BMS263
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| Drug | A chemical substance of known structure, other than a nutrient or an essential dietary ingredient, which, when administered to a living organism, produces a biological effect. Sourced from microorganisms, plants, human cells and animals, minerals and labs
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| Exogenous | Made outside the body
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| Endogenous | Made by the body itself
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| Pharmacodynamics | How a drug affects the body (it's mechanism of action)
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| Pharmacokinetics | How the body affects the drug. E.g. how the body absorbs, transports, metabolises & excretes the drug. It will affect drug action by determining which tissues the drug gets exposed to etc.
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| General Principal of Drug Action | Requires non-uniform distribution of the drug molecule within the body or tissue. Molecules must bind with particular constituents of cells and tissue to produce effect. Also involves potency and effacacy
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| Potency | How much of the drug is required to produce a response. Determined by affinity & efficacy of drug. Compared by considering the EC50. Drugs of high amount have higher affinity for receptors & occupy proportion of receptor even at low concentrations
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| EC50 | Concentration at which the drug produces 50% of its maximal response (Effective concentration at 50%)
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| Efficacy | The ability of a drug to produce its biological response
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| Drug Targets | Most are proteins. E.g. receptors (Acetylcholine receptor on muscular junction), Enzymes (Acetylcholine esterase), Carrier molecules (for sugar and amino acids) & Ion channels
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| Drug Specificity | Describes the number of effects the drug produces. Acts selectively on particular cells and tissues and shows a high degree of binding site specificity. It is reciprocal
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| Selectivity | Describes the number of molecular targets that the drug interacts with
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| Agonist | Activates a receptor. Takes place of endogenous substance. There are full and partial types. Possesses significant efficacy
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| Antagonist | A drug binds to the receptor without causing activation and prevents an agonist from binding. Has zero efficacy. Can be reversible or irreversible
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| Affinity | The strength of the interaction between a drug and its molecular
target
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| Efficacy | How big an effect the drug will have’ when all targets (receptors) are occupied. Describes the tendency of the drug-receptor complex to adopt the active rather than the resting state. The difference between full and partial agonists
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| Full Agonist | Induce maximal response when all receptors are occupied (high efficacy)
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| Partial Agonist | Have some efficacy but are unable to generate a maximal tissue response. Drugs with intermediate levels of efficacy, such that even when 100% of the receptor are occupied the tissue response is sub-maximal
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| Activation | The receptor is affected by the bound molecule in such a way as to elicit a tissue response
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| Drug Desensitisation/ Tachyphylaxis | Drug effect gradually diminishes when given continuously/ repeatedly. Develops in course of minutes. Caused by change in or translocation of receptors, exhausted mediators,increased metabolic degradation, active extrusion from cells & physiological adapt
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| Tolerance | More gradual decrease in responsiveness to a drug, taking weeks or days to develop
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| Refractoriness | The loss of the therapeutic efficacy
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| Drug Resistance | The loss of the effectiveness of antimicrobial or anti-tumour drugs
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| Change in Receptors | In regards to desensitisation. A conformation change that inhibits the efficacy of the drug. E.g. agonist binds but can no longer activate it (type 2 diabetes)
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| Translocation of Receptors | In regards to desensitisation. Receptors are internalised such that the availability of the receptors is decreased. i.e. There are less receptors for the drug to bind to. E.g. A decrease in b-adrenergic receptors can occur
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| Exhaustion of Mediators | In regards to desensitisation. Depletion of substances required for a drug response. E.g. Amphetamines cause the release of amines from neurons. Once there is a depletion of amine stores, these drugs have decreased potency
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| Increased Metabolic Degradation | In regards to desensitisation. Body produces more enzymes that catalyse the chemical degradation of drug. Usually induction of hepatic drug metabolising enzymes
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| Active Extrusion of Drug | In regards to desensitisation. Some drugs need to enter target cells to have an effect. If the target cells expel the drug, a lower intracellular concentration of the drug will occur, decreasing its potency. e.g. Cancer chemotherapy
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| Physiological Adaptation | Readjustment of homeostatic mechanisms occur to compensate for drug action. E.g. Thiazide diuretics increase production of urine, decrease BV &BP. Activation of renin-angiotensin 2 system can occur stimulating physiological mechanisms to increase BP again
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| Pharmacogenetics | The study of how genetic variability affects the response to drugs
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| Individual Response To Drugs | Inherited genes can alter drug response. Can alter pharmacodynamics and pharmacokinetics. A persons environment & stage of life can alter drug responses. Also nutrition, use of other drugs, allergic reactions & idiosyncratic reactions
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| Drug Agonism | One drug can increase the activity and/or unwanted effects of another drug. - e.g. The degradation and clearance of two drugs may involve the same enzyme
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| Drug Antagonism | One drug can decrease the activity of another drug. Four main types: Chemical antagonism, Pharmacokinetic antagonism, Block of receptor or block of receptor-effector linkage (competitive vs non-competitive), & Physiological antagonism
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| Chemical Antagonism | Refers to the uncommon situation where the two substances combine in solution; as a result, the effect of the active drug is lost. Example: The use of chelating agents (dimercaprol) that binds to heavy metals and thus reduce their toxicity
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| Pharmacokinetic Antagonism | The antagonist effectively reduces the concentration of the active drug at its site of action. The rate of metabolic degradation of the active drug may be increased
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| Competitive Antagonist | Drug binds selectively to a particular receptor without activating it, but in such a way as to prevent binding of the agonist. Can be reversible (Reversible bonds with receptor) or irreversible (Antagonist dissociates slowly or not at all from receptor)
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| Non-Competitive Antagonist | Antagonist and agonist bind to receptor at different sites, or one drug inhibits the activity of the other drug by altering cell signalling down-stream of the receptor. Antagonist blocks the chain of events that lead to a response by action of agonist
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| Physiological Antagonism | Refers to the interaction of two drugs whose opposing actions in the body tend to cancel each other. The two drugs act on separate mechanisms
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