FMGE 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 FMGE, not a summary of it.

1. 1

   General Pharmacology

   5 topics

   • Introduction to pharmacology
     • Definitions
     • Scope
     • Branches of pharmacology
   • Pharmacokinetics
     • Absorption
     • Distribution
     • Metabolism
     • Excretion of drugs
   • Pharmacodynamics
     • Mechanisms of drug action
     • Drug-receptor interactions
     • Dose-response relationships
     • Drug potency
   • Pharmacogenetics and personalized medicine
     • Genetic variation in drug response
     • Pharmacogenomic testing
     • Implications for drug therapy
   • Drug development and regulation
     • Preclinical studies
     • Clinical trials
     • Drug approval process
     • Drug scheduling
2. 2

   Autonomic Nervous System Pharmacology

   4 topics

   • Introduction to autonomic pharmacology
     • Neurotransmitters and receptors in the autonomic nervous system
   • Cholinergic drugs
     • Agonists
     • Antagonists
     • Cholinesterase inhibitors
   • Adrenergic drugs
     • Agonists
     • Antagonists
     • Adrenergic neuron blockers
   • Ganglionic and neuromuscular blocking drugs
     • Mechanism of action
     • Uses
     • Adverse effects
3. 3

   Central Nervous System Pharmacology

   7 topics

   • Introduction to CNS Pharmacology
     • Blood-brain barrier
     • Neurotransmitters in the CNS
     • Receptors in the CNS
   • Sedative-hypnotic Drugs
     • Benzodiazepines
     • Barbiturates
     • Non-benzodiazepine sedative-hypnotics
   • Antiepileptic Drugs
     • Mechanisms of action
     • Classification
     • Therapeutic uses
   • Antipsychotic Drugs
     • Typical antipsychotics
     • Atypical antipsychotics
     • Dopamine receptor antagonists
     • Serotonin-dopamine antagonists
   • Antidepressant Drugs
     • SSRIs
     • TCAs
     • MAOIs
     • Atypical antidepressants
     • Serotonin-norepinephrine reuptake inhibitors (SNRIs)
   • Analgesic and Anti-inflammatory Drugs
     • NSAIDs
     • Opioids
     • Adjuvant analgesics
   • Anxiolytic Drugs
     • Benzodiazepines
     • Buspirone
     • Selective serotonin reuptake inhibitors (SSRIs)
4. 4

   Introduction to cardiovascular pharmacology

   3 topics

   • Hemodynamics
   • Cardiac electrophysiology
   • Regulation of blood pressure
5. 5

   Endocrine Pharmacology

   5 topics

   • Introduction to Endocrine Pharmacology
     • Hormone replacement therapy
     • Hormone antagonists
     • Hormone synthesis inhibitors
   • Thyroid and Antithyroid Drugs
     • Thyroid hormones
     • Antithyroid drugs
     • Iodine preparations
   • Glucocorticoids and Mineralocorticoids
     • Mechanism of action
     • Therapeutic uses
     • Adverse effects
   • Insulin and Oral Hypoglycemic Agents
     • Mechanism of action
     • Classification
     • Therapeutic uses
   • Gonadal Hormones and Contraceptives
     • Estrogens
     • Progestins
     • Androgen receptor antagonists
     • Contraceptive methods
6. 6

   Introduction to chemotherapy

   3 topics

   • Principles of antimicrobial therapy
   • Mechanisms of antimicrobial action
   • Drug resistance
7. 7

   Chemotherapy of Neoplastic Diseases

   3 topics

   • Introduction to cancer chemotherapy
     • Principles of cancer therapy
     • Cell cycle-specific vs. cell cycle-nonspecific drugs
   • Anticancer drugs
     • Alkylating agents
     • Antimetabolites
     • Antitumor antibiotics
     • Mitotic inhibitors
     • Targeted therapies
   • Hormonal therapy
     • Hormone receptor antagonists
     • Aromatase inhibitors
     • Gonadotropin-releasing hormone analogs
8. 8

   Principles of toxicology

   3 topics

   • Mechanisms of toxicity
   • Factors affecting toxicity
   • Toxicokinetics

Pharmacology flashcards for FMGE

25 of 62 cards from the Pharmacology deck — real questions with worked answers.

1. Define bioavailability (F) and state its value for the intravenous route.

   Bioavailability is the fraction of an administered drug dose that reaches the systemic circulation unchanged. For IV administration F = 1 (100%), since the drug is placed directly into the blood.

2. What does the apparent volume of distribution (Vd) represent, and what is its formula?

   Vd is the theoretical volume needed to contain the total drug in the body at the same concentration as in plasma. Vd = Total amount of drug in body / Plasma drug concentration. A large Vd indicates extensive tissue distribution.

3. Differentiate zero-order from first-order kinetics of drug elimination.

   In zero-order kinetics a constant AMOUNT of drug is eliminated per unit time (rate independent of concentration; saturable, e.g. ethanol, phenytoin, aspirin in high doses). In first-order kinetics a constant FRACTION is eliminated per unit time (rate proportional to concentration); most drugs follow this.

4. Write the formula for drug clearance (CL) in terms of elimination rate constant and volume of distribution.

   CL = k_el × Vd, where k_el is the elimination rate constant. Clearance is the volume of plasma cleared of drug per unit time.

5. How is plasma half-life (t½) related to Vd and clearance?

   t½ = 0.693 × Vd / CL. Half-life increases with larger Vd and decreases with greater clearance.

6. After how many half-lives does a drug reach steady-state plasma concentration on continuous/repeated dosing?

   Approximately 4–5 half-lives (about 94–97% of steady state by 4–5 t½). The same number applies to nearly complete elimination after stopping the drug.

7. Define potency and efficacy in pharmacodynamics.

   Potency is the amount of drug needed to produce a given effect (reflected by EC50/ED50; lower dose = more potent). Efficacy (intrinsic activity) is the maximal effect (Emax) a drug can produce regardless of dose.

8. Compare a competitive antagonist with a non-competitive (irreversible) antagonist on the agonist dose–response curve.

   A competitive antagonist shifts the agonist curve to the RIGHT (increased EC50, unchanged Emax) and is surmountable by more agonist. A non-competitive antagonist lowers Emax (reduced maximal response) and is not surmountable.

9. Define partial agonist and give the classic analgesic example.

   A partial agonist binds the receptor and produces a submaximal response even at full occupancy (lower intrinsic activity than a full agonist) and can act as an antagonist in the presence of a full agonist. Example: buprenorphine at the opioid mu receptor.

10. What is the therapeutic index (TI) and how is it calculated?

    TI is a measure of drug safety = TD50 / ED50 (or LD50/ED50 in animals). A higher TI means a wider safety margin.

11. Name the four main signal transduction mechanisms of receptors with an example each.

    1) Ligand-gated ion channels (nicotinic, GABA-A); 2) G-protein coupled receptors (adrenergic, muscarinic); 3) Enzyme-linked/receptor tyrosine kinases (insulin); 4) Intracellular/nuclear receptors (steroids, thyroid hormone).

12. Why does sublingual administration avoid first-pass metabolism?

    Drug absorbed from the sublingual mucosa drains into the systemic venous circulation (via superior vena cava) bypassing the portal vein and liver, so it escapes hepatic first-pass metabolism. Example: sublingual nitroglycerin.

13. What is the first-pass (presystemic) effect?

    Metabolism of an orally administered drug in the gut wall and liver before it reaches the systemic circulation, reducing its bioavailability. Drugs with high first-pass: propranolol, lignocaine, GTN, morphine.

14. List the components of WHO's definition of an adverse drug reaction (ADR).

    An ADR is a response to a drug that is noxious and unintended, occurring at doses normally used in humans for prophylaxis, diagnosis, or therapy of disease. It excludes therapeutic failures and intentional overdose.

15. Classify ADRs into Type A and Type B with features.

    Type A (Augmented): dose-dependent, predictable, common, related to pharmacology, low mortality (e.g. bradycardia with beta-blocker). Type B (Bizarre): dose-independent, unpredictable, uncommon, often immunological/idiosyncratic, high mortality (e.g. penicillin anaphylaxis).

16. What is pharmacovigilance?

    The science and activities relating to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems, throughout the drug's life cycle.

17. Give the formula for pediatric dose calculation using body surface area (BSA).

    Child dose = Adult dose × (BSA of child in m² / 1.73 m²). Alternatively Young's rule: dose = adult dose × age/(age+12); Clark's rule uses weight: adult dose × (weight in lb/150).

18. Distinguish pharmacokinetic from pharmacodynamic drug interactions with an example each.

    Pharmacokinetic interactions alter absorption, distribution, metabolism, or excretion (e.g. rifampicin induces CYP3A4, lowering OCP levels). Pharmacodynamic interactions occur at the site of action without changing plasma levels (e.g. additive CNS depression from alcohol + benzodiazepine).

19. What is the mechanism and main clinical use of physostigmine versus neostigmine regarding CNS penetration?

    Both are reversible anticholinesterases. Physostigmine is a tertiary amine, crosses the blood-brain barrier, and is used for central anticholinergic (atropine) poisoning. Neostigmine is a quaternary amine, does not cross BBB, and is used for myasthenia gravis and reversal of non-depolarizing blockade.

20. Name the antidote for organophosphate poisoning and its mechanism.

    Atropine (blocks muscarinic effects) plus pralidoxime (2-PAM), which reactivates acetylcholinesterase by removing the phosphate group—effective only if given before 'aging' of the enzyme.

21. List the muscarinic effects of cholinergic stimulation (parasympathetic).

    DUMBELS: Diarrhea, Urination, Miosis, Bradycardia/Bronchoconstriction, Emesis, Lacrimation, Salivation/Sweating. Also accommodation for near vision and increased GI secretions/motility.

22. Differentiate alpha-1, alpha-2, beta-1, and beta-2 adrenergic receptor effects.

    Alpha-1: vasoconstriction, mydriasis, contraction of sphincters (Gq). Alpha-2: presynaptic inhibition of NE release, decreased central sympathetic outflow (Gi). Beta-1: increased heart rate/contractility, renin release (Gs). Beta-2: bronchodilation, vasodilation, uterine relaxation, glycogenolysis (Gs).

23. Why does adrenaline cause a 'vasomotor reversal of Dale' after an alpha-blocker?

    Adrenaline acts on both alpha (vasoconstriction) and beta-2 (vasodilation) receptors. After alpha-blockade, the unopposed beta-2 action predominates, so adrenaline causes a fall in BP instead of a rise—reversal of its pressor effect.

24. Which antihypertensive beta-blocker overdose is treated with glucagon, and why?

    Beta-blocker overdose is treated with glucagon because it increases cardiac cAMP independently of beta-receptors (via its own receptor and adenylyl cyclase), restoring heart rate and contractility.

25. State the mechanism of action of benzodiazepines and barbiturates on the GABA-A receptor.

    Benzodiazepines increase the FREQUENCY of chloride channel opening; barbiturates increase the DURATION of channel opening. Both potentiate GABA-mediated inhibition. Barbiturates can also directly open the channel at high doses (more dangerous).

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