Membership of the Royal College of Paediatrics and Child Health (MRCPCH) Foundation of Practice: Core Science, Pharmacology and Acute Care Syllabus

Foundation of Practice: Core Science, Pharmacology and Acute Care syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Foundation of Practice: Core Science, Pharmacology and Acute Care in Membership of the Royal College of Paediatrics and Child Health (MRCPCH), not a summary of it.

1. 1

   Basic and Applied Sciences in Paediatrics

   5 topics

   • Genetics and inheritance
     • Mendelian, mitochondrial and polygenic inheritance
     • Imprinting, anticipation and trinucleotide repeats
     • Karyotyping, microarray and next-generation sequencing
   • Embryology and developmental biology
     • Organogenesis and critical periods
     • Teratogenesis and fetal programming
   • Immunology and inflammation
     • Innate and adaptive immunity
     • Hypersensitivity reactions
     • Cytokines and the inflammatory cascade
   • Cellular and molecular physiology
     • Membrane transport and ion channels
     • Receptor signalling pathways
   • Microbiology and host defence
2. 2

   Clinical Pharmacology and Therapeutics

   6 topics

   • Pharmacokinetics in children
     • Age-related absorption, distribution, metabolism and excretion
     • Volume of distribution and clearance in neonates
   • Pharmacodynamics and dose-response
   • Weight and surface-area-based prescribing
     • Safe paediatric dose calculation
     • Off-label and unlicensed medicines (BNFc)
   • Adverse drug reactions and interactions
   • Therapeutic drug monitoring
     • Aminoglycosides, vancomycin and anticonvulsants
   • Antimicrobial stewardship in children
3. 3

   Fluids, Electrolytes and Nutrition

   5 topics

   • Maintenance fluid requirements and isotonic fluids
   • Assessment and correction of dehydration
     • Clinical estimation of fluid deficit
     • Hypo- and hypernatraemic dehydration
   • Electrolyte disturbances
     • Sodium, potassium, calcium and magnesium
     • Acid-base balance interpretation
   • Enteral and parenteral nutrition
   • Faltering growth and nutritional assessment
4. 4

   Recognition and Management of the Acutely Unwell Child

   6 topics

   • Structured ABCDE assessment
     • Recognising the seriously ill child
     • Paediatric early warning scores (PEWS)
   • Paediatric Basic and Advanced Life Support (APLS/EPALS)
     • Cardiac arrest rhythms and algorithms
     • Choking and airway obstruction
   • Shock recognition and management
     • Septic, hypovolaemic, cardiogenic and distributive shock
   • Status epilepticus and the convulsing child
   • Anaphylaxis management
   • Major trauma and the injured child
5. 5

   Evidence-Based Practice and Clinical Governance

   4 topics

   • Critical appraisal and study design
     • RCTs, cohort and case-control studies
     • Sensitivity, specificity and predictive values
   • Statistics for clinicians
     • Relative risk, odds ratio and number needed to treat
     • Confidence intervals and p-values
   • Audit, quality improvement and PDSA cycles
   • Guidelines, NICE and shared decision-making

Foundation of Practice: Core Science, Pharmacology and Acute Care flashcards for Membership of the Royal College of Paediatrics and Child Health (MRCPCH)

23 of 57 cards from the Foundation of Practice: Core Science, Pharmacology and Acute Care deck — real questions with worked answers.

1. What is the difference between autosomal dominant and autosomal recessive inheritance in terms of carrier status and recurrence risk?

   Autosomal dominant: one mutant allele causes disease; affected individual has 50% chance of passing it to each child; no asymptomatic carriers (vertical transmission). Autosomal recessive: two mutant alleles needed; carriers are unaffected; two carrier parents have a 25% recurrence risk per child.

2. How does X-linked recessive inheritance present in males versus females, and what is the offspring risk for a carrier mother?

   Males (hemizygous) are affected because they have one X; females are usually unaffected carriers. A carrier mother passes the mutant allele to 50% of sons (affected) and 50% of daughters (carriers). Affected fathers cannot transmit to sons but all daughters become carriers.

3. Define anticipation and give a classic paediatric example.

   Anticipation is the tendency for a trinucleotide-repeat disorder to present earlier and more severely in successive generations as the repeat expands. Classic examples: myotonic dystrophy (CTG) and Fragile X syndrome (CGG).

4. What is genomic imprinting, and which two syndromes arise from the chromosome 15q11-q13 region?

   Genomic imprinting is parent-of-origin-specific gene expression (one allele silenced by methylation). Deletion/loss of the paternal 15q11-q13 causes Prader-Willi syndrome; loss of the maternal copy causes Angelman syndrome.

5. During embryology, which three germ layers form at gastrulation, and name one major derivative of each.

   Ectoderm (epidermis, nervous system), mesoderm (muscle, bone, kidneys, heart/blood), and endoderm (gut epithelium, liver, lungs, pancreas).

6. What embryological defect underlies a neural tube defect such as spina bifida, and which vitamin reduces its risk?

   Failure of neural tube closure around days 21-28 of gestation. Periconceptional folic acid (folate) supplementation reduces the risk; standard $400\ \mu g$/day, or $5\ mg$/day for high-risk pregnancies.

7. Compare the innate and adaptive immune systems regarding specificity, speed and memory.

   Innate immunity: non-specific, immediate (minutes-hours), no memory (e.g. neutrophils, macrophages, complement). Adaptive immunity: antigen-specific, slower on first exposure (days), generates immunological memory (B and T lymphocytes).

8. List the four Gell and Coombs hypersensitivity reaction types with one example each.

   Type I (IgE-mediated immediate, e.g. anaphylaxis); Type II (antibody-mediated cytotoxic, e.g. haemolytic disease of the newborn); Type III (immune-complex, e.g. post-streptococcal glomerulonephritis); Type IV (delayed cell-mediated, e.g. contact dermatitis, TB skin test).

9. Which immunoglobulin crosses the placenta, and what is the clinical relevance to neonatal immunity?

   IgG crosses the placenta, giving passive immunity in the first months of life. Maternal IgG wanes by ~3-6 months, producing a physiological nadir of immunoglobulins before the infant's own production matures.

10. What are the cardinal signs of acute inflammation, and which mediator drives the vascular vasodilation and increased permeability?

    Rubor (redness), calor (heat), tumor (swelling), dolor (pain) and functio laesa (loss of function). Histamine (with prostaglandins, bradykinin and nitric oxide) drives vasodilation and increased vascular permeability.

11. Describe the role of the sodium-potassium ATPase pump in maintaining the resting membrane potential.

    The $\ce{Na+/K+}$-ATPase actively exports 3 $\ce{Na+}$ and imports 2 $\ce{K+}$ per ATP, maintaining high intracellular $\ce{K+}$ and low intracellular $\ce{Na+}$. This gradient, with $\ce{K+}$ leak channels, sets the negative resting membrane potential (~$-70\ mV$).

12. What is the difference between primary active transport and secondary active (cotransport) transport?

    Primary active transport uses ATP directly to move a solute against its gradient (e.g. $\ce{Na+/K+}$-ATPase). Secondary active transport uses the electrochemical gradient created by primary transport to drive another solute, via symport or antiport (e.g. $\ce{Na+}$-glucose SGLT cotransporter).

13. Outline the central dogma of molecular biology.

    Genetic information flows: $$\text{DNA} \xrightarrow{\text{transcription}} \text{mRNA} \xrightarrow{\text{translation}} \text{protein}$$ DNA replicates itself, is transcribed into RNA, which is translated into protein (with reverse transcription as an exception).

14. Distinguish exotoxins from endotoxins in microbiology.

    Exotoxins are secreted proteins from Gram-positive and Gram-negative bacteria, highly potent, often heat-labile, and can be toxoided into vaccines (e.g. diphtheria, tetanus). Endotoxin is lipopolysaccharide (LPS) in the Gram-negative outer membrane, released on lysis, heat-stable, and triggers sepsis/fever.

15. What are the main components of host defence at the mucosal surface (first line) against microbes?

    Physical/chemical barriers: intact epithelium, mucus, cilia, low gastric pH, lysozyme in secretions, antimicrobial peptides (defensins), commensal flora competition, and secretory IgA on mucosal surfaces.

16. How do the volume of distribution and total body water differ in neonates compared with adults, and how does this affect dosing of water-soluble drugs?

    Neonates have a higher total body water (~75-80% body weight vs ~60% in adults) and larger volume of distribution for water-soluble drugs. This means a higher mg/kg loading dose is often needed to achieve target plasma concentrations.

17. Why are neonates at risk of toxicity from drugs that are hepatically metabolised, and give an example.

    Immature hepatic enzyme systems (reduced phase I oxidation and phase II glucuronidation) slow drug clearance, prolonging half-life. Classic example: chloramphenicol causing grey baby syndrome due to impaired glucuronidation.

18. State the formula relating clearance, volume of distribution and elimination half-life.

    $$t_{1/2} = \frac{0.693 \times V_{d}}{CL}$$ where $V_{d}$ is the volume of distribution and $CL$ is clearance. Half-life is directly proportional to $V_{d}$ and inversely proportional to clearance.

19. Define first-order versus zero-order elimination kinetics.

    First-order: a constant fraction of drug is eliminated per unit time; rate is proportional to concentration (most drugs). Zero-order: a constant amount is eliminated per unit time regardless of concentration because enzymes are saturated (e.g. phenytoin, ethanol, high-dose salicylates).

20. Define pharmacodynamics, and explain the terms efficacy and potency.

    Pharmacodynamics is what the drug does to the body (mechanism and concentration-effect relationship). Efficacy is the maximal effect a drug can produce ($E_{max}$). Potency is the amount of drug needed to produce a given effect, reflected by $EC_{50}$ (lower $EC_{50}$ = more potent).

21. Differentiate a competitive antagonist from a non-competitive antagonist on a dose-response curve.

    A competitive antagonist shifts the agonist dose-response curve to the right (higher $EC_{50}$) but $E_{max}$ is unchanged and surmountable by more agonist. A non-competitive antagonist reduces $E_{max}$ (insurmountable) and the curve cannot be fully restored by adding agonist.

22. What is the formula for calculating body surface area (BSA) using the Mosteller method?

    $$BSA\ (m^{2}) = \sqrt{\frac{\text{height (cm)} \times \text{weight (kg)}}{3600}}$$ BSA is used for dosing drugs such as chemotherapy where weight-based dosing is less accurate.

23. Why is body-surface-area-based dosing preferred over weight-based dosing for certain drugs in children?

    BSA correlates better with physiological parameters such as cardiac output, glomerular filtration rate and metabolic rate than weight alone. It avoids overdosing in small/obese children for narrow-therapeutic-index drugs like cytotoxics, though weight-based mg/kg dosing is standard for most paediatric prescribing.

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