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psbs pcol
exam 1
| Question | Answer |
|---|---|
| pharmacology | the study of how drugs affect physiological functions |
| drugs | exogenous chemicals administered to affect biological functions |
| drug function | can only alter current cellular functions not add new ones |
| drugs can be: | small molecules (<600 kilodaltons), peptides (5-50 AAs), proteins, monoclonal antibodies |
| drug targets | receptors, enzymes, ion channels, transporters |
| affinity of drugs | how strong or how much a drug binds to the target cell |
| enzymes | convert substrates to products or metabolites |
| enzyme inhibition | compound blocks enzyme resulting in increased substrate concentration but decreased product concentration |
| types of ion channels | ligand-gated, voltage-gated |
| purpose of ion channels | allow for specific ion movement in and out of cells |
| drug effects on ion channels | increased or decreased open time of ion channels, increasing or decreasing flow along the gradient |
| drug effects on transporters | inhibit transporters to decrease intracellular substrate concentration |
| receptor structure | extracellular, transmembraned, intracelular portions |
| effects of binding to receptor | conformational changes within cell and cell membrane to activate intracellular proteins and alter cell function |
| tyrosine-kinase receptors | activation leads to phosphorylation |
| G-protein coupled receptors | proximal in transduction pathway |
| events of g-proteins | activated receptor-transducer - effector - second messenger |
| entirely intracellular receptor | usually leads to gene transcription |
| GPCR ex) | alpha and beta adrenoreceptors |
| enzyme-linked receptor ex) | insulin receptors |
| intracellular receptor ex) | steroid receptors |
| affinity | compounds binding power to receptors based on frequency |
| efficacy | compounds binding to receptor and activation it to produce desired effect |
| antagonist | binds to receptor but produces no effeect (affinity but no efficacy) |
| what antagonists do | block receptors from agonist activation |
| overuse of receptors result in | tachphylaxis or desensitization of receptor |
| cell reaction to overuse | internalization of receptor and down-regulation of receptors on the cell |
| cell reaction to underuse | externalization of receptors and up-regulation of receptors on cell surface |
| selectivity | affinity for target of interest |
| high concentrations of selective drugs results in | drug binding to non-target proteins |
| non-target protein binding causes | side effects |
| side effect | unintended response to theraputic dose of drug |
| undesirable side effects | adverse effects |
| toxic effect | results from excessive amount of drug or impaired metabolism |
| unpredictable drug effects | allergic reactions, idiosyncratic reactions (genes), teratogenic (birth defects |
| graded response | continuous and gradual; measure of magnitude of response |
| quantal response | all or nothing; frequency of response |
| dose response curves aka | concentration response curves |
| plateau of dose response curve shows | Emax or maximal effect of drug |
| response increases with | increasing dose |
| x-axis on dose response curve | potency of drug |
| y-axis on dose response curve | response or desired effect of drug |
| potentcy | amount of drug needed to cause an effect |
| the lower the ED50 | the more potent the drug |
| ED50 | effective dose needed to produce desired effect in 50% of subjects |
| dose response shift left | more potent |
| dose response shift right | less potent |
| therapeutic index | margin between therapeutic effect and lethality; measure of drug safety |
| therapeutic index calculation | TI=TD50/ED50 |
| TD50= ED50= | toxic dose; effective dose |
| therapeutic window | gap between effective and levels of drug that produce adverse effects |
| local drug delivery | eye, ear, nose, skin |
| systemic drug delivery | brain, pancreas, kidney, liver |
| intrathecal | spinal space |
| intra-articular | joint delivery |
| IV route bypasses | drug absorption, no need to move across cell layers |
| onset of action of drug depends on | rate of drug absorption |
| passive diffusion | movement of drug across a concentration gradient until equilibrium is met. |
| absorption depends on | solubility in body, stability in acids/enzymes, lipophillicity, ionic interactions |
| acidic drugs absorb better in | stomach due to more unionization |
| basic drugs absorb better in | intestine due to more basic environment |
| site of administration reflection on absorption | surface area, blood flow, gastric emptying (more absorbed in absence of food) |
| how do drugs bind to plasma proteins | reversibly |
| affinity for plasma proteins effects drugs how | higher affinity = more bound and less free drug, and vice versa |
| effect of bound drug | inactive, no effect on target receptors too large to pass through membranes |
| effect of free drug | active, can bind and effect target receptors |
| drug distribution | movement of drug from bloodstream to tissues |
| onset of action depends on | rate and extent of drug distribution, also determines maximal effect of drug |
| bloodflow to organs or tissues in order of highest to lowest | brain > liver > kidney > heart > skeletal muscle > skin > fat |
| BBB | blood brain barrier |
| harder to get drug into brain because | the brain capillaries have such tight junctions that the drug must pass through cells not just epithelium and therefore must be highly lipophillic or have an active transport protein in the brain |
| transporter proteins in endothelial cells are used to | pump out drug from cells; line organs and tissues |
| excretion of drugs is usually through | urinary excretion in the kidneys |
| 2 important processes of kidneys | glomerular filtration, tubular reabsorption |
| lipophillic molecules are ________ from kidney | reabsorbed |
| hydrophilic compounds are ________ from kidney | excreted |
| drug metabolism is | an enzymatic process to convert drug to usually inactive hydrophilic molecules for excretion |
| site of drug metabolism | usually the liver by CYP450 enzymes |
| phase 1 reactions | catalyzed by CYP450 to make the molecules more hydrophilic |
| phase 2 reactions | catalyzed by transferase enzymes to make the molecule larger and more hydrophilic |
| metabolite relationships | active to inactive (predominant), active to active, active to toxic, inactive to active (pro-drugs) |
| first pass metabolism | partial or complete inactivation of drug prior to reaching systemic circulation |
| bioavailability | percent of drug that reaches systemic circulation |
| bioavailability of IV drugs | 100% |
| bioavailability decreases if | drug is poorly absorbed, drug has high first pass metabolism |
| drugs that avoid first pass metabolism | parenteral, sublingual, pulmonary |
| metabolism is negatively altered if | drugs or diet inhibit P450 enzymes, liver disease, age (old or newborn), inherited issues |
| negative inherited traits of altered metabolism | less enzyme p450, less active enzyme |
| increased metabolism is due to | drugs, diet, inherited effects on p450 |
| if metabolism is reduced | decrease dose or frequency to prevent toxicity |
| if metabolism is increased | increase dose or frequency to achieve theraputic effects |
Created by:
lex86
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