Pharmacodynamics Flashcards Preview

Year 3: CSP & PH > Pharmacodynamics > Flashcards

Flashcards in Pharmacodynamics Deck (12):

Define 'affinity'

Mathetmatically represented as 1/Kd (dissociation constant). If the receptors have a high affinity for the ligand, the Kd will be low (takes a low concentration of ligand to bind to half of the receptors)


Define 'selectivity'

a drug’s ability to preferentially bind to certain receptors


Define 'specificity'

The number of different mechanisms involved; a high specificity involves binding to a small subset of receptors and not eliciting a large host of reactions


Define 'inverse agonist'

An agent which binds to the same receptor as an agonist, but induces a pharmacological response which opposes the agonist


Give an example of a drug which is a positive allosteric modifier



Define 'physiologic antagonism'

Occurs when two drugs acting on different receptors and pathways exert opposing actions on the same system, leading to no net response


Define 'efficacy'

the maximum effect of a drug


Define 'potency'

The concentration/dose of a drug required to produce 50% of the drug’s maximal effect (EC50). It is used as a comparative measure between drugs where different doses are needed to produce the same effect.


Define 'median inhibitory concentration'

The concentration of an antagonist that reduces a specified response to 50% of the maximal possible effect.


Define 'hysteresis'

Where the value of a physical property lags behind changes in the effect causing it i.e. the relationship between drug concentration and its effect is not direct


Define 'counter-clockwise hysteresis'

The effect can increase with time for a given drug: Sensitisation (up-regulation of receptors), distribution delay to the site of the effect, an agonistic metabolite may be formed, slow receptor kinetics, and time-dependent protein binding


Define 'clockwise hysteresis'

The measured effect decreases with time for a given drug concentration e.g. tolerance (down-regulation of receptors), disequilibrium between arterial and venous circulation, generation of an antagonistic metabolite, feedback regulation, time-dependent protein binding