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Lecture 8 Pharmacodynamics_ 2550 exam notes.docx

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Trent University
NURS 2550H
Ellen Buck- Mc Fadyen

Lecture 8 Pharmacodynamics Dose-response relationship: relationship between the size of an administered dose and the intensity of the response produced  Finds o the minimum amount of a drug we can use o maximum response a drug can cause o how much of an increase in the dose is needed for desired effect  Graded vs. All-or-nothing principle o graded: as the dosage increases, the response becomes progressively larger o all-or-nothing: drug produces only one intensity, cannot adjust  Maximum Efficacy: the largest effect a drug can produce o whichever has the highest maximum point, we would say has a greater maximum efficacy  Potency: the amount of drug we must give to elicit an effect o potent drug is the one that produces its effects at low doses o potency and maximum efficacy not related Drug-Receptor Interactions  Receptor: any functional macromolecule in a cell to which a drug binds to produce its effects o body's own receptors for hormones, neurotransmitters, and other regulatory molecules o enzymes and ribosome can be thought of target molecules  binding of a drug to its receptor is usually reversible  Drugs mimic or block the effects of these endogenous compounds at receptors o therefore drugs cannot make the body do something new, only help the body help itself  Cell membrane-embedded enzymes: drug binds to the enzyme on the outside of the membrane, causing a reaction inside the cell o insulin for example  Ligand-Gated Ion Channels: drug binds to a receptor outside of the cell, allowing ions to flow in or out of the channel (direction determined by concentration gradient) o each channel is specific for a particular ion (Na+ for example)  G protein coupled receptor systems: three components – receptor itself, G protein, and effector (ion channel or enzyme) o binding of an endogenous ligand or agonist drug activates the receptor, which in turn activates G protein, which in turn activates the effector. o rapid action  Transcription factors: o found within the cell o responses are delayed o situated on DNA in the cell's nucleus o regulates protein synthesis o can only be activated by drugs that are lipid soluble and can get through the cell membrane Selectivity of Drug Action  the more selective a drug is, the fewer side effects it will produce  for a drug to be selective, it must fit perfectly for that specific receptor  Lock and key analogy o drug resembles natural ligand of receptor o binds to it based on fit o controls rate of process by increasing or decreasing  however, sometimes some receptors are responsible for several physiological responses  selectivity does not guarantee safety  Non receptor mediated interaction o drug alters cell environment o examples: osmotic drugs, antacids, anesthetics Theories of Drug Receptor Interaction  Simple Occupancy Theory o intensity of a drug response is related to the amount of receptors it has occupied o maximum (plateau effect or maximum efficacy) will occur when all available receptors are occupied  Modified Occupancy Theory o affinity: strength of the attraction  drugs with high affinity are strongly attracted to their receptors and vice versa  related to potency: can bind to their receptors when presernt in low concentrations  effective in low doses  drugs with high affinity are very potent o intrinsic factor: ability of a drug to activate the receptor following binding  high intrinsic activity = intense receptor activation  related to maximum efficacy: by causing intense receptor activation they are able to cause intense responses  high intrinsic activity very effective o they are both independent properties o basically how strongly it binds and how well it does its j
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