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Central to PK/PD models is the concentration-effect or exposure-response relationship. [4] A variety of PK/PD modeling approaches exist to describe exposure-response relationships . PK/PD relationships can be described by simple equations such as linear model, Emax model or sigmoid Emax model . [ 5 ]
In practice, the drug concentration is measured at certain discrete points in time and the trapezoidal rule is used to estimate AUC. In pharmacology, the area under the plot of plasma concentration of a drug versus time after dosage (called “area under the curve” or AUC) gives insight into the extent of exposure to a drug and its clearance ...
There are numerous variables that influence the interpretation of drug concentration data: time, route and dose of drug given, time of blood sampling, handling and storage conditions, precision and accuracy of the analytical method, validity of pharmacokinetic models and assumptions, co-medications and, last but not least, clinical status of ...
Finally, using the Henderson-Hasselbalch equation, and knowing the drug's (pH at which there is an equilibrium between its ionized and non-ionized molecules), it is possible to calculate the non-ionized concentration of the drug and therefore the concentration that will be subject to absorption:
Toxicodynamics (TD) and pharmacodynamics (PD) link a therapeutic agent or toxicant, or toxin (xenobiotic)'s dosage to the features, amount, and time course of its biological action. [11] The mechanism of action is a crucial factor in determining effect and toxicity of the drug, taking in consideration the pharmacokinetic (PK) factors. [ 12 ]
"Metrics to characterize concentration-time profiles in single- and multiple-dose bioequivalence studies". Bioequivalence Studies in Drug Development: Methods and Applications. Statistics in Practice. Chichester, UK: John Wiley and Sons. pp. 17– 36. ISBN 978-0-470-09475-4; Chow, Shein-Chung; Liu, Jen-pei (15 October 2008).
In the simple mono-compartmental case the volume of distribution is defined as: = /, where the in practice is an extrapolated concentration at time = 0 from the first early plasma concentrations after an IV-bolus administration (generally taken around 5 min - 30 min after giving the drug).
In clinical practice, this means that it takes 4 to 5 times the half-life for a drug's serum concentration to reach steady state after regular dosing is started, stopped, or the dose changed. So, for example, digoxin has a half-life (or t 1 / 2 ) of 24–36 h; this means that a change in the dose will take the best part of a week to ...