PHC5005 Principles and Praxis of Pharmacology
The Complete Exam Bible · Sem 1 AY26/27PHC5005 Overview
- National University of Singapore
- Semester 1, AY2026/27
- Postgraduate
- 4 modular credits
- MSc in Medical Pharmacology
What this course is
PHC5005 Principles and Praxis of Pharmacology is a four-credit postgraduate course taught by the Department of Pharmacology at the National University of Singapore, whose timetable lists it under the MSc in Medical Pharmacology.
- Two examinations carry 60% The continuous assessment and the final examination are worth 30% each; two group components carry the rest.
- The quiz is free practice The PK and PD principles quiz carries no weight, and the final examination tests the same lectures.
- Name the parameter first Say whether volume, clearance or bioavailability moved before predicting any plasma level.
- Prodrugs reverse the risk A slow enzyme makes an active drug toxic but leaves a prodrug such as codeine ineffective.
How PHC5005 is assessed
| Component | Weight | Format |
|---|---|---|
| Quiz: Assessment on PK & PD Principles | 0% | Individual. Lectures 1 to 3. The Canvas page states that it does not count toward the final grade; 20 points, due 23 August. |
| Continuous Assessment (CA) | 30% | Individual. Lectures 4 to 11. Scheduled in week 7 on 29 September. |
| Final Examination (FE) | 30% | Individual. Lectures 1 to 16. Scheduled for 1 December. |
| Graded Group Presentation | 20% | Group assessment. Presentations on new modalities in weeks 11 and 12. |
| Critical Review Based on Group Presentation | 20% | Group assessment, built on the group presentation. |
The four graded weights total 100%, and the quiz on PK and PD principles is recorded at 0% in the timetable and described on its Canvas page as not counting toward the final grade. This guide claims no hurdle, minimum mark or grade descriptor for any component in either direction; confirm the current position on Canvas. The timetable lists an assessment briefing in week 5; confirm the examination format and permitted materials there or on Canvas.
Current PHC5005 dates
| Date | Item | Control |
|---|---|---|
| 23 August 2026 | PK and PD quiz due | The ungraded quiz on lectures 1 to 3, locked at 23:59. |
| 29 September 2026 | Continuous Assessment | Week 7, covering lectures 4 to 11, after the reading week of 19 to 27 September. |
| 27 October 2026 | Group presentations begin | Group presentations on new modalities, continuing on 3 November. |
| 1 December 2026 | Final Examination | Covering lectures 1 to 16, after the reading week of 14 to 20 November. |
Dates are as published in the course timetable and Canvas pages published for this offering. Confirm exact deadlines and submission settings in the live LMS.
What PHC5005 covers
Ten source-led chapters move from absorption, distribution, metabolism and excretion to dosing regimens, then from drug targets and receptor theory to population safety, and close with the genes and patient groups that change the answer.
Drug Absorption, Routes and Bioavailability
Patient and drug factors, enteral, parenteral and topical routes, first-pass metabolism and bioequivalenceWhere pharmacokinetics begins
Pharmacokinetics covers the body's handling of a drug, and the course opens it with the first of four processes: absorption, distribution, metabolism and excretion.
- Absorption as the passage of a drug from wherever it is given into the bloodstream
- Patient factors: absorptive surface, gastric emptying, gut contents, disease and age
- Drug factors: molecular size, lipid solubility, ionisation and formulation
- Enteral, parenteral and topical routes compared on speed, completeness and risk
- First-pass metabolism and the bioavailability ranges of each route
- Bioequivalence between branded and generic products
Drug Distribution and Volume of Distribution
Body water compartments, lipid solubility, tissue and protein binding, apparent volume and the loading doseFrom the bloodstream to the tissues
Distribution is the second pharmacokinetic process: the reversible movement of an absorbed drug out of plasma into the fluids and tissues of the body.
- Total body water and its intracellular, interstitial and plasma compartments
- Lipid solubility, redistribution and passage across the placenta and blood-brain barrier
- Tissue binding as a drug reservoir and a source of organ toxicity
- Plasma protein binding, displacement interactions and hypoalbuminaemia
- Blood flow and the order in which tissues receive drug
- Apparent volume of distribution: calculation and interpretation
Drug Metabolism, CYP Enzymes and Interactions
Clearance, Phase I and Phase II reactions, CYP induction and inhibition, metaboliser types and conjugation failuresElimination has two halves
The course defines elimination as the irreversible loss of a drug from the body and splits it into metabolism and excretion. Clearance is the composite measure of both: the volume of plasma cleared of drug per unit time.
- Elimination as metabolism plus excretion, and clearance as their combined measure
- Biotransformation from nonpolar to polar, with inactivation, activation and active metabolites
- Phase I functionalisation against Phase II conjugation
- CYP450 nomenclature and the dominance of CYP3A4
- Enzyme induction and inhibition as drivers of drug-drug interactions
- Metaboliser phenotypes and their consequences for active drugs and prodrugs
Renal Excretion and Dose Adjustment
Filtration, secretion and reabsorption, ion trapping, creatinine clearance thresholds and renal dosing strategiesThe last step in pharmacokinetics
Excretion is the physical process that removes a drug and its metabolites from the body for good, either unchanged or after metabolism.
- Routes of excretion and why polar compounds leave most easily
- Glomerular filtration of free drug and the normal filtration rate
- Passive tubular reabsorption and ion trapping in poisoning
- Active tubular secretion and carrier competition
- Renal blood flow, age and disease as limits on excretion
- Creatinine clearance thresholds for dose adjustment
Half-Life, Steady State and Dosing Regimens
Half-life, the plateau principle, fluctuation and accumulation, loading and maintenance doses and drug monitoringFrom parameters to a regimen
The first four chapters describe how the body handles a drug. This one turns those descriptions into dosing decisions.
- Half-life as a derived parameter of volume and clearance
- Elimination percentages after one to four half-lives
- Steady state, the plateau principle and time to plateau
- Fluctuation and accumulation as measured in the tutorial
- Loading dose, maintenance dose and the risks of loading
- Parameter changes from dehydration, organ failure and dialysis
Drug Targets, Receptors and Selectivity
Target classes, receptor families, binding forces, structure-activity, affinity and the dissociation constant, selectivityThe drug's side of the exchange
Pharmacodynamics studies how drugs act at molecular, cellular and whole-body level, and the mechanisms that produce those actions.
- Drugs as modulators of existing biological processes
- Classes of drug target and where they are located
- The four receptor families and new therapeutic modalities
- Non-covalent and covalent drug-receptor forces
- Structure-activity relationships and the pharmacophore
- Affinity and the equilibrium dissociation constant
Agonists, Antagonists and Concentration-Response
Affinity against efficacy, agonist types, the Emax model, potency, and competitive and non-competitive antagonismTwo steps to a response
A response needs two things from a drug: it must first fit and occupy its receptor, then switch it on. The course names the two abilities separately.
- Affinity and efficacy as separate properties
- Full, partial, inverse and biased agonists
- Graded concentration-response and dose-response curves
- The Emax model, EC50 as potency and Emax as efficacy
- Receptor, chemical, physiological and pharmacokinetic antagonism
- Competitive against non-competitive antagonism and allosteric modulation
Quantal Dose-Response, Therapeutic Index and Tolerance
Sources of variation, quantal curves, ED50, TD50 and LD50, the therapeutic index, hysteresis and toleranceWhy responses differ between people
The course closes its pharmacodynamics lecture by moving from a single receptor system to whole populations. It identifies four sources of individual variation in drug response.
- Pharmacodynamic, pharmacokinetic, disease and environmental sources of variation
- Graded against quantal dose-response relationships
- Log-normal distribution of individual threshold doses
- ED50, TD50 and LD50 as population medians
- The therapeutic index as a risk-benefit ratio
- Anticlockwise and clockwise hysteresis
Pharmacogenetics, CYP2D6 and Phenoconversion
Allele names, phenotype calls, codeine routing, guideline recommendations and inhibitor-driven phenoconversionGenes as a source of drug response variability
The pharmacogenetics lecture sits in the course's block on drug response variabilities, after the pharmacokinetic and pharmacodynamic foundations.
- Pharmacogenetics, pharmacogenomics and personalised medicine
- How the position of a variant changes enzyme expression or function
- CYP2D6 allele nomenclature and phenotype calls
- Codeine as a prodrug and its three metabolic routes
- Guideline-based recommendations by activity score
- Phenoconversion by CYP2D6 inhibitors and its reversibility
Pharmacokinetics in Special Populations
Pregnancy and teratogenicity, lactation, paediatric dosing rules, geriatric changes and body-weight dosing in obesityWhy standard doses fail at the edges
This lecture applies every earlier pharmacokinetic idea to five groups whose physiology differs from the adult reference: pregnant women, lactating mothers, children, older adults and people with obesity.
- Placental transfer and the criteria for teratogenicity
- FDA pregnancy risk categories and the critical developmental period
- Pharmacokinetic changes and safe prescribing in pregnancy
- Drug transfer into breast milk and the lactation risk lists
- Paediatric pharmacokinetics and dose calculation rules
- Geriatric pharmacokinetics and drug classes that need caution
Its stated aim is a comprehensive understanding of the principles that underpin the science of drugs: how drugs are absorbed, distributed, metabolised and excreted, how they act, how dose relates to response, and what decides efficacy, safety, adverse reactions and interactions.
The second half turns to praxis, the design of pharmacokinetic and pharmacodynamic studies in animals and humans and the industrial side of clinical trials.
How the principles are taught
The first week is an intensive block. Two lectures cover pharmacokinetics, one covers pharmacodynamics, and two tutorials apply them, followed by an ungraded quiz on exactly that material.
Pharmacokinetics is organised around four processes, absorption, distribution, metabolism and excretion, and then brought together in half-life, steady state and the loading and maintenance doses that follow from them. Pharmacodynamics moves from drug targets and receptors through agonism, antagonism and the concentration-response curve to population measures of safety such as the therapeutic index.
Later weeks cover receptor families, drug response variabilities from genes and special populations, interactions, adverse reactions and new therapeutic modalities.
What the guide concentrates on
This guide follows the principles block chapter by chapter.
It explains each mechanism in the course's own terms, works the calculations the lectures set, from bioavailability and volume of distribution to clearance, steady state and the Emax model, and applies them to the patients the lectures use: the elderly patient on a renally cleared drug, the child whose dose cannot simply be scaled down, the obese patient and the question of which weight to dose on, and the codeine consult in which genotype and co-medication together decide whether a painkiller works.
Where marks come from
The published assessment gives sixty per cent of the grade to two individual examinations, a continuous assessment in week seven covering lectures four to eleven and a final examination in December covering all sixteen lectures, and forty per cent to two group components built on presentations about new modalities.
The early quiz on pharmacokinetic and pharmacodynamic principles counts for nothing, which makes it the cheapest practice available for the foundations the final examination returns to.
A note on the lecture markers
Several slides in the pharmacokinetics lectures are labelled as for understanding and not counted for assessment, including the area-under-curve method for bioavailability, the creatinine clearance and renal clearance formulas, the maintenance-dose equation and long tables of enzyme substrates.
The guide keeps them, because they explain the assessed ideas, and marks them wherever they appear so that revision time can follow the lecturers' own weighting.
Worked example · free
Setting an oral loading dose from volume and bioavailability
- 2Find the amount that must be in the body.
- 2Correct for bioavailability.
- 1State why the loading dose ignores clearance.
Key terms
- Pharmacology
- The science of how chemical substances act on living systems, most often by binding molecules that regulate normal processes.
- Pharmacokinetics
- The body's handling of a drug over time through absorption, distribution, metabolism and excretion.
- Pharmacodynamics
- The drug's effects on the body, from binding at its targets to the responses that follow.
- ADME
- Shorthand for absorption, distribution, metabolism and excretion, the four processes that govern drug exposure.
- Drug Target
- The macromolecule, usually a protein, to which a drug binds to produce its effect.
- Rational Prescribing
- Choosing drug, route, dose and formulation to suit the patient, informed by pharmacokinetic and pharmacodynamic principles.
- Personalised Medicine
- Treatment that considers the genetics of the disease and the pharmacogenomic factors shaping an individual's response.
- Narrow Therapeutic Index
- A small gap between effective and toxic exposure, as with warfarin, lithium and digoxin, calling for monitoring.
- Special Population
- A patient group, such as pregnant women, children, older adults or people with obesity, whose physiology changes drug handling.
PHC5005 FAQ
How is this pharmacology course assessed?
The timetable for this offering lists five items. The continuous assessment and the final examination are individual and worth 30 per cent each; a graded group presentation and a critical review based on it are worth 20 per cent each; and a quiz on pharmacokinetic and pharmacodynamic principles carries no weight.
Which lectures does each examination cover?
The continuous assessment in week seven covers lectures four to eleven, the receptor-family lectures through drug-drug interactions. The final examination covers lectures one to sixteen, so the week-one pharmacokinetics and pharmacodynamics lectures are examined only there.
Is the early PK and PD quiz worth doing?
It counts nothing toward the grade, but it tests lectures one to three, the same foundations the final examination draws on. Treat it as a free diagnostic: every error it exposes is one you can fix before the marks start to count.
Which pharmacokinetic formulas matter most?
Volume of distribution as amount over plasma concentration, the loading dose from target concentration and volume, clearance and its link to half-life, and the steady-state level as dose rate over clearance. The lectures mark several longer formulas, such as creatinine clearance, as for understanding only.
Why do two patients respond differently to the same dose?
The course names four sources: pharmacodynamic differences in the target, pharmacokinetic differences in absorption, distribution, metabolism and excretion, disease, and environment such as diet and supplements. Its later lectures develop genetic variation and special populations as the main examples.
What does the pharmacogenetics tutorial involve?
It is a consult on codeine run in four layers. Teams decode CYP2D6 alleles, call each patient's phenotype, trace how codeine becomes morphine, apply a teaching table consistent with published CPIC guidance, and then meet patients whose co-medication changes their phenotype.
What are the group components about?
Both are built around new therapeutic modalities. Groups present in weeks eleven and twelve, and a critical review based on the presentation carries a further 20 per cent. Their marking criteria are not among the materials this guide draws on, so read them in the course materials before planning the work.
Questions students ask in each PHC5005 chapter
- Why is the small intestine the main site of absorption for most oral drugs?
- Its lining carries microvilli and a rich splanchnic blood supply, so the absorptive surface and perfusion far exceed the stomach's. Even a weak acid that is mostly unionised in gastric acid is absorbed in greater total amount further down, because area and blood flow outweigh the ionisation advantage. Chapter 01 · Drug Absorption, Routes and Bioavailability
- Can a drug really have a volume of distribution of hundreds of litres?
- The number can be that large, but the patient does not contain that much fluid. A large Vd arises when most of the dose leaves plasma for fat, muscle, bone or intracellular sites, so the plasma concentration used as the denominator is very small and the calculated ratio becomes huge. Chapter 02 · Drug Distribution and Volume of Distribution
- Is clearance the same thing as excretion?
- No. Excretion is one of the two processes that remove a drug; metabolism is the other. Clearance is the composite estimate of all elimination mechanisms, expressed as a volume of plasma cleared per unit time, so a patient with healthy kidneys can still have low clearance if liver metabolism is impaired. Chapter 03 · Drug Metabolism, CYP Enzymes and Interactions
- Why is protein-bound drug not filtered at the glomerulus?
- Filtration passes water and small solutes but holds back plasma proteins, so drug attached to albumin stays in the blood. Only the free fraction enters the tubule, which is why heavy protein binding slows renal elimination and why a change in binding changes excretion. Chapter 04 · Renal Excretion and Dose Adjustment
- Does a bigger dose reach steady state faster?
- No. The time to steady state depends on the half-life alone, four to five half-lives whatever the dose. A larger dose rate raises the height of the plateau in proportion but not the speed of approach; a loading dose is the way to reach the target sooner. Chapter 05 · Half-Life, Steady State and Dosing Regimens
- Are all drug targets receptors?
- No. Receptors are one class. Drugs also act on enzymes, transporters, pumps, structural proteins, membrane lipids and nucleic acids. The course's examples include lovastatin inhibiting HMG-CoA reductase, fluoxetine blocking serotonin reuptake and cisplatin interfering with DNA replication. Chapter 06 · Drug Targets, Receptors and Selectivity
- What is the difference between potency and efficacy?
- Potency is about how much drug is needed: a more potent drug reaches a given effect at a lower concentration, so it has a lower EC50. Efficacy is about how much effect is possible: it is the maximal response, Emax. Two drugs can share one and differ in the other. Chapter 07 · Agonists, Antagonists and Concentration-Response
- When is a quantal dose-response curve used instead of a graded one?
- When the response cannot be graded because it is all or none, such as prevention of convulsions, stopping an arrhythmia or death. The study then records how many subjects respond at each dose and plots the cumulative percentage, which is why ED50 is a population figure rather than an individual one. Chapter 08 · Quantal Dose-Response, Therapeutic Index and Tolerance
- What is the difference between pharmacogenetics and pharmacogenomics?
- Pharmacogenetics studies how genetic variation influences drug response. Pharmacogenomics goes a step further and uses genetic information to guide which drug an individual receives. Both feed personalised medicine, which considers disease genetics and pharmacogenomic factors together. Chapter 09 · Pharmacogenetics, CYP2D6 and Phenoconversion
- Why is heparin preferred over some anticoagulants in pregnancy?
- Heparin is a large molecule that does not cross the placenta, so the fetus is not exposed. Warfarin, by contrast, appears in the teratogen table for every trimester with effects that include nasal hypoplasia, bone and nervous system malformations and bleeding. Chapter 10 · Pharmacokinetics in Special Populations
How to study for the exam
Work the principles block in the order of the course: one pharmacokinetic process at a time, then the dosing chapter that joins them, then the receptor theory. After each chapter, close the book and write its key relationship and one worked number from memory. Use the ungraded quiz in the first fortnight as your baseline and the integrated practice before each examination.
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