Pharmacodynamics is the study of the biochemical and physiologic effects of drugs. The effects can include those manifested within animals, microorganisms, or combinations of organisms. Pharmacodynamics and pharmacokinetics are the main branches of pharmacology, being itself a topic of biology interested in the study of the interactions between both endogenous and exogenous chemical substances with living organisms. In particular, pharmacodynamics is the study of how a drug affects an organism, whereas pharmacokinetics is the study of how the organism affects the drug. Both together influence dosing, benefit, and adverse effects. Pharmacodynamics is sometimes abbreviated as PD and pharmacokinetics as PK, especially in combined reference. Pharmacodynamics it's a came to a greek word pharmacon means drug and dynamic means power. Pharmacodynamics is a branch of pharmacology deals with the study of drug.its came under what the drugs does to the body like machenism of action side effects advers effects. places particular emphasis on dose–response relationships, that is, the relationships between drug concentration and effect. One dominant example is drug-receptor interactions as modeled by where L, R, and LR represent ligand, receptor, and ligand-receptor complex concentrations, respectively. This equation represents a simplified model of reaction dynamics that can be studied mathematically through tools such as free energy maps.
Effects on the body
The majority of drugs either There are 7 main drug actions:
stimulating action through direct receptor agonism and downstream effects
depressing action through direct receptor agonism and downstream effects
blocking/antagonizing action, the drug binds the receptor but does not activate it
stabilizing action, the drug seems to act neither as a stimulant or as a depressant
exchanging/replacing substances or accumulating them to form a reserve
General anesthetics were once thought to work by disordering the neural membranes, thereby altering the Na+ influx. Antacids and chelating agents combine chemically in the body. Enzyme-substrate binding is a way to alter the production or metabolism of key endogenous chemicals, for example aspirin irreversibly inhibits the enzyme prostaglandin synthetase thereby preventing inflammatory response. Colchicine, a drug for gout, interferes with the function of the structural proteintubulin, while Digitalis, a drug still used in heart failure, inhibits the activity of the carrier molecule, Na-K-ATPase pump. The widest class of drugs act as ligands that bind to receptors that determine cellular effects. Upon drug binding, receptors can elicit their normal action, blocked action, or even action opposite to normal. In principle, a pharmacologist would aim for a target plasma concentration of the drug for a desired level of response. In reality, there are many factors affecting this goal. Pharmacokinetic factors determine peak concentrations, and concentrations cannot be maintained with absolute consistency because of metabolic breakdown and excretory clearance. Genetic factors may exist which would alter metabolism or drug action itself, and a patient's immediate status may also affect indicated dosage.
The therapeutic window is the amount of a medication between the amount that gives an effect and the amount that gives more adverse effects than desired effects. For instance, medication with a small pharmaceutical window must be administered with care and control, e.g. by frequently measuring blood concentration of the drug, since it easily loses effects or gives adverse effects.
Duration of action
The duration of action of a drug is the length of time that particular drug is effective. Duration of action is a function of several parameters including plasmahalf-life, the time to equilibrate between plasma and target compartments, and the off rate of the drug from its biological target.
The binding of ligands to receptors is governed by the law of mass action which relates the large-scale status to the rate of numerous molecular processes. The rates of formation and un-formation can be used to determine the equilibrium concentration of bound receptors. The equilibrium dissociation constant is defined by: where L=ligand, R=receptor, square brackets denote concentration. The fraction of bound receptors is Where is the fraction of receptor bound by the ligand. This expression is one way to consider the effect of a drug, in which the response is related to the fraction of bound receptors. The fraction of bound receptors is known as occupancy. The relationship between occupancy and pharmacological response is usually non-linear. This explains the so-called receptor reserve phenomenon i.e. the concentration producing 50% occupancy is typically higher than the concentration producing 50% of maximum response. More precisely, receptor reserve refers to a phenomenon whereby stimulation of only a fraction of the whole receptor population apparently elicits the maximal effect achievable in a particular tissue. The simplest interpretation of receptor reserve is that it is a model that states there are excess receptors on the cell surface than what is necessary for full effect. Taking a more sophisticated approach, receptor reserve is an integrative measure of the response-inducing capacity of an agonist and of the signal amplification capacity of the corresponding receptor. Thus, the existence of receptor reserve depends on the agonist, tissue and measured effect. As receptor reserve is very sensitive to agonist's intrinsic efficacy, it is usually defined only for full agonists. Often the response is determined as a function of log to consider many orders of magnitude of concentration. However, there is no biological or physical theory that relates effects to the log of concentration. It is just convenient for graphing purposes. It is useful to note that 50% of the receptors are bound when =Kd. The graph shown represents the conc-response for two hypothetical receptor agonists, plotted in a semi-log fashion. The curve toward the left represents a higher potency since lower concentrations are needed for a given response. The effect increases as a function of concentration.
Multicellular pharmacodynamics
The concept of pharmacodynamics has been expanded to include Multicellular Pharmacodynamics. MCPD is the study of the static and dynamic properties and relationships between a set of drugs and a dynamic and diverse multicellular four-dimensional organization. It is the study of the workings of a drug on a minimal multicellular system, both in vivo and in silico. Networked Multicellular Pharmacodynamics further extends the concept of MCPD to model regulatory genomic networks together with signal transduction pathways, as part of a complex of interacting components in the cell.
Toxicodynamics
Pharmacokinetics and pharmacodynamics are termed toxicokinetics and toxicodynamics in the field of ecotoxicology. Here, the focus is on toxic effects on a wide range of organisms. The corresponding models are called toxicokinetic-toxicodynamic models.