MRCS Part A 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 MRCS Part A, not a summary of it.

1. 1

   General Pharmacology

   5 topics

   • Introduction to Pharmacology
     • Definition and Scope
     • Branches of Pharmacology
     • Sources of Drugs
   • Pharmacokinetics
     • Absorption
     • Distribution
     • Metabolism
     • Excretion
   • Pharmacodynamics
     • Mechanism of Drug Action
     • Dose-Response Relationship
     • Therapeutic Index
   • Drug Receptors
     • Types of Receptors
     • Receptor Theories
     • Receptor Regulation
   • Adverse Drug Reactions
     • Types of Adverse Reactions
     • Drug Toxicity
     • Management of Adverse Reactions
2. 2

   Autonomic Nervous System Pharmacology

   2 topics

   • Cholinergic Drugs
     • Cholinergic Agonists
     • Cholinesterase Inhibitors
     • Anticholinergic Drugs
   • Adrenergic Drugs
     • Adrenergic Agonists
     • Adrenergic Antagonists
     • Indirect-Acting Adrenergic Agents
3. 3

   Cardiovascular Pharmacology

   4 topics

   • Antihypertensive Drugs
     • Diuretics
     • Beta-Blockers
     • Calcium Channel Blockers
     • ACE Inhibitors
     • ARBs
   • Antianginal Drugs
     • Nitrates
     • Beta-Blockers
     • Calcium Channel Blockers
   • Antiarrhythmic Drugs
     • Classification of Antiarrhythmics
     • Mechanism of Action
     • Clinical Uses
   • Drugs for Heart Failure
     • Cardiac Glycosides
     • Diuretics
     • ACE Inhibitors
     • Beta-Blockers
4. 4

   Central Nervous System Pharmacology

   5 topics

   • Anxiolytics and Hypnotics
     • Benzodiazepines
     • Barbiturates
     • Non-Benzodiazepine Hypnotics
   • Antidepressants
     • SSRIs
     • SNRIs
     • Tricyclic Antidepressants
     • MAO Inhibitors
   • Antipsychotics
     • Typical Antipsychotics
     • Atypical Antipsychotics
   • Antiepileptic Drugs
     • Mechanism of Action
     • Classification of Antiepileptics
     • Clinical Uses
   • Analgesics
     • Opioid Analgesics
     • Non-Opioid Analgesics
     • Adjuvant Analgesics
5. 5

   Endocrine Pharmacology

   4 topics

   • Drugs for Diabetes Mellitus
     • Insulin
     • Oral Hypoglycemic Agents
     • Non-Insulin Injectable Agents
   • Thyroid and Antithyroid Drugs
     • Thyroid Hormones
     • Antithyroid Drugs
   • Corticosteroids
     • Glucocorticoids
     • Mineralocorticoids
     • Clinical Uses and Adverse Effects
   • Sex Hormones
     • Estrogens
     • Progestins
     • Androgens
6. 6

   Chemotherapy

   4 topics

   • Antibacterial Drugs
     • Penicillins
     • Cephalosporins
     • Macrolides
     • Quinolones
     • Aminoglycosides
   • Antiviral Drugs
     • Antiretrovirals
     • Antiviral Agents for Herpesviruses
     • Antiviral Agents for Influenza
   • Antifungal Drugs
     • Azoles
     • Echinocandins
     • Polyenes
   • Anticancer Drugs
     • Alkylating Agents
     • Antimetabolites
     • Natural Products
     • Targeted Therapies
7. 7

   Respiratory Pharmacology

   3 topics

   • Drugs for Asthma
     • Beta-Agonists
     • Corticosteroids
     • Leukotriene Modifiers
   • Drugs for COPD
     • Bronchodilators
     • Phosphodiesterase-4 Inhibitors
     • Combination Therapies
   • Antitussives and Expectorants
     • Opioid Antitussives
     • Non-Opioid Antitussives
     • Expectorants
8. 8

   Gastrointestinal Pharmacology

   3 topics

   • Drugs for Peptic Ulcer Disease
     • Proton Pump Inhibitors
     • H2 Receptor Antagonists
     • Antacids
   • Antiemetic Drugs
     • Serotonin Antagonists
     • Dopamine Antagonists
     • Antihistamines
   • Laxatives and Antidiarrheal Drugs
     • Bulk-Forming Laxatives
     • Stimulant Laxatives
     • Osmotic Laxatives
     • Antidiarrheal Agents

Pharmacology flashcards for MRCS Part A

25 of 57 cards from the Pharmacology deck — real questions with worked answers.

1. Define pharmacology, and distinguish its two main branches, pharmacokinetics and pharmacodynamics.

   Pharmacology is the study of the interaction of drugs with living systems. Pharmacokinetics is what the body does to the drug (absorption, distribution, metabolism, excretion), whereas pharmacodynamics is what the drug does to the body (mechanism of action and effects).

2. What is the difference between a drug's therapeutic index and its therapeutic window?

   The therapeutic index is a ratio comparing the dose that produces toxicity to the dose that produces the desired effect, $TI = \frac{TD_{50}}{ED_{50}}$ (or $\frac{LD_{50}}{ED_{50}}$). The therapeutic window is the range of plasma concentrations between the minimum effective concentration and the minimum toxic concentration. A high TI/wide window means a safer drug.

3. What are the four processes described by the acronym ADME in pharmacokinetics?

   Absorption, Distribution, Metabolism, and Excretion.

4. Define bioavailability (F) and give the formula for oral bioavailability.

   Bioavailability is the fraction of an administered dose reaching the systemic circulation unchanged. $F = \frac{AUC_{oral}}{AUC_{IV}} \times \frac{Dose_{IV}}{Dose_{oral}}$. Intravenous administration has $F = 1$ (100%).

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

   $V_d$ is the apparent volume needed to contain the total amount of drug at the same concentration as in plasma. $V_d = \frac{\text{Total amount of drug in body}}{\text{Plasma concentration}} = \frac{Dose}{C_0}$. A large $V_d$ indicates extensive tissue distribution.

6. Distinguish zero-order from first-order elimination kinetics.

   In first-order kinetics a constant fraction of drug is eliminated per unit time (rate proportional to concentration), giving a constant half-life. In zero-order (saturation) kinetics a constant amount is eliminated per unit time regardless of concentration; e.g. ethanol, phenytoin, high-dose aspirin.

7. Give the relationship between elimination half-life ($t_{1/2}$), volume of distribution ($V_d$) and clearance (CL).

   $$t_{1/2} = \frac{0.693 \times V_d}{CL}$$ where $0.693 = \ln 2$. Half-life is directly proportional to $V_d$ and inversely proportional to clearance.

8. After how many half-lives is a drug considered essentially eliminated (or steady state reached on repeated dosing)?

   Approximately 4–5 half-lives. After 4 half-lives ~94% is eliminated, after 5 half-lives ~97%. Steady state on constant dosing is likewise reached in ~4–5 half-lives.

9. What is the difference between Phase I and Phase II reactions in drug metabolism?

   Phase I reactions (oxidation, reduction, hydrolysis; mainly cytochrome P450) introduce or unmask a functional group, often producing a more polar or active metabolite. Phase II reactions are conjugations (glucuronidation, sulfation, acetylation, methylation, glutathione) that attach an endogenous molecule to increase water solubility for excretion.

10. What is first-pass metabolism and how can it be avoided?

    First-pass metabolism is the metabolism of an orally absorbed drug by the gut wall and liver before it reaches the systemic circulation, reducing bioavailability. It can be bypassed by sublingual, rectal, transdermal, inhalational, or parenteral (IV/IM/SC) routes.

11. State the loading dose and maintenance dose formulas.

    $$\text{Loading dose} = \frac{C_{target} \times V_d}{F}$$ $$\text{Maintenance dose rate} = \frac{C_{target} \times CL}{F}$$ where $F$ is bioavailability.

12. Define pharmacodynamics terms: agonist, antagonist, and partial agonist.

    An agonist binds a receptor and produces a maximal response (full intrinsic activity). A partial agonist binds but produces only a submaximal response even at full occupancy (intrinsic activity between 0 and 1). An antagonist binds but produces no response (intrinsic activity 0) and blocks agonist action.

13. Distinguish competitive from non-competitive (irreversible) antagonism in terms of effect on the agonist dose-response curve.

    A competitive antagonist shifts the agonist dose-response curve to the right in a parallel fashion (increased $EC_{50}$) but $E_{max}$ is unchanged and surmountable by more agonist. A non-competitive/irreversible antagonist reduces $E_{max}$ (non-surmountable) and cannot be overcome by increasing agonist.

14. Define potency and efficacy, and state which parameters represent them.

    Potency is the amount of drug needed to produce a given effect, represented by $EC_{50}$ (lower $EC_{50}$ = more potent). Efficacy is the maximal effect a drug can produce, represented by $E_{max}$.

15. What does $ED_{50}$ mean and how does it relate to $LD_{50}$?

    $ED_{50}$ is the dose producing the therapeutic effect in 50% of the population; $LD_{50}$ is the dose that is lethal in 50%. The ratio $\frac{LD_{50}}{ED_{50}}$ gives the therapeutic index.

16. Name the four major types of drug (cell-surface/intracellular) receptors by signalling mechanism.

    1) Ligand-gated ion channels (ionotropic, e.g. nicotinic, GABA-A) — milliseconds; 2) G-protein-coupled receptors (metabotropic, e.g. muscarinic, adrenergic) — seconds; 3) Enzyme-linked/kinase-linked receptors (e.g. insulin, tyrosine kinase) — minutes; 4) Intracellular/nuclear receptors (e.g. steroids, thyroid hormone) — hours.

17. What second messengers are generated by $G_s$, $G_i$, and $G_q$ protein-coupled receptors?

    $G_s$ activates adenylyl cyclase, increasing cAMP. $G_i$ inhibits adenylyl cyclase, decreasing cAMP. $G_q$ activates phospholipase C, producing IP3 (releases $\ce{Ca^2+}$) and DAG (activates protein kinase C).

18. Define tachyphylaxis and distinguish it from tolerance.

    Tachyphylaxis is a rapid decrease in response after repeated doses over a short period (e.g. minutes to hours), often due to receptor desensitization or mediator depletion. Tolerance is a slower, progressive decrease in response requiring higher doses, developing over days to weeks.

19. Classify adverse drug reactions using the Rawlins-Thompson Type A vs Type B system.

    Type A (Augmented) reactions are dose-dependent, predictable, related to the drug's pharmacology, common, and low mortality (e.g. bleeding with warfarin). Type B (Bizarre) reactions are dose-independent, unpredictable, not related to known pharmacology, rare, but higher mortality (e.g. anaphylaxis, idiosyncratic reactions).

20. List the four Gell and Coombs types of hypersensitivity reactions with a drug example each.

    Type I — IgE-mediated immediate/anaphylaxis (penicillin anaphylaxis); Type II — antibody-mediated cytotoxic (methyldopa haemolytic anaemia); Type III — immune-complex mediated (serum sickness); Type IV — delayed T-cell mediated (contact dermatitis, Stevens-Johnson syndrome).

21. Where is acetylcholine the neurotransmitter in the autonomic nervous system?

    Acetylcholine acts at: all preganglionic autonomic fibres (sympathetic and parasympathetic) at nicotinic ganglionic receptors; all postganglionic parasympathetic fibres at muscarinic receptors; postganglionic sympathetic fibres to sweat glands; the adrenal medulla; and the somatic neuromuscular junction (nicotinic).

22. Contrast the effects of muscarinic agonists (parasympathetic) at the eye, heart, and secretions.

    Muscarinic stimulation causes: pupil constriction (miosis) and ciliary muscle contraction (accommodation, reduced intraocular pressure); decreased heart rate (negative chronotropy) and slowed AV conduction; and increased secretions (salivary, lacrimal, bronchial, GI) — remembered as SLUDGE effects.

23. What are the clinical features of organophosphate (irreversible anticholinesterase) poisoning and its antidotes?

    Cholinergic crisis: salivation, lacrimation, urination, defecation, GI cramps, emesis (SLUDGE), plus bronchospasm, bradycardia, miosis, muscle fasciculations and weakness. Treatment: atropine (blocks muscarinic effects) plus pralidoxime (regenerates acetylcholinesterase if given before ageing).

24. Compare the actions of atropine, glycopyrrolate and hyoscine (scopolamine) as antimuscarinics.

    All are muscarinic antagonists. Atropine crosses the blood-brain barrier (central effects, tachycardia, mydriasis). Glycopyrrolate is quaternary and does not cross the BBB (no CNS effects; used to dry secretions and block vagal reflexes). Hyoscine crosses the BBB and is strongly antiemetic/sedative (motion sickness), with more central antimuscarinic action.

25. Describe the synthesis pathway of noradrenaline (norepinephrine) and the rate-limiting step.

    $$\text{Tyrosine} \to \text{DOPA} \to \text{Dopamine} \to \text{Noradrenaline} \to \text{Adrenaline}$$ Tyrosine hydroxylase converts tyrosine to DOPA and is the rate-limiting enzyme. The final conversion of noradrenaline to adrenaline (by PNMT) occurs mainly in the adrenal medulla.

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