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MRCP Pharm: Cytochrome P450 Inducers & Inhibitors (MRCP Part 1)

TL;DR: 

For MRCP Part 1, cytochrome P450 (CYP450) questions are about recognising patterns, not memorising enzymes. Know the classic inducers and inhibitors, predict whether drug levels rise or fall, and link this to toxicity or treatment failure. If you can do that reliably, you will pick up easy marks in pharmacology stems.


Why CYP450 matters in MRCP Part 1

Drug interactions are a core safety issue in real clinical practice, and that is exactly why they feature repeatedly in MRCP Part 1. Examiners favour short vignettes where a stable patient deteriorates after a new drug is started or stopped. The correct answer often hinges on recognising whether cytochrome P450 activity has been induced or inhibited.

You are not expected to recall detailed enzyme biochemistry. Instead, MRCP Part 1 tests whether you can:

  • Identify high-risk drugs with narrow therapeutic windows

  • Anticipate predictable interactions

  • Choose the safest explanation or next step

For an overview of how pharmacology fits into the exam as a whole, see the official MRCP(UK) guidance:https://www.mrcpuk.org/mrcpuk-examinations/part-1


What the exam expects you to know (scope)

At MRCP Part 1 level, CYP450 knowledge is deliberately practical:

  • CYP450 enzymes metabolise many commonly prescribed drugs

  • Inducers increase enzyme activity → lower drug concentrations

  • Inhibitors reduce enzyme activity → higher drug concentrations

  • Clinical consequences (bleeding, seizures, pregnancy, toxicity) matter more than mechanisms

  • Interactions involving warfarin, oral contraceptives, antiepileptics, statins, and immunosuppressants are especially high yield

Authoritative reference for real-world prescribing (also aligned with exam expectations):British National Formulary (BNF): https://bnf.nice.org.uk/


High-yield CYP450 inducers (learn these cold)

These drugs increase metabolism of other medicines, reducing their effect:

  1. Rifampicin

  2. Carbamazepine

  3. Phenytoin

  4. Phenobarbital

  5. St John’s wort

  6. Chronic alcohol use (context dependent)

Exam consequence: treatment failure

  • Oral contraceptive failure → unplanned pregnancy

  • Reduced anticoagulation → thrombosis

  • Reduced steroid or immunosuppressant effect


High-yield CYP450 inhibitors (equally important)

These drugs reduce metabolism, increasing drug levels:

  1. Macrolide antibiotics (erythromycin, clarithromycin)

  2. Azole antifungals (fluconazole, ketoconazole)

  3. Amiodarone

  4. Cimetidine

  5. Protease inhibitors (e.g. ritonavir)

  6. Grapefruit juice

Exam consequence: toxicity

  • Bleeding with warfarin

  • Rhabdomyolysis with statins

  • Arrhythmias with anti-arrhythmics


One-look exam table (use for rapid revision)

Category

Typical drugs

Likely outcome in MRCP stem

Inducers

Rifampicin, carbamazepine

Loss of efficacy

Inhibitors

Macrolides, azoles

Drug toxicity

Red-flag drugs

Warfarin, statins, OCPs

Bleeding, myopathy, pregnancy

Timing clue

“Recently started”

Think inhibition first

MRCP Part 1 pharmacology revision setup with notes and practice questions

The 5 most tested clinical contexts

1. Warfarin

  • Inhibitor added → ↑ INR → bleeding

  • Inducer added → ↓ INR → thrombosis

2. Oral contraceptives

  • Enzyme induction → contraceptive failure

  • Rifampicin is the classic exam trigger

3. Antiepileptics

  • Carbamazepine and phenytoin are potent inducers

  • They reduce levels of many co-prescribed drugs

4. Statins

  • CYP3A4-metabolised statins + inhibitors → myopathy/rhabdomyolysis

5. Immunosuppressants

  • Ciclosporin and tacrolimus have narrow therapeutic windows

  • Inhibitors rapidly cause toxicity


Mini-case (MRCP Part 1 style)

A 72-year-old man with atrial fibrillation is stable on warfarin. He develops a chest infection and is prescribed clarithromycin. Four days later, he presents with epistaxis and an INR of 6.8.

What is the mechanism?

Answer: CYP450 inhibition. Explanation: Clarithromycin inhibits CYP3A4, reducing warfarin metabolism and increasing anticoagulant effect. In MRCP Part 1, macrolide + warfarin should immediately suggest raised INR and bleeding.


Common exam traps (and how to avoid them)

  • Over-learning enzyme numbers – outcomes matter more than CYP names

  • Ignoring herbal drugs – St John’s wort is examinable

  • Missing timing clues – inhibition acts quickly; induction is delayed

  • Assuming all statins are equal – CYP3A4 metabolism matters

  • Forgetting pregnancy risk – OCP failure is a classic safety question


Practical study checklist

For structured pharmacology teaching aligned to MRCP Part 1, see:https://www.crackmedicine.com/lectures/


FAQs (People Also Ask)

Do I need to memorise CYP450 isoenzymes for MRCP Part 1?

No. The exam focuses on predictable interactions and clinical consequences, not detailed enzyme pathways.

Which CYP450 interaction is most commonly tested?

Warfarin with antibiotics (especially macrolides or azoles) causing raised INR and bleeding.

Are herbal medicines tested in MRCP Part 1?

Yes. St John’s wort is a classic CYP inducer linked to treatment failure.

How are oral contraceptive interactions examined?

Usually via enzyme induction (e.g. rifampicin) leading to contraceptive failure.


Ready to start?

CYP450 questions in MRCP Part 1 are high-yield and highly predictable. Learn the classic inducers and inhibitors, anchor them to real clinical outcomes, and practise applying them to short vignettes. With a small amount of focused revision, this topic can become a reliable source of marks rather than uncertainty.


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