Pharmacodynamics and Autacoids

Flashcards covering key vocabulary and concepts in pharmacodynamics, receptors, cell signaling, and autacoids.

Pharmacodynamics

The study of the biochemical, cellular, and physiological effects of drugs and their mechanisms of action on the body.

Drug

A chemical substance of known structure that produces a biological effect.

Receptor

A molecule (usually a protein) that a drug binds to, to bring about a change in function of the biological system.

Affinity

The strength of attraction between a drug and its receptor.

Intrinsic Activity/Efficacy

The ability of a drug, once bound to the receptor, to elicit a pharmacologic response.

Potency

A relative measure of the amount of a drug required to produce a specific level of response, determined by the affinity.

Selectivity/Specificity

The measure of a receptor’s ability to respond to only one/single ligand.

Ligand

A substance that forms a complex with a biomolecule to serve a biological purpose.

Functional Modifiers

Drugs that alter normal physiological processes in the body (e.g., NSAIDs).

Replenishers

Drugs that supplement existing endogenous compounds that are deficient or lacking in concentration (e.g., Insulin).

Diagnostics

Drugs used to determine the presence or absence of disease (e.g., Tensilon test).

Chemotherapeutics

Drugs used to kill or inhibit the growth of cancer cells (anti-neoplastics) or microbes (anti-microbials).

The Receptor Concept

A component of the biological system to which a drug binds to bring about a change in the system's function.

Recognition (Receptor Function)

The receptor protein must allow for the sensing, recognition, and binding of a compound.

Transduction (Receptor Function)

The receptor must be able to transmit the message into the cell to elicit a functional response (biological or physiological).

Effectors

Molecules that translate the drug-receptor interaction into a change in cellular activity.

Saturability of Receptors

Receptors exist in finite numbers.

Selectivity of Receptors

Receptors must be selective in their ligand-binding characteristics to respond to the proper chemical signal and not to meaningless ones.

Endocrine Signaling

A chemical messenger is released into the circulation to produce effects distant from the point of release.

Paracrine Signaling

A chemical messenger is released from one cell to produce effects on a neighboring cell.

Autocrine Signaling

A chemical messenger that exerts actions on the same cell from which it is released.

Juxtacrine Signaling

A chemical messenger that remains affixed to the cell in which it is produced and exerts actions on a physically juxtaposed cell.

Synaptic Signaling

A neurotransmitter is released and acts on the postsynaptic target cell.

Uniporters

Transport proteins that move a substance from one side of the membrane to the other.

Symporters

Transport proteins that simultaneously move two substances across the membrane in the same direction.

Antiporters

Transport proteins that move one substance across the membrane in one direction while simultaneously transporting a second substance in the opposite direction.

Agonist

Drugs capable of binding to and activating a receptor.

Full Agonist

Occupies receptors to cause maximal activation; intrinsic activity = 1.

Partial Agonist

Occupies receptors but cannot elicit a maximal response; has an intrinsic activity of <1.

Antagonist

Bind to the receptor but do not initiate a response; they block the action of an agonist.

Inverse Agonist

A drug that binds to the inactive state of receptor molecules and decreases constitutive activity.

Constitutive Activity

Refers to the baseline activity of receptors or enzymes in the absence of any ligand (activating substance).

Dose-Response Theory

The increase in response to a drug depends on the increased binding of the drug to receptors.

Lock & Key Theory

The three-dimensional shape of the drug molecule acts like a key, which must fit precisely into the structure of the target (the lock) to activate it.

Efficacy

The degree to which a drug is able to induce maximal effects.

Potency

The amount of drug required to produce 50% of the maximal response that the drug is capable of inducing.

Competitive Antagonism

Combine with the same site on the receptor as the agonist, but their binding does not activate the receptor (i.e., intrinsic activity = 0).

Equilibrium Competitive

Bind reversibly to receptors at the same site as the agonist.

Non-Equilibrium Competitive

Bind irreversibly to either the same site as the agonist or an alternative site, causing a blockade of the agonist's effects.

Non-Competitive Antagonism

The antagonist acts at a site beyond the receptor for the agonist.

Functional Antagonism

Describes the ability of an agonist (rather than an antagonist) to inhibit the response to a second agonist via activation of different receptors that are physically separate.

Chemical Antagonism

Two substances combine in solution, causing the effect of the active drug to be lost.

Graded Dose-Response Curve

Expresses an individual's response to increasing doses of a given drug.

Quantal Dose-Response Curve

Relates the dosage of a drug to the frequency with which a designated response occurs within a population.

ED50 (Median Effective Dose)

The concentration or dose that causes a specified response in 50% of the population under study.

TD50 (Median Toxic Dose)

The dose required to produce a particular toxic effect in 50% of animals.

LD50 (Median Lethal Dose)

The dose required to produce a particular toxic effect (death) in 50% of animals.

Therapeutic Index (TI)

A measure of a drug’s relative safety (TD50/ED50).

Therapeutic Window

The dosage range at which a drug is both safe and effective.

Risk-Benefit Ratio

Describes the adverse effects of a drug in relation to its beneficial effects.

Autacoids

Biological factors that act like local hormones, with a short duration of action, and typically exert their effects near the site of synthesis.

Histamine

A key mediator of immediate allergic reactions and inflammatory responses; also plays roles in gastric acid secretion, chemotaxis, and neuromodulation.

H1-Antihistamines

Drugs that act primarily as inverse agonists to H1 receptors, used for allergic rhinitis and urticaria.

H2-Receptor Antagonists

Drugs that are competitive antagonists at the H2-receptor, which predominates in the gastric parietal cell. Uses: treatment of GI disorders such as heartburn and acid-induced indigestion.

Serotonin

A neurotransmitter, local hormone in the gut, component of the platelet clotting process, and plays a role in migraine headaches.

Eicosanoids

A large group of autocoids derived from the metabolism of 20-carbon, polyunsaturated long-chain fatty acids.

Arachidonic Acid (AA)

The most abundant of the eicosanoid precursors; a 20-carbon fatty acid containing four double bonds.

Neuromuscular Blockers (NMBs)

Paralytics or muscle relaxants that block cholinergic transmission between motor neurons and nicotinic receptors at the neuromuscular end plate of skeletal muscles

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDs Mechanism of Anti-inflammatory Action- Inhibition of COX-1 and COX-2: NSAIDs inhibit the enzymes that produce prostaglandin H, converting arachidonic acid to prostaglandins, TXA2, and prostacyclin.

Acetylcholine

ACh is synthesized from acetyl CoA and choline by the enzyme choline acetyltransferase (ChAT).