ABCP Diplomate key terms

The branch of pharmacology that describes what the body does to a drug over time, covering absorption, distribution, metabolism, and elimination, and how these processes determine drug concentration at the site of action.

The study of what a drug does to the body, including the relationship between drug concentration at the effect site and the resulting physiologic or clinical response, receptor interactions, and mechanisms of action.

The fraction of an administered dose of a drug that reaches systemic circulation unchanged. Intravenous administration is defined as 100 percent, and other routes are compared against it.

A theoretical volume relating the total amount of drug in the body to its plasma concentration. Large values suggest extensive tissue uptake, while small values suggest confinement to plasma water.

The volume of plasma from which a drug is completely removed per unit time. It reflects the combined activity of hepatic metabolism, renal excretion, and other elimination pathways.

The time required for the plasma concentration of a drug to decrease by half during elimination. It determines the time needed to reach steady state and the appropriate dosing interval.

The condition in which drug intake equals drug elimination, so plasma concentrations remain relatively constant with repeated dosing. It is generally reached after about four to five half-lives.

An initial larger dose given to achieve a target therapeutic concentration rapidly rather than waiting for accumulation. It is calculated from the volume of distribution and desired plasma level.

The dose given on a repeated schedule to keep drug concentrations at a desired steady-state level. It is determined primarily by clearance and the target concentration.

Presystemic elimination in which orally absorbed drug is metabolized in the intestinal wall or liver before reaching systemic circulation, reducing oral bioavailability relative to intravenous dosing.

The total drug exposure obtained by integrating plasma concentration over time after a dose. It is used to compare formulations, estimate bioavailability, and relate exposure to effect or toxicity.

Reversible attachment of drug molecules to plasma proteins such as albumin. Only the unbound fraction is pharmacologically active and available for distribution and elimination.

Biotransformation of drugs in the liver, typically through phase I reactions such as oxidation by cytochrome P450 enzymes and phase II conjugation reactions, generally producing more water-soluble metabolites.

A large family of heme-containing liver enzymes that catalyze oxidative metabolism of many drugs. Individual isoforms differ in substrate specificity and in susceptibility to inhibition or induction.

Reduction of metabolic enzyme activity by a coadministered drug, slowing clearance of substrates and raising their plasma concentrations. Inhibition usually begins quickly and can cause toxicity.

Increased synthesis or activity of metabolic enzymes after repeated exposure to a drug, accelerating clearance of substrates. The effect develops gradually over days and can reduce efficacy of coadministered drugs.

A change in a drug's exposure or effect caused by another drug, through altered absorption, metabolism, protein binding, or elimination, or through additive or opposing pharmacologic actions.

A drug that binds a receptor and activates it to produce a biologic response, mimicking the endogenous ligand. Full agonists produce maximal response, while partial agonists produce a lesser maximal effect.

A drug that binds a receptor without activating it and blocks the action of agonists. Competitive antagonists can be overcome by higher agonist concentrations, whereas noncompetitive antagonists cannot.

A ligand that activates a receptor but produces less than the maximal response even at full receptor occupancy. It can act as a functional antagonist when competing with a full agonist.

The maximal pharmacologic response a drug can produce when bound to its receptor. It is distinct from potency, which describes the concentration needed to produce a given effect.

The amount of drug required to produce a specified effect, often expressed as the concentration or dose producing half-maximal response. Lower values indicate a more potent drug.

A graph relating administered dose or concentration to the magnitude of response. Its shape reveals potency, maximal efficacy, and the steepness of the dose-effect relationship.

A ratio comparing the dose producing toxicity to the dose producing therapeutic effect. A narrow index means small dose changes can cause toxicity, so monitoring and careful titration are needed.

Measurement of plasma drug concentrations to individualize dosing, used for drugs with narrow therapeutic indices, unpredictable pharmacokinetics, or concentration-dependent toxicity, often guided by trough sampling.

A harmful or unintended response to a drug occurring at doses used for prophylaxis, diagnosis, or therapy. Reactions may be dose-related, idiosyncratic, allergic, or related to long-term use.

A clinical condition or circumstance in which a drug should not be used because the risk of harm outweighs the expected benefit, such as a known allergy or a dangerous interacting condition.

A warning that a drug should be used with special care or monitoring in certain patients, rather than being absolutely prohibited, because the balance of benefit and risk requires individual assessment.

The movement of a drug from its site of administration into the bloodstream. Rate and extent of absorption depend on route, formulation, blood flow, and physicochemical properties of the drug.

The reversible movement of a drug from blood into tissues and organs. It is influenced by blood flow, tissue affinity, protein binding, and lipid solubility, and it determines onset of effect.

A selective permeability barrier formed by tight junctions between brain capillary endothelial cells that restricts entry of many drugs into the central nervous system, favoring lipid-soluble, unbound molecules.

The tendency of a drug molecule to dissolve in fats and membranes, often estimated by its partition coefficient. Higher lipid solubility generally increases membrane passage and tissue penetration.

The path by which a drug enters the body, such as oral, intravenous, intramuscular, subcutaneous, topical, or inhaled. The route strongly influences absorption rate, bioavailability, and onset of action.

A cycle in which a drug or metabolite excreted in bile is reabsorbed from the intestine and returned to the liver, prolonging drug exposure and sometimes extending half-life considerably.

Elimination in which a constant amount of drug is removed per unit time, regardless of concentration, because metabolic pathways are saturated. Plasma levels rise disproportionately with dose increases.

Elimination in which a constant fraction of the drug present is removed per unit time, so concentrations decline exponentially. Most drugs at therapeutic doses follow this pattern.

The rise in plasma drug concentration during repeated dosing before steady state is reached. The extent depends on the dosing interval relative to the drug's half-life.

Rapidly developing reduction in response to a drug after repeated administration over a short period, often due to receptor desensitization or depletion of mediators, distinct from slower tolerance.

A gradual decrease in drug effect with continued administration, requiring higher doses to produce the original response. It may reflect pharmacokinetic changes, receptor changes, or adaptive physiologic compensation.