Fellowship of the Royal College of Anaesthetists (FRCA) Pharmacology Syllabus

Pharmacology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pharmacology in Fellowship of the Royal College of Anaesthetists (FRCA), not a summary of it.

1. 1

   Pharmacokinetics and Pharmacodynamics

   6 topics

   • Absorption, distribution, metabolism and excretion
   • Compartment models and context-sensitive half-time
     • Volume of distribution and clearance
     • Target-controlled infusion principles
   • Drug-receptor interactions
     • Agonists, antagonists, partial agonists and efficacy
     • Dose-response curves, EC50 and potency
   • Enzyme kinetics and metabolism
     • Phase I and Phase II reactions
     • Cytochrome P450 and enzyme induction/inhibition
   • Pharmacogenetics and individual variation
     • Plasma cholinesterase variants and malignant hyperthermia
   • Isomerism, chirality and stereochemistry
2. 2

   Anaesthetic Agents

   5 topics

   • Inhalational anaesthetics
     • MAC and factors affecting it
     • Uptake, distribution and the second gas effect
     • Sevoflurane, isoflurane, desflurane and nitrous oxide
   • Intravenous induction agents
     • Propofol pharmacology and infusion syndrome
     • Thiopental, ketamine and etomidate
   • Mechanisms of general anaesthesia
   • Total intravenous anaesthesia and TCI models
   • Sedative agents and benzodiazepines
3. 3

   Analgesics

   5 topics

   • Opioids
     • Receptor pharmacology and signalling
     • Morphine, fentanyl, remifentanil and oxycodone
     • Tolerance, dependence and opioid-induced hyperalgesia
   • Non-steroidal anti-inflammatory drugs
     • COX selectivity and adverse effects
   • Paracetamol pharmacology
   • Adjuvant analgesics
     • Gabapentinoids, ketamine, clonidine and dexmedetomidine
   • Local anaesthetics
     • Mechanism, pKa and differential block
     • Maximum safe doses and toxicity
     • Lipid emulsion for systemic toxicity
4. 4

   Neuromuscular and Autonomic Drugs

   6 topics

   • Depolarising neuromuscular blockers
     • Suxamethonium and its complications
   • Non-depolarising neuromuscular blockers
     • Aminosteroid and benzylisoquinolinium agents
   • Reversal agents
     • Anticholinesterases and sugammadex
   • Sympathomimetics and inotropes
     • Adrenergic agonist selectivity and clinical use
   • Anticholinergics and cholinergic drugs
   • Antihypertensives and vasodilators
5. 5

   Drugs Acting on Major Systems

   6 topics

   • Cardiovascular drugs
     • Antiarrhythmics and the Vaughan-Williams classification
     • Beta-blockers, calcium channel blockers and digoxin
   • Drugs affecting coagulation
     • Heparins, warfarin and direct oral anticoagulants
     • Antiplatelets and antifibrinolytics
   • Respiratory drugs and bronchodilators
   • Antiemetics and prokinetics
   • Endocrine drugs
     • Corticosteroids, insulin and antidiabetic agents
   • Antimicrobials relevant to anaesthesia
6. 6

   Special Topics and Toxicology

   5 topics

   • Drug interactions and adverse drug reactions
   • Anaphylaxis and drug allergy
   • Drugs in pregnancy, lactation and at the extremes of age
   • Drugs in renal and hepatic impairment
   • Antagonism, overdose and specific antidotes

Pharmacology flashcards for Fellowship of the Royal College of Anaesthetists (FRCA)

25 of 50 cards from the Pharmacology deck — real questions with worked answers.

1. Define bioavailability ($F$) and give its formula relative to an IV dose.

   Bioavailability is the fraction of an administered dose reaching the systemic circulation unchanged. $$F = \frac{\text{AUC}_{\text{oral}} \times \text{Dose}_{IV}}{\text{AUC}_{IV} \times \text{Dose}_{\text{oral}}}$$ By definition $F = 1$ (100%) for IV administration.

2. What equation relates volume of distribution to total drug amount and plasma concentration?

   $$V_d = \frac{\text{Total amount of drug in body}}{\text{Plasma concentration}}$$ A large $V_d$ implies extensive tissue distribution (e.g. lipophilic or highly tissue-bound drugs).

3. State the formula for clearance in terms of elimination rate constant and volume of distribution.

   $$Cl = k_{e} \times V_d$$ where $k_e$ is the first-order elimination rate constant. Clearance is the volume of plasma cleared of drug per unit time.

4. What is the relationship between elimination half-life, $V_d$ and clearance?

   $$t_{1/2} = \frac{0.693 \times V_d}{Cl} = \frac{\ln 2}{k_e}$$ Half-life rises with increasing $V_d$ and falls with increasing clearance.

5. List the four phases of pharmacokinetics (ADME).

   Absorption, Distribution, Metabolism (biotransformation) and Excretion. These describe what the body does to the drug.

6. Distinguish Phase I from Phase II metabolic reactions.

   Phase I reactions (oxidation, reduction, hydrolysis — often cytochrome P450) introduce or expose a reactive functional group. Phase II reactions are conjugations (glucuronidation, sulphation, acetylation, glutathione) that add a polar moiety to increase water solubility for excretion.

7. In a two-compartment model, what do the $\alpha$ and $\beta$ phases represent?

   The $\alpha$ (distribution) phase is the rapid initial fall in plasma concentration as drug redistributes from central to peripheral compartments. The $\beta$ (elimination) phase is the slower terminal decline governed by metabolism/excretion.

8. Define context-sensitive half-time.

   The time taken for the plasma (central compartment) concentration of a drug to fall by 50% after stopping a continuous infusion designed to maintain a steady concentration. It depends on infusion duration (the 'context') and is not the same as elimination half-life.

9. Why does remifentanil have a near-constant context-sensitive half-time?

   Remifentanil is metabolised by non-specific plasma and tissue esterases, giving rapid organ-independent clearance. Its context-sensitive half-time remains approximately 3–5 minutes regardless of infusion duration, so it does not accumulate.

10. Define agonist, antagonist and partial agonist at a receptor.

    An agonist binds and produces a maximal response (full intrinsic activity = 1). An antagonist binds with affinity but has no efficacy (intrinsic activity = 0), blocking agonist action. A partial agonist produces a submaximal response even at full occupancy (0 < intrinsic activity < 1).

11. Contrast competitive and non-competitive antagonism on a log dose-response curve.

    Competitive (reversible) antagonism shifts the agonist curve to the right in a parallel fashion with no reduction in maximal response (surmountable). Non-competitive antagonism reduces the maximal response and is not overcome by increasing agonist (insurmountable).

12. Define potency and efficacy.

    Potency is the amount of drug required to produce a given effect (related to $EC_{50}$ / position on the dose axis). Efficacy is the maximal achievable effect ($E_{max}$) once bound, reflecting intrinsic activity.

13. Write the Michaelis-Menten equation for enzyme reaction velocity.

    $$V = \frac{V_{max}[S]}{K_m + [S]}$$ where $V_{max}$ is maximal velocity, $[S]$ substrate concentration and $K_m$ the substrate concentration at half $V_{max}$.

14. What is the significance of $K_m$ in Michaelis-Menten kinetics?

    $K_m$ is the substrate concentration at which reaction velocity is half-maximal. A low $K_m$ indicates high enzyme affinity for substrate. When $[S] \ll K_m$ kinetics are first-order; when $[S] \gg K_m$ they are zero-order (saturated).

15. Give two examples of drugs showing zero-order (saturation) kinetics at therapeutic doses.

    Phenytoin, ethanol, and high-dose aspirin (salicylate). Their elimination enzymes saturate, so a constant amount (not a constant fraction) is eliminated per unit time, risking disproportionate accumulation.

16. What pharmacogenetic variation affects plasma cholinesterase and suxamethonium?

    Atypical (dibucaine-resistant) plasma cholinesterase due to inherited variants of the BCHE gene prolongs suxamethonium and mirivacurium action. A low dibucaine number (e.g. ~20 in homozygotes) indicates abnormal enzyme; normal is ~80.

17. What is the dibucaine number and what does a value of 80 versus 20 indicate?

    The dibucaine number is the percentage inhibition of plasma cholinesterase by dibucaine. ~80 = normal homozygous enzyme (normal suxamethonium duration). ~40–60 = heterozygous. ~20 = homozygous atypical, causing prolonged apnoea after suxamethonium.

18. Define enantiomers and explain why chirality matters in anaesthetic pharmacology.

    Enantiomers are stereoisomers that are non-superimposable mirror images (differ at a chiral centre). They can differ markedly in potency, toxicity and pharmacokinetics — e.g. levobupivacaine and ropivacaine (S-enantiomers) are less cardiotoxic than racemic bupivacaine.

19. Classify isomerism into its main structural and stereoisomeric subtypes.

    Structural (constitutional) isomerism: chain, position, functional group, and tautomerism. Stereoisomerism: geometric (cis/trans), optical (enantiomers, R/S or d/l), and diastereoisomerism. Example: isoflurane and enflurane are structural (functional-group) isomers.

20. State the Meyer-Overton correlation and its meaning for inhalational agents.

    The Meyer-Overton correlation states that anaesthetic potency correlates with lipid solubility (oil:gas partition coefficient): higher oil:gas solubility means lower MAC (greater potency). It suggested a lipid-membrane site of action.

21. Define MAC (minimum alveolar concentration).

    MAC is the alveolar concentration of a volatile agent at one atmosphere that prevents movement to a standard surgical (skin) stimulus in 50% of subjects. It is an index of potency; the lower the MAC, the more potent the agent.

22. List factors that increase and decrease MAC.

    Increase MAC: hyperthermia, chronic alcohol, hypernatraemia, infancy (peak ~6 months), MAO inhibitors, acute amphetamine/cocaine. Decrease MAC: increasing age, hypothermia, pregnancy, opioids/sedatives, acute alcohol, hyponatraemia, lithium, hypotension, nitrous oxide.

23. Why does the blood:gas partition coefficient determine speed of inhalational induction?

    A low blood:gas coefficient (e.g. desflurane 0.42, sevoflurane 0.69) means the agent is less soluble in blood, so alveolar (and brain) partial pressure rises rapidly — fast onset and offset. High solubility (e.g. halothane 2.4) gives slower induction.

24. State the induction dose and key feature of propofol.

    Propofol induction dose is approximately $1.5\text{–}2.5\ \text{mg·kg}^{-1}$ IV. It acts mainly via $GABA_A$ potentiation, causes dose-dependent hypotension and apnoea, suppresses airway reflexes, and is antiemetic. It is the agent of choice for TIVA.

25. What are the features and risks of ketamine as an induction agent?

    Ketamine ($1\text{–}2\ \text{mg·kg}^{-1}$ IV) is an NMDA-receptor antagonist producing dissociative anaesthesia. It maintains airway reflexes and respiration, is a bronchodilator, raises BP/HR (sympathomimetic), provides analgesia, but causes emergence delirium and raised secretions/ICP concerns.

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