AMC MCQ (CAT) paediatrics questions

Newborns have physiologically low levels of vitamin K-dependent clotting factors (II, VII, IX, X) because of poor placental transfer of vitamin K, immature hepatic synthesis, and sterile gut flora that normally contribute to vitamin K production. Without supplementation, this predisposes to vitamin K deficiency bleeding (haemorrhagic disease of the newborn), which can present early, classically, or late with intracranial haemorrhage. The Australian Immunisation Handbook and RACGP Red Book recommend intramuscular vitamin K (phytomenadione) 1 mg at birth for all infants to prevent this. Oral regimens exist but are less effective and require strict adherence to multiple doses.

• B. Kernicterus results from severe unconjugated hyperbilirubinaemia, not clotting factor deficiency.
• C. Haemolytic disease of the newborn is due to Rh or ABO incompatibility, unrelated to vitamin K status.
• D. Intraventricular haemorrhage relates to prematurity and fragile germinal matrix vessels, not vitamin K deficiency.
• E. Vitamin K has no role in preventing bacterial or viral neonatal infection.

This preterm infant has classic features of necrotising enterocolitis (NEC): feeding intolerance, bilious aspirates, bloody stools, abdominal distension with discoloured abdominal wall, and systemic instability with temperature instability and apnoea. The hallmark radiographic finding in NEC is pneumatosis intestinalis, gas within the bowel wall from bacterial fermentation and mucosal injury, sometimes progressing to portal venous gas, which indicates more severe disease. Pneumoperitoneum on a lateral decubitus or cross-table film indicates perforation and surgical emergency. Early recognition and staging (modified Bell's criteria) guide management, including bowel rest, nasogastric decompression and broad-spectrum antibiotics.

• A. Double bubble sign is characteristic of duodenal atresia, often associated with Down syndrome.
• B. Diffuse bowel wall thickening with absent gas is non-specific and not the classic diagnostic sign of NEC.
• D. Ground-glass appearance with air bronchograms describes neonatal respiratory distress syndrome on chest X-ray.
• E. The 'coffee bean' sign describes a sigmoid volvulus, not NEC.

Failure to sit independently by 9 months is a gross motor red flag requiring assessment. The combination of increased lower limb tone, brisk reflexes, scissoring on vertical suspension and clenched fists is characteristic of spastic cerebral palsy, which results from a non-progressive injury to the developing brain, often related to prematurity, hypoxic-ischaemic injury or antenatal factors. The diagnosis is clinical, supported by the pattern of motor delay with increased tone, and MRI brain can help identify the underlying lesion and timing of injury. Early referral for multidisciplinary therapy improves functional outcomes.

• A. Global developmental delay is a broader descriptive term and does not explain the specific findings of spasticity and hyperreflexia seen here.
• B. Spinal muscular atrophy type 1 causes profound hypotonia and areflexia ('floppy baby'), the opposite of this presentation.
• C. Duchenne muscular dystrophy causes progressive proximal weakness with hypotonia, not spasticity, and usually presents later with gait difficulty.
• E. Developmental dysplasia of the hip causes asymmetric hip abduction or leg length discrepancy, not generalised spasticity and hyperreflexia.

Non-organic (psychosocial) failure to thrive is suggested by a normal physical examination, age-appropriate development, and a feeding and social history revealing inconsistent caregiving and inadequate intake, rather than any underlying medical illness. The mechanism is inadequate caloric intake arising from disrupted feeding routines, caregiver stress or inconsistent care rather than a disease process impairing absorption, metabolism or increasing demand. Organic causes are suggested by associated symptoms such as chronic diarrhoea, dysmorphism, developmental delay or systemic findings, none of which are present here. Management involves a multidisciplinary approach addressing feeding support, parental mental health and social supports, with medical causes excluded if the history or examination suggests them.

• A. Congenital hypothyroidism would usually present with other features such as constipation, lethargy, hypotonia and coarse features, and is typically detected on newborn screening.
• C. Coeliac disease typically presents with chronic diarrhoea, abdominal distension and irritability, not seen in this well-appearing infant.
• D. Chronic renal failure would be expected to cause systemic illness, oedema or abnormal urine output, not an isolated feeding and social history.
• E. Cyanotic congenital heart disease would present with cyanosis, tachypnoea, poor feeding tolerance and often a murmur, none of which are described.

A sustained downward crossing of two or more major percentile lines on a growth chart, especially with weight falling relative to a stable length, suggests growth faltering and should prompt a careful assessment of feeding adequacy, including breastfeeding technique, frequency and effectiveness, as well as exclusion of underlying medical causes. While some crossing of percentiles can be a normal regression to the infant's genetic growth trajectory, the degree and direction of this crossing combined with disproportion between weight and length trends warrants active follow-up rather than reassurance. The RACGP Red Book recommends serial growth monitoring and timely assessment when a faltering pattern is identified, as early intervention improves outcomes. A single data point is less informative than the trend over time, which is why serial plotting on growth charts is essential.

• A. A significant drop across major percentile lines should not be dismissed as normal without assessment.
• B. Catch-down growth usually occurs in early infancy and stabilises, whereas a progressive fall with preserved length growth suggests inadequate intake rather than benign constitutional adjustment.
• C. Measurement error is possible but should not be assumed without re-measurement; the consistent trend across multiple visits makes error less likely.
• D. Chromosomal disorders are not diagnosed from growth chart patterns alone and would require clinical features and specific testing.

Lack of joint attention behaviours, such as pointing to show interest and following another person's gaze, together with reduced response to name, are core early red flags for autism spectrum disorder at 18 months. Combined with repetitive behaviours such as lining up toys and marked distress with routine changes, this pattern should prompt referral for formal developmental and autism-specific assessment. Early identification allows timely access to early intervention services, which is associated with better developmental outcomes. Walking at 13 months is within the normal range and not a red flag, and solitary play or separation anxiety at this age can be entirely typical.

• A. Walking at 13 months is within normal limits (up to 18 months) and not itself concerning for autism.
• B. Isolated mild expressive delay with normal receptive language and social communication is more typical of a speech-specific delay than autism.
• C. Separation distress at 18 months is a normal developmental stage and not an autism red flag.
• D. Solitary play is common and developmentally appropriate at 18 months and not specific to autism.

The diagnosis of ADHD requires a comprehensive assessment confirming symptoms of inattention, hyperactivity or impulsivity that are present in multiple settings, persistent for at least six months, developmentally inappropriate for age, and causing functional impairment, as outlined in DSM-5 criteria. In Australia, diagnosis and initiation of stimulant medication require assessment by a paediatrician or psychiatrist experienced in ADHD, as per state-based regulations and Therapeutic Guidelines; general practitioners typically manage ongoing care under a shared care arrangement rather than initiating diagnosis or treatment. This child's symptoms span school and home settings over 10 months with functional impact, meeting threshold criteria for specialist referral rather than reassurance. EEG and dietary elimination are not supported as diagnostic or first-line management strategies for ADHD.

• A. Stimulant medication initiation in Australia requires specialist assessment and in most states authorisation, and diagnosis should not be made solely in general practice without comprehensive evaluation.
• B. The persistence, cross-setting nature and functional impairment described exceed normal developmental variation and warrant assessment rather than reassurance.
• C. EEG is not a diagnostic test for ADHD and is not part of standard assessment criteria.
• D. Dietary elimination diets lack strong evidence as first-line management and are not recommended before specialist assessment and evidence-based management.

The Australian Immunisation Handbook provides a catch-up calculator and schedule specifically designed for children and adults who have missed or never received vaccinations, taking into account age, number of doses needed and minimum intervals between doses. This allows safe and efficient catch-up without unnecessary serological testing or specialist referral in routine cases. Live vaccines such as MMR and varicella can usually be co-administered on the same day if not contraindicated. General practitioners can manage most catch-up immunisation without specialist input unless there are complicating medical conditions.

• A. Skipping earlier missed doses would leave him inadequately protected against diseases he has never been immunised against.
• B. Specialist referral is not required for routine catch-up immunisation in an otherwise healthy child.
• C. Routine serological testing before catch-up vaccination is not recommended and would unnecessarily delay protection.
• E. The adult schedule does not provide the same antigens or timing appropriate for a young child and is not the correct catch-up pathway.

MMR is a live attenuated vaccine and is contraindicated in children with significant immunosuppression, including those receiving chemotherapy for malignancy, due to the risk of disseminated vaccine-strain infection. Live vaccines should be deferred until immune function has recovered, generally at least three to six months after completion of chemotherapy, as guided by the treating haematologist/oncologist. Household contacts should still be vaccinated to provide indirect protection. Giving a double dose does not mitigate the risk and is not a recognised strategy. Influenza vaccine (inactivated) is appropriate for this child but is not a substitute for MMR, which protects against different diseases.

• A. Doubling the dose of a live vaccine does not reduce the risk of disseminated infection and is not recommended.
• B. Giving a live vaccine during significant immunosuppression risks disseminated vaccine-strain disease.
• C. Varicella-zoster immunoglobulin is used for post-exposure prophylaxis against varicella, not as a safeguard allowing live MMR vaccination during immunosuppression.
• D. Influenza vaccine protects against a different disease and does not substitute for the measles, mumps and rubella components of MMR.

Anaphylaxis is a medical emergency, and intramuscular adrenaline is the first-line treatment, given promptly at a dose of 0.01 mg/kg of 1:1000 (10 mg/mL) solution, with a maximum single dose of 0.5 mg, injected into the anterolateral thigh because this site has reliable absorption and large muscle bulk. Delaying adrenaline in favour of antihistamines or corticosteroids increases the risk of progression to cardiovascular collapse and death. The anterolateral thigh is preferred over the deltoid because the thigh muscle mass allows more consistent absorption, particularly in children. Oxygen, calling for emergency assistance and placing the child supine with legs elevated (or left lateral if vomiting) are also required, but these do not replace adrenaline as the immediate priority.

• A. The deltoid muscle has less reliable absorption than the anterolateral thigh, especially in children, and is not the preferred site.
• B. Salbutamol may help bronchospasm but does not address the systemic features of anaphylaxis and is not a substitute for adrenaline.
• C. Antihistamines do not treat the life-threatening airway, breathing or circulatory compromise of anaphylaxis and must not delay adrenaline.
• E. Corticosteroids have a delayed onset of action and are not first-line treatment for acute anaphylaxis.

This child has mild croup, characterised by a barking cough, hoarse voice and stridor only at rest or with agitation, without chest wall retraction or significant respiratory distress. A single dose of oral dexamethasone 0.15 mg/kg reduces symptom severity, the need for further medical review and hospitalisation, and is recommended for all children with croup regardless of severity. Nebulised adrenaline is reserved for moderate to severe croup with stridor at rest accompanied by retractions or agitation, which this child does not have. Croup is a viral illness, so antibiotics are not indicated, and admission is unnecessary for mild croup that improves after corticosteroid treatment and a period of observation.

• A. Nebulised adrenaline is reserved for moderate to severe croup with respiratory distress, not mild croup.
• C. Oral dexamethasone, not nebulised budesonide, is the preferred first-line corticosteroid for croup in Australian guidelines; nebulised budesonide is an alternative only if oral therapy is not tolerated.
• D. Admission is not required for mild croup when the child is stable and can be safely discharged after treatment.
• E. Croup is caused by a virus, so antibiotics have no role in management.

This infant has bronchiolitis, a clinical diagnosis based on coryzal prodrome followed by cough, tachypnoea, chest recession and widespread crackles and wheeze, typically affecting infants under 12 months. Indications for admission include hypoxaemia (oxygen saturation below 92–94% depending on local guideline), moderate to severe respiratory distress, and inadequate oral intake, all present in this infant. Bronchodilators, corticosteroids and antibiotics have no proven benefit in bronchiolitis, as the disease is viral and the pathophysiology involves mucosal oedema and mucus plugging rather than bronchospasm or bacterial infection responsive to these agents. Chest X-ray is not routinely required and may lead to unnecessary antibiotic use if atelectasis is misinterpreted as consolidation.

• A. Bronchiolitis is a viral illness, so antibiotics are not indicated in the absence of evidence of bacterial co-infection.
• B. Corticosteroids have not been shown to improve outcomes in bronchiolitis and are not recommended.
• D. Chest X-ray is not routinely indicated in typical bronchiolitis and can lead to inappropriate antibiotic use.
• E. Bronchodilators such as salbutamol have no proven benefit in bronchiolitis and should not be used to guide discharge decisions.

This child's presentation, normal mental state, ability to speak in full sentences, mild recession, oxygen saturation above 94%, and heart rate and respiratory rate only mildly elevated for age, is consistent with a mild to moderate asthma exacerbation according to Australian paediatric asthma severity criteria. Severe exacerbations feature marked respiratory distress, inability to complete sentences, oxygen saturation below 92% and marked tachycardia, while life-threatening features include silent chest, cyanosis, exhaustion or confusion. Classification guides initial treatment intensity, including choice between intermittent and continuous bronchodilators and the need for systemic corticosteroids and escalation of care. This child does not show any features of severe or life-threatening asthma, and the clinical findings clearly support an exacerbation rather than an alternative diagnosis.

• B. Life-threatening features such as silent chest, cyanosis or exhaustion are absent in this child.
• C. There is no indication for intubation in a child who is alert, speaking normally and maintaining adequate oxygen saturation.
• D. Severe exacerbations require marked distress, inability to speak in sentences, or oxygen saturation below 92%, none of which are present here.
• E. Wheeze, recession and tachypnoea in a known asthmatic are classic features of an asthma exacerbation, so this option is incorrect.

This child has symptoms more than once a week but not daily, with occasional nocturnal symptoms, consistent with mild persistent asthma that is not adequately controlled on reliever alone. Australian guidelines recommend stepping up to a regular low-dose inhaled corticosteroid preventer at this level of symptom frequency. Low-dose ICS reduces airway inflammation, decreases exacerbation frequency and improves symptom control with a favourable safety profile at this dose in children. Long-acting beta-agonists must never be used as monotherapy due to the risk of masking worsening inflammation and increased mortality risk. High-dose combination therapy is reserved for more severe or uncontrolled disease, not as an initial step.

• A. LABA monotherapy is contraindicated in asthma due to increased risk of severe exacerbations and death
• B. High-dose ICS/LABA is excessive for this symptom frequency and skips appropriate stepwise therapy
• C. Montelukast is a less effective second-line preventer and is not first-line over inhaled corticosteroid
• E. His symptom frequency exceeds the threshold for reliever-only management and warrants a preventer

This child has the classic features of epiglottitis: abrupt onset, high fever, drooling, muffled voice, absence of cough, and toxic appearance, in an unimmunised child at risk of Haemophilus influenzae type b infection. The priority is to avoid agitating the child or examining the oropharynx, as this can precipitate complete airway obstruction. The safest approach is urgent transfer to a controlled setting (operating theatre) with anaesthetics and ENT present for airway management, usually with inhalational induction and intubation. Croup, by contrast, typically has a barking cough and preceding coryza and is treated with corticosteroids and nebulised adrenaline for severe cases, not epiglottitis.

• A. Oral antibiotics and outpatient review are inappropriate given the risk of sudden airway obstruction
• B. Examining the throat or attempting laryngoscopy outside a controlled airway setting can precipitate complete obstruction and is contraindicated
• D. This is the appropriate treatment for croup, not epiglottitis, and discharge would be unsafe in a toxic child
• E. Imaging delays definitive airway management and is unnecessary when the clinical picture is classic; it also risks deterioration during transport

Pertussis is a notifiable disease in Australia, and confirmed cases must be reported to the public health unit to allow contact tracing and prophylaxis of close contacts, particularly unvaccinated infants. Macrolides such as azithromycin are the first-line treatment for pertussis in infants, as they reduce infectivity and may shorten the clinical course if given early, despite often being started after the catarrhal phase. Infants under 6 months are at highest risk of severe disease and complications, including apnoea and encephalopathy, so antibiotics should be given promptly rather than withheld. Amoxicillin and ceftriaxone are not effective against Bordetella pertussis.

• A. A single vaccine dose given only yesterday provides no protection, and the diagnosis is already confirmed, requiring treatment and notification
• B. Antibiotics should be started as soon as pertussis is confirmed, not delayed, to reduce transmission and potentially limit severity
• D. Amoxicillin is not active against Bordetella pertussis and is not the recommended antibiotic for pertussis
• E. Ceftriaxone is not indicated for pertussis unless there is a secondary bacterial complication; prolonged isolation until full cough resolution is not required once antibiotics have been given

This presentation, fever, cough, conjunctivitis, coryza, Koplik spots, and a cephalocaudal spreading maculopapular rash in an unvaccinated child with travel history, is classic for measles. Measles is a notifiable disease in Australia, and clinical or laboratory-suspected cases require urgent notification to enable contact tracing and protection of susceptible contacts, including immunoglobulin or vaccine for exposed individuals as appropriate. Infectivity extends from about 4 days before to 4 days after rash onset, so isolation remains necessary even after the rash appears. Aciclovir has no role in measles, which is not caused by a herpesvirus, and vaccination after the child is already symptomatic does not prevent disease in this case.

• B. Isolation is still required for several days after rash onset because the child remains infectious
• C. Vaccinating this child now will not alter his current measles infection, as he is already symptomatic
• D. Aciclovir is an antiviral for herpesviruses and has no role in measles treatment
• E. The diagnosis is clinical based on the classic triad and rash pattern; biopsy is unnecessary and would delay public health action

The combination of oral vesicles/ulcers with vesicles distributed specifically on the palms and soles, in a mildly unwell child, is characteristic of hand, foot and mouth disease, most commonly caused by coxsackievirus A16 or enterovirus 71. Chickenpox typically produces a generalised, centrally distributed vesicular rash in crops at different stages, involving the trunk, scalp and face, which is absent here. Herpes gingivostomatitis causes painful oral vesicles and ulcers but does not characteristically involve the palms and soles. Scarlet fever presents with a sandpaper-textured erythematous rash and strawberry tongue, not vesicles, and impetigo produces honey-coloured crusted lesions rather than vesicles on the palms and soles.

• A. Chickenpox causes a generalised vesicular rash involving the trunk and face, not a palm-and-sole-predominant distribution
• B. Herpes gingivostomatitis affects the mouth but does not typically cause vesicles on the palms and soles
• C. Scarlet fever presents with a diffuse erythematous sandpaper rash and strawberry tongue, not oral or acral vesicles
• D. Impetigo produces honey-coloured crusted skin lesions, not vesicles affecting the oral mucosa and acral surfaces

A pregnant woman with significant exposure to parvovirus B19 and uncertain immune status should have serology performed to determine whether she is susceptible, acutely infected, or immune. IgG without IgM suggests past immunity, IgM positivity suggests recent infection requiring fetal monitoring, and seronegativity requires repeat testing and surveillance given the incubation period. If infection is confirmed, serial ultrasound monitoring for fetal anaemia and hydrops is required, but fetal blood sampling is only indicated if ultrasound shows signs of fetal compromise, not as an immediate first step. There is no effective immunoglobulin prophylaxis for parvovirus B19, and it is not associated with structural fetal malformation, so termination is not indicated.

• B. Exposure in a non-immune pregnant woman requires serological assessment, as parvovirus B19 infection in pregnancy can cause fetal anaemia and hydrops
• C. Fetal blood sampling is invasive and reserved for cases with ultrasound evidence of fetal anaemia or hydrops, not as an initial step
• D. Parvovirus B19 is associated with fetal anaemia and hydrops, not structural malformation, and does not warrant termination
• E. No effective immunoglobulin prophylaxis exists for parvovirus B19 in pregnancy

This child meets criteria for classic Kawasaki disease: fever for more than 5 days plus at least four of five principal features (conjunctival injection, oral changes, rash, extremity changes, cervical lymphadenopathy), of which he has four. The priority is to prevent coronary artery aneurysms, so intravenous immunoglobulin and high-dose aspirin should be started promptly, ideally within 10 days of fever onset, alongside a baseline echocardiogram. Echocardiography is repeated at 1-2 weeks and 6-8 weeks to monitor for coronary artery abnormalities. Delaying treatment increases the risk of coronary artery aneurysm formation.

• A. Lymph node biopsy is not part of the diagnostic pathway and would unnecessarily delay definitive treatment.
• B. Antibiotics are not indicated as this is not a bacterial infection and delay would risk coronary complications.
• C. Corticosteroid monotherapy is not first-line therapy; IVIG with aspirin is the standard initial treatment.
• D. Treatment should not be delayed for culture results; Kawasaki disease is a clinical diagnosis and early treatment reduces coronary artery risk.

This presentation with fever, non-blanching purpuric rash and signs of shock is highly suggestive of meningococcal septicaemia, a medical emergency with rapid progression and high mortality. Parenteral benzylpenicillin (or ceftriaxone if available) should be given immediately in the primary care or pre-hospital setting without waiting for investigations, followed by urgent transfer to hospital. Delaying antibiotics to perform lumbar puncture or await culture results significantly increases mortality risk. Fluid resuscitation and haemodynamic support should also be arranged during transfer.

• A. Oral antibiotics are inadequate for suspected meningococcal septicaemia; parenteral therapy must be given immediately.
• B. Lumbar puncture is contraindicated in a shocked, unstable child and would dangerously delay life-saving antibiotics.
• C. Dexamethasone is not a substitute for antibiotics in this emergency and is not indicated in the pre-hospital setting.
• E. Antibiotics must never be delayed for culture confirmation in suspected meningococcal disease due to rapid clinical deterioration.

Any infant under 3 months of age with a documented fever of 38°C or higher is considered at significant risk of serious bacterial infection, including sepsis, meningitis and urinary tract infection, regardless of how well they appear clinically. Current guidelines mandate a full septic work-up (blood culture, urine culture, and lumbar puncture unless contraindicated) with admission for empirical intravenous antibiotics while awaiting results. Clinical appearance is unreliable for excluding serious bacterial infection in this age group because neonates can decompensate rapidly. This cautious approach has been shown to reduce morbidity and mortality from missed serious infections.

• A. Oral antibiotics without a full work-up are inappropriate; infants under 3 months require admission and parenteral treatment while awaiting investigation results.
• B. Discharge without investigation is unsafe in this age group; clinical wellness does not exclude serious bacterial infection in young infants.
• C. A urine dipstick alone is insufficient; blood culture and lumbar puncture are also required to exclude bacteraemia and meningitis.
• E. A brief period of observation does not replace the need for a full septic work-up in this high-risk age group.

Hypertrophic pyloric stenosis classically presents at 3-6 weeks of age with non-bilious projectile vomiting immediately after feeds, a hungry infant, poor weight gain, a palpable 'olive' mass and visible peristalsis. The gastric outlet obstruction causes loss of hydrochloric acid and hydrogen ions, producing a hypochloraemic, hypokalaemic metabolic alkalosis, exactly as shown in this blood gas. Diagnosis is confirmed with abdominal ultrasound demonstrating pyloric muscle thickness greater than 3-4 mm and canal length greater than 15-17 mm. Management is fluid and electrolyte correction followed by pyloromyotomy.

• A. Volvulus presents acutely with bilious vomiting and a unwell, often shocked infant, not a gradually worsening history over a week.
• B. Reflux causes non-forceful regurgitation rather than projectile vomiting and does not produce a palpable mass or this alkalosis.
• D. Salt-wasting CAH causes hyponatraemia, hyperkalaemia and metabolic acidosis, the opposite electrolyte pattern seen here.
• E. Duodenal atresia presents in the neonatal period with bilious vomiting, not at 5 weeks with a palpable olive mass.

This infant has the classic triad of intermittent colicky abdominal pain, vomiting and blood-stained ('redcurrant jelly') mucus in the stool, with a palpable sausage-shaped mass, typical of intussusception. In a haemodynamically stable child without signs of perforation or peritonism, pneumatic (air) or hydrostatic (saline) enema reduction under radiological guidance is the first-line treatment and is both diagnostic and therapeutic. Ultrasound can confirm the diagnosis first if there is diagnostic uncertainty, but definitive management in a stable patient is enema reduction, not observation or immediate surgery. Surgery is reserved for failed enema reduction, peritonism, perforation or signs of bowel ischaemia.

• A. Barium follow-through is used for suspected malrotation or small bowel pathology, not as treatment for intussusception.
• B. Laparotomy is reserved for cases with peritonism, perforation, failed enema reduction or haemodynamic instability.
• C. Observation alone is inappropriate as intussusception risks bowel ischaemia and perforation without prompt treatment.
• D. While ultrasound confirms the diagnosis, outpatient review is inappropriate for a condition requiring urgent treatment.

This child shows a combination of clinical signs including tachycardia, sunken eyes, dry mucous membranes, reduced urine output, and slow skin turgor, which together with an estimated weight loss of about 6.7% indicate moderate dehydration. According to Australian paediatric guidelines, moderate dehydration (5-9%) is characterised by these findings but with the child remaining alert, which distinguishes it from severe dehydration where there is lethargy, poor perfusion and hypotension. Severe dehydration would show prolonged capillary refill greater than 3 seconds with mottled skin, deep acidotic breathing, or a decreased level of consciousness. Clinical assessment using weight change and composite signs is the recommended method; biochemistry is not required to grade dehydration clinically.

• A. The presence of tachycardia, sunken eyes, dry mucous membranes and reduced urine output excludes a diagnosis of no dehydration.
• B. Dehydration severity in children is assessed clinically using history, weight change and examination findings, not biochemistry.
• C. She remains alert with a capillary refill of only 3 seconds, which is inconsistent with decompensated shock.
• D. The constellation of signs including tachycardia and reduced skin turgor is more severe than mild dehydration.

This child has mild dehydration and is alert, tolerating oral fluids, with no signs of shock or severe dehydration. Therapeutic Guidelines and RACGP recommend oral rehydration solution as first-line treatment for mild to moderate dehydration in children who are not in shock, given in small frequent volumes to minimise vomiting, often starting at 5 mL every few minutes and increasing as tolerated. Intravenous fluids are reserved for children with severe dehydration, shock, inability to tolerate oral or nasogastric fluids, or persistent vomiting despite an adequate oral rehydration trial. Nasogastric rehydration is a reasonable second-line option if oral trial fails, but it is not the first step when the child is already tolerating oral fluids.

• B. IV fluids are unnecessary first-line therapy in a child with mild dehydration who is tolerating oral fluids and has no shock.
• C. Nasogastric rehydration is reserved for children who fail an oral rehydration trial, not as an initial step here.
• D. Discharge without any rehydration plan ignores his documented 3% dehydration and ongoing fluid losses.
• E. Admission for IV dextrose-saline is excessive for mild dehydration with successful oral tolerance already demonstrated.

In a child with symptoms suggestive of coeliac disease and a confirmed normal total IgA level, anti-tissue transglutaminase IgA (anti-tTG IgA) antibody testing is the recommended first-line serological test while the child remains on a gluten-containing diet. If the anti-tTG IgA level is strongly positive (typically more than 10 times the upper limit of normal), current paediatric guidelines allow a diagnosis without biopsy when combined with a positive anti-endomysial antibody test, but in many cases, particularly with lower titres or diagnostic uncertainty, small bowel biopsy via endoscopy remains needed to confirm villous atrophy. HLA typing is useful for excluding coeliac disease in equivocal cases or for family screening but does not confirm the diagnosis since it is present in up to 30% of the general population. Starting a gluten-free diet before serology and biopsy would compromise accurate testing, as histological and serological changes resolve on a gluten-free diet.

• A. A breath test would address isolated lactose intolerance but would not address the broader clinical picture and family history pointing to coeliac disease.
• B. Starting a gluten-free diet before serological testing risks false-negative results and should be avoided until testing is complete.
• C. Faecal calprotectin assesses intestinal inflammation suggestive of inflammatory bowel disease, not coeliac-specific serology.
• D. HLA-DQ2/DQ8 has high sensitivity but low specificity and cannot confirm the diagnosis; it is mainly used to exclude coeliac disease.

In paediatric DKA with shock or significant dehydration, initial fluid resuscitation with an isotonic crystalloid bolus (10 mL/kg 0.9% sodium chloride over 60 minutes) is the first priority to restore circulating volume before starting insulin. Rapid correction of fluid and osmolality is avoided because of the risk of cerebral oedema, which is a leading cause of death in paediatric DKA. Insulin is started after initial fluid resuscitation, typically as a low-dose intravenous infusion rather than a bolus, since boluses increase the risk of rapid osmotic shifts and cerebral oedema. Bicarbonate is not recommended in paediatric DKA as it worsens paradoxical CNS acidosis and increases cerebral oedema risk.

• A. Maintenance-only dextrose-containing fluid does not address the volume deficit and hyperglycaemia requires isotonic resuscitation first, not dextrose.
• C. Bicarbonate is not recommended in paediatric DKA and increases the risk of cerebral oedema.
• D. An insulin bolus is avoided in children as it increases the risk of cerebral oedema; insulin is given as a low-dose infusion after initial fluid resuscitation.
• E. Subcutaneous insulin has unreliable absorption in a dehydrated, poorly perfused child and intravenous insulin infusion is preferred.

A positive newborn screen for congenital hypothyroidism requires urgent confirmatory venous serum TSH and free T4, as screening tests can have false positives, but treatment must not be delayed pending confirmation if the infant cannot be seen promptly, because early treatment is critical to prevent irreversible neurodevelopmental impairment. Levothyroxine should ideally be started within the first 2 weeks of life. Imaging (ultrasound or radionuclide scan) can help determine aetiology but should not delay confirmatory blood testing and treatment. Repeating the screening test alone wastes time critical to neurodevelopmental outcome.

• A. Imaging is useful for determining aetiology but should not take priority over, or delay, confirmatory blood tests and treatment.
• C. A markedly elevated TSH on screening is a true positive until proven otherwise and must be urgently confirmed, not dismissed.
• D. Confirmatory serum testing should be obtained promptly even though treatment may need to start before results return if there is any delay.
• E. Repeating only the screening test delays definitive diagnosis and treatment, risking neurodevelopmental harm.

Up to 50% of infants with Down syndrome have congenital heart disease, most commonly atrioventricular septal defect, ventricular septal defect or patent ductus arteriosus, so all infants with trisomy 21 should have an echocardiogram performed in the neonatal period even if clinically asymptomatic. Congenital heart disease can initially be silent and may present later with failure to thrive or heart failure if missed. Coeliac disease and thyroid dysfunction are screened for later in childhood, not typically in the neonatal period. Autism spectrum disorder is not part of routine structured screening and Addison disease is not a recognised association with Down syndrome.

• A. Addison disease is not a recognised association of Down syndrome.
• B. Type 1 diabetes is not a well-established association requiring routine screening in Down syndrome.
• C. Coeliac disease screening is relevant later in childhood, not as the priority screen in early infancy.
• E. Autism spectrum disorder is not a condition with a structured early screening protocol in Down syndrome.

In a girl with signs of puberty before age 8, the initial assessment includes a bone age X-ray, which helps determine whether skeletal maturation is advanced (supporting true precocious puberty) and provides a baseline for predicting adult height. This is a simple, low-radiation, widely available first-line investigation. Hormonal tests (LH, FSH) and imaging such as pelvic ultrasound or brain MRI are important subsequent steps once precocious puberty is confirmed and to differentiate central from peripheral causes, but bone age assessment is the standard initial screening step. Karyotype is not indicated as a first step without other dysmorphic features.

• A. Karyotype is not routinely indicated for isolated precocious puberty without dysmorphic features or short stature.
• B. Pelvic ultrasound assesses ovarian/uterine maturation and is useful once precocious puberty is suspected, but bone age is typically performed first.
• D. Gonadotropin levels help confirm central precocious puberty but are usually obtained after an initial bone age assessment.
• E. Brain MRI is reserved for confirmed central precocious puberty or when neurological signs are present, not as the initial step.

Excessive cow's milk intake in toddlers displaces iron-rich solid foods and impairs intestinal absorption of non-haem iron, which is a common cause of iron deficiency anaemia in this age group. Management involves reducing cow's milk to a recommended maximum of around 500 mL per day, encouraging iron-rich solid foods, and starting oral iron supplementation (ferrous sulfate or similar) to replete iron stores. Simply continuing the current diet without intervention risks worsening anaemia and developmental effects. Soy formula alone does not correct existing iron deficiency, and transfusion is reserved for severe symptomatic anaemia, which this child does not have.

• A. Transfusion is reserved for severe, symptomatic anaemia with haemodynamic compromise, not a stable toddler with haemoglobin 92 g/L.
• B. Doing nothing and waiting 6 months risks worsening anaemia and potential developmental consequences from ongoing untreated deficiency.
• D. Dietary counselling to reduce milk volume and increase iron-rich foods is essential alongside supplementation, not supplementation alone.
• E. Switching formula type does not address the excessive milk volume or replace iron stores without supplementation.

The combination of pallor, bruising, fevers, lymphadenopathy, splenomegaly, cytopenias and circulating blasts on blood film is highly suggestive of acute lymphoblastic leukaemia, the most common childhood malignancy, and warrants urgent same-day referral to a paediatric haematology/oncology service for diagnostic confirmation (bone marrow aspirate) and staging. Delay risks life-threatening complications such as severe infection, bleeding or tumour lysis syndrome. Antibiotics alone do not address the underlying marrow failure and leukaemic process. Iron supplementation is inappropriate given the pancytopenia with blasts is not due to iron deficiency.

• A. Antibiotics do not address the underlying bone marrow infiltration causing cytopenias and circulating blasts, which requires urgent specialist assessment.
• B. A bone marrow biopsy is required urgently, not as an outpatient procedure within a month, given the risk of rapid deterioration.
• C. Iron supplementation does not address the underlying pathology; the anaemia here is due to marrow infiltration, not iron deficiency.
• E. Reassurance and delayed follow-up is inappropriate and dangerous given cytopenias with circulating blasts suggestive of leukaemia.

This presentation, isolated thrombocytopenia with petechiae and bruising following a recent viral illness, normal haemoglobin and white cell count, and no organomegaly, is classic for immune thrombocytopenic purpura (ITP), the most common cause of acquired thrombocytopenia in otherwise well children. Most children with ITP and no significant bleeding (only cutaneous petechiae/bruising) can be managed with observation and safety-netting advice, as the condition is usually self-limiting, resolving within weeks to months. Treatment (such as corticosteroids or IVIG) is reserved for significant mucosal or internal bleeding. Platelet transfusion is largely ineffective and reserved for life-threatening haemorrhage because transfused platelets are rapidly destroyed by circulating antibodies.

• A. Chemotherapy has no role in ITP, which is an autoimmune rather than malignant process.
• B. Splenectomy is reserved for chronic, refractory ITP with significant bleeding, not for initial management of a new presentation.
• D. Bone marrow biopsy is not routinely required when the clinical picture and blood film are typical for ITP without atypical features.
• E. Platelet transfusion is rapidly consumed by autoantibodies and is reserved for life-threatening bleeding, not routine ITP management.

In a young child with a painless, unilateral, non-midline-crossing abdominal mass with haematuria and hypertension, Wilms tumour (nephroblastoma) is the leading diagnosis, and abdominal ultrasound is the most appropriate initial investigation because it is readily available, avoids radiation, and can confirm the renal origin of the mass, assess for bilateral involvement, and evaluate for tumour extension into the renal vein and inferior vena cava. CT or MRI are used subsequently for staging once ultrasound suggests a renal tumour. Urine catecholamines are more relevant to neuroblastoma, which classically crosses the midline and arises from adrenal or sympathetic chain tissue.

• B. Urine catecholamines are useful for suspected neuroblastoma, which more typically crosses the midline, rather than Wilms tumour.
• C. Intravenous pyelogram has been superseded by ultrasound and CT for initial assessment of a suspected renal mass.
• D. Plain abdominal X-ray has low sensitivity and specificity for characterising an abdominal mass and is not the investigation of choice.
• E. CT with contrast is used for staging after ultrasound has confirmed a renal mass, not as the first-line investigation.

Transient synovitis typically follows a viral upper respiratory infection and presents with a well-looking, afebrile or mildly febrile child who can still partially weight-bear, with normal or only mildly elevated inflammatory markers. Septic arthritis is suggested by inability to weight-bear at all, high fever, and elevated CRP and white cell count (Kocher criteria). The age, acute onset, preceding viral illness, ability to partially weight-bear and normal inflammatory markers here favour transient synovitis, which is managed with rest and analgesia and resolves within days.

• A. Slipped upper femoral epiphysis occurs in older, often obese adolescents and presents with groin or knee pain and an externally rotated gait, not an acute illness in a preschooler.
• B. Septic arthritis usually causes inability to bear any weight, high fever and markedly raised CRP/white cell count, none of which are present here.
• C. Perthes disease presents with an insidious, often painless limp over weeks in children typically aged 4-8 years, not an acute 1-day history.
• D. Osteomyelitis typically causes bony point tenderness, high fever and systemic illness with markedly raised inflammatory markers, which are absent here.

Slipped upper femoral epiphysis classically occurs in overweight adolescent boys aged 10-16 years and presents with an insidious limp and hip, groin, thigh or referred knee pain. The pathognomonic sign is obligatory external rotation of the hip on passive flexion, with restricted internal rotation, reflecting posteroinferior displacement of the femoral epiphysis relative to the neck. Diagnosis is confirmed with anteroposterior and frog-leg lateral pelvic X-rays. It requires urgent orthopaedic referral as the hip is at risk of further slippage and avascular necrosis.

• A. Perthes disease typically affects younger children (4-8 years) and does not cause obligatory external rotation on flexion in the way SUFE does.
• C. Juvenile idiopathic arthritis usually causes joint swelling, morning stiffness and often involves multiple joints, not an isolated mechanical external rotation deformity.
• D. Osgood-Schlatter disease causes localised tenderness and swelling over the tibial tuberosity, not hip signs or restricted internal rotation.
• E. Transient synovitis presents acutely after a viral illness in younger children, not with a 3-week insidious course and the external rotation sign described.

A spiral fracture of the humerus in a pre-mobile infant, combined with rib fractures of differing ages, is highly suspicious for non-accidental injury, as pre-ambulatory infants do not sustain such fractures from typical falls and multiple fractures of different ages indicate repeated trauma. Clinicians have a mandatory reporting obligation to notify child protection authorities when non-accidental injury is suspected. The infant should be admitted for a full skeletal survey, ophthalmological assessment and multidisciplinary safeguarding assessment while safety is ensured. Discharge without investigation or reporting risks ongoing harm to the child.

• A. Delaying action risks the child returning to an unsafe environment; suspected non-accidental injury requires immediate reporting, not a 'wait and see' approach.
• B. Bone density testing is not indicated here; the pattern of injury, not bone fragility, is the key concern, and action should not be delayed for this.
• C. Discharging without reporting or further investigation ignores mandatory reporting obligations and the high suspicion of non-accidental injury.
• E. Physiotherapy does not address the acute fracture or the underlying safety concern and inappropriately delays mandatory reporting.

Early asymmetric hand use before 12 months, with unilateral increased tone, hyperreflexia and failure to meet gross motor milestones in a former preterm infant, are red flags for cerebral palsy, particularly a hemiplegic pattern related to prematurity. Early diagnosis and referral to a paediatrician and early intervention services (physiotherapy, occupational therapy) are essential, as early therapy improves functional outcomes through neuroplasticity. Hand preference this early, especially with associated tone and reflex changes, is not a normal variant and warrants prompt specialist assessment rather than reassurance.

• A. Hand preference and asymmetric reaching before 12 months, combined with abnormal tone and reflexes, is a red flag, not a normal developmental variant, and reassurance would delay needed care.
• B. Baclofen is a treatment for established spasticity and should only be initiated after specialist diagnosis and assessment, not in primary care before referral.
• D. There is no history of seizure activity described, so an EEG is not the priority investigation; the focus should be on referral for the motor findings.
• E. There is no dysmorphism or other feature suggesting a chromosomal syndrome here; the clinical picture fits a motor disorder related to prematurity.

Breath-holding spells typically occur in children aged 6 months to 5 years and are triggered by pain, frustration or anger. The pallid (reflex asystolic) type is characterised by crying, sudden pallor, loss of consciousness and brief limpness, sometimes with a short period of asystole, followed by rapid full recovery without post-ictal confusion. This is a benign, self-limiting condition related to vagal-mediated bradycardia and does not require anticonvulsant treatment, though persistent or atypical episodes warrant cardiac assessment to exclude arrhythmia. The clear emotional trigger, brief duration and rapid complete recovery without post-ictal state distinguish this from epileptic seizures.

• A. While arrhythmia can cause syncope, the clear situational trigger (frustration/crying) and recurrent pattern make a benign breath-holding spell far more likely than a primary cardiac cause.
• B. There is no fever mentioned, and febrile seizures occur in the context of fever, which is absent in this history.
• C. Absence seizures are brief staring episodes without an emotional trigger or loss of tone, and are not preceded by crying or pallor.
• D. A tonic-clonic seizure would typically involve convulsive movements, tongue biting or incontinence, and a post-ictal drowsy period, none of which occurred here.

The child has anaphylaxis with respiratory compromise (stridor, wheeze, cyanosis) and requires immediate intramuscular adrenaline, the first-line treatment that reverses vasodilation, reduces mucosal oedema and relieves bronchospasm. The recommended dose is 0.01 mg/kg of 1:1000 adrenaline, giving approximately 0.18 mg for an 18 kg child, administered into the lateral thigh muscle, which can be repeated every 5 minutes if needed. Intravenous adrenaline is reserved for refractory anaphylaxis managed by experienced clinicians in a monitored setting due to the risk of arrhythmia. Antihistamines and nebulised adrenaline are adjuncts only and do not replace intramuscular adrenaline as first-line therapy.

• A. This dose is ten times too high and risks dangerous arrhythmia and hypertension; the correct dose is 0.01 mg/kg.
• B. Intravenous adrenaline is not first-line in general practice; it is reserved for refractory anaphylaxis under specialist monitoring due to arrhythmia risk.
• C. Antihistamines do not reverse airway compromise or hypotension in anaphylaxis and must never delay administration of adrenaline.
• D. Nebulised adrenaline alone does not treat the systemic features of anaphylaxis and is not a substitute for intramuscular adrenaline.

Candidal nappy dermatitis characteristically involves the skin folds (unlike irritant dermatitis, which spares the folds) and presents with a bright red, confluent rash with satellite papules and pustules extending beyond the main rash margin. It commonly follows or coexists with irritant dermatitis and often arises after antibiotic use or in warm, moist nappy environments that favour Candida overgrowth. Treatment is with a topical antifungal such as clotrimazole, continued barrier protection and frequent nappy changes, reserving combination steroid-antifungal creams for cases with significant inflammation. Irritant dermatitis typically affects the convex surfaces in contact with the nappy and spares the skin folds, which helps distinguish the two conditions clinically.

• A. Allergic contact dermatitis to nappy materials is uncommon in this age group and would not typically produce the fold involvement with satellite pustules seen here.
• B. Irritant contact dermatitis typically spares the skin folds and affects convex surfaces exposed to urine and faeces; it does not produce satellite pustules.
• C. Psoriasis in the napkin area can mimic nappy rash but typically presents with well-demarcated, silvery scaly plaques rather than satellite pustules, and is less common than candidal infection at this age.
• D. Seborrhoeic dermatitis usually presents with greasy yellow scale, often also affecting the scalp and face, rather than satellite pustules confined to the groin folds.

Otitis media with effusion (OME) is highly prevalent in Aboriginal and Torres Strait Islander children and is a leading preventable cause of conductive hearing loss and delayed language development. Household tobacco smoke exposure, overcrowding and early childcare attendance are major modifiable risk factors that increase the frequency and persistence of OME. Reducing exposure to tobacco smoke is a key primary prevention strategy recommended by the RACGP and Australian guidelines for Aboriginal child health, alongside addressing overcrowding and promoting breastfeeding. Surgical and pharmacological interventions are reserved for persistent or complicated disease, not as first-line prevention in an asymptomatic child with uncomplicated OME.

• A. Saline irrigation has no proven role in preventing or treating otitis media with effusion.
• C. Tonsillectomy is not indicated for otitis media with effusion and does not address its underlying risk factors.
• D. Tympanostomy tubes are considered for persistent bilateral OME with hearing loss over three months, not as an initial preventive measure.
• E. Prophylactic antibiotics are not recommended for prevention of OME due to limited benefit and risk of resistance.

Jaundice occurring within the first 24 hours of life is never physiological and always requires urgent investigation, because it usually reflects a pathological process such as haemolysis from blood group incompatibility, sepsis or a red cell membrane or enzyme defect. The first step is to measure the serum bilirubin level urgently along with a blood group, direct antiglobulin test and full blood count to determine the cause and severity. Management decisions, including the need for phototherapy, depend on the bilirubin level plotted against the treatment threshold chart.

• A. Phototherapy should not be started before confirming the bilirubin level and the degree to which it exceeds the treatment threshold.
• B. Ultrasound is used to investigate conjugated hyperbilirubinaemia or suspected biliary obstruction, not as the initial step for early unconjugated jaundice.
• D. Increasing feed frequency alone is insufficient when early-onset jaundice may indicate a serious underlying cause requiring urgent biochemical assessment.
• E. Jaundice in the first 24 hours is never considered normal and cannot be safely deferred for review a day later.

Treatment threshold graphs plot bilirubin level against postnatal age in hours, with separate curves for phototherapy and exchange transfusion that account for gestational age and risk factors. A level above the phototherapy line but below the exchange line indicates that phototherapy should be started, with the bilirubin rechecked after a short interval, typically 4-6 hours, to confirm response and ensure the level is not still rising toward the exchange threshold. This approach prevents under-treatment while avoiding the more invasive exchange transfusion when it is not yet indicated.

• A. Intravenous immunoglobulin is used in haemolytic disease with rapidly rising bilirubin despite phototherapy, not as a first step based on threshold chart position alone.
• B. Exchange transfusion is reserved for levels crossing the higher exchange threshold line, which this result has not reached.
• C. A one-week interval is far too long given the level is already above the treatment threshold and bilirubin can rise rapidly over hours.
• D. A level above the phototherapy threshold requires treatment and cannot simply be discharged without intervention.

Breast milk jaundice occurs in otherwise well, thriving breastfed infants with adequate weight gain and normal feeding and elimination patterns, and is thought to result from factors in breast milk, such as beta-glucuronidase, that increase enterohepatic recirculation of bilirubin. It typically persists beyond the first week and can last several weeks, resolving spontaneously without stopping breastfeeding. This infant's good weight gain, adequate wet nappies and stooling pattern distinguish it from breastfeeding failure jaundice, which results from inadequate milk intake.

• A. Urinary tract infection would typically present with conjugated hyperbilirubinaemia and systemic signs such as fever or poor feeding, not isolated unconjugated jaundice in a well infant.
• C. Breastfeeding failure jaundice is associated with poor intake, weight loss, reduced wet nappies and infrequent stools, none of which are present here.
• D. Galactosaemia presents with conjugated hyperbilirubinaemia, vomiting, poor feeding and hepatomegaly, not an isolated unconjugated pattern in a thriving infant.
• E. Hypothyroidism can cause prolonged jaundice but is usually accompanied by lethargy, poor feeding, constipation and a hoarse cry, not seen in this well-feeding infant.

A well-appearing infant with risk factors for early-onset group B streptococcal sepsis, including inadequate intrapartum antibiotic prophylaxis and prolonged rupture of membranes, should be managed with close clinical observation and serial vital sign monitoring for at least 48 hours, as this is when most cases become symptomatic. Empirical antibiotics are reserved for infants showing clinical signs of sepsis or those with multiple high-risk factors combined with illness, not asymptomatic infants on risk factors alone. This risk-based observation approach, as recommended by Australian and international guidelines, avoids unnecessary antibiotic exposure while ensuring early detection if sepsis develops.

• B. Waiting until fever develops ignores the need for proactive monitoring, since early-onset sepsis can present with signs other than fever, such as respiratory distress or lethargy.
• C. Empirical antibiotics are not indicated in an asymptomatic, well-appearing infant based on risk factors alone without clinical signs of sepsis.
• D. Discharge without monitoring is unsafe given the combination of inadequate prophylaxis and prolonged rupture of membranes, which increases risk of early-onset sepsis.
• E. Lumbar puncture is invasive and reserved for infants with signs of sepsis or suspected meningitis, not as an initial step in an asymptomatic infant.

Infants of diabetic mothers are at risk of hypoglycaemia due to fetal hyperinsulinaemia from maternal hyperglycaemia in utero, and screening should begin with bedside capillary blood glucose testing performed before feeds in the first hours of life, as this is when the risk is highest after the maternal glucose supply is withdrawn. Testing before a feed captures the lowest, pre-feed glucose level and guides whether urgent intervention, such as additional feeding or intravenous dextrose, is needed. Screening typically continues for at least 24 hours or until stable pre-feed levels are demonstrated.

• A. Testing at a fixed time regardless of feeding does not capture the lowest pre-feed glucose level and is less useful than timing tests around feeds.
• B. Waiting until 24 hours misses the period of highest risk, which is in the first few hours after birth when hypoglycaemia is most likely to occur and cause harm.
• C. Insulin and C-peptide levels are used in investigating persistent or atypical hypoglycaemia, not as the initial screening test in this common clinical scenario.
• E. An oral glucose tolerance test assesses glucose handling over time and is not used for screening acute neonatal hypoglycaemia.

A positive Barlow or Ortolani test indicates hip instability suggestive of developmental dysplasia of the hip, and the next step is referral for hip ultrasound, which is the imaging modality of choice in infants under 4-6 months because the femoral head and acetabulum are largely cartilaginous and not well seen on X-ray. Breech presentation is itself a major risk factor for developmental dysplasia of the hip, reinforcing the need for prompt imaging rather than reassurance. Ultrasound confirms the diagnosis and guides decisions about treatment such as splinting.

• A. Treatment such as a Pavlik harness should only be started after ultrasound confirms the diagnosis and severity of dysplasia.
• B. Delaying review until 6 months risks progression of untreated dysplasia, when earlier treatment in infancy has better outcomes.
• D. Plain X-ray is unreliable in young infants because the hip joint is predominantly cartilaginous at this age and not well visualised radiographically.
• E. A positive instability test is abnormal and requires further assessment, not reassurance, despite breech presentation being a known risk factor.

Newborn bloodspot screening in Australia is recommended between 48 and 72 hours of age, as this timing allows sufficient postnatal metabolic changes to occur, improving detection of conditions such as congenital hypothyroidism, phenylketonuria, cystic fibrosis and other metabolic and genetic disorders screened on the card. Testing too early can produce false negative results because some analytes, such as thyroid stimulating hormone and phenylalanine, have not yet reached detectable abnormal levels. The test is performed on all newborns regardless of symptoms, as part of population-based screening to allow early intervention before irreversible harm occurs.

• A. Delaying testing to 2 weeks means conditions requiring urgent treatment, such as congenital hypothyroidism or phenylketonuria, may cause preventable harm before detection.
• B. At 24 hours, several screened conditions may not yet be reliably detected, increasing the risk of false negatives compared with the recommended window.
• C. Testing immediately after birth is too early and risks false negative results because many analytes have not yet reached abnormal detectable levels.
• E. Screening is performed on all newborns as a preventive measure regardless of symptoms, since the aim is to detect conditions before clinical signs appear.