This model shows the typical plasma concentration profile associated with the administration of several doses of a drug over time. It demonstrates the determinants of the fluctuation in the plasma concentrations, the accumulation of the drug over the course of therapy and the resting steady state plasma concentrations.
Most commonly people take oral doses of a drug over an extended period. This model demonstrates the unique plasma concentration profile associated with this type of drug administration. The model assumes first-order drug absorption with no lag time. Simulations can be carried out to observe how the rate and extent of absorption (bioavailability) affect the profile.
Nonlinear or capacity limited pharmacokinetics can occur whenever a process involved in the absorption, distribution or elimination of a drug becomes saturated. This model demonstrates nonlinear elimination (metabolism) using phenytoin as the model drug. Specifically, it demonstrates how increasing doses of the drug produce disproportionate increases in the plasma concentration. It also demonstrates how the model parameters, Km and Vmax influence of the plasma concentration -time profile.
The model shows the unique plasma concentration-time profile associated with the administration of a drug using multiple short infusions. It demonstrates the influence of the duration of the infusion and allows the user to practice the calculation of a suitable dose and dosing interval to achieve desired peak and trough plasma concentrations of a drug.
This is the model that is most commonly used to for the time course of drug effects in man. It assumes that the response is driven by the blood or plasma concentrations of the drug. When the model parameters are known, it can be used to predict response at anytime time after any dose.
Some drugs do not directly produce the measured drug response. Instead they act upstream, and either increase or decrease the amount of the entity that directly mediates the response (response variable). Indirect effect Model I can be used for drugs that inhibit the synthesis of the response variable. An example is warfarin which inhibits the synthesis of clotting factors.
Some drugs act by binding covalently to their receptors. As a result, the target is destroyed and its function returns only when it has been replaced by newly synthesized product. The target may be a protein, DNA, an enzyme, or a cell at any stage of development. This model has been applied to the action of the proton pump inhibitors, which bind to and destroy the H+,K+-ATPase pumps in the parietal cells of the gastric mucosa. Normal proton secretion is restored only when the pumps are replaced by newly synthesized functioning pumps (i.e., the usual turnover time of the system).
Change image Submit your own comment on the simulation. Share Comment upgrade hosting plan delete simulation Transit Compartment Model of Drug Response By Sara Rosenbaum Sim URL: https://forio.com/simulate/sarar/transit-compartment-model Sim access:Other authors can download source model Sim plan: Simulate Free Sim stats:This sim has been run 326 times. This simulation was uploaded to Forio Simulate with the isee NetSim software. More information can be found at iseesystems.com. Your Rating: 1 star2 star3 star4 star5 star Average Rating: rating(1) Click here to edit the description A delay in response to a drug can occur when it takes a long time for the drug’s initial effect to be translated into the final response (a long transduction process). The delayed response profile can be captured using a series of transit compartments.
Tolerance may be defined as a process that results in a reduction in the response to a specific drug concentration following repeated drug exposure. Tolerance could occur if an endogenous compound that plays an essential role in the response chain becomes depleted during response. This model assumes the drug stimulates the production of a response variable which becomes then becomes depleted.
This model shows the typical effect of several anticancer drugs on the number of circulating neutrophils. The drugs destroy neutrophils as they develop in the bone marrow, and its takes several days for their action to affect the circulating neutrophils. The model demonstrates how inter-individual variability in pharmacokinetics and pharmacodynamics can effect the magnitude and duration of this response.
Some drugs do not directly produce the measured drug response. Instead they act upstream, and either increase or decrease the amount of the entity that directly mediates the response (response variable). Indirect effect Model 2 can be used for drugs that inhibit the degradation of the response variable. As a result they increase the amount of the response variable.
Some drugs do not directly produce the measured drug response. Instead they act upstream, and either increase or decrease the amount of the entity that directly mediates the response (response variable). Indirect effect Model IV can be used for drugs that stimulate the degradation of the response variable. As a result they decrease the amount of the response variable.
Some drugs do not directly produce the measured drug response. Instead they act upstream, and either increase or decrease the amount of the entity that directly mediates the response (response variable). Indirect effect Model III can be used for drugs that stimulate the production of the response variable. As a result they increase the amount of the response variable.
Many drugs are removed from the body by metabolism in the liver. A drug's hepatic clearance is a measure of the liver's ability to metabolize a drug. This simulation demonstrates the characteristics of high extraction (nonrestrictive clearance, low extraction (restrictive clearance and intermediate clearance.
This simulation shows the location and functioning of the major clinically important drug transporters in the : gastrointestinal membrane; renal tubular membrane; and the membranes of the hepatocyte. Simulations demonstrate their functioning after oral and intravenous doses of a drug substrate
Use this model to see if you can use a drug's pharmacokinetic and pharmacodynamic properties to determine the initial rate of drug administration. See if you can identify potential drug-drug interactions and respond when appropriate by making appropriate modifications to the dose.
This simulation demonstrates the properties of time dependent enzyme inhibition. Specifically it shows how the inhibitor’s KI and kinact and the derived parameter kobs, control inhibition. It also demonstrates how the enzyme’s degradation rate constant controls recovery.
Lipoamide is a fictitious antipyretic (fever reducing) drug that is believed to work by reducing the synthesis of cytokines. Based on its mechanism of action and the characteristics of its response, an indirect effect model I (inhibition of kin) was used to model its effect. This model can be used to probe optimum dosing regimens of lipoamide.
This model assumes permeability controlled hepatic uptake and demonstrates the role of passive diffusion, hepatic uptake transporters, hepatic matabolism and hepatic efflux transporters on overall hepatic elimination
This simulation demonstrates the model used for the induction of the drug metabolizing enzymes. It illustrates how the inducing drug's characteristics (Emax and EC50) control the degree of induction and the rate of degradation of the enzyme controls recove..