The word pharmacology originates from the Greek terms pharmakon, meaning drug, and logos, meaning debate or investigation. The study or debate of medication and its effects on the body is therefore pharmacology. Pharmacology is often divided into two primary branches: pharmacodynamics and pharmacokinetics. The study of pharmacodynamics revolves around how drugs interact with the body - their mechanics, advantages and disadvantages, and therapeutic uses. The opposite is pharmacokinetics, which is the study of the body's activities on drugs—the absorption, distribution, storage, and disposal of medication. Pharmacogenomics, an emerging third division, is the study of how genetic composition impacts pharmacodynamics and pharmacokinetics, and consequently medication selection and administration to individual patients.
The term "drug" does not have a definite, universally agreed definition. However, it is widely understood that a drug is any external nonnutritive chemical that interferes with biological function. There are many ways drugs can influence biological processes, including physical interactions (e.g., antacids), changes in enzyme activity (e.g., enhancing or reducing), and binding to cellular structures that influence cell function (e.g., antihistamines).
The dissociation constant expresses affinity based on the intrinsic features of each specific drug-receptor combination (Kd). Kd is defined as the drug concentration at which 50% of the accessible receptors are occupied. It is possible to see the cumulative effect of receptor occupancy in a cell when a significant number of receptors on or in the cell are occupied. This results in a dose-response relationship that is inextricably coupled with drug-receptor binding.
Graded and quantal dose-response connections are the two forms of dose-response interactions. The graded dose-response curve depicts the impact (E) of different medication dosages or concentrations ([L]) on an individual, from which two crucial characteristics may be deduced: potency and effectiveness. The [L] at which a medication elicits 50% of its peak reaction is referred to as its potency (EC50). When all accessible rectors are occupied, efficacy (Emax) is the maximum effect of a medication
The quantal dose-response curve shows how a medicine affects a group of people as a function of dose, allowing three crucial features to be determined: efficacy, toxicity, and fatality. There are two types of responses: present and absent. The therapeutic window is a set of pharmacological doses that elicit a therapeutic response in a group of persons without inducing unacceptable toxic (adverse) effects. The therapeutic index (TI) can be used to quantify the therapeutic window: TI = TD50/ED50. A large therapeutic window is indicated by a large TI, such as a hundred-fold difference between TD50 and ED50. A limited therapeutic window is indicated by a tiny TI, such as a two-fold difference between TD50 and ED50.
A full agonist is a drug that binds to the active site of a receptor and produces the highest response when all receptors are activated. Partial agonists are medicines that bind to receptors near their active sites but elicit only partial responses even if all receptors are occupied, whereas antagonists are substances that suppress agonists and have no effect in the absence of them. Antagonists are classified into two types: receptor antagonists and nonreceptor antagonists.
An antagonist that competes with an agonist for the agonist binding site is known as a competitive antagonist. Agonist concentrations beyond a certain threshold can overcome competitive antagonism, making them reversible. Non-competitive antagonists bind covalently or very strongly to agonist binding sites. As a result, large agonist concentrations are unable to overcome non-competitive antagonism, which is hence irreversible.
The term "drug" does not have a definite, universally agreed definition. However, it is widely understood that a drug is any external nonnutritive chemical that interferes with biological function. There are many ways drugs can influence biological processes, including physical interactions (e.g., antacids), changes in enzyme activity (e.g., enhancing or reducing), and binding to cellular structures that influence cell function (e.g., antihistamines).
Mechanism of Drug Action
The effects of medications on the human body are regulated by pharmacodynamic processes. 8 As previously stated, drug-receptor binding leads to a plethora of complicated chemical interactions. The place on the receptor where a drug bind is referred to as its binding site. The reactivity of medication and the reactivity of a binding site both have an impact on how strongly two molecules will bind to one another. A drug's affinity for its binding site on a receptor expresses the level of interaction favorability between it and the receptor.The dissociation constant expresses affinity based on the intrinsic features of each specific drug-receptor combination (Kd). Kd is defined as the drug concentration at which 50% of the accessible receptors are occupied. It is possible to see the cumulative effect of receptor occupancy in a cell when a significant number of receptors on or in the cell are occupied. This results in a dose-response relationship that is inextricably coupled with drug-receptor binding.
Graded and quantal dose-response connections are the two forms of dose-response interactions. The graded dose-response curve depicts the impact (E) of different medication dosages or concentrations ([L]) on an individual, from which two crucial characteristics may be deduced: potency and effectiveness. The [L] at which a medication elicits 50% of its peak reaction is referred to as its potency (EC50). When all accessible rectors are occupied, efficacy (Emax) is the maximum effect of a medication
The quantal dose-response curve shows how a medicine affects a group of people as a function of dose, allowing three crucial features to be determined: efficacy, toxicity, and fatality. There are two types of responses: present and absent. The therapeutic window is a set of pharmacological doses that elicit a therapeutic response in a group of persons without inducing unacceptable toxic (adverse) effects. The therapeutic index (TI) can be used to quantify the therapeutic window: TI = TD50/ED50. A large therapeutic window is indicated by a large TI, such as a hundred-fold difference between TD50 and ED50. A limited therapeutic window is indicated by a tiny TI, such as a two-fold difference between TD50 and ED50.
A full agonist is a drug that binds to the active site of a receptor and produces the highest response when all receptors are activated. Partial agonists are medicines that bind to receptors near their active sites but elicit only partial responses even if all receptors are occupied, whereas antagonists are substances that suppress agonists and have no effect in the absence of them. Antagonists are classified into two types: receptor antagonists and nonreceptor antagonists.
An antagonist that competes with an agonist for the agonist binding site is known as a competitive antagonist. Agonist concentrations beyond a certain threshold can overcome competitive antagonism, making them reversible. Non-competitive antagonists bind covalently or very strongly to agonist binding sites. As a result, large agonist concentrations are unable to overcome non-competitive antagonism, which is hence irreversible.
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