The document discusses various aspects of pharmacodynamics, which is the study of how drugs act on the body. It describes different mechanisms of drug action including stimulation, depression, irritation, replacement, cytotoxic action, physical action, chemical action, action through enzymes, and action through receptors. It also discusses concepts like dose-response relationship, drug potency and efficacy, therapeutic index, drug combination effects like synergism and antagonism, and factors that can modify drug action.
This presentation discusses drug antagonism and neurotransmitters. It defines drug antagonism as one drug inhibiting the action of another drug, describing four types: physical, chemical, physiological/functional, and pharmacological antagonism. It then focuses on pharmacological antagonism, distinguishing between competitive and non-competitive receptor antagonism. The presentation also defines neurotransmitters as chemical signals released at synapses that activate receptors and transmit electrical signals between neurons. It classifies and describes several major neurotransmitters, including amino acids, monoamines, acetylcholine, and their functions in the brain and body. References used in creating the presentation are also listed.
This document discusses pharmacodynamics in anesthesia. It describes how drugs affect the body through mechanisms of action, drug-receptor interactions, and dose-response relationships. Factors like age, genetics, disease states can impact pharmacodynamics. Drugs act through receptor-mediated actions, with receptors on cell membranes determining effects. Receptors include ion channels, G-protein coupled receptors, and those activating protein kinases or transcription. The efficacy and potency of drugs are also discussed in relation to agonists, antagonists, competitive vs. non-competitive antagonism. Therapeutic indices compare median effective and toxic doses. Pharmacodynamics are affected by patient factors and drug properties.
The document discusses receptors and their interaction with ligands and drugs. It defines receptors as macromolecules, usually proteins, that bind ligands and initiate a cellular response. Receptors exist in two states - active and inactive - and bind agonists, antagonists, and other ligands. Agonists activate the receptor and initiate a response, while antagonists bind without activating the receptor. The affinity and efficacy of drug binding determines whether it acts as an agonist or antagonist. Competitive antagonists can be overcome by high doses of agonists, while non-competitive antagonists induce a conformational change preventing agonist binding. The document outlines the importance of receptor studies for drug development and action.
This document provides an overview of pharmacology concepts related to receptors and drug action. It defines key terms like agonists, antagonists, efficacy, and potency. It describes the four major families of pharmacologic receptors - ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, and intracellular receptors. Within each family it provides examples of receptors, the mechanism of drug action, and representative drugs. The document also distinguishes between different types of agonists, antagonists, and mechanisms of drug-receptor interactions.
Mechanism of action of drugs can occur through various pathways including biochemical, physiological, physical, chemical, enzymatic, and receptor-mediated actions. Drugs can act through membrane-bound receptors by binding with varying affinity and efficacy, and can cause effects as agonists, antagonists, partial agonists, or inverse agonists. Factors like dosage, drug potency, efficacy, interactions, tolerance, and individual patient characteristics influence a drug's effects.
This document summarizes the concepts of agonists and antagonists in receptor activation and inhibition. It defines agonists as ligands that enhance receptor activity and antagonists as those that oppose agonist action and block receptor activation. The document compares the properties and types of agonists, including full, partial, and inverse agonists, and antagonists, including competitive, non-competitive, and irreversible antagonists. It discusses how agonists and antagonists regulate signaling pathways through their effects on receptor activation and inhibition.
The document discusses pharmacodynamics, which is the study of how drugs act on the body and their mechanisms of action. It explains that most drugs act by interacting with macromolecules in the body, often proteins that normally serve as receptors for endogenous ligands. Drugs that mimic the effects of endogenous ligands are called agonists, while those that block or reduce their action are called antagonists. The specificity and effects of a drug depend on factors like its affinity for receptors and the expression of those receptors in different tissues. A drug's action is characterized by its binding to receptors and the response generated, and its potency, efficacy and affinity determine its occupational capacity of receptors.
This presentation discusses drug antagonism and neurotransmitters. It defines drug antagonism as one drug inhibiting the action of another drug, describing four types: physical, chemical, physiological/functional, and pharmacological antagonism. It then focuses on pharmacological antagonism, distinguishing between competitive and non-competitive receptor antagonism. The presentation also defines neurotransmitters as chemical signals released at synapses that activate receptors and transmit electrical signals between neurons. It classifies and describes several major neurotransmitters, including amino acids, monoamines, acetylcholine, and their functions in the brain and body. References used in creating the presentation are also listed.
This document discusses pharmacodynamics in anesthesia. It describes how drugs affect the body through mechanisms of action, drug-receptor interactions, and dose-response relationships. Factors like age, genetics, disease states can impact pharmacodynamics. Drugs act through receptor-mediated actions, with receptors on cell membranes determining effects. Receptors include ion channels, G-protein coupled receptors, and those activating protein kinases or transcription. The efficacy and potency of drugs are also discussed in relation to agonists, antagonists, competitive vs. non-competitive antagonism. Therapeutic indices compare median effective and toxic doses. Pharmacodynamics are affected by patient factors and drug properties.
The document discusses receptors and their interaction with ligands and drugs. It defines receptors as macromolecules, usually proteins, that bind ligands and initiate a cellular response. Receptors exist in two states - active and inactive - and bind agonists, antagonists, and other ligands. Agonists activate the receptor and initiate a response, while antagonists bind without activating the receptor. The affinity and efficacy of drug binding determines whether it acts as an agonist or antagonist. Competitive antagonists can be overcome by high doses of agonists, while non-competitive antagonists induce a conformational change preventing agonist binding. The document outlines the importance of receptor studies for drug development and action.
This document provides an overview of pharmacology concepts related to receptors and drug action. It defines key terms like agonists, antagonists, efficacy, and potency. It describes the four major families of pharmacologic receptors - ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, and intracellular receptors. Within each family it provides examples of receptors, the mechanism of drug action, and representative drugs. The document also distinguishes between different types of agonists, antagonists, and mechanisms of drug-receptor interactions.
Mechanism of action of drugs can occur through various pathways including biochemical, physiological, physical, chemical, enzymatic, and receptor-mediated actions. Drugs can act through membrane-bound receptors by binding with varying affinity and efficacy, and can cause effects as agonists, antagonists, partial agonists, or inverse agonists. Factors like dosage, drug potency, efficacy, interactions, tolerance, and individual patient characteristics influence a drug's effects.
This document summarizes the concepts of agonists and antagonists in receptor activation and inhibition. It defines agonists as ligands that enhance receptor activity and antagonists as those that oppose agonist action and block receptor activation. The document compares the properties and types of agonists, including full, partial, and inverse agonists, and antagonists, including competitive, non-competitive, and irreversible antagonists. It discusses how agonists and antagonists regulate signaling pathways through their effects on receptor activation and inhibition.
The document discusses pharmacodynamics, which is the study of how drugs act on the body and their mechanisms of action. It explains that most drugs act by interacting with macromolecules in the body, often proteins that normally serve as receptors for endogenous ligands. Drugs that mimic the effects of endogenous ligands are called agonists, while those that block or reduce their action are called antagonists. The specificity and effects of a drug depend on factors like its affinity for receptors and the expression of those receptors in different tissues. A drug's action is characterized by its binding to receptors and the response generated, and its potency, efficacy and affinity determine its occupational capacity of receptors.
Pharmacodynamics drug receptor interactionAnoop Kumar
1. Dr. Anoop Kumar discusses different types of drug receptor interactions including agonists, antagonists, partial agonists, and inverse agonists. He explains how these ligands can stimulate, inhibit, or modify cellular functions through receptor binding.
2. Four main classes of receptors are described: intracellular receptors, enzyme-linked receptors, ligand-gated ion channels, and G-protein coupled receptors. Intracellular receptors modify gene transcription in the nucleus. Enzyme-linked receptors dimerize and phosphorylate substrates upon ligand binding. Ligand-gated ion channels open to conduct ions when bound by ligands.
3. Specific examples like nicotinic acetylcholine receptors and GABAA receptors are given.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their effects. It describes how drugs can have therapeutic or adverse effects by stimulating, depressing, or replacing certain processes. The main targets of drugs are receptors, ion channels, enzymes, and transporter proteins. Receptors are sites that recognize signals and initiate responses. The document outlines different types of receptors like G-protein coupled, ion channel, enzyme, and nuclear receptors. It also discusses concepts like agonists, antagonists, efficacy, potency, dose-response curves, therapeutic index, and synergistic or antagonistic drug interactions.
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
The document discusses the principles of drug action and mechanisms of drug-receptor interactions. It explains that drugs can stimulate, depress, irritate or replace cellular functions. It also describes the different types of drug-receptor binding including agonists that activate receptors, antagonists that block receptor activation, and partial agonists that weakly activate receptors. The document outlines the concepts of affinity, intrinsic activity, competitive and non-competitive antagonism, and how these principles underlie drug action at the molecular level through interactions with receptors on cells.
1. Receptors are cellular macromolecules that mediate chemical signaling between and within cells. They have affinity for ligands and intrinsic activity that triggers a pharmacological response upon ligand binding.
2. Agonists have high affinity and intrinsic activity, forming active receptor complexes. Antagonists have affinity but no intrinsic activity. Partial agonists and inverse agonists have intermediate effects.
3. There are several types of receptors including ion channels, G protein-coupled, kinase-linked, intracellular, and enzymes. Long-term receptor exposure can lead to down-regulation or up-regulation depending on if it's an agonist or antagonist.
This document provides an overview of receptor pharmacology and key concepts. It defines drugs and how they act through receptors and other targets. It explains the terms agonist, antagonist, affinity, efficacy and potency. It describes competitive and non-competitive antagonism and their effects on concentration-response curves. The learning objectives are to understand these pharmacological concepts and be able to interpret graphs of drug-receptor interactions.
Outcomes:
Students must be able to demonstrate knowledge of pharmacodynamics under the following headings:
• Definition
• Structurally specific drugs
• Structurally non-specific drugs
• Receptor binding
• Agonists and antagonists
• Intracellular receptors
• Enzyme receptors
• Transport carrier receptors
• Neurotransmitters
This document discusses the mechanisms of drug action. It begins by explaining that drugs can produce effects through various mechanisms like interacting with enzymes, cell membranes, or other cellular components. It then describes four levels of drug action - molecular, cellular, tissue, and system. The document goes on to explain different types of effects like local vs systemic, primary vs side effects. It provides details on various mechanisms of drug action including physical mechanisms, chemical mechanisms, drug-receptor interactions, drug-enzyme interactions, drug-channel interactions, and miscellaneous mechanisms.
This document discusses different types of receptors including ligand gated ion channels, G-protein coupled receptors, enzyme linked receptors, and nuclear receptors. It describes receptor-drug interactions including affinity, intrinsic activity, efficacy, and potency. It defines different types of agonism and antagonism. The document provides examples and details on various receptor types and their mechanisms of action. In conclusion, extensive receptor pharmacology research has led to new drug targets, but more remains to be discovered about new receptor types and orphan receptors to further advance treatment options.
The document discusses various topics in pharmacodynamics including receptor families, dose-response relationships, and mechanisms of drug action. It describes how pharmacodynamics is the study of biochemical and physiological effects of drugs on the body and mechanisms of action. It defines key terms like receptors, ligands, ligand-receptor complexes, and major receptor families including ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, intracellular receptors, spare receptors, and desensitization of receptors.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their mechanisms of action. It describes different types of drug actions including local, systemic, and reflex actions. The mechanisms of drug action include effects on receptors as agonists, antagonists, or partial agonists. Other mechanisms are physical, chemical, interference with cell division or metabolic pathways, inhibition of enzymes, and effects on ion channels. Adverse effects are also discussed, including allergies, idiosyncrasies, side effects, overdose effects, tolerance, iatrogenic diseases, secondary effects, teratogenicity, drug dependence, and cytotoxic reactions.
THIS PPT INCLUDE PHARMACODYNAMICS AND THIS PPT IS VERY USEFUL FOR (MBBS,BDS ) STUDENTS ,POSTGRADUATE STUDENT (MD,MDS,Phd) STUDENTS TO UNDERSTAND PHARMACODYNAMICS.
1. Receptor desensitization refers to the gradual diminishing effect of a drug given continuously or repeatedly over time. It involves changes in receptors like phosphorylation, internalization, and loss of receptors from the cell surface.
2. G protein-coupled receptors (GPCRs) undergo desensitization mainly through receptor phosphorylation by G protein receptor kinases (GRKs) and arrestin binding, leading to uncoupling from G proteins and internalization.
3. Upon prolonged agonist stimulation, GRKs are activated and phosphorylate agonist-bound GPCRs, promoting arrestin binding and receptor internalization via clathrin-coated pits. This removes the receptors from the cell surface and inhibits G protein signaling
Ch02 Drug Receptor Interactions And Pharmacodynamicsaxix
This document summarizes key concepts about drug-receptor interactions and pharmacodynamics from Chapter 2. It discusses how drugs produce effects by binding to receptors on cells and tissues. It defines terms like agonists, antagonists, affinity, efficacy and potency. It also describes different types of receptors that drugs can bind to, including G-protein coupled receptors and intracellular receptors. Finally, it explains the concepts of spare receptors, desensitization, and the different types of antagonism - competitive and noncompetitive.
This document discusses drug receptor interactions. It defines a receptor as the specific cellular component that a drug binds to produce its pharmacological effects. There are four primary receptor families: ligand gated ion channels, G-protein coupled receptors, enzyme-linked receptors, and intracellular receptors. The document discusses several important interactions involved in drug-receptor complexes, including covalent bonds, ionic interactions, hydrogen bonding, charge transfer interactions, hydrophobic interactions, and van der Waals forces. It provides examples to illustrate how each interaction type can contribute to a drug binding to and activating its receptor.
This document provides an overview of drug mechanism of action. It discusses pharmacodynamics concepts like drug receptors, quantitative drug-receptor interactions, and factors that can influence drug action. It describes several mechanisms of drug action including altering endogenous ligand concentrations, regulating ion transport, and activating cellular signaling pathways. Finally, it discusses two major structural families of physiological receptors: G protein-coupled receptors and ligand-gated ion channels.
This document discusses the importance of understanding the mechanism of drug action. It explains that pharmacodynamics is the study of how drugs work in the body and affect it biochemically and physiologically. Understanding these mechanisms is important for several reasons: 1) It helps build trust between patients and their doctors by allowing doctors to explain how the drug is working, 2) Patients who understand their treatment are more likely to participate in managing their disease, and 3) Knowing the mechanisms increases doctors' confidence that drugs are being used appropriately and helps avoid interactions and adverse effects.
Here are the matches between the pharmacologic terms and their definitions:
1. Efficacy - C) This is the maximal response obtainable by a drug treatment
2. Potency - E) This is the amount of drug required to produce a desired effect
3. Tolerance - A) Decreased response to the same dose of the drug.
4. Therapeutic index - D) This is the ratio of the toxic dose to the therapeutic dose
5. Intolerance - B) When the antagonist is suddenly withdrawn, severe reaction occurs in the form of rebound or withdrawal effects
Pharmacodynamics is the study of how drugs act on the body and their mechanisms of action. It involves drug-receptor interactions and explains the relation between drug effects. Pharmacodynamics provides a basis for rational drug use and design. Drugs can act through stimulation, depression, irritation, replacement or cytotoxic effects on cells. Their main targets are receptors, ion channels, enzymes, and transporter proteins. Understanding drug-receptor interactions is important for explaining drug effects and determining their potency and efficacy. Drug interactions can enhance or reduce the effects of drugs and should be considered when administering multiple medications.
Pharmacodynamics drug receptor interactionAnoop Kumar
1. Dr. Anoop Kumar discusses different types of drug receptor interactions including agonists, antagonists, partial agonists, and inverse agonists. He explains how these ligands can stimulate, inhibit, or modify cellular functions through receptor binding.
2. Four main classes of receptors are described: intracellular receptors, enzyme-linked receptors, ligand-gated ion channels, and G-protein coupled receptors. Intracellular receptors modify gene transcription in the nucleus. Enzyme-linked receptors dimerize and phosphorylate substrates upon ligand binding. Ligand-gated ion channels open to conduct ions when bound by ligands.
3. Specific examples like nicotinic acetylcholine receptors and GABAA receptors are given.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their effects. It describes how drugs can have therapeutic or adverse effects by stimulating, depressing, or replacing certain processes. The main targets of drugs are receptors, ion channels, enzymes, and transporter proteins. Receptors are sites that recognize signals and initiate responses. The document outlines different types of receptors like G-protein coupled, ion channel, enzyme, and nuclear receptors. It also discusses concepts like agonists, antagonists, efficacy, potency, dose-response curves, therapeutic index, and synergistic or antagonistic drug interactions.
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
The document discusses the principles of drug action and mechanisms of drug-receptor interactions. It explains that drugs can stimulate, depress, irritate or replace cellular functions. It also describes the different types of drug-receptor binding including agonists that activate receptors, antagonists that block receptor activation, and partial agonists that weakly activate receptors. The document outlines the concepts of affinity, intrinsic activity, competitive and non-competitive antagonism, and how these principles underlie drug action at the molecular level through interactions with receptors on cells.
1. Receptors are cellular macromolecules that mediate chemical signaling between and within cells. They have affinity for ligands and intrinsic activity that triggers a pharmacological response upon ligand binding.
2. Agonists have high affinity and intrinsic activity, forming active receptor complexes. Antagonists have affinity but no intrinsic activity. Partial agonists and inverse agonists have intermediate effects.
3. There are several types of receptors including ion channels, G protein-coupled, kinase-linked, intracellular, and enzymes. Long-term receptor exposure can lead to down-regulation or up-regulation depending on if it's an agonist or antagonist.
This document provides an overview of receptor pharmacology and key concepts. It defines drugs and how they act through receptors and other targets. It explains the terms agonist, antagonist, affinity, efficacy and potency. It describes competitive and non-competitive antagonism and their effects on concentration-response curves. The learning objectives are to understand these pharmacological concepts and be able to interpret graphs of drug-receptor interactions.
Outcomes:
Students must be able to demonstrate knowledge of pharmacodynamics under the following headings:
• Definition
• Structurally specific drugs
• Structurally non-specific drugs
• Receptor binding
• Agonists and antagonists
• Intracellular receptors
• Enzyme receptors
• Transport carrier receptors
• Neurotransmitters
This document discusses the mechanisms of drug action. It begins by explaining that drugs can produce effects through various mechanisms like interacting with enzymes, cell membranes, or other cellular components. It then describes four levels of drug action - molecular, cellular, tissue, and system. The document goes on to explain different types of effects like local vs systemic, primary vs side effects. It provides details on various mechanisms of drug action including physical mechanisms, chemical mechanisms, drug-receptor interactions, drug-enzyme interactions, drug-channel interactions, and miscellaneous mechanisms.
This document discusses different types of receptors including ligand gated ion channels, G-protein coupled receptors, enzyme linked receptors, and nuclear receptors. It describes receptor-drug interactions including affinity, intrinsic activity, efficacy, and potency. It defines different types of agonism and antagonism. The document provides examples and details on various receptor types and their mechanisms of action. In conclusion, extensive receptor pharmacology research has led to new drug targets, but more remains to be discovered about new receptor types and orphan receptors to further advance treatment options.
The document discusses various topics in pharmacodynamics including receptor families, dose-response relationships, and mechanisms of drug action. It describes how pharmacodynamics is the study of biochemical and physiological effects of drugs on the body and mechanisms of action. It defines key terms like receptors, ligands, ligand-receptor complexes, and major receptor families including ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, intracellular receptors, spare receptors, and desensitization of receptors.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their mechanisms of action. It describes different types of drug actions including local, systemic, and reflex actions. The mechanisms of drug action include effects on receptors as agonists, antagonists, or partial agonists. Other mechanisms are physical, chemical, interference with cell division or metabolic pathways, inhibition of enzymes, and effects on ion channels. Adverse effects are also discussed, including allergies, idiosyncrasies, side effects, overdose effects, tolerance, iatrogenic diseases, secondary effects, teratogenicity, drug dependence, and cytotoxic reactions.
THIS PPT INCLUDE PHARMACODYNAMICS AND THIS PPT IS VERY USEFUL FOR (MBBS,BDS ) STUDENTS ,POSTGRADUATE STUDENT (MD,MDS,Phd) STUDENTS TO UNDERSTAND PHARMACODYNAMICS.
1. Receptor desensitization refers to the gradual diminishing effect of a drug given continuously or repeatedly over time. It involves changes in receptors like phosphorylation, internalization, and loss of receptors from the cell surface.
2. G protein-coupled receptors (GPCRs) undergo desensitization mainly through receptor phosphorylation by G protein receptor kinases (GRKs) and arrestin binding, leading to uncoupling from G proteins and internalization.
3. Upon prolonged agonist stimulation, GRKs are activated and phosphorylate agonist-bound GPCRs, promoting arrestin binding and receptor internalization via clathrin-coated pits. This removes the receptors from the cell surface and inhibits G protein signaling
Ch02 Drug Receptor Interactions And Pharmacodynamicsaxix
This document summarizes key concepts about drug-receptor interactions and pharmacodynamics from Chapter 2. It discusses how drugs produce effects by binding to receptors on cells and tissues. It defines terms like agonists, antagonists, affinity, efficacy and potency. It also describes different types of receptors that drugs can bind to, including G-protein coupled receptors and intracellular receptors. Finally, it explains the concepts of spare receptors, desensitization, and the different types of antagonism - competitive and noncompetitive.
This document discusses drug receptor interactions. It defines a receptor as the specific cellular component that a drug binds to produce its pharmacological effects. There are four primary receptor families: ligand gated ion channels, G-protein coupled receptors, enzyme-linked receptors, and intracellular receptors. The document discusses several important interactions involved in drug-receptor complexes, including covalent bonds, ionic interactions, hydrogen bonding, charge transfer interactions, hydrophobic interactions, and van der Waals forces. It provides examples to illustrate how each interaction type can contribute to a drug binding to and activating its receptor.
This document provides an overview of drug mechanism of action. It discusses pharmacodynamics concepts like drug receptors, quantitative drug-receptor interactions, and factors that can influence drug action. It describes several mechanisms of drug action including altering endogenous ligand concentrations, regulating ion transport, and activating cellular signaling pathways. Finally, it discusses two major structural families of physiological receptors: G protein-coupled receptors and ligand-gated ion channels.
This document discusses the importance of understanding the mechanism of drug action. It explains that pharmacodynamics is the study of how drugs work in the body and affect it biochemically and physiologically. Understanding these mechanisms is important for several reasons: 1) It helps build trust between patients and their doctors by allowing doctors to explain how the drug is working, 2) Patients who understand their treatment are more likely to participate in managing their disease, and 3) Knowing the mechanisms increases doctors' confidence that drugs are being used appropriately and helps avoid interactions and adverse effects.
Here are the matches between the pharmacologic terms and their definitions:
1. Efficacy - C) This is the maximal response obtainable by a drug treatment
2. Potency - E) This is the amount of drug required to produce a desired effect
3. Tolerance - A) Decreased response to the same dose of the drug.
4. Therapeutic index - D) This is the ratio of the toxic dose to the therapeutic dose
5. Intolerance - B) When the antagonist is suddenly withdrawn, severe reaction occurs in the form of rebound or withdrawal effects
Pharmacodynamics is the study of how drugs act on the body and their mechanisms of action. It involves drug-receptor interactions and explains the relation between drug effects. Pharmacodynamics provides a basis for rational drug use and design. Drugs can act through stimulation, depression, irritation, replacement or cytotoxic effects on cells. Their main targets are receptors, ion channels, enzymes, and transporter proteins. Understanding drug-receptor interactions is important for explaining drug effects and determining their potency and efficacy. Drug interactions can enhance or reduce the effects of drugs and should be considered when administering multiple medications.
Pharmacodynamics is the study of the biochemical and physiological effects of drugs and their mechanisms of action. Pharmacodynamics is often referred to as “what the drug does to the body”.
In order to exert their effects, drugs usually interact in a structurally specific way with a protein receptor or act on physiological processes within the body. This activates a secondary messenger system that produces a physiological effect. Drugs do not create new action but they can only modify (alter) the functions of cells or tissues in body. The drug–receptor complex initiates alterations in biochemical and/or molecular activity of a cell by a process called signal transduction.
Pharmacodynamics is the study of how drugs act on the body and their biochemical and physiological effects. Drugs can act through receptor-mediated or non-receptor mediated pathways. There are four main types of receptor families: ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, and nuclear receptors. Receptor-mediated actions involve drug-receptor binding which can have varying effects depending on the drug's efficacy and potency. Non-receptor mediated actions do not involve receptors and can include chemical or physical effects. Tolerance to drugs can develop with repeated use through mechanisms such as receptor regulation.
1. There are several types of drug receptors that mediate the effects of drugs, including ion channel-linked receptors, G-protein-linked receptors, enzyme-linked receptors, and intracellular receptors.
2. Drugs interact with specific receptors through precise physiochemical and spatial interactions, and this binding can lead to responses by activating ion channels, enzymes, or other intracellular signaling pathways.
3. The interaction between a drug and its receptor is described using principles from enzyme kinetics, with terms like efficacy, potency, affinity, agonists, partial agonists, and antagonists. Competitive and non-competitive antagonism can alter the response to receptor activation.
Receptors are proteins embedded in cell membranes that receive chemical signals from outside the cell. When a ligand binds to its corresponding receptor, it activates or inhibits the receptor's associated biochemical pathway. The history of receptor theory began in the mid-1800s with experiments showing chemical communication between nerves and target tissues. Today, receptors are known to include drug targets like enzymes, transporters, and ion channels. Each receptor is linked to a specific cellular signaling pathway.
This document defines key terms related to drug receptor interactions. It discusses how drugs produce their effects by binding to receptors, and defines agonists as drugs that activate receptors through both affinity and intrinsic activity. Antagonists are defined as drugs that block the action of other drugs. The document also outlines different types of antagonism and pharmacologic drug actions. Finally, it summarizes several hypotheses regarding how drugs interact with receptors, including the lock and key hypothesis.
The document discusses drug receptors and how drugs act in the body. It provides information on:
- Receptors are molecules that drugs bind to, initiating their effects. The binding is determined by the drug's chemical structure.
- Agonists activate or enhance cellular activity by binding to receptors. Antagonists bind but do not activate the receptor, instead blocking agonists from binding.
- Affinity is a drug's tightness of binding, while intrinsic activity is its ability to produce an effect once bound. These factors determine a drug's effects.
Receptors are cellular components that drugs bind to in order to produce their pharmacological effects. The ability of a drug to bind is determined by its chemical structure interacting with complementary surfaces on the receptor. When an agonist binds to a receptor, it activates or enhances the cell's activity by triggering biochemical events. Antagonists also bind receptors but do not activate the cell's activity; they prevent agonists from binding. The affinity and intrinsic activity of a drug determine which effects it produces.
Pharmacodynamics is the study of how drugs act on the body and their mechanisms of action. It includes the biochemical and physiological effects of drugs. A key concept is that drugs can act as agonists, partial agonists, antagonists, or inverse agonists depending on if they mimic endogenous compounds and what receptor states they stabilize. The potency and efficacy of a drug depends on its affinity for and ability to activate receptors. Factors like tolerance, resensitization, and downregulation also impact a drug's effects over time. Understanding pharmacodynamics is important for determining dosages, maximizing therapeutic effects, and minimizing adverse reactions.
This document discusses pharmacodynamics, which is the study of what a drug does to the body. It covers drug action, effect, and the various mechanisms of drug action including physical action, chemical action, interactions with regulatory proteins, receptors, and receptor families. It also discusses concepts like dose response curves, drug potency, efficacy, therapeutic index, synergism, and antagonism.
PRINCIPLES OF PHARMOCODYNAMICS 2 [Autosaved].pptxEmmanuelOluseyi1
The document discusses principles of pharmacodynamics, which is the study of how drugs act on the body. It explains that drugs act by interacting with receptors to cause physiological effects. The key concepts covered are: drugs must bind to receptors to have an effect; receptors determine selectivity and dose-response; and drugs can act as agonists or antagonists depending on if they activate or block receptor activity. Factors influencing drug effects and concepts of drug-receptor interactions are also summarized.
1. Pharmacodynamics is the study of how drugs act on the body, including their mechanisms of action.
2. Drugs primarily act by interacting with proteins like receptors, ion channels, enzymes, and transporters. They can also act physically or chemically.
3. Drugs can have stimulatory, depressant, replacement, or cytotoxic effects by interacting with enzymes, receptors, or through physical/chemical actions. The most common mechanism is receptor interaction.
This document summarizes key concepts in pharmacodynamics including:
- Mechanisms of drug action including receptor interactions, dose effects, and therapeutic/toxic effects
- Definitions of terms like agonist, antagonist, affinity, potency, efficacy
- Mechanisms of signal transduction between drug binding and intracellular effects
- Types of drug targets including receptors, ion channels, enzymes, and carriers
- Concepts of drug-receptor binding and interactions, dose-response curves, and agonists vs antagonists
- Factors influencing drug properties like safety, interactions, adverse effects, toxicity, idiosyncrasies, and tolerance
- Agonists, partial agonists, and inverse agonists are drug ligands that interact with receptors to elicit different cellular responses. Agonists mimic the effects of endogenous ligands, partial agonists produce submaximal effects, and inverse agonists stabilize receptors in their inactive state.
- The two-state receptor model describes receptors existing in two conformational states (active and inactive) that ligands differentially stabilize. Biased agonism occurs when ligands preferentially activate different intracellular signaling pathways.
- Key concepts include efficacy, intrinsic activity, and constitutive receptor activity. Partial agonists have efficacy below full agonists and produce submaximal responses even at full receptor occupancy. Inverse agonists suppress constitutive receptor activity.
This document discusses pharmacodynamics and drug receptors. It defines pharmacodynamics as the study of pharmacological drug effects and mechanisms of action. The objectives are to understand drug-target cell interactions and characterize a drug's full scope and sequence of action, providing a basis for rational therapeutic use and new drug development. It describes different types of drug receptors, including ligand-gated ion channels, G-protein coupled receptors, and intracellular receptors. It also discusses concepts such as agonists, antagonists, and partial agonists that act on receptors to elicit responses or block responses.
This document discusses various neurotransmitters, neuromodulators, and receptors in the nervous system. It describes:
1) Two major classes of neurotransmitter receptors - ionotropic receptors which are ligand-gated ion channels, and G protein-coupled receptors which activate intracellular second messenger systems.
2) Examples of major inhibitory and excitatory neurotransmitters like GABA, glycine, glutamate, acetylcholine, and catecholamines and their receptor properties.
3) Other substances that modulate neurotransmission like neurotrophic factors, neuromodulators, and neuromediators.
Stability Testing During Product DevelopmentAl Riyad Hasan
Stability Testing During Product Development:
Practical conduct of stability testing
Presentation and recording of results
Stability data handling and estimation of shelf life
Package Labelling
This document discusses major intra and extra-cellular fluids and electrolytes. It begins with introducing the group members and defining electrolytes. It then discusses the major physiological ions including calcium, magnesium, sodium, potassium, chloride, bicarbonate and phosphate. For each ion, it highlights their importance in the human body. The document also discusses various sodium chloride preparations, potassium chloride, and electrolytes used in acid-base therapy such as sodium acetate, sodium citrate and potassium citrate. It concludes with discussing oral rehydration therapy and salt intake relating to hypertension.
This document discusses pharmacokinetics and provides details about absorption, distribution, and bioavailability of drugs. It defines key pharmacokinetic terms and describes factors that influence absorption such as solubility, concentration, route of administration, and mechanisms of absorption including passive diffusion, active transport, and pinocytosis. Membrane permeability and drug properties like pH and lipid solubility are discussed. The document also covers volume of distribution, plasma protein binding, tissue storage, and barriers to drug distribution like the blood-brain barrier.
. Introduction to Pharmacology Course Title: Pharmacology I Course No.: PHAR 2113 Prepared by: Biswajit Biswas Reference: Goodman & Gilman’s Manual of Pharmacology and Therapeutics
2. Pharmacology Greek pharmakon : "drug“ ; and logia : "the study of“. Greek: Pharmacon (Drug) Modern Latin: Pharmacologia 18th Century: Pharmacology The branch of medicine concerned with the uses, effects, and modes of action of drugs.
3. Historic development of pharmacology Worlds oldest pharmacology - from India and China Materia medica (2735 B.C.) by Pan Tsao- contained mainly Plant and metal with few animal products Ayurveda - described by Charaka accordig to Rigveda (3000 B.C.) - includes 300 vegetable drugs , classified into 50 groups according to their effects on symptoms. Papyrus (1500 B.C.) discovered by Eber -700 drugs Modern medicine (from 450 B.C.) by Hippocrates- concept of disease as a pathologic process and organize pharmacology on the basis of observation, analysis and deduction.- use simple and efficacious drugs.
4. Allopathay (James gregory, 1753-1821) -treatment without any rational basis- use symptomatic treatment with obnoxious remedis. Homeopathy (Hanneman, 19th century)-
This document provides an overview of phytochemistry and plant drugs. It discusses several plant constituents including glycosides, carbohydrates, tannins, lipids, resins, balsams, volatile oils, and alkaloids. For each constituent, examples of plant sources are given and potential uses are described. The document also classifies different types of alkaloids based on their ring structures and provides examples of plants containing various alkaloid types.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
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This SlideShare presentation provides a comprehensive overview of the Declaration of Helsinki, a foundational document outlining ethical guidelines for conducting medical research involving human subjects.
1. Pharmacodynamics
Study of drug :
How drug exert its effects on body.
Action- effect sequence and dose effect relationship.
Modification of drug action by another drug or by other factors.
The action of a drug on the body, including receptor interactions, dose-response phenomena, and
mechanisms of therapeutic and toxic action.
What drugs do to the body.
2. Principles of drug action:
Stimulation:
Selective enhancement of the level activity of targeted cell by the drugs.
e.g. Adrenalin---------------------- Heart
Pilocarpine -----------------------salivary gland secretion
Digitoxin ---------------------------tone of heart muscles
Depression:
Selective attenuation/weakening of specialized cell activity.
e.g. Quinidine depress cardiac activity,
Barbiturate depress CNS
Certain drug causes both stimulation and depression.
e.g. Ach stimulate intestinal SM but depress SA node in heart.
3. Irritation:
Non-selective, often noxious/toxic effect and applied to less specialized tissues like, epithelium
tissue, connective tissue.
Mild irritation - therapeutic benefit: Mild bitter tonic, counter irritant
Strong irritation – cause necrosis, inflammation, and tissue damage.
Replacement:
Uses of natural metabolites or hormones in case of deficiency. e.g. Insulin, levodopa, Vit-therapy,
Iron, Immunoglobulin etc.
Cytotoxic action:
Selective cytotoxic activity for the invading parasites and cancer cell without affecting the host
cells.
Antibiotics, anticancer drugs.
4. 1. Physical action:
Mass of the drug--------bulk laxatives (bran), protective ( dimithacone)
Adsorptive properties----------------- charcoal, keolin
Radioactivity----------------------------131I
Mechanisms of action:
2. Chemical Action:
Antacid (AlOH3)-----neutralize gastric HCl.
Acidifying agent ( NH4Cl) and Alkalinizing agent (NaHCO3)----
reacts with buffer in plasma and alter urine pH
Oxidizing agents (KMnO4)----germicidal
Chelating agent (Cal. disod. Edetate)----sequester toxic metals.
5. 3. Through Enzymes:
Enzymes catalyst all biological reaction thus enzymes are very good target of drug action.
Stimulation or Inhibition.
Stimulation:
Since enzyme activity in the biological system is optimally set thus stimulation of
enzymes by drug is unusual.
Adrenalin------------------------ Adenylyl cyclase
Penicillin------------------------ Penicillinase
Inhibition:
Common mode of drug action.
A. Nonspecific inhibition
B. Specific inhibition
1. Competitive 2. Noncompetitive
6. Nonspecific inhibition:
Denatures the proteins ( 3o structure)
e.g. strong acids, heavy metal salts, alkali, alcohols, formaldehyde , phenols etc .
Specific inhibition:
Inhibits a particular enzymes, excludes others, either competitive or noncompetitive manners.
Competitive inhibition:
Drugs competitive with normal substrate for the same site and same isoenzymes.
Equilibrium type, in which if the substrate concentration sufficiently increase that can displace the drugs.
e.g. Physostigmine, neostigmine Vs Ach for Cholinestesterase
Sulfonamides Vs PABA for folate synthase
Allopurinol Vs hypoxanthin for Xanthine oxidase
7. Non- equilibrium type Inhibition, Can occur with the drugs which react with same catalytic site of the
enzyme but either form strong covalent bond or have such a higher affinity that normal substrate can not
able to displace the inhibitors.
e.g. organophosphates --- bind to the esteretic site of cholinesterase's.
Methotrexate have affinity at least 50000 time higher than DHFA for DHF reductase.
Non-competitive inhibition:
The inhibitor react with the adjacent site, not with catalytic site of the same
enzymes but alter the enzyme in such way that enzymes loses it catalytic activity.
e.g.
Acetazolamide------------------------------Carbonic anhydrase
Aspirin , Indomethacin---------------------Cyclo-oxygenase
Disulfirum----------------------------------Aldehyde dehydrogenase
Digoxin--------------------------------------Na+ K+ ATPase
8. 4. Through Receptors:
A macromolecular component of a cell, usually a protein, with which a drug interacts
to produce a response
Binding sites are situated on the surface or inside the effector cell. Specific ligands
combine with them and initiate the characteristic response.
Ligand: Molecule which attaches selectively to particular receptors or sites.
Agonist: Activates receptor to produce an effect.
Antagonist: Prevents the action of an agonist but does not have any effect of its own.
Inverse agonist: Actives a receptor to produce an opposite action to that of an agonist.
Partial agonist: Produce submaximal effect but antagonizes the action of a full agonist.
9. Drug Action Through Receptors
Receptors contain a binding site (hollow or cleft on the receptor surface) that is
recognized by the ligand.
Binding of the ligand involves intermolecular bonds.
Binding results in an lock and key phenomenon or an induced fit of the receptor
protein.
Ligand does not enter the cell. It departs the receptor unchanged and is not
permanently bound.
10. Drug Action Through Receptors
Lock and Key’ Hypothesis: “ The drug molecule must fit into the receptor AND produce
its action like a key fits into the lock AND opens it also”
Every ‘lock’ has its own ‘key’
If the ‘key’ is not precise, the ‘lock’ does not open
The ‘drug’ is the key that has to fit the target specifically and productively
Induced-Fit Hypothesis: The binding of the ligand to the receptor must cause a change in
the shape of the receptor that results in the proper alignment of the catalytic groups on its
surface.
At least two steps - e.g., step 1 is initial binding of drug with receptor and step 2 is a
change in structure of the receptor (and/or drug) so that the initial drug or a new ligand
perfectly fits with the receptor.
Receptor is flexible - can wrap around the drug.
11. Drug Action Through Receptors
Cell
Membrane
Cell
Receptor
Messenger
message
Induced fit
Cell
Receptor
Messenger
Message
Cell
Messenger
Receptor
Induced Fit Hypothesis
Lock and Key Hypothesis
12. Receptor occupation theory:
Proposed by Clark (1937)
Drug action based on occupation of receptors by specific drug.
Interaction between drug (D) and receptor (R) governed by law of mass action and
effect (E) is the direct function of the drug receptor complex (DR).
D+ R DR E
Accordingly
1. Intensity of response ∞ fraction of receptors occupied.
2. All or none action, no partial activation.
3. Drug and receptor have a rigid ‘ lock and key relationship’
13. Deviation of the theory:
By Ariens and Stephenson in 1950s - Ariens and Stephenson Hypothesis
• All receptors need not to be occupied for a maximal effect.
Histamine can produce maximum effect when most of the receptors are occupied by competitive
antagonists.
• Different drugs have different capacities to induce a response, they must occupy different
fraction of the receptor to induce equal response. So sub maximal activation of a receptor is
possible. In that case, all or none law is not applicable.
•A drug could induce change in the receptor to make it more or less favorable to combine with
the drug.
D + R --------- DR ~~> S E
S is the quantity denoting strength of stimulus.
14. Hypothesis of Paton – Rate Theory
“Effectiveness of a drug does not depend on the actual occupation of the receptor but by
obtaining proper stimulus.”
-Response is proportional to the rate of Drug-Receptor Complex formation
-Duration of receptor occupation determines if a drug is an agonist, partial agonist, or antagonist
This is also known as the Rate Theory.
Types of Receptor
G- Protein Coupled Receptors
Ligand Gated Ion Channels
Kinase Linked Receptors
Nuclear Receptors
15. Nature of Receptors
1. Receptors are regulatory macromolecules, mostly proteins,
though nucleic acids may also serve as receptors [hundreds of
receptor proteins have been isolated, purified, cloned and their
primary amino acid (AA) sequence has been worked out].
2. The cell surface receptors with their effector proteins are
considered to be floating in a sea of membrane lipids.
3. All types of receptors have a well defined common structural
motif, while the individual receptors differ in the details of amino
acid sequencing, length of intra/extracellular loops, etc.
4. Drugs act upon physiological receptors which mediate responses
to transmitters, hormones, autacoids and other endogenous
signal molecules; examples are cholinergic, adrenergic,
histaminergic, steroid, leukotriene, insulin and other receptors.
16. Regulation of Receptors
Receptors are themselves subject to many regulatory and homeostatic controls. These controls
include regulation of
1. Synthesis and degradation of the receptor by multiple mechanisms,
2. Covalent modification,
3. Association with other regulatory proteins
4. Re-localization within the cell
Down Regulation/Desensitization: Can result from temporary inaccessibility of the receptor to
agonist or from fewer receptors synthesized and available at the cell surface (e.g., down-regulation
of receptor number).
Decrease in response
Caused by prolonged use of agonist
Reduced drug effect
When initial high response is reached, the effect diminishes within seconds/minutes even in the
continued presence of the agonist
Reversible
17. Regulation of Receptors
Up Regulation/Super-sensitivity: Can result from higher receptors synthesis and available at the
cell surface (e.g., up-regulation of receptor number).
Increase in response
Caused by prolonged use of antagonist
Increase drug effect
Prolonged block by an antagonist causing fast up regulation of receptors
New receptors are highly sensitive!
Functions of receptors
Propagate regulatory signals
Amplify signals
Integrate extracellular and intracellular signals
Adapt to short term and long term changes.
18. Dose-Response Relationship
DOSE = amount of drug administered to the patient
RESPONSE = effect in the body produced by the drug
Drug + Receptor ↔ Drug-Receptor Complex Response.
i. Depends on multiple factors
ii. A drug usually has one desired effect that causes a change in a target organ or structure
iii. It will also have secondary effects because it will be absorbed by other areas of the body
iv. Main effect – the effect you want the drug to have
v. Side effects – secondary effects that may or may not be desirable or helpful
vi. Goal is to use a dose of a drug that is effective, but has minimal side effects
19. The relationship between the
concentration of drug at the
receptor site and the magnitude of
the response is called the dose-
response relationship
Dose-response curve
i. Making dosage decision
ii. Compare dosage to the percentage of
people showing different effects.
20. Potency
Absolute amount of drug required to produce an effect
More potent drug is the one that is required in lower amount to cause same effect.
Efficacy
Maximal response that can be elicited by a drug.
Agonists demonstrating high efficacy can result in a maximal effect, even when only a small fraction of the
receptors is occupied
Potency Efficacy
B<A A=B
C<A ; C=B C<A,B
D>A,B,C D<A,B; D=C
Response Drug (log conc.)
A
D
B
C
21. Therapeutic Index
The gap between the minimum therapeutic effect of
drug and the minimum adverse effect of drug is
defined as safety margin or therapeutic index of a
drug
The index used for judging drug's safety.
Therapeutic index = LD50 / ED50
ED50 (Median effective dose):The dose at which 50% of
individuals (experimental animals) exhibits specified
effect.
LD50(Median lethal dose):The dose required to
produce death in 50% of individuals.
Morphine
22. Affinity
Ability of drug to combine with the receptor.
Efficacy / intrinsic activity
Ability of a drug to activate the receptor after receptor occupation.
Agonists - both affinity and intrinsic activity/efficacy.
Competitive antagonists - have affinity but no intrinsic activity.
Partial agonists - have affinity and submaximal efficacy.
Inverse agonists - have affinity but intrinsic activity with a minus sign.
Drug action
Combination of the drug with its receptor resulting a conformational change of the receptor (in case
of agonist) or o preventing the change by the agonist ( in case of antagonist).
Drug effect
The ultimate change in the biological function due to the consequence of drug action, through a series
of intermediate steps (transduction).
23. Combination of Drugs
Combinations of two/ more drugs, simultaneously or in quick succession
1. No interference with each other’s effects
2. May oppose each other’s actions (antagonism)
3. May produce similar actions on the same organ (synergism).
Synergism
Derived from two Greek words ( Syn= together , Ergo= work, Ism)
Definition: “Drug synergy occurs when drugs can interact in ways that enhance or magnify one or
more effects, or side - effects, of those drugs.”
Positive effects:
Examples: 1) Codeine mixed with Acetaminophen or Ibuprofen to enhance the action of codeine as a
pain reliever.
2) Use of Cannabis with LSD (Lysergic acid diethylamide), where the active chemicals in cannabis
have been reported to enhance the hallucinatory experience of LSD.
24. Synergism
Negative effects:
Negative effects of synergy are a form of contraindication. For example, a combination of depressant
drugs that affect the central nervous system (CNS), such as alcohol and Valium (Diazepam), can
cause a greater reaction than simply the sum of the individual effects of each drug if they were used
separately. In this particular case, the most serious consequence of drug synergy is exaggerated
respiratory depression, which can be fatal if left untreated.
Types
1) Summation:
Definition : Combined effect of drugs which are given simultaneously is equal to the sum of
magnitude of effect produced by individual drugs.
Example: General Anesthetics
25. Synergism
Types
2) Potentiation:
Definition: Combined effect of two simultaneously given drugs is greater than the algebraic sum of
action of individual drugs.
Example: NH4Cl (Weak diuretic) potentiates the diuretic effect of Organic Mercurials.
Antagonism
Definition: Opposing action of two drugs on same biological system.
Difference between agonist and antagonist:
Agonist: Possesses both affinity and intrinsic activity.
Antagonist: Opposes the action of agonist. Possesses only affinity but no intrinsic activity.
26. Antagonism - Types
Chemical
Antagonism
Physiological
Antagonism
Pharmacological
Antagonism
Agonist-Antagonist
interaction=Agonist
loses its activity
Agonist-Antagonist act on
different receptors. Both have
opposite actions.
Antagonist prevents agonist from acting upon
its receptors.
EXAMPLES:
Antacids(NaOH ,
Al(OH)2 )
neutralize HCl
Histamine - Adrenaline
antagonism.
HISTAMINE:
*Vasodilation
*Decreases blood pressure
*Bronchoconstriction
ADRENALINE:
*Vasoconstriction
*Increases blood pressure
*Bronchodilation
Two types: 1) Competitive 2) Non-Competitive
Competitive:
1. Antagonist competes with agonist for the
same receptor site
2. Reversible phenomenon
3. Can be overcome by increasing the conc. of
agonist.
Non competitive:
1. Binds to an allosteric site other than the
agonist binding site
ii. Prevent the receptor activation by the
agonist.
27. Drug Dosage
Drug Dosage and Dose
A dose refers to a specified amount of medication taken at one time.
By contrast, dosage is the prescribed administration of a specific amount, number, and frequency
of doses over a specific period of time.
The administration of a drug or agent in prescribed amounts and at prescribed intervals.
Standard Dose: The assumed average maintenance dose per day for a drug used for its main
indication in adults.
Target Level Dose: Dose of drug administered for achieving a desired plasma/serum/tissue drug
levels in patients.
Regulated Dose: Dose of drugs which, by virtue of formulation and product design, provide drug
release in a regulated form, distinct from that of the conventional dosage forms, so that dosing of
drugs can be controlled.
Titrated Dose: The continual adjustment of a dose based on patient response. Dosages are adjusted
until the desired clinical effect is achieved.
28. Factors Modifying Drug Action
Responses of a drug varies from
(1) person to person; and
(2) also same person on different occasions such as
Individuals differ in pharmacokinetic handling of drugs
varying plasma/target site conc.
Metabolized drug Vs excreted unchanged drugs – Propranolol and Atenolol
Variation in number or state of receptors, coupling proteins or other components of
response
Variations in hormonal/neurogenic tone or concentrations – atropine, propranolol,
captopril
Categories of factors:
1. Genetic
2. Non-genetic including environmental, circumstantial and personal variables
29. Factors Modifying Drug Action
1. Body Size:
Influences the conc. of the drug attained at the site of action – obese/lean/children – Body weight
(BW) and Body Surface area (BSA)
Individual dose = BW(kg) x average adult dose;
Individual dose = BSA (m2) x average adult dose
BSA can be calculated by Dubois Formula
BSA (m2) = BW (kg) 0.425 x Height (cm) 0.725 X 0.007184
2. Age:
Young`s formula: Child dose = (Age/Age+12) x adult dose
Dilling`s formula: Child dose = (Age/20) x adult dose
3. Gender:
Females have smaller body size – required doses are lower.
Digoxin in maintenance therapy of heart failure – mortality higher in fmale.
4. Species and Race: Some strains of rabbits – resistant to atropine
5. Genetics
Determinants of drug responses – transporter, enzymes, ion channels, receptors and couplers –
controlled genetically – Individual variation of responses.
Low variants of CYP2C9 – Warfarin bleeding.
30. Factors Modifying Drug Action
6. Route of administration: Parenteral for speedy action
7. Environmental factors: Drug metabolism may get induced – exposure to insecticides, carcinogens
8. Psychological factors: Efficacy of a drug can be affected by patient`s beliefs, attitudes and
expectations – particularly CNS drugs.
Placebo: An inert substance which is given in the garb of medicine. Works by psychodynamic effects
(not pharmacodynamics) – sometimes responses equivalent to active drugs.
9. Pathological states: GIT, Liver diseases, Kidney diseases, Thyroid diseases.
10. Presence of other drugs
11. Tolerance:
Requirement of higher dose of a drug to produce a given response.
Natural: Species/individual inherently less sensitive – Rabbits to atropine and Blacks to beta –
blockers.
Acquired: Repeated use of a drug in an individual who was initially responsive become non-
responsive (tolerant) – CNS depressants.
Cross tolerance: Tolerance to pharmacologically related drugs – alcoholics to barbiturates; Morphine
and Pethidine.