NEET-SS key terms

The proportion of people who truly have a condition and are correctly identified as positive by a test. A highly sensitive test rarely misses disease, so it suits screening and rule-out purposes.

The proportion of people without a condition who are correctly identified as negative. A highly specific test seldom labels healthy people as diseased, so it is useful for confirming a diagnosis after a positive screen.

The probability that a person with a positive test result actually has the disease. It rises as disease prevalence in the tested population rises, even when sensitivity and specificity stay fixed.

The probability that a person with a negative test result genuinely does not have the disease. It increases when the condition is rare in the population being tested and falls in high-prevalence settings.

A ratio comparing the chance of a given test result in diseased versus non-diseased people. Positive and negative likelihood ratios summarise how much a result shifts the post-test probability of disease.

The number of patients who must receive an intervention for one additional person to gain the intended outcome. It is the reciprocal of the absolute risk reduction and falls as benefit grows.

The arithmetic difference in event rates between control and treated groups, expressed as a proportion or percentage. Unlike relative measures, it reflects the true clinical magnitude of benefit in the studied population.

An analysis that assigns every participant to the group they were originally randomised to, regardless of later deviations. It preserves randomisation benefits and gives a conservative, real-world estimate of effectiveness.

A range of values around an estimate within which the true population value is expected to lie with a stated probability, commonly 95%. A narrow interval implies a more precise estimate.

The process of allocating participants to study groups by chance so that known and unknown confounders are distributed evenly. It underpins the causal validity of a controlled trial.

A systematic deviation that pushes study results consistently away from the truth. Common types include selection, information, and publication bias, and they differ from random error that narrows with larger samples.

Distortion of an exposure-outcome relationship by a third variable linked to both. The confounder is not an intermediate step in the causal pathway, so analyses must adjust for it.

A statistical technique that pools results from multiple independent studies to produce a single weighted effect estimate. It increases precision but is only as trustworthy as the studies and heterogeneity within it.

A scatter plot of study effect size against a measure of its precision, used to look for publication bias. Asymmetry suggests small negative studies may be missing from the literature.

A formal procedure comparing observed data against a null hypothesis, yielding a p-value. A small p-value indicates the observed result is unlikely under the null, but does not measure effect size or importance.

A measure of how widely individual values spread around the mean of a sample. It describes variability within the data, unlike the standard error, which describes uncertainty of an estimated mean.

The number of new cases of a condition arising in a population over a defined period, divided by the population at risk. It measures the rate at which disease develops and is used for risk and causation studies.

The total number of existing cases of a condition in a population at a specific point or over a period, divided by the population size. It reflects burden of disease and is influenced by incidence and survival.

The ratio of the odds of exposure among cases to the odds of exposure among controls. It approximates the risk ratio when the outcome is rare and is commonly reported in case-control studies.

An observational design that follows a group defined by exposure status forward in time and compares disease occurrence between exposed and unexposed members. It allows direct calculation of incidence and relative risk.

An observational design that starts with people who have a disease and comparable people without it, then looks backward at past exposures. It is efficient for rare outcomes but vulnerable to recall and selection bias.

An experimental study in which participants are allocated by chance to an intervention or comparator and followed prospectively. It is the strongest design for establishing causality when properly conducted and blinded.

A test applied to apparently healthy people to detect unrecognised disease early, when treatment is more effective. It requires high sensitivity, acceptable cost, and an available intervention for detected cases.

Apparent improvement in survival after screening caused merely by earlier diagnosis, not by delayed death. It inflates survival time without changing the true time of death, so mortality is the preferred outcome.

A hierarchy ranking study designs by their vulnerability to bias, from systematic reviews of trials at the top to expert opinion at the bottom. It guides how much weight clinicians give to a piece of research.

The study of how a drug moves through the body, covering absorption, distribution, metabolism, and excretion. These processes determine the concentration-time profile and inform dosing intervals and route selection.

The apparent volume relating the total amount of drug in the body to its plasma concentration. A large value indicates extensive tissue uptake or lipophilicity and influences loading dose calculations.

The volume of plasma cleared of drug per unit time by metabolism and excretion. It determines the maintenance dose needed to sustain a target steady-state concentration during repeated dosing.

The time required for plasma drug concentration to fall by half during elimination. It governs the time to reach steady state and the interval between doses, and is prolonged in renal or hepatic impairment.

The fraction of an administered dose that reaches systemic circulation unchanged. Intravenous dosing is taken as complete, while oral bioavailability is reduced by incomplete absorption and first-pass metabolism.

Presystemic elimination of an orally absorbed drug by gut wall and liver before it enters systemic circulation. It explains why some drugs need much larger oral than intravenous doses.

A large family of hepatic enzymes that oxidatively metabolise many drugs and endogenous substances. Individual isoenzymes vary between people, causing differences in drug response and interaction risk.

An increase in metabolising enzyme activity after repeated exposure to a substance, typically developing over days to weeks. It lowers concentrations of co-administered drugs and can cause therapeutic failure.

A reduction in metabolising enzyme activity caused by a competing or binding substance, often occurring rapidly. It raises concentrations of co-administered drugs and increases the risk of toxicity.

The ratio of a drug dose producing toxicity to the dose producing the desired effect. A narrow index means small changes in concentration can cause harm, so monitoring is often required.

A molecule that binds a receptor and activates it to produce a biological response. Full agonists produce maximal effect, whereas partial agonists produce a submaximal response even at full occupancy.

A molecule that binds a receptor without activating it and blocks the action of agonists. Competitive antagonists can be overcome by more agonist, while non-competitive antagonists cannot.

A protein that recognises and binds a specific signalling molecule and converts that binding into a cellular response. Receptors mediate drug selectivity and are classified by structure and transduction mechanism.

The condition in which drug input equals elimination, so plasma concentration remains stable during repeated dosing. It is generally reached after about four to five half-lives of regular administration.