Membership of the Royal College of Physicians (MRCP UK) Acute Medicine, Clinical Pharmacology and Professional Practice Syllabus

Acute Medicine, Clinical Pharmacology and Professional Practice syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Acute Medicine, Clinical Pharmacology and Professional Practice in Membership of the Royal College of Physicians (MRCP UK), not a summary of it.

1. 1

   Acute and Critical Care Medicine

   5 topics

   • Resuscitation and the deteriorating patient
     • Advanced life support algorithms
     • NEWS2 and escalation
   • Shock states and fluid resuscitation
   • Poisoning and toxicology
     • Common overdoses and antidotes
   • Disorders of consciousness and the comatose patient
   • Environmental and physical injury
     • Hypothermia, hyperthermia and drowning
2. 2

   Clinical Pharmacology and Therapeutics

   5 topics

   • Pharmacokinetics and pharmacodynamics
   • Adverse drug reactions and interactions
   • Prescribing in renal and hepatic impairment
   • Therapeutic drug monitoring
   • Prescribing in pregnancy and the elderly
3. 3

   Geriatric Medicine and Multimorbidity

   5 topics

   • Frailty and comprehensive geriatric assessment
   • Falls, syncope and gait disorders
   • Delirium and cognitive assessment
   • Polypharmacy and deprescribing
   • Continence and pressure ulcer prevention
4. 4

   Professionalism, Ethics and Communication

   5 topics

   • Consent, capacity and the Mental Capacity Act
   • Confidentiality and information governance
   • Breaking bad news and shared decision-making
   • End-of-life decisions and DNACPR
   • Patient safety, clinical governance and duty of candour
5. 5

   Evidence-Based Medicine and Statistics

   5 topics

   • Study design and levels of evidence
   • Diagnostic test evaluation
     • Sensitivity, specificity and predictive values
   • Interpreting clinical trial outcomes
     • Relative and absolute risk, number needed to treat
   • Critical appraisal and systematic reviews
   • Screening principles and bias

Acute Medicine, Clinical Pharmacology and Professional Practice flashcards for Membership of the Royal College of Physicians (MRCP UK)

25 of 84 cards from the Acute Medicine, Clinical Pharmacology and Professional Practice deck — real questions with worked answers.

1. In the ABCDE approach to the deteriorating patient, what does each letter stand for?

   A = Airway, B = Breathing, C = Circulation, D = Disability (neurological), E = Exposure. Assess and treat each in sequence before moving on.

2. In adult advanced life support, what are the two shockable and two non-shockable rhythms?

   Shockable: ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT). Non-shockable: pulseless electrical activity (PEA) and asystole.

3. In adult ALS, what is the chest compression rate, depth, and the CPR-to-defibrillation cycle interval?

   Rate $100$–$120$ per minute, depth $5$–$6\,\text{cm}$, ratio $30:2$ (compressions:ventilations), with rhythm checks every $2$ minutes. Adrenaline $1\,\text{mg}$ IV every $3$–$5$ minutes (immediately in non-shockable; after 3rd shock in shockable).

4. What are the reversible causes of cardiac arrest (4 Hs and 4 Ts)?

   4 Hs: Hypoxia, Hypovolaemia, Hyper/hypokalaemia (and metabolic), Hypothermia. 4 Ts: Thrombosis (coronary/pulmonary), Tension pneumothorax, Tamponade (cardiac), Toxins.

5. List the four classes of haemorrhagic shock by the ATLS classification (blood loss and key signs).

   Class I: <$15\%$ loss, normal vitals. Class II: $15$–$30\%$, tachycardia, narrowed pulse pressure. Class III: $30$–$40\%$, hypotension, altered mental state. Class IV: >$40\%$, profound hypotension, oliguria/anuria, lethargy.

6. Classify the four main types of shock by haemodynamic mechanism.

   Hypovolaemic (low preload/volume), Cardiogenic (pump failure), Distributive (vasodilation: septic, anaphylactic, neurogenic), and Obstructive (PE, tamponade, tension pneumothorax).

7. In sepsis, what does the 'Sepsis Six' bundle consist of?

   Give 3: oxygen, IV fluids, IV antibiotics. Take 3: blood cultures, serum lactate, measure urine output. To be delivered within 1 hour.

8. What distinguishes warm shock from cold shock haemodynamically?

   Warm (early distributive/septic): vasodilation, warm peripheries, bounding pulse, low systemic vascular resistance, high cardiac output. Cold (cardiogenic/late shock): vasoconstriction, cold clammy peripheries, high SVR, low cardiac output.

9. What is the antidote and mechanism for paracetamol overdose, and when is it given?

   N-acetylcysteine (NAC) replenishes glutathione to detoxify NAPQI. Give based on the treatment nomogram (4-hour level), or empirically if staggered/late presentation or unknown timing. Most effective within 8 hours of ingestion.

10. Match these poisons to their antidotes: opioids, benzodiazepines, organophosphates, beta-blockers, iron, methanol/ethylene glycol.

    Opioids → naloxone; benzodiazepines → flumazenil; organophosphates → atropine + pralidoxime; beta-blockers → glucagon; iron → desferrioxamine; methanol/ethylene glycol → fomepizole (or ethanol).

11. What ECG features suggest tricyclic antidepressant (TCA) toxicity, and what is the treatment?

    Wide QRS (>$100\,\text{ms}$), tall R wave in aVR, prolonged QT, sinus tachycardia, ventricular arrhythmias. Treat with IV sodium bicarbonate to narrow QRS and correct acidosis.

12. What toxidrome is characterised by mydriasis, dry flushed skin, urinary retention, hyperthermia, and confusion?

    Anticholinergic toxidrome ('mad as a hatter, hot as a hare, dry as a bone, red as a beet, blind as a bat'). Caused by atropine, antihistamines, TCAs. Treat supportively; physostigmine in severe cases.

13. How is the anion gap calculated and what does a raised gap indicate in poisoning?

    $\text{Anion gap} = (\text{Na}^{+} + \text{K}^{+}) - (\text{Cl}^{-} + \text{HCO}_3^{-})$, normal $\approx 8$–$16\,\text{mmol/L}$. Raised gap metabolic acidosis (MUDPILES): methanol, uraemia, DKA, propylene glycol, isoniazid, lactate, ethylene glycol, salicylates.

14. What is the Glasgow Coma Scale and its component scores?

    GCS scores Eye opening (1–4), Verbal response (1–5), Motor response (1–6); total $3$ to $15$. A score $\leq 8$ indicates coma and need to consider airway protection.

15. What are the components of the brainstem death examination criteria?

    Absent: pupillary light reflex, corneal reflex, vestibulo-ocular (oculocephalic/caloric) reflex, gag/cough reflex, motor response in cranial nerve distribution, and apnoea test (no respiratory effort despite PaCO2 rise). Performed by two doctors, twice, after excluding reversible causes.

16. What is the differential framework for coma based on structural vs metabolic causes?

    Structural (focal signs, asymmetry): stroke, haemorrhage, tumour, abscess. Metabolic/diffuse (symmetrical, preserved pupillary reflexes): hypoglycaemia, hypoxia, hypercapnia, drugs, sepsis, hepatic/uraemic encephalopathy, electrolyte disturbance.

17. How does pupil size and reactivity help localise the cause of coma?

    Pinpoint reactive: opioids or pontine lesion. Fixed dilated unilateral: uncal herniation (CN III compression). Bilateral fixed dilated: severe hypoxia/brain death or anticholinergics. Reactive pupils generally suggest a metabolic cause.

18. What is the classification of hypothermia by core temperature?

    Mild $32$–$35\,^{\circ}\text{C}$ (shivering, tachycardia); Moderate $28$–$32\,^{\circ}\text{C}$ (loss of shivering, bradycardia, J waves); Severe <$28\,^{\circ}\text{C}$ (coma, arrhythmia risk, fixed pupils). 'Not dead until warm and dead.'

19. What ECG sign is characteristic of hypothermia?

    The Osborn (J) wave — a positive deflection at the J point (junction of QRS and ST segment), most prominent in inferior and lateral leads. Bradycardia and prolonged intervals also occur.

20. How are burns assessed for severity and fluid resuscitation (Parkland formula)?

    Total body surface area by 'rule of nines.' Parkland formula: $\text{fluid} = 4\,\text{mL} \times \text{weight (kg)} \times \%\text{TBSA}$ of Hartmann's over 24h, half in first 8 hours from time of burn.

21. Define zero-order and first-order kinetics in pharmacokinetics.

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

22. What is the volume of distribution ($V_d$) and how is it calculated?

    $V_d$ is the theoretical volume into which a drug distributes to give the observed plasma concentration: $V_d = \dfrac{\text{total amount of drug in body}}{\text{plasma concentration}}$. High $V_d$ means extensive tissue distribution (lipophilic drugs).

23. How are clearance, volume of distribution, and elimination half-life related?

    $t_{1/2} = \dfrac{0.693 \times V_d}{CL}$, where $CL$ is clearance. Half-life increases with larger $V_d$ and decreases with higher clearance.

24. What is bioavailability and what factors reduce it for oral drugs?

    Bioavailability ($F$) is the fraction of administered drug reaching systemic circulation unchanged; IV $F=1$. Reduced by incomplete absorption and first-pass metabolism (gut wall and hepatic). $F = \dfrac{\text{AUC}_{oral}}{\text{AUC}_{IV}}$.

25. How many half-lives are needed to reach steady state, and what is the role of a loading dose?

    Steady state is reached after approximately $4$–$5$ half-lives. A loading dose rapidly achieves the target concentration without waiting: $\text{loading dose} = C_{target} \times V_d / F$. Maintenance dose replaces eliminated drug.

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