Principles of Pharmacology – Pharmacodynamics (Week 2)

Vocabulary flashcards covering pharmacodynamics concepts from Week 2 notes.

Pharmacodynamics

The study of how a drug interacts with its molecular targets to produce pharmacological effects; what the drug does to the body.

Molecular target

A protein or molecule (receptor, enzyme, transporter, ion channel) that a drug binds to or affects to produce a response.

Receptors

Proteins that respond to chemical messengers to change cellular function; their type and signaling determine response speed.

Enzymes

Biological catalysts that speed up biochemical reactions; drugs can inhibit or induce/activate them.

Carrier molecules

Transporters and pumps that move substances across membranes; drugs can block or modulate their activity.

Ion channels

Proteins in the cell membrane that control ion flow; enable rapid ion movement down an electrochemical gradient.

Ligand-gated ion channels

Ion channels activated by ligand binding; produce very rapid responses (milliseconds).

G-protein-coupled receptors

Largest family of receptors; ligand binding activates a G-protein to trigger signal transduction (slower, seconds).

Tyrosine-kinase receptors

Receptors linked to gene transcription; activation leads to slower responses (hours) due to protein synthesis.

Nuclear receptors

Intracellular receptors that, after ligand binding, translocate to the nucleus to influence gene expression (hours).

Enzyme inhibition

Drugs reduce enzyme activity, affecting downstream biochemical processes.

Competitive inhibition

A drug competes with the natural substrate for the enzyme's active site, slowing activity (reversible; e.g., warfarin).

Non-competitive inhibition

A drug binds to a site other than the active site, changing enzyme shape and reducing activity (often irreversible, e.g., COX inhibition by aspirin).

Enzyme induction

Drugs increase production of certain enzymes (often via gene expression), increasing metabolism of other drugs.

Enzyme activation

Drugs that activate enzymes to enhance their activity (e.g., some anticoagulants affecting clotting factors).

Tachyphylaxis

Rapid, short-term loss of drug response, often due to depletion or rapid changes in signaling components.

Desensitisation

Gradual, longer-lasting decrease in receptor responsiveness after prolonged exposure to a drug or ligand.

Receptor up-regulation

Increase in receptor numbers over time in response to reduced stimulation or blockade.

Receptor down-regulation

Decrease in receptor numbers over time with persistent stimulation or high drug levels.

Agonist

A drug that binds to a receptor and activates it to produce a functional response.

Partial agonist

Binds and activates a receptor but produces a less-than-maximal response even when receptors are fully occupied.

Antagonist

Binds to a receptor but does not elicit a response (zero efficacy).

Competitive antagonist

Binds to the same active site as an agonist; reversible; effects can be overcome by increasing agonist concentration.

Dose-response

Graphical relationship between drug dose and the magnitude of its effect; used to assess potency and efficacy.

Potency

How much drug is needed to produce an effect; higher potency means a lower dose for the same effect.

Efficacy

The maximal effect a drug can produce once bound to its target.

Affinity

Strength of binding between a drug and its target.

Selectivity

The degree to which a drug acts on a specific target relative to others.

Specificity

The extent to which a drug acts on a particular target without affecting others.