Term
|
Definition
|
|
Term
| How is Langmuir's equation altered when talking about Pharmacology? |
|
Definition
| receptor instead of substrate; and LR -> stimulus -> response. With association rate constant (Ka) and dissosiation rate constant (Kd) governing the equilibrium between L + R and LR |
|
|
Term
|
Definition
| Chemical agents that interact with components of a biological system to alter the organism's function. |
|
|
Term
|
Definition
| regulatory proteins that interact with drugs or hormones and initiate a cellular response |
|
|
Term
| What are the four major types of receptors? |
|
Definition
| ion channels, G protein coupled receptors, receptor-enzymes, cytosolic nuclear receptors |
|
|
Term
| What are transducer proteins? |
|
Definition
| receptors that create an effector signal after they are activated. Signal can be amplified by post-receptor signal transduction |
|
|
Term
| What ions pass through an activated nictotinic receptor? |
|
Definition
| nicotinic receptors are nonselective cation channels |
|
|
Term
| What are the four main types of receptors? |
|
Definition
| ion channel, g protein coupled receptor, receptor-enyzmes, cytosolic-nuclear receptors |
|
|
Term
| What happens when a G protein is activated? |
|
Definition
| alpha is split from beta/gamma and GDP --> GTP |
|
|
Term
| What's another name for a g protien coupled receptor? |
|
Definition
|
|
Term
| What is the most common type of ligand that binds to cytosolic-nuclear receptors? |
|
Definition
|
|
Term
|
Definition
| initial effect of the drug on the receptor |
|
|
Term
|
Definition
| the chemical forces that cause the drug to associate with the receptor |
|
|
Term
| What is intrinsic efficacy? |
|
Definition
| the extent of functional change imparted to a receptor upon binding of a drug; aka power of drug to induce a response |
|
|
Term
| What is potency dependent upon? |
|
Definition
| receptor density, efficiency of the stimulus-response mechanism, affinity and efficacy |
|
|
Term
| What is the magnitude of effect? |
|
Definition
| asymptotic maximal response; aka efficacy |
|
|
Term
| What is magnitude of effect dependent upon? |
|
Definition
| solely upon intrinsic efficacy |
|
|
Term
| What's the difference between potency and efficacy? |
|
Definition
| potency is the ability to produce a specified effect at a certain dose while efficacy is the asymptotic maximal response |
|
|
Term
| What determines response to a drug? |
|
Definition
| intrinsic efficacy and number of receptors in the target tissue |
|
|
Term
| What are spare receptors? |
|
Definition
| receptors in certain tissues that have more receptors than necessary to produce a maximal response |
|
|
Term
| What does it mean to say a receptor is in the active state? |
|
Definition
| it is initiating cell signaling |
|
|
Term
|
Definition
| drug that binds to receptors and initiates a cellular response; has affinity and efficacy. agonists promote the active state |
|
|
Term
|
Definition
| drugs that bind to receptors but cannotinitiate a cellular response, but prevent agonsits from producing a resopnse; affinity but no efficacy. Maintain the active-inactive equilibrium (so leak current can still occur) |
|
|
Term
| What are partial agonists? |
|
Definition
| drugs that, no matter how high the dose, can not produce a full response |
|
|
Term
| What is an inverse agonist? |
|
Definition
| drug that binds to receptor to produce an effect opposite that of an agonists. Stabilizes receptors in the inactive state (no leak current) |
|
|
Term
| What's an examples of an inverse agonist? |
|
Definition
|
|
Term
| Why is it a problem to stop taking inverse agonists? |
|
Definition
| tremendous rebound effect |
|
|
Term
|
Definition
| point on a graded dose-response curve that produces a just-noticeable effect |
|
|
Term
|
Definition
| dose on a graded dose-resonse curve that produces a 50% of max response |
|
|
Term
|
Definition
| blood concentration that produces a 50% of the max response |
|
|
Term
|
Definition
| lowest dose that produces a maximal effect |
|
|
Term
| Full and partial agonists are tissue dependent upon... |
|
Definition
| receptor density, cell signaling apparatus, other receptors that are present, drug history |
|
|
Term
| A drug that has both agonist and antagonist properties could be termed a _____ |
|
Definition
|
|
Term
| What is the effect of inverse agonists on ion channels? |
|
Definition
|
|
Term
| What is the effect of inverse agonists on GPCRs? |
|
Definition
| no spontaneous or AGS activation of G-protein signaling |
|
|
Term
| What is teh effect of inverse agonists on cytosolic nuclear receptors? |
|
Definition
| inhibition of transcription/translation |
|
|
Term
| What is the effect of inverse agonists on receptor enzymes? |
|
Definition
| no spontaneous enzyme activity |
|
|
Term
| How do you compare two drugs' potencies? |
|
Definition
| ED50 of drug B/ ED50 of drug A |
|
|
Term
| How do you compare the efficacy of two drugs? |
|
Definition
| efficacy of A/Efficacy of B= relative efficacy |
|
|
Term
| What are the different types of antagonists? |
|
Definition
| competetive, noncompetitive, allosteric, and physiologic |
|
|
Term
| What is the difference between competitive and noncompetitive antagonists? |
|
Definition
competitive binds to the same site as agonist in a reversible manner
noncompetitive binds to the same site as agonist irreversibly |
|
|
Term
| What is a physiologic antagonist? |
|
Definition
| two drugs have opposite effects through differing mechanisms |
|
|
Term
| What is the ID 50 or IC 50? |
|
Definition
| 50% of max inhibitory dose (concentration) of an antagonist with a fixed dose of agonist |
|
|
Term
| What effect do competitive antagonists have on the dose reponse curve? |
|
Definition
|
|
Term
| What effect does noncompetitive inhibitors have on the dose resonse curve? |
|
Definition
| decrease ceiling (if spare receptors may shift to the right |
|
|
Term
| What effect do allosteric antagonists have on dose response curve? |
|
Definition
| you can't predict the effect |
|
|
Term
| T/F Allosteric antagonists can act on G proteins. |
|
Definition
|
|
Term
| What is a quantel dose response curve? |
|
Definition
| the percent of subjects responding at a dose is plotted. Aka concentration-percent or dose-percent curves. Used when the dose of a drug to produce a specified effect in a single patient is measured (individual effective dose or concentration) |
|
|
Term
| What is a cumulative quantal dose response curve? |
|
Definition
| where the percentage of patients responding at that dose or lower is plotted |
|
|
Term
| What is reduced responsivity? |
|
Definition
| chronic use of an agonist can result in the receptor-effector system becoming less responsive (alpha-adrenoceptor agents used a nasal decongestants) |
|
|
Term
| What is increased responsivity? |
|
Definition
| chronic disuse of a receptor-effector system can result in an increased responsiveness upon re-exposure to an agonist |
|
|
Term
| What types of drugs can cause receptor upregulation? |
|
Definition
| Antagonists slow use-dependent internalization. Inverase agonsits because they stabilize the receptor in the inactive state to prevent internalization while the cell continues to produce receptors |
|
|
Term
| What is the safety index? |
|
Definition
LD1/ED99 = lowest lethal dose/lowest max theurapeutic effect
Should be around 10 |
|
|
Term
| What is the therapeutic index? |
|
Definition
|
|
Term
| The higher the therapeutic or safety index, the more _____ the drug. |
|
Definition
| safe; safety index is always smaller than the therapeutic |
|
|
Term
| What are the different clases of drug interactions? |
|
Definition
| pharmacodynamic (pharmacologic or physiologic) or Pharmacokinetic (absorption, distribution, metabolism, excretion) |
|
|
Term
| What are pharmacodynamic interactions? |
|
Definition
| altered activity of a given drug produced by the presence of a second drug at the same receptor or at different sites on teh same organ |
|
|
Term
| Compare/contrast pharmacologic and physiologic interactions. |
|
Definition
| both are a type of pharmacodynamic interactions. Pharmacologic are at the same receptor/signaling pathway. Physiologic are via different cellular mechanisms |
|
|
Term
| What are the two types of physiologic interactions? |
|
Definition
systems interactions= occur through actions at different sites on the same organ
subcellular interactions=interactions that occur at the level of cell signaling |
|
|
Term
| Halogenated hydrocarbons and catecholamines on myocardium is an example of what type of drug interaction? |
|
Definition
|
|
Term
| What is a pharmacokinetic interaction? |
|
Definition
| altered activity produced by changes in the plasma level of a drug due to the presence of a second drug |
|
|
Term
| What are the different types of pharmacokinetic interactions? |
|
Definition
| drug absorption, distribution, metabolism, renal excretion, biliary excretion |
|
|
Term
| How can interactions affect drug absorption? |
|
Definition
| vasoconstriciton/vasodilation (epi + lidocaine), alteration of GI function (peptobismol), chemical interactions (salt formation, pH alterations of plasma alter absorption) |
|
|
Term
| What two antibiotics cause a chemical interaction at the level of absorption? |
|
Definition
| tetracyclines and sulfonamides may cause a sulfonamide salt to precipitate in the stomach |
|
|
Term
| What are the types of interactions affecting drug distribution? |
|
Definition
| plasma protein binding, blood brain barrier permeability, promiscuous transporters |
|
|
Term
| The interaction betwee wafarin and aspirin/ibuprofen can be described as... |
|
Definition
| plasma protein binding (pharmacokinetic) |
|
|
Term
| How does altering the blood brain barrier cause drug interactions? |
|
Definition
| drugs that increase permeability (like TNF) increase the effectiveness of psychoactive drugs and some analgesics |
|
|
Term
| What is an example of a promiscuous transporter commonly involved in drug drug interactions? |
|
Definition
| P-glycoprotein (gut, renal tubules, hepatocytes, BBB). and organic ion transporters in the distal tubules |
|
|
Term
| What drugs inhibit/induce P-glycoprotein? |
|
Definition
| cyclosporin A, quinidine, verapamil, itraconazole, clarithromycin all inhibit. Rifampin induces |
|
|
Term
| What are the different ways in which interactions can affect drug metabolism? |
|
Definition
| competition for metabolizing enzymes (acetominophen and alcohol with alcohol dehydrogenase), enzyme induction, enzyme inhibition |
|
|
Term
| How does St. John's wort cause drug interactions? |
|
Definition
| by inducing CYP3A which metabolizes estrone and estradiol and consequently reduces efficacy of OCs |
|
|
Term
| Give an example of enzyme inhibition drug interaction. |
|
Definition
| grapfruit juice and rifampin inhibit CYP3A4, which metabolizes midazolam, erythromycin, and many others |
|
|
Term
| In what ways to drug interactions affect renal excretion? |
|
Definition
| competition for renal transport mechanism, pH |
|
|
Term
| How does probenacid interact with rifampin? |
|
Definition
| prebenacid inhibits biliary excretion causing higher plasma concentrations of rifampin, an antibiotic used to treat tuberculosis |
|
|
Term
| Caffeine can become an analgesic when combined with... |
|
Definition
|
|
Term
| Codeine is more effective when combined with.. |
|
Definition
|
|
Term
|
Definition
| when adding one drug to another gives one of the drugs properties that it does not have alone |
|
|
