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Study of how drugs are administered, where they travel in the body, what response is produced, and what the drug's purpose is and what it will do to the body. |
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the study of drugs and their actions on living organisms. What does the drug do in the body and how does it interact with the tissues in the body. |
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The study of the metabolism and action of drugs with particular emphasis on the time required for absorption, duration of action, distribution in the body and method of excretion. |
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Study of how drugs may best be used in the treatment of illnesses. |
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the study of toxic effects from medicine, establishing antidotes and treatments of toxic manifestations and prevention of poisoning. |
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Phase 1- testing on healthy volunteers Phase 2- trials with people who have the disease for which the drug is thought to be effective Phase 3- drug used on larger number of people. Phase 4- voluntary; involves postmarked surveillance of drug's therapeutic effects. |
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- difficult to tell if there is a difference in effect between the 2, even if dosage is the same - inert ingredients may be different - key to comparison is BIOAVAILABILITY- the physiologic ability of the drug to reach its target cells and produce its effect. |
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plants, animals, minerals, synthetic, genetically engineered. |
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United States Drug Legislation |
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Controlled substance act of 1970 there are 5 classification of schedules |
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DEA : Drug Enforcement Agency Responsibility of staff NARCOTIC CONTROL |
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name of drug intended use effects on the body contraindications and precautions special considerations why its prescribed how to administer nursing process considerations r/t drug |
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a drug that interacts with receptors. It has an attraction, or affinity, for a receptor and stimulates it. |
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prevents a response from occurring |
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depends on the blood flow - Lipid soluble drugs can cross the blood brain barrier and enter the brain. |
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competes with the agonist for receptor sites - administering large doses of an agonist can overcome the antagonist's effects. |
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noncompetitive antagonist |
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binds to receptor sites and blocks the effects of the agonist - administering large doses of the agonist can't reverse its action |
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Inhibition of cyclooxyrgenase: inhibition of COX-1 can result in decreased platelet aggregation and kidney damage while inhibition of COX-2 results in decreased inflammation, fever, and pain and does not decrease platelet aggregation. |
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Therapeutic uses of NSAIDs |
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- Inflammation suppression - Analgesia for mild to moderate pain, such as with osteoarthritis and rheumatoid arthritis - fever reduction - dysmenorrhea - inhibition of platelet aggregation, which protects against ischemic stroke and myocardial infarction (aspirin) |
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- GI discomfort - impaired kidney function |
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adverse side effect of ASA |
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Salicylism -tinnitus, sweating, HA, dizziness, respiratory alkalosis |
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Occurs when aspirin is used for fever reduction in children and adolescents who have a viral illness, such as chickenpox or flu. |
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Ketorolac in patients who have advanced kidney disease |
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should be used cautiously with CV disease patients |
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Celecoxib (2nd gen NSAID) |
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suppresses inflammation, relieves pain, decreases fever, protects agains colorectal cancer.
NSAID COX-2 inhibitor - last choice for chronic pain |
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act on the mu receptors, and to a lesser degree on kappa receptors. Activation of mu receptors produces analgesia, respiratory depression, euphoria, and sedation. Where as KAPPA receptor activation produces analgesia, sedation and decreased GI motility. Activation of MU receptors can be linked to physical dependence. |
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Prototype drug for opioid agonist |
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Agonist-antagonist opioids |
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act as an ANTAGONIST ON MU receptors and AGONIST ON KAPPA receptors, except for buprenorphine, who's agonist/antagonist activity is opposite. -compared to pure opioid agonist, agonist-antagonists have the following: low potential for abuse, causing little euphoria, In fact high doses can cause adverse effects (anxiety, restlessness, mental confusion). Less respiratory depression, Less analgesic effect. |
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Prototype drug for agonist-antagonist opioids |
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interfere with the action of opioids by competing for opioid receptors. opioid antagonists have no effect in the absence of opioids. |
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Opioid antagonist prototype |
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