Paeds Flashcards
Q: What type of disorder is achondroplasia and what is it associated with?
A: Achondroplasia is an autosomal dominant disorder associated with short stature.
Q: What gene mutation causes achondroplasia?
A: A mutation in the fibroblast growth factor receptor 3 (FGFR-3) gene causes achondroplasia.
Q: What are the characteristics of abnormal cartilage in achondroplasia?
A: Characteristics include short limbs (rhizomelia) with shortened fingers (brachydactyly), large head with frontal bossing and narrow foramen magnum, midface hypoplasia with a flattened nasal bridge, ‘trident’ hands, and lumbar lordosis.
Q: What is the main risk factor for achondroplasia?
A: The main risk factor is advancing parental age at the time of conception.
Q: How is achondroplasia typically inherited?
Q: How is achondroplasia typically inherited?
A: Once present, achondroplasia is typically inherited in an autosomal dominant fashion.
Q: Is there a specific therapy for achondroplasia?
A: There is no specific therapy for achondroplasia.
Q: What treatment can benefit some individuals with achondroplasia?
A: Some individuals benefit from limb lengthening procedures, which usually involve the application of Ilizarov frames and targeted bone fractures.
Q: What causes acute epiglottitis?
A: Acute epiglottitis is caused by Haemophilus influenzae type B.
Q: Why is prompt recognition and treatment essential in acute epiglottitis?
A: Prompt recognition and treatment are essential because airway obstruction may develop.
Q: What are the features of acute epiglottitis?
A: Features include rapid onset, high temperature, generally unwell, stridor, drooling of saliva, and the ‘tripod’ position.
Q: What is the ‘tripod’ position in acute epiglottitis?
A: The ‘tripod’ position is when the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position.
Q: How is the diagnosis of acute epiglottitis made?
A: Diagnosis is made by direct visualisation by senior/airway trained staff. X-rays may be done, with a lateral view showing the ‘thumb sign’.
Q: What does a lateral view x-ray show in acute epiglottitis?
A: A lateral view in acute epiglottitis will show swelling of the epiglottis, known as the ‘thumb sign’.
Q: What does a posterior-anterior view x-ray show in croup?
A: A posterior-anterior view in croup will show subglottic narrowing, commonly called the ‘steeple sign’.
Q: What is the initial management of acute epiglottitis?
A: Initial management includes immediate senior involvement, endotracheal intubation if necessary, not examining the throat if suspected, providing oxygen, and administering intravenous antibiotics.
Q: Why should the throat not be examined if acute epiglottitis is suspected?
A: The throat should not be examined due to the risk of acute airway obstruction.
Q: What is the most common malignancy affecting children?
A: Acute lymphoblastic leukaemia (ALL) is the most common malignancy affecting children.
Q: At what age does the peak incidence of acute lymphoblastic leukaemia (ALL) occur?
A: The peak incidence of acute lymphoblastic leukaemia (ALL) occurs at around 2-5 years of age.
Q: What are some features of acute lymphoblastic leukaemia (ALL) caused by bone marrow failure?
A: Features include anaemia (lethargy and pallor), neutropaenia (frequent or severe infections), and thrombocytopenia (easy bruising, petechiae).
Q: What are some other features of acute lymphoblastic leukaemia (ALL)?
A: Other features include bone pain (secondary to bone marrow infiltration), splenomegaly, hepatomegaly, fever (present in up to 50% of new cases), and testicular swelling.
Q: What is the phenotype and marker for common ALL?
A: Common ALL has a pre-B phenotype and CD10 is present.
Q: What are the poor prognostic factors for acute lymphoblastic leukaemia (ALL)?
A: Poor prognostic factors include age < 2 years or > 10 years, WBC > 20 * 10^9/L at diagnosis, T or B cell surface markers, non-Caucasian ethnicity, and male sex.
Q: What is the most important condition to exclude in a child with an acute scrotal presentation?
A: It is essential to exclude testicular torsion, as immediate surgery is required.
Q: At what age is testicular torsion most common in children?
A: Testicular torsion is most common around puberty.
Q: At what age is an irreducible inguinal hernia most common in children?
A: An irreducible inguinal hernia is most common in children < 2 years old.
Q: Is epididymitis common in prepubescent children?
A: Epididymitis is rare in prepubescent children.
Q: What causes alpha-thalassaemia?
A: Alpha-thalassaemia is due to a deficiency of alpha chains in haemoglobin.
Q: Where are the alpha-globulin genes located?
A: The alpha-globulin genes are located on each chromosome 16.
Q: How does clinical severity in alpha-thalassaemia depend on the number of affected alpha-globulin alleles?
1 or 2 affected alleles: blood picture is hypochromic and microcytic, but Hb level is typically normal.
3 affected alleles: results in hypochromic microcytic anaemia with splenomegaly, known as Hb H disease.
4 affected alleles (homozygote): leads to death in utero (hydrops fetalis, Bart’s hydrops).
Q: What is the most common cause of ambiguous genitalia in newborns?
A: The most common cause is congenital adrenal hyperplasia.
Q: What are other causes of ambiguous genitalia?
A: Other causes include true hermaphroditism and maternal ingestion of androgens.
Q: When is the Apgar score assessed according to NICE guidelines?
A: The Apgar score is assessed at 1 and 5 minutes of age. If the score is low, it is repeated at 10 minutes.
Q: What is the score for a pulse rate > 100 in the Apgar score?
A: A pulse rate > 100 gives a score of 2.
Q: What is the score for a weak, irregular respiratory effort in the Apgar score?
A: A weak, irregular respiratory effort gives a score of 1.
Q: What does a score of 0 indicate for respiratory effort in the Apgar score?
A: A score of 0 for respiratory effort indicates nil effort.
Q: What does a score of 2 indicate for muscle tone in the Apgar score?
A: A score of 2 for muscle tone indicates active movement.
Q: What does a score of 1 indicate for muscle tone in the Apgar score?
A: A score of 1 for muscle tone indicates limb flexion.
Q: What does a score of 0 indicate for muscle tone in the Apgar score?
A: A score of 0 for muscle tone indicates flaccid muscles.
Q: What does a score of 2 indicate for reflex irritability in the Apgar score?
A: A score of 2 for reflex irritability indicates the baby cries on stimulation, sneezes, or coughs.
Q: What does a score of 1 indicate for reflex irritability in the Apgar score?
A: A score of 1 for reflex irritability indicates a grimace.
Q: What does a score of 0 indicate for reflex irritability in the Apgar score?
A: A score of 0 for reflex irritability indicates no response.
Q: What is the interpretation of a score between 0-3 on the Apgar scale?
A: A score between 0-3 is very low.
Q: What is the interpretation of a score between 4-6 on the Apgar scale?
A: A score between 4-6 is moderately low.
Q: What is the interpretation of a score between 7-10 on the Apgar scale?
A: A score between 7-10 means the baby is in a good state.
Q: What is one of the most common acute surgical problems facing children?
A: Appendicitis is one of the most common acute surgical problems facing children.
Q: What is the classical presentation of appendicitis in children?
A: The classical presentation includes central abdominal pain which later radiates to the right iliac fossa, low-grade pyrexia, and minimal vomiting.
Q: How do younger children or those with a retrocaecal/pelvic appendix present differently with appendicitis?
A: Younger children or those with a retrocaecal/pelvic appendix are more likely to present in an atypical way.
Q: What SpO2 level in children is considered consistent with a severe asthma attack?
A: SpO2 < 92% is consistent with a severe asthma attack in children.
Q: What is the PEF range for a severe asthma attack in children?
A: PEF is 33-50% of the best or predicted in a severe asthma attack.
Q: What are the symptoms indicating severe breathlessness in children with asthma?
A: Being too breathless to talk or feed.
Q: What is the heart rate for a severe asthma attack in a child over 5 years old?
A: A heart rate > 125 beats per minute is considered severe for children > 5 years.
Q: What heart rate is considered severe for children aged 1-5 years during an asthma attack?
A: A heart rate > 140 beats per minute is considered severe for children aged 1-5 years.
Q: What respiratory rate is considered severe for children older than 5 years during an asthma attack?
A: A respiratory rate > 30 breaths per minute is considered severe for children > 5 years.
Q: What respiratory rate is considered severe for children aged 1-5 years during an asthma attack?
A: A respiratory rate > 40 breaths per minute is considered severe for children aged 1-5 years.
Q: What signs indicate the use of accessory neck muscles in a severe asthma attack in children?
A: The use of accessory neck muscles is a sign of a severe asthma attack.
Q: What SpO2 level is considered life-threatening in a child with an asthma attack?
A: SpO2 < 92% is life-threatening in an asthma attack.
Q: What is the PEF for a life-threatening asthma attack in children?
A: PEF < 33% of the best or predicted is life-threatening.
Q: What physical sign indicates a life-threatening asthma attack in children?
A: A silent chest is a sign of a life-threatening asthma attack.
Q: What other signs may indicate a life-threatening asthma attack in children?
A: Poor respiratory effort, agitation, altered consciousness, and cyanosis.
Q: What should be done for children with severe or life-threatening asthma?
A: Children with severe or life-threatening asthma should be transferred immediately to the hospital.
Q: What is the first-line treatment for children with mild to moderate acute asthma?
A: Bronchodilator therapy: give a beta-2 agonist via a spacer (for children < 3 years use a close-fitting mask), 1 puff every 30-60 seconds up to a maximum of 10 puffs.
Q: What should be done if symptoms are not controlled with bronchodilator therapy?
A: If symptoms are not controlled, repeat the beta-2 agonist and refer to the hospital.
Q: What steroid therapy should be given to all children with an asthma exacerbation?
A: Steroid therapy should be given for 3-5 days.
Q: What is the usual prednisolone dose for children aged 2-5 years according to BTS guidelines?
A: The usual prednisolone dose for children aged 2-5 years is 20 mg once daily.
Q: What is the usual prednisolone dose for children aged > 5 years according to BTS guidelines?
A: The usual prednisolone dose for children aged > 5 years is 30-40 mg once daily.
Q: What is the key concept in the 2024 NICE, British Thoracic Society, and SIGN guidelines for asthma management in children?
A: The key concept is the use of maintenance and reliever therapy (MART), which involves using an inhaled corticosteroid (ICS)/formoterol combination inhaler for daily maintenance therapy and relief of symptoms as needed.
Q: What is the first step in the management of asthma in children aged 5 to 11?
A: The first step is twice-daily paediatric low-dose inhaled corticosteroid (ICS) + short-acting beta-2 agonist (SABA) as needed.
Q: If asthma symptoms are not controlled on the first step in children aged 5 to 11, what are the two management pathways?
A: The two pathways are the MART pathway and the Conventional pathway.
Q: What should be done if asthma symptoms are still not controlled on the first step in the MART pathway?
A: The next step is to use a paediatric low-dose MART + SABA as needed.
Q: What should be done if asthma symptoms are still not controlled in the MART pathway after the first step?
A: The next step is to use a paediatric moderate-dose MART + SABA as needed.
Q: What should be done if asthma symptoms are still not controlled in the Conventional pathway after the first step?
A: The next step is to add a leukotriene receptor antagonist (LTRA) to twice-daily paediatric low-dose ICS plus SABA as needed, for a trial period of 8 to 12 weeks.
Q: What should be done if asthma symptoms are still not controlled after the trial of LTRA in the Conventional pathway?
A: The next step is to switch to a twice-daily paediatric low-dose ICS/LABA (long-acting beta-2 agonist) combination inhaler plus SABA as needed, with or without a LTRA, depending on the previous trial results.
Q: What should be done if asthma symptoms are still not controlled after switching to ICS/LABA combination inhaler in the Conventional pathway?
A: The next step is to switch to a twice-daily paediatric moderate-dose ICS/LABA combination inhaler plus SABA as needed, with or without a LTRA, depending on the previous trial results.
Q: What should be done if asthma symptoms are still not controlled despite all the above steps in children aged 5 to 11?
A: A referral should be made to a respiratory specialist.
Q: What is the first step in the management of asthma in children under 5?
A: The first step is an 8 to 12-week trial of twice-daily paediatric low-dose ICS as maintenance therapy + SABA as required.
Q: What should be considered after 8 to 12 weeks of ICS treatment in children under 5?
A: Consider stopping ICS and SABA treatment after 8 to 12 weeks if symptoms are resolved, and review symptoms after a further 3 months.
Q: What is the diagnostic criteria for ADHD in children under 16?
A: For children up to the age of 16 years, six features of inattention and/or hyperactivity/impulsivity must be present.
Q: What is the diagnostic criteria for ADHD in individuals aged 17 and over?
A: For individuals aged 17 or over, five features of inattention and/or hyperactivity/impulsivity must be present.
Q: What is the management approach recommended by NICE for ADHD?
A: NICE recommends a holistic approach, including a ten-week ‘watch and wait’ period, followed by referral to secondary care if symptoms persist.
Q: What are the primary diagnostic features of inattention in ADHD?
A: Features include not following through on instructions, reluctance to engage in mentally-intense tasks, being easily distracted, difficulty sustaining tasks, and often being forgetful in daily activities.
Q: What are the primary diagnostic features of hyperactivity/impulsivity in ADHD?
A: Features include being unable to play quietly, talking excessively, not waiting their turn easily, leaving their seat when expected to sit, and interrupting or intruding on others.
Q: When is drug therapy considered in the management of ADHD?
A: Drug therapy is considered a last resort and is only available for children aged 5 years or more, typically after a period of observation and if symptoms persist.
Q: What is the first-line pharmacotherapy for ADHD in children?
A: Methylphenidate is the first-line pharmacotherapy for ADHD in children, initially given on a six-week trial basis.
Q: What are the side effects of methylphenidate in children?
A: Side effects of methylphenidate include abdominal pain, nausea, and dyspepsia. Weight and height should be monitored every 6 months in children.
Q: What should be done if a child does not respond to methylphenidate?
A: If there is inadequate response to methylphenidate, the treatment should be switched to lisdexamfetamine.
Q: What is the recommended treatment for adults with ADHD?
A: Methylphenidate or lisdexamfetamine are first-line options for adults. If no benefit is seen, a switch between these drugs is recommended.
Q: What should be done before starting pharmacotherapy for ADHD?
A: A baseline ECG should be performed before starting treatment, and a cardiologist should be consulted if there is a significant past medical or family history, or if there is any doubt.
Q: What are the clinical features of ASD?
A: Clinical features include impaired social communication and interaction, such as playing alone and difficulty with nonverbal cues, and repetitive behaviours, interests, and activities, like stereotyped motor mannerisms and rigid routines.
Q: What are some common comorbidities associated with ASD?
A: Common comorbidities include Attention Deficit Hyperactivity Disorder (35%) and epilepsy (18%).
Q: What physical characteristic is associated with ASD?
A: ASD is associated with a higher head circumference to brain volume ratio.
Q: What is the goal of treatment for Autism Spectrum Disorder (ASD)?
A: The goal is to increase functional independence and quality of life, focusing on learning and development, social skills, communication, and reducing disability and comorbidity.
Q: What are the key components of non-pharmacological therapy for ASD?
A: Non-pharmacological therapy includes early educational and behavioural interventions such as Applied Behavioural Analysis (ABA), TEACCH, ESDM, and JASPER.
Q: What are the pharmacologic interventions used for ASD?
A: Pharmacologic interventions include SSRIs (for repetitive behaviour, anxiety, and aggression), antipsychotics (for aggression and self-injury), and methylphenidate (for ADHD).
Q: How should family support and counselling be integrated into ASD management?
A: Family support and counselling should focus on parental education regarding interaction with the child and acceptance of the child’s behaviour.
Q: What is Benign Rolandic Epilepsy?
A: Benign Rolandic Epilepsy is a form of childhood epilepsy that typically occurs between the ages of 4 and 12 years.
Q: When do seizures typically occur in Benign Rolandic Epilepsy?
A: Seizures characteristically occur at night.
Q: What type of seizures are seen in Benign Rolandic Epilepsy?
A: Seizures are typically partial (e.g., paraesthesia affecting the face), but secondary generalisation may occur, with tonic-clonic movements.
Q: How does the child appear between seizures in Benign Rolandic Epilepsy?
A: The child is otherwise normal.
Q: What is seen on an EEG in Benign Rolandic Epilepsy?
A: The EEG characteristically shows centrotemporal spikes.
Q: What is the prognosis for a child with Benign Rolandic Epilepsy?
A: The prognosis is excellent, with seizures typically stopping by adolescence.
Q: What is biliary atresia?
A: Biliary atresia is a pediatric condition involving the obliteration or discontinuity within the extrahepatic biliary system, causing obstruction in bile flow, leading to neonatal cholestasis.
Q: What is the epidemiology of biliary atresia?
A: Biliary atresia occurs in 1 in every 10,000-15,000 live births and is more common in females than males. It is unique to neonatal children, with perinatal form presenting in the first two weeks and postnatal form within 2-8 weeks.
Q: What are the types of biliary atresia?
Type 1: Proximal ducts patent, but common duct obliterated.
Type 2: Atresia of the cystic duct and cystic structures in the porta hepatis.
Type 3: Atresia of the left and right ducts to the level of the porta hepatis, occurring in >90% of cases.
Q: What are the clinical features of biliary atresia?
A: Symptoms include jaundice extending beyond the physiological two weeks, dark urine, pale stools, and abnormal growth, although appetite may be normal.
Q: What are the signs of biliary atresia?
A: Jaundice, hepatomegaly with splenomegaly, abnormal growth, and cardiac murmurs (if associated cardiac abnormalities are present).
Q: What are some investigations for biliary atresia?
A: Serum bilirubin (high conjugated bilirubin), liver function tests, serum alpha 1-antitrypsin, sweat chloride test, ultrasound of the biliary tree, and percutaneous liver biopsy with intraoperative cholangioscopy.
Q: What is the definitive treatment for biliary atresia?
A: Surgical intervention, such as dissection of abnormalities and creation of anastomosis, is the only definitive treatment.
Q: What are some complications of biliary atresia?
A: Unsuccessful anastomosis, progressive liver disease, cirrhosis, and eventual hepatocellular carcinoma.
Q: What is the prognosis for biliary atresia?
A: The prognosis is good if surgery is successful. If surgery fails, liver transplantation may be required within the first two years of life.
Q: What is bronchiolitis?
A: Bronchiolitis is a condition characterized by acute bronchiolar inflammation, commonly caused by respiratory syncytial virus (RSV) in 75-80% of cases.
Q: What is the epidemiology of bronchiolitis?
A: Bronchiolitis is the most common cause of serious lower respiratory tract infection in infants under 1 year old, with 90% of cases occurring in infants aged 1-9 months, peaking at 3-6 months. The incidence is higher in winter.
Q: What are the common causes of bronchiolitis?
A: RSV is the pathogen in 75-80% of cases. Other causes include mycoplasma, adenoviruses, and secondary bacterial infections.
Q: What makes bronchiolitis more serious?
A: It is more serious in children with bronchopulmonary dysplasia, congenital heart disease, or cystic fibrosis.
Q: When should a child with bronchiolitis be immediately referred to the hospital?
A: Immediate referral is necessary if the child has apnoea, appears seriously unwell, shows severe respiratory distress (e.g., grunting, marked chest recession, respiratory rate >70), has central cyanosis, or oxygen saturation is persistently <92%.
Q: What are the features of bronchiolitis?
A: Initial coryzal symptoms (mild fever), followed by dry cough, increasing breathlessness, wheezing, fine inspiratory crackles, and feeding difficulties due to dyspnoea.
Q: When should clinicians consider referring a child with bronchiolitis to the hospital?
A: Consider referral if the respiratory rate is >60 breaths/minute, the child has difficulty breastfeeding or inadequate oral intake (50-75% of usual volume), or there is clinical dehydration.
Q: How is bronchiolitis investigated?
A: Immunofluorescence of nasopharyngeal secretions can detect RSV.
Q: What is the management for bronchiolitis?
A: Management is supportive, including humidified oxygen for oxygen saturation <92%, nasogastric feeding if oral intake is insufficient, and suction for excessive upper airway secretions.
Q: What is caput succedaneum?
A: Caput succedaneum is oedema of the scalp at the presenting part of the head, typically the vertex, often due to mechanical trauma during delivery or use of ventouse (vacuum) delivery.
Q: What are the features of caput succedaneum?
A: It presents as a soft, puffy swelling due to localized oedema that crosses the suture lines.
Q: What is the treatment for caput succedaneum?
A: No treatment is needed as it typically resolves on its own.
Q: How does caput succedaneum differ from cephalohaematoma?
A: Unlike caput succedaneum, cephalohaematoma is a collection of blood beneath the periosteum and does not cross suture lines.
Q: What is a cephalohaematoma?
A: A cephalohaematoma is a swelling on the newborn’s head due to bleeding between the periosteum and skull, typically developing several hours after delivery.
Q: What is the most common site affected by cephalohaematoma?
A: The most common site affected is the parietal region of the skull.
Q: What complication may arise from a cephalohaematoma?
A: Jaundice may develop as a complication due to the breakdown of blood.
Q: What is cerebral palsy?
A: Cerebral palsy is a disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain.
Q: How long does a cephalohaematoma take to resolve?
A: A cephalohaematoma can take up to 3 months to resolve.
Q: What are the antenatal causes of cerebral palsy?
A: Antenatal causes include cerebral malformation and congenital infections such as rubella, toxoplasmosis, and CMV.
Q: What are the intrapartum causes of cerebral palsy?
A: Intrapartum causes include birth asphyxia and trauma.
Q: What are the postnatal causes of cerebral palsy?
A: Postnatal causes include intraventricular haemorrhage, meningitis, and head trauma.
Q: What are some possible manifestations of cerebral palsy?
A: Possible manifestations include abnormal tone early in infancy, delayed motor milestones, abnormal gait, and feeding difficulties.
Q: What are the subtypes of spastic cerebral palsy?
A: The subtypes include hemiplegia, diplegia, and quadriplegia, which involve increased tone resulting from damage to upper motor neurons.
Q: What are some non-motor problems associated with cerebral palsy?
A: Non-motor problems can include learning difficulties (60%), epilepsy (30%), squints (30%), and hearing impairment (20%).
Q: What causes dyskinetic cerebral palsy?
A: Dyskinetic cerebral palsy is caused by damage to the basal ganglia and the substantia nigra, leading to athetoid movements and oro-motor problems.
Q: What causes ataxic cerebral palsy?
A: Ataxic cerebral palsy is caused by damage to the cerebellum, resulting in typical cerebellar signs.
Q: What is the management approach for cerebral palsy?
A: A multidisciplinary approach is needed, with treatments for spasticity including oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopaedic surgery, and selective dorsal rhizotomy. Anticonvulsants and analgesia may also be required.
Q: When is a person with chickenpox infectious?
A: A person with chickenpox is infectious 4 days before the rash appears, until 5 days after the rash first appeared.
Q: How is chickenpox transmitted?
A: Chickenpox is highly infectious and spreads via the respiratory route. It can also be caught from someone with shingles.
Q: What causes chickenpox?
A: Chickenpox is caused by primary infection with varicella zoster virus.
Q: What is shingles?
A: Shingles is a reactivation of the dormant varicella zoster virus in the dorsal root ganglion.
Q: What are the common clinical features of chickenpox?
A: Chickenpox often presents with fever, an itchy rash that starts on the head/trunk before spreading, initially macular, then papular, and then vesicular. Systemic upset is usually mild.
Q: What is the management for chickenpox?
A: Management is supportive, including keeping the child cool, trimming nails, and using calamine lotion.
Q: What is a common complication of chickenpox?
A: A common complication is secondary bacterial infection of the lesions, which may be exacerbated by NSAIDs.
Q: What rare complications can occur with chickenpox?
A: Rare complications include pneumonia, encephalitis (especially with cerebellar involvement), disseminated haemorrhagic chickenpox, arthritis, nephritis, and pancreatitis.
Q: What should be given to immunocompromised patients and newborns with peripartum exposure to chickenpox?
A: Immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG). If chickenpox develops, IV aciclovir should be considered.
Q: How long should a child with chickenpox be excluded from school?
A: School exclusion is advised until all lesions are dry and have crusted over, usually about 5 days after the onset of the rash.
Q: What ongoing health surveillance occurs in children?
A: Ongoing health surveillance includes monitoring growth, vision, and hearing, as well as providing advice on immunisations, diet, and accident prevention.
Q: What happens during the first month of child health surveillance?
A: The first month involves the heel-prick test, midwife visits, and health visitor input.
Q: What happens at the GP examination at 6-8 weeks?
A: The GP examination at 6-8 weeks includes an assessment of the child’s development and overall health, alongside routine immunisations.
Q: What is involved in the preschool child health surveillance?
A: The preschool health surveillance includes a national orthoptist-led programme for pre-school vision screening.
Q: What are the main symptoms of mumps?
A: Mumps presents with fever, malaise, muscular pain, and parotitis (earache). Initially, parotitis is unilateral and becomes bilateral in 70% of cases.
Q: What are the features of rubella?
A: Rubella causes a pink maculopapular rash that starts on the face and spreads to the whole body, usually fading by the 3-5 day. It is also associated with suboccipital and postauricular lymphadenopathy.
Q: What are the clinical features of chickenpox?
A: Chickenpox presents with fever initially, followed by an itchy rash starting on the head/trunk and spreading. The rash progresses from macular to papular to vesicular. Systemic upset is usually mild.
Q: What are the key features of measles?
A: Measles starts with a prodrome of irritability, conjunctivitis, and fever. Koplik spots (white spots on buccal mucosa) are seen, followed by a rash that starts behind the ears and spreads to the whole body, initially discrete maculopapular, then becoming blotchy and confluent.
Q: What are the clinical features of scarlet fever?
A: Scarlet fever is a reaction to erythrogenic toxins produced by Group A haemolytic streptococci. It presents with fever, malaise, tonsillitis, “strawberry” tongue, and a rash with fine punctate erythema sparing the area around the mouth (circumoral pallor).
Q: What are the symptoms of erythema infectiosum (fifth disease or ‘slapped-cheek syndrome’)?
A: Erythema infectiosum, caused by parvovirus B19, presents with lethargy, fever, headache, and a characteristic “slapped-cheek” rash that spreads to the proximal arms and extensor surfaces.
Q: What are the symptoms of hand, foot, and mouth disease?
A: Hand, foot, and mouth disease, caused by the coxsackie A16 virus, presents with mild systemic upset (sore throat, fever) and vesicles in the mouth and on the palms and soles of the feet.
Q: What are the key features of Patau syndrome (trisomy 13)?
A: Patau syndrome is characterized by microcephaly, small eyes, cleft lip/palate, polydactyly, and scalp lesions.
Q: What are the main features of Edward’s syndrome (trisomy 18)?
A: Edward’s syndrome presents with micrognathia, low-set ears, rocker bottom feet, and overlapping of fingers.
Q: What are the main features of Noonan syndrome?
A: Noonan syndrome is characterized by a webbed neck, pectus excavatum, short stature, and pulmonary stenosis.
Q: What are the key features of Fragile X syndrome?
A: Fragile X syndrome presents with learning difficulties, macrocephaly, long face, large ears, and macro-orchidism.
Q: What are the key features of Pierre-Robin syndrome?
A: Pierre-Robin syndrome involves micrognathia, posterior displacement of the tongue (which may cause upper airway obstruction), and cleft palate.
Q: What are the main features of Prader-Willi syndrome?
A: Prader-Willi syndrome presents with hypotonia, hypogonadism, and obesity.
Q: What are the key features of William’s syndrome?
A: William’s syndrome is characterized by short stature, learning difficulties, a friendly and extrovert personality, transient neonatal hypercalcaemia, and supravalvular aortic stenosis.
Q: Which congenital heart defect is more common in adults, VSD or ASD?
A: Atrial septal defect (ASD) is more commonly diagnosed in adults, as it typically presents later in life compared to ventricular septal defects (VSD).
Q: What are the key features of Cri du chat syndrome (chromosome 5p deletion syndrome)?
A: Cri du chat syndrome presents with a characteristic cry due to larynx and neurological problems, feeding difficulties, poor weight gain, learning difficulties, microcephaly, micrognathism, and hypertelorism.
Q: What is congenital diaphragmatic hernia (CDH) and how common is it?
A: CDH is a condition where abdominal viscera herniate into the chest due to incomplete diaphragm formation. It occurs in around 1 in 2,000 newborns.
Q: Which congenital heart defect is more common at birth, tetralogy of Fallot or transposition of the great arteries (TGA)?
A: At birth, transposition of the great arteries (TGA) is more common, while tetralogy of Fallot typically presents later, around 1-2 months of age.
Q: How is coeliac disease diagnosed?
A: Diagnosis is confirmed by a jejunal biopsy showing subtotal villous atrophy. Anti-endomysial and anti-gliadin antibodies are also useful screening tests.
Q: What are the problems associated with cleft lip and palate?
A: Problems include feeding difficulties (orthodontic devices may help), speech issues (75% of children develop normal speech with speech therapy), and an increased risk of otitis media for cleft palate babies.
Q: What is the typical management for cleft lip and palate?
A: Cleft lip is repaired earlier, typically within the first week to three months of life, and cleft palates are repaired between 6-12 months of age.
Q: What are the most common causes of acyanotic congenital heart disease?
A: The most common causes of acyanotic congenital heart disease are ventricular septal defects (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), coarctation of the aorta, and aortic valve stenosis.
Q: What are the most common causes of cyanotic congenital heart disease?
A: The most common causes of cyanotic congenital heart disease are tetralogy of Fallot, transposition of the great arteries (TGA), and tricuspid atresia.
Q: What are the characteristic features of rubella in congenital infections?
A: The characteristic features of rubella include sensorineural deafness, congenital cataracts, congenital heart disease (e.g., patent ductus arteriosus), glaucoma, cerebral calcification, chorioretinitis, and hydrocephalus.
Q: What are the characteristic features of toxoplasmosis in congenital infections?
A: The characteristic features of toxoplasmosis include growth retardation, hepatosplenomegaly, purpuric skin lesions, ‘salt and pepper’ chorioretinitis, microphthalmia, cerebral palsy, anaemia, and visual impairment.
Q: Does pulmonary valve stenosis cause cyanosis, and what affects its presence?
A: The presence of cyanosis in pulmonary valve stenosis depends on the severity of the stenosis and any coexisting defects.
Q: What is the pathophysiology of cleft lip and palate?
A: Cleft lip results from failure of the fronto-nasal and maxillary processes to fuse, while cleft palate results from failure of the palatine processes and nasal septum to fuse. It has a polygenic inheritance, and maternal antiepileptic use increases the risk.
Q: What are the typical features of coeliac disease in children?
A: Features may coincide with the introduction of cereals and include failure to thrive, diarrhoea, abdominal distension, and anaemia in older children. Many cases are not diagnosed until adulthood.
Q: What is the prognosis for newborns with congenital diaphragmatic hernia (CDH)?
A: Despite modern medical interventions, only around 50% of newborns with CDH survive.
Q: What are the characteristic features of cytomegalovirus (CMV) in congenital infections?
A: The characteristic features of cytomegalovirus include sensorineural deafness, microcephaly, cerebral palsy, learning disability, encephalitis/seizures, pneumonitis, hepatosplenomegaly, anaemia, jaundice, and cerebral palsy.
Q: Which is the most common congenital infection in the UK?
A: Cytomegalovirus (CMV) is the most common congenital infection in the UK.
Q: What are the Fraser Guidelines for providing contraceptives to patients under 16 years old?
A: The Fraser Guidelines state that contraceptive treatment can be provided to those under 16 if: they understand the advice, cannot be persuaded to inform their parents, are likely to have sexual intercourse, their health may suffer without treatment, and their best interests require contraceptive advice or treatment.
Q: How is maternal infection typically characterized in cytomegalovirus?
A: Maternal infection with cytomegalovirus is usually asymptomatic.
Q: What is the legal age for a child to give consent to treatment?
A: Children under 16 years can consent to treatment if deemed competent (e.g., under Fraser guidelines), but they cannot refuse treatment deemed in their best interest. Between 16-18 years, competence is presumed. Children over 18 years can consent or refuse treatment.
Q: What is the frequency of bowel movements considered a sign of constipation in children under 1 year old?
A: Fewer than 3 complete stools per week (type 3 or 4 on the Bristol Stool Form Scale), except for exclusively breastfed babies after 6 weeks of age.
Q: What should be considered when diagnosing constipation in children?
A: Exclude secondary causes, such as neurological problems, abdominal distension, and faltering growth. Idiopathic constipation can be diagnosed if no red or amber flags are present.
Q: What are some common causes of constipation in children?
A: Dehydration, low-fibre diet, medications (e.g., opiates), anal fissure, over-enthusiastic potty training, hypothyroidism, Hirschsprung’s disease, hypercalcaemia, learning disabilities.
Q: What are the first-line treatments for faecal impaction in children?
A: Polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain), with an escalating dose regimen. If no disimpaction after 2 weeks, add a stimulant laxative.
Q: What should be included in maintenance therapy for constipation in children?
A: Movicol Paediatric Plain as first-line; if no response, add a stimulant laxative. If not tolerated, substitute with another laxative (e.g., lactulose or docusate) and continue for several weeks after regular bowel habits are established.
Q: What management strategies should be considered for young infants (under 6 months) with constipation?
A: For bottle-fed infants, offer extra water between feeds and try gentle abdominal massage. For breast-fed infants, constipation is unusual, and organic causes should be considered.
Q: What additional interventions can help in managing constipation in weaned infants?
A: Offer extra water, diluted fruit juice, fruits, and if not effective, consider adding lactulose.
Q: When does cow’s milk protein intolerance/allergy typically present in infants?
A: In the first 3 months of life, especially in formula-fed infants.
Q: What are common features of cow’s milk protein intolerance/allergy in infants?
A: Regurgitation, vomiting, diarrhoea, urticaria, atopic eczema, irritability, crying (colic), wheeze, chronic cough, and in rare cases, angioedema and anaphylaxis.
Q: What formula should be used for infants with severe cow’s milk protein allergy (CMPA) or those who do not respond to eHF?
A: Amino acid-based formula (AAF).
Q: What are the main diagnostic methods for cow’s milk protein intolerance/allergy?
A: Clinical improvement with elimination of cow’s milk protein, skin prick/patch testing, total IgE, and specific IgE (RAST) for cow’s milk protein.
Q: What is the first-line formula replacement for formula-fed infants with mild-moderate symptoms of CMPI/CMPA?
A: Extensive hydrolysed formula (eHF).
Q: How should a breastfeeding mother manage cow’s milk protein intolerance/allergy in their baby?
A: Continue breastfeeding while eliminating cow’s milk protein from the maternal diet. Calcium supplements may be prescribed to prevent deficiency.
Q: What is the approach for testing tolerance to milk in children with cow’s milk protein intolerance/allergy?
A: A challenge is often performed in a hospital setting due to the risk of anaphylaxis.
Q: What is the typical prognosis for children with cow’s milk protein intolerance/allergy?
A: Most children resolve CMPI, with around 55% of children with IgE mediated intolerance becoming milk-tolerant by age 5, and most children with non-IgE mediated intolerance becoming milk-tolerant by age 3.
Q: When is croup more commonly seen?
A: Croup is more common in the autumn.
Q: What is croup and what causes it?
A: Croup is an upper respiratory tract infection seen in infants and toddlers, characterised by stridor caused by laryngeal oedema and secretions. Parainfluenza viruses account for the majority of cases.
Q: At what age is croup most common?
A: Peak incidence occurs between 6 months and 3 years.
Q: Why should the throat not be examined in a child with croup?
A: Examining the throat may precipitate airway obstruction.
Q: What are the characteristic features of croup?
A: Barking, seal-like cough, worse at night, stridor, fever, coryzal symptoms, increased work of breathing (e.g. retraction).
Q: When should a child with croup be admitted to hospital?
A: Any child with moderate or severe croup, those <3 months of age, with known upper airway abnormalities, or if there is uncertainty about the diagnosis.
Q: How is the severity of croup graded?
Mild: Occasional barking cough, no audible stridor at rest, no or mild retraction, happy child.
Moderate: Frequent barking cough, audible stridor at rest, mild retraction, placatable child.
Severe: Frequent barking cough, prominent stridor, marked retractions, significant distress, tachycardia.
Q: What are the differential diagnoses to consider in a child with croup?
A: Acute epiglottitis, bacterial tracheitis, peritonsillar abscess, and foreign body inhalation.
Q: What signs may be seen on a chest x-ray in a child with croup?
A: A posterior-anterior view will show subglottic narrowing, known as the ‘steeple sign’.
Q: What is the recommended first-line management for croup?
A: A single dose of oral dexamethasone (0.15 mg/kg) to all children, regardless of severity.
Q: What are the emergency treatments for severe croup?
A: High-flow oxygen and nebulised adrenaline.
Q: What is the difference between peripheral and central cyanosis in the neonatal period?
A: Peripheral cyanosis, such as on the hands and feet, is common in the first 24 hours of life and may occur when the baby is crying or unwell. Central cyanosis occurs when the concentration of reduced haemoglobin exceeds 5g/dl.
Q: When may peripheral cyanosis be observed in neonates?
A: Peripheral cyanosis is very common in the first 24 hours of life, especially when the baby is crying or unwell.
Q: How can central cyanosis be clinically recognised in neonates?
A: Central cyanosis is recognised when the concentration of reduced haemoglobin in the blood exceeds 5g/dl.
Q: What is the nitrogen washout test (hyperoxia test), and how does it help in diagnosing cyanosis?
A: The nitrogen washout test involves giving 100% oxygen for 10 minutes and then measuring arterial blood gases. A pO2 of less than 15 kPa indicates cyanotic congenital heart disease.
Q: What are the causes of cyanotic congenital heart disease in neonates?
A: Causes include tetralogy of Fallot (TOF), transposition of the great arteries (TGA), and tricuspid atresia.
Q: What is the initial management for suspected cyanotic congenital heart disease in neonates?
A: Initial management includes supportive care and the administration of prostaglandin E1 (e.g., alprostadil) to maintain a patent ductus arteriosus in ductal-dependent congenital heart defects.
Q: What is acrocyanosis and when is it commonly seen in neonates?
A: Acrocyanosis refers to cyanosis around the mouth and extremities, seen in healthy newborns. It is common and may persist for 24 to 48 hours after birth.
Q: How can acrocyanosis be differentiated from other causes of peripheral cyanosis in neonates?
A: Acrocyanosis occurs immediately after birth in healthy infants and is not associated with significant pathology. It typically resolves within 24 to 48 hours.
Q: What is cystic fibrosis and what causes it?
A: Cystic fibrosis (CF) is an autosomal recessive disorder caused by a defect in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, leading to increased viscosity of secretions, affecting organs like the lungs and pancreas.
Q: What is the most common genetic mutation in cystic fibrosis in the UK?
A: In the UK, 80% of cystic fibrosis cases are due to the delta F508 mutation on the long arm of chromosome 7.
Q: What organisms are commonly found in patients with cystic fibrosis?
A: Common organisms that colonise CF patients include Staphylococcus aureus, Pseudomonas aeruginosa, Burkholderia cepacia, and Aspergillus.
Q: What are some causes of a false positive sweat test?
A: Causes of a false positive sweat test include malnutrition, adrenal insufficiency, glycogen storage diseases, nephrogenic diabetes insipidus, hypothyroidism, hypoparathyroidism, G6PD deficiency, and ectodermal dysplasia.
Q: What is the sweat test used for in diagnosing cystic fibrosis?
A: The sweat test measures sweat chloride levels; patients with cystic fibrosis have abnormally high sweat chloride. A normal value is < 40 mEq/l, and CF is indicated by a value > 60 mEq/l.
Q: What is the most common reason for a false negative sweat test?
A: The most common reason for a false negative sweat test is skin oedema, often due to hypoalbuminaemia or hypoproteinaemia secondary to pancreatic exocrine insufficiency.
Q: What are the common presenting features of cystic fibrosis in the neonatal period?
A: Common presenting features in the neonatal period include meconium ileus (around 20%) and, less commonly, prolonged jaundice.
Q: What are common presenting features of cystic fibrosis in early childhood?
A: Recurrent chest infections (40%), malabsorption with steatorrhoea and failure to thrive (30%), and liver disease (10%) are common presenting features.
Q: What is a key part of the daily management for cystic fibrosis?
A: Regular chest physiotherapy and postural drainage, at least twice daily, along with deep breathing exercises.
Q: Where are dermoid cysts most commonly located?
A: Common locations include the midline of the neck, external angle of the eye, and posterior to the pinna of the ear.
Q: What supplements should cystic fibrosis patients take?
A: Vitamin supplementation and pancreatic enzyme supplements with meals.
Q: What are some other features of cystic fibrosis?
A: Other features include short stature, diabetes mellitus, delayed puberty, rectal prolapse, nasal polyps, male infertility, and female subfertility.
Q: What other sites may dermoid cysts develop in, aside from the skin?
A: Dermoid cysts can also develop in the ovary, where they are considered teratomas.
Q: What is a dermoid cyst?
A: A cutaneous dermoid cyst develops at sites of embryonic developmental fusion, often found in the midline of the neck, external angle of the eye, and posterior to the ear, containing inclusions like hair follicles.
Q: What dietary recommendation is given to patients with cystic fibrosis?
A: A high-calorie diet, including high fat intake, is recommended.
Q: What is a contraindication for lung transplantation in cystic fibrosis patients?
A: Chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation.
What drugs can you use in CF
Lumacaftor/Ivacaftor
Q: Why should cystic fibrosis patients minimize contact with each other?
A: To prevent cross-infection with Burkholderia cepacia complex and Pseudomonas aeruginosa.
Q: What is the key feature of dermoid cysts?
A: Dermoid cysts typically have multiple inclusions, such as hair follicles, that bud out from their walls.
Q: What is a desmoid tumour?
A: A desmoid tumour is a type of fibrous tumour, either classified as low-grade fibrosarcoma or non-aggressive fibrous tumour, often presenting as large, infiltrative masses.
Q: How are desmoid tumours categorized?
A: Desmoid tumours are categorized into abdominal, extra-abdominal, and intra-abdominal types, based on their location.
Q: What does developmental delay refer to?
A: Developmental delay refers to a significant lag in a child’s physical, cognitive, behavioural, emotional, or social development relative to established growth milestones.
Q: What is an example referral point for developmental delay in a child?
A: Examples include not smiling at 10 weeks, not sitting unsupported at 12 months, or not walking at 18 months.
Q: What does hand preference before 12 months potentially indicate?
A: Hand preference before 12 months may indicate cerebral palsy.
Q: What are the most common causes of gross motor problems in children?
A: Common causes include variations of normal development, cerebral palsy, and neuromuscular disorders like Duchenne muscular dystrophy.
Q: What should be checked if a child has speech and language problems?
A: Hearing should always be checked, along with considering other causes such as environmental deprivation or general developmental delay.
Q: What are some common differential diagnoses for developmental delay?
A: Differential diagnoses include Autism Spectrum Disorder (ASD), cerebral palsy, Fragile X syndrome, Down syndrome, and fetal alcohol spectrum disorders (FASDs).
Q: What is the initial management approach for a child with suspected developmental delay?
A: The initial management involves a clinical examination, investigations (genetic testing, neuroimaging, hearing/vision assessments), referrals for specialist assessments, and early intervention services.
Q: What is developmental dysplasia of the hip (DDH)?
A: DDH is a condition where the hip joint does not develop properly, and is gradually replacing the term ‘congenital dislocation of the hip’ (CDH). It affects around 1-3% of newborns.
Q: What are the risk factors for DDH?
A: Risk factors include female sex, breech presentation, positive family history, firstborn children, oligohydramnios, birth weight > 5 kg, and congenital calcaneovalgus foot deformity.
Q: Is DDH more common in one hip?
A: DDH is slightly more common in the left hip, and around 20% of cases are bilateral.
Q: Which infants require a routine ultrasound examination for DDH?
A: Infants with a first-degree family history of hip problems, breech presentation at or after 36 weeks gestation, or multiple pregnancies require routine ultrasound examination.
Q: How are DDH cases screened in infants?
A: DDH is screened using the Barlow and Ortolani tests at the newborn check and six-week baby check.
Q: What does the Barlow test assess in DDH?
A: The Barlow test attempts to dislocate an articulated femoral head.
Q: What does the Ortolani test assess in DDH?
A: The Ortolani test attempts to relocate a dislocated femoral head.
Q: What factors are important in clinical examination for DDH?
A: Important factors include symmetry of leg length, the level of knees when hips and knees are flexed, and restricted abduction of the hip in flexion.
Q: What is the first-line imaging for DDH in infants under 4.5 months old?
A: Ultrasound is generally used to confirm the diagnosis if DDH is clinically suspected.
Q: What is the first-line imaging for DDH in infants over 4.5 months old?
A: X-ray is the first-line investigation in infants older than 4.5 months.
Q: What is the management for most unstable hips in DDH?
A: Most unstable hips will spontaneously stabilize by 3-6 weeks of age.
Q: What is the treatment for DDH in children younger than 4-5 months?
A: The Pavlik harness (a dynamic flexion-abduction orthosis) is used for children younger than 4-5 months.
Q: What is the treatment for DDH in older children?
A: Older children may require surgery for DDH management.
Q: What fine motor milestone is expected at 3 months?
A: At 3 months, the infant reaches for objects, holds a rattle briefly if given to hand, and is visually alert, particularly to human faces. They can fixate and follow objects to 180 degrees.
Q: What fine motor milestone is expected at 6 months?
A: At 6 months, the infant holds objects in a palmar grasp, passes objects from one hand to another, and is visually insatiable, looking around in all directions.
Q: What fine motor milestone is expected at 9 months?
A: At 9 months, the infant points with their finger and demonstrates an early pincer grip.
Q: What is the expected tower building milestone for an 18-month-old?
A: At 18 months, the child is expected to build a tower of 3 blocks.
Q: What fine motor milestone is expected at 12 months?
A: At 12 months, the infant has a good pincer grip and can bang toys together.
Q: What is the expected tower building milestone for a 15-month-old?
A: At 15 months, the child is expected to build a tower of 2 blocks.
Q: What is the expected tower building milestone for a 2-year-old?
A: At 2 years, the child is expected to build a tower of 6 blocks.
Q: What is the expected tower building milestone for a 3-year-old?
A: At 3 years, the child is expected to build a tower of 9 blocks.
Q: What drawing milestone is expected at 2 years?
A: At 2 years, the child is expected to copy a vertical line.
Q: What drawing milestone is expected at 18 months?
A: At 18 months, the child is expected to make a circular scribble.
Q: What drawing milestone is expected at 3 years?
A: At 3 years, the child is expected to copy a circle.
Q: What drawing milestone is expected at 4 years?
A: At 4 years, the child is expected to copy a cross.
Q: What drawing milestone is expected at 5 years?
A: At 5 years, the child is expected to copy a square and triangle.
Q: What book milestone is expected at 15 months?
A: At 15 months, the child looks at a book and pats the page.
Q: What book milestone is expected at 18 months?
A: At 18 months, the child turns pages, several at a time.
Q: What book milestone is expected at 2 years?
A: At 2 years, the child turns pages, one at a time.
Q: What is considered abnormal in hand preference before 12 months?
Q: What is considered abnormal in hand preference before 12 months?
Q: What gross motor milestone is expected at 3 months?
A: At 3 months, there is little or no head lag when being pulled to sit, and the infant has good head control when lying on their abdomen.
Q: What gross motor milestone is expected at 6 months?
A: At 6 months, the infant lies on their abdomen with arms extended, lies on their back and lifts and grasps their feet, pulls themselves to sitting, and has a straight back when held in sitting. The infant also rolls from front to back.
Q: What gross motor milestone is expected at 7-8 months?
A: At 7-8 months, the infant sits without support. (Referral is required at 12 months if not achieved.)
Q: What gross motor milestone is expected at 9 months?
A: At 9 months, the infant pulls to standing and begins crawling.
Q: What gross motor milestone is expected at 12 months?
A: At 12 months, the infant cruises (walks while holding onto furniture) and walks with one hand held.
Q: What gross motor milestone is expected at 13-15 months?
A: At 13-15 months, the infant walks unsupported (Referral is required at 18 months if not achieved).
Q: What gross motor milestone is expected at 18 months?
A: At 18 months, the child squats to pick up a toy.
Q: What gross motor milestone is expected at 2 years?
A: At 2 years, the child runs and walks upstairs and downstairs while holding onto the rail.
Q: What gross motor milestone is expected at 3 years?
A: At 3 years, the child rides a tricycle using pedals and walks up stairs without holding onto the rail.
Q: What gross motor milestone is expected at 4 years?
A: At 4 years, the child hops on one leg.
Q: What is considered a normal variant in crawling before walking?
A: While most children crawl on all fours before walking, some children may ‘bottom-shuffle,’ which is a normal variant that runs in families.
Q: What social milestone is expected at 6 weeks?
A: At 6 weeks, the infant smiles. (Referral is required at 10 weeks if not achieved.)
Q: What social milestone is expected at 3 months?
A: At 3 months, the infant laughs and enjoys friendly handling.
Q: What social milestone is expected at 6 months?
A: At 6 months, the infant is not shy.
Q: What social milestone is expected at 9 months?
A: At 9 months, the infant becomes shy and takes everything to their mouth.
Q: What feeding milestone is expected at 6 months?
A: At 6 months, the infant may put their hand on the bottle when being fed.
Q: What feeding milestone is expected between 12-15 months?
A: Between 12-15 months, the child drinks from a cup and uses a spoon, developing these skills over the next 3 months.
Q: What feeding milestone is expected at 2 years?
A: At 2 years, the child becomes competent with a spoon and does not spill when using a cup.
Q: What feeding milestone is expected at 3 years?
A: At 3 years, the child uses both a spoon and fork.
Q: What feeding milestone is expected at 5 years?
A: At 5 years, the child uses a knife and fork.
Q: What dressing milestone is expected between 12-15 months?
A: Between 12-15 months, the child helps with getting dressed or undressed.
Q: What dressing milestone is expected at 18 months?
A: At 18 months, the child can take off their shoes and hat but is unable to replace them.
Q: What dressing milestone is expected at 2 years?
A: At 2 years, the child can put on a hat and shoes.
Q: What dressing milestone is expected at 4 years?
A: At 4 years, the child can dress and undress independently, except for laces and buttons.
Q: What play milestone is expected at 9 months?
A: At 9 months, the infant plays ‘peek-a-boo.’
Q: What play milestone is expected at 12 months?
A: At 12 months, the infant waves ‘bye-bye’ and plays ‘pat-a-cake.’
Q: What play milestone is expected at 18 months?
A: At 18 months, the child plays contentedly alone.
Q: What play milestone is expected at 2 years?
A: At 2 years, the child plays near others, but not yet with them.
Q: What play milestone is expected at 4 years?
A: At 4 years, the child plays with other children.
Q: What speech and hearing milestone is expected at 3 months?
A: At 3 months, the infant quietens to their parent’s voice, turns towards sound, and squeals.
Q: What speech and hearing milestone is expected at 6 months?
A: At 6 months, the infant says double syllables like ‘adah’ and ‘erleh.’
Q: What speech and hearing milestone is expected at 9 months?
A: At 9 months, the infant says ‘mama’ and ‘dada’ and understands ‘no.’
Q: What speech and hearing milestone is expected at 12 months?
A: At 12 months, the child knows and responds to their own name.
Q: What speech and hearing milestone is expected between 12-15 months?
A: Between 12-15 months, the child knows about 2-6 words and understands simple commands like ‘give it to mummy.’ (Referral is needed at 18 months.)
Q: What speech and hearing milestone is expected at 2 years?
A: At 2 years, the child combines two words and points to parts of the body.
Q: What speech and hearing milestone is expected at 2½ years?
A: At 2½ years, the child has a vocabulary of about 200 words.
Q: What speech and hearing milestone is expected at 3 years?
A: At 3 years, the child talks in short sentences (3-5 words), asks ‘what’ and ‘who’ questions, identifies colours, and counts to 10 with little appreciation of numbers.
Q: What speech and hearing milestone is expected at 4 years?
A: At 4 years, the child asks ‘why’, ‘when’, and ‘how’ questions.
Q: What is the most common cause of gastroenteritis in children in the UK?
A: The most common cause of gastroenteritis in children in the UK is rotavirus.
Q: What is the typical duration of diarrhoea and vomiting in children?
A: Diarrhoea usually lasts for 5-7 days and stops within 2 weeks. Vomiting usually lasts for 1-2 days and stops within 3 days.
Q: What are the clinical features of dehydration in children?
A: Clinical dehydration features include sunken eyes, dry mucous membranes, tachycardia, tachypnoea, normal peripheral pulses, normal capillary refill time, and reduced skin turgor.
Q: What are the clinical features of shock in children?
A: Clinical shock features include decreased level of consciousness, cold extremities, pale or mottled skin, tachycardia, tachypnoea, weak peripheral pulses, prolonged capillary refill time, and hypotension.
Q: Which children are at increased risk of dehydration?
A: Children at increased risk of dehydration include those younger than 1 year (especially those under 6 months), low birth weight infants, those who have passed six or more diarrhoeal stools in 24 hours, those who have vomited three or more times, and those who haven’t been offered or tolerated fluids.
Q: What features suggest hypernatraemic dehydration in children?
A: Features of hypernatraemic dehydration include jittery movements, increased muscle tone, hyperreflexia, convulsions, drowsiness, or coma.
Q: When should a stool culture be performed in children with diarrhoea and vomiting?
A: Stool culture should be done if you suspect septicaemia, there is blood/mucus in the stool, or if the child is immunocompromised. Consider it if the child has recently been abroad, diarrhoea hasn’t improved by day 7, or there is diagnostic uncertainty.
Q: What is the management for children with no evidence of dehydration?
A: For children with no dehydration, continue breastfeeding, encourage fluid intake, and discourage fruit juices and carbonated drinks.
Q: What is the management for children with suspected dehydration?
A: For suspected dehydration, give 50 ml/kg of low osmolarity oral rehydration solution (ORS) over 4 hours, continue breastfeeding, and supplement with usual fluids, avoiding fruit juices and carbonated drinks.
Q: What is the most common cause of chronic diarrhoea in infants in the developed world?
A: The most common cause is cows’ milk intolerance.
