Glossary
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Absorption: The first stage of pharmacokinetics: medications enter the body and travel from the site of administration into the body’s circulation.
Adverse effect: An unintended and potentially dangerous pharmacological effect that occurs when a medication is administered correctly.
Affinity: The strength of binding between drug and receptor.
Agonist: A drug or ligand that binds to a “receptor” and produces an effect. Agonists may be full or partial.
Antagonist: A molecule that prevents the action of other molecules, often by competing for a cellular receptor; opposite of agonist. Antagonists may be further described as competitive, non-competitive, or irreversible.
Bioavailability: The presence of a drug in the bloodstream after it is administered. Bioavailability varies with route of administration.
Blood–brain barrier (BBB): A nearly impenetrable barricade built from a tightly woven mesh of capillaries tightly woven together to protect the brain from potentially dangerous substances such as poisons or viruses.
Clearance: The ratio of the rate of elimination of a drug to the plasma concentration of the drug.
Competitive antagonists: A drug that competes for the same binding site with an agonist, and their binding is mutually exclusive.
CYP (Cytochrome) 450 family: Enzymes responsible for most drugs; there are many isoforms of CYP.
Distribution: The second stage of pharmacokinetics; the process by which medication is distributed throughout the body.
Dose-Response: As the dose of a drug increases, the response should also increase. The slope of the curve is characteristic of the particular drug–receptor interaction.
Dose-response curve: Graph showing the relationship between the effectiveness and drug concentration most often expressed as a log.
Duration: The length of time that a medication is producing its desired therapeutic effect.
Efficacy: The maximum effect of which the drug is capable.
Excretion: The final stage of pharmacokinetics; the process whereby drug byproducts and metabolites are eliminated from the body.
First-order kinetics: When a drug follows a first-order pattern of elimination pharmacokinetics, the elimination rate depends on the plasma concentration. As the plasma concentration increases, so does the rate of elimination.
First-pass effect: The inactivation of orally or enterally administered drugs in the liver and intestine. Blood containing the absorbed drug passes through the liver and goes through chemical reactions that can deactivate a substantial amount of the drug and decrease its bioavailability and efficacy.
Half-life: A drug's half-life (t1/2) is the measure of time it takes for the concentration of a drug to be reduced by half.
Induction: Increased synthesis of drug-metabolizing enzymes.
Inhibition: Decreased synthesis of drug-metabolizing enzymes or interference with how an enzyme works
Intermediate metabolizer: Reduced metabolic activity.
LD50: Lethal dose of a drug for 50% of the population in an animal study.
Mechanism of action: How a medication works at a cellular level within the body.
Metabolism: The breakdown of a drug molecule via enzymes in the liver (primarily) or intestines (secondarily).
Non-competitive antagonists: A drug that binds to an allosteric (non-agonist) site on the receptor to prevent activation of the receptor.
Normal metabolizer: Normal metabolic activity.
Onset: When a medication first begins to work and exerts a therapeutic effect.
P-glycoprotein: a membrane protein that transports a variety of substances, including drugs, across epithelial membranes.
Peak: When the maximum concentration of a drug is in the bloodstream.
Phase I reactions: CYP450 enzyme reactions that convert the parent drug into a metabolite that is more polar and more water soluble, making the drug easier to eliminate. These enzymes are not highly selective for their substrate, so a few isoforms metabolize thousands of drugs.
Phase II reactions: Reactions that increase the water solubility of a drug.
Pharmacodynamics: The study of how drugs act at target sites of action in the body.
Pharmacogenetics: A branch of pharmacology that studies individual variation in the DNA sequence in drug metabolism and response.
Pharamacogenomics: A branch of pharmacology that studies population variation in the DNA sequence in drug metabolism and response.
Pharmacokinetics: The study of how the body absorbs, distributes, metabolizes, and eliminates drugs.
Pharmacology: The science dealing with the actions of drugs on the body.
Pharmacy: The science of the preparation of drugs.
Poor metabolizer: Little to no functional metabolic activity.
Potency: The drug dose required to produce a specific intensity of effect.
Rapid metabolizer: Increased metabolic activity.
Selectivity: A “selective” drug binds to a primary and predictable site to create one desired effect. A “non-selective” drug can bind to many different and unpredictable receptor sites with potential side effects.
Side effect: Effect of a drug, other than the desired effect, sometimes in an organ other than the target organ.
Single nucleotide polymorphism (SNP): a DNA sequence variation that occurs when a single nucleotide in DNA is different from the reference sequence.
Steady state: When the rate of drug elimination equals the rate of administration.
Therapeutic index: A quantitative measurement of the relative safety of a drug that compares the amount of drug that produces a therapeutic effect with the amount of drug that produces a toxic effect. A medication with a large therapeutic index is safer than a medication with a small therapeutic index. TI= LD50/ED50.
Therapeutic window: The dosing window is the safe range between the minimum therapeutic concentration and the minimum toxic concentration of a drug; the range in which the most effective treatment will occur.
Ultra-rapid metabolizer: Substantially increased metabolic activity.
Zero-order kinetics: A process that describes how a drug's metabolism or elimination rate remains constant, regardless of the drug's concentration.