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Pharm Exam 1
| Term | Definition |
|---|---|
| drug | any chemical that can affect living processes |
| pharmacology | the study of drugs and how they affect living systems |
| clinical pharmacology | the study of drugs in humans |
| pharmacotherapeutics | the use of drugs to diagnose, prevent, or treat an illness or prevent pregnancy; HOW a medication works to treat an illness |
| important properties of an ideal drug | effectiveness, safety, selectivity |
| safety | cannot produce harmful effects even if administered in very high doses |
| selectivity | elicits only the response for which it is given; IDEAL=localized effect |
| patient education | best way to educate is to ask for patient to demonstrate and explain |
| additional properties of ideal drugs | reversible action, predictability, ease of administration, freedom from drug interactions, low cost, chemical stability, simple generic name |
| sources of individual variation | physiological (age, gender, weight), pathological (diminished organ -kidney and liver- function), genetic (predisposed to reaction), drug interactions |
| therapeutic objective | provide maximum benefit with minimum harm |
| application of nursing process in drug therapy | pre administration assessment, evaluation and interventions, implementation, and patient education |
| identifying high risk patients | tools: patient history, physical exam, baseline lab results types: liver and kidney impairment, genetic factors, drug allergies, pregnancy, older adult or pediatric age group |
| chemical drug name | nomenclature of chemistry of a drug |
| generic drug name | assigned by US Adopted Names Council, one per drug (ex: Acetaminophen) |
| trade/brand drug name | assigned by company, easier for/more known by public, single drug can have multiple brand names (ex: Tylenol) |
| sources of drug information | people, newsletters, reference books, and the internet |
| stages of new drug development | 1. preclinical testing (animals) 2. clinical testing (humans) - a.) phase 1: healthy human volunteers to test drugs, b.) phase 2-3: drugs are tested in patients, c.) drug sent to FDA for approval, d.) phase 4: post marketing surveillance |
| limitations of testing procedure | failure to detect all adverse effects because - only small # of patients are given drug during clinical trials, not representative of population (excluding women and children), patients in trials take drug for short amount of time |
| chemically equivalent preparations | drug preparations that contain the same amount of identical chemical compound |
| bioavailability | preparations containing drugs absorbed at the same rate and to the same extent |
| tablets | drug plus binders and fillers pressed together |
| enteric-coated preparations | coated with material designed to not get dissolved in the stomach but in the intestine (protected from acid and pepsin in stomach, protects stomach from drugs causing gastric discomfort, DO NOT CRUSH) |
| sustained-release preparations | capsules filled with tiny spheres that contain drug and individual spheres with coatings that dissolve at variable rates (allow for less doses, DO NOT CRUSH) |
| clinical significance of plasma drug levels | cannot measure drug concentrations at sites of action, but can measure plasma drug concentrations (amount of drug present in plasma has a direct correlation to the therapeutic and toxic response) |
| latent period | responses cannot occur until plasma drug levels have reached minimum effective concentration |
| minimum effective concentration | plasma drug level below that at which therapeutic effects will not occur |
| toxic concentration | plasma level at which toxic effect begins |
| therapeutic range | range of plasma drug levels between MEC and toxic concentration (goal = therapeutic range) |
| narrow therapeutic range | less safe, requires more precise dosage |
| wide therapeutic range | safer, dosage doesn't have to be as exact |
| multiple dosing | drug accumulation |
| plateau drug levels | if second dose is administered before all of prior dose has been eliminated, total body stores of that drug will be higher after the second dose than the first |
| peak concentration | highest dose level (below toxic level) |
| trough concentration | lowest dose level (above minimum effective concentration) |
| techniques to reduce fluctuations | 1. administer drugs by continuous infusion 2. administer depot preparations (slow and steady release of drug) 3. reduce size of dose and dosing interval |
| half-life | time required for amount of drug in the body to decrease by 50% |
| parenteral IV medications | no barriers, instant and complete absorption pattern and drug movement |
| advantages of parenteral IV meds | rapid onset (15-30 mins), control of drug levels in blood, use of large fluid volumes over time, permits use of irritant drugs |
| disadvantages of parenteral IV meds | high cost, difficulty, and inconvenience, irreversibility, risk of infection |
| risks and cautions of IV meds | most drugs must be injected slowly over 1+ mins, fluid overload, infection, embolism, infiltration, extravasation, site infection, sepsis, occlusion |
| parenteral IM and subQ meds | capillary wall around muscles and tissues is a barrier, rapid or slow absorption pattern |
| advantages to parenteral IM and subQ meds | best for parenteral administration of poorly soluble drugs, depot preparations |
| disadvantages to parenteral IM and subQ meds | discomfort and inconvenience, bleeding risk for patients on anticoagulants |
| albumin | most abundant protein in plasma, remains in bloodstream, can't exit pores in capillary wall, protein made by liver that drugs attach to |
| protein binding | % of drug molecules bound to albumin is determined by strength of attraction between albumin and the drug |
| binding competition | attached drugs have no therapeutic effect, non-attached drugs rise to toxic levels and excessive free-flowing concentration |
| patients who are prone to adverse reactions | cancer, HIV, and liver patients with low albumin |
| maximal efficacy | largest effect that a drug can produce (match to patient's needs) |
| intrinsic activity | ability of a drug to activate a receptor upon binding (potency) |
| potency | amount of drug that must be given to elicit a response (strength of drug) - higher potency = lower dose required to produce effect |
| affinity | strength of attraction between a drug and its receptor |
| pharmacodynamic tolerance | decreased responsiveness to a drug due to repeated administration |
| tachyphylaxis | development of tolerance due to repeated dosing over short period of time |
| metabolic tolerance | how body metabolizes medications, tolerance from accelerated drug metabolism |
| therapeutic index | measure of a drug's safety (small therapeutic index = unsafe versus large therapeutic index = safe) |
| agonists | activate receptors by mimicking the action of body's regulatory molecules, has an affinity and high intrinsic activity, can increase or decrease function |
| antagonists | prevent receptor activation, have no effect without presence of agonist |
| partial agonists | can act as agonist or antagonist, have moderate intrinsic activity, maximal effect is lower than full agonist |
| non-competitive | binds irreversibly to receptors but not permanent, reduces total # of receptors for agonists = reduces maximal response that agonist can illicit, cannot be overcome |
| competitive | bind reversibly, highest concentration between agonist and antagonist will win, can be overcome |
| inducing agents | increase dose of paired drug (paired drug metabolizes faster) |
| consequences of inducing agents | intensification of effects and potential interactions, reduction of effects and inhibitory interactions |
| minimizing drug-drug interactions | decrease # of drugs patient takes, obtain thorough drug history, adjust dosage and timing, monitor early signs of toxicity |
| idiosyncratic effect | uncommon drug response resulting from a genetic predisposition |
| paradoxical effect | opposite of intended response (happens in very young and very old patients) |
| carcinogenic effect | cancer-causing effect |
| teratogenic effect | drug-induced birth defect |
Created by:
kpaveg
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