https://en.wikivet.net/api.php?action=feedcontributions&feedformat=atom&user=Phlancelot 2026-08-16T08:37:46Z User contributions MediaWiki 1.35.0 https://en.wikivet.net/index.php?title=Pharmacodynamics&diff=138047 2012-05-04T13:29:27Z

<p>Phlancelot: /* Agonists */</p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |sublink1 = Basic Concepts of Pharmacology<br /> |subtext1 = Basic Concepts of Pharmacology<br /> |pagetype = Drugs<br /> }}<br /> '''Pharmacodynamics is the actions of drugs on the body.'''<br /> <br /> For drugs to act upon the body they must be able to exert some chemical influence upon a cell to result in a physiological response. They are capable of doing this by binding to a target molecule (usually proteins).<br /> <br /> There are four main targets which drugs to bind to:<br /> <br /> * '''Receptors''' - these are protein molecules that are capable of responding to endogenous chemical signals. They are usually found on the cell membrane, in the cytoplasm or on the nucleus and other organelles.<br /> * '''Enzymes''' - both intracellular and extracellular ones.<br /> * '''Ion Channels'''<br /> * '''Transport proteins'''<br /> <br /> <br /> ==Agonists==<br /> <br /> An agonist can be defined as '''a drug that binds to a target molecule and results in activation of the receptor and thus a tissue response'''.<br /> <br /> * An agonist forms a complex with the receptor. This complex is '''dynamic''' as the agonist will continously associate and dissociate with the receptor. The agonist will continue to do this and thus produce a response, until the concentration of the agonist is reduced to a level at which binding no longer occurs.<br /> <br /> <br /> * The rate of complex formation is dependent on two factors: '''agonist concentration''' and the '''number of free receptors'''.<br /> <br /> <br /> * The '''affinity''' of a drug to a receptor varies and can be compared using the '''equilibrium constant or K&lt;sub&gt;A&lt;/sub&gt;'''.<br /> <br /> This can be defined as the concentration of a drug which results in 50% of receptors being bound in equilibrium or when '''K&lt;sub&gt;1&lt;/sub&gt;=K&lt;sub&gt;-1&lt;/sub&gt;'''.<br /> <br /> &lt;big&gt;'''Drug + Number of Free Receptors = Drug-Receptor Complexes'''&lt;/big&gt;<br /> <br /> Where '''K&lt;sub&gt;1&lt;/sub&gt;''' is the rate constant in a forward direction (association rate constant)<br /> and '''K&lt;sub&gt;-1&lt;/sub&gt;''' is the rate constant in a backward direction (dissociation rate constant)<br /> <br /> Therefore a drug that has a higher affinity to a receptor has a lower '''K&lt;sub&gt;A&lt;/sub&gt;''' value.<br /> <br /> <br /> * The biological response resulting from an agonist binding is proportional to the number of receptors occupied. The size of a response can be measured and plotted against the dose/concentration of the agonist. As the size of a response normally increases in a non-linear manner (until the maximum is reached) the response is normally plotted against the log of the concentration.<br /> <br /> <br /> '''Please Insert Appropriate Graphs'''<br /> [[File:Dose-Response Curve.png|thumb|dose-response curve used to calculate EC50]]<br /> <br /> From these graphs two figures can be achieved, the '''ED50''' or '''EC50'''. The ED50 is the effective dose at which 50% of a maximal response occurs or 50% of individuals respond. The EC50 is the same but is the effective concentration. Agonists with higher affinities will have a lower concentration and so EC50 than an agonist with a lower affinity. The first drug is therfore said to be more '''potent'''.<br /> <br /> <br /> The '''potency''' of a drug is very important clinically as it will determine the dose needed to have the desired clinical effect. Often if a drug is more potent it is usally more selective to which target molecules it binds to.<br /> <br /> <br /> ===Full and Partial Agonists===<br /> <br /> * A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.<br /> <br /> <br /> * A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.<br /> <br /> <br /> The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist. <br /> <br /> It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.<br /> <br /> <br /> ===Inverse Agonists===<br /> <br /> These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therefore have a negative efficacy.<br /> <br /> ===Effector Linkage Mechanisms===<br /> <br /> Once the agonist binds to the receptor the cell response can be formed in three different ways:<br /> * By the opening of a ligand gated ion channel<br /> * By an intracellular second messenger system<br /> * By DNA transcription<br /> <br /> ==Antagonists==<br /> <br /> An antagonist can be defined as '''a drug that inhibits the action of an agonist'''.<br /> <br /> Antagonists bind to similar receptors as agonist but crucially they don't activate any intracellular events and so there is no tissue response. It's effect is produced by reducing the amount or capability of an agonist to bind to it's target molecule. <br /> <br /> Antagonists like agonists bind to receptors in a dynamic fashion, and so it is the antagonists affinity to the receptor that determines it's inhibitory response. The amount of inhibition thus depends on the concentration of the drug at the target site and the number of free receptor sites.<br /> <br /> ===Competitive Antagonism===<br /> <br /> ====Reversible Competitive Antagonism====<br /> <br /> Here the antagonist competes with the agonist for the occupation of the receptor site. Since less agonist is able to bind to the target molecule the size of the tissue response will decrease. As the dose/concentration of the antagonist increases so the size of the tissue response will further decrease.<br /> <br /> The formation of receptor complexes is dynamic in it's nature and so if the agonist' dose/concentration is increased it will out-compete the antagonist for receptor occupation and the size of the tissue response will start to increase. Therefore the antagonists action is reversible.<br /> <br /> <br /> ====Irreversible Competitive Antagonism====<br /> <br /> This form of antagonism essentially works in the same manner as above except for one crucial difference. The antagonist forms very strong bonds to the receptor sit meaning that it dissociates very slowly or not at all. This means that increasing the amount of agonist present is unable to out-compete the antagonist as receptor sites are always full. <br /> <br /> <br /> A partial agonist can effectively act as an antagonist when it is present in very high concentrations as it out-competes the full agonist for the receptor site. <br /> <br /> <br /> ===Non-Competitive Antagonism===<br /> <br /> Here the agonist binds to its receptor but the antagonist acts further along the sequence of events resulting in a tissue response. As this chain is blocked the agonist is incapable of producing a response.<br /> <br /> <br /> ===Pharmacokinetic Antagonism===<br /> <br /> The antagonist reduces the effect of another drug by reducing its absorption or increasing its rate of metabolism or increasing its rate of excretion. <br /> <br /> <br /> ===Self-antagonism===<br /> <br /> If some drugs are repeatedly given its effect can decrease. This is called '''tachyphylaxis''' or '''desensitisation'''. If a gradual decrease in response to a drug occurs this is called '''tolerance''' and if the drug loses total therapeutic efficacy it is deemed '''refractory'''. Many types of mechanisms occur to cause this phenomenon, the most important include:<br /> <br /> * change in receptor type<br /> * loss of receptors<br /> * exhaustion of cell mediators<br /> * increased metabolic degradation of the drug<br /> * physiological adaptation<br /> * active extrusion of the drug from cells<br /> <br /> ===Chemical Antagonism===<br /> <br /> This is where the interaction of two drugs results in the failure of an biological activity.<br /> <br /> <br /> ===Physiological Antagonism===<br /> <br /> This occurs when two drugs have opposing actions on the body and so their actions cancel each other out.</div>

Phlancelot https://en.wikivet.net/index.php?title=Pharmacodynamics&diff=138046 2012-05-04T13:26:16Z

<p>Phlancelot: /* Agonists */</p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |sublink1 = Basic Concepts of Pharmacology<br /> |subtext1 = Basic Concepts of Pharmacology<br /> |pagetype = Drugs<br /> }}<br /> '''Pharmacodynamics is the actions of drugs on the body.'''<br /> <br /> For drugs to act upon the body they must be able to exert some chemical influence upon a cell to result in a physiological response. They are capable of doing this by binding to a target molecule (usually proteins).<br /> <br /> There are four main targets which drugs to bind to:<br /> <br /> * '''Receptors''' - these are protein molecules that are capable of responding to endogenous chemical signals. They are usually found on the cell membrane, in the cytoplasm or on the nucleus and other organelles.<br /> * '''Enzymes''' - both intracellular and extracellular ones.<br /> * '''Ion Channels'''<br /> * '''Transport proteins'''<br /> <br /> <br /> ==Agonists==<br /> <br /> An agonist can be defined as '''a drug that binds to a target molecule and results in activation of the receptor and thus a tissue response'''.<br /> <br /> * An agonist forms a complex with the receptor. This complex is '''dynamic''' as the agonist will continously associate and dissociate with the receptor. The agonist will continue to do this and thus produce a response, until the concentration of the agonist is reduced to a level at which binding no longer occurs.<br /> <br /> <br /> * The rate of complex formation is dependent on two factors: '''agonist concentration''' and the '''number of free receptors'''.<br /> <br /> <br /> * The '''affinity''' of a drug to a receptor varies and can be compared using the '''equilibrium constant or K&lt;sub&gt;A&lt;/sub&gt;'''.<br /> <br /> This can be defined as the concentration of a drug which results in 50% of receptors being bound in equilibrium or when '''K&lt;sub&gt;1&lt;/sub&gt;=K&lt;sub&gt;-1&lt;/sub&gt;'''.<br /> <br /> &lt;big&gt;'''Drug + Number of Free Receptors = Drug-Receptor Complexes'''&lt;/big&gt;<br /> <br /> Where '''K&lt;sub&gt;1&lt;/sub&gt;''' is the rate constant in a forward direction (association rate constant)<br /> and '''K&lt;sub&gt;-1&lt;/sub&gt;''' is the rate constant in a backward direction (dissociation rate constant)<br /> <br /> Therefore a drug that has a higher affinity to a receptor has a lower '''K&lt;sub&gt;A&lt;/sub&gt;''' value.<br /> <br /> <br /> * The biological response resulting from an agonist binding is proportional to the number of receptors occupied. The size of a response can be measured and plotted against the dose/concentration of the agonist. As the size of a response normally increases in a non-linear manner (until the maximum is reached) the response is normally plotted against the log of the concentration.<br /> <br /> <br /> '''Please Insert Appropriate Graphs'''<br /> [[File:Dose-Response Curve.png|thumb|Add caption here]]<br /> <br /> From these graphs two figures can be achieved, the '''ED50''' or '''EC50'''. The ED50 is the effective dose at which 50% of a maximal response occurs or 50% of individuals respond. The EC50 is the same but is the effective concentration. Agonists with higher affinities will have a lower concentration and so EC50 than an agonist with a lower affinity. The first drug is therfore said to be more '''potent'''.<br /> <br /> <br /> The '''potency''' of a drug is very important clinically as it will determine the dose needed to have the desired clinical effect. Often if a drug is more potent it is usally more selective to which target molecules it binds to.<br /> <br /> <br /> ===Full and Partial Agonists===<br /> <br /> * A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.<br /> <br /> <br /> * A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.<br /> <br /> <br /> The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist. <br /> <br /> It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.<br /> <br /> <br /> ===Inverse Agonists===<br /> <br /> These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therefore have a negative efficacy.<br /> <br /> ===Effector Linkage Mechanisms===<br /> <br /> Once the agonist binds to the receptor the cell response can be formed in three different ways:<br /> * By the opening of a ligand gated ion channel<br /> * By an intracellular second messenger system<br /> * By DNA transcription<br /> <br /> ==Antagonists==<br /> <br /> An antagonist can be defined as '''a drug that inhibits the action of an agonist'''.<br /> <br /> Antagonists bind to similar receptors as agonist but crucially they don't activate any intracellular events and so there is no tissue response. It's effect is produced by reducing the amount or capability of an agonist to bind to it's target molecule. <br /> <br /> Antagonists like agonists bind to receptors in a dynamic fashion, and so it is the antagonists affinity to the receptor that determines it's inhibitory response. The amount of inhibition thus depends on the concentration of the drug at the target site and the number of free receptor sites.<br /> <br /> ===Competitive Antagonism===<br /> <br /> ====Reversible Competitive Antagonism====<br /> <br /> Here the antagonist competes with the agonist for the occupation of the receptor site. Since less agonist is able to bind to the target molecule the size of the tissue response will decrease. As the dose/concentration of the antagonist increases so the size of the tissue response will further decrease.<br /> <br /> The formation of receptor complexes is dynamic in it's nature and so if the agonist' dose/concentration is increased it will out-compete the antagonist for receptor occupation and the size of the tissue response will start to increase. Therefore the antagonists action is reversible.<br /> <br /> <br /> ====Irreversible Competitive Antagonism====<br /> <br /> This form of antagonism essentially works in the same manner as above except for one crucial difference. The antagonist forms very strong bonds to the receptor sit meaning that it dissociates very slowly or not at all. This means that increasing the amount of agonist present is unable to out-compete the antagonist as receptor sites are always full. <br /> <br /> <br /> A partial agonist can effectively act as an antagonist when it is present in very high concentrations as it out-competes the full agonist for the receptor site. <br /> <br /> <br /> ===Non-Competitive Antagonism===<br /> <br /> Here the agonist binds to its receptor but the antagonist acts further along the sequence of events resulting in a tissue response. As this chain is blocked the agonist is incapable of producing a response.<br /> <br /> <br /> ===Pharmacokinetic Antagonism===<br /> <br /> The antagonist reduces the effect of another drug by reducing its absorption or increasing its rate of metabolism or increasing its rate of excretion. <br /> <br /> <br /> ===Self-antagonism===<br /> <br /> If some drugs are repeatedly given its effect can decrease. This is called '''tachyphylaxis''' or '''desensitisation'''. If a gradual decrease in response to a drug occurs this is called '''tolerance''' and if the drug loses total therapeutic efficacy it is deemed '''refractory'''. Many types of mechanisms occur to cause this phenomenon, the most important include:<br /> <br /> * change in receptor type<br /> * loss of receptors<br /> * exhaustion of cell mediators<br /> * increased metabolic degradation of the drug<br /> * physiological adaptation<br /> * active extrusion of the drug from cells<br /> <br /> ===Chemical Antagonism===<br /> <br /> This is where the interaction of two drugs results in the failure of an biological activity.<br /> <br /> <br /> ===Physiological Antagonism===<br /> <br /> This occurs when two drugs have opposing actions on the body and so their actions cancel each other out.</div>

Phlancelot https://en.wikivet.net/index.php?title=Pharmacodynamics&diff=138045 2012-05-04T13:08:00Z

<p>Phlancelot: /* Agonists */</p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |sublink1 = Basic Concepts of Pharmacology<br /> |subtext1 = Basic Concepts of Pharmacology<br /> |pagetype = Drugs<br /> }}<br /> '''Pharmacodynamics is the actions of drugs on the body.'''<br /> <br /> For drugs to act upon the body they must be able to exert some chemical influence upon a cell to result in a physiological response. They are capable of doing this by binding to a target molecule (usually proteins).<br /> <br /> There are four main targets which drugs to bind to:<br /> <br /> * '''Receptors''' - these are protein molecules that are capable of responding to endogenous chemical signals. They are usually found on the cell membrane, in the cytoplasm or on the nucleus and other organelles.<br /> * '''Enzymes''' - both intracellular and extracellular ones.<br /> * '''Ion Channels'''<br /> * '''Transport proteins'''<br /> <br /> <br /> ==Agonists==<br /> <br /> An agonist can be defined as '''a drug that binds to a target molecule and results in activation of the receptor and thus a tissue response'''.<br /> <br /> * An agonist forms a complex with the receptor. This complex is '''dynamic''' as the agonist will continously associate and dissociate with the receptor. The agonist will continue to do this and thus produce a response, until the concentration of the agonist is reduced to a level at which binding no longer occurs.<br /> <br /> <br /> * The rate of complex formation is dependent on two factors: '''agonist concentration''' and the '''number of free receptors'''.<br /> <br /> <br /> * The '''affinity''' of a drug to a receptor varies and can be compared using the '''equilibrium constant or K&lt;sub&gt;A&lt;/sub&gt;'''.<br /> <br /> This can be defined as the concentration of a drug which results in 50% of receptors being bound in equilibrium or when '''K&lt;sub&gt;1&lt;/sub&gt;=K&lt;sub&gt;-1&lt;/sub&gt;'''.<br /> <br /> &lt;big&gt;'''Drug + Number of Free Receptors = Drug-Receptor Complexes'''&lt;/big&gt;<br /> <br /> Where '''K&lt;sub&gt;1&lt;/sub&gt;''' is the rate constant in a forward direction (association rate constant)<br /> and '''K&lt;sub&gt;-1&lt;/sub&gt;''' is the rate constant in a backward direction (dissociation rate constant)<br /> <br /> Therefore a drug that has a higher affinity to a receptor has a lower '''K&lt;sub&gt;A&lt;/sub&gt;''' value.<br /> <br /> <br /> * The biological response resulting from an agonist binding is proportional to the number of receptors occupied. The size of a response can be measured and plotted against the dose/concentration of the agonist. As the size of a response normally increases in a non-linear manner (until the maximum is reached) the response is normally plotted against the log of the concentration.<br /> <br /> <br /> '''Please Insert Appropriate Graphs'''<br /> <br /> From these graphs two figures can be achieved, the '''ED50''' or '''EC50'''. The ED50 is the effective dose at which 50% of a maximal response occurs or 50% of individuals respond. The EC50 is the same but is the effective concentration. Agonists with higher affinities will have a lower concentration and so EC50 than an agonist with a lower affinity. The first drug is therfore said to be more '''potent'''.<br /> <br /> <br /> The '''potency''' of a drug is very important clinically as it will determine the dose needed to have the desired clinical effect. Often if a drug is more potent it is usally more selective to which target molecules it binds to.<br /> <br /> <br /> ===Full and Partial Agonists===<br /> <br /> * A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.<br /> <br /> <br /> * A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.<br /> <br /> <br /> The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist. <br /> <br /> It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.<br /> <br /> <br /> ===Inverse Agonists===<br /> <br /> These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therefore have a negative efficacy.<br /> <br /> ===Effector Linkage Mechanisms===<br /> <br /> Once the agonist binds to the receptor the cell response can be formed in three different ways:<br /> * By the opening of a ligand gated ion channel<br /> * By an intracellular second messenger system<br /> * By DNA transcription<br /> <br /> ==Antagonists==<br /> <br /> An antagonist can be defined as '''a drug that inhibits the action of an agonist'''.<br /> <br /> Antagonists bind to similar receptors as agonist but crucially they don't activate any intracellular events and so there is no tissue response. It's effect is produced by reducing the amount or capability of an agonist to bind to it's target molecule. <br /> <br /> Antagonists like agonists bind to receptors in a dynamic fashion, and so it is the antagonists affinity to the receptor that determines it's inhibitory response. The amount of inhibition thus depends on the concentration of the drug at the target site and the number of free receptor sites.<br /> <br /> ===Competitive Antagonism===<br /> <br /> ====Reversible Competitive Antagonism====<br /> <br /> Here the antagonist competes with the agonist for the occupation of the receptor site. Since less agonist is able to bind to the target molecule the size of the tissue response will decrease. As the dose/concentration of the antagonist increases so the size of the tissue response will further decrease.<br /> <br /> The formation of receptor complexes is dynamic in it's nature and so if the agonist' dose/concentration is increased it will out-compete the antagonist for receptor occupation and the size of the tissue response will start to increase. Therefore the antagonists action is reversible.<br /> <br /> <br /> ====Irreversible Competitive Antagonism====<br /> <br /> This form of antagonism essentially works in the same manner as above except for one crucial difference. The antagonist forms very strong bonds to the receptor sit meaning that it dissociates very slowly or not at all. This means that increasing the amount of agonist present is unable to out-compete the antagonist as receptor sites are always full. <br /> <br /> <br /> A partial agonist can effectively act as an antagonist when it is present in very high concentrations as it out-competes the full agonist for the receptor site. <br /> <br /> <br /> ===Non-Competitive Antagonism===<br /> <br /> Here the agonist binds to its receptor but the antagonist acts further along the sequence of events resulting in a tissue response. As this chain is blocked the agonist is incapable of producing a response.<br /> <br /> <br /> ===Pharmacokinetic Antagonism===<br /> <br /> The antagonist reduces the effect of another drug by reducing its absorption or increasing its rate of metabolism or increasing its rate of excretion. <br /> <br /> <br /> ===Self-antagonism===<br /> <br /> If some drugs are repeatedly given its effect can decrease. This is called '''tachyphylaxis''' or '''desensitisation'''. If a gradual decrease in response to a drug occurs this is called '''tolerance''' and if the drug loses total therapeutic efficacy it is deemed '''refractory'''. Many types of mechanisms occur to cause this phenomenon, the most important include:<br /> <br /> * change in receptor type<br /> * loss of receptors<br /> * exhaustion of cell mediators<br /> * increased metabolic degradation of the drug<br /> * physiological adaptation<br /> * active extrusion of the drug from cells<br /> <br /> ===Chemical Antagonism===<br /> <br /> This is where the interaction of two drugs results in the failure of an biological activity.<br /> <br /> <br /> ===Physiological Antagonism===<br /> <br /> This occurs when two drugs have opposing actions on the body and so their actions cancel each other out.</div>

Phlancelot https://en.wikivet.net/index.php?title=Pharmacodynamics&diff=138044 2012-05-04T13:07:13Z

<p>Phlancelot: /* Agonists */</p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |sublink1 = Basic Concepts of Pharmacology<br /> |subtext1 = Basic Concepts of Pharmacology<br /> |pagetype = Drugs<br /> }}<br /> '''Pharmacodynamics is the actions of drugs on the body.'''<br /> <br /> For drugs to act upon the body they must be able to exert some chemical influence upon a cell to result in a physiological response. They are capable of doing this by binding to a target molecule (usually proteins).<br /> <br /> There are four main targets which drugs to bind to:<br /> <br /> * '''Receptors''' - these are protein molecules that are capable of responding to endogenous chemical signals. They are usually found on the cell membrane, in the cytoplasm or on the nucleus and other organelles.<br /> * '''Enzymes''' - both intracellular and extracellular ones.<br /> * '''Ion Channels'''<br /> * '''Transport proteins'''<br /> <br /> <br /> ==Agonists==<br /> <br /> An agonist can be defined as '''a drug that binds to a target molecule and results in activation of the receptor and thus a tissue response'''.<br /> <br /> * An agonist forms a complex with the receptor. This complex is '''dynamic''' as the agonist will continously associate and dissociate with the receptor. The agonist will continue to do this and thus produce a response, until the concentration of the agonist is reduced to a level at which binding no longer occurs.<br /> <br /> <br /> * The rate of complex formation is dependent on two factors: '''agonist concentration''' and the '''number of free receptors'''.<br /> <br /> <br /> * The '''affinity''' of a drug to a receptor varies and can be compared using the '''equilibrium constant or K&lt;sub&gt;A&lt;/sub&gt;'''.<br /> <br /> This can be defined as the concentration of a drug which results in 50% of receptors being bound in equilibrium or when '''K&lt;sub&gt;1&lt;/sub&gt;=K&lt;sub&gt;-1&lt;/sub&gt;'''.<br /> <br /> &lt;big&gt;'''Drug + Number of Free Receptors = Drug-Receptor Complexes'''&lt;/big&gt;<br /> <br /> Where '''K&lt;sub&gt;1&lt;/sub&gt;''' is the rate constant in a forward direction (association rate constant)<br /> and '''K&lt;sub&gt;-1&lt;/sub&gt;''' is the rate constant in a backward direction (dissociation rate constant)<br /> <br /> Therefore a drug that has a higher affinity to a receptor has a lower '''K&lt;sub&gt;A&lt;/sub&gt;''' value.<br /> <br /> <br /> * The biological response resulting from an agonist binding is proportional to the number of receptors occupied. The size of a response can be measured and plotted against the dose/concentration of the agonist. As the size of a response normally increasee in a non-linear manner (until the maximum is reached) the response is normally plotted against the log of the concentration.<br /> <br /> <br /> '''Please Insert Appropriate Graphs'''<br /> <br /> From these graphs two figures can be achieved, the '''ED50''' or '''EC50'''. The ED50 is the effective dose at which 50% of a maximal response occurs or 50% of individuals respond. The EC50 is the same but is the effective concentration. Agonists with higher affinities will have a lower concentration and so EC50 than an agonist with a lower affinity. The first drug is therfore said to be more '''potent'''.<br /> <br /> <br /> The '''potency''' of a drug is very important clinically as it will determine the dose needed to have the desired clinical effect. Often if a drug is more potent it is usally more selective to which target molecules it binds to.<br /> <br /> <br /> ===Full and Partial Agonists===<br /> <br /> * A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.<br /> <br /> <br /> * A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.<br /> <br /> <br /> The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist. <br /> <br /> It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.<br /> <br /> <br /> ===Inverse Agonists===<br /> <br /> These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therefore have a negative efficacy.<br /> <br /> ===Effector Linkage Mechanisms===<br /> <br /> Once the agonist binds to the receptor the cell response can be formed in three different ways:<br /> * By the opening of a ligand gated ion channel<br /> * By an intracellular second messenger system<br /> * By DNA transcription<br /> <br /> ==Antagonists==<br /> <br /> An antagonist can be defined as '''a drug that inhibits the action of an agonist'''.<br /> <br /> Antagonists bind to similar receptors as agonist but crucially they don't activate any intracellular events and so there is no tissue response. It's effect is produced by reducing the amount or capability of an agonist to bind to it's target molecule. <br /> <br /> Antagonists like agonists bind to receptors in a dynamic fashion, and so it is the antagonists affinity to the receptor that determines it's inhibitory response. The amount of inhibition thus depends on the concentration of the drug at the target site and the number of free receptor sites.<br /> <br /> ===Competitive Antagonism===<br /> <br /> ====Reversible Competitive Antagonism====<br /> <br /> Here the antagonist competes with the agonist for the occupation of the receptor site. Since less agonist is able to bind to the target molecule the size of the tissue response will decrease. As the dose/concentration of the antagonist increases so the size of the tissue response will further decrease.<br /> <br /> The formation of receptor complexes is dynamic in it's nature and so if the agonist' dose/concentration is increased it will out-compete the antagonist for receptor occupation and the size of the tissue response will start to increase. Therefore the antagonists action is reversible.<br /> <br /> <br /> ====Irreversible Competitive Antagonism====<br /> <br /> This form of antagonism essentially works in the same manner as above except for one crucial difference. The antagonist forms very strong bonds to the receptor sit meaning that it dissociates very slowly or not at all. This means that increasing the amount of agonist present is unable to out-compete the antagonist as receptor sites are always full. <br /> <br /> <br /> A partial agonist can effectively act as an antagonist when it is present in very high concentrations as it out-competes the full agonist for the receptor site. <br /> <br /> <br /> ===Non-Competitive Antagonism===<br /> <br /> Here the agonist binds to its receptor but the antagonist acts further along the sequence of events resulting in a tissue response. As this chain is blocked the agonist is incapable of producing a response.<br /> <br /> <br /> ===Pharmacokinetic Antagonism===<br /> <br /> The antagonist reduces the effect of another drug by reducing its absorption or increasing its rate of metabolism or increasing its rate of excretion. <br /> <br /> <br /> ===Self-antagonism===<br /> <br /> If some drugs are repeatedly given its effect can decrease. This is called '''tachyphylaxis''' or '''desensitisation'''. If a gradual decrease in response to a drug occurs this is called '''tolerance''' and if the drug loses total therapeutic efficacy it is deemed '''refractory'''. Many types of mechanisms occur to cause this phenomenon, the most important include:<br /> <br /> * change in receptor type<br /> * loss of receptors<br /> * exhaustion of cell mediators<br /> * increased metabolic degradation of the drug<br /> * physiological adaptation<br /> * active extrusion of the drug from cells<br /> <br /> ===Chemical Antagonism===<br /> <br /> This is where the interaction of two drugs results in the failure of an biological activity.<br /> <br /> <br /> ===Physiological Antagonism===<br /> <br /> This occurs when two drugs have opposing actions on the body and so their actions cancel each other out.</div>

Phlancelot https://en.wikivet.net/index.php?title=Pharmacodynamics&diff=138043 2012-05-04T13:06:48Z

<p>Phlancelot: /* Agonists */</p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |sublink1 = Basic Concepts of Pharmacology<br /> |subtext1 = Basic Concepts of Pharmacology<br /> |pagetype = Drugs<br /> }}<br /> '''Pharmacodynamics is the actions of drugs on the body.'''<br /> <br /> For drugs to act upon the body they must be able to exert some chemical influence upon a cell to result in a physiological response. They are capable of doing this by binding to a target molecule (usually proteins).<br /> <br /> There are four main targets which drugs to bind to:<br /> <br /> * '''Receptors''' - these are protein molecules that are capable of responding to endogenous chemical signals. They are usually found on the cell membrane, in the cytoplasm or on the nucleus and other organelles.<br /> * '''Enzymes''' - both intracellular and extracellular ones.<br /> * '''Ion Channels'''<br /> * '''Transport proteins'''<br /> <br /> <br /> ==Agonists==<br /> <br /> An agonist can be defined as '''a drug that binds to a target molecule and results in activation of the receptor and thus a tissue response'''.<br /> <br /> * An agonist forms a complex with the receptor. This complex is '''dynamic''' as the agonist will continously associate and dissociate with the receptor. The agonist will continue to do this and thus produce a response, until the concentration of the agonist is reduced to a level at which binding no longer occurs.<br /> <br /> <br /> * The rate of complex formation is dependent on two factors: '''agonist concentration''' and the '''number of free receptors'''.<br /> <br /> <br /> * The '''affinity''' of a drug to a receptor varies and can be compared using the '''equilibrium constant or K&lt;sub&gt;A&lt;/sub&gt;'''.<br /> <br /> This can be defined as the concentration of a drug which results in 50% of receptors being bound in equilibrium or when '''K&lt;sub&gt;1&lt;/sub&gt;=K&lt;sub&gt;-1&lt;/sub&gt;'''.<br /> <br /> &lt;big&gt;'''Drug + Number of Free Receptors = Drug-Receptor Complexes'''&lt;/big&gt;<br /> <br /> Where '''K&lt;sub&gt;1&lt;/sub&gt;''' is the rate constant in a forward direction (association rate constant)<br /> and '''K&lt;sub&gt;-1&lt;/sub&gt;''' is the rate constant in a backward direction (dissociation rate constant)<br /> <br /> Therefore a drug that has a higher affinity to a receptor has a lower '''K&lt;sub&gt;A&lt;/sub&gt;''' value.<br /> <br /> <br /> * The biological response resulting from an agonist is proportional to the number of receptors occupied. The size of a response can be measured and plotted against the dose/concentration of the agonist. As the size of a response normally increasee in a non-linear manner (until the maximum is reached) the response is normally plotted against the log of the concentration.<br /> <br /> <br /> '''Please Insert Appropriate Graphs'''<br /> <br /> From these graphs two figures can be achieved, the '''ED50''' or '''EC50'''. The ED50 is the effective dose at which 50% of a maximal response occurs or 50% of individuals respond. The EC50 is the same but is the effective concentration. Agonists with higher affinities will have a lower concentration and so EC50 than an agonist with a lower affinity. The first drug is therfore said to be more '''potent'''.<br /> <br /> <br /> The '''potency''' of a drug is very important clinically as it will determine the dose needed to have the desired clinical effect. Often if a drug is more potent it is usally more selective to which target molecules it binds to.<br /> <br /> <br /> ===Full and Partial Agonists===<br /> <br /> * A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.<br /> <br /> <br /> * A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.<br /> <br /> <br /> The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist. <br /> <br /> It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.<br /> <br /> <br /> ===Inverse Agonists===<br /> <br /> These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therefore have a negative efficacy.<br /> <br /> ===Effector Linkage Mechanisms===<br /> <br /> Once the agonist binds to the receptor the cell response can be formed in three different ways:<br /> * By the opening of a ligand gated ion channel<br /> * By an intracellular second messenger system<br /> * By DNA transcription<br /> <br /> ==Antagonists==<br /> <br /> An antagonist can be defined as '''a drug that inhibits the action of an agonist'''.<br /> <br /> Antagonists bind to similar receptors as agonist but crucially they don't activate any intracellular events and so there is no tissue response. It's effect is produced by reducing the amount or capability of an agonist to bind to it's target molecule. <br /> <br /> Antagonists like agonists bind to receptors in a dynamic fashion, and so it is the antagonists affinity to the receptor that determines it's inhibitory response. The amount of inhibition thus depends on the concentration of the drug at the target site and the number of free receptor sites.<br /> <br /> ===Competitive Antagonism===<br /> <br /> ====Reversible Competitive Antagonism====<br /> <br /> Here the antagonist competes with the agonist for the occupation of the receptor site. Since less agonist is able to bind to the target molecule the size of the tissue response will decrease. As the dose/concentration of the antagonist increases so the size of the tissue response will further decrease.<br /> <br /> The formation of receptor complexes is dynamic in it's nature and so if the agonist' dose/concentration is increased it will out-compete the antagonist for receptor occupation and the size of the tissue response will start to increase. Therefore the antagonists action is reversible.<br /> <br /> <br /> ====Irreversible Competitive Antagonism====<br /> <br /> This form of antagonism essentially works in the same manner as above except for one crucial difference. The antagonist forms very strong bonds to the receptor sit meaning that it dissociates very slowly or not at all. This means that increasing the amount of agonist present is unable to out-compete the antagonist as receptor sites are always full. <br /> <br /> <br /> A partial agonist can effectively act as an antagonist when it is present in very high concentrations as it out-competes the full agonist for the receptor site. <br /> <br /> <br /> ===Non-Competitive Antagonism===<br /> <br /> Here the agonist binds to its receptor but the antagonist acts further along the sequence of events resulting in a tissue response. As this chain is blocked the agonist is incapable of producing a response.<br /> <br /> <br /> ===Pharmacokinetic Antagonism===<br /> <br /> The antagonist reduces the effect of another drug by reducing its absorption or increasing its rate of metabolism or increasing its rate of excretion. <br /> <br /> <br /> ===Self-antagonism===<br /> <br /> If some drugs are repeatedly given its effect can decrease. This is called '''tachyphylaxis''' or '''desensitisation'''. If a gradual decrease in response to a drug occurs this is called '''tolerance''' and if the drug loses total therapeutic efficacy it is deemed '''refractory'''. Many types of mechanisms occur to cause this phenomenon, the most important include:<br /> <br /> * change in receptor type<br /> * loss of receptors<br /> * exhaustion of cell mediators<br /> * increased metabolic degradation of the drug<br /> * physiological adaptation<br /> * active extrusion of the drug from cells<br /> <br /> ===Chemical Antagonism===<br /> <br /> This is where the interaction of two drugs results in the failure of an biological activity.<br /> <br /> <br /> ===Physiological Antagonism===<br /> <br /> This occurs when two drugs have opposing actions on the body and so their actions cancel each other out.</div>

Phlancelot https://en.wikivet.net/index.php?title=Pharmacodynamics&diff=138042 2012-05-04T13:03:58Z

<p>Phlancelot: </p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |sublink1 = Basic Concepts of Pharmacology<br /> |subtext1 = Basic Concepts of Pharmacology<br /> |pagetype = Drugs<br /> }}<br /> '''Pharmacodynamics is the actions of drugs on the body.'''<br /> <br /> For drugs to act upon the body they must be able to exert some chemical influence upon a cell to result in a physiological response. They are capable of doing this by binding to a target molecule (usually proteins).<br /> <br /> There are four main targets which drugs to bind to:<br /> <br /> * '''Receptors''' - these are protein molecules that are capable of responding to endogenous chemical signals. They are usually found on the cell membrane, in the cytoplasm or on the nucleus and other organelles.<br /> * '''Enzymes''' - both intracellular and extracellular ones.<br /> * '''Ion Channels'''<br /> * '''Transport proteins'''<br /> <br /> <br /> ==Agonists==<br /> <br /> An agonist can be defined as '''a drug that binds to a target molecule and results in activation of the receptor and thus a tissue response'''.<br /> <br /> * An agonist forms a complex with the receptor. This complex is '''dynamic''' as the agonist will continously associate and dissociate with the receptor. The agonist will continue to do this and thus produce a response, until the concentration of the agonist is reduced to a level at which binding no longer occurs.<br /> <br /> <br /> * The rate of complex formation is dependent on two factors: '''agonist concentration''' and the '''number of free receptors'''.<br /> <br /> <br /> * The '''affinity''' of a drug to a receptor varies and can be compared using the '''equilibrium constant or K&lt;sub&gt;A&lt;/sub&gt;'''.<br /> <br /> This can be defined as the concentration of a drug which results in 50% of receptors being bound in equilibrium or when '''K&lt;sub&gt;1&lt;/sub&gt;=K&lt;sub&gt;-1&lt;/sub&gt;'''.<br /> <br /> &lt;big&gt;'''Drug + Number of Free Receptors = Drug-Receptor Complexes'''&lt;/big&gt;<br /> <br /> Where '''K&lt;sub&gt;1&lt;/sub&gt;''' is the rate constant in a forward direction (association rate constant)<br /> and '''K&lt;sub&gt;-1&lt;/sub&gt;''' is the rate constant in a backward direction (dissociation rate constant)<br /> <br /> Therefore a drug that has a higher affinity to a receptor has a lower '''K&lt;sub&gt;A&lt;/sub&gt;''' value.<br /> <br /> <br /> * The biological response of resulting from an agonist is proportional to the number of receptors occupied. The size of a response can be measured and plotted against the dose/concentration of the agonist. As the size of a response normally increasee in a non-linear manner (until the maximum is reached) the response is normally plotted against the log of the concentration.<br /> <br /> <br /> '''Please Insert Appropriate Graphs'''<br /> <br /> From these graphs two figures can be achieved, the '''ED50''' or '''EC50'''. The ED50 is the effective dose at which 50% of a maximal response occurs or 50% of individuals respond. The EC50 is the same but is the effective concentration. Agonists with higher affinities will have a lower concentration and so EC50 than an agonist with a lower affinity. The first drug is therfore said to be more '''potent'''.<br /> <br /> <br /> The '''potency''' of a drug is very important clinically as it will determine the dose needed to have the desired clinical effect. Often if a drug is more potent it is usally more selective to which target molecules it binds to.<br /> <br /> <br /> ===Full and Partial Agonists===<br /> <br /> * A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.<br /> <br /> <br /> * A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.<br /> <br /> <br /> The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist. <br /> <br /> It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.<br /> <br /> <br /> ===Inverse Agonists===<br /> <br /> These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therefore have a negative efficacy.<br /> <br /> ===Effector Linkage Mechanisms===<br /> <br /> Once the agonist binds to the receptor the cell response can be formed in three different ways:<br /> * By the opening of a ligand gated ion channel<br /> * By an intracellular second messenger system<br /> * By DNA transcription<br /> <br /> ==Antagonists==<br /> <br /> An antagonist can be defined as '''a drug that inhibits the action of an agonist'''.<br /> <br /> Antagonists bind to similar receptors as agonist but crucially they don't activate any intracellular events and so there is no tissue response. It's effect is produced by reducing the amount or capability of an agonist to bind to it's target molecule. <br /> <br /> Antagonists like agonists bind to receptors in a dynamic fashion, and so it is the antagonists affinity to the receptor that determines it's inhibitory response. The amount of inhibition thus depends on the concentration of the drug at the target site and the number of free receptor sites.<br /> <br /> ===Competitive Antagonism===<br /> <br /> ====Reversible Competitive Antagonism====<br /> <br /> Here the antagonist competes with the agonist for the occupation of the receptor site. Since less agonist is able to bind to the target molecule the size of the tissue response will decrease. As the dose/concentration of the antagonist increases so the size of the tissue response will further decrease.<br /> <br /> The formation of receptor complexes is dynamic in it's nature and so if the agonist' dose/concentration is increased it will out-compete the antagonist for receptor occupation and the size of the tissue response will start to increase. Therefore the antagonists action is reversible.<br /> <br /> <br /> ====Irreversible Competitive Antagonism====<br /> <br /> This form of antagonism essentially works in the same manner as above except for one crucial difference. The antagonist forms very strong bonds to the receptor sit meaning that it dissociates very slowly or not at all. This means that increasing the amount of agonist present is unable to out-compete the antagonist as receptor sites are always full. <br /> <br /> <br /> A partial agonist can effectively act as an antagonist when it is present in very high concentrations as it out-competes the full agonist for the receptor site. <br /> <br /> <br /> ===Non-Competitive Antagonism===<br /> <br /> Here the agonist binds to its receptor but the antagonist acts further along the sequence of events resulting in a tissue response. As this chain is blocked the agonist is incapable of producing a response.<br /> <br /> <br /> ===Pharmacokinetic Antagonism===<br /> <br /> The antagonist reduces the effect of another drug by reducing its absorption or increasing its rate of metabolism or increasing its rate of excretion. <br /> <br /> <br /> ===Self-antagonism===<br /> <br /> If some drugs are repeatedly given its effect can decrease. This is called '''tachyphylaxis''' or '''desensitisation'''. If a gradual decrease in response to a drug occurs this is called '''tolerance''' and if the drug loses total therapeutic efficacy it is deemed '''refractory'''. Many types of mechanisms occur to cause this phenomenon, the most important include:<br /> <br /> * change in receptor type<br /> * loss of receptors<br /> * exhaustion of cell mediators<br /> * increased metabolic degradation of the drug<br /> * physiological adaptation<br /> * active extrusion of the drug from cells<br /> <br /> ===Chemical Antagonism===<br /> <br /> This is where the interaction of two drugs results in the failure of an biological activity.<br /> <br /> <br /> ===Physiological Antagonism===<br /> <br /> This occurs when two drugs have opposing actions on the body and so their actions cancel each other out.</div>

Phlancelot https://en.wikivet.net/index.php?title=Pharmacodynamics&diff=138041 2012-05-04T12:59:14Z

<p>Phlancelot: </p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |sublink1 = Basic Concepts of Pharmacology<br /> |subtext1 = Basic Concepts of Pharmacology<br /> |pagetype = Drugs<br /> }}<br /> '''Pharmacodynamics is the actions of drugs on the body.'''<br /> <br /> For drugs to act upon the body they must be able to exert some chemical influence upon a cell to result in a physiological response. They are capable of doing this by binding to a target molecule (usually proteins).<br /> <br /> There are four main kinds of targets for the drugs to bind to:<br /> <br /> * '''Receptors''' - these are protein molecules that are capable of responding to endogenous chemical signals. They are usually found on the cell membrane, in the cytoplasm or on the nucleus and other organelles.<br /> * '''Enzymes''' - both intracellular and extracellular ones.<br /> * '''Ion Channels'''<br /> * '''Transport proteins'''<br /> <br /> <br /> ==Agonists==<br /> <br /> An agonist can be defined as '''a drug that binds to a target molecule and results in activation of the receptor and thus a tissue response'''.<br /> <br /> * An agonist forms a complex with the receptor. This complex is '''dynamic''' as the agonist will continously associate and dissociate with the receptor. The agonist will continue to do this and thus produce a response, until the concentration of the agonist is reduced to a level at which binding no longer occurs.<br /> <br /> <br /> * The rate of complex formation is dependent on two factors: '''agonist concentration''' and the '''number of free receptors'''.<br /> <br /> <br /> * The '''affinity''' of a drug to a receptor varies and can be compared using the '''equilibrium constant or K&lt;sub&gt;A&lt;/sub&gt;'''.<br /> <br /> This can be defined as the concentration of a drug which results in 50% of receptors being bound in equilibrium or when '''K&lt;sub&gt;1&lt;/sub&gt;=K&lt;sub&gt;-1&lt;/sub&gt;'''.<br /> <br /> &lt;big&gt;'''Drug + Number of Free Receptors = Drug-Receptor Complexes'''&lt;/big&gt;<br /> <br /> Where '''K&lt;sub&gt;1&lt;/sub&gt;''' is the rate constant in a forward direction (association rate constant)<br /> and '''K&lt;sub&gt;-1&lt;/sub&gt;''' is the rate constant in a backward direction (dissociation rate constant)<br /> <br /> Therefore a drug that has a higher affinity to a receptor has a lower '''K&lt;sub&gt;A&lt;/sub&gt;''' value.<br /> <br /> <br /> * The biological response of resulting from an agonist is proportional to the number of receptors occupied. The size of a response can be measured and plotted against the dose/concentration of the agonist. As the size of a response normally increasee in a non-linear manner (until the maximum is reached) the response is normally plotted against the log of the concentration.<br /> <br /> <br /> '''Please Insert Appropriate Graphs'''<br /> <br /> From these graphs two figures can be achieved, the '''ED50''' or '''EC50'''. The ED50 is the effective dose at which 50% of a maximal response occurs or 50% of individuals respond. The EC50 is the same but is the effective concentration. Agonists with higher affinities will have a lower concentration and so EC50 than an agonist with a lower affinity. The first drug is therfore said to be more '''potent'''.<br /> <br /> <br /> The '''potency''' of a drug is very important clinically as it will determine the dose needed to have the desired clinical effect. Often if a drug is more potent it is usally more selective to which target molecules it binds to.<br /> <br /> <br /> ===Full and Partial Agonists===<br /> <br /> * A full agonist is defined as an agonist that is capable of producing the maximal response of a tissue. To achieve this the number of receptors occupied varies and in some cases very few receptors need occupying. This is called the '''spare receptor hypothesis''' and is very relevant when thinking about multiple drugs working at the same receptor site simultaneously.<br /> <br /> <br /> * A partial agonist is unable to produce the maximum tissue response however great the dose or concentration of the drug. It must be remembered that a partial agonistmay have a greater, lesser or equal affinity to a receptor site compared to a full agonist.<br /> <br /> <br /> The difference between the full and partial agonist is it's '''efficacy'''. This is defined as the strength of the tissue response that results from the formation of a agonist-receptor complex. The efficacy of the partial agonist is lower than that of the full agonist. <br /> <br /> It is still unclear why molecules that are chemically very similar have differing efficacies. Only now are the mechanisms behind it being gradually understand. This however doesn't mean that we ignore efficacy. It is of great practical importance as some drugs of equal affinity for a specific receptor may have widely differing efficacy.<br /> <br /> <br /> ===Inverse Agonists===<br /> <br /> These are agonists that bind to receptors that are continuely activated (even if no ligand is present) and result in the reduction of the level of activation. They therefore have a negative efficacy.<br /> <br /> ===Effector Linkage Mechanisms===<br /> <br /> Once the agonist binds to the receptor the cell response can be formed in three different ways:<br /> * By the opening of a ligand gated ion channel<br /> * By an intracellular second messenger system<br /> * By DNA transcription<br /> <br /> ==Antagonists==<br /> <br /> An antagonist can be defined as '''a drug that inhibits the action of an agonist'''.<br /> <br /> Antagonists bind to similar receptors as agonist but crucially they don't activate any intracellular events and so there is no tissue response. It's effect is produced by reducing the amount or capability of an agonist to bind to it's target molecule. <br /> <br /> Antagonists like agonists bind to receptors in a dynamic fashion, and so it is the antagonists affinity to the receptor that determines it's inhibitory response. The amount of inhibition thus depends on the concentration of the drug at the target site and the number of free receptor sites.<br /> <br /> ===Competitive Antagonism===<br /> <br /> ====Reversible Competitive Antagonism====<br /> <br /> Here the antagonist competes with the agonist for the occupation of the receptor site. Since less agonist is able to bind to the target molecule the size of the tissue response will decrease. As the dose/concentration of the antagonist increases so the size of the tissue response will further decrease.<br /> <br /> The formation of receptor complexes is dynamic in it's nature and so if the agonist' dose/concentration is increased it will out-compete the antagonist for receptor occupation and the size of the tissue response will start to increase. Therefore the antagonists action is reversible.<br /> <br /> <br /> ====Irreversible Competitive Antagonism====<br /> <br /> This form of antagonism essentially works in the same manner as above except for one crucial difference. The antagonist forms very strong bonds to the receptor sit meaning that it dissociates very slowly or not at all. This means that increasing the amount of agonist present is unable to out-compete the antagonist as receptor sites are always full. <br /> <br /> <br /> A partial agonist can effectively act as an antagonist when it is present in very high concentrations as it out-competes the full agonist for the receptor site. <br /> <br /> <br /> ===Non-Competitive Antagonism===<br /> <br /> Here the agonist binds to its receptor but the antagonist acts further along the sequence of events resulting in a tissue response. As this chain is blocked the agonist is incapable of producing a response.<br /> <br /> <br /> ===Pharmacokinetic Antagonism===<br /> <br /> The antagonist reduces the effect of another drug by reducing its absorption or increasing its rate of metabolism or increasing its rate of excretion. <br /> <br /> <br /> ===Self-antagonism===<br /> <br /> If some drugs are repeatedly given its effect can decrease. This is called '''tachyphylaxis''' or '''desensitisation'''. If a gradual decrease in response to a drug occurs this is called '''tolerance''' and if the drug loses total therapeutic efficacy it is deemed '''refractory'''. Many types of mechanisms occur to cause this phenomenon, the most important include:<br /> <br /> * change in receptor type<br /> * loss of receptors<br /> * exhaustion of cell mediators<br /> * increased metabolic degradation of the drug<br /> * physiological adaptation<br /> * active extrusion of the drug from cells<br /> <br /> ===Chemical Antagonism===<br /> <br /> This is where the interaction of two drugs results in the failure of an biological activity.<br /> <br /> <br /> ===Physiological Antagonism===<br /> <br /> This occurs when two drugs have opposing actions on the body and so their actions cancel each other out.</div>

Phlancelot https://en.wikivet.net/index.php?title=Basic_Concepts_of_Pharmacology&diff=138040 2012-05-04T12:21:59Z

<p>Phlancelot: </p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |pagetype = Drugs<br /> }}<br /> Pharmacology can be defined as the effect of drugs on living systems. Drugs can mimic or inhibit the natural processes of the body; it is therefore crucial to understand how these processes work to truely understand the effect of a drug. As such the principles of pharmacology touch on all aspects of veterinary medicine and are essential to grasp to fully appreciate drug use in practice. <br /> <br /> Drugs mainly exert their effects on the body by binding to a target molecule. A few drugs used in veterinary medicine depend upon their physical properties; an example of this would be the use of liquid paraffin in a horse with an impacted colic. <br /> <br /> The way that drugs interact with the body can be divided into two strict catergories:<br /> <br /> * [[Pharmacodynamics]] - the action that drugs have upon the body<br /> <br /> * [[Pharmacokinetics]] - the actions that the body has upon drugs<br /> <br /> Often combinations of drugs can enhance their power over a certain disease process but often a combination can cause deleterious effects on the body. <br /> [[Adverse Drug Reactions|Adverse drug reactions]] are a common aspect of the veterinary profession. It can be a challenge to recognise the signs of an adverse reaction as they can affect several organ systems simultaneously and can occur over varying periods of time.<br /> <br /> ==Literature Search==<br /> [[File:CABI logo.jpg|left|90px]]<br /> <br /> <br /> Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).<br /> &lt;br&gt;&lt;br&gt;&lt;br&gt;<br /> [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093142606.pdf ''' Review of how drugs work.''' Fajt, V. R.; The North American Veterinary Conference, Gainesville, USA, Large animal proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 311-314, 4 ref. - '''Full Text Article''']<br /> <br /> [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093142604.pdf ''' Review of how drugs move through the body.''' Fajt, V. R.; The North American Veterinary Conference, Gainesville, USA, Large animal proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 307-310, 2 ref. - '''Full Text Article''']<br /> <br /> [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093142607.pdf ''' How to evaluate drug information.''' Fajt, V. R.; The North American Veterinary Conference, Gainesville, USA, Large animal proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 315-317, 1 ref. - '''Full Text Article''']</div>

Phlancelot https://en.wikivet.net/index.php?title=Basic_Concepts_of_Pharmacology&diff=138039 2012-05-04T12:13:31Z

<p>Phlancelot: </p> <hr /> <div>{{review}}<br /> {{toplink<br /> |linkpage =WikiDrugs<br /> |linktext =WikiDrugs<br /> |pagetype = Drugs<br /> }}<br /> Pharmacology can be defined as the effect of drugs on living systems. Drugs can mimic or inhibit the natural processes of the body; it is therefore crucial to understand how these processes work to truely understand the effect of a drug. As such the principles of pharmacology touch on all aspects of veterinary medicine and are essential to grasp to fully appreciate drug use in practice. <br /> <br /> Drugs mainly exert their effects on the body by binding to a target molecule. A few drugs used in veterinary medicine depend upon their physical properties; an example of this would be the use of liquid paraffin in a horse with an impacted colic. <br /> <br /> The way that drugs interact with the body can be divided into two strict catergories:<br /> <br /> * [[Pharmacodynamics]] - the action that drugs have upon the body<br /> <br /> * [[Pharmacokinetics]] - the actions that the body has upon drugs (remember 'ADME' - Absorption, Distribution, Metabolism, Elimination)<br /> <br /> Often combinations of drugs can enhance their power over a certain disease process but often a combination can cause deleterious effects on the body. <br /> [[Adverse Drug Reactions|Adverse drug reactions]] are a common aspect of the veterinary profession. It can be a challenge to recognise the signs of an adverse reaction as they can affect several organ systems simultaneously and can occur over varying periods of time.<br /> <br /> ==Literature Search==<br /> [[File:CABI logo.jpg|left|90px]]<br /> <br /> <br /> Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).<br /> &lt;br&gt;&lt;br&gt;&lt;br&gt;<br /> [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093142606.pdf ''' Review of how drugs work.''' Fajt, V. R.; The North American Veterinary Conference, Gainesville, USA, Large animal proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 311-314, 4 ref. - '''Full Text Article''']<br /> <br /> [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093142604.pdf ''' Review of how drugs move through the body.''' Fajt, V. R.; The North American Veterinary Conference, Gainesville, USA, Large animal proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 307-310, 2 ref. - '''Full Text Article''']<br /> <br /> [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093142607.pdf ''' How to evaluate drug information.''' Fajt, V. R.; The North American Veterinary Conference, Gainesville, USA, Large animal proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 315-317, 1 ref. - '''Full Text Article''']</div>

Phlancelot https://en.wikivet.net/index.php?title=Talk:Computer_Aided_Learning&diff=132539 2011-11-30T13:38:14Z

<p>Phlancelot: Blanked the page</p> <hr /> <div></div>

Phlancelot https://en.wikivet.net/index.php?title=Talk:Computer_Aided_Learning&diff=132201 2011-11-23T13:19:09Z

<p>Phlancelot: Created page with &quot;I would like to create sort of stepwise dichotomous key for identifying bacterial isolates from the lab. I thought about doing this with an object oriented programming approach b...&quot;</p> <hr /> <div>I would like to create sort of stepwise dichotomous key for identifying bacterial isolates from the lab. I thought about doing this with an object oriented programming approach but it might take more time for me to re-learn how to write such code and perhaps it would be more useful as an online resource.<br /> <br /> My idea was to make a bunch of final pages with names of specific bacteria species and have each of these contain a number of attributes. The user would begin with a list of all possible bacteria and a series of interactive prompts would allow him/her to refine the list. For instance one obvious test would be a gram stain. If it was negative then only show those species that are gram negative. From there you could have prompts including if the species was catalase or oxidase positive/negative and so on. The final page would link to WikiVet's article on that particular organism to integrate better with the system.<br /> <br /> This is very much just an idea at this stage and I'm not sure how to go about implementing it exactly. I'd need to do some research on object oriented approaches with HTML. Just thought I'd throw this up in case anyone else thinks it could be useful or has ideas on how to make it more useful?</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114956 2011-05-04T14:13:31Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=Phollandprofile.jpg<br /> }}<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114955 2011-05-04T14:11:27Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=Phollandprofile.jpg<br /> }<br /> }<br /> This is just a test to see if my wiki editing skills are up to par!<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114954 2011-05-04T14:11:05Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=Phollandprofile.jpg<br /> <br /> <br /> <br /> }<br /> <br /> This is just a test to see if my wiki editing skills are up to par!}<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114953 2011-05-04T14:10:47Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=Phollandprofile.jpg<br /> <br /> This is just a test to see if my wiki editing skills are up to par!<br /> <br /> }}<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114952 2011-05-04T14:06:57Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=Phollandprofile.jpg<br /> }}<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=File:Phollandprofile.jpg&diff=114951 2011-05-04T14:05:42Z

<p>Phlancelot: {{Information |Description =a photo of paul holland for profile use |Source =HTC desire vignette photo |Author =Paul Holland |Date =May 4th 2011 |Permission = |other_versions = }}</p> <hr /> <div>== Summary ==<br /> {{Information<br /> |Description =a photo of paul holland for profile use<br /> |Source =HTC desire vignette photo<br /> |Author =Paul Holland<br /> |Date =May 4th 2011<br /> |Permission =<br /> |other_versions =<br /> }}<br /> <br /> == Licensing ==<br /> {{cc-zero}}</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114949 2011-05-04T14:00:03Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=<br /> }}<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114948 2011-05-04T13:59:09Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Hometown= Vancouver, BC, Canada<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=<br /> }}<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=User:Phlancelot&diff=114947 2011-05-04T13:58:18Z

<p>Phlancelot: </p> <hr /> <div>&lt;!--Go to 'Help:Personalise User Page' for help customising your user page--&gt;<br /> {{UserPage<br /> |Name=Paul Holland<br /> |Occupation= Veterinary Student &lt;!--Word Specific &amp; Case Sensitive--&gt;<br /> |School= UK - Glasgow<br /> |Year= 2014<br /> |Email=0902558H@student.gla.ac.uk<br /> |Image=<br /> }}<br /> [[Category:UK - Glasgow Graduates]]<br /> [[Category:2014 Graduate - UK - Glasgow]]</div>

Phlancelot https://en.wikivet.net/index.php?title=UK_-_School_of_Veterinary_Medicine,_Glasgow&diff=111186 2011-03-08T17:52:48Z

<p>Phlancelot: </p> <hr /> <div>{{Vetschool<br /> |Introduction=Introductory text here<br /> |History=Input text<br /> |Education=Input text<br /> |Research=Input text<br /> |Clinical=Input text<br /> <br /> |Image3=click this link to upload THIRD image.jpg<br /> |Image2=click this link to upload SECOND image.jpg<br /> |MainImage=click this link to upload MAIN image.jpg<br /> |School=University of Glasgow School of Veterinary Medicine<br /> |Established=1862<br /> |Location=Glasgow<br /> |Principal= Name<br /> |Students=595<br /> |Undergraduates= 500<br /> |Postgraduates= 95<br /> |Website=http://www.gla.ac.uk/schools/vet<br /> |Contact= 464 Bearsden Road, Glasgow, G61 1QH, Scotland<br /> +44 (0) 141 330 5700<br /> enquiries@vet.gla.ac.uk<br /> }}<br /> __NOTOC__<br /> [[Category:Europe]]</div>

Phlancelot https://en.wikivet.net/index.php?title=Cystic_Kidney&diff=108751 2011-02-21T18:57:46Z

<p>Phlancelot: </p> <hr /> <div>* Also known as polycystic kidney. <br /> * Can be seen in many different species.<br /> * Can have a hereditary basis. <br /> * The cysts may be single or multiple. <br /> * Results from the failure of development of the tubular system in nephrons.<br /> * Severely affected animals may die of renal failure early in life.<br /> ** The affected kidney does not have enough functional reserve, and so small infections can have a serious effect on renal function.<br /> <br /> <br /> *Among the most commonly encountered malformations of the kidney.<br /> *Can be congenital or acquired.<br /> **Congenital cysts are common incidental findings in both pigs and calves. Simple cysts generally cause no problems verses polycystic kidneys which can disrupt the renal architecture and lead to compromised function. Persian cats and Cairn terriers are predisposed.<br /> *** Kidney nephrons and collecting ducts have different embryological origins.<br /> *** If their connection fails to develop during development, polycycstic disease may result (especially common in cats).<br /> **Acquired cysts can occur as a sequel to chronic renal disease involving interstitial fibrosis.<br /> <br /> <br /> [[Category:Urinary System - Pathology]]<br /> [[Category:To Do - GenPath]]</div>

Phlancelot