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Paediatrics Flashcards

1
Q

IV fluid choice in children

A

o Neonates = 10% glucose
o Older = 0.9% NaCl + 5% glucose (+/- KCl)

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2
Q

Fluid maintenance in neonates

A

o Day 1 = 60ml/kg/day
o Day 2 = 90ml/kg/day
o Day 3 = 120ml/kg/day
o Day 4 = 150ml/kg/day

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3
Q

Fluid maintenance in children

A

o (Age+4) x2 = weight in kg (approx)
o First 10kg = 100ml/kg
o Next 10kg = 50ml/kg
o Every other kg = 20ml/kg

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4
Q

Fluid deficit in children

A
  • Dehydrated = 50ml/kg extra over 24/48 hrs
  • Shocked = 100ml/kg extra over 24/48 hrs
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5
Q

Fluid bolus in children

A

20ml/kg of 0.9% NaCl

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6
Q

Presentation of bronchopulmonary dysplasia (chronic lung disease of prematurity)

A
  • Low oxygen saturations
  • Increased work of breathing
  • Poor feeding and weight gain
  • Crackles and wheezes on chest auscultation
  • Increased susceptibility to infection
  • Requires oxygen therapy after reaching 36 wks gestational age
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7
Q

Prevention of chronic lung disease of prematurity

A
  • Corticosteroids to mothers that show signs of premature labour
  • CPAP rather than intubation and ventilation
  • Caffeine to stimulate respiratory effort
  • Not over oxygenating with supplementary O2
  • Surfactant
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8
Q

Causes of cleft lip and palate

A
  • Benzodiazepines
  • Antiepileptics
  • Rubella
  • Trisomy 18, 13-15
  • Pierre robin short mandible = causes intermittent short airway obstruction
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9
Q

Management of cleft lip

A
  • Feeding with special teats may be needed before plastic surgery
  • Lip repair at 3m and palate at 6m
    o Avoid NICU as decreased bonding
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10
Q

Risk factors for meconium aspiration syndrome

A
  • Post-term deliveries (>42 wks)
  • Maternal hypertension
  • Pre-eclampsia
  • Chorioamnionitis
  • Smoking
  • Substance abuse
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11
Q

Complications of meconium aspiration syndrome

A
  • Airway obstruction
  • Surfactant dysfunction
  • Pulmonary vasoconstriction
  • Infection
  • Chemical pneumonitis
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12
Q

Causes of hypoxic-ischaemic encephalopathy

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord = compression of cord during birth
  • Nuchal cord = cord wrapped around neck of baby
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13
Q

Sarnat staging of hypoxic-ischaemic encephalopathy

A
  • Mild = Poor feeding, general irritability and hyper-alert
  • Moderate = Poor feeding, lethargic, hypotonic and seizures
  • Severe = Reduced consciousness, apnoeas, flaccid and reduced/absent reflexes
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14
Q

Management of Hypoxic-ischaemic encephalopathy

A

Therapeutic hypothermia

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15
Q

Risk factors for necrotising enterocolitis

A
  • Very LBW or very premature
  • Formulae feeds
  • Respiratory distress and assisted ventilation
  • Sepsis
  • Patent ductus arteriosus and other congenital heart disease
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16
Q

Presentation of necrotising enterocolitis

A
  • Intolerance to feeds
  • Vomiting (green bile)
  • Generally unwell
  • Distended tender abdomen
  • Absent bowel sounds
  • Blood in stools
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17
Q

AXR in necrotising enterocolitis

A

o Dilated loops of bowel
o Bowel wall oedema
o Pneumatosis intestinalis = gas in bowel wall
o Pneumoperitoneum = free gas in peritoneal cavity
o Gas in portal veins
o Rigler sign = air both inside and outside bowel wall
o Football sign = air outlining falciform ligament

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18
Q

Causes of neonatal hypoglycaemia

A
  • Preterm birth
  • Maternal DM
  • IUGR
  • Hypothermia
  • Neonatal sepsis
  • Inborn errors of metabolism
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19
Q

Management of neonatal hypoglycaemia

A
  • Asymptomatic
    o Encourage normal feeding
    o Monitor blood glucose
  • Symptomatic or very low blood glucose
    o Admit to neonatal unit
    o IV 10% dextrose
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20
Q

Risk factors for neonatal jaundice

A
  • Premature neonates = immature liver
  • Low infant birth weight
  • Male
  • Visible bruising
  • Maternal age >25
  • Maternal DM
  • Ethnicity = Asian, European, native American
  • Sibling born with jaundice requiring phototherapy
  • Dehydration
  • Poor caloric intake/increased neonatal weight loss
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21
Q

Causes of neonatal jaundice

A
  • Increased production
    o Haemolytic disease of newborn
    o ABO incompatibility (<24hrs)
    o Haemorrhage
    o Intraventricular haemorrhage
    o Cephalo-haematoma
    o Polycythaemia
    o Sepsis and disseminated intravascular coagulation
    o G6PD deficiency (<24 hrs)
  • Decreased clearance
    o Prematurity
    o Neonatal cholestasis
    o Extrahepatic biliary atresia
    o Endocrine disorders (hypothyroid and hypopituitary)
    o Gilbert syndrome
  • Physiological (2-14 days)
    o Breastfeeding (benign and self-limiting)
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22
Q

Criteria for admission of neonatal jaundice

A
  • Emergency admission if signs of bilirubin encephalopathy
  • Urgent admission (seen within 2 hrs) if jaundice appears <24hrs old
  • Urgent admission (seen within 6 hrs)
    o Jaundice first appeared >7 days old
    o Neonate unwell (lethargy, fever, vomiting, irritability)
    o Gestational age <35 wks
    o Prolonged jaundice suspected = <37wks >21 days jaundice or >37 wks with >14 days jaundice
    o Feeding problems or concerns about weight
    o Pale stools and dark urine
  • Community care  Record bilirubin level within 6 hrs and manage following local protocol
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23
Q

Treatment of neonatal jaundice

A
  • None if bilirubin level below threshold
  • Phototherapy
    o Rebound bilirubin measured 12-18 hrs after
  • Exchange transfusions
  • Early surgical treatment
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24
Q

Complications of neonatal jaundice

A
  • Kernicterus = brain damage caused by excessive bilirubin levels
    o Cerebral palsy
    o Learning disability
    o Deafness
  • Acute/chronic bilirubin encephalopathy (neurotoxicity)
    o Atypical sleepiness
    o Poor feeding
    o Irritability
    o Vomiting
    o Hypotonia followed by hypertonia
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25
Q

Presentation of biliary atresia

A
  • Persistent jaundice (>14 days if term or >21 days if preterm)
    High conjugated bilirubin
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26
Q

Management of biliary atresia

A

Kasai protoenterostomy

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27
Q

Principles of neonatal resuscitation

A
  • Warm the baby
    o Get baby dry = vigorous drying helps stimulate breathing
    o Warm delivery rooms
    o Management under heat lamp
    o Babies <28wks placed in plastic bag still wet and managed under heat lamp
  • Calculate APGAR score
    o Done at 1, 5, 10 mins whilst resuscitation continues
    o Used as indicator of progress over first minutes after birth
    o Helps guide neonatal resuscitation efforts
  • Stimulate breathing
    o Dry vigorously with towel
    o Place baby’s head in neutral position to keep airway open
     Towel under shoulders
    o If gasping or unable to breath, check airway obstruction and consider aspiration under direct visualisation
  • Inflation breaths
    o Given when neonate is gasping or not breathing despite adequate initial stimulation
    o 2 cycles of 5 inflation breaths (lasting 3s each) can be given to stimulate breathing and heart rate
    o If no response and HR low, 30s of ventilations breath can be used
    o If still no response, chest compressions can be used, coordinated with ventilation breaths
    o Maintain neutral head position and get good seal around mouth and nose
    o Look for rise and fall in chest
    o Air should be used in term/near term babies and mix air and oxygen should be used in pre-term babies
    o O2 sats monitored throughout and aim for gradual rise to 95%
  • Chest compressions
    o Start if HR remains below 60bpm despite resuscitation and inflation breaths
    o Chest compressions performed at 3:1 ratio with ventilation breaths
  • Severe situations
    o IV drugs and intubation should be considered
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28
Q

What is APGAR

A

Appearance
Pulse
Grimmace (response to stimulation)
Activity (muscle tone)
Respiration

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29
Q

Benefits of delayed cord clamping

A

o Improved haemoglobin
o Improved iron stores
o Improved BP
o Reduction in intraventricular haemorrhage
o Reduction in necrotising enterocolitis

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30
Q

Risk factors for neonatal sepsis

A
  • Vaginal GBS colonisation
  • GBS sepsis in previous baby
  • Maternal sepsis, chorioamnionitis or fever >38
  • Prematurity
  • Early rupture of membranes
  • Prolonged rupture of membranes
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31
Q

Red flags for neonatal sepsis

A
  • Confirmed/suspected sepsis in mother
  • Signs of shock
  • Seizures
  • Term baby needing mechanical ventilation
  • Respiratory distress starting >4 hrs after birth
  • Presumed sepsis in another baby in multiple pregnancy
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32
Q

Management of neonatal sepsis

A
  • If 1+ risk factor/clinical feature = monitor obs and clinical condition for min 12 hrs
  • Antibiotics if 2+ risk factors/clinical features or single red flag
  • Abx given within 1 hrs of decision to start them
  • 1st line = benzylpenicillin and gentamycin
    o Stop Abx if clinically well, blood cultures neg 36 hrs after and CRP <10
  • Check CRP again at 24 hrs
  • Check blood culture results at 36 hrs
  • Check CRP again at 5 days if still on Tx
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33
Q

Management of neonatal respiratory distress syndrome

A
  • CXR = ground-glass appearance and indistinct heart border
  • Antenatal steroids (dexamethasone) given with suspected/confirmed preterm labour
  • Supplementary oxygen = keep sats between 91-95%
  • Intubation and ventilation
  • Endotracheal surfactant
  • CPAP via nasal mask
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34
Q

Presentation of retinopathy of prematurity

A
  • Scarring
  • Retinal detachment
  • Blindness
  • Plus disease = tortuous vessels and hazy vitreous humour
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35
Q

Management of retinopathy of prematurity

A
  • Transpupillary laser photocoagulation  Halt and reverse neovascularisation
  • Cryotherapy
  • Injections of VEGF inhibitors
  • Surgery (if retinal detachment)
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36
Q

Presentation of congenital varicella syndrome

A

o Fetal growth restriction
o Microcephaly, hydrocephalus, learning disability
o Scars and significant skin changes following dermatomes
o Limb hypoplasia (underdeveloped limbs)
o Cataracts and inflammation in eye = chorioretinitis

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37
Q

Presentation of congenital rubella syndrome

A

o Congenital cataracts
o Congenital heart disease (PDA and pulmonary stenosis)
o Learning disability
o Hearing loss (sensorineural deafness)
o Growth retardation
o Hepatosplenomegaly
o Purpuric skin lesions
o Salt and pepper chorioetinitis
o Microphthalmia
o Cerebral palsy

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38
Q

Presentation of ASD

A
  • Childhood (can be asymptomatic)
    o SoB
    o Difficulty feeding
    o Poor weight gain
    o Lower resp tract infections
  • Adulthood  Dyspnoea, HF, Stroke
  • Mid-systolic crescendo-decrescendo murmur at upper left sternal border
  • Fixed split second heart sound
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39
Q

Risk factors for VSD

A
  • Down’s syndrome
  • Turner’s syndrome
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40
Q

Presentation of VSD

A
  • Poor feeding and failure to thrive
  • Dyspnoea, Tachypnoea
  • Pan-systolic murmur
  • Systolic thrill
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41
Q

Presentation of PDA

A
  • Shortness of breath
  • Difficulty feeding and Poor weight gain
  • Lower resp tract infections
  • Murmur = continuous crescendo-decrescendo “machinery” sound
  • Left subclavicular thrill
  • Large volume, bounding, collapsing pulse
  • Wide pulse pressure
  • Heaving apex beat
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42
Q

Management of PDA

A
  • Monitored until 1 year of age
  • Indomethacin or ibuprofen
    o Given to neonate
    o Inhibits prostaglandin synthesis
  • After 1 year unlikely to close spontaneously = trans-catheter/surgical closure
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43
Q

Risk factors of coarctation of aorta

A

Turner’s syndrome

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44
Q

Presentation of coarctation of aorta

A
  • Weak femoral pulses
  • Systolic murmur
  • Tachypnoea and increased work of breathing
  • Poor feeding
  • Grey and floppy baby
  • LV heave
  • Underdeveloped left arm
  • Underdevelopment of legs
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45
Q

Presentation of aortic stenosis

A
  • Mild = asymptomatic
  • Fatigue
  • Shortness of breath
  • Dizziness
  • Fainting
  • Sx worse on exertion
  • Ejection systolic murmur in aortic area
    o Crescendo-decrescendo character
    o Radiates to carotids
  • Ejection click before murmur
  • Palpable thrill
  • Slow rising pulse and narrow pulse pressure
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46
Q

Associations of pulmonary stenosis

A
  • Tetralogy of Fallot
  • William syndrome
  • Noonan syndrome
  • Congenital rubella syndrome
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47
Q

Presentation of pulmonary stenosis

A
  • Mild = asymptomatic
  • Fatigue on exertion
  • Shortness of breath
  • Dizziness
  • Fainting
  • Ejection systolic murmur over pulmonary area
  • Palpable thrill
  • Right ventricular heave
  • Raised JVP with giant a waves
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48
Q

Management of pulmonary stenosis

A
  • Asymptomatic = watching and waiting
  • Symptomatic
    o Balloon valvuloplasty via venous catheter
    o Open heart surgery
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49
Q

Presentation of innocent murmurs

A
  • Soft, short, systolic murmur
  • Symptomless
  • Situation dependent
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50
Q

Concerning features of mumrurs

A
  • Murmur louder than 2/6
  • Diastolic murmurs
  • Louder on standing
  • Failure to thrive
  • Feeding difficulty
  • Cyanosis
  • Shortness of breath
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51
Q

Features of tetralogy of fallot

A
  • Ventricular septal defect
  • Right ventricular hypertrophy
  • Pulmonary stenosis
  • Overriding aorta
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52
Q

Triggers of tet spells

A
  • Waking
  • Physical exertion
  • Crying
  • Pain
  • Fever
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53
Q

Presentation of TOF

A
  • Cyanosis
  • Ejection systolic murmur due to pulmonary stenosis
  • Right sided aortic arch
  • Severe episodes  Reduced consciousness, Seizures, Death
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54
Q

CXR in TOF

A

Boot shaped heart

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55
Q

Associations of transposition of great arteries

A
  • Ventricular septal defect
  • Coarctation of aorta
  • Pulmonary stenosis
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56
Q

Presentation of transposition of great arteries

A
  • Cyanosis at or within few days of birth
  • Respiratory distress
  • Tachycardia
  • Poor feeding
  • Poor weight gain
  • Sweating
  • Single loud S2
  • Prominent loud ventricular impulse
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57
Q

CXR in transposition of great arteries

A

Egg-on-side appearance of heart

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58
Q

What is Ebstein’s anomaly

A

Tricuspid valve set lower in right side of heart causing bigger right atrium and smaller right ventricle

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59
Q

Cause of rheumatic fever

A

Group A strep (strep pyogenes)

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60
Q

Jones diagnostic criteria for rheumatic fever

A
  • 2 Major or 1 major and 2 minor plus evidence of preceding strep infection
    o Scarlet fever
    o Throat swab
    o Serum ASO titre
  • Major criteria
    o Carditis = changed murmur, CCF, cardiomegaly, friction rub, +ve echo
    o Polyarthritis
    o Erythema marginatum
    o Subcutaneous nodules
    o Sydenham’s chorea
  • Minor criteria
    o Fever
    o ESR >20mm or CRP increased
    o Arthralgia (pain but no swelling)
    o ECG: PR interval >0.2s
    o Previous rheumatic fever or rheumatic heart disease
  • Joints  Knees, ankles, elbows, wrists may be very tender but no sequelae
  • Echo criteria
    o Mitral regurg jet is: >1cm, holosytolic, visible in 2 planes, mosaic pattern
  • MacCallum plaque
    o Base of posterior mitral leaflet
    o Aortic, pulmonary, tricuspid valves are affected in descending order of frequency
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61
Q

Management of rheumatic fever

A
  • Rest/immobilisation helps joints and heart
  • NSAIDs
  • Oral Phenoxymethylpenicillin (for pharyngitis) preceded by one dose of benzylpenicillin
  • Sydenham’s chorea  Unless mild consider prednisolone for 4wks then taper
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62
Q

What is PANDAS

A

Paediatric autoimmune neuropsychiatric disorders associated with strep infections
o Suspect this in those with tics/Tourettes and OCD
o Anorexia nervosa may also be feature

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63
Q

Causes of childhood obesity

A
  • Imbalance between energy intake and expenditure
  • Dietary and Exercise
  • Sleep deprivation
  • Socioeconomic background
  • Genetics
  • Ethnicity = Asian
  • Female
  • Taller children
  • Medication = sodium valproate, carbamazepine, mirtazapine, steroids
  • High/low birth weight
  • Intrauterine exposure to gestational diabetes or maternal obesity
  • Hypothyroidism
  • Cushing’s syndrome
  • Growth hormone deficiency
  • Prader-Willi Syndrome
  • Down’s syndrome
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64
Q

Complications of childhood obesity

A
  • Insulin resistance
  • Type 2 DM
  • Sleep apnoea
  • Orthopaedic problems
    o Slipped upper femoral epiphyses
    o Blout’s disease
    o Musculoskeletal pains
  • Non-alcoholic fatty liver disease
  • Psychosocial morbidity = poor self-esteem, bullying
  • PCOS
  • Vitamin D deficiency
  • Atherosclerosis
  • Early onset CVD
  • Cancers = breast, bowel
  • Subfertility
  • Hypertension
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65
Q

Causes of hypogonadotropic hypogonadism

A
  • Abnormal functioning of hypothalamus or pituitary gland
  • Previous damage to hypothalamus or pituitary
  • GH deficiency
  • Hypothyroidism
  • Hyperprolactinaemia
  • Serious chronic conditions (cystic fibrosis, IBD)
  • Excessive exercise or dieting (delay menstruation in girls)
  • Constitutional delay in growth and development
  • Kallmann syndrome
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66
Q

Presentation of Kallmann syndrome

A
  • Failure to start puberty
  • Reduced or absent sense of smell (anosmia)
  • Hypogonadism, cryptorchidism
  • Normal or above average height
  • Cleft lip/palate and visual/hearing defects
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67
Q

Causes of hypergonadotropic hypogonadism

A
  • Previous damage to gonads (testicular torsion, cancer, infections)
  • Congenital absence of testes or ovaries
  • Kleinfelter’s syndrome
  • Turner’s syndrome
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68
Q

What is precocious puberty

A

Development of secondary sexual characteristics earlier than normal

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69
Q

Presentation of precocious puberty

A
  • Girls
    1. Thelarche = first stage of breast development
    2. Adrenarche = first stage of pubic hair development
    3. Menarche = onset of menstrual periods (2yrs after start)
  • Boys
    o Bilateral testes enlargement
    o Pubic hair growth
    o Penis enlargement
  • Other symptoms
    o Gynaecomastia in boys
    o Short stature
    o Disproportioned growth of one area compared to other
    o Polyuria
    o Polydipsia
    o Sleep
    o Temperature regulation
    o Visual disturbance
  • Testes
    o Small testes  adrenal cause
    o Bilateral enlargement  gonadotrophin release from intracranial lesion
    o Unilateral enlargement  gonadal tumour
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70
Q

Puberty staging

A

Tanner

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71
Q

Congenital cause of testicular torsion

A

Belt-clapper deformity

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72
Q

PResentation of testicular torsion

A
  • Abdominal pain
  • Sudden severely painful, inflamed testis
    o makes walking uncomfortable
    o Pain often comes on during sport or physical activity
    o With intermittent torsion the pain may have passed on presentation
    o But if severe and lie is horizontal then prophylactic fixing may be wise
    o Very tender, hot and swollen
    o Testis may lie high and transversely
  • Nausea and vomiting
  • Prehn’s sign = elevation of testes does not relief pain
  • Cremasteric reflex lost
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73
Q

Management of testicular torsion

A
  • Urgent surgical exploration
    o If surgery performed in <6 hrs, salvage rate = 90-100%
    o If >24 hours = 0-10%
  • Orchidectomy = removal of testis
  • Bilateral fixation
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74
Q

Management of undescended testis

A
  • Unilateral
    o Referral from around 3m
    o Urological surgeon before 6m
    o Early (at 1yr) fixing within scrotum = Orchidopexy
  • Bilateral
    o Review within 24 hrs
    o May need urgent endocrine and genetic investigations
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75
Q

Congenital causes of deafness

A

o Maternal rubella or CMV infection in pregnancy
o Genetic deafness
o Down’s syndrome

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76
Q

Red flags for abdominal pain

A
  • Persistent or bilious vomiting
  • Severe chronic diarrhoea
  • Fever
  • Rectal bleeding
  • Weight loss or faltering growth
  • Dysphagia
  • Night time pain
  • Abdominal tenderness
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77
Q

What is intussusception

A
  • Bowel telescopes into itself
  • Thickens overall bowel and narrow lumen at folded area
  • Obstruction to passage of faeces through bowel
  • Proximal to or at level of ileo-caecal valve
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78
Q

Presentation of intussusception

A
  • Severe, colicky abdo pain  Draw knees up
  • Pale, lethargic and unwell child
  • Redcurrant jelly stool (late sign)
  • Vomiting (bilious = green)
  • Diarrhoea
  • RUQ mass on palpation = sausage-shaped
  • Intestinal obstruction
  • Tender abdomen and guarding
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79
Q

Investigations of intussusception

A

Abdominal USS = Target or bull’s eye sign

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80
Q

Management of intussusception

A
  • 1st line = reduction by air insufflation under radiological control
  • Therapeutic enemas to try to reduce intussusception = contrast/water/air pumped into colon force folded bowel out
  • Surgical reduction (if signs of peritonitis)
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81
Q

What is meckel’s diverticulum

A

Congenital diverticulum of small intestine

82
Q

Red flags for constipation

A
  • Not passing meconium within 48 hrs of birth
  • Neurological signs/sx (lower limbs)
  • Vomiting
  • Ribbon stool
  • Abnormal anus
  • Abnormal lower back or buttocks
  • Failure to thrive
  • Acute severe abdominal pain and bloating/distension
83
Q

Amber flags for constipation

A
  • Faltering growth
  • Disclosure or evidence that raises concerns over possibility of child maltreatment
84
Q

Causes of constipation

A
  • Functional constipation
  • Hirschsprung’s disease
  • Cystic fibrosis
  • Hypothyroidism
  • Spinal cord lesions
  • Sexual abuse
  • Intestinal obstruction
  • Anal stenosis/fissure
  • Cows milk intolerance
  • Medication = opiates
  • Hypercalcaemia
85
Q

Mangement of idiopathic constipation

A
  • Correct any reversible factors = high fibre diet and good hydration
  • Faecal impaction present
    o 1st line = polyethylene glycol 2250 + electrolytes (Movicol Paediatric plain)
    o Add stimulant laxative (after 2 wks if no improvement)
    o Substitute for lactulose
    o Parent education = can increase Sx of soiling and abdo pain
  • Maintenance therapy
    o Continue long term Movicol and slowly weaned off as child develops normal, regular bowel habit
  • Encourage and praise visiting toilet = scheduling visits, bowel diary and star charts
  • Infants not yet weaned
    o Bottle fed = give extra water in between feeds, gentle abdo massage, bicycling of legs
    o Breast fed = consider organic causes
  • Infants have/being weaned
    o Extra water, diluted fruit juice, fruits
    o Consider adding lactulose
86
Q

What is hirschsprung’s disease

A

Nerve cells of myenteric plexus are absent in distal bowel and rectum
- Nerve plexus responsible for stimulating peristalsis of large bowel
- Without stimulation bowel loses motility and stops being able to pass food along its length

87
Q

Presentation of Hirschsprung’s disease

A
  • Neonatal = Delay in passing meconium (more than 24 hrs)
  • Chronic constipation since birth
  • Abdominal pain and distention
  • Vomiting
  • Poor weight gain and failure to thrive
88
Q

Investigations of hirschsprung’s disease

A
  • Abdo XR = intestinal obstruction
  • PR = stool ejection
  • Full thickness Rectal biopsy (GS) = histology shows absence of ganglionic cells
89
Q

Management of Hirschsprung’s disease

A
  • Fluid resuscitation
  • 1st line = Rectal washouts initially
  • Anorectal pull through procedure
  • Management of intestinal obstruction
  • Definitive = Surgical removal of aganglionic section of bowel
90
Q

Associations of congenital diaphragmatic hernia

A
  • Other malformations (neural tube)
  • Trisomy 18
  • Chromosome deletions
  • Pierre Robin
91
Q

Presentation of congenital diaphragmatic hernia

A
  • Impaired lung development (pulmonary hypoplasia and pulmonary hypertension)
  • Difficult resuscitation at birth
  • Respiratory distress shortly after birth
  • Bowels sounds in one hemithorax
  • pH <7.3
  • Cyanosis augar badly = lung hypoplasia
  • Heart sounds displaced medially
  • Abdominal wall appears concave
92
Q

Vomiting red flags

A
  • Not keeping any feed down = pyloric stenosis/intestinal obstruction
  • Projectile/forceful vomiting = pyloric stenosis/intestinal obstruction
  • Bile stained vomit = obstruction
  • Haematemesis/melaena = peptic ulcer, oesophagitis or varices
  • Abdominal distention = obstruction
  • Reduced consciousness/bulging fontanelles/neurological signs = meningitis/ raised ICP
  • Respiratory sx = aspiration/ infection
  • Blood in stools = gastroenteritis or cows milk protein allergy
  • Signs of infection = pneumonia, UTI, tonsillitis, otitis or meningitis
  • Rash, angioedema and other signs of allergy = cows milk
  • Apnoeas = serious underlying pathology
93
Q

Management of GORD

A
  • Advise
    o Small, frequent meals
    o Burping regularly to help milk settle
    o Not over-feeding
    o Keep baby upright after feeding (not lying flat)
  • More problematic cases
    o Thickened milk/formula
    o Gaviscon mixed with feeds
    o PPI = Omeprazole if unexplained feeding difficulties, distressed behaviour or faltering growth
    o Metoclopramide
  • Rare severe cases  Surgical fundoplication
94
Q

Presentation of pyloric stenosis

A
  • Presents in first few weeks of life (4-6 wks)
  • Projectile vomiting (typically 30 mins after feed)
  • Hungry baby
  • Non bile stained
  • Constipation and dehydration
  • Thin, pale and failing to thrive
  • See peristalsis of abdomen after feeding
  • Firm, round, palpable mass felt in upper abdo
95
Q

Investigations of pyloric stenosis

A
  • Blood gas = metabolic alkalosis with low chloride and potassium
  • Abdo USS = thickened pylorus
96
Q

Management of pyloric stenosis

A

Laparoscopic pyloromyotomy (Ramstedt’s operation)

97
Q

Presentation of Cow’s milk protein allergy

A

Colic symptoms = irritability, crying
Regurgitation and vomiting
Blood/mucus in stools
Faltering growth
Diarrhoea
Urticaria, atopic eczema
Rarely angioedema and anaphylaxis

98
Q

Management of CMPA

A

Exclusively breastfed
* Continue breastfeeding
* Exclude cow’s milk protein from mothers diet
* Use eHF when breastfeeding stops until 12m and at least for 6m
Formula fed
* 1st line = change to hypoallergenic extensively hydrolysed formula
* amino acid formula
* 10% also intolerant to soya milk

99
Q

Presentation of intestinal malrotation

A

If volvulus = bile stained vomiting in first day of life

100
Q

Management of volvulus

A

Ladd’s procedure

101
Q

Presentation of oesophageal atresia

A

Antenatal = polyhydramnios
Respiratory distress
Distended abdomen
Choking and problems with swallowing
Difficulty feeding and overflow saliva
Cyanotic spells Following aspiration

102
Q

Association of duodenal atresia

A

Downs syndrome
Other intestinal atresia
VACTERL association

103
Q

Presentation of duodenal atresia

A

Antenatal = polyhydramnios
Distended abdomen
Non-bilious/bilious vomiting

104
Q

Investigations of duodenal atresia

A

XR = double bubble

105
Q

Presentation of haemolytic disease of newborn

A

Jaundice (<24 hrs)
Infection
Yellow vernix
CCF (oedema, ascites)
Hepatosplenomegaly
Progressive anaemia
Bleeding
CNS signs (Kernicterus)
Hypoalbuminaemia
Maternal diabetes
Thalassaemia

106
Q

Management of haemolytic disease of newborn

A

Exchange transfusion
* If Hb <7g/dL, give 1st volume of the exchange transfusion as packed cells
* Subsequent precise exchanges according to response
* Keep baby warm
Phototherapy
under phototherapy lights
Giving Rh negative mothers anti-D immunoglobulin
ABO incompatibility = Exchange transfusion may be needed

107
Q

Complication of haemolytic disease of newborn

A

Hydrops fetalis

108
Q

Infectivity of chickenpox

A
  • Infectivity 4 days before rash and 5 days after rash appeared
  • Incubation = 10-21 days
109
Q

Groups at high risks of complications from chickenpox

A
  • Immunocompromised
  • Preterm babies
  • Steroid use
  • <1 yrs old
  • Adults and adolescents >14
  • Pregnant women
110
Q

Presentation of chickenpox

A
  • Fever initially
  • Generalised itchy rash
    o Erythematous, raised
    o Starts on trunk/face and spreads outwards affecting whole body over 2-5 days
    o Blistering lesions (macules  papules  vesicles)
  • General fatigue and malaise
  • Mild systemic upset
  • URTI symptoms
  • Shingles  Reactivated chicken pox
111
Q

Mangement of chickenpox

A
  • Supportive
    o Keep cool, trim nails
    o School exclusion and avoid high risk groups until all lesions crusted over (5 days)
    o Itching = calamine lotion, chlorphenamine
  • Higher risk groups  IV Acyclovir 5 days
112
Q

Complications of chickenpox

A
  • Secondary bacterial infection  Necrotising fasciitis
    o Increased with NSAID use
  • Rarely
    o Conjunctival lesions
    o Pneumonia
    o Encephalitis
    o Shingles
113
Q

Cause of glandular fever

A

EBV

114
Q

PResentation of glandular fever

A
  • Classic triad = sore throat, lymphadenopathy, pyrexia
  • Malaise, anorexia, headache
  • Palatal peteciae
  • Splenomegaly
  • Hepatitis
  • Lymphocytosis
  • Haemolytic anaemia
  • Maculopapular pruritic rash (if taking amoxicillin/ampicillin)
115
Q

Investigations of glandular fever

A

Monospot test (in week 2)

116
Q

Management of glandular fever

A
  • Usually resolves in 2-4 wks
  • Supportive
    o Rest, fluids, avoid alcohol
    o Simple analgesia
    o Avoid playing contact sports for 4 wks (splenic rupture)
117
Q

Cause of hand, foot and mouth disease

A

Coxsackie 16

118
Q

Presentation of HFM disease

A
  • Mild systemic upset (sore throat and fever)
  • Oral ulcer
  • Vesicles on palms and soles
119
Q

Management of HFM disease

A
  • Self-resolves 7-10 days
  • Supportive  Simple analgesia, Hydration, Reassurance
  • Keep unwell children off school but no exclusion required
120
Q

Cause of impetigo

A
  • Staphylococcus aureus (bullous)
  • Streptococcus pyogenes
121
Q

Presentation of impetigo

A
  • Non-bullous impetigo
    o Typically occurs around nose or mouth
    o Exudate from lesions dries to form golden crust
  • Bullous impetigo
    o 1-2cm fluid filled vesicles to form on skin
    o Vesicles grow in size then burst forming golden crust
    o Heal without scarring
    o Lesions are painful and itchy
    o Feverish and generally unwell
122
Q

Management of impetigo

A
  • Contagious so children kept off school until lesions healed or treated with Abx for at least 48 hrs
  • Advise not to touch or scratch lesions, hand hygiene, avoid sharing face towels and cutlery
  • Non-bullous
    o Antiseptic cream (hydrogen peroxide 1% cream)
    o Topical fusidic acid
  • Bullous  Flucloxacillin (oral or IV)
123
Q

Complications of impetigo

A
  • Cellulitis
  • Sepsis
  • Scarring
  • Post streptococcal glomerulonephritis
  • Staphylococcus scalded skin syndrome
  • Scarlet fever
124
Q

Cause of measles

A

RNA paramyxovirus

125
Q

Presentation of measles

A
  • Prodrome = cough, coryza, conjunctivitis, cranky
  • High temp until 5 days after rash starts
  • Koplik spots on palate (classic presentation)
    o Spots often fade as rash appears
    o behind ears, on day 3-5, spread down body, merging
  • Diarrhoea
126
Q

Management of measles

A
  • Isolate
  • Ensure adequate nutrition
    o Continue breastfeeding even during diarrhoea
    o Pass nasogastric feeding tube if intake poor
  • Vitamin A
    o Developing world
    o CI = pregnancy, known not to be deficient
  • Treat secondary bacteria infection (otitis media/pneumonia)
  • Admission considered in immunosuppressed or pregnant
  • Notifiable disease
  • Vaccinate contacts within 72 hrs if unvaccinated
127
Q

Complications of measles

A
  • More common if <5 yrs or >20yrs
  • Otitis media
  • Croup and tracheitis (infants)
  • Pneumonia (cause of death)
  • Encephalitis (older patients)
  • Subacute sclerosing parencephalitis (chronic – develops 7-13 yrs after)
  • Febrile convulsions
  • Keratoconjunctivits, corneal ulceration
  • Appendicitis
  • Myocarditis
128
Q

Presentation of mumps

A
  • Fever
  • Malaise
  • Muscular pain
  • Parotitis  Ear ache, Pain on eating
129
Q

Presentation of rubella

A
  • Pink Maculopapular rash on face which spreads to whole body
  • Suboccipital and post-auricular lymphadenopathy
130
Q

Presentation of molluscum contagiosum

A
  • Pinkish or pearly white papules with central umbilication (5mm diameter)
  • Lesions appear in clusters in areas anywhere on body (except palms of hands and soles of feet)
131
Q

Management of molluscum

A
  • Self-care advice
    o Reassure that self-limiting
    o Spontaneous resolution within 18m
    o Avoid sharing towels, clothing and baths with uninfected people
    o Encourage not to scratch
    o Exclusion from school not necessary
  • Treatment
    o Not usually recommended
    o Simple trauma
    o Cryotherapy
    o Emollient and mild topic corticosteroid
    o Antibiotic if infected
132
Q

Cause of 6th disease (roseola infantum)

A

HHV 6

133
Q

Presentation of 6th disease

A
  • High fever (precedes rash by few days)
  • Maculopapular rash
  • Nagayama spots
  • Febrile convulsions
  • Diarrhoea
  • Cough
134
Q

Presentation of scalded skin syndrome

A
  • Generalised patches of erythema on skin  similar appearance to burn or scalded
  • Skin looks thin and wrinkled
  • Formation of fluid filled blisters (bullae)
  • Blisters burst and leave very sore, erythematous skin below
  • Nikolsky sign = gentle rubbing of skin causes it to peel away
  • Systemic: Fever, Irritability, Lethargy, Dehydration
135
Q

Cause of scarlet fever

A

Group A strep

136
Q

Presentation of scarlet fever

A
  • Red-pink blotchy macular rash starting on trunk and spreads outwards
  • Rough sandpaper skin
  • Sore throat (tonsilitis)
  • Strawberry tongue
  • Fever (lasts 24-48 hrs)
  • Red, flushed cheeks
  • Cervical lymphadenopathy
  • Systemic: Lethargy, Malaise, Headache, N+V
137
Q

Management of scarlet fever

A
  • Phenoxymethylpenicillin for 10 days immediately
    o Azithromycin if penicillin allergy
  • Notifiable disease
  • Keep children off school until 24 hrs after starting Abx
138
Q

Complications of scarlet fever

A
  • Otitis media
  • Rheumatic fever
  • Acute glomerulonephritis
  • Invasive complications  Bacteraemia, Meningitis, Necrotising fasciitis
139
Q

Cause of slapped cheek syndrome

A

Parovirus B19

140
Q

Cause of stevens Johnson syndrome

A
  • Medications
    o Anti-epileptics
    o Antibiotics
    o Allopurinol
    o NSAIDs
  • Infections
    o Herpes simplex
    o Mycoplasma pneumonia
    o Cytomegalovirus
    o HIV
141
Q

Presentation of stevens johnson syndrome

A
  • Non-specific symptoms = fever, cough, sore throat, sore mouth, sore eyes, itchy skin
  • Painful Purple/red rash with blistering
    o Affects less than 10% body surface area
    o Spreads across skin
    o Shedding of top layer of skin
    o Can happen to lips and mucous membranes
    o Ulcerated
  • Inflamed eyes
  • Affect urinary tract, lungs, internal organs
142
Q

Risk factors for developmental dysplasia of hip

A
  • 1st born (tighter, unstretched uterus)
  • Breech position (incl CS)
  • Sibling/ FH of DDH
  • Swaddling
  • Macrosomia
  • Oligohydramnios
  • Congenital calcaneovalgus foot deformity
143
Q

Presentation of developmental dysplasia of hip

A
  • Asymmetrical skin folds
  • Limb length discrepancy
  • Less mobility/flexibility
  • Limping, toe walking, waddling
144
Q

Investigations for developmental displasia fo hip

A
  • Screening at 6-8wks
    o Barlow’s test (dislocate)
    o Ortolani’s test (relocate)
    o Symmetry of leg length
    o Level of knees when hips and knees are bilaterally flexed
    o Restricted abduction of hip in flexion
  • US at 6w
    o 1st degree relative with DDH
    o Breech
    o Other RF
  • 6m > US
  • 6m < XR
145
Q

Management of developmental dysplasia of hip

A
  • Observation  Most unstable hips spontaneously stabillise by 3-6 wks
  • Pavlik harness (constant, few months)
    o Children younger than 4-5m
  • Abduction brace (if harness fails/ineffective)
  • Surgical reduction/fixation
146
Q

Presentation of transient synovitis

A

Recent viral URTI (sx occur within few wks)
Limp
Refusal to weight bear
Groin or hip pain
Mild low grade temp

147
Q

Management of transient synovitis

A

Simple analgesia
Exclude other pathology
Clear safety net advice to attend A&E if Sx worsen or develop fever
Follow up at 48 hrs and 1 wk

148
Q

PResentation of juvenile idiopathic arthritis

A

Joint swelling/inflammation/pain/stiffness
Fever
Limp
Fatigue
Lymphadenopathy
Hepatosplenomegaly
Blurry/gritty eyes (uveitis)
Salmon-pink Rash
Appetite loss and weight loss

149
Q

Differential of limping child

A
  • Septic arthritis/osteomyelitis
  • Juvenile idiopathic arthritis
  • Trauma
  • Development dysplasia of hip
  • Perthes disease
  • Slipped upper femoral epiphysis
150
Q

What is Osgood-Schlatter’s disease

A

Inflammation at tibial tuberosity where patella ligament inserts

151
Q

PResentation of osgood-schlatter

A

Gradual onset
Anterior knee pain
Usually unilateral (can be bilateral)
Pain exacerbated by physical activity, kneeling and on extension of knee
Visible or palpable hard and tender lump at tibial tuberosity

152
Q

What is osteogeneis imperfecta

A

Brittle bone disease – group of disorders of collagen metabolism resulting in bone fragility and fractures

153
Q

Presentation of osteogenesis imperfecta

A

Increased fragility
* Frequent fractures following minor trauma
* Abuse
* Crush fractures (vertebrae)
Bone deformity = bowed legs
Joint issues
Scoliosis
Short stature
Weak teeth/ dental caries
Blue sclera
Hearing loss (deafness secondary to otosclerosis)

154
Q

What is perthes disease

A

Idiopathic avascular necrosis of proximal femoral epiphysis

155
Q

Presentation of perthes disease

A

Insidious onset
Painless limp (worsens)
Intermittent hip, knee, groin or thigh pain
Gait disturbance
Hip stiffness and loss of int rot and abd
Reduced range of hip movement
Limb length discrepancy
Muscle wasting

156
Q

Management of perthes disease

A

Keep femoral head within acetabulum: cast, braces
If <6 yrs = observation
Resolve symptoms
* NSAIDs
* Traction
* Crutches
Restore ROM
* Physio
* Muscle lengthening
Surgery (if older and with moderate results)
* Osteotomy

157
Q

Presentation of rickets

A

Lethargy
Bone pain
Swollen wrists ‘ricket rosary’
Bone deformity
Poor growth
Dental problems
Muscle weakness
Pathological or abnormal fractures
Bowing of legs (curve outwards)
Knock knees (legs curve inwards)
Rachitic rosary (ends of ribs expand at costochondral junctions, causing lumps along chest)
Craniotabes (soft skull, with delayed closure of sutures and frontal bossing)
Delayed teeth (underdevelopment of enamel)
Harrison’s sulcus

158
Q

Risk factors for slipper upper femoral epiphysis

A

Adolescence
Male
Obesity
History of radiotherapy to area
Puberty
Downs syndrome
Hypothyroidism
Hypopituitary
GH deficiency

159
Q

Presentation of SUFE

A

Groin and thigh pain
Limp = antalgic gait, externally rotated foot
Loss of internal rotation of leg in flexion
Knee pain
Present for wks/mnths
Prefer to sit with affected leg crossed over other

160
Q

Causes of global developmental delay

A
  • Down’s syndrome
  • Fragile X syndrome
  • Fetal alcohol syndrome
  • Rett syndrome
  • Metabolic disorders
161
Q

Causes of gross motor delay

A
  • Cerebral palsy
  • Ataxia
  • Myopathy
  • Spina bifida
  • Visual impairment
162
Q

Causes of fine motor delay

A
  • Dyspraxia
  • Cerebral palsy
  • Muscular dystrophy
  • Visual impairment
  • Congenital ataxia
163
Q

Causes of hearing, speech and language delay

A
  • Specific social circumstances
  • Hearing impairment
  • Learning disability
  • Neglect
  • Autism
  • Cerebral palsy
164
Q

Presentation of ADHD

A

Inattention
* Does not follow through on instructions
* Reluctant to engage in mentally-intense tasks
* Easily distracted
* Finds it difficult to sustain tasks
* Finds it difficult to organise tasks or activities
* Often forgetful of daily activities
* Often loses things necessary for tasks or activities
* Often dose not seem to listen when spoken directly
Impulsivity/Hyperactivity
* Unable to play quietly
* Talks excessively
* Dose not wait their turn easily
* Will spontaneously leave their seat when expected to sit
* Is often ‘on the go’
* Often interruptive or intrusive to others
* Will answer prematurely before a question has been finished
* Will run and climb in situations where it is not appropriate
Different presentation in girls (underdiagnosis)

165
Q

Medication for ADHD

A

Methylphenidate (Ritalin) = 6wk trial
* S/E = abdo pain, nausea, dyspepsia, stunted growth
* Monitor weight and height every 6m
2nd line - Lisdexamfetamine (Elvanse)
Atomoxetine (Strattera)
Guanfacine (Intuniv)
Clonidine

166
Q

Severity of ADHD

A

Connor’s

167
Q

Presentation of Autism Spectrum Disorder

A

Impaired reciprocal social interaction
* Children frequently play along (relatively uninterested in being with other children)
* Fail to regulate social interaction with nonverbal cues (eye gaze, facial expression, gestures)
* Fail to form and maintain appropriate relationships = become socially isolated
Repetitive behaviours, interests, activities
* Stereotyped and repetitive motor mannerisms, inflexible adherence to non-functional routines or rituals
* Children noted to have particular ways of going about everyday activities
Impaired communication and language
Spectrum (can be high functioning)
Higher head circumference to brain volume ratio

168
Q

Red flags for child abuse

A
  • Disclosure by child
  • Odd story, incongruent with injuries, odd mode of injury, odd set of signs
  • Delayed presentation to doctor, taken by someone other than parents
  • History inconsistent with child’s development
  • Efforts to avoid full examination
  • Psychological sequelae from sexual/emotional abuse
  • Unexplained fractures (forearm, rib)
  • Rare for non-ambulant baby to sustain accidental fracture
  • Buttock, perineum or face injury, intracranial bleeds, torn lingual frenulum, vitreous/retinal bleeds, hyphaemia, lens dislocation, bulging fontanelle, increased head circumference + xanthochromia
  • Cigarette burns, whip marks, bruised non-mobile baby, signs of suffocation, fingermark bruising, perforated pharynx, bite marks
  • Torn frenulum
  • Failure to thrive
  • STIs
169
Q

Severity of AKI in children

A

Paediatric RIFLE criteria
* Risk
* Injury
* Failure
* Loss of kidney function
* End-stage renal failure

170
Q

Types of nocturnal enuresis

A

Primary = never been continent through night (at least 2x per week for 3m)
Secondary = been continent for at least 6m before

171
Q

Causes of nocturnal enuresis

A

Constipation
Abuse/emotional upset
UTI
Diabetes mellitus
Renal failure

172
Q

Management of nocturnal enuresis

A

Parental advice
* diet, fluid intake, toilet patterns, lifting and waking
* Punishment and disapproval ineffective
Conservative measures
* Restricting fluid intake before bedtime and irritating fluids (orange juice)
* Double voiding at night
* Waking child to pass urine once in night
* Introduce reward system for agreed behaviours
* Clear constipation
Use bed-wetting (enuresis) alarm = trial for 4 wks
* 1st line for children <7
If all unsuccessful or >7
* Desmopressin 1-2 hrs before bed
* Do not drink after medication as increases risk of cerebral oedema

173
Q

Cause of bronchiolitis

A

Respiratory syncytial virus

174
Q

Presentation of bronchiolitis

A
  • Coryzal sx = runny/snotty nose, sneezing, mucus in throat, watery eyes
  • Dry cough
  • Poor feeding with increasing dyspnoea
  • Mild fever
  • Apnoeas
  • Wheeze and fine inspiratory crackles on auscultation
  • Signs of respiratory distress
    o Use of accessory muscles
    o Intercostal and subcostal recessions
    o Nasal flaring
    o Head bobbing
    o Tracheal tugging
    o Cyanosis
    o Abnormal airway noises
    o Tachypnoea
175
Q

Maangement of bronchiolitis

A
  • Supportive management
    o Ensuring adequate intake = NG tube/IV fluids
    o Saline nasal drops and nasal suctioning = clear nasal secretions
    o Supplementary oxygen = if sats below 92%
    o Ventilatory support if required
  • Palivizumab (monoclonal antibody) = monthly injection as prevention
176
Q

Cause of Croup

A

parainfluenza virus

177
Q

Presentation of Croup

A
  • Increased work of breathing
  • “Barking” cough, occurring in clusters of coughing episodes
  • Hoarse voice
  • Stridor
  • Low grade fever
  • Respiratory distress
  • Sx worse at night and increase with agitation
  • Preceded by non-specific upper RTI (12-72 hrs) = coryzal Sx
  • Usually resolves within 24hrs but may last up to 1wk
178
Q

Management of croup

A
  • All children with croup = Single dose oral dexamethasone
  • Managed at home  fluids and rest, Infection control, Simple Analgesia
  • Safety-net parents
    o Child very pale, grey or blue for more than few secs
    o Unusually sleepy or unresponsive
    o Having trouble breathing
    o Upset while struggling to breath
    o Unable to talk or drooling
  • Admission for
    o >60 breaths/min or high fever or toxic appearance
    o <6m age
    o Known upper airway abnormalities (Laryngomalacia, Downs)
    o Uncertainty about diagnosis
  • Severe croup
    o Oxygen
    o Nebulised budesonide
    o Nebulised adrenalin
    o Intubation and ventilation
179
Q

CXR in epiglottis

A

Steeple sign = subglottic narrowing

180
Q

Presentation of diptheria

A
  • Sore throat
  • Swollen tonsils  bull neck
  • Low grade fever
  • Pseudomembrane formation
  • Polyneuritis (starting with cranial nerves)
  • Shock = myocarditis, toxaemia, cardiac conducting system involvement
  • Dysphagia
  • Muffled voice
  • Bronchopneumonia
  • Airway obstruction preceded by brassy cough
  • Nasal discharge with excoriated upper lip
  • Motor palatal paralysis also occurs causing fluids to escape from nose on swallowing
181
Q

Management of diptheria

A
  • IM penicillin
  • Diphtheria antitoxin = 10 000-30 000 units IM
  • Erythromycin
  • Contacts <2 receive erythromycin syrup 7 days
  • Keep away from pregnant women
182
Q

Cause of whooping cough

A

Bordetella pertussis

183
Q

Presentation of whooping cough

A

acute cough lasting >14 days without another apparent cause and 1+ of:
o Paroxysmal cough
o Inspiratory whoop
o Post-tussive vomiting
o Undiagnosed apnoeic attacks in young infants

184
Q

Maangement of whooping cough

A
  • Oral Clarithromycin if onset of cough within previous 21 days
  • Admit if <6m
  • Notifiable disease
  • May need ventilating
  • Household contacts offered antibiotic prophylaxis
  • School exclusion: 48 hrs after commencing Abx
185
Q

Cause of epiglottitis

A

Haemophilus influenza type B (HiB)

186
Q

Presentation of epiglottitis

A
  • Rapid onset
  • Fever
  • Stridor
  • Pooling/drooling saliva
  • Sore throat
  • Muffled voice/cry
  • Dysphagia
  • Tripod stance: sitting and lean forward, extend neck
  • NO COUGH
  • Respiratory distress  respiratory retractions and cyanosis
187
Q

Management of epiglottitis

A
  • Intubate (or tracheostomy)
  • Antibiotics = cephalosporins
  • Dexamethasone
  • Fluid resuscitation
188
Q

Presentation of viral induced wheeze

A
  • Viral Sx = fever, cough, coryzal Sx 1-2 days before
  • Shortness of breath
  • Signs of respiratory distress
  • Expiratory wheeze throughout chest
189
Q

Management of viral induced wheeze

A
  • Encourage smoking parents to stop
  • Moderate
    1. Short acting beta 2 agonist (salbutamol) via spacer
    2. Intermittent leukotriene receptor antagonist (montelukast) and/or inhaled corticosteroids
  • Severe
    o Oxygen if required
    o Aminophylline infusion
    o Consider IV salbutamol
190
Q

Angelman syndrome

A

Fascination with water
Happy demeanour

191
Q

Down’s syndrome

A

Hypotonia
Brachycephaly (small head with flat back)
Short neck
Short stature
Flattened face and nose
Prominent epicanthic folds
Upward sloping palpable fissures
Single palmar crease
Brushfield spots in iris
Protruding tongue
Small low-set ears

192
Q

Antenatal screening for Down’s syndrome

A
  • 1st line = combined USS and maternal blood test (11-14/40)
  • Nuchal thickness >6mm
  • Beta-HCG = higher is greater risk
  • Pregnancy-associated plasma protein-A = lower is greater risk
193
Q

Complication’s of Down’s syndrome

A

Learning disability
Recurrent otitis media
Deafness (Eustachian tube abnormalities)
Visual problems (myopia, strabismus, cataracts)
Hypothyroidism
Cardiac defects = endocardial cushion defect (ASD, VSD, PDA, ToF)
Atlantoaxial instability
Acute lymphoblastic Leukaemia
Dementia (Alzheimer’s)
Duodenal atresia
Hirschsprung’s disease
Subfertility
Repeated respiratory infections

194
Q

Edward’s syndrome (trisomy 18)

A

Micrognathia
Low set ears
Rocker bottom feet
Overlapping of fingers

195
Q

Patau syndrome (13)

A

Microcephalic small eyes
Cleft lip/palate
Polydactyly
Scalp lesions

196
Q

Fragile X syndrome

A

Long, narrow face
Large ears
Large testicles after puberty
Hypermobile joints

197
Q

Klinefelter’s syndrome (47XXY)

A

Appear normal until puberty
Taller height
Wider hips
Gynaecomastia
Weaker muscles
Small testicles
Reduced libido
Shyness
Infertility
Subtle learning difficulties (speech and language)

198
Q

Marfan syndrome

A

Tall stature
Long neck
Long limbs
Long fingers (arachnodactyly)
High arch palate
Hypermobility
Pectus carinatum or pectus excavatum
Downward sloping palpable fissures

199
Q

Noonan syndrome

A

Short stature
Broad forehead
Downward sloping eyes with ptosis
Hypertelorism (wide space between eyes)
Prominent nasolabial folds
Low set ears
Webbed neck
Widely spaced nipples

200
Q

Prader-Willli syndrome

A

Constant insatiable hunger that leads to obesity
Neonatal hypotonia

201
Q

Turner syndrome (45X0)

A

Short stature
Webbed neck
High arching palate
Downward sloping eyes with ptosis
Broad chest with widely spaced nipples
Cubitus valgus
Underdeveloped ovaries with reduced function
Late or incomplete puberty

202
Q

William syndrome

A

Broad forehead
Starburst eyes
Flattened nasal bridge
Long philtrum
Wide mouth with widely spaced teeth
Small chin
Very sociable trusting personality

Finals (23 decks)

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