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53 Cards in this Set
- Front
- Back
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pharmocolgy
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the study of drugs
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pharmacotherapeutics
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use of specific drugs to treat, prevent, diagnose disease
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pharmacokinetics
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how the body interacts with drugs; absorption, distribution, metabolism, elimination
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pharmacodynamics
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analysis of what and how (mechanisms of action) the drug affects the body
what the drug does to the patient |
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toxicology
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study of harmful effects of chemicals
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metabolism
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process by which the body breaks down and converts medication into active chemical substances
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absorption
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movement of drug into the bloodstream
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elimination
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removal of the drug from the body via the kidney and urine
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distribution
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transfer of drug from one area of the body to another, including the target tissue
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intravenous administration
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100% active drug, immediate effect (if distributed to site of action)
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intramuscular administration
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usually 100% effective, takes 30-60 minutes, administered via syringe/needle
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oral administration
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variable effect of how much drug reaches the system (0-100%), takes 1-2 hours
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schedule I controlled substances
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LSD, heroine, marijuana, morphine
highest potential for abuse, limited to research purposes physician/dentist, FDA approval necessary |
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schedule II controlled substances
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high potential for abuse and addiction (pain meds.)
physician/dentist |
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schedule III controlled substances
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lower potential for abuse, but still possibility of developing moderate physical or psychological dependency
physician/dentist |
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schedule IV controlled substances
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lower abuse potential than III, limited possible dependency
physician/dentist nurse practitioner/PA |
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schedule V controlled substances
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lowest abuse potential
physician/dentist nurse practitioner/PA |
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lipophilic/lipid soluble drugs
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diffuse across plasma membrane
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hydrophilic/water soluble
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requires mediated transport process to be carried into the cell
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agonist interaction with receptors
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activates receptor, drug binds to receptor and elicits maximal response
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antagonist interaction with receptors
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do not initiate cellular change, can prevent the binding and actions of agonists, aka blockers/inhibitors, bind to all available receptors
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partial agonist
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drug that binds to available receptors and elicits less than a maximal response
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competitive antagonist
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inhibition can be overcome by increasing the concentration of agonist at receptor site
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non-competitive agonist
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binds to receptor at a site different than agonist binding site, causes conformational changes in receptor therefore preventing binding and/or activation by agonist
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ceiling effect
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aka maximal efficacy, plateau in response along dose-response curve, no further increase in response
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minimum effective concentration MEC
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the lowest plasma concentration required to cause measurable response, lowest dose to cause change
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minimum toxic concentration MTC
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minimum lethal dose
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onset time
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length of time before medicine starts to work
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duration of activity
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time period when plasma concentration is above MEC
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therapeutic index
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ratio of dose to achieve toxic response vs. therapeutic response
TI > safer TI=toxic dose/effective dose |
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potency
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the more potent a drug is the lower the dose to produce the same effect as a drug with a lesser potency
may be cheaper, less needed (but may not...) NOT the same as max efficacy |
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median effect dose
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the dose at which 50 percent of the population responds to a drug in a specified manner (desired)
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median toxic dose
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the dose at which 50 percent of the population responds to a drug in a specified manner (adverse)
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therapeutic window
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well defined range of acceptable concentrations, receive therapeutic effects, and avoid toxicity
drugs with low TI should be monitored* |
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growth fraction
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ratio of proliferating cells to resting (G0) cells
high growth fraction= disseminated cancers low growth fraction= solid tumors |
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alkylating agents
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inhibit cell growth and division by reacting with DNA
S phase & metaphase of mitosis cytotoxic agent |
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antimetabolites
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prevent cell growth by competing for components needed to make nucleic acids
S phase cytotoxic agent |
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antitumor antibiotics
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inhibit cell growth by binding to DNA and interfere with DNA dependent RNA synthesis
cytotoxic agent |
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mitotic inhibitors (plant alkaloids)
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disrupt cell mitosis, prevent cell division
two types: vinca alkaloids, taxoids cytotoxic agent |
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tpoisomerase inhibitors
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prevents repair of DNA strand
cytotoxic agent |
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glucocorticoid steroids
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used w/ other drugs, useful for lympohoid tissue cancers, long term treatment = bad,
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endogenous corticosteriods
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natural.
primary (cortisol- regulates blood sugar, holds back immune response, released as a result of stress) |
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exogenous corticosteriods
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synthetic.
interfere with nuetrophil chemotaxis; stops neutrophils from sticking to vessel walls and causing inflammation peaks at 4-6 hours after dosage |
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1st line of defense
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intact skin, mucous membrane, cilia, GI tract
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2nd line of defense
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inflammatory response
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3rd line of defense
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immune response
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bacteriocidal
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kill organisms
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bacteriostatic
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slow or stop growth/division and allow host to eliminate
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gram (-)
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thicker cell wall (90%), stains dark purple
easier to kill |
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gram (+)
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thinner cell wall (10%), stains pink
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empirical diagnosis
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treatment derived from practical experience/inference
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specific & sensitive
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test to determine actual treatment necessary
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selective toxicity
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treatment that kills/damages pathogen, but causes minimal/no damage to healthy cells
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