BMS263
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| show | 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 | show 🗑
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| show | Made by the body itself
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| show | How a drug affects the body (it's mechanism of action)
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| Pharmacokinetics | show 🗑
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| show | 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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| show | 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 | show 🗑
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| show | The ability of a drug to produce its biological response
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| Drug Targets | show 🗑
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| Drug Specificity | show 🗑
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| Selectivity | show 🗑
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| Agonist | show 🗑
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| show | 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 | show 🗑
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| show | 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 | show 🗑
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| show | 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 | show 🗑
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| show | 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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| show | More gradual decrease in responsiveness to a drug, taking weeks or days to develop
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| show | The loss of the therapeutic efficacy
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| show | The loss of the effectiveness of antimicrobial or anti-tumour drugs
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| show | 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 | show 🗑
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| Exhaustion of Mediators | show 🗑
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| show | 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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| show | 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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| show | 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 | show 🗑
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| show | 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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| show | 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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| show | 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 | show 🗑
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| Pharmacokinetic Antagonism | show 🗑
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| Competitive Antagonist | show 🗑
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| show | 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 | show 🗑
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Created by:
Mandyrox300
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