This document discusses pharmacodynamics, which refers to how drugs act on the body. It describes different types of drug actions like stimulation, depression, irritation, and replacement. The mechanisms of drug action are either receptor-mediated or non-receptor mediated. Non-receptor mediated mechanisms include physical actions like osmosis, chemical actions like acids neutralizing gastric acid, and actions through enzymes, ion channels, antibody production, and transporters. Receptor-mediated mechanisms involve drugs binding to receptors on cells and can be agonists, antagonists, partial agonists, or inverse agonists. The main receptor families are ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, and nuclear receptors.
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.
This document discusses the basic types and mechanisms of drug action. It describes five basic types of drug action: stimulation, depression, irritation, replacement, and cytotoxic action. It then provides examples and explanations of each type. The document also discusses the mechanisms of drug action, including interaction with target biomolecules like enzymes, ion channels, transporters, and receptors. Agonists, antagonists, and other receptor interactions are explained in detail. Non-receptor mechanisms like changing physical properties and cell membrane permeability are also covered.
This presentation includes basic concepts about pharmacodynamics. It discusses about:
Definition of Pharmacodynamics
Types of drug tragets
Stay tuned for more!
This document discusses different types of receptors including ion channel receptors, G protein-coupled receptors, kinase linked receptors, and intracellular receptors. It defines key concepts such as receptor, affinity, intrinsic activity, and defines different types of ligands including agonists, antagonists, and partial agonists. It also discusses receptor mechanisms, types of G proteins, desensitization, up-regulation, down-regulation, spare receptors, and some receptor-related diseases.
This document discusses the principles and mechanisms of drug action. It defines pharmacodynamics as the study of physiological and biological effects of drugs and their mechanisms of action. Drugs can act through various mechanisms including physical action, chemical action, and by interacting with functional proteins like ion channels, carrier molecules, enzymes, and receptors. Receptors are macromolecules that drugs can bind to in order to produce their effects, and drugs are classified based on their interactions with receptors as agonists, antagonists, partial agonists, or inverse agonists.
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 pharmacodynamics and receptors. It discusses receptor occupation theory and the dual nature of receptors. It focuses on G-protein coupled receptors (GPCRs), describing their structure, classification, mechanism of activation, and major effector systems. GPCRs represent the largest family of receptors and signal through G-proteins to modulate adenylyl cyclase, phospholipase C, ion channels, and guanylate cyclase. The document also briefly mentions biased signaling at GPCRs and different receptor types including ion channel-coupled receptors, kinase-linked receptors, and intracellular receptors.
This document discusses pharmacodynamics, which refers to how drugs act on the body. It describes different types of drug actions like stimulation, depression, irritation, and replacement. The mechanisms of drug action are either receptor-mediated or non-receptor mediated. Non-receptor mediated mechanisms include physical actions like osmosis, chemical actions like acids neutralizing gastric acid, and actions through enzymes, ion channels, antibody production, and transporters. Receptor-mediated mechanisms involve drugs binding to receptors on cells and can be agonists, antagonists, partial agonists, or inverse agonists. The main receptor families are ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, and nuclear receptors.
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.
This document discusses the basic types and mechanisms of drug action. It describes five basic types of drug action: stimulation, depression, irritation, replacement, and cytotoxic action. It then provides examples and explanations of each type. The document also discusses the mechanisms of drug action, including interaction with target biomolecules like enzymes, ion channels, transporters, and receptors. Agonists, antagonists, and other receptor interactions are explained in detail. Non-receptor mechanisms like changing physical properties and cell membrane permeability are also covered.
This presentation includes basic concepts about pharmacodynamics. It discusses about:
Definition of Pharmacodynamics
Types of drug tragets
Stay tuned for more!
This document discusses different types of receptors including ion channel receptors, G protein-coupled receptors, kinase linked receptors, and intracellular receptors. It defines key concepts such as receptor, affinity, intrinsic activity, and defines different types of ligands including agonists, antagonists, and partial agonists. It also discusses receptor mechanisms, types of G proteins, desensitization, up-regulation, down-regulation, spare receptors, and some receptor-related diseases.
This document discusses the principles and mechanisms of drug action. It defines pharmacodynamics as the study of physiological and biological effects of drugs and their mechanisms of action. Drugs can act through various mechanisms including physical action, chemical action, and by interacting with functional proteins like ion channels, carrier molecules, enzymes, and receptors. Receptors are macromolecules that drugs can bind to in order to produce their effects, and drugs are classified based on their interactions with receptors as agonists, antagonists, partial agonists, or inverse agonists.
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 pharmacodynamics and receptors. It discusses receptor occupation theory and the dual nature of receptors. It focuses on G-protein coupled receptors (GPCRs), describing their structure, classification, mechanism of activation, and major effector systems. GPCRs represent the largest family of receptors and signal through G-proteins to modulate adenylyl cyclase, phospholipase C, ion channels, and guanylate cyclase. The document also briefly mentions biased signaling at GPCRs and different receptor types including ion channel-coupled receptors, kinase-linked receptors, and intracellular receptors.
Pharmacodynamics is the study of how drugs act on the body and biological system, including receptor interactions and mechanisms of action. Most drugs act by binding to receptors, and spare receptors allow a maximal response even when not all receptors are occupied, as only a portion need to be bound. Agonists activate receptors to produce a response, with full agonists having maximal efficacy and partial agonists having less efficacy than full agonists. Antagonists block the action of agonists without activating the receptors themselves.
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.
Drugs produce their effects by interacting with target biomolecules like enzymes, ion channels, transporters, and receptors. The main types of drug action are stimulation, depression, irritation, and replacement. Drugs can stimulate or inhibit enzymes, affect the opening of ion channels, inhibit transporters, and act as agonists, antagonists, or partial agonists at receptors. The drug effect is the ultimate change in biological function that occurs through a series of steps after the initial drug-receptor interaction or prevention of interaction.
RECEPTORS – what are they?
Langley (1878) suggested presence of specific interaction mechanisms/sites after observing SPECIFIC antagonistic interactions between ‘Pilocarpine & Atropine’
RECEPTORS -
Macromolecular PROTEIN/PEPTIDE structures
On the Cell Surface, or Transcellular or Intra-cellular
Have SPECIFIC 3-D structure & Binding properties
Regulate critical Cell Functions – e.g. Enzyme activity Permeability of cell (wall, membrane, etc) Ion Channels activity Carrier functions Template Function, etc.
Monomeric - with separate receptor- & DNA-binding domains
This document discusses approaches to rational design of enzyme inhibitors. It begins by explaining how natural products have historically been used as medicines by targeting enzymes. The concept of the "magic bullet" introduced targeted chemotherapy. Modern strategies use assays, crystal structures, site-directed mutagenesis, and molecular docking. The document then classifies enzymes and their inhibition mechanisms, including reversible competitive, uncompetitive, and non-competitive inhibition as well as irreversible inhibition. It discusses using enzyme inhibitors in medicine and research by targeting specific enzymes.
The document discusses the molecular mechanisms of action of drugs. It describes four main ways drugs produce effects in the body: 1) by acting on receptors, 2) by inhibiting carriers, 3) by modulating or blocking ion channels, and 4) by inhibiting enzymes. It focuses on describing the different types of protein targets for drug action, including receptors, ion channels, enzymes, and carrier molecules. It provides details on the structure and function of receptors, the main types of receptor families, and concepts such as receptor heterogeneity, subtypes, and the actions of agonists and antagonists.
ENZYME INHIBITION MORE INTERESTING IN CHEMISTRY WAYShikha Popali
WHAT ARE EWNZYMES? HERE IT IS EXPLAIN WITH ITS KINETICS AND LATER ENZYME INHIBITION. WHERE IT ALSO INCLUDES THE CLASSIFICATION OF ENZYME INHIBITORS, AVAILABLE IN MEDICINE WITH ITA BASIC REASEARCH.
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 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.
This document summarizes the mechanism of drug action. It discusses pharmacodynamics, which is the study of drug effects and mechanisms of action. It describes different types of drug action including stimulation, depression, irritation, replacement, and cytotoxic action. It also discusses the site of drug action including extracellular, cellular, and intracellular sites. It explains concepts such as drug receptors, agonists, antagonists, and different receptor types including G protein-coupled receptors and second messenger systems like cAMP, PKA, PKG, PDEs, and EPACs.
This document discusses drug receptor interactions, including definitions of key terms like drug, receptor, antagonist, and pA2 value. It describes how drugs bind to receptors and can act as agonists or antagonists. Quantitative aspects of drug-receptor interactions are covered, including dose-response curves, potency, and therapeutic indices. Factors that contribute to variability in individual responses are also summarized. Binding studies and docking simulations are introduced as methods to study these interactions.
A comprehensive presentation on Enzymology :Types of Enzyme inhibition & Therapeutic uses for MBBS ,BDS, B Pharm & Biotechnology students to facilitate self- study.
This document provides an overview of receptors in drug design. It begins by discussing the historical concept of receptors proposed by Langley and Ehrlich. Key terms like ligand, affinity, intrinsic activity, and signal transduction are introduced. The molecular biology of receptors is explained, including their structure as membrane proteins with binding sites, and mechanisms of signal transduction like controlling ion channels or activating signal proteins. Different types of receptor-ligand interactions are covered, such as those between agonists, antagonists, irreversible antagonists, and allosteric modulators. Finally, major receptor theories including Clark's occupancy theory, two-state model, and rate theory are summarized.
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.
This document discusses enzyme induction and inhibition. It defines enzymes as biological catalysts that speed up reactions without being permanently altered. Enzyme activity can be altered by small molecules binding to the active site or other sites. Inhibitors reduce enzymatic reaction rates by blocking the active site without destroying enzymes, and can be reversible or irreversible. Inhibitors are classified as competitive, non-competitive, uncompetitive, or mixed based on whether they bind to the active site or other sites and how they impact substrate binding and catalysis. Enzyme induction increases enzyme production and activity through a homeostatic regulatory mechanism, often by combining with a regulatory protein to increase gene expression.
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 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 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 discusses enzyme inhibition as it relates to drug discovery. It begins by providing background on the target-based approach to drug discovery, noting that enzymes are excellent drug targets. It then discusses different drug discovery approaches and the multi-stage drug discovery process. Several sections provide examples of enzyme inhibitors that are used as drugs to treat various diseases and medical conditions. The mechanisms of reversible and irreversible enzyme inhibition are also summarized. Finally, specific classes of enzyme inhibitors are discussed in more detail, such as kinase inhibitors, ACE inhibitors to treat hypertension, and statin drugs to lower cholesterol.
The document discusses the mechanisms of drug action, summarizing that most drugs produce their effects by interacting with specific protein targets in the body. It identifies the main categories of protein targets as enzymes, ion channels, transporters, and receptors. For each category, examples are given of drugs that act through these mechanisms, such as enzymes being stimulated or inhibited, drugs blocking ion channels, inhibiting transporters, and acting through receptor occupation and receptor subtypes.
This document discusses pharmacodynamics and drug interactions. It begins by defining pharmacodynamics as the study of how drugs act on living tissues and their mechanism of action. It then describes the common protein targets of drugs, including enzymes, ion channels, carriers, and receptors. Various examples are provided of how drugs can interact with these targets. The document also discusses drug interactions, including synergism through addition or potentiation, and antagonism through different mechanisms. It covers interactions that can occur during absorption, distribution, metabolism, and excretion of drugs. Enzyme induction and inhibition are provided as key examples of metabolic interactions.
Pharmacodynamics is the study of how drugs act on the body and biological system, including receptor interactions and mechanisms of action. Most drugs act by binding to receptors, and spare receptors allow a maximal response even when not all receptors are occupied, as only a portion need to be bound. Agonists activate receptors to produce a response, with full agonists having maximal efficacy and partial agonists having less efficacy than full agonists. Antagonists block the action of agonists without activating the receptors themselves.
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.
Drugs produce their effects by interacting with target biomolecules like enzymes, ion channels, transporters, and receptors. The main types of drug action are stimulation, depression, irritation, and replacement. Drugs can stimulate or inhibit enzymes, affect the opening of ion channels, inhibit transporters, and act as agonists, antagonists, or partial agonists at receptors. The drug effect is the ultimate change in biological function that occurs through a series of steps after the initial drug-receptor interaction or prevention of interaction.
RECEPTORS – what are they?
Langley (1878) suggested presence of specific interaction mechanisms/sites after observing SPECIFIC antagonistic interactions between ‘Pilocarpine & Atropine’
RECEPTORS -
Macromolecular PROTEIN/PEPTIDE structures
On the Cell Surface, or Transcellular or Intra-cellular
Have SPECIFIC 3-D structure & Binding properties
Regulate critical Cell Functions – e.g. Enzyme activity Permeability of cell (wall, membrane, etc) Ion Channels activity Carrier functions Template Function, etc.
Monomeric - with separate receptor- & DNA-binding domains
This document discusses approaches to rational design of enzyme inhibitors. It begins by explaining how natural products have historically been used as medicines by targeting enzymes. The concept of the "magic bullet" introduced targeted chemotherapy. Modern strategies use assays, crystal structures, site-directed mutagenesis, and molecular docking. The document then classifies enzymes and their inhibition mechanisms, including reversible competitive, uncompetitive, and non-competitive inhibition as well as irreversible inhibition. It discusses using enzyme inhibitors in medicine and research by targeting specific enzymes.
The document discusses the molecular mechanisms of action of drugs. It describes four main ways drugs produce effects in the body: 1) by acting on receptors, 2) by inhibiting carriers, 3) by modulating or blocking ion channels, and 4) by inhibiting enzymes. It focuses on describing the different types of protein targets for drug action, including receptors, ion channels, enzymes, and carrier molecules. It provides details on the structure and function of receptors, the main types of receptor families, and concepts such as receptor heterogeneity, subtypes, and the actions of agonists and antagonists.
ENZYME INHIBITION MORE INTERESTING IN CHEMISTRY WAYShikha Popali
WHAT ARE EWNZYMES? HERE IT IS EXPLAIN WITH ITS KINETICS AND LATER ENZYME INHIBITION. WHERE IT ALSO INCLUDES THE CLASSIFICATION OF ENZYME INHIBITORS, AVAILABLE IN MEDICINE WITH ITA BASIC REASEARCH.
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 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.
This document summarizes the mechanism of drug action. It discusses pharmacodynamics, which is the study of drug effects and mechanisms of action. It describes different types of drug action including stimulation, depression, irritation, replacement, and cytotoxic action. It also discusses the site of drug action including extracellular, cellular, and intracellular sites. It explains concepts such as drug receptors, agonists, antagonists, and different receptor types including G protein-coupled receptors and second messenger systems like cAMP, PKA, PKG, PDEs, and EPACs.
This document discusses drug receptor interactions, including definitions of key terms like drug, receptor, antagonist, and pA2 value. It describes how drugs bind to receptors and can act as agonists or antagonists. Quantitative aspects of drug-receptor interactions are covered, including dose-response curves, potency, and therapeutic indices. Factors that contribute to variability in individual responses are also summarized. Binding studies and docking simulations are introduced as methods to study these interactions.
A comprehensive presentation on Enzymology :Types of Enzyme inhibition & Therapeutic uses for MBBS ,BDS, B Pharm & Biotechnology students to facilitate self- study.
This document provides an overview of receptors in drug design. It begins by discussing the historical concept of receptors proposed by Langley and Ehrlich. Key terms like ligand, affinity, intrinsic activity, and signal transduction are introduced. The molecular biology of receptors is explained, including their structure as membrane proteins with binding sites, and mechanisms of signal transduction like controlling ion channels or activating signal proteins. Different types of receptor-ligand interactions are covered, such as those between agonists, antagonists, irreversible antagonists, and allosteric modulators. Finally, major receptor theories including Clark's occupancy theory, two-state model, and rate theory are summarized.
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.
This document discusses enzyme induction and inhibition. It defines enzymes as biological catalysts that speed up reactions without being permanently altered. Enzyme activity can be altered by small molecules binding to the active site or other sites. Inhibitors reduce enzymatic reaction rates by blocking the active site without destroying enzymes, and can be reversible or irreversible. Inhibitors are classified as competitive, non-competitive, uncompetitive, or mixed based on whether they bind to the active site or other sites and how they impact substrate binding and catalysis. Enzyme induction increases enzyme production and activity through a homeostatic regulatory mechanism, often by combining with a regulatory protein to increase gene expression.
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 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 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 discusses enzyme inhibition as it relates to drug discovery. It begins by providing background on the target-based approach to drug discovery, noting that enzymes are excellent drug targets. It then discusses different drug discovery approaches and the multi-stage drug discovery process. Several sections provide examples of enzyme inhibitors that are used as drugs to treat various diseases and medical conditions. The mechanisms of reversible and irreversible enzyme inhibition are also summarized. Finally, specific classes of enzyme inhibitors are discussed in more detail, such as kinase inhibitors, ACE inhibitors to treat hypertension, and statin drugs to lower cholesterol.
The document discusses the mechanisms of drug action, summarizing that most drugs produce their effects by interacting with specific protein targets in the body. It identifies the main categories of protein targets as enzymes, ion channels, transporters, and receptors. For each category, examples are given of drugs that act through these mechanisms, such as enzymes being stimulated or inhibited, drugs blocking ion channels, inhibiting transporters, and acting through receptor occupation and receptor subtypes.
This document discusses pharmacodynamics and drug interactions. It begins by defining pharmacodynamics as the study of how drugs act on living tissues and their mechanism of action. It then describes the common protein targets of drugs, including enzymes, ion channels, carriers, and receptors. Various examples are provided of how drugs can interact with these targets. The document also discusses drug interactions, including synergism through addition or potentiation, and antagonism through different mechanisms. It covers interactions that can occur during absorption, distribution, metabolism, and excretion of drugs. Enzyme induction and inhibition are provided as key examples of metabolic interactions.
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.
This document discusses pharmacodynamics and the mechanisms of drug action. It defines pharmacodynamics as the study of biochemical and physiological effects of drugs and their mechanisms of action at organ and cellular levels. It describes the major mechanisms as:
1) Interaction with biomolecules like enzymes, ion channels, transporters, and receptors. Most drugs target these proteins.
2) At the receptor level, drugs can act as agonists, antagonists, partial agonists, or inverse agonists depending on their affinity and intrinsic activity.
3) The receptor occupation theory explains how drug-receptor binding results in a functional response based on concepts of affinity, intrinsic activity, and two-state receptor models.
This document summarizes pharmacodynamics, which is the study of how drugs act on the body and their mechanisms of action and side effects. It discusses the different types of drug actions including stimulation, depression, irritation, replacement, and cytotoxic actions. It then describes the various mechanisms of drug action, including physical, chemical, enzymatic, through ion channels, antibody production, and interactions with receptors. Finally, it discusses the different types of receptors that drugs can act on like G protein-coupled receptors and ion channel receptors.
Principles and mechanisms of drug action. Receptor theories and classification of receptors, regulation of receptors. drug
receptors interactions signal transduction mechanisms, G protein–coupled receptors, ion channel receptor, transmembrane enzyme linked receptors,
transmembrane receptor and receptors that regulate
transcription factors, dose response relationship, therapeutic index, combined effects of drugs and factors modifying drug action.
This document discusses biological drug targets and summarizes key points about receptors and drug-receptor interactions. It begins with an introduction to biological drug targets and explains that drugs produce their effects by binding to receptors and causing biochemical or physical changes. It then discusses the main types of receptors - ligand-gated ion channels, G-protein coupled receptors, kinase-linked receptors, and nuclear receptors. Theories of drug-receptor interaction are also summarized, including occupancy theory, rate theory, induced fit theory, and others. Finally, the document briefly introduces artificial enzymes as synthetic molecules that can mimic the functions of natural enzymes.
1) Drugs act by interacting with discrete target molecules like enzymes, ion channels, transporters, and receptors located inside or on the surface of cells.
2) The main types of drug actions are stimulation, depression, irritation, replacement, cytotoxic effects, and modification of immune status. Drugs can stimulate, depress, or irritate specialized cells.
3) The major mechanisms of drug action involve altering the activity of enzymes, opening or closing ion channels, inhibiting transporters, and activating or blocking cell surface receptors. This leads to changes in second messenger signaling and gene expression that ultimately cause a pharmacological response.
1. Enzyme activity can be regulated through several mechanisms including allosteric regulation, feedback inhibition, proenzymes, and protein modification.
2. Allosteric enzymes have effector molecules that bind and induce a conformational change that increases or decreases enzyme activity. Feedback inhibition occurs when a metabolic end product inhibits an earlier enzyme.
3. Proenzymes are inactive precursors that are activated by proteolytic cleavage. Protein modification like phosphorylation can also regulate enzymes by changing their structure.
3 Enzymes.pptx Enzymes, it's types and functionAbdulGhayur1
Enzymes are biological molecules that catalyze chemical reactions and increase their rates. They are selective for specific substrates and only catalyze a few reactions. Enzymes work by lowering activation energy and can accelerate reactions by millions of times. They are not consumed in reactions and do not alter equilibrium. Enzyme activity is affected by factors like temperature, pH, inhibitors, and more. The lock and key and induced fit models describe how enzymes and substrates interact specifically in the active site. Cofactors like metal ions and coenzymes are required for some enzyme activity. Enzymes perform critical functions in cell signaling, movement, and metabolism and are targets of drugs and involved in diseases.
This document discusses mechanisms of drug action, including drug-receptor interactions and signal transduction. It describes the major receptor families - ligand-gated ion channels, G-protein coupled receptors, enzyme-linked receptors, and intracellular receptors. It provides examples of specific receptors like nicotinic acetylcholine and insulin receptors. The document also covers concepts like dose-response curves, potency, efficacy, intrinsic activity, affinity, desensitization of receptors, and characteristics of signal transduction.
This document discusses the pharmacodynamics of drug action at the molecular level. It describes how drugs act by interacting with receptors, usually proteins, in the body. It explains the key and lock model of drug-receptor binding and discusses different types of bonds involved like covalent, electrostatic, hydrophobic, and hydrogen bonds. It classifies receptors based on their agonists and antagonists as well as the signaling pathways they activate, such as G-protein coupled receptors, ligand-gated ion channels, receptors with associated enzymes, cytokine receptors, and intracellular receptors.
This document discusses pharmacodynamics, which refers to what a drug does to the body. It defines key terms and covers topics like the sites and types of drug action, mechanisms of drug action including receptor-mediated actions, and factors that can modify a drug's action. Specifically, it explains that drugs can act through extracellular, cellular, or intracellular sites. Their actions include stimulation, inhibition, replacement, irritation, and cytotoxic effects. Drugs act through mechanisms like interactions with enzymes, ion channels, transporters, receptors, or through physical/chemical properties. Receptor-mediated actions involve drug-receptor binding and complexes that can result in agonism, antagonism, or other effects. Finally, it lists factors like age,
Mechanism of drug action,drug receptor phrmacologyReena Gollapalli
includes various types of receptors, mechanism of action, factors modifying drug action,principles of drug action,all types of drug receptor complex interactions very useful to students and post graduates..
This document discusses pharmacodynamics, which refers to how drugs act on the body. It covers several mechanisms of drug action, including receptor-mediated and non-receptor mediated effects. Receptor-mediated actions can be further broken down based on the type of receptor, such as ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, nuclear receptors, and Jak-Stat binding receptors. Non-receptor mediated effects occur through physical, chemical, or enzymatic actions. The document also briefly discusses concepts of drug affinity, intrinsic activity, and the combination effects of synergism and antagonism.
This document discusses pharmacodynamics and drug receptors. It defines key terms like receptors, ligands, agonists, and antagonists. It describes the four major classifications of drug receptors based on general characteristics, location, consequences of interaction, and secondary messengers involved. It explains the five major transmembrane signaling mechanisms between receptors and effectors, including receptors that directly activate intracellular effectors, membrane-spanning enzymes, ion channels, and those linked to G proteins. The document provides examples to illustrate drug action through different receptor types and signaling pathways.
Pharmacodynamics covers how drugs act on the body. Drugs can act through receptor-mediated or non-receptor mediated mechanisms. Receptor-mediated actions involve drug binding to receptors, which then trigger signal transduction pathways. The main receptor families are ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, and nuclear receptors. Drugs can have different effects depending on their affinity and efficacy at receptors. Tolerance can develop with repeated drug use through pharmacokinetic or pharmacodynamic changes. Therapeutic dosing aims to achieve drug concentrations within the therapeutic window for maximum benefit.
This document discusses pharmacodynamics and the mechanisms of drug action. It explains that pharmacodynamics is the study of how drugs act on the body and their effects, focusing on drug-receptor interactions and the biochemical and physiological impacts of drugs. Various mechanisms are described, including stimulation, depression, irritation, and replacement effects. The key mechanisms of drug action are interactions with receptors, ion channels, enzymes, and transporter proteins. Different types of receptors - ligand-gated ion channels, G-protein coupled receptors, kinase-linked receptors, and nuclear receptors - are also outlined.
Pharmacodynamics covers how drugs act on the body. Drugs can act through receptor-mediated or non-receptor mediated mechanisms. Receptor-mediated actions involve drug binding to receptors, which then trigger signal transduction pathways. There are various types of receptors including ion channels, G-protein coupled receptors, and nuclear receptors. Drug effects are determined by factors like affinity, efficacy, and intrinsic activity. Individual drug responses can be modified by pharmacokinetic and pharmacodynamic factors such as age, weight, disease states, genetic differences, and drug interactions.
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Mistry Shivangi, M.pharm in Pharmacology, Assitant professor in Bhagwan Mahavir College of PHarmacy. definition, epidermiology, etiology, symptoms, pathophysiology and treatment....
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
2. MECHANISM OF DRUG ACTION
• Drug action : Drug action is the initial interaction of a drug with cells at the
site of action & the resultant physiological & biochemical consequences
are the drug effect.
• Majority of drugs produce their effect by interacting with a discrete target
biochemolecule, which usually is protein .
• Protein that are targets of drug action can be grouped into four major
categories :
1. Enzyme
2. Ion channel
3. Transporters
4. Receptor
4. • Drugs can either increase or decrease the rate of enzymatically
mediated reactions.
• Enzyme stimulation : it is increase affinity for the substrate .
• enzyme stimulation is relevant to some natural metabolites only ,
e.g. pyridoxine acts as a co- factor & increase decarboxylase activity.
• Several enzyme are stimulated through receptor & second
messenger, e.g. adrenaline stimulates hepatic glycogen
phosphorylase through beta- receptor & second messenger.
• Enzyme inhibition :
• (A) Non-specific inhibition : They alter the tertiary structure of any
enzyme with which they come in contact & thus inhibit it.
• E.g. Heavy metal salts, strong acid & alkalies, alcohol, formaldehyde,
phenol.
5. • (B) specific inhibition : (a) competitive inhibition :
• Equilibrium type : The drug being structurally similar with the normal
substrate for catalytic binding site of enzyme so that the product is not formed
or non-functional product is formed.
• E.g . - physostigmine & neostigmine compete with Ach for cholinesteras.
- sulfonamide compete with PABA for bacterial folate synthetase.
• Non-equilibrium type : it’s type of enzyme inhibition can also occur with drug
which react with same catalytic site of enzyme but either form strong covalent
bonds or have such high affinity for enzyme that normal substrate is not able
to displace the inhibition.
• E.g. - Organophosphate react covalently with esteretic site of the enzyme
cholinesteras.
- Methotrexate has 50,000 time higher affinity for dihydrofolate
reductase than normal substrate DHFA.
6. • (b) Non-competitive : The inhibitor reacts with adjacent & not with
catalytic site, but alter enzyme in such a way that it loses it’s catalytic
property.
• E.g - Omeprazole :- H+ k+ ATPase.
- Digoxin :- Na+ K+ ATPase.
• 2. ION CHANNEL :
• Protein which acts as ion selective channels participate in
transmembrane signaling & regulate intracellular ionic composition.
• Drugs can affect ion channel either through specific receptor ( ligand gated ion channels, G-
protein operated ion channels) or by directly binding channels & affecting ion movement.
• E.g. - quinine block myocardial Na+ channel.
- dofetilide & amiodarone bolck myocardial delayed rectifier K+ channels.
7.
8. 3. TRANSPORTERS :
• Several substrate are translocated across membrane by binding
to specific transporters.
• Many drugs produce their action by directly interacting with
carrier of transpoter protein to inhibit going physiological
transport of metabolites.
• E.g. - amphetamine selectively block dopamine reuptake in
Brian neurons by vesicular amine transporter.
- reserpine block granular reuptake of noradrenaline &
5-HT by vesicular amine transporter.
12. • (A) Receptor occupation theory : Clark (1937) propounded theory of
drug action based on occupation of receptor by specific drugs & that
pace of cellular function can be altered by interaction of receptor with
drug.
• Agonist :- it’s have both affinity & max. intrinsic activity.
- E.g. adrenaline, histamine, morphine.
• Competitive antagonist :- it’s have affinity but no intrinsic activity.
- E.g. propranolol, atropine.
• Partial agonist :- it’s have affinity & submax. Intrinsic activity.
- E.g. pentazocine.
• Inverse agonist :- it’s have affinity but negative intrinsic activity.
- E.g. benzodiazepine receptor.
13. (B) The two-state receptor model :-
• The receptor is believed to exit in two interchangeable state :
Ra(active) & Ri(inactive) which are in equilibrium.