Locomotor, Nutrition, Developmental problems Flashcards

1
Q

Kocher criteria for Septic arthritis

A

WCC>12000
ESR/CRP elevated
Non-Wx bearing
Temp>38

ALL 4= 99% Septic Arthritis

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2
Q

Epidemiology of septic arthritis

A

50% in first 2 years of life
2x more common in Boys
Underlying joint disease or prosthetic joints or bacteraemia increase risk

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3
Q

Presentation of septic arthritis

A
Likely < 3 years old 
75% Lower limb (Knees>Hip>Ankle)
Acute, hot swollen joint 
Pain on passive movement 
Pseudoparalysis 
Cannot weight bear
Systemic symptoms
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4
Q

Diagnosis of septic arthritis

A

Joint aspiration under GA + USS guided
Then Gram stain and culture of synovial fluid
+/- FBC, ESR, CRP, Blood cultures

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5
Q

X-ray findings in septic arthritis

A

Initially normal +/- Widened joint spaces B/C effusion

Later will have space narrowing, erosive changes, subluxation, dislocation

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6
Q

Management of septic arthritis

A

Abx after aspiration
-IV up to 3/52 followed by oral for 4-6/52
Surgical involvement if recurrent or affecting hip
Splintage improves pain
Physio to avoid stiffness

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7
Q

Indications for a LP in septic arthritis

A

If H.Influ then do an LP as there is increased incidence of meningitis

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8
Q

What is developmental dysplasia of the hip

A

Abnormal formation of the hip joint where there is a shallow acetabulum that doesn’t cover the femoral head sufficiently

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9
Q

Risk Factors for DDH

A
FEMALE (6X more likely)
Breech delivery
FHx
1st born
Oligohydramnios 
Other joint problems 
High birth Wx
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10
Q

Screening for DDH

A

1st day- Hips examined

6 weeks USS

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11
Q

How are Breech babies screened for DDH

A

All have USS

Same if 1st degree relative with DDH

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12
Q

Presentation of DDH

A

From birth or shortly after
Delay in walking
Waddling gait (like a pregnant lady)
Shortened affected leg

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13
Q

Barlow and Ortolani tests

A

Tests for DDH

Barlow- Press hips posteriorly when flexed to attempt to dislocate

Ortolani- Hips flexed and then abducted to try and relocate the dislocated hip

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14
Q

Management of DDH

A

Most spontaneously stabilise at 3-6 weeks therefore use double nappies until this point

No success + <6 months= Bracing with Pavlik harness for 3/12

Then consider surgery if above fails

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15
Q

Complications of DDH

A

OA, Lower back pain

Also a risk of re-dislocation and/or avascular necrosis

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16
Q

Commonest cause of hip pain in 3-10 years

A

Reactive arthritis/Irritable hip

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17
Q

Presentation of irritable hip/reactive arthritis

A
Slight limp and hip pain 
Hx viral infection 
No systemic symptoms 
Likely single joint 
No pain at rest but pain O/E
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18
Q

What features would likely indicate septic arthritis over reactive arthritis in a child with limp

A
Systemically unwell 
Fever
Night pain and pain on rest
Cannot Wx bear
> 2 weeks 
Very elevated inflammatory markers
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19
Q

When would you discharge a child with reactive arthritis?

A

Non-dramatic physical signs
X-rays and bloods normal

Advise NSAIDS and rest

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20
Q

Reiter’s syndrome

A

Form of reactive arthritis
“Cant see, can’t wee, can’t climb a tree”

Uveitis, urethritis and arthritis

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21
Q

Classification of JIA

A
Objective arthritis in >/= 1 joint for at least 6 weeks 
\+/- Swelling, warmth, reduced movement 
< 16 years 
Nil other cause found 
Most common in girls under 4 years
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22
Q

Oligoarticular/Pauarticular JIA vs Polyarticular JIA vs Still’s disease

A
Oligo/Pau= Up to 4 joints affected. Most common.
Poly= >4 joints affected
Still's= Systemic onset JIA
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23
Q

Presentation of JIA

A

Joints- Painful, swollen, stiff on mornings, cartilage erosion
Walk on toes
Hepato/Splenomegaly

Still’s= + Fever, salmon-pink rash, Uveitis, Wx loss, Anorexia

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24
Q

Likely Blood result changes in Still’s disease

A

Leukocytes, ESR, CRP and platelets can be raised
HB can be low

Can be similar in non-systemic JIA

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25
Q

Rh and Anti-nuclear factor in JIA

A

Rh can be -ve or +ve

Anti-nuclear factor +ve in 70% Pauarticular JIA

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26
Q

Management of JIA

A

Mild exercise alongside rest each day
Physio and splints
NSAIDS and hot baths +/- Steroid injections

Long term: Methotrexate, Sulfasalazine, oral corticosteroids

Surgery to preserve joint function

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27
Q

Osteomyelitis presentation

A

Fever, Swelling, erythema and severe bony pain
Child will stop using the affected limb

Lucency and periosteal thickening can sometimes be seen on an X-ray

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28
Q

What does a child under 3 years with an acute limp need?

A

A secondary care assessment

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29
Q

Benign idiopathic nocturnal limb pain of childhood (Growing pains)

A

Preschool children (~3-5 years) or 8-12 years
Pain at night and no limp by the day
No interference with normal activities
Meeting motor milestones

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30
Q

Most common age range irritable hip is seen

A

2-8 years

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31
Q

When are Bow legs normal

A

< 3 years

Surgical referral for Blout’s disease if > 4 years

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32
Q

ALL and limp

A

ALL can cause pathological fractures and thereby lead to limp/pain/tenderness
Therefore always have malignancy as a differential

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33
Q

Osgood Schlatters

A

Knee pain in active children

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34
Q

Red flags indicating an organic cause of limp

A
Day and night pain 
There on weekends and vacations 
Interruption of normal activities- ask about play
Unilateral 
Localised to a join 
Unremitting 
Refusal to walk
Systemic manifestations 
Wx loss, bruising, night sweats, hepatosplenomegaly 
Pain on passive internal rotation
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35
Q

Reassuring features indicating a non-organic cause of limp

A
Painless passive internal rotation 
Pain only at night/school days
No interference with normal activities 
Bilateral 
Pain located between joints
Not systemic 
Pain without limp is also reassuring
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36
Q

What is Perthe’s disease

A

Osteochondritis of the femoral head

Can be caused by or develop into avascular necrosis

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37
Q

Risk factors for Perthe’s disease

A

MALE
Short
Trisomy 21

Think a child in Primary school

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38
Q

Presentation of Perthe’s disease

A

Short child 4-8 years who is hyperactive
Progressive hip pain over weeks
Reduced movement, discrepancy in leg length
Limp
Can be bilateral

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39
Q

What gait is classically seen in Perthe’s disease

A

Trendelenberg gait- Unaffected side rises above affected side

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40
Q

X-ray of perthe’s disease

A

Sub-chondral linear lucency

Widened joint space early on

Collapsed deformity later on

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41
Q

Management of Perthe’s disease

A

< 6 years= Observation

If older then try physio and strengthening then callipers (non-wx bearing device) if good imaging

surgery if above fails

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42
Q

What is Slipper upper femoral epiphysis

A

Femoral head epiphysis displaced postero-inferiorly

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43
Q

Risk factors for SUFE

A
Secondary school age (10-16 years)
Obese
Hypothyroidism 
Trauma 
Pelvic RT
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44
Q

Presentation of SUFE

A

Pain, Limp, Reduced movement
Externally rotated hip +/- shorter length
Can be bilateral and thereby look like a ‘normal hip on x-ray’

If Unilateral look for Klein’s line on X-ray- Inferolateral displacement “melting ice cream appearance”

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45
Q

Management of SUFE

A

Surgical fixation/closure to prevent AVN and chondrolysis

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46
Q

Normal calorie requirements

A

150mls/kg/day until around 6/12

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47
Q

How many mls per oz

A

30mls: 1 oz

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48
Q

Maintenance fluids

A

1st 10kg= 100mls/kg/day
2nd 10kg= 50mls/kg/day
subsequent kgs= 20mls/kg/day

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49
Q

Common causes of malabsorption

A
GORD
Chronic infection
CF
Immunodeficiency 
Eating disorder
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50
Q

Definition of malnutrition

A

BMI<18.5

or

> 10% Wx loss over 3/12

Indicated by falling across two centile lines on serial Hx and Wx (or <3rd centile)

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51
Q

Kwashiokor vs Marasmus malnutrition

A

Kwashiokor- Severe protein/AA deficiency: Abd distension and growth retardation

Marasmus- Severe calorie deficiency where height is preserved but they have a wasted appearance

(Generally a mix of the two)

52
Q

Refeeding syndrome

A

Respiratory and cardiac failure induced by electrolyte imbalance as a consequence of rapid large feeding after a period of minimal feeding

53
Q

Feeding options for severe malnutrition

A

Parenteral (IV) or enteral (GI) feeding

54
Q

What is Ricket’s

A

Vitamin D deficiency that occurs before fusion of epiphysial plates during growth
Disrupts mineralisation of said plates

55
Q

What happens to Calcium and Phosphate levels during progression of Vit D deficiency/ Rickets

A

Initially- Low Ca2+ and normal Phos

Then Normal Ca2+ as compensatory hyperparathyroidism

Finally low Ca2+ and low phosphate
This is advanced bone disease with clinical features

56
Q

Radiological findings in rickets/Vit D deficiency

A

Widening at the end of the long bones

Cupped and ragged surfaces

57
Q

Key features of Rickets

A
Frontal bossing 
Ankle and Wrist swelling 
Delayed closure of fontanelles 
Harrison's sulcus below ribs 
Dental hypoplasia 
Leg bowing 
Pectus carinatum 
Craniotabes (bones in cranium collapse under pressure)
Rachitic rosary (expansion of the anterior rib ends at the costochondral junctions)
58
Q

Treatment of Vit D deficiency/Rickets

A

Colacalciferol- 6 weeks

Then need maintenance

59
Q

Genetics of vitamin D dependent rickets

A

Type 1 and 2 are autosomal recessive

Type 1 cannot activate vit D due to enzyme deficiency
Type 2 is end organ resistance to vitamin D

Both present early in life

60
Q

Strongest RF for Down’s syndrome

A

High maternal age

61
Q

Tone features in Down’s syndrome

A

Hypotonia and marked head lag

62
Q

Facial features in Down’s syndrome

A
Small low set ears
Upslanting palpebral fissures
Prominent epicanthic folds
Protuding tongue 
White Brushfield's spots on iris
Flat occiput 
Short neck
63
Q

Limb/Motor features in Down’s syndrome

A
Short broad hands
Single palmar crease
Wide sandle gap
Atlantoaxial instability 
Short
64
Q

Most common heart defect associated with Down’s syndrome

A

AVSD

65
Q

Conditions associated with Down’s syndrome

A
Congential HD
GI- Pyloric stenosis, Atresia, Hirschsprung's, Umbilical hernias, GORD, Coeliac's
DDH
Eczema
Deafness
Cataracts
Leukaemia (1%)
Infections 
Hypo/Hyperthyroidism 
Alzheimer's disease + other dementias
66
Q

Referrals needed in a newly diagnosed child with Down’s syndrome

A

Cardiac assessment
Hip USS for DDH (~6 weeks)
Audiology for ?Deafness
Ophthalmic assessment

67
Q

Median age of death for Down’s syndrome and prognostic information

A

Mid-50s

Much improved as ,10yrs in 1970s
Majority semi-independent
Big risk of AD in 40+

68
Q

Amblyopia

A

Eye fails to achieve visual acuity even with prescription glasses/lenses
Feature of squint when eye has not received clear images in a sensitive period of development

69
Q

3 key features of squint

A

Eye misalignment (Stabismus)
Diplopia
Amblyopia

70
Q

Causes of squint

A

Number 1 is idiopathic

Also consider: Retinoblastoma, Glaucoma, CN palsy, Retinal disease

71
Q

Paralytic vs Non-paralytic squint

A

Non-paralytic= Squint constant in all directions of gaze typically an imbalance of extraocular muscles, convergent or divergent but can be latent where it manifests when tired

Paralytic (Rare)= CN palsy, CN3 is down and out therefore squint varies with direction of gaze

72
Q

Past what age should a squint always be investigated?

A

Beyond 12 weeks

73
Q

How do you investigate a squint?

A

Full Ophthalmic examination including cover test

74
Q

What is involved in an ophthalmic examination?

A
Acuity
Colour
Fields
Pupils + Reflexes
Cover test
Movements 
Fundoscopy
75
Q

Assessing visual acuity

A

Snellen chart at 6m

Fine print reading

76
Q

Assessing colour in ophthalmic examination

A

Ishihara to identify number

77
Q

Assessing visual fields

A

Red hot pin

1) Blind spot
2) Peripheral vision

78
Q

Assessing pupils in an ophthalmic examination

A

Size, shape, symmetry
Direct and consensual pupillary reflex
Accommodation
RAPD- look for dilatation

79
Q

Assessing eye movements in an ophthalmic examination

A

Draw H

80
Q

Cover test

A

Shine light in eye- can they see one or multiple sources of light

Cover one eye and observe for movement

81
Q

Temporal movement in cover test

A

Esotropia

Convergent squint

82
Q

Nasal movement in cover test

A

Exotropia

Divergent squint

83
Q

Fundoscopy

A

1% Tropicamide
Red reflex at 30cm
Then look closer

84
Q

Hypertropia

A

One eye misaligned superiorly

85
Q

Management of squint

A

Correct refractive error with spectacles
Patching good eye prevents ambylopia
Surgery to realign rectus muscle

86
Q

Features of CN3 palsy

A

Pupil dilated
Partial ptosis
Eye is “down and out”

87
Q

Key features of ASD

A

Abnormal impaired development before 3 years
Poor verbal and non-verbal communication
Obsessive repetitive interests
Reduced imaginative play
Difficulties with reciprocal social interaction

88
Q

Problems associated with ASD

A
Epilepsy
Visual/Auditory impairment 
Mental health problems 
Learning disability
PKU, FXS, TS, TORCHES
89
Q

What does 3/60 mean in term of visual acuity?

A

Would have to stand 3 metres to see what a normal person would see at 60 metres

90
Q

Definition of partially sighted and blindness

A

Partially sighted= <6/60

Blind= <3/60

91
Q

Causes of blindness

A
Genetic- Retinoblastoma, cataracts etc
Congenital Rubella syndrome 
Perinatal insult
Post-natal insult
Vitamin A deficiency
92
Q

Key signs of blindness in a newborn/infant

A

Not smiling by 6 weeks
Delayed reaching/Pincer grip (Fine pincer >12 months)
Eye rubbing/irritation
Eyes move and/or look abnormal

93
Q

Auditory impairment screening

A

Newborns have otoacoustic emission test

Can also use auditory brainstem response test

Audiology assessment at 7-9 months if abnormal

94
Q

How does hearing impairment manifest?

A

Nil response to sound
Delayed speech
Behavioural problems
Associated neurology/pathology like LD or blindness

95
Q

Most mild-moderate hearing loss is caused by…

A

Otitis media

Therefore conductive

96
Q

Causes of sensorineural deafness

A
Mostly genetic 
Rubella
Perinatal insult 
Post-natal infections like meningitis 
Some drugs like Amnioglycosides
97
Q

Management of sensorineural hearing loss

A

Sit at front of classroom etc
Hearing aids
Cochlear implants
Makaton if associated learning difficulty

98
Q

Causes of conductive deafness

A

Middle ear disease + Glue ear

ET dysfucntion

99
Q

Management of Conductive deafness

A

Can try Grommets

Amplification with hearing aids

100
Q

Cause of FXS

A

Repeat expansion on the FMR1 gene (>200 CGC repeats)

X-linked and dominant

101
Q

Features of FXS

A

LD (IQ<70) therefore delayed milestones

High forehead, large testicles, large jaws/ears, facial asymmetry, prominent ears

Connective tissue problems= MV prolapse

Echolalia and Perseveration

Epilepsy

102
Q

Causes of developmental delay

A
Genetic/Syndromes- Down's, Fragile X, ASD etc
Perinatal injury
Fetal alcohol syndrome 
TORCHES 
Congential hypothyroidism 
PKU
Leucomalacia 
Neurofibromatosis, TS, Sturge-Weber
Post-natal insult- Meningitis etc
NTDs and Hydrocephalus
103
Q

Dealing with temper tantrums/aggression

A
Stay calm
Ignore bad behaviour
Reward good behaviour- them not doing it initially 
Avoid precipitants like hunger/tiredness
Star chart with child involvement
104
Q

Managing anxiety in children

A

CBT is best… hierachial desensitisation and skills acquisition alongside family involvement

105
Q

Between what ages is normal attachment present

A

6-36 months

106
Q

What are the two types of attachment disorder?

A

Disinhibited

Reactive

107
Q

Disinhibited attachment disorder

A

Caused by early institutional style care or care by a variety of carers
Child is unduly friendly with strangers and forms superficial relationships early

108
Q

Reactive attachment disorder

A

Caused by abuse
Fearful and hypervigilant, not responsive to reassurance
Does not respond appropriately to social interaction

109
Q

What are the 4 types of behavioural interaction seen in attachment disorder

A

A- Insecure avoidant- no reaction to separation/union, suppresses distress

B-Securely attached- distress upon separation, happy upon reunion

C- Insecure ambivalent- stressed upon separation, angry upon reunion

D- Disorganised- mix of A and C

110
Q

Key features of ADHD

A

Inattention
Hyperactivity
Impulsivity

111
Q

Diagnostic features of ADHD

A

Presents at a young age

Impulsivity, Hyperactivity, Inattention

Pervasive (>1 setting) and excessive vs norm for that age

112
Q

Management of ADHD

A
Strict routines
Praise concentration 
Positive reinforcement 
Mindfullness/CBT
Family involvement 
Ritalin
113
Q

Ritalin/Methyphenidate in ADHD

A

Stimulates inhibitory output
Inhibits re-uptake of Dopamine and NorA

Monitor growth 6/12 as it can perturb this and also cause Wx loss

114
Q

Self-harm red flags

A
Significant suicidal ideation 
Hopelessness
Violent methods
Escalating frequency/severity
Disengagement from services
No support system
115
Q

Epidemiology of self harm/suicide

A

self harm more common in females

Suicide more common in males

116
Q

Hx of a self-harm event

A
Explore acute event- Before, During, After
Background of self harm
Suicidal screen and ongoing intent
MSE
SHx/DHx etc
117
Q

Management of ODs/Self-harm in children

A

Admit all ODs overnight to be seen by CAHMS next day

<16 years + self-harm= Admit overnight

16+= Admit to adult ward

118
Q

What 3 features typically make up an eating disorder?

A

Low Wx
Fear of gaining Wx
Desire to be thin

119
Q

Diagnostic criteria for Anorexia Nervosa

A

Restriction of energy intake
Intense fear of gaining Wx despite being underweight
Disturbance in the way one’s body shape/Wx is experienced

120
Q

Common sequela of Anorexia Nervosa

A
Hypokalaemia 
Low Sex hormones
Impaired Glucose tolerance
Hypercholesterolaemia 
Hypercarotenemia= Yellow Skin
Low T3
121
Q

1st line management for Anorexia Nervosa/ Bulimia Nervosa

A

Family therapy

122
Q

Epidemilogy of eating disorders

A

Bulimia more common than Anorexia

Bulimia rare in <13s

123
Q

Diagnostic features of Bulimia

A

Recurrent binges with no control
Recurrent purges to compensate
Above >/=1 time a week for >/=3 months
Self-evaluation entirely based on body shape

124
Q

Below what age can people not refuse treatment?

A

<18 years

Although can still consent

125
Q

Trisomy 18

A

Edward’s syndrome

2nd most common autosomal trisomy

126
Q

Trisomy 13

A

Patau’s syndrome