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100+ Free MRCPCH TAS Practice Questions

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A neonate with ambiguous genitalia and salt-wasting crisis is found to have congenital adrenal hyperplasia. Which enzyme deficiency accounts for over 90% of cases?

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D
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Sample MRCPCH TAS Practice Questions

Try these sample questions to test your MRCPCH TAS exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A neonate with a patent ductus arteriosus is treated with intravenous ibuprofen to promote ductal closure. Which pharmacological action explains why this drug closes the duct?
A.Activation of guanylate cyclase increasing cyclic GMP
B.Stimulation of prostaglandin E2 receptors in ductal smooth muscle
C.Blockade of beta-adrenergic receptors in the ductal wall
D.Inhibition of cyclo-oxygenase, reducing prostaglandin E2 synthesis
Explanation: Patency of the ductus arteriosus is maintained by prostaglandin E2. NSAIDs such as ibuprofen and indomethacin inhibit cyclo-oxygenase (COX), lowering prostaglandin synthesis and allowing the duct to constrict and close. This is the basis for their use in haemodynamically significant PDA.
2Neonates handle many drugs differently from adults. Compared with adults, which pharmacokinetic feature is characteristic of the term neonate?
A.Reduced volume of distribution for water-soluble drugs
B.Increased total body water as a proportion of body weight
C.Faster hepatic glucuronidation of drugs such as morphine
D.Higher plasma albumin concentration than in adults
Explanation: Neonates have a higher proportion of total body water (around 75-80% of body weight versus ~60% in adults), which increases the volume of distribution of water-soluble drugs and often requires higher per-kilogram loading doses. Immature hepatic enzymes and lower albumin further alter handling.
3A child is started on phenytoin for seizures. Plotting serum concentration against dose shows that small dose increases cause disproportionately large rises in plasma level. What does this pattern indicate?
A.First-order elimination kinetics
B.Zero-order (saturable) elimination kinetics
C.Extensive enterohepatic recirculation
D.Rapid renal tubular secretion
Explanation: Phenytoin shows saturable (zero-order) kinetics: once the metabolising enzymes are saturated, a fixed amount is cleared per unit time regardless of concentration, so small dose increments produce large, non-linear rises in plasma level. This is why phenytoin requires careful dose titration and therapeutic drug monitoring.
4Salbutamol is given to a child with acute asthma. Through which receptor and second messenger does it relieve bronchospasm?
A.Histamine H1 receptor blockade preventing mast cell degranulation
B.Muscarinic M3 receptor blockade reducing acetylcholine effect
C.Alpha-1 adrenoceptor activation causing vasoconstriction
D.Beta-2 adrenoceptor activation increasing intracellular cyclic AMP
Explanation: Salbutamol is a selective beta-2 adrenoceptor agonist. Receptor activation stimulates adenylate cyclase, raising intracellular cyclic AMP, which relaxes airway smooth muscle and produces bronchodilation. Beta-2 agonists are first-line bronchodilators in acute asthma.
5A 6-year-old develops an acute dystonic reaction (oculogyric crisis and torticollis) shortly after receiving metoclopramide for vomiting. Which drug is the most appropriate immediate treatment?
A.Intravenous adrenaline
B.Intravenous procyclidine (an anticholinergic)
C.Oral diazepam alone
D.Intramuscular naloxone
Explanation: Acute dystonia from dopamine antagonists such as metoclopramide reflects a relative cholinergic-dopaminergic imbalance in the basal ganglia. An anticholinergic such as procyclidine (or benzatropine) rapidly reverses the reaction. Children are more susceptible to extrapyramidal effects, which is why metoclopramide use is restricted in young patients.
6Gentamicin is prescribed for a neonate with suspected sepsis, with serum levels monitored. Which property best explains why aminoglycosides are dosed using extended intervals and trough-level monitoring?
A.They show time-dependent killing with no post-antibiotic effect
B.They show concentration-dependent killing and dose-related ototoxicity and nephrotoxicity
C.They are extensively metabolised by hepatic cytochrome P450
D.They have a very large therapeutic index
Explanation: Aminoglycosides exhibit concentration-dependent bactericidal activity and a post-antibiotic effect, favouring higher peak, less frequent dosing. Because they cause dose-related, accumulation-dependent ototoxicity and nephrotoxicity, trough levels are monitored to ensure adequate clearance between doses. They have a narrow therapeutic index.
7A teenager taking carbamazepine is also started on a macrolide. The carbamazepine level rises and she develops toxicity. What is the mechanism of this interaction?
A.The macrolide induces cytochrome P450 enzymes, increasing carbamazepine clearance
B.The macrolide inhibits cytochrome P450 (CYP3A4), reducing carbamazepine metabolism
C.The macrolide displaces carbamazepine from renal binding sites
D.Carbamazepine inhibits gastric absorption of the macrolide
Explanation: Macrolides such as erythromycin and clarithromycin inhibit CYP3A4, which is responsible for carbamazepine metabolism. Reduced clearance raises carbamazepine levels and precipitates toxicity (ataxia, diplopia, drowsiness). Recognising P450 enzyme inhibitors and inducers is a core TAS pharmacology theme.
8Which statement about paracetamol overdose and its antidote in children is correct?
A.The toxic metabolite is conjugated paracetamol-glucuronide
B.Toxicity is caused directly by paracetamol binding to hepatocyte DNA
C.Activated charcoal is contraindicated within one hour of ingestion
D.N-acetylcysteine works by replenishing hepatic glutathione
Explanation: In overdose, the minor oxidative pathway produces the reactive metabolite NAPQI, which depletes hepatic glutathione and damages hepatocytes. N-acetylcysteine restores glutathione stores and provides sulfhydryl groups to detoxify NAPQI, preventing hepatic necrosis when given promptly.
9Digoxin is occasionally used in paediatric heart failure. Which cellular mechanism underlies its positive inotropic effect?
A.Activation of beta-1 adrenoceptors on cardiomyocytes
B.Direct opening of L-type calcium channels by digoxin
C.Inhibition of the sarcolemmal Na+/K+-ATPase, raising intracellular calcium
D.Inhibition of phosphodiesterase increasing cyclic AMP
Explanation: Digoxin inhibits the Na+/K+-ATPase, raising intracellular sodium. This reduces the gradient driving the Na+/Ca2+ exchanger, so more calcium remains intracellularly, increasing contractility. Hypokalaemia potentiates toxicity because potassium competes with digoxin at the same pump.
10A drug has an elimination half-life of 8 hours and is given by regular dosing without a loading dose. Approximately how long will it take to reach steady-state plasma concentration?
A.About 8 hours
B.About 16 hours
C.About 40 hours
D.About 5 days
Explanation: Steady state is reached after approximately 4-5 half-lives. With an 8-hour half-life, 5 half-lives is about 40 hours. A loading dose can achieve therapeutic levels faster but does not change the time to steady state, which depends only on the half-life.

About the MRCPCH TAS Exam

MRCPCH Theory and Science (TAS), formerly Part 1B, is one of three theory exams required for Membership of the Royal College of Paediatrics and Child Health. It tests the basic scientific, physiological and pharmacological principles underpinning clinical practice and the principles of evidence-based practice. The paper has 100 SBA questions and lasts 2 hours.

Assessment

100 Single Best Answer (SBA) questions in a single computer-based paper, with no negative marking.

Time Limit

2 hours

Passing Score

No fixed percentage. The pass mark is set for each diet by criterion-referenced (Angoff) standard setting; since the 2025.2 diet, Angoff judges make two judgments to agree the pass mark.

Exam Fee

2026: TAS single paper UK 365 GBP / international 455 GBP; combined FOP and TAS UK 659 GBP / international 804 GBP. (Royal College of Paediatrics and Child Health (RCPCH))

MRCPCH TAS Exam Content Outline

12%

Pharmacology and therapeutics

Pharmacokinetics, receptor mechanisms, drug interactions, toxicology and paediatric prescribing science.

12%

Physiology

Fetal, neonatal, cardiovascular, respiratory, renal and acid-base physiology underpinning practice.

10%

Genetics and dysmorphology

Inheritance patterns, chromosomal abnormalities, mutations, imprinting and genetic testing.

10%

Statistics and evidence-based practice

Diagnostic test metrics, study design, measures of association, confidence intervals and critical appraisal.

8%

Infection and immunology

Immunoglobulins, hypersensitivity, immunodeficiency, vaccines and antimicrobial mechanisms.

7%

Metabolism and acid-base

Inborn errors of metabolism, glucose and ammonia handling, anion gap and acid-base disturbances.

6%

Embryology and development

Embryological origins of malformations and normal developmental milestones.

6%

Cardiology science

Cardiac action potential, shunt physiology, cardiac output and cardiovascular pharmacology.

6%

Endocrinology and growth

Hormonal regulation of growth, puberty, calcium, adrenal and thyroid physiology.

6%

Haematology and oncology

Haemoglobinopathies, coagulation, childhood malignancy and oncological emergencies.

5%

Neurology and neurodevelopment

Neurotransmitters, CSF physiology and neuropharmacology.

5%

Respiratory science

Surfactant, gas transport, control of breathing and blood gas interpretation.

4%

Nephro-urology

Renal tubular function, nephrotic physiology, erythropoietin and fetal renal physiology.

3%

Nutrition

Vitamin D and rickets, refeeding syndrome and breast milk immunology.

How to Pass the MRCPCH TAS Exam

What You Need to Know

  • Passing score: No fixed percentage. The pass mark is set for each diet by criterion-referenced (Angoff) standard setting; since the 2025.2 diet, Angoff judges make two judgments to agree the pass mark.
  • Assessment: 100 Single Best Answer (SBA) questions in a single computer-based paper, with no negative marking.
  • Time limit: 2 hours
  • Exam fee: 2026: TAS single paper UK 365 GBP / international 455 GBP; combined FOP and TAS UK 659 GBP / international 804 GBP.

Keys to Passing

  • Complete 500+ practice questions
  • Score 80%+ consistently before scheduling
  • Focus on highest-weighted sections
  • Use our AI tutor for tough concepts

MRCPCH TAS Study Tips from Top Performers

1Focus on the science behind clinical conditions: drug mechanisms and pharmacokinetics, receptors, physiology, genetics and embryology, rather than management protocols, which are tested more in FOP and AKP.
2Master core statistics and evidence-based practice (sensitivity/specificity, predictive values, number needed to treat, confidence intervals, study design), as these recur reliably and are scoring opportunities.
3Practise timed SBAs at roughly 72 seconds per question and review every answer's reasoning; remember there is no negative marking, so attempt every question.

Frequently Asked Questions

How many questions are on the MRCPCH TAS exam and how long is it?

TAS consists of 100 Single Best Answer (SBA) questions and lasts 2 hours. It is taken as a single computer-based paper with no negative marking.

What does the MRCPCH TAS exam test?

TAS (formerly Part 1B) tests the basic scientific, physiological and pharmacological principles underpinning clinical practice, plus the principles of evidence-based practice, including statistics and study design.

How is the TAS pass mark determined?

There is no fixed pass percentage. The pass mark is set for each exam diet using criterion-referenced Angoff standard setting; since the 2025.2 diet, Angoff judges make two judgments to agree the pass mark.

How much does the MRCPCH TAS exam cost in 2026?

For 2026 the single TAS paper costs 365 GBP in the UK and 455 GBP internationally. Sitting FOP and TAS combined costs 659 GBP in the UK and 804 GBP internationally.