Pharmacodynamics 2020
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bind to receptors and produce a response- effects of various types 2. Antagonists bind to receptors without producing a response and by occupying the receptors they prevent action of agonists.
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Dose response curvevpp
The documents discuss graded dose response curves which depict the relationship between drug dose and magnitude of effect. The potency of a drug refers to the amount needed to produce a response, which can be measured by the dose required to produce half the maximum effect. Effectiveness considers both response and safety, which is measured by the therapeutic index - the ratio of lethal to effective doses. Quantal dose response curves plot the percentage of a population responding at given doses and are useful in determining therapeutic indices.
Drug receptor interactions
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Dose response relationship
This document discusses dose-response relationships and dose-response curves. It defines dose as the amount of drug administered and response as the effect on the body. The relationship between dose and response can be illustrated with a dose-response curve, which is typically a rectangular hyperbola. Dose-response curves are used to determine the appropriate dose of a drug and compare effects across doses and individuals. The document also discusses factors like potency, efficacy, thresholds, and how dose-response curves can be graded or quantal depending on the type of response measured.
Drug antagonism
Drug Antagonism
The effect of one drug blocked (or inhibited) due to another drug is said to be antagonism. In other word, an interaction between two or more drugs that have opposite effects on the body. Drug antagonism may block or reduce effectiveness of one or more of the drugs.
e.g., atropine blocks the action of acetylcholine
Types of antagonism
1. Pharmacological antagonism: Competitive and Non-Competitive
2. Physiological antagonism
3. Chemical antagonism
Competitive Antagonism
If both the agonist and the antagonist compete for the same receptor in a reversible manner, they are said to be “competitive.” The antagonist drug interacts with the receptor and blocks it. Therefore it does not produce pharmacological action. The extent of antagonism depends on number of receptors occupied by the both drugs (agonist and antagonist), their affinity for receptors and their concentration. The increase in concentration of either one of these drugs can displace the other from receptor binding sites. Drugs interact with their receptors by weak bonds i.e. ionic bond or Hydrogen bond or Vander wal force. Hence duration of action of drug is short. Both agonist and antagonist have chemical resemblance (structural similarity).
Overview of Pharmacodynamics
Pharmacodynamics is the study of how drugs act on the body and biological system, including the receptors to which they bind, and their mechanisms of action and effects. Most drugs act by interacting with receptors, which are usually proteins, though some drugs can act without directly binding to receptors. The relationship between the dose level of a drug and its therapeutic effects or toxic side effects can be shown using dose-response curves and is important for understanding a drug's safety and efficacy.
Consequences of drug receptor interactions
Receptors are macromolecular structures, usually located on cell surfaces, that have specific binding sites for chemical ligands. When a ligand binds to a receptor, it triggers a series of biochemical events that lead to a cellular response. There are two main types of receptor-ligand interactions: agonism, where ligand binding activates the receptor and elicits a response, and antagonism, where ligand binding blocks receptor activation and prevents the response. The affinity, efficacy, and potency of receptor-ligand interactions determine their pharmacological effects. Understanding dose-response relationships and therapeutic indices provides insights into drug safety and effectiveness.
Pharmacodynamics II Dose-Response Relationships
This document discusses general principles of drug therapy, including:
1) Dose-response relationships and how drug effects are related to the dose and concentration of the drug. Higher doses result in greater drug effects until a maximum effect is reached.
2) Time-response relationships, where the drug effect occurs only after a certain amount of time as the drug accumulates and binds to receptors in the body.
3) Different types of drug-receptor interactions including agonists that activate receptors, antagonists that block receptors, and concepts like potency, efficacy, competitive vs. noncompetitive antagonism.
4) Factors that can influence individual responses to drugs like tolerance from repeated use and differences in drug
Quantitative aspects of drug receptor interaction
This document provides an overview of quantitative aspects of drug receptor interactions, including concentration-binding relationships and dose-response relationships. It discusses graded dose-response curves and how they are used to quantify drug agonism and antagonism. Parameters like EC50, Emax, and pA2 values are extracted from graded curves to characterize drug potency and efficacy. Quantal dose-response curves are also covered, which analyze population variability in drug response and are used to determine values like ED50 and LD50 for evaluating drug safety. The document concludes by emphasizing the importance of quantifying these relationships for understanding and comparing drug behavior.
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The documents discuss graded dose response curves which depict the relationship between drug dose and magnitude of effect. The potency of a drug refers to the amount needed to produce a response, which can be measured by the dose required to produce half the maximum effect. Effectiveness considers both response and safety, which is measured by the therapeutic index - the ratio of lethal to effective doses. Quantal dose response curves plot the percentage of a population responding at given doses and are useful in determining therapeutic indices.
Drug receptor interactions
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Dose response relationship
This document discusses dose-response relationships and dose-response curves. It defines dose as the amount of drug administered and response as the effect on the body. The relationship between dose and response can be illustrated with a dose-response curve, which is typically a rectangular hyperbola. Dose-response curves are used to determine the appropriate dose of a drug and compare effects across doses and individuals. The document also discusses factors like potency, efficacy, thresholds, and how dose-response curves can be graded or quantal depending on the type of response measured.
Drug antagonism
Drug Antagonism
The effect of one drug blocked (or inhibited) due to another drug is said to be antagonism. In other word, an interaction between two or more drugs that have opposite effects on the body. Drug antagonism may block or reduce effectiveness of one or more of the drugs.
e.g., atropine blocks the action of acetylcholine
Types of antagonism
1. Pharmacological antagonism: Competitive and Non-Competitive
2. Physiological antagonism
3. Chemical antagonism
Competitive Antagonism
If both the agonist and the antagonist compete for the same receptor in a reversible manner, they are said to be “competitive.” The antagonist drug interacts with the receptor and blocks it. Therefore it does not produce pharmacological action. The extent of antagonism depends on number of receptors occupied by the both drugs (agonist and antagonist), their affinity for receptors and their concentration. The increase in concentration of either one of these drugs can displace the other from receptor binding sites. Drugs interact with their receptors by weak bonds i.e. ionic bond or Hydrogen bond or Vander wal force. Hence duration of action of drug is short. Both agonist and antagonist have chemical resemblance (structural similarity).
Overview of Pharmacodynamics
Pharmacodynamics is the study of how drugs act on the body and biological system, including the receptors to which they bind, and their mechanisms of action and effects. Most drugs act by interacting with receptors, which are usually proteins, though some drugs can act without directly binding to receptors. The relationship between the dose level of a drug and its therapeutic effects or toxic side effects can be shown using dose-response curves and is important for understanding a drug's safety and efficacy.
Consequences of drug receptor interactions
Receptors are macromolecular structures, usually located on cell surfaces, that have specific binding sites for chemical ligands. When a ligand binds to a receptor, it triggers a series of biochemical events that lead to a cellular response. There are two main types of receptor-ligand interactions: agonism, where ligand binding activates the receptor and elicits a response, and antagonism, where ligand binding blocks receptor activation and prevents the response. The affinity, efficacy, and potency of receptor-ligand interactions determine their pharmacological effects. Understanding dose-response relationships and therapeutic indices provides insights into drug safety and effectiveness.
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This document discusses general principles of drug therapy, including:
1) Dose-response relationships and how drug effects are related to the dose and concentration of the drug. Higher doses result in greater drug effects until a maximum effect is reached.
2) Time-response relationships, where the drug effect occurs only after a certain amount of time as the drug accumulates and binds to receptors in the body.
3) Different types of drug-receptor interactions including agonists that activate receptors, antagonists that block receptors, and concepts like potency, efficacy, competitive vs. noncompetitive antagonism.
4) Factors that can influence individual responses to drugs like tolerance from repeated use and differences in drug
Quantitative aspects of drug receptor interaction
This document provides an overview of quantitative aspects of drug receptor interactions, including concentration-binding relationships and dose-response relationships. It discusses graded dose-response curves and how they are used to quantify drug agonism and antagonism. Parameters like EC50, Emax, and pA2 values are extracted from graded curves to characterize drug potency and efficacy. Quantal dose-response curves are also covered, which analyze population variability in drug response and are used to determine values like ED50 and LD50 for evaluating drug safety. The document concludes by emphasizing the importance of quantifying these relationships for understanding and comparing drug behavior.
Combined effects of Drugs, Pharmacology
The document discusses different types of interactions that can occur when two or more drugs are taken together. It describes additive or summation effects when the effects of the drugs combine in an additive fashion. It also explains drug synergism, where the combined effect is greater than the sum of the individual drug effects. Additionally, it covers drug antagonism, where the combined effect is less than additive due to one drug opposing or decreasing the effects of another drug. The types of antagonism discussed include competitive, non-competitive, chemical, physiological, and physical antagonism.
Ic50
Plate-based proliferation assays are used in oncology drug discovery to evaluate the potency of compounds and sensitivity of cell lines. A dose-response curve describes the relationship between increasing drug concentration and the resulting change in response. To determine the IC50, which is the dose that inhibits 50% of the response, one should test at least three doses around the estimated proper dose, use a negative control, and blank wells. The assay is run and optical densities are determined using assays like MTS, MTT, or Orangu, with the data exported to Excel. The ODs are normalized to the mean control and inhibition curves are constructed to find the IC50.
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- Drug dose response relationships can be graded/quantitative or quantal/all-or-none. Graded responses increase continuously with dose while quantal responses produce a fixed effect.
- The therapeutic index compares a drug's median lethal dose to its median effective dose, providing a measure of its margin of safety. Higher therapeutic indices indicate a drug is safer.
- Factors like additive effects or synergism between drugs in combination therapy can impact their overall dose response relationship and safety profile.
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This document discusses key concepts in toxicology related to dose-response relationships. It explains that there is usually a relationship between the amount of a toxic substance received (dose) and the resulting toxic response. Important assumptions are that below a certain dose there is no measurable response, and increasing the dose beyond a maximum response level does not increase the effect. Dose-response curves are used to estimate thresholds for toxic effects like LD50, which is the dose at which 50% of subjects show a lethal response. The therapeutic index compares a substance's toxic dose to its therapeutic dose as a measure of its safety margin. The document also discusses non-traditional dose-response curves like U-shaped and hormetic relationships.
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it's our aim to provide notes for pharmacy students without any charge. So that we make pharmacy education easier.
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This document discusses key concepts in medicinal chemistry including receptor interactions, drug potency and efficacy, and the stereochemical effects of drug enantiomers. Specifically, it defines receptor down-regulation as a decrease in receptor numbers induced by an agonist, and receptor up-regulation as the opposite, an agonist-induced increase in receptor numbers. It also explains that drug potency depends on both affinity, the ability of a drug to bind a receptor, and efficacy, the intensity of response produced by an agonist occupying receptors. Finally, it notes some stereoselective differences in the absorption, distribution, metabolism and excretion of drug enantiomers.
Combined effect of drugs
Combined drugs can have additive, supraadditive, or antagonistic effects. Additive effects occur when two drugs act in the same direction and their individual effects are added together without increasing side effects. Supraadditive effects happen when the combination is greater than the sum of the individual effects, such as when one drug inhibits the breakdown or metabolism of another. Antagonism occurs when one drug decreases or abolishes the effects of another drug through physical, chemical, physiological, or receptor-based mechanisms. Antagonism can be competitive or non-competitive depending on whether the drugs bind to the same receptor site.
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This presentation discusses drug antagonism, which occurs when one drug inhibits the action of another drug. There are four types of antagonism: physical, chemical, physiological/functional, and pharmacological. Pharmacological antagonism can be competitive or non-competitive. Competitive antagonism occurs when two drugs bind to the same receptor site, such that increasing the concentration of one drug can overcome the effects of the other. Non-competitive antagonism occurs when an antagonist binds to a site other than the agonist site and prevents receptor activation by the agonist. Examples of competitive and non-competitive antagonism in receptor pharmacology are provided.
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Pharmacodynamics 2. AGONIST AND ANTIDONIST
Drugs may interact in three ways when taken together: synergism, where their combined effect is greater than the sum of their individual effects; additivity, where their effects simply add up; and antagonism, where one drug decreases or abolishes the effect of another. Synergism can occur through potentiation or when drug effects are additive. Antagonism can occur via physical, chemical, physiological, receptor-based, competitive, or irreversible mechanisms. Pharmacogenomics studies an individual's genetic basis for drug response to guide optimal treatment, while pharmacoeconomics compares costs and outcomes of different treatment options.
Molecular mechanisms of drugs
1. Drug-receptor interactions involve drugs binding reversibly to receptors via various interactions like ionic bonds or hydrogen bonds.
2. When a drug binds a receptor, it can either activate the receptor like an agonist to produce a biological response, or have no effect like an antagonist.
3. Different theories describe drug-receptor interactions, like occupation theory which says response is proportional to receptor occupancy, or induced fit theory where binding causes conformational changes in the receptor and drug.
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- When two drugs exhibit a constant potency ratio in producing an effect, their combination will produce a linear additive isobole that can distinguish synergistic and antagonistic interactions.
- The additive isobole is based on the historical concept of dose equivalence.
- When one drug is a partial agonist, the additive isobole calculated using dose equivalence requires large enough doses to produce the maximum effect, resulting in non-linear isoboles.
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Quantitative structure-activity relationships (QSARs) attempt to establish mathematical relationships between biological activity and measurable physicochemical parameters of drugs. These parameters represent properties like lipophilicity, size, and shape. QSAR studies relate parameter values to biological activity using regression analysis to generate equations. These equations can then be used to predict activity and guide the synthesis of new analogs. Key parameters include lipophilicity, represented by partition coefficients, electronic effects, represented by Hammett constants, and steric effects, represented by Taft constants. Lipophilicity shows an optimal value for activity that balances solubility in aqueous and lipid phases.
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Hope you I'll know about Electronic Parameters of Drugs.If you need more information please refer some books.
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This document summarizes key concepts about allosteric drug effects. It defines important terminology like alpha, beta, and cooperativity. It explains that allosteric molecules can bind to sites on proteins and induce conformational changes that affect the protein's activity. This allows allosteric drugs to have unique effects compared to orthosteric drugs, including modulating but not fully activating or inhibiting receptor function. The document also describes how to detect and quantify allosteric effects using models to fit binding data.
Pharmacology pdf
This document discusses key concepts in pharmacology including:
- Pharmacodynamics is the study of what drugs do to the body, how they act on receptors and their downstream effects. Pharmacokinetics describes how the body affects drugs through absorption, distribution, metabolism and excretion.
- Dose-response curves can be graded, showing the change in effect with increasing dose on a linear scale, or quantal, showing the percentage of a population exhibiting an effect.
- The therapeutic window is the difference between the effective dose (ED50) and the toxic (TD50) or lethal dose (LD50). Understanding dose-response helps optimize drug safety and efficacy.
Comparison of reversible and irreversible antagonists (Dose-response.pptx
This document compares reversible (competitive) and irreversible (non-competitive) antagonists and their effects on dose-response curves. It discusses that competitive antagonists reduce potency by lowering the affinity for receptors but do not change maximum efficacy. In contrast, non-competitive antagonists reduce both potency and maximum efficacy by interacting with receptors in a different area than the active site. The document also introduces concepts like ED50, TD50, LD50, efficacy, potency, agonists, partial agonists, and spare receptors.
Pharmacodynamics revised
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
Affinity and Efficacy
The document discusses key concepts related to how ligands bind to proteins and receptors. It defines important terms like:
1) Equilibrium dissociation constant (Keq), which represents the concentration of ligand that occupies 50% of receptor sites. Keq is inversely related to affinity.
2) Potency, which refers to the concentration of a drug needed to produce a given effect. It is determined by receptor affinity.
3) Efficacy, which represents a drug's ability to induce a physiological response through a receptor. Full agonists elicit the maximum response while partial agonists have lower efficacy.
Lecture 1 Pharmacodynamics
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.
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The document discusses different types of interactions that can occur when two or more drugs are taken together. It describes additive or summation effects when the effects of the drugs combine in an additive fashion. It also explains drug synergism, where the combined effect is greater than the sum of the individual drug effects. Additionally, it covers drug antagonism, where the combined effect is less than additive due to one drug opposing or decreasing the effects of another drug. The types of antagonism discussed include competitive, non-competitive, chemical, physiological, and physical antagonism.
Ic50
Plate-based proliferation assays are used in oncology drug discovery to evaluate the potency of compounds and sensitivity of cell lines. A dose-response curve describes the relationship between increasing drug concentration and the resulting change in response. To determine the IC50, which is the dose that inhibits 50% of the response, one should test at least three doses around the estimated proper dose, use a negative control, and blank wells. The assay is run and optical densities are determined using assays like MTS, MTT, or Orangu, with the data exported to Excel. The ODs are normalized to the mean control and inhibition curves are constructed to find the IC50.
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"DRUG RESPONSE CURVE & THERAPEUTIC" it's a topic in which detail information about How Drug Response when taken in body & effect of various drugs on body with there Response Curve is Given.
Dose response relationship
- Drug dose response relationships can be graded/quantitative or quantal/all-or-none. Graded responses increase continuously with dose while quantal responses produce a fixed effect.
- The therapeutic index compares a drug's median lethal dose to its median effective dose, providing a measure of its margin of safety. Higher therapeutic indices indicate a drug is safer.
- Factors like additive effects or synergism between drugs in combination therapy can impact their overall dose response relationship and safety profile.
Dose response relationship
This document discusses key concepts in toxicology related to dose-response relationships. It explains that there is usually a relationship between the amount of a toxic substance received (dose) and the resulting toxic response. Important assumptions are that below a certain dose there is no measurable response, and increasing the dose beyond a maximum response level does not increase the effect. Dose-response curves are used to estimate thresholds for toxic effects like LD50, which is the dose at which 50% of subjects show a lethal response. The therapeutic index compares a substance's toxic dose to its therapeutic dose as a measure of its safety margin. The document also discusses non-traditional dose-response curves like U-shaped and hormetic relationships.
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it's our aim to provide notes for pharmacy students without any charge. So that we make pharmacy education easier.
Third year lecture 8
This document discusses key concepts in medicinal chemistry including receptor interactions, drug potency and efficacy, and the stereochemical effects of drug enantiomers. Specifically, it defines receptor down-regulation as a decrease in receptor numbers induced by an agonist, and receptor up-regulation as the opposite, an agonist-induced increase in receptor numbers. It also explains that drug potency depends on both affinity, the ability of a drug to bind a receptor, and efficacy, the intensity of response produced by an agonist occupying receptors. Finally, it notes some stereoselective differences in the absorption, distribution, metabolism and excretion of drug enantiomers.
Combined effect of drugs
Combined drugs can have additive, supraadditive, or antagonistic effects. Additive effects occur when two drugs act in the same direction and their individual effects are added together without increasing side effects. Supraadditive effects happen when the combination is greater than the sum of the individual effects, such as when one drug inhibits the breakdown or metabolism of another. Antagonism occurs when one drug decreases or abolishes the effects of another drug through physical, chemical, physiological, or receptor-based mechanisms. Antagonism can be competitive or non-competitive depending on whether the drugs bind to the same receptor site.
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This presentation discusses drug antagonism, which occurs when one drug inhibits the action of another drug. There are four types of antagonism: physical, chemical, physiological/functional, and pharmacological. Pharmacological antagonism can be competitive or non-competitive. Competitive antagonism occurs when two drugs bind to the same receptor site, such that increasing the concentration of one drug can overcome the effects of the other. Non-competitive antagonism occurs when an antagonist binds to a site other than the agonist site and prevents receptor activation by the agonist. Examples of competitive and non-competitive antagonism in receptor pharmacology are provided.
QSAR.pptx
Dr. Manjoor Ahamad Syed is an Assistant Professor in the Department of Medicinal Chemistry at Mettu University in Ethiopia. QSAR attempts to identify physicochemical properties of drugs that affect biological activity using a mathematical equation. Key physicochemical properties include hydrophobicity, electronic effects, and steric effects. QSAR involves synthesizing compounds to vary a property, plotting biological activity vs the property, and using linear regression to determine the best correlation line. The approach has been used to design many successful drug classes.
Pharmacodynamics 2. AGONIST AND ANTIDONIST
Drugs may interact in three ways when taken together: synergism, where their combined effect is greater than the sum of their individual effects; additivity, where their effects simply add up; and antagonism, where one drug decreases or abolishes the effect of another. Synergism can occur through potentiation or when drug effects are additive. Antagonism can occur via physical, chemical, physiological, receptor-based, competitive, or irreversible mechanisms. Pharmacogenomics studies an individual's genetic basis for drug response to guide optimal treatment, while pharmacoeconomics compares costs and outcomes of different treatment options.
Molecular mechanisms of drugs
1. Drug-receptor interactions involve drugs binding reversibly to receptors via various interactions like ionic bonds or hydrogen bonds.
2. When a drug binds a receptor, it can either activate the receptor like an agonist to produce a biological response, or have no effect like an antagonist.
3. Different theories describe drug-receptor interactions, like occupation theory which says response is proportional to receptor occupancy, or induced fit theory where binding causes conformational changes in the receptor and drug.
Isobologram
- When two drugs exhibit a constant potency ratio in producing an effect, their combination will produce a linear additive isobole that can distinguish synergistic and antagonistic interactions.
- The additive isobole is based on the historical concept of dose equivalence.
- When one drug is a partial agonist, the additive isobole calculated using dose equivalence requires large enough doses to produce the maximum effect, resulting in non-linear isoboles.
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Quantitative structure-activity relationships (QSARs) attempt to establish mathematical relationships between biological activity and measurable physicochemical parameters of drugs. These parameters represent properties like lipophilicity, size, and shape. QSAR studies relate parameter values to biological activity using regression analysis to generate equations. These equations can then be used to predict activity and guide the synthesis of new analogs. Key parameters include lipophilicity, represented by partition coefficients, electronic effects, represented by Hammett constants, and steric effects, represented by Taft constants. Lipophilicity shows an optimal value for activity that balances solubility in aqueous and lipid phases.
Electronic Parameters used for quantifying Drug - Introduction
Hope you I'll know about Electronic Parameters of Drugs.If you need more information please refer some books.
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This document summarizes key concepts about allosteric drug effects. It defines important terminology like alpha, beta, and cooperativity. It explains that allosteric molecules can bind to sites on proteins and induce conformational changes that affect the protein's activity. This allows allosteric drugs to have unique effects compared to orthosteric drugs, including modulating but not fully activating or inhibiting receptor function. The document also describes how to detect and quantify allosteric effects using models to fit binding data.
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- Dose-response curves can be graded, showing the change in effect with increasing dose on a linear scale, or quantal, showing the percentage of a population exhibiting an effect.
- The therapeutic window is the difference between the effective dose (ED50) and the toxic (TD50) or lethal dose (LD50). Understanding dose-response helps optimize drug safety and efficacy.
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This document compares reversible (competitive) and irreversible (non-competitive) antagonists and their effects on dose-response curves. It discusses that competitive antagonists reduce potency by lowering the affinity for receptors but do not change maximum efficacy. In contrast, non-competitive antagonists reduce both potency and maximum efficacy by interacting with receptors in a different area than the active site. The document also introduces concepts like ED50, TD50, LD50, efficacy, potency, agonists, partial agonists, and spare receptors.
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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
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The document discusses key concepts related to how ligands bind to proteins and receptors. It defines important terms like:
1) Equilibrium dissociation constant (Keq), which represents the concentration of ligand that occupies 50% of receptor sites. Keq is inversely related to affinity.
2) Potency, which refers to the concentration of a drug needed to produce a given effect. It is determined by receptor affinity.
3) Efficacy, which represents a drug's ability to induce a physiological response through a receptor. Full agonists elicit the maximum response while partial agonists have lower efficacy.
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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.
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Parmacodynamics.pptx
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.
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The document discusses drug receptors and how drugs act in the body. It provides information on:
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- 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.
dynamics.ppt
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.
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1. The document discusses key concepts related to how drugs act including affinity, efficacy, potency, graded and quantal dose-response relationships.
2. It explains that affinity refers to a drug's tendency to bind receptors, efficacy is a drug's ability to produce a maximum response, and potency is the concentration needed to produce 50% of a drug's effect.
3. The document also discusses factors that modify drug action such as age, metabolism, and genetic factors. It emphasizes that drug potency determines dosage while efficacy impacts clinical effectiveness.
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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.
pharmacodynamics
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their biochemical effects. It covers topics like dose-response relationships, drug-receptor interactions, and variability in drug responses. Receptors are important sites of drug action that allow for selectivity. Drugs can act as agonists, antagonists, or partial agonists at receptors. The therapeutic index is a measure of a drug's safety based on its lethal and effective doses. Understanding pharmacodynamics helps nurses educate patients and evaluate drug effects.
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Pharmacodynamics 2020
- 1. Principles of pharmacodynamics Adnan mansour jasim alqasim green university
- 2. Receptors
- 3. Regulatoryproteins–receptors drugsactonreceptorsasagonistsorantagonists 1. Agonists bind to receptors and produce a response- effects of various types 2. Antagonists bind to receptors without producing a response and by occupying the receptors they prevent action of agonists.
- 5. 1. Agonists (cont.) • Affinity - tendency to bind to the receptors (attraction between receptor and drug) • Efficacy - ability once bound, to initiate changes, which lead to effect (is the capacity of drug to activate a receptor) Full agonists - can produce maximal effect when all receptors are occupied (high efficacy) Partial agonists - can produce only submaximal effects even when all receptors are occupied
- 7. 2. Antagonists • competitive antagonism antagonists are able to displace the agonists from the receptors (one drug can be displaced by another drug), may be abolished by adding an excess of agonist. a. reversible b. ireversible antagonist dissociates very slowly or not
- 8. 2. Antagonists (cont.) non-competitive antagonism a. form bonds with the receptors usually at sites other than the endogenous agent. b. in some cases binding may be covalent and ireversible c. cannot be overcom by higher concentration of agonist
- 10. Log-concentration-effect curve c 10-8 10-7 10-6 10-5 10-4 potency (affinity) 50% EC50 efficacy slope of the curve
- 11. Typical dose-response curve for drug showing differences in potency and efficacy. (EC50 = drug dose that shows fifty percent of maximal response.) Drug A is more potent than Drug B, but both show the same efficacy. Drug C shows lower potency and lower efficacy than Drugs A and B. Drug A Drug B Drug C Log drug concentration EC50 for Drug A EC50 for Drug B EC50 for Drug C 0 50 100 Biologiceffect (according to Lippincott´s Pharmacology, 2006)
- 12. Therapeutic index The ratio of the dose that produces toxicity to the dose that produces a clinically desired or effective response in a population of individuals: Therapeutic index = LD50/ED50 or TD50/ED50 TD50 = the dose that produces a toxic effect in half the population, LD50 = the dose that produces a death in half the population ED50 = the dose that produces a therapeutic or desired response in half the population. The therapeutic index = a measure of a drug's safety – a large value = there is a wide margin between doses that are effective and toxic.