Acetaminophen

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Narcotic Agonists - Darvocet (proproxyphene)

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The narcotic agonists are drugs that react with the opioid receptors throughout the body to cause analgesia, sedation, or euphoria. Anticipated effects other than analgesia are mediated by the types of opioid receptors affected by each drug. Because of the potential for the development of physical dependence while taking these drugs, the narcotic agonists are classified as controlled substances. The degree of control is determined by the relative ability of each drug to cause physical dependence. The available narcotic agonists are listed in .
Therapeutic Actions and Indications
The narcotic agonists act at specific opioid receptor sites in the CNS to produce analgesia, sedation, and a sense of well-being. They are used as antitussives and as adjuncts to general anesthesia to produce rapid analgesia, sedation, and respiratory depression. Indications for narcotic agonists include relief of severe acute or chronic pain, preoperative medication, analgesia during anesthesia, and specific individual indications depending on their receptor affinity. (Box 26.2 describes how to calculate dosage for one narcotic agonist.)
In deciding which narcotic to use in any particular situation, it is important to consider all of these aspects and to select the drug that will be most effective in each situation with the least adverse effects for the patient . For instance, if an analgesic that is long-acting but not too sedating is desired for an outpatient, hydrocodone might fit those objectives.
Contraindications and Cautions
The narcotic agonists are contraindicated in the following conditions: presence of any known allergy to any narcotic agonist; pregnancy, labor, or lactation because of potential adverse effects on the fetus or neonate, including respiratory depression; diarrhea caused by poisons because depression of GI activity could lead to increased absorption and toxicity; and after biliary surgery or surgical anastomoses because of the adverse effects associated with GI depression and narcotics.
Caution should be used in patients with respiratory dysfunction, which could be exacerbated by the respiratory depression caused by these drugs; recent GI or genitourinary (GU) surgery; acute abdomen or ulcerative colitis, which could become worse with the depressive effects of the narcotics; head injuries, alcoholism, delirium tremens, or cerebral vascular disease, which could be exacerbated by the CNS effects of the drugs; and liver or renal dysfunction, which could alter the metabolism and excretion of the drugs.
Adverse Effects
The most frequently seen adverse effects associated with narcotic agonists relate to their effects on various opioid receptors. Respiratory depression with apnea, cardiac arrest, and shock may result from narcotic-caused CNS respiratory depression. Orthostatic hypotension is commonly seen with some narcotics. Such GI effects as nausea, vomiting, constipation, and biliary spasm may occur as a result of CTZ stimulation and negative effects on GI motility. Neurological effects such as light-headedness, dizziness, psychoses, anxiety, fear, hallucinations, pupil constriction, and impaired mental processes may occur as a result of the stimulation of CNS opioid receptors in the cerebrum, limbic system, and hypothalamus. GU effects, including ureteral spasm, urinary retention, hesitancy, and loss of libido, may be related to direct receptor stimulation or to CNS activation of sympathetic pathways. In addition, sweating and dependence (both physical and psychological) are possible, more so with some agents than with others.

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Nonsteroidal Anti-inflammatory Drugs - Motrin/Nuprin (ibuprofen)

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Therapeutic Actions and Indications
The anti-inflammatory, analgesic, and antipyretic effects of the NSAIDs are largely related to inhibition of prostaglandin synthesis. The NSAIDs block two enzymes, known as cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is present in all tissues and seems to be involved in many body functions, including blood clotting, protecting the stomach lining, and maintaining sodium and water balance in the kidney. COX-1 turns arachidonic acid into prostaglandins as needed in a variety of tissues. COX-2 is active at sites of trauma or injury when more prostaglandins are needed, but it does not seem to be involved in the other tissue functions. By interfering with this part of the inflammatory reaction, NSAIDs block inflammation before all of the signs and symptoms can develop. Most NSAIDs also block various other functions of the prostaglandins, including protection of the stomach lining, regulation of blood clotting, and water and salt balance in the kidney. The COX-2 inhibitors are thought to act only at sites of trauma and injury to more specifically block the inflammatory reaction. The adverse effects associated with most NSAIDs are related to blocking of both of these enzymes and changes in the functions that they influence—GI integrity, blood clotting, and sodium and water balance. The COX-2 inhibitors are designed to affect only the activity of COX-2, the enzyme that becomes active in response to trauma and injury. They do not interfere with COX-1, which is needed for normal functioning of these systems. Consequently, these drugs should not have the associated adverse effects seen when both COX-1 and COX-2 are inhibited. Experience has shown that the COX-2 inhibitors still have some effect on these other functions, and patients should still be evaluated for GI effects, changes in bleeding time, and water retention. Recent studies suggest that they may block some protective responses in the body, such as vasodilation and inhibited platelet clumping, which could lead to cardiovascular problems.
The NSAIDs are indicated for relief of the signs and symptoms of rheumatoid arthritis and osteoarthritis, for relief of mild to moderate pain, for treatment of primary dysmenorrhea, and for fever reduction.
Contraindications and Cautions
The NSAIDs are contraindicated in the presence of allergy to any NSAID or salicylate, and celecoxib is also contraindicated in the presence of allergy to sulfonamides. Additional contraindications are cardiovascular dysfunction or hypertension, because of the varying effects of the prostaglandins; peptic ulcer or known GI bleeding, because of the potential to exacerbate the GI bleeding; and pregnancy or lactation, because of potential adverse effects on the neonate or mother. Caution should be used with renal or hepatic dysfunction, which could alter the metabolism and excretion of these drugs, and with any other known allergies, which indicate increased sensitivity.
Adverse Effects
Patients receiving NSAIDs often experience nausea, dyspepsia, GI pain, constipation, diarrhea, or flatulence caused by direct GI effects of the drug. The potential for GI bleeding often is a cause of discontinuation of the drug. Headache, dizziness, somnolence, and fatigue also occur frequently and could be related to prostaglandin activity in the CNS. Bleeding, platelet inhibition, and even bone marrow depression have been reported with chronic use and probably are related to the blocking of prostaglandin activity. Rash and mouth sores may occur, and anaphylactoid reactions ranging to fatal anaphylactic shock have been reported in cases of severe hypersensitivity.
Clinically Important Drug–Drug Interactions
There often is a decreased diuretic effect when these drugs are taken with loop diuretics; there is a potential for decreased antihypertensive effect of beta-blockers if these drugs are combined; and there have been reports of lithium toxicity, especially when combined with ibuprofen. Patients who receive these combinations should be monitored closely, and appropriate dosage adjustments should be made by the prescriber.

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Glucocorticoids - Predisone

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Therapeutic Actions and Indications
Glucocorticoids enter target cells and bind to cytoplasmic receptors, initiating many complex reactions that are responsible for anti-inflammatory and immunosuppressive effects. Hydrocortisone, cortisone, and prednisone also have some mineralocorticoid activity and affect potassium, sodium, and water levels in the body.
Glucocorticoids are indicated for the short-term treatment of many inflammatory disorders, to relieve discomfort, and to give the body a chance to heal from the effects of inflammation. They block the actions of arachidonic acid, which leads to a decrease in the formation of prostaglandins and leukotrienes. Without these chemicals, the normal inflammatory reaction is blocked. They also impair the ability of phagocytes to leave the bloodstream and move to injured tissues, and they inhibit the ability of lymphocytes to act within the immune system, including a blocking of the production of antibodies. They can be used to treat local inflammation as topical agents, intranasal or inhaled agents, intra-articular injections, and ophthalmic agents. Systemic use is indicated for the treatment of some cancers, hypercalcemia associated with cancer, hematological disorders, and some neurological infections. When combined with mineralocorticoids, some of these drugs can be used in replacement therapy for adrenal insufficiency.
Contraindications and Cautions
These drugs are contraindicated in the presence of any known allergy to any steroid preparation; in the presence of an acute infection which could become serious or even fatal if the immune and inflammatory responses are blocked; and with lactation because the anti-inflammatory and immunosuppressive actions could be passed to the baby.
Caution should be used in patients with diabetes because the glucose-elevating effects disrupt glucose control; acute peptic ulcers because steroid use is associated with the development of ulcers; other endocrine disorders which could be sent into imbalance; or pregnancy.
Adverse Effects
The adverse effects associated with the glucocorticoids are related to the route of administration that is used. Systemic use is associated with endocrine disorders; fluid retention and potential congestive heart failure (CHF); increased appetite and weight gain; fragile skin and loss of hair; weakness and muscle atrophy as protein breakdown occurs and protein is not built; and increased susceptibility to infections and the development of cancers (with long-term use). Children are at risk for growth retardation associated with suppression of the hypothalamic–pituitary system. Local use is associated with local inflammations and infections, as well as burning and stinging sensations.
Clinically Important Drug–Drug Interactions
Therapeutic and toxic effects increase if corticosteroids are given with erythromycin, ketoconazole, or troleandomycin. Serum levels and effectiveness may decrease if corticosteroids are combined with salicylates, barbiturates, phenytoin, or rifampin.

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Nonsteroidal Anti-inflammatory Drugs - Motrin/Nuprin (ibuprofen)

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Implementation with Rationale
Administer with food if GI upset is severe; provide small, frequent meals to alleviate GI effects.
Administer drug as indicated; monitor dosage to avoid toxic levels.
Monitor for severe reactions to avoid problems and provide emergency procedures (gastric lavage, induction of vomiting, charcoal) if they occur.
Arrange for supportive care and comfort measures (rest, environmental control) to decrease body temperature or to alleviate inflammation.
Ensure that the patient is well hydrated during therapy to decrease the risk of toxicity.
Provide thorough patient teaching, including measures to avoid adverse effects and warning signs of problems, as well as proper administration, to increase knowledge about drug therapy and to increase compliance with drug regimen.
Offer support and encouragement to deal with the drug regimen.
Evaluation
Monitor patient response to the drug (improvement in condition being treated, relief of signs and symptoms of inflammation).
Monitor for adverse effects (GI upset, CNS changes, bleeding).
Evaluate effectiveness of teaching plan (patient can name drug, dosage, adverse effects to watch for, specific measures to avoid adverse effects).
Monitor effectiveness of comfort measures and compliance with the drug regimen.

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Glucocorticoids - Predisone

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Implementation with Rationale
Administer drug daily at 8 to 9 AM to mimic normal peak diurnal concentration levels and thereby minimize suppression of the hypothalamic–pituitary axis.
Space multiple doses evenly throughout the day to try to achieve homeostasis.
Use minimal dose for minimal amount of time to minimize adverse effects.
Taper doses when discontinuing from high doses or from long-term therapy to give the adrenal glands a chance to recover and produce adrenocorticoids.
Arrange for increased dosage when the patient is under stress to supply increased demand for corticosteroids associated with the stress reaction.
Use alternate-day maintenance therapy with short-acting drugs whenever possible to decrease the risk of adrenal suppression.
Do not give live virus vaccines when the patient is immunosuppressed because there is an increased risk of infection.
Protect the patient from unnecessary exposure to infection and invasive procedures because the steroids suppress the immune system and the patient is at increased risk for infection.
Assess the patient carefully for any potential drug– drug interactions to avoid adverse effects.
Provide thorough patient teaching, including measures to avoid adverse effects; warning signs of problems; and the need for regular evaluation, including blood tests, to enhance patient knowledge of drug therapy and promote compliance. Explain the need to protect the patient from exposure to infections to prevent serious adverse effects.
Evaluation
Monitor patient response to the drug (relief of signs and symptoms of inflammation, return of adrenal function to within normal limits).
Monitor for adverse effects (increased susceptibility to infections, skin changes, endocrine dysfunctions, fatigue, fluid retention, peptic ulcer, psychological changes).
Evaluate the effectiveness of the teaching plan (patient can name drug, dosage, adverse effects to watch for, specific measures to avoid adverse effects).
Monitor the effectiveness of comfort measures and compliance with the regimen

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Narcotic Agonists - Darvocet (proproxyphene)

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Implementation with Rationale
Provide a narcotic antagonist and equipment for assisted ventilation on standby during IV administration to support the patient in case severe reaction occurs.
Monitor injection sites for irritation and extravasation to provide appropriate supportive care if needed.
Monitor timing of analgesic doses. Prompt administration may provide a more acceptable level of analgesia and lead to quicker resolution of the pain.
Use extreme caution when injecting a narcotic into any body area that is chilled or has poor perfusion or shock because absorption may be delayed. After repeated doses, an excessive amount is absorbed all at once.
Use additional measures for relief of pain, such as back rubs, stress reduction, hot packs, and ice packs to increase the effectiveness of the narcotic and reduce pain.
Reassure patients that the risk of addiction is minimal. Most patients who receive narcotics for medical reasons do not develop dependency syndromes.
Provide thorough patient teaching, including drug name and prescribed dosage, measures for avoidance of adverse effects, warning signs that may indicate possible problems, and the need for monitoring and evaluation, to enhance patient knowledge about drug therapy and to promote compliance. (See Critical Thinking Scenario 26-1.)
Offer support and encouragement to help the patient cope with the drug regimen.
Evaluation
Monitor patient response to the drug (relief of pain, cough suppression, sedation).
Monitor for adverse effects (CNS changes, GI depression, respiratory depression, constipation).
Evaluate the effectiveness of the teaching plan (patient can give the drug name and dosage and describe possible adverse effects to watch for, specific measures to prevent adverse effects, and warning signs to report).
Monitor the effectiveness of comfort measures and compliance with the regimen.