Lebanon Pharmacy Colloquium key terms

The fraction of an administered dose of unchanged drug that reaches systemic circulation. Intravenous dosing defines F = 1; oral products are compared against it to compute extent of absorption.

The absence of a significant difference in the rate and extent of absorption between two pharmaceutically equivalent products. Regulators typically require 90% confidence intervals for AUC and Cmax within 80–125%.

Presystemic biotransformation of an orally absorbed drug in gut wall or liver before it reaches systemic circulation, lowering oral bioavailability. Drugs with extensive first-pass loss often need higher oral doses or alternative routes.

An inactive or less active chemical derivative that is converted in the body to the active drug, usually to improve absorption, stability, or targeting. Examples include ester prodrugs hydrolysed by esterases.

Elimination in which a constant amount of drug is removed per unit time regardless of concentration, because eliminating enzymes are saturated. Plasma concentration falls linearly, and half-life lengthens as dose rises.

Elimination in which a constant fraction of the drug present is removed per unit time, so plasma concentration decays exponentially. Half-life is constant and independent of dose for most drugs at therapeutic concentrations.

The time required for plasma concentration to fall by half during first-order elimination. It determines dosing interval and time to steady state, which is roughly four to five half-lives.

The volume of plasma from which drug is completely removed per unit time. It links dose rate to steady-state concentration and reflects combined hepatic, renal, and other elimination pathways.

The condition during repeated dosing when drug input equals elimination, so plasma concentration fluctuates around a constant mean. It is reached after about four to five half-lives of unchanged dosing.

An apparent volume relating the amount of drug in the body to its plasma concentration. A large Vd indicates extensive tissue distribution; Vd helps calculate loading doses.

An initial larger dose given to reach therapeutic concentration rapidly, calculated from target concentration and volume of distribution. Maintenance doses then replace ongoing elimination.

Measurement of plasma drug concentrations to individualise dosing for drugs with narrow therapeutic indices, poor concentration-response correlation, or unpredictable kinetics. Interpretation requires sampling time and clinical context.

A small ratio between toxic and effective doses, meaning minor concentration changes risk toxicity or failure. Such drugs demand careful dosing, monitoring, and cautious substitution between products.

A ligand that binds a receptor and activates it, producing a biological response. Full agonists achieve maximal response; partial agonists produce submaximal effects even at full occupancy.

A ligand that binds the receptor without activating it and can be overcome by higher agonist concentrations. It shifts the agonist dose-response curve rightward without reducing maximal response.

The agonist concentration producing half of its maximal response, reflecting potency. A lower EC50 means higher potency; it is distinct from affinity and from Kd measured in binding studies.

The systematic link between a molecule's chemical features and its biological activity. Medicinal chemists use it to modify functional groups and optimise potency, selectivity, and pharmacokinetic behaviour.

The spatial arrangement of chemical features essential for a molecule to bind a target and produce activity. It guides scaffold hopping and virtual screening during lead optimisation.

A set of guidelines predicting oral drug-likeness: molecular weight under 500, logP under 5, hydrogen-bond donors under 5, and acceptors under 10. Violations suggest poorer absorption likelihood.

The property of a molecule that is non-superimposable on its mirror image, usually due to a carbon with four different substituents. Enantiomers can differ markedly in potency, kinetics, and toxicity.

An equimolar mixture of two enantiomers that is optically inactive. Because enantiomers may have different pharmacological and toxicological profiles, racemic drugs require careful evaluation.

Adjusting an herbal preparation to a defined marker or active constituent content to ensure batch-to-batch consistency. It may use chemical markers, chromatographic fingerprints, or biological assays.

A characteristic constituent used to identify or quantify an herbal extract, whether or not it is the active principle. Markers support quality control and detection of adulteration.

The study of medicinal substances of natural origin, covering their botany, chemistry, cultivation, extraction, and quality control. It underpins development and regulation of herbal medicinal products.

A change in drug effect caused by a botanical product, often through enzyme or transporter modulation. St John's wort inducing CYP3A4 and reducing oral contraceptive efficacy is a classic example.

A harmful or unintended response to a medicine at doses normally used for prevention, diagnosis, or treatment. Reactions are classified by mechanism, including dose-related, idiosyncratic, and hypersensitivity types.

The science of detecting, assessing, understanding, and preventing adverse effects or other drug-related problems. Activities include spontaneous reporting, signal detection, and risk management planning.

The process of identifying a new or incompletely documented safety concern from case reports or databases. Disproportionality statistics flag potential signals that require clinical and epidemiological assessment.

A product marketed after patent or exclusivity expiry, containing the same active substance and shown to be bioequivalent to the reference product. It is approved on evidence of quality and equivalence rather than new efficacy trials.

The condition in which two products contain the same amount of the same active substance in identical dosage forms meeting compendial standards. It does not by itself prove therapeutic equivalence.

The quality-assurance system ensuring medicinal products are consistently produced and controlled to quality standards. It covers premises, personnel, documentation, validation, and complaint handling.

An official compendium of drug quality standards, tests, and monographs recognised by a regulatory authority. It provides legally binding specifications for identity, purity, and assay.

The testing and sampling activities confirming that materials and products meet specifications. It differs from quality assurance, which covers the whole system ensuring quality is built in.

A medicine whose sale or supply is restricted by law because of abuse potential, toxicity, or dependence risk. Dispensing requires prescription, special records, and secure storage.

The mandatory elements a valid prescription must contain, such as prescriber details, patient identity, drug name, dose, and date. Missing elements make dispensing unlawful and require clarification.

The professional duty to protect patient health information from unauthorised disclosure. It may be overridden only by law, patient consent, or serious public health risk.

The responsible provision of drug therapy to achieve definite outcomes that improve a patient's quality of life. It involves identifying, resolving, and preventing medication-related problems collaboratively.

A structured process comparing a patient's current medicines with newly prescribed ones at transitions of care. It aims to prevent omissions, duplications, and dosing errors.

A structured dialogue giving patients the information and skills needed to use medicines correctly. It covers indication, dose, administration, expected effects, and when to seek help.

The extent to which a patient's behaviour matches agreed recommendations from a prescriber. It is influenced by regimen complexity, side effects, beliefs, and cost, and is distinct from persistence.

A preventable mistake occurring during prescribing, transcribing, dispensing, or administration of a medicine. Reporting and root-cause analysis help identify system failures rather than blaming individuals.

The study of costs and consequences of pharmaceutical products and services. Analyses include cost-minimisation, cost-effectiveness, cost-utility, and cost-benefit to inform resource allocation.

A health outcome measure combining length of life with quality of life, where one year in perfect health equals 1. It is used in cost-utility analysis to compare interventions.

The number of patients who must be treated for one additional patient to benefit. It equals the reciprocal of the absolute risk reduction and reflects clinical impact.

The number of new cases of a condition arising in a defined population during a specified period. It measures risk of developing disease and differs from prevalence.

The proportion of a population affected by a condition at a given time or over a period. It reflects both incidence and duration of disease.

A substance that counteracts the toxic effect of a poison through chemical, pharmacological, or physiological mechanisms. Examples include activated charcoal, naloxone, and N-acetylcysteine.