Intro & PNS drugs
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| What is a drug? (ch 1) | any chemical that can affect living processes
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| What is pharmacology? (ch 1) | the study of drugs and their interactions with living systems
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| What is clinical pharmacology? (ch 1) | the study of drugs in humans (includes patients and healthy volunteers)
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| What are therapeutics (or pharmacotherapeutics)? (ch 1) | the use of drugs to diagnose, prevent, or treat disease or to prevent pregnancy
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| What are the three most important properties of an ideal drug? (ch 1) | Effectiveness, Safety, Selectivity
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| Effectiveness (ch 1) | elicits responses for which it is given *most important property of drug
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| Safety (ch 1) | cannot produce harmful effects (risk never be eliminated)
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| Selectivity (ch 1) | elicits only the response for which it is given *no such thing as a wholly selective drug because all drugs cause side effects
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| Therapeutic objective (ch 1) | provide maximum benefit with minimal harm
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| 3 factors that determine intensity of drug responses (ch 1) | Administration, Pharmacokinetics, Pharmacodynamics
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| Administration (ch 1) | drug dosage, route, timing --- impt determinants of drug responses
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| 4 processes of Pharmacokinetics (ch 1) | drug absorption, distribution, metabolism, excretion (impact of the body on drugs)
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| Pharmacodynamics (ch 1) | impact of drugs on the body
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| Why must we tailor drug therapy to the individual? (ch 1) | Individual variation
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| What are 4 sources of individual variation? (ch 1) | physiologic, pathologic, genetic variables & drug interactions
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| age, gender & weight are what type of variation? (ch 1) | physiologic variables
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| diminished function of kidneys & liver (major organs of drug elimination) = what type of variation? (ch 1) | pathologic variables
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| predisposition to unique drug reactions = what type of variation? (ch 1) | genetic factors
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| Beyond 5 rights, what are three key things to remember? (ch 2) | Check order for error, Know what drugs are contraindicated for pt, Anticipate possible reactions & prepare to respond
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| 3 goals of pre administration assessment (ch 2) | 1. collect baseline data, 2. ID high-risk patients, 3. assess patient's capacity for self-care
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| 3 tools to ID high risk patients (ch 2) | 1. patient history, 2. physical exam, 3. lab data
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| 4 tips to reduce adverse effects (ch 2) | Know 1. major adverse effects drug can produce, 2. when reax likely to occur, 3. early signs of an adverse reax, 4. interventions that can minimize discomfort & harm
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| When should you question a drug's appropriateness? (ch 2) | 1. no actions know to benefit pt diagnosis, 2. pt failed to respond to drug in the past, 3. pt had serious adverse reax in the past, 4. pt has condition or is using a drug that contraindicates prescribed drug
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| Federal Pure Food and Drug Act of 1906 (ch 3) | set standards for drug quality, purity, labeling
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| Food Drug, and Cosmetic Act 1938 (ch 3) | after 100 people died by taking med with diethylene glycol, req all new drugs to undergo testing for safety, with results reviewed by FDA- only drugs judged safe would receive FDA approval for marketing
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| Harris-Kefauver Amendment 1962 (ch 3) | after thalidomide tragedy (sedative caused birth defects), all drugs must be proved effective- first law to demand that drugs must offer some benefit, + rigorous testing for new drugs
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| Controlled Substances Act 1970 (ch 3) | set of rules for manufacture and distribution for drugs w/ potential for abuse, Schedules I-V, I = no accepted medical use in US
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| 1992 FDA approved accelerated approval for what drugs? (ch 3) | drugs for AIDS and cancer
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| Prescription Drug User Fee Act (PDUFA) 1992 (ch 3) | fees fund adt'l reviewers, speed up review timetables, drugs reach market sooner
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| FDA Modernization Act (FDAMA) 1997 (ch 3) | fast-track system for AIDS, cancer & serious + life-threatening diseases, manufacturers must inform pts 6 mo before stop making drug, clinical trial database required to allow for informed decisions, off-label uses - use that has not been evaluated by FDA
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| Best Pharmaceuticals for Children Act (BPCA) 2002 & Pediatric Research Equity Act (PREA) 2003 (ch 3) | designed to promote much-needed research on drug efficacy & safety in children
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| FDA Amendments Act (FDAAA) 2007 (ch 3) | FDA includes rigorous oversight of drug safety AFTER a drug has been approved.. require postmarketing safety studies, order changes in label to include new safety information,
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| Family Smoking Prevention & Tobacco Control Act 2009 (ch 3) | allows FDA to regulate cigarettes (responsible for 1 in 5 deaths in US each year)
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| 3 features of randomized controlled trials (RCTs) (ch 3) | use of controls, randomization, blinding (to minimize influence of personal bias on the results)
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| 2 principle steps of new drug testing (ch 3) | preclinical testing & clinical testing
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| 4 phases of clinical trials (ch 3) | 1. healthy volunteers, 2 & 3, 500-5000 patients, a few hundred take for more than 3-6 months, 4. postmarking surveillance
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| limitations of testing (ch 3) | women (barred from most trials until 1977), minorities, children
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| Guideline for discretion regarding new drugs (ch 3) | "Be neither the first to adopt the new nor the last to abandon the old"
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| 3 types of drug names (ch 3) | chemical, generic, trade/proprietary
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| 3 ways to cross a cell membrane (ch 4) | through channels/pores, passage w/ aid of transport system, direct penetration of membrane itself
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| What can cross membrane via channels or pores? (ch 4) | only small ions such as potassium & sodium
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| P-Glycoprotein is a transport system that transports a wide variety of drugs _________ (ch 4) | out of cells (e.g., transports drugs from liver into bile, from kidneys into urine, from placenta into maternal blood, from intestines into intestinal lumen, from brain capillaries into blood)
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| To directly penetrate a membrane, a drug must be (ch 4) | lipid soluble (lipophilic)
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| non-lipid-soluble molecules cannot penetrate membranes= 2 types (ch 4) | polar molecules & ions
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| polar molecules, will dissolve in what? (ch 4) | uneven distribution of charge, no net charge, will dissolve in polar solvents (not in non polar lipid bilayer of cell membrane)
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| ions, can ions cross membranes? (ch 4) | have a net electrical charge, except for very small molecules, ions are unable to cross membranes?
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| quaternary ammonium compounds (ch 4) | contain at least one atom of nitrogen, always positive charge, unable to cross most membranes
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| acids tend to ionize in ______ media (ch 4) | basic (alkaline)
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| bases tend to ionize in _____ media (ch 4) | acidic
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| Asprin in the stomach remains _______, but _____ in the intestines (ch 4) | Asprin is nonionized in stomach, can be absorbed across the membranes that separate stomach from the bloodstream, acid ionized in small intestine, absorption impeded
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| What is ion trapping/pH partitioning? (ch 4) | drug molecules will accumulate on side where pH most favors their ionization
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| What is absorption? (ch 4) | mvmt of drug from its site of administration into the blood (rate determines how soon effects will begin, amt determines how intense effects will be)
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| 5 factors affecting drug absorption (ch 4) | rate of dissolution, surface area, blood flow, lipid solubility, pH partitioning
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| 2 major routes of administration (ch 4) | enteral (GI tract), parenteral (by injection-IV, subcut, intramuscular)
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| IV advantages (ch 4) | no barriers to absorption, absorption instantaneous & complete, rapid onset, control, permits use of large fluid volumes, permits use of irritant drugs
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| IV disadvantages (ch 4) | high cost, difficulty, inconvenience, fluid overload, infection, embolism, imptce of reading labels (formulations of drug specific to route)
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| IM- barrier to absorption, rate determined by what? (ch 4) | water solubility of drug & blood flow to site of injection
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| IM advantages (ch 4) | can be used for parenteral admin of poorly soluble drugs, can deposit suspension, can use drugs with poor water solubility, can administer "depot preparations" in which drug is absorbed slowly over extended time
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| IM disadvantages (ch 4) | discomfort, inconvenience (pain, local tissue injury, possible nerve damage), bleeding risk *** contraindicated for pt with anticoagulant therapy***
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| subQ advantages (ch 4) | no significant barriers to absorption, readily enters blood by passing through spaces between cells of capillary wall, suitable for poorly soluble drugs and depot preparations
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| subQ disadvantages (ch 4) | discomfort, inconvenience, potential for injury
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| PO barriers to absorption (ch 4) | **GI tract epithelium**, capillary wall (po may be absorbed from stomach, intestine, or both), for some drugs, P-glycoprotein may reduce intestinal absorption (p 30) **absorption pattern highly variable**
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| Factors that can influence absorption following oral administration (ch 4) | 1. solubility & stability of drug, 2. gastric & intestinal pH, 3. gastric emptying time, 4. food in gut, 5. coadministration of other drugs, 6. special coatings on drug preparation (p 30)
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| enterohepatic recirculation (ch 4) *limited to drugs that have undergone glucuronidation | repeating cycle in which a drug moves from the liver via bile duct into the duodenum and then via portal blood back to the liver (p. 30, 37) *drugs can remain in the body much longer than they otherwise would
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| PO advantages (ch 4) | safer than injection! no risk of fluid overload, infection, embolism; potentially reversible by using activated charcoal
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| PO disadvantages (ch 4) | absorption highly variable, difficult to control concentration of drug @ site of action-- onset, intensity, duration of responses; Oral admin can inactivate certain drugs FIRST-PASS (e.g.. penicillin G, insulin, nitroglycerin), pt req, local GI irritation
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| first-pass effect (PO) (ch 4, p. 36) | drugs pass through liver, rapid hepatic inactivation of certain oral drugs (e.g. nitroglycerin rapidly metabolized in liver, so given sublingually)
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| chemical equivalence (ch 4) | drug preparation contains same amount of the identical compound(drug)
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| bioavailability (ch 4) | the drug preparation they contain is absorbed at the same rate and to the same extent
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| tablet = mixture of drug + ____ + _____ (ch 4) | tablet = drug plus binders and fillers, differ in rates of disintegration & dissolution, causing difference in bioavailability-- onset & intensity differ
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| ER designed to dissolve in the _______ not the ________ (ch 4) | ER designed to dissolve in intestine, not stomach
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| ER disadvantages (ch 4) | can be even more variable than standard tablets, b/c variations in gastric emptying time, coatings may fail to dissolve, allowing to pass through GI tract without being absorbed at all
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| SR advantages & disadvantages (ch 4) | advantages: permit reduction in number of daily doses, relatively steady drug levels over extended period, disadvantages: high cost, potential for variable absorption
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| distribution (ch 4) | movement of drugs throughout the body
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| distribution determined by 3 major factors: (ch 4) | blood flow to tissues (abcesses & tumors = problems), ability of drug to exit the vascular system (only lipid-soluble can pass BBB), ability of drug to enter cells
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| Placental drug transfer (ch 4) | lipid-soluble, nonionized compounds readily pass from maternal bloodstream into blood of fetus e.g. opioids, heroin - child will be born drug dependent, will need treatment to prevent withdrawal
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| Protein binding (ch 4) | Warfarin, gentamicin bind to albumen in plasma, competition for binding can increase amount of free drug, increasing toxicity
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| Factors that determine ability of drug to cross cell membranes (ch 4) | lipid solubility, presence of transport system, or both
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| metabolism/ biotransformation, where? (ch 4) | enzymatic alteration of drug structure (most takes place in liver)
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| P450 hepatic microsomal enzyme system (ch 4) | group of 12 closely related enzyme families, 3 (CYP1-3) metabolize drugs, other 9 metabolize endogenous compounds, steroids & fatty acids
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| Six possible consequences of drug metabolism (ch 4) | 1. accelerated renal excretion, 2. drug inactivation, 3. increased therapeutic action, 4. activation of "prodrugs," 5. increased toxicity, 6. decreased toxicity
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| Special considerations in drug metabolism (ch 4) | age, induction& inhibition of drug-metabolizing enzymes,
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| excretion (ch 4) | removal of drugs from the body
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| What is the most important organ for drug excretion? (ch 4) | kidney!
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| 3 steps of renal drug excretion: (ch 4) | 1. gomerular filtration, 2. passive tubular reabsorption, 3. active tubular secretion
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| pH dependent ionization- used to promote excretion of poisons or toxic doses, ASA example? (ch 4) | For ASA poisoning, give agent to elevate urine pH (more alkaline), since aspirin acidic, acids tend to ionize in basic media, causes more aspirin molecules in urine to become ionized, less drug passively reabsorbed, more excreted
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| Plasma drug levels (ch 4) | used to regulate drug responses
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| minimum effective concentration (MEC) (ch 4) | plasma drug level below which therapeutic effects will not occur (to be of benefit, drug must be present in concentrations at or above MEC)
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| toxic concentration (ch 4) | plasma level at which toxic effects begin (doses must be kept small enough so that toxic concentration is not reached)
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| therapeutic range (ch 4) | range of plasma drug levels, falling between MEC and toxic concentration
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| extent of delay between admin and onset of effects determined by: (ch 4) | rate of absorption
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| duration of effects determined by (ch 4) | metabolism & excretion
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| drug half-life determined by (ch 4) | time required for amt of drug in body to decrease by 50%
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| half-life of morphine (ch 4) | 3 hours (p. 40)
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| plateau (steady) (ch 4) | when amount eliminated between doses equals dose administered (p. 40)
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| time to plateau (ch 4) | approximately 4 half-lives
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| 3 techniques to reduce fluctuations in drug levels (ch 4) | drugs by continuous infusion, admin depot prep, reduce size of dose and dosing interval
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| loading dose (ch 4) | large initial dose
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| decline from plateau (ch 4) | most (94%) of the drug in the body will be eliminated over an interval equal to about four half-lives
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| pharmacodynamics (ch 5) | what drugs do to the body and how they do it
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| maximal efficacy * impt quality of drug (ch 5) | largest effect that a drug can produce (indicated by height of dose-response curve) *high maximal efficacy not always more desirable-- match intensity of response to patient's needs -- furosamide high efficacy, dehyd., but hydrocholorothaliazide lower
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| potency (ch 5) | how much drug must be administered to elicit a desired response (e.g.. morphine more potent than meperidine- demerol) *not impt quality of drug
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| Agonists (ch 5) | molecules that activate receptors
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| antagonists (ch 5) | prevent receptor activation by endogenous regulatory molecules and drugs
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| noncompetitive antagonists (ch 5) | bind irreversibly to receptors- reduce maximal response agonist can elicit (wear off in a few days)
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| competitive antagonists (ch 5) | bind reversibly to receptors- produce receptor blockade by competing with agonists for receptor binding
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| partial agonists (ch 5) | only moderate intrinsic activity, maximal effect that partial agonist can produce is lower than that of a full agonist
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| Receptor-less drugs (ch 5) | antacids, antiseptics, saline laxatives, chelating agents
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| ED50 (ch 5) | dose that will produce a predefined intensity of response in 50% of population
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| therapeutic index (ch 5) | measures drug safety
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| potentiative interaction (ch 6) | intensify effects
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| admin on empty stomach (ch 6) | 1 hr before or 2 hrs after meal p. 61
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