ACVCP key terms

The study of what the body does to a drug over time, covering absorption, distribution, metabolism, and elimination. It links a dose to the resulting drug concentrations in blood and tissues.

The study of what a drug does to the body, including its mechanism of action, receptor interactions, and the relationship between drug concentration and the intensity of effect produced.

The fraction of an administered dose that reaches systemic circulation unchanged. Intravenous dosing is defined as 100 percent, while oral bioavailability is usually lower due to incomplete absorption or first-pass metabolism.

A calculated apparent volume relating the amount of drug in the body to its plasma concentration. A large value suggests extensive tissue distribution rather than confinement to blood plasma.

The volume of plasma from which a drug is completely removed per unit time. It determines the maintenance dose needed to sustain a target steady-state concentration.

The time required for the plasma concentration of a drug to decline by half during elimination. It guides dosing intervals and estimates how long to reach steady state or drug withdrawal.

The condition in which drug intake equals drug elimination, so plasma concentrations remain stable across repeated doses. It is generally reached after about four to five half-lives of consistent dosing.

An initial larger dose given to rapidly achieve therapeutic drug concentrations before maintenance dosing sustains them. It is calculated from the volume of distribution and the desired target concentration.

The repeated dose calculated to replace the amount of drug eliminated between doses, keeping concentrations at steady state. It depends on clearance and the chosen dosing interval.

Metabolism of an orally absorbed drug by the intestinal wall or liver before it reaches systemic circulation. It can greatly reduce oral bioavailability and is bypassed by intravenous or some other routes.

The total drug exposure obtained by integrating plasma concentration over time after a dose. It reflects the extent of absorption and is used to compare formulations and calculate clearance.

A ratio comparing the dose producing toxicity with the dose producing the desired effect. A low index means the safe and effective dose ranges are close, requiring careful dosing and monitoring.

The drug concentration that produces half of the maximal achievable response in a test system. It expresses potency, with a lower value indicating a more potent drug.

A drug that binds a receptor and activates it to produce a biological response. Full agonists produce maximal effect, while partial agonists produce a lesser response even at full occupancy.

A drug that binds a receptor without activating it, blocking the effects of agonists. Competitive antagonists can be overcome by more agonist, while noncompetitive antagonists cannot.

A graph plotting the magnitude of drug effect against dose or concentration. Its shape reveals potency, maximal efficacy, and the steepness of the response relationship.

A drug whose effective and toxic concentrations lie close together, so small dosing errors can cause harm. Such drugs often require therapeutic drug monitoring and individualized dosing.

Measuring plasma drug concentrations to individualize dosing, typically for drugs with narrow therapeutic ranges or unpredictable kinetics. Timing of samples relative to dosing is critical for interpretation.

An inactive compound that is converted in the body to an active drug, usually through metabolism. This strategy can improve absorption, reduce irritation, or target drug release.

Chemical alteration of drugs by liver enzymes, often in two phases: functionalization reactions then conjugation. It usually produces more water-soluble metabolites that are easier to excrete.

An increase in drug-metabolizing enzyme activity caused by repeated exposure to a substance. It accelerates metabolism of affected drugs, potentially lowering their concentrations and reducing efficacy.

A decrease in drug-metabolizing enzyme activity caused by another substance. It slows metabolism of affected drugs, potentially raising concentrations and increasing risk of toxicity.

An alteration in a drug's effect caused by another drug, a food, or a supplement. Interactions may be pharmacokinetic, changing absorption or elimination, or pharmacodynamic, changing the response at the target.

An unintended and harmful response to a drug given at normal doses. Reactions may be dose-dependent and predictable or idiosyncratic and unrelated to the expected pharmacology.

A condition or circumstance in which a drug should not be used because the risk of harm outweighs the potential benefit. Absolute contraindications prohibit use, while relative ones require caution.

The period after the last drug administration during which residues may remain in edible tissues or milk, so the animal or product cannot enter the food supply. It is set by regulatory authorities.

Using an approved drug in a manner not described on its label, such as a different species, dose, or indication. It requires a valid veterinarian-client-patient relationship and careful residue considerations.

The professional relationship required before a veterinarian may prescribe or dispense drugs, especially for extra-label use. It involves assuming responsibility for the animal's care with the owner's agreement.

A coordinated effort to use antimicrobials responsibly, optimizing dose, duration, and drug choice to cure infection while limiting resistance development and unnecessary exposure.

The lowest antimicrobial concentration that prevents visible growth of a bacterial isolate in vitro. It guides drug selection and dosing when compared with achievable tissue concentrations.

The ability of microorganisms to survive and grow despite exposure to antimicrobial concentrations that would normally inhibit or kill them. It can be intrinsic or acquired through mutation or gene transfer.

Laboratory identification of an infectious organism and determination of which antimicrobials inhibit it. Results guide targeted therapy, though in vitro results must be interpreted with clinical context.

Starting antimicrobial treatment based on clinical suspicion and likely pathogens before culture results are available. It is later adjusted according to laboratory findings and patient response.

A class of analgesic and anti-inflammatory drugs that inhibit cyclooxygenase enzymes, reducing prostaglandin synthesis. They can cause gastrointestinal and renal adverse effects, especially with prolonged use or dehydration.

The enzyme that converts arachidonic acid into prostaglandins and related mediators. Its isoforms, often called COX-1 and COX-2, differ in tissue distribution and roles in health and inflammation.

A steroid hormone or synthetic analog that binds intracellular receptors to alter gene transcription, producing anti-inflammatory and immunosuppressive effects. Long-term use can cause endocrine and metabolic side effects.

A drug-receptor interaction in which the antagonist can dissociate from the receptor, so its effect can be overcome by increasing agonist concentration. Competitive antagonism is the classic example.

An interaction in which one drug reduces another's effect by acting at the same or a related physiologic target, rather than by altering the other drug's concentration.

A condition or circumstance suggesting a drug should be used cautiously, with monitoring or dose adjustment, because the risk of harm may be increased but use is not absolutely prohibited.