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Pharmacodynamics

BMS263

TermDefinition
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
Exogenous Made outside the body
Endogenous Made by the body itself
Pharmacodynamics How a drug affects the body (it's mechanism of action)
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.
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
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
EC50 Concentration at which the drug produces 50% of its maximal response (Effective concentration at 50%)
Efficacy The ability of a drug to produce its biological response
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
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
Selectivity Describes the number of molecular targets that the drug interacts with
Agonist Activates a receptor. Takes place of endogenous substance. There are full and partial types. Possesses significant efficacy
Antagonist A drug binds to the receptor without causing activation and prevents an agonist from binding. Has zero efficacy. Can be reversible or irreversible
Affinity The strength of the interaction between a drug and its molecular target
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
Full Agonist Induce maximal response when all receptors are occupied (high efficacy)
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
Activation The receptor is affected by the bound molecule in such a way as to elicit a tissue response
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
Tolerance More gradual decrease in responsiveness to a drug, taking weeks or days to develop
Refractoriness The loss of the therapeutic efficacy
Drug Resistance The loss of the effectiveness of antimicrobial or anti-tumour drugs
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)
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
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
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
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
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
Pharmacogenetics The study of how genetic variability affects the response to drugs
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
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
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
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
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
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)
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
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
Created by: Mandyrox300
 

 



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