Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
pharm basics c.2
Pharmacology basic concepts/processes ch.2
| Question | Answer |
|---|---|
| Absorption | process that occurs from time drug enters body to time it enters bloodstream to be circulated. Onset of drug action determined by rate of absorption. Intensity by extent of absorption. variables - dose, route, blood flow, GI function, food/drugs. |
| Agonist vs antagonist | drugs that mimic effects of naturally occurring hormones, neurotransmitters and other substances. vs. drugs that inhibit cell function by occupying receptor sites. |
| Metabolism | method by which drugs are inactivated or biotransformed by body. most often active > inactive metabolites - then exreted. biotransformation -some drugs not active until metabolized. convert fat soluble drugs to water soluble to be excreted by kidneys. |
| Bioavailability | portion of drug dose that reaches systemic circulation and is available to act on body cells. |
| Distribution | transport of drug molecules within body; after drug injected/absorbed into blood, carried by blood and tissue fluids to site of action, metabolism and excretion. |
| Enterohepatic recirculation | some drugs are excreted into bile, reabsorbed from small intestine, RETURNED TO THE LIVER, metabolized and eventually excreted in urine. |
| Enzyme induction | drugs stimulate liver to product more drug-metabolizing enzymes. Increased drug metabolism. Can lead to need for higher dosage for same effect. Takes 1-3 weeks after inducing agent started, bc new enzyme proteins must be synthesized. |
| Enzyme inhibition | Decreased drug metabolism. Often occurs when 2+ drugs administered, compete for same metabolizing enzymes. Smaller doses needed to avoid adverse effects from drug accumulation. Occurs within hours/days of starting an inhibiting agent. |
| Excretion | rid drug from body. Effectiveness req's circulatory system/ organs (kidneys, bowel, lungs and skin). Most by kidneys and eliminated (unchanged or metabolites) in urine. Some in bile. lungs - anesthetic gases. impairment - accumulation of drugs |
| First Pass effect | presystemic metabolism - drugs mostly metabolized by liver, with only a part of dose reaching systemic circulation for distribution to sites of action. |
| Hypersensitivity | allergy-occurs w/ drug in susceptible pts. unpredictable/unrelated to dose. Previously exposed to drug or similar (antigen) & developed antibodies. Readminister -drug reacts w/ antibodies cause cell damage & release histamine + other>produce reactions |
| Anaphylactic shock | life threatening hypersensitivity reaction characterized by respiratory distress and cardiovascular collapse. Occurs within minutes after drug administration and requires emergency treatment with epinephrine. |
| Pharmacokinetics | drug mov't through body to reach sites of action, metabolism and excretion. |
| pathways of drug movement across cell membranes | direct penetration (lipid-soluble drug dissolve in lipid layer of membrane). protein channels (small ions na+ K+ can use channel - gating mechanism). carrier proteins (transport molecules from one side to other. selective based on structure) |
| Mechanisms of drug transport in the body | passive diffusion ( mov't higher to lower concentration), facilitated diffusion (drugs combine with carrier substance before mov't) and active transport ( lower to higher concentration. carrier substance and release of cellular energy). |
| Protein binding | drugs form compound w/ plasma proteins (albumin) act as carriers. pharmacologically inactive bc of large size. free or unbound portion acts on body cells. dec. in plasma drug level > release of bound drug. reduce toxicity risk maintain blood levels. |
| blood-brain barrier | prevents drug distribution to central nervous system. |
| prodrugs | inactive until metabolized. |
| serum drug levels | lab measurement of amt of drug in blood at particular time. reflects dosage, absorption, bioavailability, half life and rates of metabolism and excretion. indicates onset, peak and duration of drug action. |
| MEC | minimum effective concentration - must be present before drug exerts effects on cells |
| therapeutic range | serum drug level between MEC and toxicity. |
| Importance of measuring serum drug levels in clinical practice | when drug has narrow margin of safety (therapeutic and toxicity levels close to one another) ex. digoxin, lithium). document level assoc. w/ dosage, therapeutic effect/adverse reaction. monitor unexpected. drug overdose suspected. |
| serum half life | elimination half life. time req'd for serum concentration of drug to dec. by 50%. determined by drug's rate of metabolism and excretion. related to time it takes (ex. weeks) for drug to be effective and after discontinued still in body. |
| Pharmacodynamics | drug actions on target cells and resulting alterations in cellular biochemical reactions and functions (what does in body) |
| Receptor theory of drug action | drugs can change rate of cellular metabolism, change permeability of cell membranes to 1+ ions, modify synthesis, release or inactivation of neurohormones that regulate processes. |
| Nonreceptor drug actions | drugs don't use receptor sites. rare. ex. antacid - act chemically to neutralize acid raising pH of gastric fluid. ex. osmotic diuretics - inc. osmolarity of plasma pull h2o out of tissue into blood. ex. structurally similar to nutrients req'd |
| Dosage recommendations | those that produce particular responses in 50% of people tested. Mixture of therapeutic and adverse effects. |
| Route of administration affect on drug action | influences absorption and distribution |
| intervention to combat drug-diet interactions | give medications 1 hr before or 2 hrs after eating to minimize interactions that decrease drug absorption. |
| basic cause of many drug-drug interactions | altered drug metabolism. enzymes competing for binding sites. |
| drug-drug interactions that can increase therapeutic or adverse effects of drug | additive effects, synergism, interference and displacement. |
| additive effects | occur when 2 drugs with similar pharmacologic actions are taken. |
| synergism | occurs when 2 drugs w/ different sites or mechanisms of action produce greater effects when taken together. |
| Interference | one drug may alter the metabolism of a second drug, intensifying effects. Same effect as taking larger dose of drug whose metabolism is inhibited or slowed. |
| Displacement | one drug is displaced from plasma protein-binding sites by a second drug which increases effects of the displaced drug. BC displaced drug, becomes pharacologically active. Same as takin glarger dose of displaced drug. |
| Drug-drug interactions where effects are decreased | antidote (antagonizes toxic effects of another drug) when drugs combine and produce nonabsorbable compounds decreasing intestinal absorption. activation of drug-metabolizing enzymes in liver inc. metabolism rate of any drug dec. effects. |
| Patient related variables | age (neonates, infants, elder), weight (dose, distribution), genetic/ethnic characteristics, gender, pathologic condition, psychological considerations |
| Pharmacogenetics | study of genetic variations that result in interindividual differences in drug response. |
| Explain main effect of cardiovascular disorder on pharmacokinetic processes | interfere with processes by decreasing blood flow to sites of administration, action, metabolism (liver) and excretion (kidneys) |
| Explain effect of GI disorders, hepatic disorders and renal disorders on pharmacokinetic processes | GI - absorption, Hepatic - metabolism, Renal - excretion |
| Thyroid disorder effect on pharmacokinetic processes | Hyperthyroidism speeds metabolism, shorten drug action /hasten elimination. Hypothyroidism slows metabolism, prolongs drug action slows elimination. |
| Placebo response | inactive substance. Used in clinical trials to compare med. tested with "dummy" med. Recipients often report both therapeutic and adverse effects from placebo. Attitudes/expectations related to drug or placebo influence patient responses/compliance. |
| Drug tolerance | accustomed to drug over time so larger doses needed for same effect. To pharmacologic action of drugs (alcohol, analgesics). If from pharmacologically related drugs = cross-tolerance. ex. alcohol tolerance > larger amt of sedative for same effect (ct) |
| Tolerance and cross-tolerance attributed to... | activation of drug metabolizing enzymes in liver, which accelerate metabolism and excretion. and dec. sensitivity or # of receptor sites. |
| adverse effects of drugs | any undesired responses to drug administration. range: rare, mild, severe, localized, widespread. |
| side effects | adverse effects that often occur with usual therapeutic doses of drugs. more likely and severe with larger doses. |
| Black box warning (bbw) | fda required warning on label or in literature describing the serious or life-threatening adverse effect that may occur with drug. Strongest fda warning |
| CNS effects | result from cns stimulation (agitation, disorientation, seizures) or cns depression (sedation, coma, impaired circulation). |
| GI effects | nausea, vomiting, constipation/diarrhea. local irritation or stimulation of brain centers. increased peristalsis cause diarrhea. more serious bleed/ulcer or severe diarrhea/colitis (antibiotics) |
| Hematologic effects | excessive bleeding, clots, bone marrow depression (anticancer drugs), anemia, leukopenia, agranulocytosis, thrombocytopenia - commone/ life threatening. excessive bleed assoc. w/ anticoagulants and thrombolytics. |
| Hepatic effects | hepatitis, liver dysfunction/failure, biliary tract disorder - life threatening. most drugs circulated to liver some toxic to liver cells. drugs can cause abnormal values in liver function tests w/o clinical signs of liver dysfunction. |
| Nephrotoxicity | nephritis, renal insufficiency/failure - occurs w/ several antimicrobial agents, nonsteroidal anti-inflammatory agents and others. may interfere w/ drug excretion, causing accumulation and inc. adverse effects. |
| Drug Fever | drugs cause fever many ways. - allergic reaction, damaging tissues, interfering w/ dissipation of heat, acting on temperature-regulation center in brain. most common allergic. |
| Idiosyncrasy | unexpected reaction to drug that occurs first time given. attributed to genetic characteristics that alter drug-metabolizing enzymes. |
| Drug Dependence | w/ mind-altering drugs - such as opioid analgesics. may be physiologic or psychological. physiologic - unpleasant physical symptoms when dose reduced or drug withdrawn. Psychological dependence leads to excessive preoccupation w/ drugs and drug-seeking |
| Carcinogenicity | ability of substance to cause caner. results from drug-induced alterations in cellular dna |
| teratogenicity | ability of substance to cause abnormalfetal development when taken by pregnant women. antiepileptic drugs and "statin" cholesterol-lowering drugs. |
| drug toxicity | poisoning/overdose - results from excesive amts of drug may damage tisues. from single large dose or prolonged smaller doses. |
| management of drug toxicity | monitor/support vital functions - drugs, flushing, activated charcoal "universal antidote" |
Created by:
FSclafani
Popular Pharmacology sets