment
epaderm ointment

238
Q

what is the theory for using topical steroids for eczema

A

general rule is to use the weakest steroid for the shortest period of time to get the skin under control
- thicker the skin the stronger the steroid required

239
Q

what are side effects that can happen with use of steroids in eczema

A

can lead to thinning of the skin
makes the skin more prone to flares, bruising, tearing, stretch marks and enlarged blood vessels (telangiectasia)

240
Q

what is the steroid ladder used in eczema from least to most strong

A

Mild: hydrocortisone 0.5, 1 and 2.5 %
moderate: Eumovate (clobetasone butyrate 0.05%)
potent: Betnovate (betamethasone 0.1%)
very potent: Dermovate (clobetasol propionate 0.05%)

241
Q

what is the most common bacterial infection that can occur in eczema

A

most common is staph. aureus

242
Q

how is bacterial infection treated in eczema

A

oral antibiotics - flucloxacillin
more severe cases may need admission and IV antibiotics

243
Q

what is eczema herpeticum

A

this is a viral skin infection in patients with eczema caused by HSV or VZV

244
Q

what is the most common causative organism in eczema herpeticum

A

Herpes simplex virus 1
may be associated with a coldsore

245
Q

how does eczema herpeticum present

A

patient that suffers with eczema that has developed a widespread, painful, vesicular rash
systemic symptoms such as fever, lethargy, irritability, and reduced oral intake
there will usually be lymphadenopathy

246
Q

what does the rash look like in eczema herpeticum

A

widespread - can affect any area of the body
erythematous
painful
can be itchy
vesicles containing pus which burst and leave small punched out ulcers with a red base

247
Q

what is the management of eczema herpeticum

A

viral swabs can confirm the diagnosis
treatment is with aciclovir - in milder cases use oral and in severe cases use IV

248
Q

what are complications of eczema herpeticum

A

life threatening when not treated correctly, particularly in those immunocompromised
bacterial superinfection can occur

249
Q

what is stephens johnson syndrome

A

disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of the skin

250
Q

what is the difference between stevens-johnson syndrome and toxic epidermal necrolysis

A

they are a spectrum of the same pathology
SJS affects less than 10% of the body surface
TEN affects more than 10% of the body surface

251
Q

what are causes of stephen-johnson syndrome

A

medications: anti-epileptics, antibiotics, allopurinol, NSAIDS
infections: herpes simplex, mycoplasma pneumonia, cytomegalovirus, HIV

252
Q

how does stephen-johnson syndrome present

A

dependent on severity
starts nonspecific such as fever, cough, sore throat, sore mouth, sore eyes, itchy skin
then develop a purple or red rash that spreads across the skin and starts to blister
few days after blistering starts the skin starts to break away and shed
eyes can become inflamed and ulcerated
can affect urinary tract, lungs and internal organs

253
Q

what is the management of stephen-johnson syndrome

A

medical emergency
nutritional care, antiseptics, analgesia
steroids
immunoglobulins
immunosuppressants

254
Q

what are complications of stephen-johnson syndrome

A

secondary infection: breaks in skin can lead to bacterial infection, cellulitis and sepsis
permanent skin damage
visual complications: sore eyes, scarring or blindness

255
Q

what is urticaria

A

also known as hives - small itchy lumps that appear on the skin
can be localised or widespread

256
Q

what are the two types of uritcaria

A

acute
chronic

257
Q

what is the pathophysiology of urticaria

A

urticaria is caused by release of histamine and other pro-inflammatory chemicals by mast cells in the skin
- can be part of an allergic reaction in acute
- can be due to autoimmune reaction in chronic

258
Q

what are causes of acute urticaria

A

allergies to food, medications or animals
contact with chemicals, latex or stinging nettles
medications
viral infections
insect bites
dermatographism (rubbing of skin)

259
Q

what causes chronic urticaria

A

autoimmune condition where autoantibodies target mast cells, and can be sub-classified into:
chronic idiopathic
chronic inducible
autoimmune

260
Q

what is chronic idiopathic urticaria

A

it is recurrent episodes of chronic urticaria without a clear underlying cause or trigger

261
Q

what is chronic inducible urticaria

A

episodes of urticaria that can be induced by certain triggers such as:
sunlight
temperature change
exercise
strong emotions
hot or cold weather
pressure (dermatographism)

262
Q

what is autoimmune urticaria

A

it is chronic urticaria which is associated with an underlying autoimmune condition such as SLE

263
Q

what is the management of urticaria

A

antihistamines are the main treatment - fexofenadine
oral steroids can be used in severe flares
in very problematic cases referral is needed and specialised treatment may be given: anti-leukotrienes (montelukast) ,omalizumab and cyclosporin

264
Q

what are birthmarks

A

they are marks on the skin that are present at birth or can show up soon after, which cosmetically change the appearance of the skin

265
Q

what are the types of birthmarks

A

vascular birthmarks: made of blood vessels
pigmented birthmarks: cluster of melanocyte cells

266
Q

what are types of vascular birthmarks

A

hemangiomas
port wine stains
salmon patches/stork bites

267
Q

what is a strawberry hemangioma

A

they consist of small closely packed blood vessels which develop after several weeks and are often rapidly growing

268
Q

where might hemangiomas commonly present

A

face, scalp. back or chest

269
Q

what is a cavernous hemangioma

A

it is similar to a strawberry hemangioma but extends deeper below the surface of the skin

270
Q

what are port wide stain birthmarks

A

flat, purple to red birthmarks made of dilated blood capillaries, which most often appear on the face
port wine stains are permanent and may darken over time

271
Q

what are salmon patches/stork bite birthmarks

A

these marks are capillaries which are visible through the childs skin
they are most common on the forehead, eyelids, upper lip, between the eyebrows and back of the neck

272
Q

what are the different types of pigmented birthmarks

A

dermal melanocytosis (mongolian spots)
pigmented nevi
congenital nevi
cafe-au-lait spots

273
Q

what are the dermal melanocytosis birthmark

A

this is a bluish birthmark which can look like a bruise
they often appear on the buttocks and the lower back

274
Q

what are pigmented nevi

A

these are raised growths on the skin that are the same colour as you natural skin tone/brown/black
moles can appear anywhere on the skin

275
Q

what are congenital nevi

A

these are moles which are present at birth and have a slightly higher chance of becoming skin cancer, depending on the size

276
Q

what are cafe-au-lait spots

A

they are light tan or light brown spots that are usually oval in shape
they appear at birth but bight develop in the first few years of a childs life
multiple spots might be a sign of an underlying condition called neurofibromatosis

277
Q

what causes birthmarks

A

blood vessels not forming as expected
melanocyte cells growing in clusters
genetic predisposition
underlying medical condition

278
Q

how are birthmarks diagnosed

A

physical examination
if its deep in the skin may image it - MRI, ultrasound or CT
skin biopsy may be necessary

279
Q

what are the treatment options for removing a birthmark

A

cryotherapy
laser removal
surgical removal
injections of cortisone

280
Q

what is psoriasis

A

it is a chronic autoimmune condition that causes recurrent symptoms of psoriatic skin lesions

281
Q

what are symptoms of psoriasis

A

patches of psoriasis are dry, flaky, scaly and faintly erythematous skin lesions
can appear in raised and rough plaques
commonly over extensor surfaces of the elbows, knees and scalp

282
Q

what are types of psoriasis

A

plaque psoriasis
guttate psoriasis
pustular psoriasis
erythematous psoriasis

283
Q

what are features of plaque psoriasis

A

thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp
plaques are 1cm-10cm
most common in adults

284
Q

what are features of guttate psoriasis

A

it is the second most common
commonly occurs in children
presents with small raised papules across he trunk and limb
mildly erythematous
scaly
over time the papules can become plaques

285
Q

what are causes of guttate psoriasis

A

streptococcal throat infection
stress
medications

286
Q

what are features of pustular psoriasis

A

severe form where pustules form around areas of erythematous skin
patients can be systemically unwell
treated as medical emergency

287
Q

what are the features of erythrodermic psoriasis

A

rare severe form
extensive erythematous inflamed areas covering most of the surface area of the skin
skin comes away in large patches
medical emergency

288
Q

how does psoriasis present

A

in children the distribution and presentation may differ than in adults
plaques are likely to be smaller, soften and less prominent

289
Q

what are signs which are suggestive of psoriasis

A

Auspitz sign: small points of bleeding where plaques are scraped off
Koebner phenomenon: development of psoriatic lesions to areas of skin affected by trauma
residual pigmentation of skin after lesions resolve

290
Q

what is the management of psoriasis

A

topical steroids
topical vitamin D analogues (calcipotriol)
topical dithranol
topical calcineurin inhibitors (tacrolimus) are usually only used in adults
phototherapy with narrow band UV B light in extensive guttate psoriasis
where topical treatments fail children may be started on unlicensed systemic treatment under specialist guidance: methotrexate, cyclosporin, retinoids, biologics

291
Q

what are two products containing steroid and vitamin D that care used in psoriasis

A

Dovobet
Enstilar
These not licensed in children and will be guided by a specialist.

292
Q

what are other conditions that are associated with psoriasis

A

nail psoriasis: nail pitting, thickening, discolouration, ridging and onycholysis
psoriatic arthritis
psychosocial issues
obesity, hyperlipidaemia, hypertension, T2DM

293
Q

what causes acne valgaris

A

caused by chronic inflammation with or without localised infection, in pockets within the skin known as pilosebaceous unit.
Acne results from increased production of sebum, trapping of keratin and blockage of the pilosebaceous unit leading to swelling and inflammation

294
Q

what are the pilosebaceous units

A

these are tiny dimples in the skin that contain the hair follicles and sebaceous glands. The sebaceous glands produce the natural skin oils and a waxy substance known as sebum

295
Q

why is acne exacerbated by puberty

A

because androgenic hormones increased the production of sebum

296
Q

what are comedones

A

these are swollen and inflamed units in acne

297
Q

how does acne vulgaris present

A

red, inflamed and sore spots on the skin, typically distributed across the face, upper chest and back
has macules, papules and pustules
comedomes - skin coloured papules
blackheads
ice pick scars - small indentations in the skin that remain after acne lesions heal
hypertrophic scars - small lumps in the skin that remain after acne lesions heal
rolling scars - irregular wave like irregularities of the skin that remain after acne lesions heal

298
Q

how is acne managed

A

reduce symptoms of acne, reduce risk of scarring
- topical benzoly peroxide: reduces inflammation and helps unblock skin, toxic to P.acnes bacteria
- topical retinoids: slow production of sebum
- topical antibiotics such as clindamycin
- oral antibiotics such as lymecycline
- oral contraceptive pill

299
Q

what is used as an effective last line treatment for acne

A

oral retinoids
- need careful follow up and monitoring and reliable contraception in females

300
Q

what COCP is the most effective for acne

A

Co-cyprindiol (dianette)
- it has higher risk of thromboembolism so treatment is usually discontinued once acne is controlled and is not prescribed long term

301
Q

what is isotretinoin

A

it is a retinoid which is very effective at clearing the skin

302
Q

what is the mode of action of isotretinoin

A

it reduces the production of sebum
reduces inflammation
reduces bacterial growth

303
Q

what are side effects of isotretinoin

A

dry skin and lips
photosensitivity of the skin to sunlight
depression, anxiety, aggression and suicidal ideation - screen for mental health issues prior
rarely stephens-johnson syndrome and toxic epidermal necrolysis

304
Q

what are the six viral exanthemas diseases

A

first disease: measles
second disease: scarlet fever
third disease: Rubella
fourth disease: Dukes’ disease
fifth disease: Parvovirus B19
sixth disease: roseola infantum

305
Q

what causes measles

A

measles virus

306
Q

when do measles symptoms start after exposure

A

10-12 days after exposure

307
Q

what are koplik spots

A

these are greyish white spots on the buccal mucosa, and appear 2 days after fever in measles

308
Q

where does the rash start in measles

A

the rash starts on the face, classically behind the ears 3-5 days after the fever
it then spreads to the rest of the body

309
Q

how long does measles last

A

it is self resolving after 7-10 days of symptoms

310
Q

how long should children with measles isolate for

A

children should be isolated until 4 days after their symptoms resolve

311
Q

what are complications of measles

A

pneumonia
diarrhoea
dehydration
encephalitis
meningitis
hearing loss
vision loss
death

312
Q

what bacteria is scarlet fever often associated with

A

group A streptococcus infection, usually tonsilitis

313
Q

what causes scarlet fever

A

it is caused by an exotoxin produced by the streptococcus pyogenes bacteria

314
Q

what is the characteristic rash in scarlet fever

A

red-pink, blotchy macular rash with rough
sandpaper skin
starts on the trunk and spreads outward

315
Q

what are features of scarlet fever

A

rash
flushed red cheeks
fever
lethargy
sore throat
strawberry tongue
cervical lymphadenopathy

316
Q

what is the treatment for scarlet fever

A

phenoxymethylpenicillin for 10 days

317
Q

how long should children with scarlet fever be off school for

A

until 24 hours after starting antibiotics

318
Q

what causes rubella

A

the rubella virus

319
Q

how soon after infection so rubella symptoms start

A

2 weeks after exposure

320
Q

what are the symptoms of rubella

A

milder erythematous rash than measles
rash starts on face and spreads to the rest of the body, lasting 3 days
mild fever
joint pain
sore throat
lymphadenopathy behind ears and back of neck

321
Q

how long should children stay off school with rubella

A

for at least 5 days after the rash appears

322
Q

what are the complications of rubella

A

thrombocytopenia
encephalitis
in pregnancy can be dangerous and lead to congenital rubella which causes deafness, blindness and congenital heart disease

323
Q

what causes slapped cheek syndrome

A

parvovirus B 19

324
Q

what is the disease course of slapped cheek syndrome

A

starts with mild fever, coryza and non specific viral symptoms
then 2-5 days in a rash appears as a diffuse bright red rash on both cheeks
few days later a mildly erythematous lace like rash appears on the trunk and limbs

325
Q

how long do children with slapped cheek syndrome need to stay off school for

A

infectious prior to the rash forming but once the rash has formed they are no longer infectious and dont need to stay off school

326
Q

what patients are at risk of complications when infected with parvovirus B19

A

immunocompromised
pregnant patients
sickle cell anaemia
thalassemia
hereditary spherocytosis
haemolytic anaemia

327
Q

what are the complications of parvovirus B19

A

aplastic anaemia
encephalitis or meningitis
pregnancy complications including fetal death
rarely hepatitis, myocarditis or nephritis

328
Q

what causes roseola infantum

A

HHV 6 and less frequently HHV7

329
Q

what is the pattern of illness with roseola infantum

A

presents 1-2 weeks after infection with a high fever (up to 40o) lasting 3-5 days
coryzal symptoms
when the fever settles the rash appears for 1-2 days consisting of a mild erythematous rash across the arms, legs, trunk and face. It is not itchy

330
Q

what is the min complication of roseola infantum

A

febrile convulsions

331
Q

what is parvovirus B19 infection known as

A

slapped cheek syndrome or erythema infectiosum

332
Q

what is erythema multiforme

A

it is a erythematous rash caused by a hypersensitivity reaction

333
Q

what are the most common causes of erythema multiform

A

viral infections and medications
associated with herpes simplex virus and mycoplasma pneumonia

334
Q

how does erythema multiform present

A

it produces a widespread, itchy, erythematous rash
produces characteristic target lesions - red rings within larger rings
doesnt usually affect mucous membraned but can cause a sore mouth
may be associated with mild fever, stomatitis, muscle and joint aches, headaches and flu like illness

335
Q

what is the management of erythema multiforme

A

need to identify the underlying cause and treat that
when there is no clear cause - chest x ray (look for cause)
usually it is mild and will resolve spontaneously without further treatment
in severe cases it may need hospital admission for treatment with IV fluids, analgesia, steroids

336
Q

what causes chicken pox

A

Varicella zoster virus

337
Q

how does chickenpox present

A

widespread, erythematous, raised, vesicular blistering lesions
rash normally starts on the face or trunk and spreads outward affecting the whole body over 2-5 days
eventually lesions scab over

338
Q

what is often the first symptom of chicken pox

A

fever

339
Q

when does a patient with chicken pox stop being infectious

A

after all the lesions have crusted over

340
Q

what are complications of chickenpox

A

bacterial superinfection
dehydration
conjunctival lesions
pneumonia
encephalitis

341
Q

what can happen if chickenpox is caught during pregnancy

A

if the woman is not immune, and catches it before 28 weeks it can cause developmental issues in the fetus
chickenpox around the time of delivery can lead to life threatening neonatal infection treated with VZ immunoglobulins and aciclovir

342
Q

what is the management of chickenpox

A

normally self limiting
aciclovir can be used in immunocompromised patients, adults and adolescents over 14 presenting within 24 hours, neonates and those at risk of complications
symptoms of itching can be treated with calcamine lotion and chlorphenamine (antihistamine)

343
Q

what is the cause of hand foot and mouth disease

A

coxsackie A virus

344
Q

how does hand foot and mouth present

A

illness typically starts with viral respiratory tract symptoms
after 1-2 days small mouth ulcers appear followed by blistering red spots across the body, notably on the hands, feet and mouth
painful mouth ulcers on tongue are also present

345
Q

what is the management of hand foot and mouth

A

no treatment - management is supportive with adequate fluid intake and simple analgesia such as paracetamol if required
the rash and illness resolve spontaneously without treatment after a week to 10 days

346
Q

what are complications of hand, foot and mouth

A

dehydration
bacterial superinfection
encephalitis

347
Q

what advice should be given to help the spread of hand foot and mouth

A

as its highly contagious advise should be given such as:
avoiding sharing towels and bedding
washing hands
careful handling dirty nappies

348
Q

what is molluscum contagiosum

A

it is a viral skin infection caused by the molluscum contagiosum virus which it a type of poxvirus

349
Q

what are features of molluscum contagiosum

A

small flesh coloured papules that characteristically have a central dimple
they typically appear in crops of multiple lesions in a local area
it spreads through direct contact or by sharing items like towels or bedsheets

350
Q

how do the papules in molluscum contagiosum resolve

A

by themselves without treatment however this can take up to 18 months

351
Q

what is the management for molluscum contagiosum

A

no treatment or change in lifestyle is required
avoid sharing towels or other close contact with lesions to minimise the risk of spreading
rarely bacterial superinfection occurs in the lesions due to scratching and this may need antibiotics such as fuscidic acid or flucloxacillin

352
Q

in an immunocompromised patient with molluscum contagiosum what treatment options may be given

A

topical potassium hydroxide, benozyl peroxide, podophyllotoxin imiquimod or tretinoin
surgical removal and cryotherapy

353
Q

what is pityriasis rosea

A

it is a generalised self limiting rash that has an unknown cause. it may be caused by a virus such as HHV6 or 7 but no definitive cause has been established

354
Q

how does pityriasis rosea present

A

there may be prodromal symptoms prior to the rash such as headache tiredness, LOA and flu like symptoms
the rash then starts with a herald patch (faint red or pink scaly oval lesion 2cm or more) which normally presents on the torso
then the rash appears which is a widespread faint red/pink slightly scaly oval shaped lesions. seen as christmas tree rash on the torso
may have a generalised itch, pyrexia, headache and lethargy

355
Q

what is the disease course of pityriasis rosea

A

resolves without treatment within 3 months
can leave a discolouration of the skin where the lesions were but this will resolve within another few months

356
Q

what is the management for pityriasis rosea

A

no treatment for the rash
patient education and reassurance
can have symptomatic treatment if bothered by itching such as emollients, topical steroids or sedating antihistamines at night (chlorphenamine)

357
Q

what is seborrhoeic dermatitis

A

this is an inflammatory skin condition that affects the sebaceous glands, affecting skin where there are a lot of these glands such as the scalp, nasolabial folds and the eyebrows

358
Q

how does seborrhoeic dermatitis present

A

erythema
dermatitis
crusted dry skin
in infants it causes a crusted cry flaky scalp often called cradle cap

359
Q

what is thought to be the cause of seborrhoeic dermatitis

A

Malassezia yeast colonisation is thought to have a role and the condition improves with antifungal treatment

360
Q

what is infantile seborrhoeic dermatitis

A

it is a self limiting condition which causes a crusted flaky scalp

361
Q

what is the first line treatment for infantile seborrhoeic dermatitis

A

applying baby oil, vegetable oil or olive oil, and gently brushing the scalp and then washing off
when this isnt effective white petroleum jelly can be used overnight to soften crusted areas

362
Q

how is infantile seborrhoeic dermatitis treated if oil/emollients are not working

A

topical anti-fungal cream such as clotrimazole or miconazole used for up to 4 weeks

363
Q

what is seborrhoeic dermatitis of the scalp

A

this is a condition which presents with faky itchy skin on the scalp, with more severe cases causing more dense oily scaly brown crusting
- commonly in adolescents and adults rather than children

364
Q

what is the first line treatment forseborrhoeic dermatitis of the scalp

A

ketoconazole shampoo, left on for 5 minutes before washing off
topical steroids may be sued if there is severe itching

365
Q

what is seborrhoeic dermatitis of the face and body

A

this is a condition which presents with red, flaky, crusted itching skin, commonly affecting the eyelids, nasolabial folds, ears, upper chest and back

366
Q

what is the treatment for seborrhoeic dermatitis of the face and body

A

anti-fungal cream such as clotrimazole or miconazole used for up to 4 weeks
localised areas may benefit from topical steroids such as hydrocortisone 1%

367
Q

what is ringworm

A

this is a fungal infection of the skin
also known as tinea and dermatophytosis

368
Q

what are the specific names of fungal infections depending on the areas they infect

A

tinea capitis - ringworm affecting the scalp
tinea pedis - ringworm affecting the feet
tinea cruris - ringworm of the groin
tinea corporis - ringworm on the body
onychomycosis - fungal nail infection

369
Q

how does ringworm present

A

itchy rash that is erythematous, scaly and well demarcated
often one or several rings or circular shaped areas that spread outward, with a well demarcated edge
edge is more prominent and red

370
Q

how does tinea capitis present

A

normal ringworm presentation plus well demarcated hair less
also be itching, dryness and erythema of the scalp

371
Q

how does tinea pedis present

A

white or red flaky, cracked, itchy patches between the toes
skin may split and bleed

372
Q

how does onychomycosis present

A

thickened, discoloured and deformed nails

373
Q

what is the management for ringworm

A

antifungal medications
- creams: clotrimazole or miconazole
- shampoo: ketoconazole
- oral medications: fluconazole, griseofulvin and itraconazole

374
Q

how are fungal nail infections treated

A

with amoroline nail lacquer for 6 -12 months
Resistant cases may need oral terbinafine, however the patient will need their LFTs monitoring before and whilst taking this.

375
Q

what can help with the inflammation and itching in ringworm

A

mild topical steroids: hydrocortisone 1% (often combined with miconazole 2%)

376
Q

what simple advice can be given to people with ringworm to help recovery, prevent spread and avoid recurrence

A

Wear loose breathable clothing
Keep the affected area clean and dry
Avoid sharing towels, clothes and bedding
Use a separate towel for the feet with tinea pedis
Avoid scratching and spreading to other areas
Wear clean dry socks every day

377
Q

what is tinea incognito

A

it is a more extensive and less well recognised fungal skin infection that results from the use of steroids to treat an initial fungal infection
This often occurs when the initial presentation of ringworm was misdiagnosed as dermatitis and a topical steroid was prescribed. The steroid improves the itching and inflammation but accelerates the growth of the fungal infection by dampening the immune response in the local area

378
Q

what is the presentation of tinea incognito

A

less recognisable as ringworm as there is a less demarcated boarder and fewer scales

379
Q

what is nappy rash

A

it is a contact dermatitis in the nappy area usually caused by friction between the skin and the nappy and contact with urine and faeces in a dirty nappy

380
Q

what are risk factors for nappy rash

A

delayed changing of nappies
irritant soap products and vigorous cleaning
certain types of nappies (poorly absorbent ones)
diarrhoea
oral antibiotics predispose to candida infection
pre-term infants

381
Q

how does nappy rash present

A

sore, red, inflamed skin in the nappy area
rash appears in individual patches on exposure areas of the skin
tends to spare the skin creases
skin may be uncomfortable, itchy and infant may be in distress
longstanding rash may lead to erosions and ulceration

382
Q

how can you tell the difference between nappy rash and candidal infection

A

candida (thrush) in the nappy area is a common finding, signs that would point to candida rather than nappy rash are:
- rash extending into the skin folds
- larger red macules
- well demarcated scaly border
- circular pattern to the rash spreading outward
- satellite lesions which are smaller patches of rash or pustules near to the main rash
- may have oral thrush as well

383
Q

what is the management of nappy rash

A

simple measures to improve skin health:
Switching to highly absorbent nappies (disposable gel matrix nappies)
Change the nappy and clean the skin as soon as possible after wetting or soiling
Use water or gentle alcohol free products for cleaning the nappy area
Ensure the nappy area is dry before replacing the nappy
Maximise time not wearing a nappy
infection with candida or bacteria warrants treatment with antifungal or antibiotic (fusidic acid cream or flucloxacillin)

384
Q

what are complications of nappy rash

A

Candida infection
Cellulitis
Jacquet’s erosive diaper dermatitis
Perianal pseudoverrucous papules and nodules

385
Q

what is scabies

A

scabies is tiny mites called sarcoptes scabiei that burrow under the skin causing infection and intense itching. They lay eggs in the skin, leading to further infection and symptoms

386
Q

how does scabies present

A

can take up to 8 weeks for any symptoms to appear after the initial infection
incredibly itchy small red spots, possibly with track marks where the mites have burrows
classic location of the rash is between the finger webs but can spread to the whole body

387
Q

what is the management of scabies

A

permethrin cream - applied to the shole body, completely covering the skin. the cream should be left on for 8-12 hours and then washed off. this should be repeated a week later to catch all the eggs that survived the first treatment and have now hatched
oral ivermectin as a sngle dose can be repeated a week later for difficult to treat/crusted scabies

388
Q

what advice should be given to people diagnosed with scabies

A

All clothes, bedclothes, towels and other materials in contact with scabies need to be washed on a hot wash to destroy the mites. Thorough hoovering of carpets and furniture is also essential.

389
Q

what can be given to people with scabies to help with the itching

A

Crotamiton cream and chlorphenamine at night

390
Q

what is crusted scabies

A

it is a serious infestation with scabies in patients that are immunocompromised
it is extremely contagious
rather than individual spots and burrows they have patches of red skin that turn into scaly plaques

391
Q

what are headlice

A

they are the pediculus humanus capitis parasite which causes infestations of the scalp

392
Q

how are headlice transmitted

A

head to head contact or by sharing equipment like combs or towels

393
Q

how does head lice present

A

itchy scalp
can see visible eggs and lice on examination

394
Q

what is the management for head lice

A

dimeticone 4% applied to hair and left to dry - left on for 8 hrs and then washed off. this is then repeated 7 days later to catch any like that have hatched since the treatment
fine combs can be used

395
Q

what are non blanching rashes

A

these are rashes caused by bleeding under the skin, and can be described as petechiae (<3mm) and purpura (3-10mm)

396
Q

what are causes of a non blanching rash

A

meningococcal septicaemia or other bacterial sepsis
Henoch-schonlein purpura
idiopathic thrombocytopenic purpura
acute leukaemias
haemolytic uraemic syndrome
mechanical: strong coughing, vomiting or breath holding
traumatic: non accidental injury, occlusion of blood in an area
viral illness: influenza and enterovirus

397
Q

what investigations should be done if a child presents with a non blanching rash

A

FBC, U+E, CRP, ESR
coagulation screen
blood culture
meningococcal PCR
lumbar puncture
blood pressure
urine dipstick

398
Q

what is erythema nodosum

A

this is a condition where red lumps appear across the patients shins, caused by inflammation of the subcutaneous fat on the shins

399
Q

what causes erythema nodosum

A

a hypersensitivity reaction and is associated with a number of triggers and underlying conditions

400
Q

what are trigger that can cause erythema nodosum

A

streptococcal throat infections
gastroenteritis
mycoplasma pneumoniae
tuberculosis
pregnancy
medications such as the OCP and NSAIDS

401
Q

what chronic diseases is erythema nodosum associated with

A

inflammatory bowel disease
sarcoidosis
lymphoma
leukaemia

402
Q

how does erythema nodosum present

A

red, inflamed, subcutaneous nodules across both shins
nodules are raised and can be painful and tender
often will settle over time and appear as bruises

403
Q

what investigations should be done in someone with erythema nodosum

A

diagnosis is based on clinical presentation
Inflammatory markers (CRP and ESR)
Throat swab for streptococcal infection
Chest xray can help identify mycoplasma, tuberculosis, sarcoidosis and lymphoma
Stool microscopy and culture for campylobacter and salmonella
Faecal calprotectin for inflammatory bowel disease

404
Q

how is erythema nodosum managed

A

conservatively with rest and analgesia
steroids can be used to settle the inflammation

405
Q

what is impetigo

A

it is a superficial bacterial infection usually caused by staphylococcus aureus bacteria (can also be caused by streptococcus pyogenes)

406
Q

how does impetigo occur

A

when bacteria enters via a break in the skin
- healthy skin or can be related to eczema or dermatitis

407
Q

what is non bullous impetigo

A

typically occurs around the nose and mouth, and has exudate from lesions that dries to form a golden crust

408
Q

how is non bullous impetigo treated

A

topical fusidic acid can be used
antiseptic cream (hydrogen peroxide 1%) can be used in localised non bullous impetigo
oral flucloxacillin can be used in more widespread or severe impetigo

409
Q

what advice should be given about how to reduce spread of impetigo

A

Patients should be given advice about not touching or scratching the lesions, hand hygiene and avoiding sharing face towels and cutlery. They need to be off school until all the lesions have healed or they have been treated with antibiotics for at least 48 hours.

410
Q

what is bullous impetigo

A

it is aways caused by staphylococcus aureus bacteria, and causes 1-2cm fluid filled vesicles to form on the skin which grow and then burst causing a golden crust

411
Q

what type of impetigo is more common in neonates and children under 2

A

bullous impetigo

412
Q

what are symptoms of bullous impetigo

A

lesions - golden crust, painful, itchy
feverish
malaise
can cause staphylococcus scalded skin syndrome

413
Q

what is the treatment of bullous impetigo

A

antibiotics - flucloxacillin

414
Q

what are complications of impetigo

A

Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever

415
Q

what is staphylococcus scalded skin syndrome

A

this is a condition caused by a type of staphylococcus aureus bacteria that produces epidermolysis toxins. These break down proteins that holds skin together

416
Q

how does scalded skin syndrome present

A

generalised patches of erythema on the skin
then the skin looks thin and wrinkles
then there is formation of bullae which burst and leave very sore erythematous skin below
gentle rubbing of the skin causes it to peel away
will have generalised symptoms: fever, irritability, lethargy, dehydration

417
Q

what is Nickolsky sign

A

where very gentle rubbing of the skin causes it to peel away. This is positive in SSSS.

418
Q

what is the management of scalded skin syndrome

A

IV antibiotics
fluid and electrolyte balance is key

419
Q

what is pityriasis versicolour

A

it is a yeast infection of the skin which causes flaky discoloured patches on the chest and back

420
Q

who are most likely to get pityriasis versicolour

A

commonly affects young adults
slightly more common in men than women
can also affect children, adolescents and older adults

421
Q

what are risk factors for pityriasis versicolour

A

it is more common in hot humid climates
it affects those who heavily perspire
may be clear in winter months and recur in the summer

422
Q

what causes pityriasis versicolour

A

fungi in the genus Malassezia which are a part of the normal microbiota
most common are M. globosa, M. restricta and M. sympodialis

423
Q

how do Malassezia cause pityriasis

A

One theory implicates a tryptophan-dependent metabolic pathway.
The yeasts induce enlarged melanosomes (pigment granules) within basal melanocytes in the brown type of pityriasis versicolor.
The white or hypopigmented type of pityriasis versicolor is thought to be due to a chemical produced by malassezia that diffuses into the epidermis and impairs the function of the melanocytes.
The pink type of pityriasis versicolor is mildly inflamed, due to dermatiits induced by malassezia or its metabolites.

424
Q

what are the clinical features of pityriasis versicolour

A

affects the neck, trunk and/or arms
patches may be coppery brown, paler than surrounding skin or pink
pale patches are more common in darker skin
normally asymptomatic but may have mild itching

425
Q

how is Pityriasis versicolour diagnosed

A

wood lamp (black light) examination - yellow-green fluorescence may be seen
dermoscopy of the patches - pallor, background faint pigment network and scale
microscopy of skin scraping
fungal culture
skin biopsy

426
Q

what is the treatment of pityriasis versicolour

A

mild - topical antifungals: selenium sulfide shampoo, topical azole cream/shampoo, terbinafine gel
applied to skin for 5-15 minutes and then washed off - daily for for one week and then weekly for one month
systemic measures - oral: fluconazole
prevention - selenium sulfide shampoo every month once the rash has cleared

427
Q

what is rosacea

A

it is a long term skin condition that mainly affects the face - redness

428
Q

what are the symptoms of rosacea

A

redness across the nose, cheeks, forehead, chin, neck and chest that comes and goes
usually lasts minutes each time
face may also feel warm, hot and painful
burning or stinging feeling when using water or skincare products
may cause tiny broken blood vessels on face
dry skin and swelling around the eyes
yellow-orange patches on the skin
sore eyelids or crusts around the roots of the eyelashes
thickened skin mainly around the nose

429
Q

what are triggers for rosacea

A

It’s not known what causes rosacea, but some things can make symptoms worse.
Common triggers for rosacea include:
alcohol
spicy foods
hot drinks
sunlight
hot or cold temperatures
aerobic exercise, like running
being stressed

430
Q

what is the treatment for rosacea

A

cant be cured but can control symptoms
creams: brimonidine gel to reduce redness, creams such as azelaic acid or metronidazole
antibiotics for 6-16 weeks: doxycycline
dermatology referral

431
Q

what can be done to help with rosacea

A

wear a high SPF sunscreen of at least SPF 30 every day
try to avoid heat, sunlight or humid conditions if possible
try to cover your face in cold weather
use gentle skincare products for sensitive skin
clean your eyelids at least once a day if you have blepharitis
take steps to manage stress

432
Q

if a child presents with a imp/hip pain and has a fever what is the management

A

they need to be referred for same day assessment even if transient synovitis is suspected

433
Q
A

Phase 3a Jemima (16 decks)

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