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pharmacodynamics relationship between the drug concentration at the site of action and pharmacologic response including biochemical and physiologic effect that influence interaction of drug molecule with the receptor- this interaction causes a pharmacologic response
affinity occupation of drug to receptor the tendency of a drug to bind to its receptor
efficacy activation of drug via receptor the tendency of bound drug to elicit response
occupation theory drug molecule interacts with a receptor with a single binding site to produce a pharmacologic response
rate theory pharmacologic response depends on the rate of association of the drug and receptor complex
according to rate theory what will an agonist do? an agonist with associate rapidly to form a receptor complex, which dissociated rapidly to produce a response
according to rate theory an antagonist will associate rapidly to form drug-receptor complex and dissociate SLOWLY to maintain antagonist response
spare receptors unoccupied receptors are assumed to be present at the site of action, because a maximal pharmacologic response may be obtained when only a small fraction of the receptors are occupied by drug receptors
potency drug concentration needed to obtain specific pharmacologic effect
classes of drug antagonism pk, reversibe, irreversible, chemical, physiological
pharmacokinetic antagonism when an antagonist effectively reduces the concentration of active drug at its site of action by altering its rate of absorption or metabolic degradation or excretion
reversible antagonism response still reaches max
irreversible antagonism maximal response is not reached
chmical antagonism when two substances combine that results in a loss of activity of drug substance
physiological antagonism interaction of two drugs whose opposing actions in the body tend to cancel each other
drug tolerance quantitative change in the sensitivity of the drug to the receptor site
how is drug tolerance demonstrated demonstrated by a decrease in pharmacodynamic effect after repeated exposure to the same drug
two mechanisms of drug tolerance pharmacokinetic tolerance, pharmacodynamic tolerance
pharmacokinetic tolerance changes in drug disposition due to altered metabolism or elimination
pharmacodynamic tolerance change or loss of receptors, exhaustion of mediators
tachyphylaxis the rapid development of tolerance after administration of a single or few doses of the drug- acute desensitization
physical dependency demonstrated by the appearance of withdrawal symptoms after cessation of the drug use
factors that affect drug dependency amount, duration, and total dose of drug used
adverse drug response hypersensitivity and allergic responses- not full explained by pd or pk
pd models express the relationship between pharmacologic effect and dose in mathematical equations- rate of change
Maximum effect model empirical (hyperbolic) model that relates pharmacologic response to drug concentrations, incorporated the law of diminishing returns
Sigmoid Emax model describes pharmacologic response to drug concentration curves that are s-shaped- extension of max effect model
hysteresis loop plasma verse pharmacologic response relationship is complex- identical plasma drug concentrations can result significantly different responses depending on the time due to tolerance metabolite deactivation, reduced response or translocation of receptors
pk-pd models related pharmacological effects to the plasma drug concentration close to the receptor site
what do pk-pd models predict dose-response curve for onset, magnitude, and duration of effect and help to estimate therapeutic dosage regimens
what do pk-pd models combine combine a pk model describing drug concentration vs time relation with pd model that describes concentration vs effect with a statistical model describing inter and intra-individual variation
ultimately pk-pd models predict predict time-course and variability of effect vs time
types of pk-pd models pk-pd models at steady state, and non-stead state and time-dependent pk-pd modles
pk-pd models at steady state when concentrations of drug at the site of action are constant and the pd parameters are time-invariant, the system is kinetically at steady state
non-steady state and time depended pk-pd models when the concentrations of drug and pd parameters are changing with time, the system is not at a steady state
types of pk-pd models at steady state fixed effect, linear, log-linear, Emax, sigmoid Emax models
fixed effect model relates drug concentration with statistical likelihood of one or several effects to be present or absent "quantal effect model"
linear model assumes direct proportionality between drug concentration and drug effect
log-linear model when concentration-effect relationship is hyperbolic
Emax model based on classical receptor theory, sigmoidal Emax model is extension
non-steady state and time-dependent pk-pd models effect compartment, physiological indirect response models
effect compartment model it includes a hypothetical effect compartment as an additional compartment of pk compartment model and represents the active drug concentration at the effect site- the rate constant for the transfer between central and effect compartment is negligible
physiological indirect response model for drugs whose mechanism of action consists of either inhibition or stimulation of a physiological process involved in the elaboration of clinical expression of the observed effect
Created by: 1614571257



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