Pharmacodynamics Flashcards

A drug that antagonizes the same physiological effect as another drug but acts via a completely different receptor is called a:

Answer: Physiological antagonist

A physiological antagonist produces an opposing effect through action at a different receptor system (e.g., epinephrine counteracts histamine-induced bronchoconstriction via different receptors).

Desensitization of G-protein coupled receptors after agonist binding is primarily initiated by:

Answer: Phosphorylation by G-protein coupled receptor kinases (GRKs) followed by arrestin binding

GRKs phosphorylate the activated GPCR, promoting arrestin binding which sterically uncouples the receptor from its G protein, causing acute desensitization.

The Kd (dissociation constant) for a drug-receptor interaction reflects:

Answer: The drug concentration at which 50% of receptors are occupied

Kd is the concentration of drug at which half the receptors are occupied; a lower Kd indicates higher affinity between the drug and receptor.

Which type of receptor is directly linked to an ion channel and produces the fastest response to agonist binding?

Answer: Ligand-gated ion channel (ionotropic receptor)

Ligand-gated ion channels (e.g., nicotinic ACh receptors, GABA-A) directly open upon ligand binding, producing ionic flux within milliseconds — the fastest receptor-mediated response.

Chemical antagonism occurs when:

Answer: A drug directly binds and inactivates another drug in solution

Chemical antagonism involves a direct chemical interaction between two drugs that renders one or both inactive (e.g., protamine sulfate neutralizing heparin).

If two full agonists at the same receptor are given together and produce greater than additive effects, this is termed:

Answer: Synergism

Synergism (also called supra-additive effect) describes a combined effect greater than the sum of the individual drugs' effects when given alone.

Receptor tyrosine kinases (RTKs) transduce signals by:

Answer: Dimerizing and autophosphorylating tyrosine residues to initiate intracellular cascades

Ligand binding causes RTK monomers to dimerize, triggering autophosphorylation of tyrosine residues that serve as docking sites for downstream signaling proteins (e.g., RAS-MAPK, PI3K-Akt pathways).