Paeds Flashcards

1
Q

Differentials for Stridor in kids <6months

A
  • Laryngomalacia
  • Laryngeal cyst, haemangioma or web
  • Laryngeal stenosis
  • Vocal cord paralysis
  • Vascular ring
  • Gastro-oesophageal reflux
  • Hypocalcaemia (laryngeal tetany)
  • Respiratory papillomatosis
  • Subglottic stenosis

Croup and epiglottis less common in <6 months olds

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2
Q

Differential diagnosis of acute stridor in kids >6months to 5yrs

A
  • Laryngotracheobronchitis
  • Inhaled foreign body
  • Anaphylaxis
  • Epiglottitis
  • Rare causes include:
    – Bacterial tracheitis
    – Severe tonsillitis with very large tonsils
    – Inhalation of hot gases (e.g. house fire)
    – Retropharyngeal abscess

Croup typically occurs in children aged 6 months to 5 years. It is characterized by an
upper respiratory tract infection that is followed by a barking-type cough, a hoarse
voice, stridor and a low-grade fever. Croup is most commonly caused by the parainfluenza virus.

The upper airway of a child with stridor should not be examined as this may
precipitate total obstruction.

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3
Q

Treatment for croup

A

Supportive care + PO dex/pred +/- nebulised adrenaline

If unsuccesful ventilation, intubation and ENT emergency tracheostomy

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4
Q

Indications for hospital referral

A
  • Apnoeic episodes (commonest in babies 2 months and may be the presenting feature)
  • Intake 50 per cent of normal in preceding 24 hours
  • Cyanosis
  • Severe respiratory distress – grunting, nasal flaring, severe recession, respiratory rate 70/min
  • Congenital heart disease, pre-existing lung disease or immunodeficiency
  • Significant hypotonia, e.g. trisomy 21 – less likely to cope with respiratory compromise
  • Survivor of extreme prematurity
  • Social factors
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5
Q

Key points about bronchiolitis

A

Bronchiolitis is a viral lower respiratory tract infection, generally affecting children under 12 months of age.

It is a clinical diagnosis, based on typical history and examination. No investigations are typically performed for management.

Peak severity is usually at around day two to three of the illness with resolution over 7–10 days.

Usually self-limiting, often requiring no treatment or interventions.

The cough may persist for weeks.

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6
Q

Differential diagnosis of a recurrent or persistent cough in childhood

A
  • Recurrent viral URTIs – very common in all age groups but more so in infants
    and toddlers
  • Asthma – unlikely without wheeze or dyspnoea
  • Allergic rhinitis – often nocturnal due to ‘post-nasal drip’
  • Chronic non-specific cough – probably post-viral with increased cough receptor
    sensitivity
  • Post-infectious – a ‘pertussis (whooping cough)-like’ illness can continue for
    months following pertussis, adenovirus, mycoplasma and chlamydia
  • Recurrent aspiration – gastro-oesophageal reflux
  • Environmental – especially smoking, active or passive
  • Suppurative lung disease – cystic fibrosis or primary ciliary dyskinesia
  • Tuberculosis
  • Habit
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7
Q

Presentations of cystic fibrosis

A

Neonatal
* Meconium ileus
* Intestinal atresia
* Hepatitis/prolonged jaundice

Infant
* Rectal prolapse (may be recurrent)
* Failure to thrive
* Malabsorption and vitamin deficiency (A, D, E, K)

Older children
* Recurrent chest infections
* ‘Difficult’ asthma
* Haemoptysis
* Nasal polyps
* Distal intestinal obstruction syndrome
* Liver disease
* Diabetes mellitus

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8
Q

Diagnosis and management of Cystic Fibrosis

A

Diagnosis can be made by the sweat test, which will demonstrate elevated sweat sodium and chloride concentrations, and by genetic testing.

National newborn screening using blood spots collected on day 5 of life are now tested for immunoreactive trypsinogen (at
the same time as testing for phenylketonuria, congenital hypothyroidism and sickle cell
disease). This is now leading to the identification of cases before the onset of clinical disease.

Once a child is diagnosed with CF, he or she will need multidisciplinary team management under the supervision of a paediatric respiratory consultant. Optimal care will aim
to maintain lung function by treating respiratory infections and removing mucus from the airways with physiotherapy, and to maintain adequate growth and nutrition with
pancreatic enzyme and nutritional supplements.

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9
Q

Signs of impending respiratory failure

A
  • Exhaustion (this is a clinical impression)
  • Unable to speak or complete sentences
  • Colour – cyanosis +/- pallor
  • Hypoxia despite high-flow humidified oxygen
  • Restlessness and agitation are signs of hypoxia, especially in small children
  • Silent chest – so little air entry that no wheeze is audible
  • Tachycardia
  • Drowsiness
  • Peak expiratory flow rate (PEFR) persistently <30 per cent of predicted for height
    (tables are available) or personal best. Children <7 years cannot perform PEFR
    reliably and technique in sick children is often poor
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10
Q

Doses for acute asthma

A

Doses:
Salbutamol (100 mcg/puff) dose:
<6 years old: 6 puffs MDI
6 years or older: 12 puffs MDI

Ipratropium bromide (21 mcg/puff) dose:
<6 years old: 4 puffs MDI
6 years or older: 8 puffs MDI

Oral prednisolone
2 mg/kg (max 60 mg) initially, only continuing with 1 mg/kg daily for further 1-2 days if there is ongoing need for regular salbutamol

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11
Q

Management of pneumonia in a child

A
  • Oxygen to maintain saturation at 92 per cent
  • Adequate pain relief for pleuritic pain
  • Intravenous antibiotics according to local guidelines, e.g. co-amoxiclav
  • Initial fluid restriction to two-thirds maintenance to help correct the hyponatraemia.Fluid restrict even if no hyponatraemia, as SIADH may still develop
  • Fluid balance, regular urea and electrolytes – adjust fluids accordingly. Weigh
    twice daily
  • Physiotherapy, e.g. bubble blowing. Encourage mobility
  • Monitor for development of a pleural effusion. If the chest X-ray is suspicious,
    an ultrasound will be diagnostic. If present, a longer course of antibiotics is
    recommended to prevent empyema (a purulent pleural effusion). A chest drain
    may be necessary if there is worsening respiratory distress, mediastinal shift on
    the chest X-ray, a large effusion or failure to respond to adequate antibiotics
  • Ensure adequate nutrition – children have often been anorectic for several days.
    Low threshold for supplementary feeds probably via nasogastric tube
  • Organise immunization programme before discharge
  • Arrange a follow-up chest X-ray in 6–8 weeks for those with lobar collapse and/
    or an effusion. If still abnormal, consider an inhaled foreign body
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12
Q

Differential diagnosis of chest pain in children

A
  • Trauma, e.g. fractured rib
  • Exercise, e.g. overuse injury
  • Idiopathic
  • Psychological, e.g. anxiety
  • Costochondritis
  • Pneumonia with pleural involvement
  • Asthma
  • Severe cough
  • Pneumothorax
  • Reflux oesophagitis
  • Sickle cell disease with chest crisis and/or pneumonia
  • Rare: pericarditis, angina, e.g. from severe aortic stenosis, osteomyelitis, tumour
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13
Q

Congenital cardiac lesions presenting with neonatal collapse

A
  • Severe aortic coarctation
  • Aortic arch interruption
  • Hypoplastic left heart syndrome
  • Critical aortic stenosis
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14
Q

Differential diagnosis of a collapsed neonate

A
  • Infection – e.g. group B Streptococcus, herpes simplex
  • Cardiogenic – e.g. hypoplastic left heart syndrome, supraventricular tachycardia
  • Hypovolaemic – e.g. dehydration, bleeding
  • Neurogenic – e.g. meningitis, subdural haematoma (‘shaken baby’)
  • Lung disorder – e.g. congenital diaphragmatic hernia (late presentation)
  • Metabolic – e.g. propionic acidaemia, methylmalonic acidaemia
  • Endocrine – e.g. panhypopituitarism
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15
Q

Features of heart failure in a baby

A
  • Tachycardia
  • Tachypnoea
  • Hepatomegaly
  • Poor feeding
  • Sweating
  • Excessive weight gain (acutely)
  • Poor weight gain (chronically)
  • Gallop rhythm
  • Cyanosis
  • Heart murmur
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16
Q

Clinical findings in innocent murmurs in children

A
  • Asymptomatic
  • No thrills or heaves
  • Normal heart sounds, normally split with no added clicks
  • Quiet and soft
  • Systolic (isolated diastolic murmurs are never innocent)
  • Short, ejection (pansystolic murmurs are pathological)
  • Single site with no radiation to neck, lung fields or back
  • Varies with posture (decreases or disappears when patient sits up, loudest when
    they’re lying)
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17
Q

Causes of a funny turn

A
  • Epileptic seizure: Aura, incontinence, tongue biting, family history
  • Cardiac arrhythmia: Palpitations, sudden collapse, exercise-related
  • Neurally mediated syncope: Preceding stimulus, dizziness, nausea
  • Panic attack: Hyperventilation, paraesthesia, carpopedal spasm
  • Breath-holding attack: Usually a toddler, upset/crying
  • Reflex anoxic seizure: Usually infant/toddler, painful stimulus
  • Pseudoseizures: Psychological problems

Other causes
- Hypoglycaemia
- Other metabolic derangements
- Drugs, alcohol

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18
Q

biochemical criteria for diagnosis of DKA

A
  • Serum glucose >11 mmol/L
  • Venous pH <7.3 or Bicarbonate <15 mmol/L
  • Presence of ketonaemia/ketonuria
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19
Q

Differentials of familial tall stature

A
  • Marfan
  • Klinefelter (47, XXY) syndrome,
  • Endocrine cause is e.g. sexual precocity, thyrotoxicosis or growth hormone excess
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20
Q

Clinical signs suggesting a pathological cause for short stature

A
  • Extreme short stature – on or below 0.4th centile.
  • Short for family size – outside target range for parents
  • Short and relatively overweight – suggests an endocrinopathy
  • Short and very underweight – suggests poor nutrition malabsorption
  • Growth failure – crossing the centiles downwards
  • Dysmorphic features
  • Skeletal disproportion – charts available for ratio between sitting height
    and leg length. Significant disproportion suggests a skeletal dysplasia, e.g.
    achondroplasia
  • Signs of systemic disease, e.g. clubbing
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21
Q

Surgical operation for pyloric stenosis

A

Ramstedt’s pyloromyotomy.

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22
Q

Causes of rectal bleeding

A
  • Gastroenteritis
  • Anal fissure
  • Intussusception
  • Cow’s milk protein allergy
  • Meckel’s diverticulum
  • Inflammatory bowel disease
  • Polyp
  • Clotting abnormality
  • Sexual abuse
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23
Q

Causes of chronic diarrhoea (14 days)

A

Infection
* Bacterial (Salmonella, Campylobacter)
* Protozoal (e.g. Giardia)
* Post-gastroenteritis diarrhoea

Malabsorption
* Lactose intolerance
* Cow’s milk protein intolerance
* Cystic fibrosis
* Coeliac disease

Gastrointestinal disorders
* Crohn’s disease
* Ulcerative colitis

Miscellaneous
* Toddler’s diarrhoea/irritable bowel syndrome
* Drugs (e.g. laxatives, antibiotics, chemotherapy)
* Immunodeficiency

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24
Q

Indications for surgery in Crohns Disease

A

Surgery is considered when medical therapy fails.

Indications include:
- intractabledisease with growth failure,
- obstruction (due to strictures or adhesions), abscess drainage,
- fistula,
- intractable haemorrhage and
- perforation.

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25
Q

Signs of dehydration in children

A
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26
Q

Fluid requirement in a child

A

Fluid requirement for 24 hours = maintenance x correction of deficit x replacement of ongoing losses

Maintenance fluid = 100 mL/kg for first 10 kg body weight, 50 mL/kg for next 10 kg, 20 mL/kg thereafter

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27
Q

Causes of right lower quadrant pain

A
  • Appendicitis
  • Mesenteric adenitis
  • Urinary tract infection
  • Gastroenteritis
  • Crohn’s disease
  • Ovulation pain: ‘mittelschmerz’
  • Ovarian cyst/torsion
  • Ectopic pregnancy
  • Pelvic inflammatory disease
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28
Q

Clinical tests for appendicitis

A

McBurney’s sign involves tenderness with palpation of McBurney’s point, which is located at one-third of the distance from the anterior superior iliac spine to the umbilicus.

Rovsing’s sign is positive when palpation in the left lower quadrant (LLQ) causes referred pain in the RLQ

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29
Q

Differential diagnosis of chronic abdominal pain

A
  • Psychosomatic
  • Urinary tract infections
  • Constipation
  • Gastro-oesophageal reflux
  • Coeliac disease
  • Inflammatory bowel disease
  • Cow’s milk intolerance
  • Abnormal renal anatomy, e.g. pelviureteric junction obstruction
  • Abdominal migraine
  • Peptic ulcer
  • Sexual or other abuse
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30
Q

Causes of constipation

A
  • Dietary
  • Dehydration
  • Anal fissure/stenosis
  • Hirschsprung’s disease
  • Intestinal obstruction e.g. stricture post-necrotizing enterocolitis
  • Spinal cord lesion
  • Cystic fibrosis (meconium ileus equivalent)
  • Cow’s milk intolerance
  • Drugs, e.g. opiates, vincristine, lead poisoning
  • Hypothyroidism
  • Sexual abuse
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31
Q

Causes of failure to thrive

A

Inadequate intake of food
* Poor feeding
* Mechanical problem such as a cleft palate or bulbar palsy

Malabsorption
* Coeliac disease
* Cystic fibrosis

Excessive loss of nutrients
* Vomiting due to gastro-oesophageal reflux
* Protein-losing enteropathy, e.g. cow’s milk protein intolerance

Increased nutrient requirement
* Congestive cardiac failure
* Chronic infection, e.g. HIV

Miscellaneous causes
* Dysmorphic syndromes, e.g. Russell–Silver syndrome
* Inborn errors of metabolism

Psychosocial
* Child abuse and neglect
* Emotional and social deprivation

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32
Q

Causes of jaundice

A

Early onset (first 24 hours, haemolytic jaundice)
* Rhesus haemolytic disease
* ABO incompatibility
* G6PD deficiency (commonest in those of African, Asian, or Mediterranean
descent)
* Hereditary spherocytosis

Normal onset
* Physiological (all newborns get a degree of jaundice peaking at 4–5 days)
* Bruising
* Polycythaemia
* Causes of early jaundice

Late onset (14 days, prolonged jaundice)
* Persistence of a pathological earlier jaundice
* Breast milk jaundice
* Neonatal hepatitis
* Biliary atresia
* Hypothyroidism
* Galactosaemia

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33
Q

Differential diagnosis of abdominal pain and jaundice

A

Pre-hepatic
* Abdominal pain is an uncommon feature
* Possible causes: malaria, sickle cell crisis

Hepatic
* Often pale stools and dark urine will be present
* Acute hepatitis due to infection, drugs, toxins

Posthepatic
* Pale stools and dark urine
* Bile duct stones, cholecystitis, choledochal cyst
* Cholangitis must be considered in a febrile child

34
Q

Children at risk of inguinal hernia

A
  • Preterm infants – especially those with very low birth weight (30 per cent
    affected)
  • Boys – outnumber girls 6:1 because ovaries do not leave the abdominal cavity
  • Infants with chronic lung disease
  • Children with conditions associated with abnormal abdominal fluid or increased
    intra-abdominal pressure
  • Children with developmental urogenital anomalies
  • Infants with disorders of sexual differentiation – phenotypically female infants
    with inguinal hernias, especially bilateral, should be examined carefully to
    exclude complete androgen insensitivity syndrome, an extremely rare but
    crucial diagnosis
35
Q

Symptoms of a urinary tract infection

A
  • Infant – fever, vomiting, lethargy, irritability, poor feeding
  • Older child – frequency, dysuria, abdominal pain or loin pain, fever
36
Q

Investigations for red urine post infection

A

The following investigations should be performed:
* throat swab
* anti-streptolysin O titre (ASOT), C3 and C4 – ASOT is raised and C3 is reduced in post-streptococcal glomerulonephritis
* ESR and ANA – will be abnormal in vasculitides, e.g. SLE
* abdominal X-ray and renal US – will demonstrate normality of kidneys and help exclude calculi.

37
Q

Causes of haematuria

A
  • urinary tract infection
  • nephritis – post-streptococcal glomerulonephritis
    – Henoch–Schönlein purpura
    – IgA nephropathy
    – nephrotic syndrome (20 per cent have haematuria at presentation)
  • calculi
  • trauma
  • haematological – clotting disorders, haemolytic uraemic syndrome
  • anatomical causes – polycystic kidneys, hydronephrosis
  • tumours, e.g. Wilms’ tumour
  • drugs, e.g. cyclophosphamide, aspirin
  • factitious illness
  • recurrent benign haematuria (a diagnosis by elimination)
38
Q

Diagnosis of nephrotic syndrome

A

**Oedema: **typically periorbital, abdominal and lower limbs
Proteinuria: ≥ 3+ protein on urine dipstick, or a urine protein / creatinine ratio (uPCR) >200mg/mmol
Hypoalbuminemia: serum albumin <25g/l

39
Q

Investigations for nephrotic syndrome

A
  • Blood
    – cholesterol and triglyceride levels (elevated in nephrotic syndrome)
    – anti-streptolysin O titre (ASOT) and C3/C4 levels to investigate the possibility of
    post-streptococcal disease
    – antinuclear antibody (ANA), which may be positive in vasculitides such as SLE
    – hepatitis B antibodies if from an at-risk population, as this is a rare cause of nephrotic syndrome
    – measles and Varicella zoster antibodies (these are important to know as children who are on immunosuppressive therapy such as steroids are more vulnerable to these conditions)
    – blood culture if febrile
  • Urine – microscopy and culture, spot urine protein/creatinine ratio (will be 2 in nephrotic syndrome).
40
Q

Causes of nocturnal enurisis

A

Primary nocturnal enuresis indicates that he has never achieved dryness at night and three mechanisms may contribute to this:
- lack of arousal from sleep,
- bladder instability or
- low functional bladder capacity, and nocturnal polyuria due to low vasopressin levels.

Secondary enuresis indicates that he had previously achieved dryness at night for at least 6 months and something has happened to cause bedwetting again. Secondary causes include:
- constipation,
- urinary tract infection,
- diabetes mellitus or
- psychosocial stresses, such as bullying or a recent parental separation

41
Q

Management options for primary nocturnal enuresis

A
  • Self help measures – regular daytime fluid intake and voiding, avoid caffeinated drinks
  • Enuresis clinic support
  • Nocturnal polyuria – desmopressin (synthetic analogue of antidiuretic hormone)
  • Lack of arousal – enuresis alarm with star chart
  • Bladder instability – bladder retraining, anticholinergic medication
42
Q

Causes of hypertension in children (use the mnemonic – CREED)

A
  • Cardiological, e.g. coarctation of the aorta
  • Renal, e.g. glomerulonephritis, renal artery stenosis
  • Essential
  • Endocrine, e.g. thyrotoxicosis, Cushing’s disease, phaeochromocytoma
  • Drugs, e.g. steroids, contraceptive pill, amphetamines
43
Q

Clinical presentation of measles

A

Commencing with a catarrhal prodrome
phase of fever, conjunctivitis, cough and coryza, preceding development of the rash 3–5 days later. During the catarrhal phase, Koplik’s spots may be seen as small white spots on the buccal mucosa.

Although pathognomonic of measles, they can be very hard to find and have usually disappeared within 1 day of the rash starting.

The rash is maculopapular and starts around the hairline and behind the ears, spreading downwards across the body. It often becomes confluent on the upper body, resulting in a blotchy appearance.

Usually children with measles are very miserable.

44
Q

Differential diagnosis of measles

A
45
Q

Complications of measles

A
  • Pneumonia
  • Corneal ulceration
  • Suppurative otitis media
  • Gastroenteritis
  • Febrile convulsions
  • Encephalomyelitis (rare) and subacute sclerosing panencephalitis (very rare)
46
Q

Non-specific symptoms occuring in children with malaria

A
  • Fever
  • Diarrhoea
  • Vomiting
  • Cough
  • Tachypnoea
  • Headache
  • Lethargy
  • Coma
  • Jaundice
  • Haematuria
  • Myalgia
  • Pallor
47
Q

Diagnosis of Kawasaki Disease

A

Kawasaki’s disease is a vasculitis. This disorder occurs mainly in young children (80 per cent <5 years). It is diagnosed clinically.

Criteria for diagnosis are:
* The presence of a fever for 5 or more days and four of the following five features:
– non-purulent conjunctivitis
– cervical lymphadenopathy
– skin rash
– erythema of the oral and pharyngeal mucosa
– erythema and swelling of the hands and feet (followed a week later by skin
desquamation).

Accompanying features are a raised WCC, CRP and ESR. In the second week of the illness a thrombocytosis usually develops.

48
Q

Causes of a prolonged fever (apart from Kawasaki)

A
  • Infections, e.g. tuberculosis, HIV
  • Malignant diseases, e.g. lymphoma
  • Autoimmune diseases, e.g. juvenile idiopathic arthritis
  • Miscellaneous, e.g. drugs, inflammatory bowel disease
49
Q

Examples of factors predisposing to recurrent infections

A
50
Q

Causes of weight loss

A
  • Inadequate nutrition/neglect
  • Gastro-oesophageal reflux
  • Coeliac disease
  • Inflammatory bowel disease
  • Cystic fibrosis
  • Anorexia nervosa
  • Cardiac failure
  • Chronic renal failure
  • Diabetes mellitus
  • Malignancy
  • Infections, e.g. tuberculosis, HIV
51
Q

Common causes of an itchy rash in a child

A
  • eczema – very common, often involves face, elbow and knee flexures
  • seborrhoeic dermatitis – affects infants, often in association with cradle cap
  • scabies – itchy where mite has burrowed
  • insect bites – affects uncovered areas such as arms and legs
  • drug allergy
  • urticaria – idiopathic or secondary to allergens, consists of wheal (raised and white)
    and flare (red)
  • fungal infections – e.g. tinea capitis or tinea pedis (athlete’s foot)
  • chickenpox.
52
Q

Differential diagnosis of pancytopenia

A

Bone marrow failure
* Inherited – all rare. Commonest is Fanconi’s anaemia. Excess chromosome
breaks. Defective DNA repair, decreased cell survival and susceptible to oxidant
stress. Associated physical abnormalities, e.g. skeletal (absent thumbs), short
stature. Only cure is a BM transplant.
* Acquired
– viral, e.g. hepatitis, herpes, Epstein–Barr
– drugs – idiosyncratic, e.g. chloramphenicol, anticonvulsants, or predictable,
e.g. chemotherapy; 80 per cent are ‘idiopathic aplastic anaemia’.

Bone marrow infiltration
* Malignancy, e.g. leukaemia or neuroblastoma. Rarely myelofibrosis and
myelodysplasia.

53
Q

Investigation of pancytopenia

A
  • Blood film – detailed morphology of all cell lines
  • Red cell indices – the anaemia in AA is normocytic or mildly macrocytic
  • Reticulocytes – <20 x 10^9
    /L suggests severe aplastic anaemia
  • Viral titres – hepatitis, Epstein–Barr, parvovirus (usually causes red cell aplasia)
  • Chromosomes for breakage analysis
  • BM aspirate and trephine – to assess morphology and cellularity of the cells and to exclude infiltration. In AA it is hypocellular but the remaining cells are normal
54
Q

Causes of purpura in a child

A
  • Infections
  • Thrombocytopenia secondary to ITP, leukaemia or chemotherapy
  • Henoch–Schönlein purpura (HSP) and other vasculitides
  • Vomiting or coughing
  • Trauma
  • Clotting disorders
  • Drugs, e.g. steroids
55
Q

Complications of sickle cell disease in children

A
  • Painful crises, avascular necrosis of the hips and shoulders
  • Chest syndrome, abdominal syndrome, girdle syndrome
  • Splenic sequestration, aplastic anaemic crisis
  • Stroke, retinal vein occlusion
  • Priapism, haematuria, enuresis, chronic renal failure
  • Pigment gallstones, cholecystitis, biliary colic
  • Hyposplenism, sepsis, osteomyelitis
  • Delayed puberty
56
Q

Contributing factors to infection in children with cancer

A
  • Neutropenia – the more severe (0.5 109/L) and prolonged, the greater the risk.
    There may be loss of the inflammatory response, e.g. insufficient white blood cells
    to form an abscess
  • Mucositis – following radiotherapy or chemotherapy. Can affect the whole
    gastrointestinal tract. There is a risk that intestinal bacteria will breach the gut
    wall and enter the bloodstream
  • Indwelling central lines – crucial for giving chemotherapy and blood sampling,
    but significant source of infection, both blood-borne and at exit site
  • Frequent hospital admissions
  • Poor nutrition
  • Generalized immunosuppression, inhibiting the usual host defences – viruses that rarely cause severe illness in immunocompetent children can be lifethreatening in oncology patients, e.g. varicella, measles and cytomegalovirus.

Chemotherapy also predisposes children to ‘opportunistic infections’ – organisms that only infect an immunocompromised host. Prophylaxis against Pneumocystis carinii is included in protocols for cancers where the chemotherapy regimen is particularly immunosuppressive

57
Q

Poor prognostic factors in acute lymphoblastic leukaemia

A
  • Total white cell count >100 x 10^9 /L at presentation
  • Outside age range 2–10 years
  • Male sex
  • T-cell (15 per cent) or mature B-cell (1 per cent) origin (Common-ALL (85 per cent) from B-cell progenitors has best prognosis)
  • Certain chromosome abnormalities – hypodiploidy, presence of Philadelphia chromosome (Others, e.g. hyperdiploidy, confer a favourable prognosis)
  • CNS disease at presentation
  • Slow response to treatment, 5% blasts persisting on day 28 BM Overall prognosis for ALL is excellent with a 5-year survival 80 per cent.
58
Q

Causes of a limp in a child

A

* 0–3 years
– Trauma, e.g. fracture (may be accidental or non-accidental)
– Infection: septic arthritis, osteomyelitis or discitis
– Malignancy
– Developmental dysplasia of the hip
– Neuromuscular disease, e.g. cerebral palsy

* 4–10 years
– Trauma
– Transient synovitis (irritable hip)
– Infection – septic arthritis, osteomyelitis or discitis
– Perthe’s disease
– Juvenile idiopathic arthritis
– Malignancy, e.g. leukaemia
– Neuromuscular disease, e.g. cerebral palsy

* 10–18 years
– Trauma
– Infection: septic arthritis, osteomyelitis or discitis
– Slipped upper femoral epiphysis
– Juvenile idiopathic arthritis
– Malignancy, e.g. osteogenic sarcoma

59
Q

Imaging for osteomyelitis

A
  • Plain X-rays – excludes trauma. In osteomyelitis, bones are unlikely to be abnormal until 10–14 days after onset. In arthritis they are often normal but may show widening of joint space +/- local soft tissue or fat changes
  • Ultrasound (US) – highly sensitive in detecting joint effusion and guiding aspiration. It may demonstrate swelling and distortion of soft tissues and subperiosteal region
  • MRI – the best technique to differentiate between soft tissue and bone infection; also to detect a joint effusion where US is normal. However, the boy will need sedation or general anaesthetic at this age
  • Technetium (99mTc) bone scan – accumulates as ‘hot spots’ in areas of increased bone turnover so useful in osteomyelitis, especially multifocal. Infection close
    to growth plates can limit specificity
60
Q

Differential diagnosis of chronic polyarthritis

A
  • Connective tissue disorder – juvenile idiopathic arthritis (JIA), systemic lupus erythematosus, dermatomyositis, psoriatic arthritis
  • Infection – bacterial causes are unlikely with this chronic history. Viruses such as hepatitis and also Lyme disease should be excluded
  • Malignant disorders – children with leukaemia can have joint pain due to metaphyseal marrow expansion months before peripheral blood count changes. A bone marrow examination may be indicated
  • Inflammatory bowel disease – can present with arthritis
  • Vasculitis – Henoch–Schönlein purpura
61
Q

Relative contraindications to a lumbar puncture

A
  • Prolonged or focal seizure
  • Focal neurological signs
  • A widespread purpuric rash
  • A Glasgow Coma Scale score 13
  • Abnormal posture or movement e.g. decerebrate posture
  • An inappropriately low pulse, raised blood pressure and irregular breathing (suggesting impending brain herniation)
  • Thrombocytopenia or clotting disorder
  • Pupillary dilatation
  • Papilloedema
  • Hypertension
62
Q

Causes of macrocephaly

A
63
Q

Differential diagnosis of coma in children

A
  • Hypoxic-ischaemic brain injury, e.g. following a respiratory arrest
  • Epileptic seizure/postictal state
  • Trauma, e.g. intracranial haemorrhage, cerebral oedema
  • Infections, e.g. meningitis, encephalitis, abscess
  • Metabolic – renal and hepatic failure, hypoglycaemia, diabetic ketoacidosis, inborn errors
  • Poisoning
  • Vascular lesions, e.g. stroke
64
Q

AVPU scoring

A

The AVPU score is a score used for the rapid assessment of the conscious level of a child (especially 5 years of age).
A = Alert,
V= responds to Voice,
P= responds only to Pain,
U= Unresponsive to all stimuli.

**P or less corresponds to a GCS of 8 or less.

65
Q

Examples of causes of learning difficulties

A

Congenital causes
* Chromosome disorder
* Fragile X syndrome
* Duchenne muscular dystrophy
* Congenital infection
* Fetal alcohol syndrome

Acquired causes
* Traumatic brain injury
* Meningitis
* Psychosocial deprivation

66
Q

Causes of acute stroke in childhood

A
  • Haematological abnormalities – SCD, polycythaemia, leukaemia, disorders of coagulation
  • Cardiac disease – congenital, especially cyanotic and acquired, e.g. endocarditis or Kawasaki disease. Usually embolic
  • Infection – meningitis, local head and neck infections or bacteraemia
  • Intracerebral vascular pathology – ruptured aneurysm, arteriovenous malformation
  • Autoimmune disease – systemic lupus erythematosus, juvenile idiopathic arthritis, sarcoidosis
  • Metabolic disease – homocystinuria, mitochondrial disorders
  • Trauma
67
Q

Differential diagnosis of chronic headaches

A
  • Tension headaches – commonest of all, described as a ‘band’ or ‘pressure’ and bilateral. Usually otherwise asymptomatic. May last weeks and tend to worsen
    as day progresses. Child is otherwise healthy
  • Sinusitis – percussing over affected sinuses causes pain and discomfort
  • Refractive errors – ensure vision has been checked recently
  • Raised intracranial pressure – a brain tumour is most parents’ underlying worry. Unlike migraine and tension headaches, pain is worse when lying down. It is almost always accompanied by other abnormal symptoms, e.g. change in
    behaviour, or neurological signs, e.g. papilloedema
  • Solvent or drug abuse
  • Hypertension – blood pressure must be checked
68
Q

Differential diagnosis of back pain in children

A
  • Developmental abnormalities – spondylolysis (defect in pars interarticularis), spondylolisthesis (spondylolysis with anterior slippage of affected vertebra), scoliosis
  • Traumatic – vertebral stress fractures, muscle spasm due to overuse, e.g. in athletes and gymnasts, prolapsed intervertebral disc
  • Neoplastic – primary benign or malignant vertebral or spinal cord tumours, leukaemias or lymphomas, metastases, e.g. neuroblastoma
  • Infection – discitis (common before 6 years), vertebral osteomyelitis
  • Rheumatological – pauciarticular juvenile rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis
69
Q

Causes of developmental regression

A
70
Q

Features of conductive and sensorineural hearing loss

A
71
Q

Features of anorexia nervosa and bulimia nervosa

A
72
Q

Physical complications of anorexia nervosa

A
  • Cardiovascular – bradycardia, hypotension, conduction abnormalities
  • Neurological – cognitive impairment, poor concentration
  • Renal – fluid and electrolyte abnormalities, pre-renal failure
  • Endocrine – amenorrhoea, delayed/arrested puberty, osteoporosis
  • Gastrointestinal – abnormal motility and absorption, damage from purgatives
  • Haematological – anaemia, thrombocytopenia, leucopenia
  • Skin – dry skin, lanugo hair, brittle nails
73
Q

Complications of premature birth

A
  • Respiratory – RDS, pneumothorax, apnoea, chronic lung disease
  • Cardiovascular – patent ductus arteriosus
  • Neurological – periventricular haemorrhage, periventricular leucomalacia
  • Gastrointestinal – necrotizing enterocolitis, gastro-oesophageal reflux
  • Infection – group B Streptococcus, nosocomial infection
  • Metabolic – hypoglycaemia, jaundice, rickets
  • Iatrogenic – extravasation injury, pressure sores
74
Q

Causes of unexpected respiratory distress in the term newborn

A
  • Transient tachypnoea of the newborn
  • Pneumothorax
  • Congenital pneumonia, sepsis
  • Lung malformations, congenital diaphragmatic hernia
  • Oesophageal atresia, tracheo-oesophageal fistula
  • Choanal atresia, other upper airway malformations
  • Congenital heart disease
  • Anaemia, polycythaemia
  • Cerebral haemorrhage
75
Q

Causes of apnoea in a newborn

A
  • Apnoea of prematurity
  • Lung disease, e.g. respiratory distress syndrome
  • Congenital heart disease
  • Sepsis
  • Hypoglycaemia
  • Hypothermia
  • Sedative drugs (administered to mother in labour, or to baby)
  • Neurological insults – cerebral haemorrhage, oedema or seizures
  • Anaemia
  • Gastro-oesophageal reflux
76
Q

Causes of a sudden desaturation in a ventilated neonate

A
  • no chest movement
    – ventilator not working or tubing disconnected or kinked
    – endotracheal tube blocked or dislocated
  • chest movement decreased or asymmetrical
    – pneumothorax
    – worsening respiratory disease
  • chest movement normal
    – right-to-left shunt, e.g. across a patent ductus arteriosus
    – large periventricular haemorrhage
    – severe sepsis
77
Q

Causes of jaundice

A

Early onset (first 24 hours, haemolytic jaundice)
* Rhesus haemolytic disease
* ABO incompatibility
* G6PD deficiency (commonest in those of African, Asian, or Mediterranean descent)
* Hereditary spherocytosis

Normal onset
* Physiological (all newborns get a degree of jaundice peaking at 4–5 days)
* Bruising
* Polycythaemia
* Causes of early jaundice

Late onset (14 days, prolonged jaundice)
* Persistence of a pathological earlier jaundice
* Breast milk jaundice
* Neonatal hepatitis
* Biliary atresia
* Hypothyroidism
* Galactosaemia

78
Q

Causes of a floppy infant

A
79
Q

Complications of birth asphyxia

A
80
Q

Causes of congenital malformations

A
  • Genetic
    – chromosomal abnormalities, e.g. 22q11 deletion (DiGeorge syndrome)
    – gene defects, e.g. CHD7 (chromodomain helicase DNA-binding protein 7
    mutations causing CHARGE syndrome)
  • Environmental
    – maternal factors, e.g. diabetes (cardiac malformations)
    – prescribed drugs, e.g. phenytoin (fetal hydantoin syndrome)
    – recreational drugs, e.g. alcohol (fetal alcohol syndrome)
    – environmental toxins, e.g. dioxins (central nervous system anomalies)
    – infections (e.g. rubella, cytomegalovirus)
  • Sporadic
81
Q

Characteristic dysmorphic features of trisomy 21

A
  • Hypotonia
  • Flat face
  • Upward slanting palpebral fissures
  • Epicanthic folds
  • White speckles in the iris (Brushfield spots)
  • Short broad hands
  • Single palmar and plantar fissures (Simian crease)

There are several associated features, the commonest of which are low IQ (average IQ about 50), congenital heart disease, duodenal atresia and short stature.

82
Q

Causes of hypocalcaemia in infancy

A
  • Prematurity
  • Hypoxic ischaemic encephalopathy (HIE)
  • Hypoparathyroidism – transient (associated with prematurity, HIE or maternal diabetes) or permanent
  • Hypomagnesaemia – magnesium facilitates release of parathormone (PTH)
  • Exchange transfusion – citrate in transfused blood chelates calcium to prevent clotting
  • Familial activating mutations of the calcium-sensing receptor – the calcium level at which PTH is released is lower than normal; some cases labelled as ‘familial hypoparathyroidism’ are probably this disorder
  • Maternal hypercalcaemia – suppresses fetal PTH
  • Maternal vitamin D deficiency
  • In older children, vitamin D deficiency is the commonest cause, but the ALP would be high due to the increased bone turnover in rickets