Membership of the Royal College of Paediatrics and Child Health (MRCPCH) General Paediatrics and Systems Medicine Flashcards

24 sample cards from the General Paediatrics and Systems Medicine deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. How are the causes of acute kidney injury (AKI) classified, with paediatric examples?

   Pre-renal (hypovolaemia, sepsis, dehydration — commonest), renal/intrinsic (HUS, glomerulonephritis, ATN, nephrotoxins), and post-renal (obstruction — posterior urethral valves, stones).

2. How is hypertension defined in children and what is the commonest secondary cause?

   BP $\geq 95^{\text{th}}$ percentile for age, sex and height on $\geq 3$ occasions. Unlike adults, most paediatric hypertension is secondary — the commonest cause is renal/renovascular disease (e.g. reflux nephropathy, renal artery stenosis, coarctation).

3. What defines primary nocturnal enuresis and the first-line interventions?

   Involuntary night-time wetting in a child $\geq 5$ years who has never been reliably dry. First-line after lifestyle/fluid advice: enuresis alarm; desmopressin for short-term/rapid control (e.g. sleepovers) or alarm failure.

4. How do you quantify clinically significant proteinuria in children?

   Early-morning urine protein:creatinine ratio (uPCR) $> 20\,\text{mg/mmol}$ is abnormal; nephrotic-range is $> 250\,\text{mg/mmol}$. A 24-h collection $> 40\,\text{mg/m}^2/\text{h}$ is nephrotic. Orthostatic proteinuria is benign (absent in early-morning sample).

5. State the biochemical diagnostic criteria for diabetic ketoacidosis (DKA) in children.

   Hyperglycaemia (blood glucose $>11\,\text{mmol/L}$), ketonaemia ($\geq 3\,\text{mmol/L}$) or significant ketonuria, and acidosis (venous $\text{pH} < 7.3$ or bicarbonate $< 15\,\text{mmol/L}$).

6. What is the most feared complication of DKA treatment in children and how is its risk reduced?

   Cerebral oedema (the leading cause of DKA death in children). Risk reduced by cautious fluid rehydration over 48 h, delaying insulin until 1 h after fluids start, and avoiding rapid falls in glucose/osmolality; treat with hypertonic saline or mannitol.

7. How are the principal causes of congenital hypothyroidism and acquired hypothyroidism in children distinguished?

   Congenital: thyroid dysgenesis/agenesis (commonest), dyshormonogenesis, iodine deficiency — detected on newborn screening (raised TSH), must be treated early to prevent intellectual disability. Acquired: most often autoimmune (Hashimoto) thyroiditis.

8. Define short stature and list the key 'pathological' patterns to recognise on a growth chart.

   Height below the $2^{\text{nd}}$ centile (or $-2$ SD), or crossing down $\geq 2$ centiles. Pathological clues: low height velocity, height well below mid-parental target, or disproportion. Causes: familial/constitutional delay (commonest, normal velocity) vs endocrine (GH deficiency, hypothyroid), Turner syndrome, chronic disease.

9. Define precocious puberty and contrast central (gonadotrophin-dependent) vs peripheral types.

   Onset of secondary sexual characteristics before age 8 (girls) or 9 (boys). Central (GnRH-dependent): early HPG-axis activation, raised LH/FSH, often idiopathic in girls. Peripheral (GnRH-independent): sex steroids from gonad/adrenal/tumour, suppressed LH/FSH (e.g. CAH, McCune–Albright).

10. Describe the typical presentation of classic salt-wasting congenital adrenal hyperplasia (21-hydroxylase deficiency).

    Autosomal recessive 21-hydroxylase deficiency causes cortisol/aldosterone deficiency with androgen excess. Females: virilised/ambiguous genitalia. Both sexes: salt-wasting adrenal crisis at 1–3 weeks with hyponatraemia, hyperkalaemia, hypoglycaemia; raised 17-hydroxyprogesterone.

11. What clinical clues should prompt suspicion of an inborn error of metabolism in a neonate/infant?

    Encephalopathy/lethargy, poor feeding and vomiting after a symptom-free interval, hypoglycaemia, metabolic acidosis with raised anion gap, hyperammonaemia, unusual odour, and a history of consanguinity or unexplained sibling deaths.

12. Use red cell indices to classify the anaemias and give a paediatric example of each.

    Microcytic (low MCV): iron deficiency (commonest), thalassaemia. Normocytic: acute blood loss, haemolysis, anaemia of chronic disease. Macrocytic (high MCV): $\text{B}_{12}$/folate deficiency, hypothyroidism.

13. Contrast the inheritance and lab findings of haemophilia A vs von Willebrand disease.

    Haemophilia A: X-linked recessive Factor VIII deficiency — prolonged APTT, normal PT/platelets, deep bleeds/haemarthroses. von Willebrand disease: autosomal dominant — mucocutaneous bleeding, prolonged bleeding time/APTT, low vWF and reduced platelet adhesion.

14. What is the commonest childhood malignancy, its peak age, and classic presenting features?

    Acute lymphoblastic leukaemia (ALL), peak age 2–5 years. Presents with marrow failure: anaemia (pallor, lethargy), thrombocytopenia (bruising/petechiae), neutropenia (infection), plus bone pain, hepatosplenomegaly and lymphadenopathy.

15. What are the 'red flag' features of lymphadenopathy in a child that suggest malignancy?

    Nodes $>2\,\text{cm}$, hard/matted/fixed, non-tender, supraclavicular location, persistent $>4$–$6$ weeks or progressively enlarging, plus systemic 'B' symptoms (fever, night sweats, weight loss) or hepatosplenomegaly.

16. Distinguish neuroblastoma from Wilms tumour (nephroblastoma) as childhood abdominal masses.

    Neuroblastoma: arises from adrenal/sympathetic chain, may cross the midline, raised urinary catecholamines (VMA/HVA), under age 5. Wilms tumour: arises from kidney, usually does not cross midline, haematuria, associated with WT1 syndromes (WAGR, Beckwith–Wiedemann).

17. List the 'traffic light' / NICE red features that mark a febrile child as high risk for serious illness.

    Pale/mottled/blue skin, no response to social cues / appears ill / weak high-pitched cry, grunting, RR $>60$, moderate–severe chest indrawing, reduced skin turgor, non-blanching rash, bulging fontanelle, neck stiffness, status/focal seizures, age $<3$ months with temp $\geq 38^{\circ}\text{C}$.

18. What are the commonest causes of bacterial meningitis by age group in children?

    Neonates: Group B Streptococcus, E. coli, Listeria. Infants/children: Neisseria meningitidis and Streptococcus pneumoniae; Haemophilus influenzae type b now rare due to vaccination.

19. Interpret typical CSF findings in bacterial vs viral meningitis.

    Bacterial: cloudy, raised neutrophils (polymorphs), high protein, LOW glucose (CSF:plasma ratio $<0.4$), high opening pressure. Viral: clear, lymphocytes, normal/mildly raised protein, normal glucose.

20. Match these childhood exanthems to their classic features: measles, rubella, erythema infectiosum, roseola, scarlet fever.

    Measles: Koplik spots, descending maculopapular rash, coryza/conjunctivitis. Rubella: pink rash + suboccipital lymphadenopathy. Erythema infectiosum (parvovirus B19): 'slapped cheek'. Roseola (HHV-6): high fever then rash as fever resolves. Scarlet fever (Group A Strep): sandpaper rash, strawberry tongue, perioral sparing.

21. How does primary pulmonary tuberculosis typically present in children and what is the standard treatment regimen?

    Often asymptomatic or with chronic cough, fever, weight loss, lymphadenopathy (Ghon focus + hilar nodes = primary/Ghon complex). Treatment: 2 months of Rifampicin, Isoniazid, Pyrazinamide, Ethambutol (RIPE), then 4 months Rifampicin + Isoniazid.

22. List the routine UK childhood immunisations given at 8, 12 and 16 weeks.

    8 weeks: 6-in-1 (DTaP/IPV/Hib/HepB), MenB, rotavirus. 12 weeks: 6-in-1, pneumococcal (PCV), rotavirus. 16 weeks: 6-in-1, MenB. (MMR given at 1 year.)

23. What is the difference between live-attenuated and inactivated vaccines, with examples, and a key contraindication?

    Live-attenuated (MMR, BCG, rotavirus, nasal flu, varicella): weakened organism giving strong durable immunity but contraindicated in significant immunosuppression/pregnancy. Inactivated/subunit (6-in-1, PCV, HPV): cannot replicate, safer in immunocompromise but often need boosters.

24. What pattern of infections suggests a primary immunodeficiency, and which type is most common?

    Recurrent, Severe, Persistent, Unusual organisms/sites infections plus failure to thrive and family history ('SPUR'). Antibody (B-cell) deficiencies (e.g. selective IgA deficiency, common variable immunodeficiency) are the commonest, causing recurrent sinopulmonary bacterial infections.

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