Paediatrics Flashcards

1
Q

Nocturnal Enuresis Management?

A
  1. General
  2. Enuresis alarm
  3. Desmopressin
  4. Others (Imipramine, Oxybutynin)
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2
Q

Nocturnal Enuresis General Management?

A
  1. Fluid intake
  2. Toileting patterns
  3. Lifting and waking
  4. Reward systems e.g. star charts
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3
Q

Nocturnal Enuresis underlying causes?

A
  1. Constipation
  2. Diabetes
  3. UTI if recent onset
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4
Q

Desmopressin MOA?

A

Vasopressin analogue

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5
Q

Desmopressin side effect?

A

Hyponatraemia

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6
Q

‘Other’ Nocturnal Enuresis management?

A
  1. Imipramine
  2. Oxybutynin
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7
Q

Imipramine MOA?

A

TCA

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8
Q

Oxybutynin MOA?

A

Anticholinergic

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9
Q

Nocturnal Enuresis Classification?

A
  1. Primary = never achieved continence
  2. Secondary = dry for at least 6m before
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10
Q

Desmopressin for NE preferable?

A

Short term control e.g. sleepovers

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11
Q

Child development referral points?

A
  1. Doesnt smile at 10 weeks
  2. Cannot sit unsupported at 12 months
  3. Cannot walk at 18 months
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12
Q

Hand preference before 12 monthsa?

A

Abnormal, ?Cerebral Palsy

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13
Q

Probability of septic arthritis in children criteria?

A

Kocher’s criteria

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14
Q

Kocher’s criteria (1 point each)?

A
  1. Non weight bearing
  2. Fever > 38.5
  3. WCC > 12
  4. ESR > 40
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15
Q

Kocher’s criteria score interpretation?

A
  1. Very low risk
  2. 3% probability
  3. 40% probability
  4. 93% probability
  5. 99% probability
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16
Q

Septic arthritis children epidemiology?

A
  1. 4-5/100,000 children
  2. 2M:1F
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17
Q

Septic arthritis most commonly affected joints?

A

Hip, knee, ankle

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18
Q

Septic arthritis symptoms x4?

A
  1. Joint pain
  2. Limp
  3. Fever
  4. Systemically unwell: lethargy
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19
Q

Septic arthritis signs x3?

A
  1. Swollen
  2. Red joint
  3. Minimal movement of affected joint
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20
Q

Septic Arthritis Ix?

A
  1. Joint aspiration (for culture, WCCs)
  2. Bloods (raised inflammatory markers)
  3. Blood cultures
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21
Q

Kawasaki disease diagnosis?

A

Fever for >5 days + 4/5 of:
1. Bilateral conjunctivitis
2. Cervical lymphadenopathy
3. Cracked lips/strawberry tongue
4. Oedema/desquamation of hands/feet
5. Polymorphic rash

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22
Q

Kawasaki disease management?

A
  1. High dose aspirin
  2. IVIG
  3. Echo
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23
Q

Kawasaki disease complication?

A

Coronary artery aneurysm

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24
Q

Why is aspirin C/I in children?

A

Reye’s syndrome

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25
Q

CXR in TTN?

A

Hyperinflation and fluid in the horizontal fissure

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26
Q

TTN pathophysiology?

A

Delayed resorption of fluid in the lungs

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27
Q

Commonest cause of respiratory distress in newborns?

A

TTN

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28
Q

What mode of birth is TTN more common in?

A

C-sections (lung fluid not being squeezed out during passage through the birth canal)

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29
Q

TTN Management?

A
  1. Observation
  2. Supportive care
  3. Supplementary oxygen may be required
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30
Q

When does TTN usually settle?

A

1-2 days

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31
Q

Even if you suspect TTN what should be done?

A

Baby screened and treated for sepsis

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32
Q

RDS CXR findings?

A

Ground glass appearance and low volume lungs

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33
Q

Meconium aspiration syndrome CXR findings?

A

Asymmetric patchy opacities

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34
Q

Patau syndrome genetics?

A

Trisomy 13

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35
Q

Patau syndrome features?

A
  1. Microcephalic, small eyes
  2. Cleft lip/palate
  3. Polydactyly
  4. Scalp lesions
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36
Q

Edward’s syndrome genetics?

A

Trisomy 18

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37
Q

Edward’s syndrome features?

A
  1. Micrognathia
  2. Low set ears
  3. Rocket bottom feet
  4. Overlapping of fingers
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38
Q

Fragile X features?

A
  1. Learning difficulties
  2. Macrocephaly
  3. Long face
  4. Large ears
  5. Macro-orchidism
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39
Q

Noonan syndrome features?

A
  1. Webbed neck
  2. Pectus excavatum
  3. Short stature
  4. Pulmonary stenosis
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40
Q

Pierre-Robin syndrome features?

A
  1. Micrognathia
  2. Posterior displacement of the tongue (may result in upper airway obstruction)
  3. Cleft palate
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41
Q

Prader-Willi syndrome features?

A
  1. Hypotonia
  2. Hypogonadism
  3. Obesity
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42
Q

William’s syndrome features?

A
  1. Short stature
  2. Learning difficulties
  3. Friendly, extrovert personality
  4. Transient neonatal hypercalcaemia
  5. Supravalvular aortic stenosis
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43
Q

Cri du chat syndrome genetics?

A

Chromosome 5p deletion

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44
Q

Cri du chat syndrome features?

A
  1. Characteristic cry due to larynx and neurological problems
  2. Feeding difficulties and poor weight gain
  3. Learning difficulties
  4. Microcephaly and micrognathism
  5. Hypertelorism
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45
Q

Difference between Pierre-Robin and Treacher-Collins syndrome?

A

TC syndrome is AD so usually FHx of similar problems

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46
Q

Acute epiglottitis cause?

A

Haemophilus Influenzae type B

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47
Q

Why acute epiglottitis decreased?

A

Introduction of HiB vaccine

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48
Q

Acute epiglottitis features x5?

A
  1. Rapid onset
  2. High temp, generally unwell
  3. Stridor
  4. Drooling of saliva
  5. Tripod position
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49
Q

Acute epiglottitis Ix?

A

XR if concern about foreign body

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50
Q

Acute epiglottitis XR findings?

A

Lateral view will show swelling of epiglottis = Thumb sign

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51
Q

Croup XR findings?

A

PA view will show subglottic narrowing = Steeple sign

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52
Q

Croup Rx?

A
  1. Immediate senior involvement, endotracheal intubation may be necessary to protect airway
  2. Oxygen
  3. IV Abx
  4. Do NOT examine throat
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53
Q

Asthma 5-16 y/o Rx?

A
  1. SABA
  2. SABA + Low dose Inhaled ICS
  3. SABA + LD ICS + LTRA
  4. SABA + LD ICS + LABA
  5. SABA + MART
  6. SABA + MD ICS + MART
  7. SABA + (HD ICS as part of fixed dose regime or MART/trial of additional drug e.g. theophylline/refer to expert)
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54
Q

When should you prescribe SABA + LD ICS in asthma 5-16 y/o?

A
  1. Not controlled on previous step OR
  2. Newly diagnosed asthma with >=3/week or night time waking
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55
Q

Asthma <5 y/o Rx?

A
  1. SABA
  2. SABA + 8 week MD ICS (3 offshoots)
  3. SABA + LD ICS + LTRA
  4. Stop LTRA and refer to paediatric asthma specialist
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56
Q

Asthma <5y/o Step 2 Offshoots?

A
  1. If symptoms did not resolve during the trial period, review whether an alternative diagnosis is likely
  2. If symptoms resolved then reoccurred within 4 weeks of stopping ICS treatment, restart the ICS at a paediatric low dose as first-line maintenance therapy
  3. If symptoms resolved but reoccurred beyond 4 weeks after stopping ICS treatment, repeat the 8‑week trial of a paediatric moderate dose of ICS
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57
Q

What is MART?

A
  1. Maintenance and Reliever Therapy
  2. A form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required
  3. MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)
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58
Q

LD ICS dose?

A

<= 200mcg budesonide or equivalent

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59
Q

MD ICS dose?

A

200-400mcg budesonide or equivalent

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60
Q

HD ICS dose?

A

> 400mcg budesonide of equivalent

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61
Q

DDH risk factors?

A
  1. 6F:1M
  2. Breech
  3. FHx
  4. Firstborn
  5. Oligohydramnios
  6. > 5kg
  7. Congenital calcaneovalgus foot deformity
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62
Q

DDH hip preference?

A
  1. Left hip
  2. 20% bilateral
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63
Q

DDH screening?

A
  1. Clinically at newborn and 6 week baby check using Barlow and Ortolani Tests
  2. US for 3 conditions
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64
Q

DDH US screening at 6 weeks?

A
  1. 1st degree FHx of hip problems in early life
  2. Breech presentation at or after 36 weeks gestation, irrespective of presentation at birth or mode of delivery
  3. Breech presentation at delivery if earlier than 36 weeks
    4 Multiple pregnancy
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65
Q

DDH clinical examination?

A
  1. Barlow = dislocate an articulated femoral head
  2. Ortolani = relocate a dislocated femoral head
  3. Others = leg length symmetry, level of knees when hips and knees bilaterally flexed, restricted abduction of the hip in flexion
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66
Q

DDH imaging?

A
  1. US if clinically suspected
  2. If Infant > 4.5 months then XR 1st line
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67
Q

DDH Rx?

A
  1. Most unstable hips will spontaneously stabilise by 3-6 weeks of age
  2. Pavlik harness (dynamic flexion-abduction orthosis) in children younger than 4-5 months
  3. Older children may require surgery
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68
Q

Serum markers in severe asthma?

A

IL-6 and MMP-9

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69
Q

Commonest cause of vomiting in infancy?

A

GORD

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70
Q

GORD risk factors?

A
  1. Pre-term delivery
  2. Neurological disorders
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71
Q

GORD features?

A
  1. Typically develops before 8 weeks
  2. Vomiting/regurgitation following feeds
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72
Q

GORD diagnosis?

A

Clinical

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73
Q

GORD Rx?

A
  1. 30 degree head up during feed
  2. Sleep on back
  3. Smaller and more frequent feeds
  4. Trial of thickened formula
  5. Trial of alginates (Gaviscon), not at same time as thickening agents
  6. PPI with certain criteria
  7. Metoclopramide only used with specialist advice
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74
Q

GORD PPI criteria?

A
  1. Unexplained feeding difficulties (refusing feeds/gagging/choking)
  2. Distressed behaviour
  3. Faltering growth
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75
Q

GORD complications?

A
  1. Distress
  2. FTT
  3. Aspiration
  4. Frequent OM
  5. Dental erosion in older children
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76
Q

GORD fundoplication consideration?

A

If severe complications e.g. FTT and Medical Rx ineffective

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77
Q

Bronchiolitis most common cause?

A

RSV in 75-80%

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78
Q

Bronchiolitis epidemiology?

A

90% in 1-9m, peak incidence 3-6 months

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79
Q

What protects newborns against RSV?

A

Maternal IgG

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80
Q

Other causes of bronchiolitis?

A
  1. RSV
  2. Mycoplasma, adenovirus
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81
Q

When is bronchiolitis more severe?

A
  1. Premature (bronchopulmonary dysplasia)
  2. Congenital heart disease
  3. Cystic fibrosis
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82
Q

Bronchiolitis features?

A

Coryzal symptoms incl. mild fever precede:
1. Dry cough
2. Increasing SOB
3. Wheezing, fine inspiratory crackles

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83
Q

Bronchiolitis referral criteria?

A
  1. Apnoea
  2. Looks unwell
  3. Respiratory distress
  4. RR > 70 breaths/min
  5. Central cyanosis
  6. SpO2 <92%
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84
Q

Bronchiolitis Ix?

A

Immunofluorescence of nasopharyngeal secretions may show RSV

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85
Q

Bronchiolitis Rx?

A

Supportive
1. Humidified oxygen via head box if SpO2 <92%
2. NG feed if indicated
3. Suction sometimes used for excessive upper airway secretionsWh

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86
Q

What should be recorded in all febrile children?

A
  1. Temp
  2. HR
  3. RR
  4. CRT
  5. Signs of dehydration
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87
Q

CF genetics?

A

AR CTFR gene, encoded cAMP-regulated chloride channel

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88
Q

4 organisms which may colonise CF patients?

A
  1. S. aureus
  2. P. aeruginosa
  3. B. cepacia
  4. Aspergillus
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89
Q

Hand, foot and mouth disease cause?

A

Coxsackie A16 and Enterovirus 71

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90
Q

HFM disease features?

A
  1. Mild systemic upset = sore throat, fever
  2. Oral ulcers
  3. Vesicles on palms and soles of the feet
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91
Q

HFM disease Rx?

A
  1. Symptomatic (hydration and analgesia)
  2. No link to cattle disease
  3. Do not need to be excluded from school
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92
Q

Immunisations at birth?

A

BCG if risk factor

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93
Q

Immunisations at 2 months?

A
  1. ‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
  2. Oral rotavirus vaccine
  3. Men B
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94
Q

Immunisations at 3 months?

A
  1. ‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
  2. Oral rotavirus vaccine
  3. PCV
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95
Q

Immunisations at 4 months?

A
  1. ‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
  2. Men B
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96
Q

Immunisations at 12-13 months?

A
  1. Hib/Men C
  2. MMR
  3. PCV
  4. Men B
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97
Q

Immunisations at 2-8 years?

A

Flu vaccine (annual)

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98
Q

Immunisations at 3-4 years?

A
  1. ‘4-in-1 pre-school booster’ (diphtheria, tetanus, whooping cough and polio)
  2. MMR
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99
Q

Immunisations at 12-13 years?

A

HPV vaccine

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100
Q

Immunisations at 13-18 years?

A
  1. ‘3-in-1 teenage booster’ (tetanus, diphtheria and polio)
  2. Men ACWY
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101
Q

Croup main cause?

A

Parainfluenza virus

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102
Q

Croup epidemiology?

A

6m - 3y
More common in autumn

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103
Q

Croup features?

A
  1. Stridor
  2. Barking cough (worse at night)
  3. Fever
  4. Coryzal symptoms
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104
Q

Croup admission features?

A
  1. Any child with moderate or severe croup
  2. <6 m/o
  3. Known upper airway abnormalities e.g. laryngomalacia, Down’s
  4. Uncertainty about diagnosis
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105
Q

Croup Rx?

A

Single dose oral dexamethasone 0.15mg/kg to all children regardless of severity

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106
Q

Emergency croup Rx?

A
  1. High flow O2
  2. Nebulised adrenaline
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107
Q

Hypospadia characteristics?

A
  1. Ventral urethral meatus
  2. Hooded prepuce
  3. Chordee in more severe forms
  4. Urethral meatus may open more proximally in more severe variants
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108
Q

Hypospadia managament?

A
  1. Referral to specialist when identified
  2. Corrective surgery usually at 12 m/o
  3. Essential not circumcised prior
  4. Rx may not be needed in very distal disease
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109
Q

Commonest gynaecological disorder in girls?

A

Vulvovaginitis

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110
Q

Vulvovaginitis Rx?

A
  1. Advise about hygiene
  2. Soothing creams may be useful
  3. Topical Abx/antifungals
  4. Oestrogen cream in resistant cases
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111
Q

When does mucoid white vaginal discharge disappear?

A

3m of age

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112
Q

CMPI/CMPA epidemiology?

A

3-6% of all children and typically presents in the first 3 months of life in formula-fed infants, although rarely it is seen in exclusively breastfed infants

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113
Q

CMPI vs. CMPA IgE status?

A

Both IgE mediated (immediate) and delayed (non-IgE mediated reactions are seen)
CMPI = mild-moderate delayed reactions
CMPA = immediate reactions

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114
Q

CMPI/CMPA features?

A
  1. Regurgitation and vomiting
  2. Diarrhoea
  3. Urticaria, atopic eczema
  4. ‘Colic’ symptoms: irritability, crying
  5. Wheeze, chronic cough
  6. Rarely angioedema and anaphylaxis may occur
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115
Q

CMPI/CMPA Dx?

A

Often clinical, e.g. improvement with CMP elimination

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116
Q

CMPI/CMPA Ix?

A
  1. Skin prick/patch testing
  2. Total IgE and specific IgE (RAST) for cow’s milk protein
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117
Q

CMPI/CMPA management classification?

A
  1. Formula fed
  2. Breastfed
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118
Q

CMPI/CMPA formula fed management?

A
  1. Extensive hydrolysed formula (eHF) milk is the first-line replacement formula for infants with mild-moderate symptoms
  2. Amino acid-based formula (AAF) in infants with severe CMPA or if no response to eHF
  3. Around 10% of infants are also intolerant to soya milk
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119
Q

CMPI/CMPA breastfed management?

A
  1. Continue breastfeeding
  2. Eliminate cow’s milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers whose babies have, or are suspected to have, CMPI, to prevent deficiency whilst they exclude dairy from their diet
  3. Use eHF milk when breastfeeding stops, until 12 months of age and at least for 6 months
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120
Q

CMPI prognosis?

A
  1. CMPI usually resolves in most children
  2. In children with IgE mediated intolerance around 55% will be milk tolerant by the age of 5 years
  3. In children with non-IgE mediated intolerance most children will be milk tolerant by the age of 3 years
  4. A challenge is often performed in the hospital setting as anaphylaxis can occur.
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121
Q

Labial adhesion definition?

A

Fusion of the labia minora in the midline

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122
Q

Labial adhesion epidemiology?

A
  1. 3m - 3y/o
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123
Q

Labial adhesion features?

A

Majority of cases are symptomatic
1. Micturition problems incl. vaginal pooling
2. On examination thin semitranslucent adhesions covering the vaginal opening between the labia minora are seen, which sometimes cover the vaginal opening completely

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124
Q

Labial adhesion Rx?

A
  1. Usually conservative (spontaneous resolution around puberty)
  2. If associated problems e.g. UTI –> oestrogen cream
  3. If this fails surgical intervention may be warranted
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125
Q

Labial adhesion cause?

A

Low level of oestrogen

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126
Q

Umbilical embryology?

A

During development the umbilicus has two umbilical arteries and one umbilical vein. The arteries are continuous with the internal iliac arteries and the vein is continuous with the falciform ligament (ductus venosus). After birth, the cord dessicates and separates and the umbilical ring closes.

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127
Q

Umbilical hernia?

A
  1. 20% neonates
  2. Majority will close within 12m-3y
  3. Strangulation rare
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128
Q

Paraumbilical hernia?

A
  1. Defect in linea alba close to umbilicus
  2. Edge more clearly defined than umbilical hernia
  3. Less likely to resolve than umbilical hernia
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129
Q

Omphalitis?

A
  1. Infection of the umbilicus, usually S. Aureus
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130
Q

Why is omphalitis dangerous?

A

Infection may spread through umbilical vessels with risk of portal pyaemia and portal vein thrombosis

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131
Q

Omphalitis Rx?

A

Topical and systemic Abx

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132
Q

Umbilical granuloma?

A
  1. Cherry red lesions surrounding the umbilicus, may bleed on contact and be a site of seropurulent discharge
  2. Infection is unusual
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133
Q

Umbilical granuloma Rx?

A
  1. Regular application of salt to wound
  2. Chemical cautery with topically applied silver nitrate
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134
Q

Persistent urachus?

A
  1. Urinary discharge from umbilicus
  2. Caused by persistence of urachus which attaches to the bladder
  3. Associated with other urogenital abnormalities
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135
Q

Persistent vitello-intestinal duct?

A
  1. Umbilical discharge that discharges small bowel content
  2. Complete persistence of duct is rare
  3. More common is persistence of part of duct (Meckel’s)
  4. Best imaged using contrast study to delineate anatomy
  5. Managed by laparotomy and surgical closure
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136
Q

Jaundice in first 24 hours?

A

Always pathological

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137
Q

Causes of Jaundice in first 24 hours?

A
  1. Rhesus haemolytic disease
  2. ABO haemolytic disease
  3. Hereditary spherocytosis
  4. G6PDD
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138
Q

Causes of jaundice from 2-14 days?

A
  1. Common (up to 40%), usually physiological. Due to more RBCs, more fragile RBCs, and less developed liver function
  2. More commonly seen in breastfed babies
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139
Q

Jaundice after 14 days Ix?

A

Prolonged jaundice screen (>21 days if premature)
1. Conjugated and unconjugated bilirubin
2. DAT (Coombs)
3. FBC, U&E, LFT, TFT, blood film
4. Urine for MC&S and reducing sugars

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140
Q

Meningococcal septicaemia benzylpenicillin community doses?

A
  1. <1 y/o = 300mg
  2. 1-10 y/o = 600mg
  3. > 10 years = 1200mg
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141
Q

Brushfield spots?

A

Down’s syndrome

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142
Q

Coloboma?

A
  1. Defect causing gap in lens, iris or retina
  2. Associated with Patau syndrome
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143
Q

Down’s features?

A
  1. Face = upslanting palpebral fissures, epicanthic folds, Brushfield spots in iris, protruding tongue, small low-set ears, round/flat face
  2. Flat occiput
  3. Single palmar crease, sandal gap
  4. Hypotonia
  5. Congenital heart defects (40-50%)
  6. Duodenal atresia
  7. Hirschprung’s disease
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144
Q

Down’s cardiac complications?

A
  1. Endocardial cushion defect (most common, 40%, AKA atrioventricular septal canal defect)
  2. VSD (30%)
  3. Secundum ASD (10%)
  4. Tetralogy of Fallot (5%)
  5. Isolated PDA (5%)
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145
Q

Down’s fertility?

A
  1. Males = almost always infertile due to impaired spermatogenesis
  2. Females = usually subfertile and have an increased incidence of problems with pregnancy and labour
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146
Q

Down’s other features?

A
  1. LD
  2. Short stature
  3. Repeated respiratory infections and glue ear
  4. ALL
  5. Hypothyroidism
  6. Alzheimer’s disease
  7. Atlanto-axial instability
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147
Q

5 normal lower limb variants in children?

A
  1. Flat feet (pes planus)
  2. In toeing
  3. Out toeing
  4. Bow legs (genu varum)
  5. Knock knees (genu valgum)
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148
Q

Flat feet mushkies?

A
  1. Present at all ages
  2. Absent medial arch on standing
  3. Typically resolves b/w 4-8 y/o, orthotics not recommended, parental reassurance appropriate
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149
Q

In toeing mushkies?

A
  1. Typically presents in 1st year
  2. Possible causes = metatarsus adductus, internal tibial torsion, femoral anteversion
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150
Q

Out toeing mushkies?

A
  1. Common in infancy and usually resolves by 2 y/o
  2. Usually due to external tibial tosion
  3. Intervention may be appropriate if doesnt resolve as increases risk of patellofemoral pain
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151
Q

Bow legs mushkies?

A
  1. Presents in 1st-2nd year
  2. Increased intercondylar distance
  3. Typically resolves by age of 4-5 years
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152
Q

Knock knees mushkies?

A
  1. Presents in 3rd-4th year
  2. Increased intermalleolar distance
  3. Typically resolves spontaneously
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153
Q

Most common cause of cyanotic CHD?

A

Tetralogy of Fallot

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154
Q

Tetralogy of Fallot time of presentation?

A

1-2 months, although may not be picked up until 6 months old

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155
Q

ToF x4?

A
  1. VSD
  2. RVH
  3. PS
  4. OA
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156
Q

Features of ToF?

A
  1. Right to left shunt
  2. Ejection systolic murmur due to PS
  3. Right sided aortic arch in 25%
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157
Q

ToF Cyanosis mushkies?

A
  1. Unrepaired TOF infants may develop episodic hypercyanotic ‘tet’ spells due to near occlusion of the right ventricular outflow tract
  2. Features of tet spells include tachypnoea and severe cyanosis that may occasionally result in loss of consciousness
  3. They typically occur when an infant is upset, is in pain or has a fever
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158
Q

ToF CXR?

A

Boot shapes heart

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159
Q

ToF ECG?

A

RVH

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160
Q

ToF management?

A
  1. Surgical repair often undertaken in two parts
  2. Cyanotic episodes may be helped by BB to reduce infundibular spasm
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161
Q

Chondromalacia patellae mushkies?

A
  1. Softening of the cartilage of the patella
  2. Common in teenage girls
  3. Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
  4. Usually responds to physiotherapy
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162
Q

Osgood-Schlatter disease (tibial apophysitis) mushkies?

A
  1. Seen in sporty teenagers
  2. Pain, tenderness and swelling over the tibial tubercle
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163
Q

Osteochondritis dissecans mushkies?

A
  1. Pain after exercise
  2. Intermittent swelling and locking
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164
Q

Patellar subluxation mushkies?

A
  1. Medial knee pain due to lateral subluxation of the patella
  2. Knee may give way
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165
Q

Patellar tendonitis mushkies?

A
  1. More common in athletic teenage boys
  2. Chronic anterior knee pain that worsens after running
  3. Tender below the patella on examination
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166
Q

Causes of snoring in children?

A
  1. Obesity
  2. Nasal problems (polyps, deviated septum, hypertrophic nasal turbinates)
  3. Recurrent tonsillitis
  4. Down’s syndrome
  5. Hypothyroidism
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167
Q

Respiratory distress syndrome (RDS) AKA?

A
  1. Surfactant lung deficient disease (SDLD)
  2. Hyaline membrane disease (HMD)
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168
Q

SDLD cause?

A

Insufficient surfactant production and structural immaturity of the lungs

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169
Q

SDLD prevalence?

A
  1. 50% born at 26-28 weeks
  2. 25% born at 30-31 weeks
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170
Q

Risk factors for SDLD?

A
  1. Male sex
  2. Diabetic mothers
  3. C-section
  4. Second born of premature twins
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171
Q

SDLD CXR?

A

Ground glass appearance with indistinct heart border

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172
Q

SDLD clinical features?

A

Similar to respiratory distress in the newborn i.e. tachypnoea, intercostal recession, expiratory grunting and cyanosis

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173
Q

SDLD management?

A
  1. Prevention during pregnancy = maternal corticosteroids to induce fetal lung maturations
  2. Oxygen
  3. Assisted ventilation
  4. Exogenous surfactant given via endotracheal tube
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174
Q

Caffeine in newborn babies?

A

Used as a respiratory stimulant

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175
Q

Sildafenil in neonates?

A

Pulmonary hypertension

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176
Q

Speech and hearing 3m?

A

Quietens to parents voice, turns towards sound, squeals

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177
Q

Speech and hearing 9m?

A

Mama and Dada
Understands no

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178
Q

Speech and hearing 12m?

A

Knows and responds to own name

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179
Q

Speech and hearing 12-15m?

A

Knows 2-6 words, understands simple commands

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180
Q

Speech and hearing 2y?

A

Combines two words, points to parts of the body

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181
Q

Speech and hearing 2.5y?

A

Vocabulary of 200 words

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182
Q

Speech and hearing 3y?

A

Talks in short sentences (e.g. 3-5 words)
Asks ‘what’ and ‘who’ questions
Identifies colours
Counts to 10 (little appreciation of numbers though)

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183
Q

Speech and hearing 4y?

A

Asks why, when, how questions

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184
Q

Gross motor 3m?

A

Little or no head lag on being pulled to sit
Lying on abdomen, good head control
Held sitting, lumbar curve

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185
Q

Gross motor 6m?

A

Lying on abdomen, arms extended
Lying on back, lifts and grasps feet
Pulls self to sitting
Held sitting, back straight
Rolls front to back

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186
Q

Gross motor 7-8 months?

A

Sits without support (refer at 12 months)

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187
Q

Gross motor 9m?

A

Pulls to standing, crawls

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188
Q

Gross motor 12m?

A

Cruises, walks with one hand held

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189
Q

Gross motor 13-15m?

A

Walks unsupported (refer at 18 months)

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190
Q

Gross motor 18m?

A

Squats to pick up a toy

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191
Q

Gross motor 2y?

A

Runs
Walks upstairs and downstairs holding on to rail

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192
Q

Gross motor 3y?

A

Rides a tricycle using pedals
Walks up stairs without holding on to rail

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193
Q

Gross motor 4y?

A

Hops on one leg

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194
Q

When should you consider pneumonia over bronchiolitis?

A

High fever (>39 degrees) and/or persistently focal crackles

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195
Q

Most common cause of nephrotic syndrome in children?

A

Minimal change disease

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196
Q

Nephrotic syndrome triad?

A
  1. Proteinuria (>1g/m^2 per 24 hours)
  2. Hypoalbuminaemia (<25g/l)
  3. Oedema
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197
Q

Minimal change disease management?

A

90% cases responding to high dose oral steroids

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198
Q

Minimal change disease peak incidence age?

A

2-5 y/o

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199
Q

Other features of nephrotic syndrome?

A
  1. Hyperlipidaemia
  2. Hypercoagulable state (due to loss of antithrombin III)
  3. Predisposition to infection (due to loss of Igs)
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200
Q

ADHD epidemiology?

A
  1. 2x autism, 4M:1F
  2. Most diagnosed 3-7 y/o
  3. Possible genetic component
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201
Q

ADHD triad?

A
  1. Inattention
  2. Hyperactivity
  3. Impulsivity
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202
Q

ADHD diagnosis?

A
  1. 6 features up to 16 y/o
  2. 5 features > 17 y/o
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203
Q

ADHD management?

A
  1. Ten week watch and wait period
  2. If persists then referral to secondary care
  3. Mild/moderate = parents attending education and training programmes
  4. Methylphenydate on a 6 week trial basis
  5. If inadequate response switch to lisdexamfetamine
  6. Dexamfetine if cant tolerate lisdexamfetamine side effects
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204
Q

Age at which methylphenidate can be started?

A

> 5 y/o

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205
Q

Methylphenidate MOA?

A

CNS stimulant which primarily acts as a dopamine/noradrenaline reuptake inhibitor

206
Q

Methylphenidate s/e?

A

Abdominal pain, nausea, dyspepsia

207
Q

Methylphenidate monitoring?

A

Weight and height monitored every 6 months

208
Q

Adult ADHD medication?

A
  1. Methyphenidate or lisdexamfetamine are first line options, switch between these drugs if no benefit is seen after a trial of the other
209
Q

Methylphenidate heart effects?

A
  1. Cardiotoxic
  2. Perform baseline ECG before Rx, refer to cardiologist if any doubt
210
Q

Gastroschisis definition?

A

Congenital defect in the anterior abdominal wall just lateral to the umbilical cord

211
Q

Gastroschisis managament?

A
  1. Vaginal delivery may be attempted
  2. Newborns should go to theatre ASAP after delivery e.g. within 4 hours
212
Q

Exomphalos (omphalocoele) definition?

A

Abdominal continents protrude through the anterior abdominal wall but are covered in an amniotic sac formed by the amniotic membrane and peritoneum

213
Q

Exomphalos associations?

A
  1. Beckwith-Wiedamann syndrome
  2. Down’s syndrome
  3. Cardiac and kidney malformations
214
Q

Exomphalos management?

A
  1. C-section indicated to reduce risk of sac rupture
  2. Staged repair may be undertaken as primary closure may be difficult due to high intra-abdominal pressure
215
Q

Is gastroschisis associated with other tings?

A

Tends to be a stand-alone medical condition

216
Q

What is palivizumab?

A

mAb used to prevent RSV in those at increased risk of disease

217
Q

SUFE mushkies?

A
  1. Typically obese boys 10-15 years
  2. Displacement of femoral head epiphysis postero-inferiorly
  3. May present acutely following trauma or more commonly with chronic, persistent symptoms
218
Q

SUFE features?

A
  1. Hip, groin or medial thigh or knee pain
  2. Loss of internal rotation of the leg in flexion
  3. Bilateral slip in 20% cases
219
Q

SUFE Ix?

A

AP and lateral (typically frog-leg) views diagnostic

220
Q

SUFE Rx?

A

Internal fixation: typically a single cannulated screw placed in the centre of the epiphysis

221
Q

Aortic stenosis associations?

A
  1. William’s syndrome
  2. Coarctation of the aorta
  3. Turner’s syndrome
222
Q

Management of aortic stenosis in children?

A
  1. Aim is to avoid or delay valve replacement if possible
  2. If gradient across valve is >60mmh Hg then balloon valvotomy may be indicated
223
Q

Meconium aspiration syndrome mushkies?

A
  1. More common in post-term, 44% in babies born after 42 weeks
  2. Higher rates occur in Hx of maternal HTN, pre-eclampsia, chorioamnionitis, smoking or substance abuse
224
Q

Milk ladder?

A
  1. Malted milk biscuits
  2. Digestive biscuits
  3. Chocolate and yoghurt
225
Q

Haemorrhagic disease of the newborn mushkies?

A
  1. Newborn babies relatively deficient in Vit K, may result in impaired production of clotting factors which can lead to HDN
226
Q

Increased risk of HDN?

A
  1. Breastfed babies
  2. Maternal use of antiepileptics
227
Q

How to reduce risk of HDN?

A

All newborns in Uk are offered Vitamin K

228
Q

Measuring BP in children?

A
  1. Correct cuff size is approximately 2/3 the length of the upper arm
  2. 4th Korotkoff sound is used to measure the diastolic blood pressure until adolescence, when the 5th Korotkoff sound can be used
  3. Results should be compared with a graph of normal values for age
229
Q

Most common cause of HTN in younger children?

A

Secondary HTN, with renal parenchymal disease accounting for up to 80%

230
Q

Causes of HTN in children?

A
  1. Renal = parenchymal/vascular disease
  2. Coarctaction of the aorta
  3. Phaeochromocytoma
  4. Congenital adrenal hyperplasia
  5. Essential/Primary (more common as children become older)
231
Q

Bartter’s syndrome definition?

A

Autosomal recessive cause of severe hypokalaemia due to defective chloride absorption at the NaK2Cl cotransported in the ascending loop of Henle, associated with normotension

232
Q

Bartter’s syndrome features?

A
  1. Usually presents in childhood with e.g. failure to thrive
  2. Polyuria, polydipsia
  3. Hypokalaemia
  4. Normotension
  5. Weakness
233
Q

Meningitis cause in neonatal to 3m?

A
  1. GBS
  2. E. coli and other gram -ves
  3. Listeria monocytogenes
234
Q

Meningitis cause in 1m to 6y?

A
  1. N. meningitidis
  2. S. pneumoniae
  3. H. Influenzae
235
Q

Meningitis cause in >6 years?

A
  1. N. meningitidis
  2. S. pneumoniae
236
Q

Chickenpox muskies?

A
  1. Fever initially
  2. Itchy, rash starting on head/trunk before spreading. Initially macular then papular then vesicular
  3. Systemic upset is usually mild
237
Q

Measles mushkies?

A
  1. Prodrome: irritable, conjunctivitis, fever
  2. Koplik spots: white spots (‘grain of salt’) on buccal mucosa
  3. Rash: starts behind ears then to whole body, discrete maculopapular rash becoming blotchy & confluent
238
Q

Mumps mushkies?

A
  1. Fever, malaise, muscular pain
  2. Parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%
239
Q

Rubella mushkies?

A
  1. Rash: pink maculopapular, initially on face before spreading to whole body, usually fades by the 3-5 day
  2. Lymphadenopathy: suboccipital and postauricular
240
Q

Erythema infectiosum mushkies?

A
  1. Also known as fifth disease or ‘slapped-cheek syndrome’
  2. Caused by parvovirus B19
  3. Lethargy, fever, headache
  4. ‘Slapped-cheek’ rash spreading to proximal arms and extensor surfaces
241
Q

Scarlet fever mushkies?

A
  1. Reaction to erythrogenic toxins produced by Group A haemolytic streptococci
  2. Fever, malaise, tonsillitis
  3. ‘Strawberry’ tongue
  4. Rash - fine punctate erythema sparing the area around the mouth (circumoral pallor)
242
Q

When does TGA tend to present?

A

Within first 24 hour of life

243
Q

Umbilical hernia associations?

A
  1. Afro-Caribbean infants
  2. Down’s syndrome
  3. Mucopolysaccharide storage disease
244
Q

RDS with CPAP risk?

A

Pneumothorax

245
Q

Contraindications to LP?

A

Any signs of ICP
1. Focal neurological signs
2. Papilloedema
3. Significant bulging of the fontanelle
4. DIC
5. Signs of cerebral herniation

246
Q

LP in meningococcal septicaemia?

A

Contraindicated - blood cultures and PCR for meningococcus should be obtained

247
Q

Meningitis management?

A
  1. Abx
  2. Steroids
  3. IVF
  4. Cerebral monitoring (mechanical ventilation if respiratory impairment)
  5. Public health notification and antibiotic prophylaxis of contacts (ciprofloxacin preferred over rifampicin)
248
Q

Meningitis Abx?

A
  1. < 3m = IV Amoxicillin/ampicillin + IV Cefotaxime
  2. > 3m = IV Cefotaxime (or ceftriaxone)
249
Q

Meningitis steroids?

A
  1. Not for children under 3 years
  2. Dexamathasone considered if LP: frankly purulent, >1000/microlitre, protein >1g/litre, bacteria on gram stain
250
Q

Benign Rolandic epilepsy age?

A

4-12 years

251
Q

Benign Rolandic Epilepsy features?

A
  1. Night time
  2. Typically partial but secondary generalisation may occur
  3. Child is otherwise normal
252
Q

Benign Rolandic Epilepsy EEG?

A

Centro-temporal spikes

253
Q

Bengin Rolandic Epilepsy prognosis?

A

Excellent, seizures stopping by adolescence

254
Q

Precocious puberty definition?

A

Development of secondary sexual characteristics before 8 years in females and 9 years in males

255
Q

Thelarche?

A

Breast development

256
Q

Adrenarche?

A

Pubic hair development

257
Q

Precocious puberty classification?

A
  1. Gonadotrophin dependent (central/true)
  2. Gonadotrophin independent (pseudo/false)
258
Q

Gonadotrophin dependent precocious puberty?

A
  1. Due to premature activation of the hypothalamo-pituitary-gonadal axis
  2. FSH and LH raised
259
Q

Gonadotrophin independent precocious puberty?

A
  1. Due to excess sex hormones
  2. FSH and LH low
260
Q

Male precocious puberty mushkies?

A

Uncommon and usually has an organic cause, testes:
1. Bilateral enlargement = gonadotrophin release from intracranial lesion
2. Unilateral enlargement = gonadal tumour
3. Small tests = adrenal cause (tumour or hyperplasia)

261
Q

Female precocious puberty causes?

A
  1. Usually idiopathic or familial and follows normal sequence of puberty
  2. Organic = rare, associated with rapid onset, neurological symptoms and signs and dissonance e.g. McCune-Albright Syndrome
262
Q

Precocious puberty definition?

A

Development of secondary sexual characteristics before 8 years in girls and 9 year in boys

263
Q

Pyloric stenosis epidemiology?

A
  1. 4/1000
  2. 4M:1F
  3. 10% FHx
  4. 1st borns more commonly affected
264
Q

Pyloric stenosis presentation age?

A
  1. Usually in 2nd-4th weeks of life with vomiting, although rarely may present later at up to 4 months
265
Q

Pyloric steneosis features?

A
  1. Projectile vomiting, 30 mins after feed
  2. Constipation and dehydration
  3. Palpable mass in upper abdomen
266
Q

Pyloric stenosis gas?

A

Hypochloraemic, hypokalaemic metabolic alkalosis

267
Q

Pyloric stenosis diagnosis?

A

Ultrasound

268
Q

Pyloric stenosis management?

A

Ramstedt’s Pyloromyotomy

269
Q

Paediatric BLS 2015 changes?

A
  1. Lay rescuers should use 30:2, if there are two or more rescuers with duty to respond then 15:2
  2. Infant <1 y/o, child 1y-puberty
270
Q

Paediatric BLS algorithm?

A
  1. 5 rescue breaths
  2. Check for signs of circulation (infants use brachial or femoral pulse, children use femoral pulse)
  3. 15:2 compressions at 100-120/min, depress the lower half of the sternum by at least one-third of the anterior–posterior dimension of the chest (which is approximately 4 cm for an infant and 5 cm for a child). In children: compress the lower half of the sternum. In infants: use a two-thumb encircling technique for chest compression
271
Q

IgE mediated allergy investigation?

A

Skin prick test or blood tests for specific IgE antibodies to the suspected foods and likely co-allergens

272
Q

Non IgE mediated allergy investigation?

A

Eliminate the suspected allergen for 2-6 weeks, then reintroduce. NICE advise to ‘consult a dietitian with appropriate competencies about nutritional adequacies, timings and follow-up’

273
Q

Commonest cause of death in 1st year of life?

A

SIDS. Most common at 3m of age.

274
Q

SIDS main RFs?

A
  1. Prone sleeping
  2. Parental smoking
  3. Bed sharing
  4. Hyperthermia and head covering
  5. Prematurity
275
Q

SIDS side RFs?

A
  1. Male sex
  2. Multiple births
  3. Social classes IV and V
  4. Maternal drug use
  5. Incidence increases in winter
276
Q

SIDS protective factors?

A
  1. Breastfeeding
  2. Room sharing
  3. Dummies
277
Q

Following cot death siblings?

A

Siblings should be screened for potential sepsis and IEM

278
Q

NEC features?

A
  1. Initial symptoms = feeding intolerance, abdominal distension and bloody stools
  2. Can quickly progress to abdominal discoloration, perforation and peritonitis
279
Q

NEC AXR?

A
  1. Bilateral bowel loops (often asymmetrical)
  2. Bowel wall oedema
  3. Pneumatosis intestinalis (intramural gas)
  4. Portal venous gas
  5. Pneumoperitoneum resulting from perforation
  6. Rigler’s sign
  7. Football sign = air outlining the falciform ligament
280
Q

Dance’s sign?

A

Emptiness in the right lower

281
Q

Dance’s sign?

A

Emptiness in the right lower quadrant in intussusception

282
Q

Measles overview?

A
  1. RNA paramyxovirus
  2. One of the most infectious known viruses
  3. Spread by aerosol transmission
  4. Infective from prodrome until 4 days after rash starts
  5. Incubation period = 10-14 days
283
Q

Measles features?

A
  1. Prodromal phase = irritable, conjunctivitis, fever
  2. Koplik spots = typically develop before the rash, white spots on the buccal mucosa (grains of salt)
  3. Eash = starts behind ears then whole body, discrete maculopapular rash becoming blotchy and confluent, desquamation that typically spares the palms and soles and may occur after a week
  4. Diarrhoea in 10%
284
Q

Measles Dx?

A

IgM antibodies can be detected within a few days of rash onset

285
Q

Measles Dx?

A

IgM antibodies can be detected within a few days of rash onsetMeasles management/

286
Q

Measles Rx?

A
  1. Mainly supportive
  2. Admission may be considered in immunosuppressed or pregnant patients
  3. Notifiable disease –> inform public health
287
Q

Measles complications?

A
  1. Otitis media = most common
  2. Pneumonia = most common cause of death
  3. Encephalitis = 1-2 weeks after
  4. SSPE = 5-10 years
  5. Febrile convulsions, keratoconjunctivitis, corneal ulceration, diarrhoea, increased incidence of appendicitis, myocarditis
288
Q

Measles management of contacts?

A
  1. If a child not immunized against measles comes into contact with measles then MMR should be offered (vaccine-induced measles antibody develops more rapidly than that following natural infection)
    this should be given within 72 hours
289
Q

Seborrhoeic dermatitis areas?

A
  1. Scalp (cradle cap)
  2. Nappy area
  3. Face
  4. Limb flexures
290
Q

Seborrhoiec dermatitis management?

A
  1. Mild-moderate = baby shampoo and baby oils
  2. Severe = mild topical steroids e.g. 1% hydrocortisone
291
Q

Seborrhoiec dermatitis prognosis?

A

Tends to resolve spontaneously by around 8m of age

292
Q

Child health surveillance schedule?

A
  1. Antenatal = ensure intrauterine growth, check for maternal infections e.g. HIV, US scan for foetal abnormalities, blood tests for NTDs
  2. Neonatal = Clinical examination of newborn, Newborn Hearing Screening Programme e.g. oto-acoustic emissions test, Give mother Personal Child Health Record
  3. 1st month = Heel-prick test day 5-9 - hypothyroidism, PKU, metabolic diseases, cystic fibrosis, medium-chain acyl Co-A dehydrogenase deficiency (MCADD)
    Midwife visit up to 4 weeks*
  4. Following months = Health visitor input
    GP examination at 6-8 weeks
    Routine immunisations
  5. Pre-school = National orthoptist-led programme for pre-school vision screening to be introduced
  6. Ongoing = Monitoring of growth, vision, hearing, Health professionals advice on immunisations, diet, accident prevention
293
Q

Scarlet fever definition?

A

Reaction to erythrogenic toxins produced by GAS (usually pyogenes)

294
Q

Scarlet fever age?

A

2-6 years, peak at 4 years

295
Q

Scarlet fever spread?

A

Respiratory by inhaling or ingesting respiratory droplets or by direct contact with nose and throat discharges

296
Q

Scarlet fever features?

A

Incubation period of 2-3 days and typically presents with:
1. Fever
2. Pharyngitis
3. Strawberry tongue
4. Sandpaper rash over extremities, spares palms and soles
5. Cervical lymphadenopathy

297
Q

Scarlet fever diagnosis?

A

Throat swab but Abx should be commenced immediately

298
Q

Scarlet fever management?

A
  1. Oral pencillin V for 10 days
  2. Pen allergy = azithromycin
  3. Can return to school 24 hours after starting Abx
  4. Notifiable disease
299
Q

Scarlet fever complications?

A
  1. Otitis media = most common complication
  2. Rheumatic fever = 20 days after
  3. Acute glomerulonephritis = 10 days after
  4. Invasive = bacteraemia, meningitis, necrotising fasciitis
300
Q

Usual bowel frequency?

A

Mean of 3 times a day for infants to under 6m old to once a day after 3y of age

301
Q

Constipation red flags?

A
  1. Reported from birth or first few weeks of life
  2. Meconium >48 hours
  3. Ribbon stools
  4. Faltering growth
  5. Previously unknown or undiagnosed weakness in legs, locomotor delat
  6. Abdominal distension
  7. Disclosure of evidence that raises concerns over possibility of child maltreatment
302
Q

Features which suggest faecal impaction?

A
  1. Symptoms of severe constipation
  2. Overflow soiling
  3. Faecal mass palpable in the abdomen (DRE should only be carried out by a specialist)
303
Q

Faecal impaction management?

A
  1. Movicol escalating dose regimen
  2. Stimulant if no disimpaction after 2w
  3. Stimulant +/- lactulose if movicol not tolerated
  4. Inform families that disimpaction treatment can initially increase symptoms of soiling and abdominal pain
304
Q

Constipation maintenance therapy?

A
  1. Movicol
  2. Add stimulant laxative if no response
  3. Stimulant +/- lactulose/docusate if movicol not tolerated
  4. Continue medication at maintenance dose for several weeks after regular bowel habit is established, then reduce the dose gradually
305
Q

Hypotonia classification?

A
  1. Central
  2. Neurological and muscular problems
306
Q

Hypotonia associated with encephalopathy in the newborn period?

A

HIE

307
Q

Central causes of hypotonia?

A
  1. Down’s
  2. Prader-Willi
  3. Hypothyroidism
  4. Cerebral palsy (hypotonia may precede the development of spasticity)
308
Q

Neurological and muscular causes of hypotonia?

A
  1. SMA
  2. GBS
  3. Myasthenia gravis
  4. Muscular dystrophy
  5. Myotonic dystrophy
  6. Spina bifida
309
Q

Contraindications to MMR?

A
  1. Severe immunosuppression
  2. Allergy to neomycin
  3. Children who have received another live vaccine by injection within 4 weeks
  4. Pregnancy should be avoided for at least 1 month following vaccination
  5. Immunoglobulin therapy within the past 3 months (there may be no immune response to the measles vaccine if antibodies are present)
310
Q

MMR adverse effects?

A

Malaise, fever and rash may occur after the first dose of MMR. This typically occurs after 5-10 days and lasts around 2-3 days

311
Q

How long between MMR doses?

A
  1. 3m to maximise response
  2. 1m if >10 y/o
  3. If urgent then 1m can be used in younger children e.g. outbreak at school
312
Q

Obtaining consent in children?

A
  1. At 16 years or older a young person can be treated as an adult and can be presumed to have capacity to decide
  2. Under the age of 16 years children may have capacity to decide, depending on their ability to understand what is involved
  3. Where a competent child refuses treatment, a person with parental responsibility or the court may authorise investigation or treatment which is in the child’s best interests (but not in Scotland)
313
Q

Contraceptives to under 16y/o?

A

All 5 of Fraser guidelines:
1. Understands
2. Cant be persuaded to inform parents
3. Will have sex anyways
4. Will suffer without it
5. Best interests

314
Q

Perthes’ disease definition?

A

Degenerative condition affecting the hip joints of children, typically between the ages of 4-8 years. It is due to avascular necrosis of the femoral head, specifically the femoral epiphysis. Impaired blood supply to the femoral head causes bone infarction.

315
Q

Perthes’ disease epidemiology?

A
  1. 5x more common boys
  2. 10% bilateral
316
Q

Perthes disease features?

A
  1. Hip pain (develops progressively over a few weeks)
  2. Limp
  3. Stiffness and reduced ROM
317
Q

Perthes disease Ix?

A
  1. XR = early changes include widening of joint space, later changes include decreased femoral head size/flattening
  2. Technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms persist
318
Q

Perthes disease complications?

A
  1. Osteoarthritis
  2. Premature fusion of growth plates
319
Q

Perthes disease classification?

A

Catterall staging
1. Clinical and histological features only
2. Sclerosis with or without cystic changes and preservation of the articular surface
3. Loss of structural integrity of the femoral head
4. Loss of acetabular integrity

320
Q

Perthes disease management?

A
  1. Keep femoral head in acetabulum = cast, braces
  2. <6y/o = observation
  3. Older = surgical management with moderate results
  4. Operate on severe deformities
321
Q

Perthes disease prognosis?

A

Most cases will resolve with conservative management. Early diagnosis improves outcomes.

322
Q

Growing pain epidemiology?

A

M=F, 3-12 y/o

323
Q

Growing pain features?

A
  1. Never present at the start of the day after the child has woken
  2. No limp
  3. No limitation of physical activity
  4. Systematically well
  5. Normal physical examination
  6. Motor milestones normal
  7. Symptoms are often intermittent and worse after a day of vigorous activity
324
Q

PDA mushkies?

A
  1. Acyanotic, can result in differential cyanosis if uncorrected
  2. Connection b/w pulmonary trunk and ascending aorta
  3. Usually DA closes with first breaths due to increased pulmonary flow which enhances prostaglandins clearance
  4. More common in premature babies, born at high altitude or maternal rubella infection in the first trimester
325
Q

PDA features?

A
  1. Left subclavicular thrill
  2. Continuous machinery murmur
  3. Large volume, bounding, collapsing pulse
  4. Wide pulse pressure
  5. Heaving apex beat
326
Q

PDA management?

A
  1. Indomethacin or ibuprofen = given to neonate, inhibits prostaglandin synthesis, closes in the majority of cases
  2. If associated with another CHD amenable to surgery then Prostaglandin E1 is useful to keep the duct open until after surgical repair
327
Q

Cyanotic CHD?

A
  1. ToF
  2. TGA
  3. Tricuspid atresia
328
Q

Acyanotic CHD?

A
  1. VSD (more common)
  2. ASD (more common in adults as present later)
  3. PDA
  4. Coarctation of the aorta
  5. Aortic stenosis
329
Q

Epstein’s pearl?

A

A congenital cyst found in the mouth. They are common on the hard palate, but may also be seen on the gums where the parents may mistake it for an erupting tooth. No treatment is generally required as they tend to spontaneously resolve over the course of a few weeks.

330
Q

Bohn’s nodules?

A

Mucous gland cysts, frequently located on the buccal or lingual aspects of the alveolar ridges and rarely on the palate.

331
Q

Congenital ranula?

A

A translucent, firm papule or nodule found on the anterior floor of mouth, lateral to lingual frenulum

332
Q

Alveolar lymphangioma?

A

Bluish fluid-filled lesions on the alveolar ridges, not seen on the palate

333
Q

Duct dependent cardiac lesions?

A
  1. ToF
  2. Ebstein’s anomaly
  3. Pulmonary atresia/stenosis
334
Q

Duct dependent cardiac lesion management?

A

Keep duct open with prostaglandins

335
Q

X-linked recessive who is affected?

A

Only males (Turner’s is the exception)

336
Q

X-linked recessive transmission?

A

Transmitted by heterozygote females (carriers) and male to male transmission is not seen

337
Q

X-linked recessive affected male’s children?

A

Unaffected sons and carrier daughters

338
Q

X-linked recessive carrier female’s children?

A

Each male child of a heterozygous female carrier has a 50% chance of being affected whilst each female child of a heterozygous female carrier has a 50% chance of being a carrier

339
Q

Transient synovitis age?

A

3-8 years old

340
Q

Transient synovitis features?

A
  1. Limp/refusal to weight bear
  2. Groin or hip pain
  3. Low-grade fever is present in a minority of patients (high fever should raise suspicion of septic arthritis)
341
Q

Transient synovitis management?

A

Self-limiting, requiring only rest and analgesia

342
Q

Fever, drooling and stridor?

A

Acute epiglottitis

343
Q

Headache in children epidemiology?

A

Equally common in boys and girls until puberty and then strong 3:1 female preponderance

344
Q

Most common cause of primary headache in children?

A

Migraine without aura

345
Q

Acute migraine management?

A
  1. Ibuprofen
  2. Triptans if >12 y/o, sumatriptan (nasal) is only one with proven efficacy
346
Q

Triptan s/e?

A

Tingling, heat and heaviness/pressure sensation

347
Q

Migraine prophylaxis?

A

In practice, pizotifen and propranolol should be used as first line preventatives in children. Second line preventatives are valproate, topiramate and amitryptiline

348
Q

2nd most common cause of headache in children?

A

Tension-type headache

349
Q

Eczema prevalence?

A

Eczema occurs in around 15-20% of children and is becoming more common. It typically presents before 2 years but clears in around 50% of children by 5 years of age and in 75% of children by 10 years of age

350
Q

Eczema features?

A
  1. Itchy, erythematous rash
  2. In infants face and trunk are often affected
  3. In younger children, eczema often occurs on the extensor surfaces
  4. In older children, more typical distribution seen, with flexor surfaces and the creases of the face and neck
351
Q

Eczema management?

A
  1. Avoid irritants
  2. Simple emollients
  3. Topical steroids
  4. Wet wrapping
  5. In severe cases, oral ciclosporin may be used
352
Q

What is wet wrapping?

A

Large amounts of emollient and sometimes topical steroids applied under wet bandages

353
Q

Eczema simple emollient mushkies?

A
  1. Large quantities should be prescribed (e.g. 250g / week), roughly in a ratio of with topical steroids of 10:1
  2. If a topical steroid is also being used the emollient should be applied first followed by waiting at least 30 minutes before applying the topical steroid
  3. Creams soak into the skin faster than ointments
  4. Emollients can become contaminated with bacteria - fingers should not be inserted into pots (many brands have pump dispensers)
354
Q

Congenital heart disease presentation?

A
  1. Antenatal = 18-20 week fetal anomaly scan
  2. Murmur = routine newborn examination
  3. Cyanosis
  4. HF
355
Q

Presentation of HF in neonates?

A

Poor feeding, SOB, sweating, hepatomegaly

356
Q

Rocker-bottom feet?

A

Edward’s

357
Q

Most common cause of pneumonia in children?

A

S. pneumoniae

358
Q

Pneumonia Rx?

A
  1. Amoxicillin first line
  2. Macrolides may be added if no response to first line therapy
  3. Macrolides if mycoplasma or chlamydia suspected
359
Q

Pneumonia associated with influenza Rx?

A

Co-amoxiclav

360
Q

Roseola infantum AKA?

A
  1. Exanthem subitum
  2. Sixth disease
361
Q

Roseola infantum cause?

A

HHV6

362
Q

Roseola infantum features?

A
  1. High fever lasting a few days followed by:
  2. Maculopapular rash
  3. Nagayama spots (papular enanthem on the uvula and soft palate)
  4. Febrile convulsions in 10-15%
  5. Diarrhoea and cough are also commonly seen
363
Q

Other consequences of HHV6 infection?

A
  1. Aseptic meningitis
  2. Hepatitis
364
Q

5 red rashes of childhood?

A
  1. Measles
  2. Parvovirus B19
  3. Rubella
  4. Scarlet fever
  5. Roseola infantum
365
Q

Turner’s syndrome prevalence?

A

1 in 2500

366
Q

Turner’s syndrome cause?

A

Presence of only one sex chromosome (X) or a deletion of the short arm of one of the X chromosomes

367
Q

Turner’s syndrome features?

A
  1. Short
  2. Shield chest with widely spaced nipples
  3. Webbed neck
  4. Bicuspid aortic valve/coarctation of aorta
  5. Primary amenorrhoea
  6. Cystic hygroma
  7. High arched palate
  8. Short 4th metacarpal
  9. Multiple pigmented naevi
  10. Lymphoedema in neonates esp. in feet
368
Q

Turner’s syndrome bloods?

A
  1. elevated gonadotrophin levels
  2. Hypothyroidism more common
369
Q

Turner’s syndrome bloods?

A
  1. Elevated gonadotrophin levels
  2. Hypothyroidism more common
370
Q

Most common renal abnormality in Turner’s syndrome?

A

Horseshoe kidney

371
Q

AI disease in Turner’s?

A

Increased incidence, esp. autoimmune thyroiditis and Crohn’s disease

372
Q

Fine motor and vision 3m?

A

Fixes and follow to 180 degrees, reaches for object

373
Q

Fine motor and vision 6m?

A

Palmer grasp, passes from one hand to another

374
Q

Fine motor and vision 9m?

A

Points with finger, early pincer

375
Q

Fine motor and vision

A

Good pincer, bangs toys together

376
Q

Nappy rash causes?

A
  1. Irritant dermatitis
  2. Candida dermatitis
  3. Seborrhoeic dermatitis
  4. Psoriasis
  5. Atopic eczema
377
Q

Irritant dermatitis mushkies?

A
  1. Most common cause, due to irritant effect of urinary ammonia and faeces
  2. Creases are charactersically spared
378
Q

Candida dermatitis mushkies?

A
  1. Erythmatous rash which involves the flexures and has satellite lesions
379
Q

General nappy rash management?

A
  1. Disposable preferable to towel nappies
  2. Expose napkin area to air when possible
  3. Apply barrier cream (zinc and castor oil)
  4. Mild steroid cream (1% hydrocortisone in severe cases
380
Q

Candidal nappy rash management?

A
  1. Topical imidazole
  2. Cease use of barrier cream until candida has settled
381
Q

Autosomal recessive conditions tend to be?

A

Metabolic (except for inherited ataxias)

382
Q

Autosomal dominant conditions tend to be?

A

Structural (except for Gilbert’s, hyperlipidaemia Type II)

383
Q

Tuberous sclerosis inheritance?

A

AD

384
Q

Contraindications to immunisation?

A
  1. Confirmed anaphylactic reaction to a previous dose of a vaccine containing the same antigens
  2. Confirmed anaphylactic reaction to another component contained in the relevant vaccine e.g. egg protein
385
Q

Vaccine should be delayed?

A

Febrile illness/intercurrent infection

386
Q

Contraindications to live vaccines?

A
  1. Pregnancy
  2. Immunosuppression
387
Q

When should DTP vaccine be deferred?

A

In children with evolving or unstable neurological condition

388
Q

Babies born prematurely vaccination?

A

According to chronological age

389
Q

Babies born prior to 28 weeks gestation immunisations?

A

First set at hospital due to risk of apnoea

390
Q

G6PDD inheritance?

A

X-linked recessive

391
Q

Perinatal mortality rate?

A

Stillbirths + early neonatal deaths (within 7 days) per 1,000 births after 24 weeks gestation

392
Q

Maternal mortality rate?

A

Deaths in pregnancy, labour and 6 weeks after/total maternities x 1000

393
Q

Stillbirth rate?

A

Babies born dead after 24 weeks / total births (live + stillborn) x 1000

394
Q

Neonatal death rate?

A

Babies dying between 0-28 days / total live births x 1000

395
Q

Fetus lost prior vs. after 20 weeks?

A

Miscarriage vs. stillbirth

396
Q

Shaken baby syndrome triad?

A
  1. Retinal haemorrhages
  2. Subdural haematoma
  3. Encephalopathy
397
Q

Risk of Down’s syndrome with increasing maternal age?

A
  1. 20 = 1/1500
  2. 30 = 1/800
  3. 35 = 1/270
  4. 40 = 1/100
  5. 45 = 1/50
398
Q

Down’s syndrome genetics?

A
  1. Nondisjunction = 94%
  2. Robertsonian translocation (usually onto 14) = 5%
  3. Mosaicism = 1%
399
Q

Coeliac disease presentation age?

A

<3 y/o

400
Q

Coeliac disease incidence?

A

1 in 100

401
Q

Coeliac disease HLA association?

A
  1. HLA-DQ2 = 95%
  2. HLA-DQ8 = 80%
402
Q

Coeliac disease features?

A
  1. Failure to thrive
  2. Diarrhoea
  3. Abdominal distension
  4. Older children may present with anaemia
  5. Many cases not diagnosed to adulthood
403
Q

Coeliac disease diagnosis?

A
  1. Jejunal biopsy = subtotal villous atrophy
  2. Anti-endomysial and anti-gliadin antibodies are useful screening tests
404
Q

Caput succadeneum?

A
  1. Present at birth
  2. Crosses suture lines
  3. Resolves within days
405
Q

Cephalohaematoma?

A
  1. Several hours after birth
  2. Most commonly in parietal region, doesn’t cross suture lines
  3. Resolves in months
406
Q

Subgaleal haematoma?

A
  1. Between periosteum and epicranial aponeurosis
  2. 12-72 hours post delivery
  3. Ventouse-assissted deliveries
407
Q

Threadworm organism?

A

Enterobius vermicularis

408
Q

Threadworm infestation features?

A
  1. Asymptomatic in 90%
  2. Perianal itching, esp. at night
  3. Girls may have vulval symptoms
409
Q

Threadworm Dx?

A

Sellotape to perianal area and sending for microscopy. However most treated empirically

410
Q

Threadworm management?

A
  1. Mebendazole single dose (>6m) and hygeine measures for all members of household
411
Q

Anticipation?

A

Early onset in trinucleotide repeat disorders in successive generations

412
Q

Fragile X x3?

A

CGG

413
Q

Myotonic dystrophy x3?

A

CTG

414
Q

Friedrich’s ataxia x3?

A

GAA

415
Q

Does friedrich’s ataxia show anticipation?

A

No

416
Q

Fever followed later by rash?

A

Roseola infantum

417
Q

Microcephaly definition?

A

Occipital-frontal circumference <2nd centile

418
Q

Microcephaly causes?

A
  1. Normal variation
  2. Familial
  3. Congenital infection
  4. HIE
  5. FAS
  6. Patau’s
  7. Craniosynostosis
419
Q

APGAR criteria?

A

1, 5, 10 mins if low
1. Appearance
2. Pulse
3. Grimace
4. Activity
5. Respiration

420
Q

Urinary tract imaging?

A
  1. Infants <6m with first UTI responding to treatment should have US within 6 weeks
  2. Children >6m with first UTI responding to treatment do not require imaging unless features suggestive of an atypical infection
421
Q

Features of atypical UTI?

A
  1. Seriously ill
  2. Poor urine flow
  3. Abdominal or bladder mass
  4. Raised creatinine
  5. Septicaemia
  6. Failure to respond to treatment with Abx within 48h
  7. Infection with non-E.coli organisms
422
Q

Most common congenital cardiac abnormality in Down’s?

A

AVSD aka endocardial cushion defect

423
Q

Most common ocular malignancy in children?

A

Retinoblastoma

424
Q

Average age of onset of retinoblastoma?

A

18 months

425
Q

Retinoblastoma pathophysiology?

A
  1. AD
  2. Loss of function of the Rb TS gene on Chr 13
  3. 10% of cases are hereditary
426
Q

Retinoblastoma features?

A
  1. Absence of red reflec, replaced by white pupil (leukocoria)
  2. Strabismus
    3 Visual problems
427
Q

Retinoblastoma management?

A
  1. External beam radiation
  2. Chemotherapy
  3. Photocoagulation
428
Q

Retinoblastoma management?

A

Excellent, 90% survive into adulthood

429
Q

mall testes inprecocious puberty?

A

Adrenal cause

430
Q

Sexual aggression during childhood?

A

Testotoxicosis

431
Q

Whooping cough organism?

A

Bordatella pertussis

432
Q

Pertussis immunisation?

A
  1. Infants are routinely immunised at 2, 3, 4 months and 3-5 years. Newborn infants are particularly vulnerable, which is why the vaccination campaign for pregnant women was introduced
  2. Neither infection nor immunisation results in lifelong protection - hence adolescents and adults may develop whooping cough despite having had their routine immunisations
433
Q

Pertussis Dx?

A

Cough lasting >14 days without another cause plus one of:
1. Paroxysmal cough
2. Inspiratory whoop
3. post-tussive vomiting
3. Undiagnosed apnoeic attacks in young infants

434
Q

Pertussis FBC?

A

Marked lymphocytosis

435
Q

Pertussis Dx?

A
  1. Per nasal swab for BP, may take several days or weeks to come back
  2. PCR and serology now increasingly used
436
Q

Pertussis Rx?

A
  1. <6m admitted
  2. Notifiable
  3. Macrolide if onset of cough within 21 days
  4. Household contacts offered pantibiotic prophylaxis
  5. Abx not shown to alter course of illness
  6. School exclusion = 48 hours after commencing Abx (or 21 days from onset of symptoms if no Abx)
437
Q

Pertussis complications?

A
  1. Subconjunctival haemorrhage
  2. Pneumonia
  3. Bronchiectasis
  4. Seizures
438
Q

Pregnancy pertussis vaccination?

A

Between 16-32 weeks pregnant

439
Q

Risk of threadworm transmission in families?

A

75%

440
Q

Plagiocephaly?

A

Parallellogram shaped head

441
Q

Craniosynostosis?

A

Premature fusion of skull bones

442
Q

Newborn head molding management?

A

Can be left alone but document clearly

443
Q

Mama and Dada?

A

9-10 months

444
Q

Homocystinuria inheritance?

A

Autosomal recessive

445
Q

When is neonatal blood spot screening performed?

A

5-9 days of life

446
Q

Neonatal blood spot conditions?

A

congenital hypothyroidism
cystic fibrosis
sickle cell disease
phenylketonuria
medium chain acyl-CoA dehydrogenase deficiency (MCADD)
maple syrup urine disease (MSUD)
isovaleric acidaemia (IVA)
glutaric aciduria type 1 (GA1)
homocystinuria (pyridoxine unresponsive) (HCU)

447
Q

Friedrich’s ataxia inheritance?

A

Autosomal recessive

448
Q

Hearing tests in children?

A
  1. Newborn = otocaustic emission tests as part of newborn hearing screening programme –> auditory brainstem response if abnormal
  2. 6-9 months = distraction test, done by health visitor
  3. > 2.5 years = speech discrimination tests e.g. Kendall Toy test, McCormick Toy Test
  4. > 3y = Pure tone audiometry, done at school entry
449
Q

MMR vaccine type?

A

Live attenuated

450
Q

Sitting without support?

A

Should be achieved around 7-8m, refer if still not achieved by 12m

451
Q

Acrocyanosis?

A

Peripheral cyanosis around the mouth and extremities, common in neonates, esp. in first 24-48 hours of life

452
Q

How to distinguish cardiac from non-cardiac causes of cyanosis?

A

Nitrogen washout test (hyperoxia test)
1. The infant is given 100% oxygen for ten minutes after which arterial blood gases are taken. A pO2 of less than 15 kPa indicates cyanotic congenital heart disease

453
Q

ITP definition?

A

Immune-mediated reduction in the platelet count. Abs directed against the glycoprotein IIb/IIIa or Ib-V-IX complex

454
Q

ITP type of reaction?

A

Type II hypersensitivity reaction

455
Q

ITP features?

A
  1. Bruising
  2. petechial or purpuric rash
  3. Bleeding is less common and typically presents as epistaxis or gingival bleeding
456
Q

ITP Ix?

A
  1. FBC = isolated thrombocytopenia
  2. Blood film
  3. Bone marrow exam if atypical features (e.g. lymph node enlargement/splenomegaly, high/low white cells, failure to resolve/respond to treatment)
457
Q

ITP management?

A
  1. Usually none = resolves in 80% children within 6m
  2. Avoid activities resulting in trauma
  3. If plt count v. low (<10) or bleeding –> oral/IV steroids, IVIG, plt transfusion in emergencies)
458
Q

VUR?

A

Abnormal backflow of urine from the bladder into the ureter and kidney. It is a relatively common abnormality of the urinary tract in children and predisposes to urinary tract infection (UTI), being found in around 30% of children who present with a UTI. As around 35% of children develop renal scarring it is important to investigate for VUR in children following a UTI

459
Q

VUR pathophysiology?

A
  1. Ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
  2. Therefore shortened intramural course of the ureter
  3. Vesicoureteric junction cannot, therefore, function adequately
460
Q

VUR presentation?

A
  1. Antenatal = hydronephrosis on US
  2. Recurrent childhood UTIs
  3. Reflux nephropathy = chronic pyelonephritis secondary to VUR, renal scar may produce renin –> HTN
461
Q

VUR Dx

A
  1. MCUG
  2. DMSA to look for renal scarring
462
Q

VUR grading?

A
  1. Into ureter, no dilatation
  2. Into pelvis on micturition, no dilatation
  3. Mild/moderate dilatation of ureter, renal pelvis and calyces
  4. Dilation of renal pelvis and calyces with moderate ureteral tortuosity
  5. Gross dilatation of the ureter, pelvis anc calyces with ureteral tortuosity
463
Q

Bulging tympanic membrane?

A

Acute otitis media

464
Q

Scarlet fever back to school?

A

24 hours after commencing Abx

465
Q

Whooping cough back to school?

A

2 days after commencing Abx or 21 days from onset of symptoms if no Abx

466
Q

Measles back to school?

A

4 days from onset of rash

467
Q

Rubella back to school?

A

5 days from onset of rash

468
Q

Chickenpox back to school?

A

All lesions crusted over

469
Q

Mumps back to school?

A

5 days from onset of swollen glands

470
Q

D&V back to school?

A

48 hours from symptom settled

471
Q

Impetigo back to school?

A

Until lesions are crusted and healed, or 48 hours after commencing antibiotic treatment

472
Q

Scabies back to school?

A

Until treated

473
Q

Influenza back to school?

A

Until recovered

474
Q

When is chickenpox infectious?

A

2 days before rash appears to 5 days after onset of rash

475
Q

Cephalohaematoma location?

A

Between cranial bone and periossteal membrane

476
Q

Subgaleal bleed location?

A

Subaponeurotic space

477
Q

Caput succedaneum location?

A

Subcutaneous tissue

478
Q

When can child usually run?

A

2y

479
Q

TGA cause?

A

Failure of the aorticopulmonary septum to spiral during septation

480
Q

Maternal risk factor for TGA?

A

Diabetic mothers

481
Q

TGA clinical features?

A
  1. Tachypnoea
  2. Cyanosis
  3. Loud single S2
  4. Prominent RV impulse
  5. Egg on side appearnce on CXR
482
Q

TGA management?

A
  1. Maintenance of DA with PGs
  2. Surgical correction is definite treatment
483
Q

Most common malignancy affecting children?

A

ALL, accounts for 80% childhood leukaemias, peak 2-5 y/o, M>F

484
Q

ALL features?

A
  1. Anaemia = lethargy and pallor
  2. Neutropenia = frequent or severe infections
  3. Thrombocytopenia = easy bruising, petechiae
  4. Bone pain
  5. Splenomegaly, hepatomegaly
  6. Testicular swelling
  7. Fever in up to 50% new cases
485
Q

ALL types?

A
  1. Common ALL = 75%, CD10 present, pre-B phenotype
  2. T-cell ALL (20%)
  3. B-cell ALL (5%)
486
Q

ALL poor prognostic factors?

A
  1. Age < 2 years or > 10 years
  2. WBC > 20 * 109/l at diagnosis
  3. T or B cell surface markers
  4. Non-Caucasian
  5. Male sex
487
Q

Wilms’ tumour typical age?

A

<5y/o, median age 3 y/o

488
Q

Wilms’ associations?

A
  1. Beckwith-Wiedemann syndrome
  2. WAGR syndrome
  3. Hemihypertrophy
  4. Around one-third of cases are associated with a loss-of-function mutation in the WT1 gene on chromosome 11
489
Q

Wilms’ features?

A
  1. Abdominal mass (most common presenting feature)
  2. Painless haematuria
  3. Flank pain
  4. Anorexia, fever
  5. Unilateral in 95% cases
  6. Metastases foud in 20% pts (most common lung)
490
Q

Wilms’ management?

A
  1. Nephrectomy
  2. Chemotherapy
  3. Radiotherapy if advanced disease
  4. Prognosis: good, 80% cure rate
491
Q

2-5 y/o asthma prednisolone dose?

A

20mg OD (1-2mg/kg OD)

492
Q

> 5 y/o asthma prednisolone dose?

A

30-40mg OD (1-2mg/kg OD)

493
Q

<2 y/o asthma prednisolone dose?

A

10mg OD

494
Q

Most common cause of meningococcal disease?

A

Meningitis B

495
Q

Meningitis B dose timings?

A
  1. 2 months
  2. 4 months
  3. 12-13 months
496
Q

Chickenpox management?

A
  1. Keep cool, trim nails
  2. Calamine lotion
  3. School exclusion until all lesions crusted over/5 days after rash onset
  4. Immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG). If chickenpox develops then IV aciclovir should be considered
497
Q

Chickenpox complications?

A
  1. Pneumonia
  2. Encephalitis (cerebellar may be seen)
  3. Disseminated haemorrhagic chickenpox
  4. Arthritis, nephritis, pancreatitis
  5. Group A strep infection –> Necrotising fasciitis
498
Q

Diffuse enlargement of thyroid gland in puberty?

A

Normal

499
Q

Male puberty mushkies?

A
  1. First sign is testicular growth at around 12 years of age (range = 10-15 years)
  2. Testicular volume > 4 ml indicates onset of puberty
  3. Maximum height spurt at 14
500
Q

Female puberty mushkies?

A
  1. First sign is breast development at around 11.5 years of age (range = 9-13 years)
  2. Height spurt reaches its maximum early in puberty (at 12) , before menarche
  3. Menarche at 13 (11-15)
  4. There is an increase of only about 4% of height following menarche
501
Q

Venous hum?

A

Due to the turbulent blood flow in the great veins returning to the heart. Heard as a continuous blowing noise heard just below the clavicles

502
Q

Still’s murmur?

A

Innocent, Low-pitched sound heard at the lower left sternal edge

503
Q

Most common cause of hypothyroidism in UK?

A

Autoimmune thyroiditis

504
Q

Most common cause of hypothyroidism in developing world?

A

Iodine deficiency

505
Q

Congenital diaphragmatic hernia?

A

Congenital diaphragmatic hernia (CDH) occurs in around 1 in 2,000 newborns. It is characterised by the herniation of abdominal viscera into the chest cavity due to incomplete formation of the diaphragm. This can result in pulmonary hypoplasia and hypertension which causes respiratory distress shortly after birth.

506
Q

Congenital diaphragmatic hernia pathophysiology?

A

Failure of pleuroperitoneal canal to close completely

507
Q

Congenital diaphragmatic hernia prognosis?

A

Only 50% with CDH survive

508
Q

Obesity management in children NICE recommendations?

A
  1. Tailored clinical intervention at 91st centile or above
  2. Assessing for comorbidities if BMI at 98th centile or above
509
Q

Obesity associations?

A

Female, Asian, Tall

510
Q

Causes of obesity in children?

A
  1. Lifestyle (most common)
  2. GH deficiency
  3. Hypothyrodism
  4. Down’s
  5. Cushing’s
  6. Prader-Willi