MDG5204 Advanced Topics in Fundamental and Applied Pharmacology
The Complete Exam Bible · Sem 1 AY26/27MDG5204 Overview
- National University of Singapore
- Semester 1, AY2026/27
- Postgraduate
- 4 Units
- Closed-book final examination
What the course sets out to do
MDG5204 is a graduate course taught by the Department of Pharmacology at the Yong Loo Lin School of Medicine.
- Assessed by A closed-book final examination at 60%, a journal club presentation at 30%, and attendance and participation at 10%.
- Pass the quiz first A PK/PD quiz score of at least 16 out of 20 is the condition for sitting the final examination.
- Write in points Each examination answer is marked one factual point per mark, so plan ten distinct facts before writing.
- Attendance The overview sets a minimum attendance requirement of 80%, which does not apply to part-time students.
How MDG5204 is assessed
| Component | Weight | Format |
|---|---|---|
| Final Examination (Semi-structured / Essays) | 60% | Closed book, Tuesday 24 November 2026, 1 to 3pm. Structured essay questions: choose 6 of 8, each worth 10% of total marks at one factual point per mark. |
| Journal club / Seminar | 30% | Individual or team of two, about 15 to 20 minutes, in six sessions from 20 October to 5 November. Content 15%, presentation 10%, delivery 5%; a pair shares the content mark. |
| Attendance / Class participation | 10% | Each presenter is asked at least one question and each questioner is rated, 5% each. Attendance of at least 80% is required, but not of part-time students. |
| Class Quiz on PK / PD · hurdle | Based on the consolidated pharmacokinetics and pharmacodynamics lectures. At least 16 out of 20 is needed to proceed, and a student who does not pass cannot take the final examination. Due 31 August 2026 at 23:30 on Canvas; the overview states 30 August. |
The three weighted components total 100%. The PK/PD quiz is the stated pass condition: a score of at least 16 out of 20 is needed to sit the final examination. The Canvas quiz page says the quiz does not count toward the final grade, while the course overview groups quiz, attendance and participation under the 10% component; the pass mark is the same on both. The overview also sets a minimum attendance requirement of 80%, which does not apply to part-time students. No minimum mark for the examination or the journal club appears in the course materials reviewed here, so confirm the current position on Canvas.
Current MDG5204 dates
| Date | Item | Control |
|---|---|---|
| 31 August 2026 | PK/PD quiz due | Canvas states 23:30 on 31 August; the course overview gives 30 August, so aim for the earlier date. |
| 15 October 2026 | Examination briefings | A briefing on the computer-based examination platform, followed by a briefing on the final examination itself. |
| 20 October 2026 | Journal clubs begin | Six sessions run from 20 October to 5 November, with each topic released about three weeks before its session. |
| 24 November 2026 | Final examination | Closed book, 1 to 3pm; the venue is listed as to be confirmed. |
Dates are as published in the timetable and course overview published for this offering. Confirm exact deadlines and submission settings in the live LMS.
What MDG5204 covers
Eleven chapters follow the course from the four pharmacokinetic processes and the dosing arithmetic that joins them, through receptor pharmacology, to the nervous system, Parkinson disease and ischaemic stroke.
Drug Absorption, Routes and Bioavailability
Factors that change absorption, enteral against parenteral routes, first-pass metabolism, bioavailability from AUC and bioequivalenceWhere the course begins
The foundations theme opens with the four processes that decide what happens to a dose between the moment it is given and the moment it is gone.
- Absorption defined as transfer from the point of dosing into the blood
- Patient factors: absorptive surface, gastric emptying, gut contents, disease and demographics
- Drug factors: lipid solubility, size, ionisation, solubility and formulation
- Enteral, parenteral and topical routes compared on speed and completeness
- First-pass metabolism and the drugs whose route it changes
- Bioavailability from the ratio of oral to intravenous AUC, and bioequivalence of generics
Drug Distribution and the Volume of Distribution
Body water compartments, lipid solubility and redistribution, apparent volume of distribution, loading dose and protein bindingFrom the blood into the body
Distribution is what happens after absorption: the drug leaves the plasma and moves into interstitial fluid, into cells and into tissues.
- Distribution defined through the apparent volume a drug seems to occupy
- Total body water, intracellular and extracellular fluid and plasma as reference volumes
- Lipid solubility, blood flow and redistribution to muscle and fat
- Apparent volume of distribution calculated from an intravenous dose
- Loading dose from target concentration, volume and bioavailability
- Plasma protein binding, displacement interactions and tissue binding
Drug Metabolism and Cytochrome P450 Interactions
Phase I and Phase II reactions, CYP inducers and inhibitors, metaboliser phenotypes and the conjugation failures taught as casesWhy drugs are metabolised
The properties that let a drug cross membranes, lipid solubility above all, are the properties that stop the kidney removing it.
- Biotransformation from nonpolar to polar and why it is needed for excretion
- Phase I oxidation, reduction and hydrolysis against Phase II conjugation
- Cytochrome P450 nomenclature and the dominance of CYP3A4
- Enzyme inducers and inhibitors and the direction of each interaction
- Poor, extensive and ultrarapid metabolisers and prodrug activation
- Glucuronidation, glutathione and acetylation failures and who metabolises less
Renal Excretion and Dose Adjustment
Filtration, reabsorption and secretion, ion trapping, carrier competition, creatinine clearance and renal dose adjustmentThe last pharmacokinetic process
Excretion is the irreversible physical removal of a drug and its metabolites from the body.
- Excretion routes and why the kidney dominates
- Glomerular filtration of free drug and the normal filtration rate
- Tubular reabsorption of unionised, lipid-soluble drug
- Ion trapping and the use of urinary pH in poisoning
- Active tubular secretion and probenecid competition with penicillin
- Creatinine clearance thresholds and the two dose-adjustment strategies
Clearance, Half-Life and Steady-State Dosing
Clearance as metabolism plus excretion, half-life, the plateau principle, loading and maintenance doses and drug monitoringTwo numbers that summarise elimination
Clearance is the course's measure of how efficiently the body removes a drug.
- Clearance as metabolism plus excretion and its units
- Half-life and its dependence on volume of distribution and clearance
- The four-to-five half-life rule for elimination and accumulation
- Steady state, the plateau principle and the therapeutic window
- Loading dose from volume and maintenance dose from clearance
- Therapeutic drug monitoring and the drugs that need it
Drug Targets, Receptors and Selectivity
Protein and nucleic acid targets, receptor families, binding forces, the pharmacophore and selectivity against specificityFrom kinetics to dynamics
Pharmacodynamics is the study of what a drug does to the body: its biochemical, cellular and physiological actions and the molecular mechanisms behind them.
- Drugs modulate existing biology rather than creating new processes
- Protein and nucleic acid targets with one drug example for each
- New modalities from monoclonal antibodies to gene silencing
- Four receptor-effector families and the forces of drug binding
- Structure-activity relationships and the pharmacophore
- Selectivity against specificity, beta-blockers, antihistamines and hERG
Dose-Response, Agonism and Antagonism
Affinity and efficacy, EC50 and Emax, agonist types, the kinds of antagonism, quantal curves and the therapeutic indexBinding follows the law of mass action
The course treats drug-receptor binding as a reversible reaction whose rate depends on the concentrations of drug and receptor.
- Law of mass action, KD and affinity
- Occupancy against activation: efficacy and intrinsic activity
- Full, partial, inverse and biased agonists
- EC50 and Emax on graded concentration-response curves
- Receptor, chemical, physiological and pharmacokinetic antagonism
- Quantal curves, ED50, TD50, LD50 and the therapeutic index
Neurotransmission and Basal Ganglia Motor Circuits
Resting and action potentials, transmitter release and termination, the main transmitters and the direct and indirect pathwaysNeuropharmacology as its own layer
The second theme applies the pharmacology of the first to the nervous system. Neuropharmacology asks how chemical substances change the way the nervous system works, how it is built and its chemistry.
- Neuropharmacology defined and why complexity limits prediction
- Resting membrane potential and the ion-channel sequence of the action potential
- Calcium-triggered transmitter release, termination and autoreceptors
- Glutamate, GABA, acetylcholine and dopamine
- Direct and indirect basal ganglia pathways
- Dopamine acting through D1 and D2 receptors in the striatum
Parkinson Disease and the Blood-Brain Barrier
Motor signs and pathology, the circuit explanation, dopaminergic drug strategies, barrier structure and routes into the brainThe disease the circuits predict
Parkinson disease is the course's main example of neurodegeneration. Its motor features are resting tremor, bradykinesia, rigidity and postural instability.
- Motor features and the protein-clearance failure behind Parkinson disease
- Loss of nigrostriatal dopamine and its effect on both motor pathways
- Levodopa with carbidopa and its long-term limits
- COMT inhibitors, MAO-B inhibitors and dopamine agonists
- Functions and structure of the blood-brain barrier
- Diffusion, carriers, efflux and strategies for delivering drugs to the brain
Ischaemic Stroke: Mechanisms and Acute Treatment
Definition and mechanisms, the Singapore burden, risk factors, imaging first, thrombolysis and neuroprotectionA major cause of death and disability
The stroke lecture opens with its scale.
- The burden of stroke in Singapore as the course presents it
- The WHO definition and the transient ischaemic attack
- Rupture against occlusion and the ischaemic cascade
- Modifiable and non-modifiable risk factors
- Arterial territories and the circle of Willis
- Imaging first, thrombolysis within the window and failed neuroprotection
Stroke Research: Animal Models, Genetics and Biomarkers
MCAO and other rodent models, the translation gap and strain differences, genome-wide association studies and stroke biomarkersHow new stroke treatments are sought
The research half of the stroke lecture asks how the field looks for new treatments, and it describes stroke research as multimodal.
- Research axes: in vitro and in vivo, basic and translational, human and animal
- Global and focal models and the intraluminal MCAO procedure
- Measuring infarcts with TTC staining and behavioural tests
- Why hundreds of neuroprotectants failed to translate
- Genome-wide association studies and monogenic stroke genes
- Biochemical biomarkers and the MMP-9 finding
It aims to give an in-depth understanding of advanced topics in three areas, general pharmacology, neuropharmacology and cancer pharmacology, through lectures and journal clubs led by clinical and basic science experts.
The course overview frames its audience as life-science and biomedical graduate students who need depth both inside and outside their own research, and it asks them to carry ideas from the lectures back into their own work.
How the lectures are organised
The timetable groups the teaching into three themes.
The foundations theme opens the semester with combined lectures on pharmacokinetics, covering absorption, distribution, metabolism and excretion, and on pharmacodynamics. The second theme, on excitable membranes, channels and neurotransmission, treats the brain as a drug target and moves through neurodegeneration to stroke.
The third theme, on signal transduction and cell proliferation, covers cancer biology, non-coding RNA, HDAC inhibitors, signalling kinases, the cell cycle, GPCRs, immune signalling and precision oncology. Journal club sessions follow the lectures.
This guide covers the first two themes in eleven chapters; the cancer lectures should be revised directly from their slides.
The ideas that hold the foundations together
Pharmacokinetics asks how the body handles a drug, and pharmacodynamics asks how the drug acts on the body.
On the kinetic side, two numbers summarise almost everything: the volume of distribution, which sets the loading dose, and clearance, which sets the maintenance dose and, together with the volume, the half-life. On the dynamic side, affinity decides whether a drug occupies its receptor and efficacy decides what happens once it does, which is why potency and maximal effect are read from different axes of the same curve.
The neuropharmacology chapters then use both halves at once: levodopa works in Parkinson disease because a transporter carries it across the blood-brain barrier, and the only proven acute stroke drug is limited by timing and by haemorrhage risk.
What is assessed
Three components carry the grade: a closed-book final examination worth 60%, a journal club presentation worth 30%, and attendance and class participation worth 10%.
The examination consists of structured essay questions, with six answered from eight offered, each worth 10% of the course total at one factual point per mark. The journal club is an individual or paired presentation of about 15 to 20 minutes, marked on content, presentation and delivery.
Before any of this, a quiz on the pharmacokinetics and pharmacodynamics lectures acts as a gatekeeper: a score of at least 16 out of 20 is needed, and a student who does not pass cannot take the final examination. The overview also sets a minimum attendance requirement of 80%, which does not apply to part-time students.
Where the published details differ
Two details differ between course documents.
The overview gives the quiz deadline as 30 August 2026, while the Canvas assignment page gives 31 August at 23:30, so the earlier date is the safer target. The Canvas page also says the quiz does not count toward the final grade, while the overview lists it within the 10% for participation, quiz and attendance; the pass mark of 16 out of 20 is the same on both.
Some older course pages still show dates from earlier years, and this guide uses the 2026/2027 timetable throughout.
Worked example · free
Designing an oral regimen from Vd, clearance and bioavailability
- 2Compute the half-life from Vd and CL.
- 1State the time to steady state without loading.
- 2Compute the oral loading dose, correcting for F.
- 3Compute the dose rate and the oral maintenance dose per interval.
Key terms
- Pharmacokinetics
- The body’s handling of a drug over time: its absorption, distribution, metabolism and excretion.
- Pharmacodynamics
- What a drug does to the body: its targets, its mechanism of action and the relation between concentration and effect.
- Bioavailability
- The fraction of an administered dose that reaches the systemic circulation, 100% by definition for an intravenous dose.
- First-Pass Metabolism
- Metabolism of an oral drug in the gut wall and liver before it reaches the systemic circulation, lowering bioavailability.
- Volume of Distribution
- The volume that would hold the total amount of drug in the body at the concentration measured in plasma.
- Clearance
- The volume of plasma cleared of drug per unit time, combining metabolism and excretion.
- Half-Life
- The time for the plasma concentration to fall by half, set by the volume of distribution and clearance.
- Steady State
- The plateau reached with repeated dosing when the rate of elimination equals the rate of administration.
- Therapeutic Index
- The ratio of the dose toxic to half a population to the dose effective in half, TD50 over ED50.
- Partial Agonist
- A ligand that activates its receptor but falls short of the full system response however high its concentration.
- Competitive Antagonist
- A drug that binds the agonist site reversibly, shifting the concentration-response curve right without lowering its maximum.
- Blood-Brain Barrier
- The tight-junction seal of brain capillaries and choroid plexus that limits which drugs reach neurons.
MDG5204 FAQ
How is this course assessed?
Three components make up the grade: a closed-book final examination worth 60%, a journal club presentation worth 30%, and attendance and class participation worth 10%. The examination is structured essays, answering six of eight questions. Before any of these, a quiz on pharmacokinetics and pharmacodynamics must be passed to be allowed to sit the examination.
What are the pass conditions for the quiz and for attendance?
A student who scores below 16 out of 20 cannot take the final examination, which carries 60% of the grade, so the quiz acts as a gatekeeper. Canvas lists the deadline as 31 August at 23:30 and the overview as 30 August. Separately, the overview sets a minimum attendance requirement of 80%, which does not apply to part-time students.
What does the final examination look like?
It is closed book and runs for two hours on the afternoon of 24 November 2026. Eight structured essay questions are offered and six must be answered. Each carries 10% of the total at one factual point per mark, which rewards listing separate facts over fluent prose. A briefing on the computer-based platform is held on 15 October.
Why does oral bioavailability differ so much between drugs?
Two things intervene between swallowing and the circulation: incomplete absorption across the gut, and metabolism in the gut wall and liver on first passage. Drugs that are poorly lipid soluble or heavily metabolised on that passage, such as nitroglycerin, reach the circulation in small fractions, while others arrive almost intact.
What is the volume of distribution actually telling you?
It reports how widely a drug spreads relative to its plasma concentration, not a physical space. A value near plasma volume suggests the drug stays in the vessels, a value near total body water suggests even spread, and a value far above body water means tissue binding. Its practical use is choosing a loading dose.
How do enzyme inducers and inhibitors change another drug's effect?
An inducer raises expression of the metabolising enzyme, so a co-prescribed substrate is cleared faster, its level falls and treatment can fail, as with rifampin and oral contraceptives. An inhibitor blocks the enzyme, so the substrate accumulates and toxicity becomes likely, as with grapefruit juice and a CYP3A4-dependent statin.
What is the difference between potency and efficacy?
Potency is how much drug is needed for a given effect, read as the EC50 on the horizontal axis; a lower EC50 means higher potency. Efficacy is the largest effect the drug can produce, read as Emax on the vertical axis. Two drugs can share one and differ in the other.
How is the journal club presentation marked?
Out of 30%: content carries 15% for scientific, thorough and thoughtful work, presentation 10% for clear slides that favour figures and tables over text, and delivery 5% for speed, clarity and timing. Individuals present for about 15 minutes and pairs for about 20; a pair shares the content mark but is marked individually on the rest.
Questions students ask in each MDG5204 chapter
- Why does a drug given by mouth take longer to act than the same drug given intravenously?
- An intravenous dose is already in the circulation, while an oral dose must dissolve, cross the gut wall and pass the liver before it arrives. Gastric emptying, food and gut motility all slow that journey, which is why an oral antihypertensive can take about an hour to show any effect. Chapter 01 · Drug Absorption, Routes and Bioavailability
- Why can the volume of distribution be larger than the whole body?
- Because it is calculated rather than measured. When a drug binds strongly to tissue, very little remains in plasma, and dividing the amount in the body by that small concentration produces a large number. It signals extensive tissue uptake, not a body of that size. Chapter 02 · Drug Distribution and the Volume of Distribution
- Why does grapefruit juice matter for someone taking a statin?
- Grapefruit juice inhibits CYP3A4, the enzyme that metabolises several statins. With the enzyme blocked, the statin is cleared more slowly and its plasma level rises, increasing the risk of dose-related adverse effects. The juice changes the handling of the drug rather than having an effect of its own. Chapter 03 · Drug Metabolism and Cytochrome P450 Interactions
- Why does protein binding reduce renal filtration of a drug?
- The glomerulus filters plasma water and small solutes, and a drug bound to albumin is carried as part of a large protein that is not filtered. Only the unbound fraction passes into the tubule, so extensive binding slows renal elimination unless the drug is also actively secreted. Chapter 04 · Renal Excretion and Dose Adjustment
- Why does it take four to five half-lives to reach steady state?
- Accumulation approaches the plateau in the same exponential way that elimination approaches zero, covering half the remaining distance each half-life. After four to five half-lives the level is within a few per cent of the plateau, which the course treats as steady state for practical purposes. Chapter 05 · Clearance, Half-Life and Steady-State Dosing
- Why do most drugs have side effects even when they are well designed?
- Most drugs are selective rather than specific: they prefer one target but bind others at higher concentrations. As concentration rises that preference weakens, so off-target binding produces effects unrelated to the intended one, as with dry mouth from older antihistamines. Chapter 06 · Drug Targets, Receptors and Selectivity
- Can a drug have high affinity but low efficacy?
- Yes. A partial agonist binds strongly, with high affinity, but activates the receptor only weakly, so it cannot reach the full response of the system. An antagonist is the extreme case: it can bind with high affinity while having no efficacy at all. Chapter 07 · Dose-Response, Agonism and Antagonism
- Why does the inside of a resting neuron sit at a negative voltage?
- The resting membrane is far more permeable to potassium than to sodium, so potassium leaking out leaves the inside negative, and the sodium-potassium pump maintains the gradients. The result is a resting potential of about minus 70 mV, from which depolarisation starts. Chapter 08 · Neurotransmission and Basal Ganglia Motor Circuits
- What causes the motor symptoms of Parkinson disease?
- Degeneration of dopaminergic neurons in the substantia nigra pars compacta removes dopamine input to the striatum. Both basal ganglia pathways then shift towards greater inhibition of the thalamus, reducing cortical drive and producing slowness, rigidity, tremor at rest and postural instability. Chapter 09 · Parkinson Disease and the Blood-Brain Barrier
- What does time is brain mean in practice?
- Once an artery is blocked, the ischaemic cascade progresses minute by minute and tissue that could be saved is lost. Treatment that restores flow, such as thrombolysis, is only offered within a narrow window of about 3 to 4.5 hours, so delay directly reduces what can be rescued. Chapter 10 · Ischaemic Stroke: Mechanisms and Acute Treatment
- Why is middle cerebral artery occlusion the most used stroke model?
- The middle cerebral artery is the vessel most often affected in human ischaemic stroke, and the intraluminal suture method produces reproducible infarcts with a penumbra without opening the skull, while allowing reperfusion to be controlled. Its main weakness is that it involves no clot, so it suits thrombolytic studies poorly. Chapter 11 · Stroke Research: Animal Models, Genetics and Biomarkers
How to study for the exam
Rebuild the dosing arithmetic of the first five chapters by hand until you can produce every equation from memory, because it underpins the foundations questions and the quiz you must pass. Then, for each neuropharmacology topic, pair every mechanism with one named drug, since a mechanism with its example is worth two points in the examination format.
Your AI Pharmacology tutor for MDG5204
Stuck on a hard MDG5204 question? Sia is AskSia’s AI Pharmacology tutor — ask any MDG5204 Advanced Topics in Fundamental and Applied Pharmacology question and get a clear, step-by-step explanation grounded in how the course is actually taught and assessed. Read this whole study guide free, then take your hardest questions to Sia.
