Lehne's Pharmacology for Nursing Care: Application of Pharmacology in Nursing Practice Flashcards

D
Pharmacotherapeutics is the study of the use of drugs to diagnose, treat, and prevent conditions. Clinical pharmacology is concerned with all aspects of drug-human interactions. Drug efficacy measures the extent to which a given drug causes an intended effect. Pharmacokinetics is the study of the impact of the body on a drug.

C
A major benefit of drugs that are easy to administer is that patients taking them are more likely to comply with the drug regimen. Drugs that are easy to give may have the other attributes listed, but those properties are independent of ease of administration.

C
A drug is effective if it produces the intended effects, even if it also produces side effects. Patients who understand both the risks and benefits of taking a medication are more likely to comply with the drug regimen.

B, C, D
In addition to predictability, ease of administration, and chemical stability, other properties include a reversible action so that any harm the drug may cause can be undone and a simple generic name, because generic names are usually complex and difficult to remember and pronounce.

C, D, E
The family medical history can indicate genetic factors that may affect a patient's response to a medication. Patients of different ages can respond differently to medications. The patient's illness can affect how drugs are metabolized. The chemical stability of the medication and the ease of administration are properties of drugs.

D
It is not within the nurse's scope of practice to change the dose of a medication without an order from a prescriber. Asking the patient to demonstrate inhaler use helps the nurse to evaluate the patient's ability to administer the medication properly and is part of the nurse's evaluation. Assessing tobacco smoke exposure helps the nurse determine whether nondrug therapies, such a smoke avoidance, can be used as an adjunct to drug therapy. Performing a physical assessment helps the nurse evaluate the patient's response to the medication.

B
Tylenol is the trade name and acetaminophen is the generic name for the same medication. It is important to teach patients to be aware of the different names for the same drug to minimize the risk of overdose. Over-the-counter (OTC) medications and prescription medications may be taken together unless significant harmful drug interactions are possible. Even though no drug interactions are at play in this case, both drugs contain acetaminophen, which could lead to toxicity.

C
The assessment part of the nursing process involves gathering information before beginning treatment, and this includes asking about other medications the patient may be taking. Monitoring serum drug levels, watching for drug interactions, and checking vital signs after giving the medication are all part of the evaluation phase.

B
The nursing diagnosis for this patient is severe pain. Acetaminophen is given for mild to moderate pain, so the nurse should ask the prescriber to order a stronger analgesic medication. Asking the patient to tell the nurse what has helped in the past is part of an initial assessment and should be done preoperatively and not when the patient is having severe pain. Because the patient is having severe pain, acetaminophen combined with nondrug therapies will not be sufficient. Increasing the frequency of the dose of a medication for mild pain will not be effective.

A
Because insulin must be given correctly to control symptoms and because an overdose can be fatal, it is most important for the patient to know how to administer it. Asking for a demonstration of technique is the best way to determine whether the patient has understood the teaching. When a patient is receiving a lot of new information, the information presented first is the most likely to be remembered. The other teaching points are important as well, but they are not as critical and can be taught later.

A
Assessing the patient's pain after administering the medication is an important part of the nursing process when giving medications, but it is not part of the six rights of drug administration. Checking to see when the last dose was given helps ensure that the medication is given at the right time. Consulting a drug manual helps ensure that the medication is given in the right dose. Documenting the reason for a pain medication is an important part of the right documentation—the sixth right.

A
When evaluating the effectiveness of a drug, it is important to determine whether the patient is using the drug as ordered. Asking the patient to tell the nurse how many tablets are taken and how often helps the nurse determine compliance. Assessing current pain does not yield information about how well the medication is working unless the patient is currently taking it. The nurse should gather as much information about compliance, symptoms, and drug effectiveness as possible before contacting the prescriber. Biofeedback may be an effective adjunct to treatment, but it should not be recommended without complete information about drug effectiveness.

A
The individual with impaired kidney function would be at risk of having the drug accumulate to a toxic level because of potential excretion difficulties. Cystitis is an infection of the bladder and not usually the cause of excretion problems that might lead to an adverse reaction from a medication. A respiratory tract infection would not predispose a patient to an adverse reaction, because drugs are not metabolized or excreted by the lungs. A 9-year-old boy would not have the greatest predisposition to an adverse reaction simply because he is a child; nor does an ear infection put him at greater risk.

A
The drug manual indicates that this drug should be given with caution to elderly patients. Getting information about liver function before giving the drug establishes baseline data that can be compared with post-treatment data to determine whether the drug is affecting the liver. Giving the correct dose at the correct interval helps to minimize risk, but without baseline information, the effects cannot be determined. The drug is not contraindicated.

D
Prurient and wheezing are signs of a possible allergic reaction, which can be fatal; therefore, the medication should not be given and the prescribes should be notified. When patients are having a potentially serious reaction to a medication, the nurse should not continue giving the medication. Antihistamines may help the symptoms of an allergic reaction, but the first priority is to stop the medication. Obtaining a chest radio-graph is not helpful

D
With PRN medications, the schedule is not fixed and the administration of these medications depends on the patient's condition. It is the nurse's responsibility to assess the patient's condition and then give the appropriate PRN medication. In this case, the patient has severe pain and should receive MS IV. Either 1 mg or 2 mg may be given, but the nurse must evaluate the effectiveness of the pain medication within 15 to 30 minutes to help determine subsequent doses. Acetaminophen-hydrocodone is not appropriate because it is ordered for moderate pain and this patient reports severe pain. Giving MS IV every hour is not appropriate for a PRN medication unless the patient's condition warrants it.

D
In the planning step, the nurse delineates specific interventions directed at solving or preventing problems. When creating the care plan, the nurse defines goals, sets priorities, and establishes criteria for evaluating success. The assessment step involves collecting data about the patient. The evaluation step involves evaluating the medication effectiveness. The implementation step identifies actions that are taken to administer the drug.

B, C, D
Age, genetic factors, and gender influence an individual patient's ability to absorb, metabolize, and excrete drugs; therefore, these factors must be assessed before a medication is administered. A patient's ability to swallow pills, although it may determine the way a drug is administered, does not affect the physiologic response. Height does not affect response; weight and the distribution of adipose tissue can affect the distribution of drugs.

A
Amoxicillin is the generic name, and the suffix "-cillin" indicates that it belongs to the penicillin class of antibiotics. Tylenol, Cipro, and Motrin are all trade names without segments that indicate their pharmacologic class.

B
The FDAAA was passed to enable the Food and Drug Administration to continue oversight of a drug after granting it approval so that changes in labeling could be made as necessary and postmarketing risks could be tracked and identified. A provision of the FDA Modernization Act (FDAMA), passed in 1997, allows drug companies to promote their products for off-label uses as long as they promise to conduct studies to support their claims. Regulations to permit accelerated approval of drugs for life-threatening diseases were adopted in 1992 by the FDA. The requirement that drug companies notify patients 6 months before removing a drug from the market is a provision of the FDAMA.

A
Randomization helps prevent allocation bias, which can occur when researchers place subjects with desired characteristics in the study group and other subjects in the control group so that differences in outcome are actually the result of differences in subjects and not treatment. Comparing treatment outcome to no treatment outcome is the definition of a controlled study. The last two options describe the use of blinding in studies; blinding ensures that researchers or subjects (or both) are unaware of which subjects are in which group so that preconceptions about benefits and risks cannot bias the results.

B
Preclinical testing must be completed before drugs can be tested in humans. In this stage, drugs are evaluated for toxicities, pharmacokinetic properties, and potentially useful effects. Some drugs can be used in patients before completion of Phase III studies, but this is after preclinical testing is complete. Clinical trials proceed in stages, and each stage has guidelines defining how a new drug may be used and which patients may receive it. Postmarketing surveillance takes place after a drug is in general use.

D
All drug trials are limited by a relatively small group of subjects who may not have all the characteristics of people who will be using the drug; therefore, some side effects go undetected until the drug is in use. Although drug trials are very expensive, this is only an indirect reason they do not detect all side effects before approval. In theory, well-designed drug trials, using blinded studies, minimize or eliminate subject bias. Designing studies to prove desired results is unethical.

B
Nonproprietary, or generic, names are assigned by the U.S. Adopted Names Council, which ensures that each drug has only one name. Trade names, or brand names, are approved by the FDA and are easier to remember. Some nonproprietary names contain syllables that identify the classification, although not all do. Drug names are not supposed to identify the use for the drug, although some brand names do so.

C
Enteric-coated drugs are preparations that have been coated with a material that dissolves in the intestines, not the stomach. This coating is used either to protect the drug from stomach acid and pepsin or to protect the stomach from a drug that can cause gastric upset. Sublingual forms often are used for drugs that undergo rapid inactivation during the first pass through the hepatic circulation so that the drug can be absorbed directly into the systemic circulation. Parenteral routes are more costly and less safe than oral administration and should not be used unless necessary. A sustained-release preparation is used to release the drug into the body over a specific period to reduce the number of daily doses required to sustain therapeutic drug levels.

C
Even if two brands of a drug are chemically equivalent (i.e., they have identical amounts of the same chemical compound), they can have different effects in the body if they differ in bioavailability. Tablets made by different manufacturers contain different binders and fillers, which disintegrate and dissolve at different rates and affect the bioavailability of the drug. Two brands may be chemically equivalent and still differ in bioavailability, which is not determined by the amount of drug in the dose.

C
A drug with a narrow therapeutic range is more difficult to administer safely, because the difference between the minimum effective concentration and the toxic concentration is small. Patients taking these medications must have their plasma drug levels monitored closely to ensure that they are getting an effective dose that is not toxic. Administering medications at longer intervals only increases the time required to reach effective plasma drug levels. Drugs that have a narrow therapeutic range may be given by any route and do not differ from other medications in the amount of time it takes for them to take effect, which is a function of a drug's half-life and dosing frequency.

A
A large initial dose is often used as a loading dose to help get serum drug levels to plateau levels more quickly. Larger doses do not prevent first pass effects in drugs susceptible to this type of metabolism. Tapering of doses sometimes is used to prevent rebound or withdrawal effects and is done by stepping down the amount of drug with each dose. Tubular reabsorption is a process that allows drugs to be reabsorbed from the urine into the blood

B
Parenteral routes include the intravenous, intramuscular, and subcutaneous routes. Enteral routes include oral administration, including pills and liquid suspensions. Enteral routes are safer, cheaper, and easier to use. Parenteral routes are used when rapid absorption, precise control of plasma drug levels, and prevention of digestive inactivation are important.

D
Penicillin G is inactivated by digestive enzymes in the stomach and cannot be given orally. It does not have a narrow therapeutic range.

B
It takes four half-lives for a drug to reach plateau. Total body stores reach their peak at the beginning of the fifth dose of a drug if all doses are equal in amount; in this case, this will be at 8:00 AM the following day.

C
The intravenous route is the fastest route of absorption and the one most appropriate for a patient in extreme pain. With the oral route, the medication would take at least 45 minutes to be effective, too long for a patient in extreme pain. With the intramuscular route, the medication would take at least 15 minutes to be effective; although faster than the oral route, this is not as fast as the intravenous route. A Duragesic patch would be the most inappropriate route because of the long drug half-life. This is a more appropriate route for long-term use.

C
Glucuronidation of some drugs in the liver allows drugs to enter the bile, pass into the duodenum, and then be hydrolyzed to release the free drug. This is a repeating cycle of enterohepatic recirculation, which allows drugs to remain in the body longer. Glucuronidated drugs that are more resistant to hydrolysis are excreted in the feces. Glucuronidation occurs in the enterohepatic circulation and not in the renal circulation.

C
Gentamicin binds to albumin, but only weakly, and in the presence of another drug that binds to albumin, it can rise to toxic levels in blood serum. A loading dose increases the initial amount of a drug and is used to bring drug levels to the desired plateau more quickly. A drug that is not completely dissolved carries a risk of causing embolism. A drug given at a frequency longer than the drug half-life will likely be at subtherapeutic levels and not at toxic levels.

D
The phenomenon of pH-dependent ionization can be used to accelerate renal excretion of drugs. When children have been exposed to toxic amounts of aspirin, they can be treated, in part, by giving an agent that elevates urinary pH, leading to less passive reabsorption of the now ionized molecules of aspirin and, hence, more excretion. Elevating the pH of the blood and urine does not affect absorption in the stomach. Ionization of aspirin does not affect lipid solubility or protein binding.

B
As blood flows through the glomerular capillaries, fluids and small molecules are forced through the pores of the capillary wall. Large molecules, such as drugs bound to albumin, remain behind in the blood. Active tubular secretion requires active transport systems to pump molecules from one side of the membrane to another. Passive tubular reabsorption allows substances in high concentrations in the tubule to be reabsorbed into the blood, and lipid-soluble drugs readily cross this membrane by passive reabsorption. pH-dependent ionization affects drugs that ionize in either acid or alkaline environments.

B, C, D
Immature renal function causes infants to excrete drugs more slowly, and infants are at risk for toxicity until renal function is well developed. Infants' livers are not completely developed, and they are less able to metabolize drugs efficiently. Because the blood-brain barrier is not well developed in infants, caution must be used when administering CNS drugs. Lipid-soluble drugs may be excreted in breast milk if the mother is taking them, but breast-feeding does not affect medications given directly to the infant. Oral medications may be given safely to infants as long as they are awake and can swallow the drug.

A
The symptoms indicate toxicity, and even though the dose is safe and effective in most cases, an individual patient may have toxic effects with a standard dose. The nurse should contact the prescriber to discuss the next steps. Delaying a dose without a change in order is not within the scope of practice for a nurse. The nurse should not give a dose of a medication when toxicity is suspected, because additional drug will compound the symptoms. Antiemetics are useful for counteracting drug side effects, but they should not be used when the patient's symptoms indicate toxicity.

C
Continual exposure to an agonist would cause the cell to become less responsive or desensitized. The body does not produce antagonists as a response to a medication. Receptor site selectivity is determined by physiologic factors and not by the substances that bind to them. Medications do not cause more receptors to be produced.

C
A narrow therapeutic index indicates that a drug is relatively unsafe and should be monitored closely. The nurse should have a blood level drawn to confirm suspicions of toxicity. The nurse would not have the antibiotic changed, because there is no cause at this time. The patient is unlikely to be experiencing an allergic reaction, because the antibiotic has been in the system for 10 days. The patient shows no signs of anaphylaxis, so oxygen and an antagonist are not indicated.

D
Morphine is a medication that is selective to receptor type that regulates more than one process. Because it is selective to receptor type, it does not bind to different types of receptors. Constipation is a normal side effect and is not significant for toxicity.

B
When a drug binds to a receptor, it mimics or blocks the actions of the usual endogenous regulatory molecules, either increasing or decreasing the rate of the physiologic activity normally controlled by that receptor. It does not alter the activity of the receptor and does not give the receptor a new function

C
Naloxone acts by blocking the action of opioids at opioid receptors. An opioid agonist would increase the effects of morphine. Naloxone does not affect serum pH or excretion of opioids. Naloxone does not alter the sensitivity of opioid receptors.

B, C, E
Affinity refers to the strength of the attraction between a drug and its receptor. Drugs with high affinity are strongly attracted to their receptors, and the affinity of a drug and its receptors is reflected in its potency. Affinity and intrinsic activity are independent properties. Drugs with low affinity are weakly attracted to their receptors.

A, B, D
Antiseptics, antacids, and chelating agents are all receptorless drugs that do not depend on the body's processes for effects; these agents react with other molecules. Broad-spectrum antibiotics and topical analgesics bind with receptors to produce desired effects, and these processes can be influenced by individual patient variables.

D
A potentiative effect is one in which one drug intensifies the effects of another. Both warfarin and aspirin suppress blood clotting, and the combination may increase the risk of bleeding, which is an intensified adverse effect. Creation of a unique effect is a rare occurrence in which the combination of two drugs creates a response not seen with either drug when given alone. Increased therapeutic effects are a type of potentiative effect; however, in this case the combination of two drugs would increase the desired effects. An inhibitory effect is a type of pharmacodynamic effect that occurs when an antagonist drug inhibits the action of an agonist drug at the same receptor site.

C
A respiratory rate of 8 breaths per minute indicates respiratory depression, which is a significant adverse effect indicating morphine toxicity. Naloxone blocks the actions of morphine at cell receptor sites and is given to quickly reverse the effects. This patient does not have signs of an allergic response, which would include shortness of breath, a rapid respiratory rate, and wheezing. The tachycardia might be a sign of worsening pain, but the toxic effects must be treated first. Patients who are sleeping are not always pain free.

A
Naloxone is used when a narcotic overdose has occurred. As a narcotic antagonist, it provides a beneficial inhibitory interaction. An antacid blocking tetracycline's antibiotic effects would not be beneficial, but rather detrimental to the desired effects of the tetracycline. Alcohol would not block the effects of opiates, but would contribute to CNS depression. Cholestyramine and certain other adsorbent drugs, which are administered orally but do not undergo absorption, can adsorb other drugs onto themselves, thereby preventing absorption of the other drugs into the blood.

C
An inducing agent stimulates the synthesis of CYP isoenzymes, which may increase the metabolism of other drugs as much as two- to threefold, thereby lowering the level of those drugs in the body and requiring higher doses to maintain drug effectiveness.

B
Patients taking oral contraceptives along with phenobarbital, which is used to treat seizures, will have lower levels of the contraceptive, because phenobarbital is an inducing agent, which causes an increase in the metabolism of oral contraceptives. Grapefruit juice inhibits the metabolism of some drugs, leading to toxic effects. Dairy products interfere with the absorption of tetracyclines, because the calcium binds with the drug to form an insoluble complex. Laxatives reduce the absorption of some drugs by speeding up the transit time through the gut.

D
Sodium bicarbonate increases the pH of interstitial fluid and plasma, allowing the acidic aspirin ions to move outside the cells and thus removing them from the site where they have toxic effects. It does not have laxative effects and does not alter the rate of passage through the gut. It is not a CYP isoenzyme inducer and therefore has no effect on drug metabolism. It does not alter renal excretion of aspirin.

D
Grapefruit juice inhibits CYP3A4, which lowers the metabolism of some drugs, leading to toxic effects of drugs affected by these isoenzymes. Foods can alter all pharmacokinetic and pharmacodynamic processes. Not all medications are absorbed better on an empty stomach; some require certain foods to enhance absorption. Patient comfort is a concern, but it is not as important as more severe and possibly life-threatening food and drug interactions.

B
Aged cheeses are rich in tyramine, which interacts with MAO inhibitors to raise blood pressure to life-threatening levels. Patients taking MAO inhibitors should be taught to avoid tyramine-rich foods. Chianti wine contains tyramine, but other alcoholic beverages do not. Brussels sprouts and cabbage are foods rich in vitamin K, which can interfere with the effects of warfarin. Grapefruit juice inhibits CYP3A4 and interferes with the metabolism of many medications.

B
Drugs that induce PGP can increase drug export from cells of the intestinal epithelium into the intestinal lumen, thus decreasing absorption of the drug. PGP inducers also increase drug elimination and decrease brain and fetal drug exposure.

A, B
Calcium channel blockers and selective serotonin reuptake inhibitors have been shown to reach increased and/or toxic levels when taken with grapefruit juice. Grapefruit juice is not contraindicated with aminoglycosides, beta blockers, or penicillins.

A, B, D
When two drugs bind to the same site on plasma albumin, coadministration of those drugs produces competition for binding. As a result, binding of one or both agents is reduced, causing plasma levels of free drug to rise. The increase in free drug can intensify the effect, but it usually undergoes rapid elimination. The increase in plasma levels of free drug is rarely sustained.

A, B, D
Over-the-counter medications add to drug interactions, and a thorough history of all medications taken by the patient is essential to minimize adverse drug reactions. Cytochrome P450 levels yield important information about a patient's ability to metabolize drugs and can help predict whether drugs will reach toxic levels or be ineffective. A diet history allows providers to anticipate significant known food-drug interactions. Limiting calcium intake is necessary only if the patient is taking drugs known to interact with calcium, such as tetracycline. Asking for PRN medications to treat drug reactions may only compound the risk, because the risk of drug interactions increases with the number of medications taken.

A, D
The absorption of some drugs can be significantly reduced by food; these drugs should be taken on an empty stomach, which is 1 hour or more before a meal or at least 2 hours after a meal. An 8-hour fast is not necessary; the patient does not need to miss a meal to take the medication; and it is not reasonable to have the patient on thin liquids for 12 hours.

A
Not all adverse drug reactions (ADRs) can be detected during clinical trials, and nurses should be alert to any effects that may result from drug administration. Because nausea is not a serious effect and because it is not yet known whether the drug is the cause of this patient's nausea, the nurse should administer the medication and observe the patient for recurrence of the symptom. It is not necessary to hold the drug, because nausea is not a serious side effect. The MEDWATCH program should be notified when there is a greater suspicion that the drug may have caused the nausea if the nausea occurs with subsequent doses. Until there is greater suspicion that the drug actually caused this patient's nausea, giving an antiemetic is not indicated.

C
Combining a hepatotoxic drug with certain other drugs may increase the risk of hepatotoxicity. When even therapeutic doses of acetaminophen are taken with alcohol, the acetaminophen can cause liver damage. Patients should be cautioned not to drink alcohol; even two drinks with acetaminophen can produce this effect. Hydrocodone does not contribute to hepatotoxicity. Ibuprofen is not indicated for postoperative pain unless the pain is mild. Limiting wine to one or two glasses per day still increases the risk of hepatotoxicity.

D
The correct answer is a complete order; it contains the medication, dose, route, and time. "qd" is no longer an accepted abbreviation; it should be written out as "daily" or "every day." The order of "20 mg daily" does not specify the route to be used.

D
A side effect is a secondary drug effect produced at therapeutic doses. This patient received the correct dose of the drug and developed shortness of breath, which, in this case, is a drug side effect. To experience an allergic reaction, a patient must have prior exposure to a drug and sensitization of the immune response. An idiosyncratic effect results from a genetic predisposition to an uncommon drug response. An iatrogenic response occurs when a drug causes symptoms of a disease.

B
A drug that causes disease-like symptoms is known to be iatrogenic. Nurses should be prepared for this possibility and be prepared to withdraw the drug if necessary and treat the symptoms. Such effects are not teratogenic. Patients with a genetic predisposition to respond differently to drugs are known to have idiosyncratic effects. Iatrogenic effects, even when known, are not typically expected side effects.

D
Drug-induced liver injury can progress from undetectable to advanced between routine tests; therefore, routine testing does not always prevent liver failure. Patients taking known hepatotoxic drugs should avoid other drugs, such as acetaminophen, that can cause liver damage. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are liver enzymes that are routinely monitored when a patient is taking hepatotoxic drugs. Nausea, vomiting, and abdominal pain are signs of liver injury and should be reported.

A
Both sertraline and azithromycin prolong the QT interval, and when taken together, they increase the risk of fatal dysrhythmias. Because the antibiotic is used for a short time, it is correct to consider using a different antibiotic. Reducing the dose of sertraline does not alter the combined effects of two drugs that lengthen the QT interval. Sertraline should not be stopped abruptly, so withholding it during antibiotic therapy is not indicated.

C
When a drug is administered that has known toxic side effects, the nurse is responsible for monitoring all organ systems potentially affected by the drug. Not all toxic side effects warrant discontinuation of the drug, and a nurse cannot discontinue a drug without an order from the provider. Complete blood counts are indicated only for drugs that affect the blood. Some drugs need to be discontinued, so teaching a patient to treat symptoms is not correct in all cases.

C
Boxed warnings (also known as black box warnings) are used to alert providers to potential side effects and to ways to prevent or reduce harm from these side effects. A boxed warning is placed on any drug that, although useful, has serious side effects; this is a way to keep drugs on the market while protecting patients. Many of these drugs are used in situations that are not life threatening. The boxed warning provides a concise summary and not a detailed explanation of drug side effects. The boxed warning does not include antidotes to toxicity.

B, C, E
Ninety percent of fatal medication errors fall into three categories: human factors, communication mistakes, and name confusion. Giving a drug IV (intravenously) instead of IM (intramuscularly) is an example of a human factor; writing a prescription so that it is illegible is an example of a communication mistake; and giving a drug with a name that sounds like the name of another drug is an example of name confusion. Confusion of drugs with similar packaging and using a faulty device also can cause fatal drug errors, but these factors do not fall into the categories that account for 90% of fatal errors.

A, C, E
To help prevent medication errors, it is important to create an environment for tracking errors that is nonpunitive so that caregivers can learn from mistakes and work together to change systems appropriately. Helping patients be active, informed members of the healthcare team is a useful tool in this process. Using electronic order entry helps eliminate confusion from poor handwriting and allows built-in systems to warn caregivers about possible overdoses, side effects, and drug interactions; it also helps ensure the right dose at the right time to the right patient. An approach that focuses on those who make mistakes by naming, blaming, and shaming is not productive and often results in personnel who cover up mistakes instead of working to make things better.

A, C, E
Patients at increased risk for adverse drug events include the very young, the very old, and those who have serious illnesses. Females, children, and young adults taking single medications do not have increased risks for adverse events.

B
The full extent of placebo effects, if they truly occur, is not well documented or understood, although a decrease in pain as a placebo effect has been demonstrated to some extent. To foster a beneficial placebo effect, it is important for all members of the healthcare team to present an optimistic and realistic assessment of the effects of the drug the patient is taking. If the nurse tells an anxious patient that the medication being given is not as strong as what has been given, the patient is likely to have lowered expectations of the effectiveness of the drug, causing a negative placebo effect. Lowered expectations do not mean that the patient will give up on the drug entirely; in fact, the patient may actually fill the prescription and then take more drug than what is prescribed to get a better effect.

C
Each patient's genetic makeup can determine how that patient responds to drugs quantitatively and qualitatively, and this is the most likely cause of individual variation when the same drug is given at the same dose. The bioavailability of a drug is determined by the drug's composition and varies across formulations of the drug. The patients in this example were given the same drug. The nurse was administering the medication to the patients, so compliance is not an issue. Nothing in this example indicates that a placebo effect was in play.

B
Pharmacogenomics is the study of the ways genetic variations affect individual responses to drugs through alterations in genes that code for drug-metabolizing enzymes and drug receptors. For some drugs, the FDA requires genetic testing, and for others, this testing is recommended but not required. Genetic testing does not determine a drug's therapeutic index; this is a measure of a drug's safety based on statistics of the drug's use in the general population (see Chapter 5). Any distinct physiologic differences in drug response among various racial populations are related to genetic differences and do not affect psychosocial differences in drug responses. Genetic testing is recommended to identify how a patient will respond to a drug and not to design a drug specific to an individual.

C
The most common source of genetic variation in drug response is related to alterations in drug metabolism and is determined by genetic codes for various drug-metabolizing isoenzymes. There are known genetic differences in codes for drug target sites, but these are not as numerous as those for metabolic isoenzymes. Hypersensitivity potential is also genetically determined, but variations produce differences in adverse reactions to drugs and not in drug effectiveness. Psychosocial responses vary for many less measurable reasons, such as individual personalities and variations in cultures.

C
Pharmacodynamic tolerance results when a patient takes a drug over a period of time. Adaptive processes occur in response to chronic receptor occupation. The result is that the body requires increased drug, or an increased MEC, to achieve the same effect. This patient is getting adequate pain relief, so there is no negative placebo effect. Tachyphylaxis is a form of tolerance that can be defined as a reduction in drug responsiveness brought on by repeated dosing over a short time; this occurs over several months. Barbiturates induce synthesis of hepatic enzymes that cause increased metabolism of the drug, but it does not increase the MEC.

A
Women with a deficiency of the CYP2D6 gene lack the ability to convert tamoxifen to its active form, endoxifen, and will not benefit from this drug. Another drug should be used to treat this patient's breast cancer. Increasing the dose, reducing the dose, or monitoring serum drug levels will not make this drug more effective in these women.

B
Until 1997 almost all clinical drug trials were performed in men. Women may have more toxic effects with some drugs and fewer toxic effects with others. Not all drugs are influenced by hormonal changes. Women metabolize some drugs more slowly and other drugs more quickly. Unless drug trials are performed in both women and men, the effects of drugs in women will not be clear.

D
Older patients and those who are malnourished are at increased risk for low serum albumin. Since warfarin binds to albumin, such patients are at increased risk for elevated warfarin levels, which can cause increased bleeding. The nurse should request albumin levels and coagulation studies.

A, C
Older adults and infants are the two groups most sensitive to drugs because of differences in organs that absorb, metabolize, and excrete drugs. In the older adult, organ degeneration accounts for these differences, whereas in infants the differences are related to organ immaturity. Racial and gender differences tend to be related to genetic differences and not race and gender per se. These groups are more sensitive to drug effects in some cases and less sensitive in other cases.

D
Morphine and its antagonist, naloxone, act directly at the same receptors. Morphine causes activation, and naloxone prevents activation. Neither morphine nor naloxone acts to alter transmitter reuptake, release, or storage.

A
Local anesthetics are drugs that work by altering axonal conduction. Any drug affecting axonal conduction would be nonselective, because axonal conduction of impulses is essentially the same in all neurons. In contrast, drugs that affect synaptic transmission can be highly selective, because each transmitter has different effects on receptor sites. Most PNS drugs work on synaptic transmission processes. Through their effects on transmitters, they influence receptor activity.

A
Drugs that directly activate receptors are called agonists, so this drug will directly activate the receptor site. Drugs that are nonselective activate a variety of receptor sites. A selective agonist would directly activate specific receptors to affect a specific process. An antagonist would prevent receptor activatio

C
Drugs that increase transmitter synthesis increase receptor activation. Other drugs that alter transmitter synthesis can decrease synthesis and would cause decreased receptor activation. Drugs that affect transmitter production do not exert their effects on axonal conduction. The amount of transmitter produced does not directly affect transmitter storage. Some drugs that alter transmitter synthesis cause the synthesis of transmitter molecules that are more effective than the transmitter itself.

A
Drugs that interfere with transmitter storage reduce receptor activation, because disruption of storage decreases the amount of transmitter available for release. Because this transmitter increases the heart rate, the result will be a decrease in the heart rate. Inotropic effects control the force of contraction, not the rate of contraction. Decreased transmitter storage would result in decreased receptor activation. Tachycardia would occur if transmitter availability were increased.

A
Acetylcholine is a neurotransmitter that activates receptors that increase skeletal muscle contraction. Botulinum toxin inhibits the release of this transmitter. It does not interfere with storage, reuptake, or synthesis of acetylcholine.

C
Antihistamines bind to receptors to prevent activation by histamine; this makes antihistamines antagonist drugs. Antihistamines do not activate receptors. Agonist drugs activate receptors; they are not antidotes.

D
Drugs that interfere with termination of transmitter action do so by blocking transmitter reuptake or inhibiting transmitter degradation, resulting in increased receptor activation, because more of the transmitter remains available. Diffusion of the transmitter occurs naturally, but it is a slow process with little clinical significance. Drugs that alter this process cause a decrease in reuptake, not an increase. The effect of drugs that interfere with termination of transmitter action is increased activation.

A
A beta1 agonist increases the patient's heart rate and blood pressure and is used in heart failure. Beta1 agonists would not be used for kidney, respiratory, or liver failure.

B
The sympathetic nervous system does not regulate digestive functions of the body—the parasympathetic nervous system does; further education is needed. The sympathetic nervous system regulates the cardiovascular system, the fight-or-flight response, and the body temperature; no further education is needed.

B
Beta agonists are used for asthma because of their beta2 effects on bronchial smooth muscle, causing dilation. Beta1 effects cause tachycardia and hypertension. Beta receptors do not exert effects on the bladder.

D
Acetylcholine (ACh) is destroyed by acetylcholinesterase, an enzyme that degrades ACh into two inactive products: acetate and choline. Choline is taken up into the nerve terminal. ACh activates three receptor sites: nicotinicN, nicotinicM, and muscarinic. ACh has effects throughout the peripheral nervous system (PNS) and is used at most junctions in the PNS.

C
Norepinephrine (NE) is the most common neurotransmitter released by all postganglionic neurons of the sympathetic nervous system except those going to sweat glands where ACh is the neurotransmitter. NE acts on alpha1, alpha2, and beta1 receptors to increase the force and rate of cardiac contraction, thus increasing cardiac output. ACh would increase sweating. Bronchodilation occurs when epinephrine activates beta2 receptors on bronchial smooth muscle. NE affects alpha1 receptors to dilate the pupils.

B
Cholinergic stimulation by ACh causes increased salivation, increased gastrointestinal (GI) motility, and relaxation of the bladder trigone and sphincter. Anticholinergic medications inhibit these responses, causing dry mouth, constipation, and urinary retention. Alpha-adrenergic agents effect processes in the sympathetic nervous system, causing peripheral vasoconstriction and pupil dilation, among other effects. The effects of beta-adrenergic medications are seen mostly in the heart and blood vessels. The sympathetic nervous system has both cholinergic and adrenergic transmitters.

B
Beta2 activation would result in relaxation of uterine smooth muscle, not contraction; this statement indicates a need for further teaching. Bronchodilation is an effect of beta2 activation; no further teaching is needed. Beta2 activation does result in glycogenolysis; no further teaching is needed. Beta2 activation does result in vasodilation of skeletal muscle; no further teaching is needed.

C
Beta2 agonists cause relaxation of uterine muscle, slowing or stopping the contractions that precipitate labor. An alpha1 agonist would have effects on the heart and arterioles. Anticholinergic drugs generally are given for their effects on the urinary and GI tracts and do not affect uterine muscle. A beta2 antagonist would cause increased constriction of uterine muscle.

D
A beta agonist dilates respiratory smooth muscle, but as a side effect, it can stimulate the heart. A heart rate of 110 beats per minute is a concern, because this medication may further increase the already elevated heart rate. A pulse oximetry reading of 88% is a concern, but the medication causes bronchodilation and increased oxygenation; this should increase the pulse oximetry reading. A blood pressure of 100/60 mm Hg is on the low side, but this medication may actually cause an increase in blood pressure as a side effect; this should not concern the nurse before administration of the medication. A respiratory rate of 28 breaths per minute is elevated; however, this medication should increase oxygenation by bronchodilation, and the patient's respiratory rate should decrease once oxygenation has improved. Therefore, this should not concern the nurse.

B
Pilocarpine is a muscarinic agonist used mainly for topical therapy of glaucoma to reduce intraocular pressure. Pilocarpine is not indicated for the treatment of excessive secretions and mucus; in fact, pilocarpine is used to treat dry mouth. Pilocarpine does not inhibit muscular activity in the bladder. Pilocarpine is not used to prevent hypertensive crisis.

B
Physostigmine is indicated for muscarinic antagonist toxicity. Atropine is a drying agent and would only complicate the drying action that arises from the muscarinic antagonist. An acetylcholinesterase activator would only contribute to dryness that arises from the muscarinic antagonist. Ephedrine is not indicated for muscarinic antagonist toxicity.

A
Bethanechol is contraindicated in patients with active or latent asthma, because activation of muscarinic receptors in the lungs causes bronchoconstriction. It increases the tone and motility of the gastrointestinal (GI) tract and is not contraindicated in patients with reflux. It causes vasodilation and would actually lower blood pressure in a hypertensive patient. It causes dysrhythmias in hyperthyroid patients.

D
Benadryl is an antihistamine, and even though it is not classified as a muscarinic antagonist, it has anticholinergic effects. Giving it with a muscarinic antagonist greatly enhances these effects, so it should not be used. Muscarinic antagonists cause dry mouth, and patients should be taught to use sugar-free gum or candies to help with this. Muscarinic antagonists can cause constipation, and laxatives may be used. Medication applied topically can be transferred to others who come in contact with the skin, so the site should be covered.

C
The transdermal patch is applied weekly and may be the best option for a patient who is more likely to forget to take a daily medication. The transdermal preparation has fewer side effects than the systemic dose, so it is less likely to increase this patient's constipation. The syrup has a high incidence of dry mouth and other anticholinergic side effects. The extended-release tablets must be given daily, and this patient may not remember to take them. PTNS is used after behavioral and drug therapies have failed.

B
This patient is showing signs of antimuscarinic toxicity, caused by the atropine given during surgery. The most effective antidote is physostigmine, which inhibits acetylcholinesterase, allowing acetylcholine to build up at cholinergic junctions and compete with the antimuscarinic agent for receptor binding. Activated charcoal is useful only if an antimuscarinic agent has been ingested, because it impedes absorption from the GI tract. Because this patient's psychotic symptoms are caused by an antimuscarinic agent, physostigmine should be given to treat the cause; an antipsychotic medication would only treat the symptom. Ipratropium bromide is an antimuscarinic agent and would only compound the effects. This patient's respiratory rate is only mildly elevated.

B
Bethanechol is being investigated for treatment for gastroesophageal reflux disease (GERD) because of its effects on esophageal motility and the lower esophageal sphincter. Bethanechol stimulates acid secretion and could intensify ulcer formation. Bethanechol can cause hypotension. Because bethanechol increases the motility and tone of intestinal smooth muscle, the presence of an obstruction could lead to bowel rupture.

C
By blocking muscarinic receptors in the eye, atropine causes paralysis of the iris sphincter, which prevents constriction of the pupil; consequently, the eye cannot adapt to bright light. This also causes an elevation in intraocular pressure, which increases the risk of glaucoma. However, it is not an indication for wearing darkened glasses. Muscarinic agonists cause miosis; atropine causes mydriasis. The effect of relaxing ciliary muscles focuses the eye for far vision, causing blurred vision

D
The dosing for pilocarpine, when used for dry mouth associated with head and neck cancers, is 5 mg three times daily, which may be titrated up to 10 mg three times daily. Tachycardia and constipation are side effects of atropine. Sweating occurs with low doses of pilocarpine. Higher doses, such as this, are associated with the full range of muscarinic effects.

B
Catecholamines undergo rapid degradation by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT). Consequently, they have a brief duration of action, and continuous infusion often is required to maintain the drug's effects. Catecholamines cannot be used orally. Catecholamines do not cross the blood-brain barrier; noncatecholamines do. Noncatecholamines are not degraded by MAO.

B
Dopamine would cause an increase in urine output, because cardiac output is increased as a result of the increase in blood pressure. The effectiveness of dopamine would not be measured by a decrease in pulse, because dopamine's primary effect is to increase blood pressure. Dopamine's effectiveness would not be evaluated by a weight gain. Dopamine's effectiveness would not be evaluated by improved gastric motility.

D
Receptor specificity is relative, not absolute, and is dose dependent. At low doses, selectivity is maximal, and selectivity declines as the dose increases. Dopamine is the only drug in this class that acts on dopamine receptors, but it also has effects on alpha and beta receptors. Epinephrine is the least selective of this class.

B
Epinephrine prolongs absorption of the anesthetic, because it is an alpha1 agonist. It is frequently combined with a local anesthetic for this purpose, so that the amount of anesthetic required may be reduced. Local anesthetics do not induce hypertension; therefore, epinephrine would not be needed to prevent it. Epinephrine does not act as an antiemetic and would not reduce anesthetic-induced nausea. Epinephrine is not used to reduce the pain of an injection.

C
The nurse would be concerned if the patient's peripheral IV were edematous, because this could signal infiltration of the solution into the tissues. Dopamine can cause necrosis if it extravasates. Dopamine is indicated to increase the patient's blood pressure; this blood pressure reading is acceptable. When dopamine is effective at increasing cardiac output, it also causes an increase in urine output. Headache is not a contraindication to the use of dopamine.

A
Tachycardia is a response to activation of beta1 receptors. It can occur when large doses of albuterol are used and selectivity decreases. The nurse should question the patient about the number of inhalations used. Isoproterenol can cause hyperglycemia in diabetic patients. Isoproterenol has more side effects than albuterol. Tremors are an expected side effect and are not an indication for stopping the drug.

A
After using the Epi-Pen, it is important that the individual get medical attention as quickly as possible. The effects of epinephrine fade in 10 to 20 minutes, and the anaphylactic reaction can be biphasic and prolonged. Epinephrine is sensitive to heat, but storing the device in the refrigerator can compromise the injection mechanism; the device should be stored at room temperature in a dark place. Individuals who need an Epi-Pen must have the device with them at all times; any delay in treatment can be fatal, because anaphylaxis can occur within minutes after exposure. The Epi-Pen contains 2 mL of epinephrine, but only 0.3 mL is injected; the device will not be empty with a successful injection.

A
The vasoconstrictive effects of alpha1-adrenergic agonists, such as epinephrine, help produce hemostasis in skin and mucous membranes. These agents can increase blood pressure but are not the primary drugs used except in emergency situations. Alpha1 receptors in the radial muscles of the iris, not vasoconstriction, cause mydriasis. Reflex bradycardia is a side effect and not a clinical use of these agents.

C
Isoproterenol is used for shock because of its actions on beta1 receptors in the heart. It has a positive inotropic effect, which improves cardiac output and thus increases tissue perfusion. Isoproterenol does not affect alpha1 receptors. Although it activates beta2 receptors to cause bronchodilation, this is not indicated for the treatment of shock.

B
Epinephrine is used to treat anaphylactic shock because of its ability to activate multiple adrenergic receptor types. Activation of beta1 receptors helps to increase cardiac output and improve blood pressure as well as suppress glottal edema. Activation of beta2 receptors helps to counteract bronchoconstriction. Activation of alpha1 receptors also causes vasoconstriction, which improves blood pressure. Isoproterenol may also be given parenterally but does not activate multiple receptor types. Other adrenergic agonists, such as albuterol, are more specific to beta2 receptors and have fewer side effects.

A
Although albuterol affects the beta2 receptors, at higher doses it may also activate beta1 receptors, causing an increase in the heart rate. Bronchodilation does not lower the blood pressure, and activation of beta1 receptors actually may increase it. Tachycardia is a common side effect. The inhaled route reduces the likelihood of systemic side effects.

A, B, E
Angina, dysrhythmias, and tachycardia are the most common adverse effects of dopamine; general anesthetics can increase the likelihood of dysrhythmias. Dopamine elevates blood pressure by increasing cardiac output. Diuretics complement the beneficial effects of dopamine on the kidney, so urine output would be increased, not decreased.

C
Cardiac output is decreased as a result of the venous dilation caused by alpha-adrenergic antagonists. Alpha-adrenergic antagonists block alpha1 receptors on arterioles and veins. When alpha1 receptors on arterioles are blocked by alpha-adrenergic antagonists, a direct effect on arterial pressure occurs. When alpha1 receptors on veins are blocked by alpha-adrenergic antagonists, an indirect effect on arterial pressure occurs.

A
Manipulation of the adrenal tumor in patients with pheochromocytoma can cause a massive catecholamine release. Alpha-adrenergic antagonists are given to reduce the risk of acute hypertension during surgery. These agents do not prevent secretion of catecholamines; they block catecholamine receptor sites. They do not act on the tissue of the adrenal medulla. They are given chronically in patients who have inoperable tumors.

C
Because metoprolol may mask the signs of hypoglycemia, the patient should monitor the blood glucose closely and report changes to the prescriber. Metoprolol does have an indirect effect on diabetes mellitus and/or insulin requirements in that it may mask the signs of hypoglycemia, causing the patient to make a healthcare decision based on the drug-to-drug interaction rather than actual physiologic factors. The patient should not increase the insulin, because metoprolol will cause a decrease in blood glucose, increasing the risk of a hypoglycemic reaction. The patient should not reduce the dose of insulin when taking metoprolol, because this might alter serum glucose levels.

C
Orthostatic hypotension is a common side effect of this class of drugs and is most severe with the first dose. Administering the first dose at bedtime eliminates the risk associated with this first-dose effect. Tachycardia is an expected side effect; if severe, it can be treated with other medications. Patients should not drive during the first 12 to 24 hours after taking these agents, because fainting and dizziness may occur, but they may drive after that. Dizziness is not an indication for stopping the drug; patients who experience dizziness are instructed to sit or lie down until symptoms pass.

D
A beta blocker, such as propranolol, should not be given if the pulse is lower than 60 beats per minute; therefore, the nurse should withhold the dose and notify the prescriber. Administering the dose as prescribed would not be appropriate, because the patient's pulse rate is too slow at this time. The dose should be withheld and the prescriber notified. The patient's heart rate is slow, and atropine may be necessary if the bradycardia persists, but the first step is to withhold the dose of propranolol. Withholding the dose and documenting the pulse rate is an appropriate but incomplete nursing intervention. The nurse must notify the prescriber to obtain further orders related to the medication.

D
Phentolamine can cause orthostatic hypotension, reflex tachycardia, nasal congestion, and inhibition of ejaculation. Overdose can produce profound hypotension. When this occurs, blood pressure can be elevated with norepinephrine. Epinephrine should not be used because, in the presence of alpha1 blockade, the ability of epinephrine to promote vasodilation by activation of beta2 receptors may outweigh its ability to cause vasoconstriction, causing further lowering of blood pressure. Norepinephrine does not activate beta2 receptors. Beta blockers may be used to treat severe reflex tachycardia. This patient has significant hypotension, so it is not correct to continue to monitor without notifying the provider.

C
Phentolamine has actions on both alpha1 and alpha2 receptors; it is not selective for alpha1 receptors only. It blocks both epinephrine- and norepinephrine-mediated vasoconstriction. It is used to prevent tissue necrosis after extravasation of drugs such as norepinephrine and other drugs that produce alpha1-mediated vasoconstriction. Side effects include tachycardia and hypotension.

B
The signs and symptoms describe left-sided heart failure, in which the blood normally handled by the left ventricle and forced out through the aorta into the body backs up into the lungs, producing respiratory signs and symptoms. The patient's signs and symptoms are not indicative of bronchoconstriction, which would cause wheezing and diminished breath sounds. Rebound cardiac excitation occurs when the beta blocker is withdrawn, not during administration of the drug. The patient's heart rate is elevated, so sinus bradycardia is not present.

A
Alfuzosin is used for BPH and does not interfere with ejaculation. All of the other drugs have ejaculatory side effects. Prazosin may be useful for BPH, but it is not approved for this use.

B
Blockade of beta1 receptors in the heart reduces cardiac work by reducing the heart rate, the force of contraction, and the velocity of impulse conduction through the AV node. Beta blockers result in bronchoconstriction, not bronchodilation. They do not increase blood flow to the heart. Cardiac output is decreased, not increased.

C
Use of beta blockers during pregnancy can affect a newborn for several days after birth. Newborns are at risk for bradycardia, respiratory distress, and hypoglycemia. Hyperglycemia, hyperthyroidism, and tachycardia are not expected residual effects.

A
Patients taking propranolol can develop heart failure because of the suppression in myocardial contractility. Patients should be taught to watch for signs, which include shortness of breath, night coughs, and swelling of the extremities. Use of these agents with calcium channel blockers is contraindicated, because the effects are identical and excessive cardiosuppression can occur. Shortness of breath should be reported to the provider, but abrupt cessation of the drug can cause rebound cardiac excitability. Propranolol reduces the heart rate and should not be given if the pulse is less than 60 beats per minute.

A
When taken prophylactically, beta blockers can reduce the frequency of migraine attacks. Beta blockers do not provide complete relief from migraines. They do not reduce the duration of migraines. They are not effective for treating a migraine once the migraine has begun.

B, C, E
Adverse effects of alpha blockade include reflex tachycardia, nasal congestion, and hypernatremia. Other adverse effects include orthostatic hypotension and inhibition of ejaculation. Hypertension and ejaculation are not adverse effects of alpha blockade.

A, B, E
Beta blockers are used to treat cardiac dysrhythmias, heart failure, and stage fright. They are used to treat hypertension and hyperthyroidism.

A
Xerostomia is a common side effect of clonidine and is often uncomfortable enough that patients stop using the drug. Counseling patients to chew sugar-free gum and take frequent sips of liquid can help alleviate this discomfort. Drowsiness is common, but this side effect becomes less intense over time. Patients should be counseled to avoid hazardous activities in the first weeks of therapy if they feel this effect. The hypertensive effects of clonidine are not posture dependent, as they are with the peripheral alpha-adrenergic blockers, so orthostatic hypotension is minimal with this drug. Clonidine causes euphoria, hallucinations, and sedation in high doses and can cause anxiety or depression, although the last two effects are less common. The drug should not be stopped abruptly because of the risk of rebound hypertension, so patients experiencing unpleasant central nervous system (CNS) effects should consult their provider about withdrawing the medication slowly.

D
Hepatotoxicity is a serious adverse effect of methyldopa and is an indication for withdrawal of the drug to prevent fatal hepatic necrosis. Jaundice is a sign of liver toxicity. Patients should undergo periodic liver function tests while taking the drug. Liver function usually improves when the drug is withdrawn. A positive Coombs' test result is not an indication for withdrawal of the drug in itself. About 5% of patients with a positive Coombs' test result develop hemolytic anemia; withdrawal of the drug is indicated for those patients. Methyldopa does not have analgesic effects. Xerostomia and orthostatic hypotension are known side effects of methyldopa but usually are not serious.

A
CNS depression, evidenced in this patient by drowsiness, is common in about 35% of the population. These responses become less intense with continued drug use. Orthostatic hypotension is less likely with clonidine, because its antihypertensive effects are not posture dependent. The experience of drowsiness does not indicate abuse potential. The patient should not discontinue the medication abruptly because of the potential for rebound hypertension; the patient should contact the prescriber before stopping the medication.

C
Methyldopa does not reduce the heart rate or cardiac output, so its hypotensive actions are not the result of cardiac depression. The drug is not, in itself, an alpha2 agonist. When taken up into brainstem neurons, it is converted into methylnorepinephrine, which is an alpha2 agonist; it is not effective until converted to this active compound. Its hypotensive effects are the result of vasodilation, not cardiosuppression.

A
Reserpine can produce severe depression, which may persist for months during drug therapy and after the drug is withdrawn. Reserpine can stimulate the secretion of gastric acid, which can cause ulcers; it also can increase the tone and motility of intestinal smooth muscle, which can cause cramps and diarrhea. Reserpine can cause orthostatic hypotension, so patients should be counseled to rise slowly when standing up and to sit or lie down if they feel dizzy. Reserpine works by depleting norepinephrine, and the processes necessary for this may take 1 to 2 weeks.

A
CNS depression is common with clonidine, but this effect lessens over time. Constipation is also a common side effect. Patients who take most of the daily amount at bedtime can minimize daytime sedation. Transdermal forms of clonidine do not alter adverse effects. Patients who are abusing clonidine often experience euphoria and hallucinations along with sedation, but they generally find these effects desirable and would not complain about them to a healthcare provider. Clonidine should not be withdrawn abruptly, because serious rebound hypertension can occur.

A
Patients who abuse cocaine, opioids, and other such drugs also frequently abuse clonidine, so this agent would not be the best choice for this patient. The other drugs do not share this abuse potential.

D
Transdermal patches are to be changed every 7 days. Medication administered by patch has the same therapeutic effect and adverse effects as that given by other routes, except that localized skin reactions may occur and are common with clonidine patches. The patch should be applied to intact, hairless skin on the upper arm or torso.

A
Kapvay ER is used to treat ADHD and is given as a single dose at bedtime. This form of clonidine is not used for hypertension, severe pain, or treatment of Tourette's syndrome.

A, B, C
A positive Coombs' test result occurs in 10% to 20% of patients who take methyldopa chronically. A few of these patients (5%) develop hemolytic anemia. Blood should be drawn for a Coombs' test and an H&H before treatment is started and at intervals during treatment. Because methyldopa is associated with liver disorders, liver function tests should be performed before therapy is started and periodically during treatment. Clonidine, not methyldopa, is contraindicated during pregnancy. A urinalysis is not indicated.

A, B, D
Clonidine has three approved uses: treatment of ADHD, hypertension, and severe pain. It has investigational uses for management of opioid withdrawal and for smoking cessation

A
It is thought that beneficial responses to central nervous system (CNS) drugs are delayed because they result from adaptive changes as the CNS modifies itself in response to prolonged drug exposure, and that the responses are not the result of the direct effects of the drugs on synaptic functions. The blood-brain barrier prevents protein-bound and highly ionized drugs from crossing into the CNS, but it does not slow the effects of drugs that can cross the barrier. Tolerance is a decreased response to a drug after prolonged use.

D
With adaptation of the central nervous system to prolonged exposure to CNS drugs, many adverse effects diminish and therapeutic effects remain. Adaptation helps explain how tolerance and physical dependence occur, as the brain adapts to the presence of the drug. Therapeutic effects can take several weeks to manifest, because they appear to work by initiating adaptive changes in the brain.

A
The blood-brain barrier can prevent some drugs and some toxic substances from entering the CNS. The blood-brain barrier in infants is not fully developed, so infants are more sensitive to CNS drugs and often require lower doses. The blood-brain barrier prevents highly ionized and protein-bound drugs from crossing into the CNS and allows lipid-soluble drugs and those that can cross via specific transport systems to enter.

D
The deficiencies in knowledge about how CNS transmitters and receptors work make systematic development of CNS drugs difficult. Testing in healthy subjects often leads either to no effect or to paradoxical effects. Medical knowledge of the neurochemical and physiologic changes underlying mental illness is incomplete. The development of CNS drugs depends less on knowledge of how the CNS functions and how these drugs affect that process and more on how administering one of these agents leads to changes in behavior.

B
When tolerance develops, a dose increase may be needed, because a decreased response may occur with prolonged use. Psychologic dependence involves cravings for drug effects and does not define tolerance. Physical dependence occurs when the drug becomes necessary for the brain to function "normally," meaning the patient should be weaned from the drug slowly to prevent an abstinence syndrome. Patients may have a decreased sensitivity to drug side effects over time as the brain adapts to the medication.

A
The blood-brain barrier is not fully developed at birth, making infants much more sensitive to CNS drugs than older children and adults. CNS symptoms may include sedation and drowsiness. The first-past effect and GI absorption affect metabolism and absorption of drugs, and renal filtration affects elimination of drugs, all of which may alter drug levels.

B, C, D, E
Acetylcholine and histamines are not monoamines.

A, B, E
CNS drugs have medical uses for pain management, anesthesia, and seizure control. Depression and euphoria are side effects that can contribute to abuse of these drugs.

C
A full therapeutic response with levodopa may take several months to develop. Until the true effect of the dose is seen, it is not necessary to change to another drug, increase the dose, or change the drug regimen.

A
Levodopa combined with carbidopa is the initial drug of choice to treat motor symptoms. Amantadine is the only drug recommended to treat dyskinesias. Entacapone and rasagiline are used to treat abrupt loss of effect, or "off" times. Drug therapy does not slow the progression of the disease.

D
Patients beginning therapy with levodopa/carbidopa should expect therapeutic effects to occur after several months of treatment. Levodopa is so effective that a diagnosis of PD should be questioned if the patient fails to respond in this time frame. Adding a dopamine agonist is not indicated. The "on-off" phenomenon occurs when therapeutic effects are present. Increasing the dose of levodopa/carbidopa is not indicated.

A
This patient is describing abrupt loss of effect, or the "off" phenomenon, which is treated with entacapone or another COMT inhibitor. Amantadine is used to treat dyskinesias. A direct-acting dopamine agonist is useful for gradual loss of effect, which occurs at the end of the dosing interval as the dose is wearing off. Shortening the dosing interval does not help with abrupt loss of effect.

C
Because levodopa activates the chemoreceptive trigger zone (CTZ) of the medulla, causing nausea and vomiting (N/V), the patient may need to take a lower dose temporarily until tolerance develops. A meal helps slow absorption to minimize this side effect. A high protein intake contributes to abrupt loss of effect, so meals should be low in protein. Taking a dose on an empty stomach increases absorption and also N/V. An increased dose with a high-protein snack increases N/V and also abrupt loss of effect. Dopamine increases N/V, because it activates the CTZ of the medulla.

A
Levodopa can cause movement disorders, generally within the first year of therapy. If they occur, a lower dose of levodopa may be required to alleviate them. Clozapine is an antipsychotic used to treat levodopa-induced psychoses. Movement disorders generally occur as the dose of levodopa increases. Surgery is a last option for treating movement disorders, after amantadine fails.

C
Postural hypotension is common early in treatment and can be reduced by increasing the intake of salt and water. An alpha-adrenergic agonist, not an antagonist, can help. Amantadine is used to treat levodopa-induced dyskinesias. Drug holidays are used when adverse effects increase with long-term use of levodopa; the drug holiday allows beneficial effects to be achieved with lower doses, which reduces the incidence of side effects.

D
Adding carbidopa to levodopa does not reduce the incidence of dyskinesias or psychosis. In fact, carbidopa can increase the intensity and the speed of onset of these effects. Carbidopa inhibits decarboxylation of levodopa in the intestine and peripheral tissues, leading to more levodopa in the CNS. Carbidopa cannot cross the blood-brain barrier, so it does not have this action in the CNS. Peripheral side effects are reduced, including nausea, vomiting, and cardiovascular effects.

A
A few patients taking pramipexole have experienced sleep attacks, or an overwhelming and irresistible sleepiness that comes on without warning. Dizziness, hallucinations, and dyskinesias are listed as side effects of pramipexole and other dopamine agonists.

B
Carbidopa inhibits decarboxylation of levodopa in the intestine and peripheral tissues, leading to more levodopa in the CNS. Carbidopa cannot cross the blood-brain barrier, so it does not have this action in the CNS. Carbidopa is not given with high-protein meals. Carbidopa does not have dopamine-like effects. Carbidopa does not affect abrupt loss of effect.

A
Pramipexole has been associated with impulse control disorders, and this risk increases in patients with a history of alcohol abuse or compulsive behaviors. Pramipexole increases the risk of hypotension and sleep attacks, so a history of hypertension or insomnia would not be cautionary. Unlike with levodopa, the risk of psychoses is not increased.

D
Trimethobenzamide can be used as an antiemetic in patients treated with apomorphine. Serotonin receptor agonists (eg, ondansetron) and dopamine receptor antagonists (eg, prochlorperazine) cannot be used, because they increase the risk of serious postural hypotension. Levodopa only increases nausea and vomiting.

C
Bromocriptine is used to treat levodopa-induced dyskinesias and has dose-dependent psychologic side effects. The nurse should suggest reducing the dose of this drug to minimize these side effects. Adding an antipsychotic medication is not indicated. Cabergoline is not approved for this use. Reducing the dose of levodopa/carbidopa is not indicated.

D
To date, there is no definitive proof that any drug can protect dopaminergic neurons from progressive degeneration. Levodopa has shown neuroprotective effects, but studies have demonstrated toxic effects in the doses required for this purpose. MAO-B inhibitors have shown benefits, but only in animal studies. Vitamin E was once theorized to offer this protection, but recent studies have provided good evidence that this is not the case.

B
Rotigotine is a nonergot dopamine agonist, which is given by starting with a 2-mg dose that is increased by 2 mg each week until the lowest effective dose is reached. It should not be stopped abruptly but should be decreased by 2 mg per week until tapered off. It undergoes extensive first-pass metabolism, so it is not given orally and is currently available as a transdermal patch.

B
When amantadine is added to therapy to treat dyskinesias associated with levodopa, it often loses effectiveness after several months. If the effects diminish, they can be restored by either increasing the dosage or by interrupting treatment for several weeks. The maximum dosage of amantadine is 400 mg/day, so it is incorrect to increase the dose. Altered renal function would result in drug toxicity, not ineffectiveness of the drug. It is not necessary to order another drug until determining whether the effectiveness can be restored.

A
Transdermal fentanyl is indicated only for persistent, severe pain in patients already opioid tolerant. Hydrocodone, a combination product, has actions similar to codeine and is not used for severe, chronic pain. Meperidine is not recommended for continued use because of the risk of harm caused by the accumulation of a toxic metabolite. Pentazocine is an agonist-antagonist opioid and is less effective for pain; moreover, when given to a patient who is already opioid tolerant, it can precipitate an acute withdrawal syndrome.

D
Opioid toxicity is characterized by coma, respiratory depression, and pinpoint pupils. Although pupils are constricted initially, they may dilate as hypoxia progresses, which also causes blood pressure to drop. This patient has a respiratory rate of fewer than 12 breaths per minute, dilated pupils, and low blood pressure; the patient also is showing signs of central nervous system (CNS) depression. The nurse should prepare to give naloxone and should watch the patient closely for respiratory collapse. Patients with opioid dependence show withdrawal symptoms when the drug is discontinued. When postoperative patients have adequate analgesia without serious side effects, encouraging patients to turn, cough, and breathe deeply is appropriate. This patient is probably relatively pain free, but providing emergency treatment is the priority.

B
Oxycodone is useful for moderate to severe pain, and a continued-release preparation may give more continuous relief. Dosing is every 12 hours, not PRN. A combination product is not recommended with increasing pain, because the nonopioid portion of the medication cannot be increased indefinitely. This patient does not demonstrate drug-seeking behaviors. Physical dependence is not an indication for withdrawing an opioid, as long as it is still needed; it indicates a need for withdrawing the drug slowly when the drug is discontinued.

C
This patient is developing tolerance, which occurs over time and is evidenced by the need for a larger dose to produce the effect formerly produced by a smaller dose. This patient should be encouraged to request an increased dose. PRN dosing is less effective than scheduled, around-the-clock dosing. The risk of respiratory depression decreases over time as patients develop tolerance to this effect. Benzodiazepines are CNS depressants and should not be given with opioids, because they increase the risk of oversedation.

C
Use of morphine or other opioids during delivery can cause respiratory depression in the neonate, because the drug crosses the placenta. Infants should be monitored for respiratory depression and receive naloxone if needed. Opioids given during delivery do not contribute to birth defects in the newborn. Excessive crying and sneezing and tremors and hyperreflexia are signs of neonatal opioid dependence, which occurs with long-term opioid use by the mother during pregnancy and not with short-term use of these drugs during labor.

C
Opioids can induce spasm of the common bile duct and can cause biliary colic. For patients with existing biliary colic, morphine may intensify the pain. It is important to treat pain, however, and certain opioids, such as meperidine, which cause less smooth muscle spasm, may be given. Ibuprofen is used for mild to moderate pain and is not appropriate for this patient. Nonpharmacologic methods are appropriate when used as adjunctive therapy with an opioid.

D
The classic triad of symptoms of opioid overdose are coma, respiratory depression, and pinpoint pupils. The pupils may dilate as hypoxia worsens, and this symptom, along with continued respiratory depression (fewer than 12 breaths per minute), indicates worsening hypoxia. Fentanyl is a strong opioid, so this is not likely to be a mild overdose, because the patient was wearing two patches. Fentanyl continues to be absorbed even after the patches are removed because of residual drug in the skin, so the drug levels are not likely to be decreasing. The patient does not have improved ventilation, because the respiratory rate is still fewer than 12 breaths per minute.

D
Pentazocine is an agonist-antagonist opioid, and when given to a patient who is physically dependent on morphine, it can precipitate withdrawal. Yawning and sweating are early signs of opioid withdrawal. Pentazocine does not produce euphoria, hypotension, or respiratory depression.

A
Patients using the buprenorphine transdermal patch should be cautioned against heat, heating pads, hot baths, saunas, and prolonged sun exposure. The skin should be cleaned with water only. The patch should stay on for 7 days before a new patch is applied. Patients should remove hair by clipping, not shaving.

A
The nurse should instruct parents not to activate the PCA when their child is sleeping because that can lead to drug overdose. Postoperative pain should be treated appropriately with medications that are effective. Nonopioid medications are not sufficient to treat postoperative pain. Patients should be encouraged to use the PCA as needed so that pain can be controlled in a timely fashion. PRN dosing is not as effective as dosing that is continuous, so a basal dose should be given as well as a PRN dose.

A
Methadone prolongs the QT interval. It does not prolong the P-R interval, cause AV block, or produce an elevated QRS complex.

A
Patients who develop tolerance to opioids will develop tolerance to its analgesic, euphoric, and sedative effects and will also develop tolerance to respiratory depression. Very little tolerance develops to constipation.

A, B, D
Respiratory depression, constipation, and urinary retention are common adverse effects of opioid analgesics. It is important to count respirations before giving the drug and periodically thereafter to make sure that respiratory depression has not occurred. Increased physical activity, increased fluid intake, and increased fiber help alleviate constipation. It is important to assess the patient's abdomen and palpate the bladder to make sure that urinary retention has not occurred. Patients taking morphine often experience hypotension, not hypertension. Methylnaltrexone is given as a last resort to treat constipation, because it blocks mu receptors in the intestine.

B, C, E
Individual effects of morphine may be beneficial, detrimental, or both. Cough suppression is usually beneficial; suppression of bowel motility and vasodilation can be either beneficial or detrimental. Biliary colic and urinary retention are always detrimental side effects.

C
Sexual dysfunction may be managed by having the patient take a drug holiday, which involves discontinuing medication on Fridays and Saturdays. Cutting the tablet in half anytime to reduce the dosage is an inappropriate way to manage drug administration effectively. In addition, it does not describe a drug holiday. The patient should not take the drug every other day, nor should it be discontinued for a week at a time, because this would diminish the therapeutic levels of the drug, thereby minimizing the therapeutic effects. In addition, neither of those options describe a drug holiday.

C
This patient has symptoms of major depression, which include depressed mood, loss of pleasure in usual activities, insomnia, weight loss, and feelings of fatigue. For a diagnosis of major depression, these symptoms must be present most of the day, nearly every day, for at least 2 weeks. Grief and sadness and situational depression are common responses to the death of a loved one, but this patient's symptoms go beyond this normal response. This patient does not show signs of hypomania.

D
Patients with severe depression benefit more from a combination of drug therapy and psychotherapy than from either component alone, so this patient should ask the provider about nondrug therapies. Once a drug has been selected for treatment, it must be used for 4 to 8 weeks before its efficacy can be assessed. Until a drug has been used at least 1 month without success, it should not be considered a failure. Adding a second medication, changing to a different medication, and increasing the dose of this medication should all be reserved until the current drug is deemed to have failed after at least 4 weeks.

C
Patients with depression often think of suicide, and during treatment with antidepressants, these thoughts often increase for a time. Patients whose risk of suicide is especially high should be hospitalized. All antidepressants carry this risk, so changing medication is not recommended. Discontinuing the medication is not recommended. More frequent clinic visits are recommended for patients with a low to moderate risk of suicide.

B
Abrupt discontinuation of selective serotonin reuptake inhibitors (SSRIs) can cause a withdrawal syndrome, so these drugs should be withdrawn gradually. After symptoms are in remission, treatment should continue for 4 to 9 months to prevent relapse; these drugs are not taken indefinitely. It is incorrect to counsel the patient to stop taking the drug without tapering it. Drug holidays are used to minimize sexual dysfunction side effects, not to monitor symptoms.

C
Bruxism is a side effect of SSRIs and can result in headache and jaw pain. Patients who experience these signs should be evaluated for bruxism by a dentist, who can determine whether the patient may benefit from use of a mouth guard. Headache and jaw pain are not signs of extrapyramidal side effects. Discontinuing the antidepressant is not indicated, because depression may return. Stress-relieving methods and relaxation techniques are not recommended, because these symptoms occur during sleep.

D
MAOIs increase 5-HT availability, thus greatly increasing the risk of serotonin syndrome. MAOIs should be withdrawn at least 14 days before an SSRI is started. An SSRI should never be given at the same time as an MAOI. It is not necessary to wait 5 weeks before starting an SSRI.

A
Use of venlafaxine late in pregnancy can result in a neonatal withdrawal syndrome characterized by irritability, abnormal crying, tremor, respiratory distress, and possibly seizures. Poor appetite and disturbed sleep are not part of this withdrawal syndrome. Serotonin syndrome is not likely. Sustained mydriasis occurs as an adverse effect in patients taking the drug.

B
Duloxetine can cause elevation of serum transaminases, indicating liver disease. Patients with existing liver disease or alcohol abuse should not receive this drug. This side effect is not likely with desvenlafaxine or venlafaxine. Escitalopram is an SSRI.

C
TCAs can adversely affect cardiac function, and these effects can be serious in patients with preexisting cardiac impairment. TCAs do block receptors for histamine, acetylcholine, and norepinephrine; they do block the uptake of norepinephrine and 5-HT; and they do have other uses besides depression.

A
For many patients, taking the entire dose of a TCA at bedtime is advantageous for facilitating adherence, minimizing daytime sedation, and promoting sleep. However, older adult patients are at greater risk for cardiotoxicity and may experience intolerable effects on the heart if the entire dose is taken at once; therefore, twice-daily dosing is recommended in the elderly.

C
Orthostatic hypotension can occur with TCAs. Patients should be advised to sit or lie down if they feel lightheaded to prevent falls. Foods containing tyrosine cause adverse effects in patients taking MAOIs. Patients taking TCAs should be counseled to avoid all alcohol. Because TCAs cause sedation, the medication should be taken at bedtime.

C
Patients taking an MAOI should be counseled to follow strict dietary restrictions and to avoid all foods containing tyramine. Patients who consume such foods when taking an MAOI experience a hypertensive episode. Antihypertensive medications, given with an MAOI, will result in hypotension. Grapefruit juice does not alter the metabolism of an MAOI. SSRIs and MAOIs, when administered together, cause a serotonin syndrome

A
Bupropion does not cause weight gain, sexual dysfunction, or sedation, so it may be a useful adjunct to or substitute for an SSRI when those side effects become intolerable. Imipramine causes sedation. Isocarboxazid is an MAOI and is not used unless other drugs are ineffective. Trazodone causes sedation.

A
Women who experience depressive symptoms after childbirth can be screened using a quick test: the Edinburgh Postnatal Depression Scale, which may be administered 6 to 8 weeks after delivery. Reassuring her that her feelings are normal does not acknowledge her concerns; also, without objective screening, this reassurance may not be warranted. Increased sleep and activity may help, but screening is necessary to determine the severity of the depression. Until the patient is diagnosed as having postpartum depression, an SSRI is not indicated.

C
Sertraline is safer than other antidepressants for nursing women when used to treat postpartum depression. It is not necessary for her to stop nursing while taking the medication. Colic and poor weight gain occur with fluoxetine, which is not safe for nursing mothers.

A, B, C
Patients who overdose with a TCA should have cardiac monitoring, because cardiac side effects can occur. Cholinesterase inhibitors are given to counteract anticholinergic side effects. Gastric lavage followed by activated charcoal can reduce absorption of the TCA. Sedative drugs would only increase the sedative effects of the TCA. Procainamide causes cardiac depression and is not recommended to treat TCA dysrhythmias.

A, B, C
Patients who have not responded to SSRIs or TCAs, patients with atypical depression, and patients with bulimia nervosa are candidates for MAOIs. MAOIs contribute to hypotension and therefore are contraindicated in patients with hypotension. MAOIs are not recommended for the treatment of postpartum depression.

A
All beneficial and most adverse effects of benzodiazepines occur from depressant actions in the central nervous system (CNS); the various effects depend on the site of action. Anterograde amnesia is the result of effects in the hippocampus and the cerebral cortex. Benzodiazepines act at multiple sites in the CNS. Muscle relaxant effects are the result of actions on supraspinal motor areas in the CNS. Benzodiazepines promote sleep through effects on cortical areas and on the sleep-wakefulness "clock."

D
Benzodiazepines potentiate the actions of GABA, and because the amount of GABA in the CNS is finite, these drugs' depressive effect on the CNS is limited. Benzodiazepines depress the CNS but not to the extent that barbiturates do. Benzodiazepines are weak respiratory depressants at therapeutic doses and moderate respiratory depressants at toxic doses. Barbiturates mimic GABA; therefore, because they produce CNS depression, this effect is limited only by the amount of barbiturate administered.

D
Flurazepam has a half-life of 2 to 3 hours; however, its metabolite has a long half-life, so giving the drug results in long-lasting effects. Barbiturates, not benzodiazepines, are commonly associated with residual, or hangover, effects. A paradoxical reaction to a sedative would manifest as insomnia, euphoria, and excitation, not drowsiness. Tolerance means that the patient would need increased amounts of a drug to get the desired effects and would not have prolonged effects of the medication.

D
Benzodiazepines are given to ease withdrawal from alcohol because of cross-dependence with these drugs and alcohol, enabling the benzodiazepine to suppress withdrawal symptoms. Alcohol and benzodiazepines can potentiate one another. The benzodiazepine does not potentiate withdrawal symptoms. Benzodiazepines relieve muscle spasms, but this is not why they are given for alcohol withdrawal.

A
This patient is describing complex sleep-related behavior, which occurs when patients carry out complex behaviors while taking benzodiazepines but have no memory of their actions. These actions can occur with normal doses but are more likely with excessive doses or when benzodiazepines are combined with alcohol or other CNS depressants, so the nurse is correct in evaluating this possibility. The duration of the benzodiazepine does not contribute to this phenomenon. Paradoxical effects of benzodiazepines include insomnia, excitation, euphoria, anxiety, and rage. Anterograde amnesia occurs when patients have impaired recall of events that occur after dosing.

C
Patients taking benzodiazepines for anxiety sometimes develop paradoxical responses to the drug, which include insomnia, excitation, euphoria, heightened anxiety, and rage. A missed dose would trigger withdrawal symptoms, which would include anxiety, insomnia, sweating, tremors, and dizziness. Because this is a paradoxical reaction to the drug, a longer-acting drug would make the symptoms worse. This is not caused by overdose, which would manifest as drowsiness, lethargy, and confusion, so a drug level is not warranted.

C
When benzodiazepines are administered IV, severe effects, including profound hypotension, respiratory arrest, and cardiac arrest, can occur. Respiration should be monitored, and the airway must be managed if necessary. Flumazenil [Romazicon] is a competitive benzodiazepine receptor antagonist and is used to reverse the sedative effects but may not reverse respiratory depression. Gastric lavage would not be effective, because the benzodiazepine has been given IV. Without further indication of the ingestion of other drugs, toxicology testing is not a priority.

C
Because time has elapsed, enough medication is present in the system to warrant treatment for systemic effects. A central nervous system stimulant is contraindicated, and intravenous fluids do not address the overdose. Although activated charcoal may assist in absorption of medication in the gut, flumazenil will be effective only for the benzodiazepines. Naloxone, a narcotic antagonist, is not effective for barbiturates and benzodiazepines.

C
Zaleplon [Sonata] works well for people who have trouble falling asleep and, because of its short duration of action, can be taken late at night without causing a hangover or next-day sedation early in the morning. Zolpidem [Ambien] has a longer duration and is a good choice for patients who have difficulty maintaining sleep. Flurazepam has a long duration of action. Trazodone causes daytime grogginess.

A
Phenobarbital and mephobarbital are used for seizure disorders and suppress seizures at doses that are nonsedative. Phenobarbital is a long-acting barbiturate. At therapeutic doses, sedative effects do not occur. Paradoxical drug effects are associated with benzodiazepines and in older adults and debilitated patients with barbiturates.

C
Trazodone is an atypical antidepressant with sedative actions and can be used to prolong sleep duration. It is useful for treating insomnia related to antidepressants such as Prozac. Ramelteon is not a drug of choice to treat patients who have difficulty maintaining sleep. Patients who are depressed or at increased risk for suicide should not take barbiturates, because overdose can readily cause death. Alcohol is contraindicated when taking barbiturates. Alternative remedies have not shown effectiveness in treating insomnia.

B
Research has shown that cognitive behavioral therapy is superior to drug therapy for short-term and long-term management of chronic insomnia in older adults. Alternative remedies have not been proven effective. Barbiturates may elicit paradoxical effects in elderly patients. Triazolam does not help to maintain sleep.

B
Rules for sleep fitness recommend getting out of bed if unable to fall asleep in 20 minutes and doing something relaxing and then returning to bed when drowsy. Eating a large meal will increase insomnia. Drinking alcohol helps some people to fall asleep but causes fragmented sleep. Taking a nap reduces feelings of drowsiness at bedtime.

B, C
Benzodiazepines are indicated to relieve the symptoms of general anxiety and to suppress the central nervous system, thereby suppressing seizures and/or seizure activity. Benzodiazepines cause sleepiness, not sleep deprivation. Benzodiazepines do not cause tardive dyskinesia. Benzodiazepines relax muscles; they do not increase muscle spasms.

A, B, E
Eszopiclone [Lunesta], flurazepam, and extended-release zolpidem [Ambien CR] help with difficulty falling asleep and difficulty maintaining sleep. Temazepam is useful for maintaining sleep only. Triazolam helps with difficulty falling asleep but does not maintain sleep.

A
Furosemide, a potent diuretic, is used when rapid or massive mobilization of fluids is needed. This patient shows severe signs of congestive heart failure with respiratory distress and pulmonary edema and needs immediate mobilization of fluid. Hydrochlorothiazide and spironolactone are not indicated for pulmonary edema, because their diuretic effects are less rapid. Mannitol is indicated for patients with increased intracranial pressure and must be discontinued immediately if signs of pulmonary congestion or heart failure occur.

C
This patient has an irregular, rapid heartbeat that might be caused by a dysrhythmia. This patient's serum potassium level is low, which can trigger fatal dysrhythmias, especially in patients taking digoxin. Furosemide contributes to loss of potassium through its effects on the distal nephron. Potassium-sparing diuretics often are used in conjunction with furosemide to prevent this complication. This patient's serum glucose and sodium levels are normal and of no concern at this point, although they can be affected by furosemide. The oxygen saturation is somewhat low and needs to be monitored, although it may improve with diuresis.

C
Spironolactone is a non-potassium-wasting diuretic; therefore, if the patient has a serum potassium level of 6 mEq/L, indicating hyperkalemia, an order for this drug should be questioned. Bumetanide, furosemide, and hydrochlorothiazide are potassium-wasting diuretics and would be appropriate to administer in a patient with hyperkalemia.

D
Spironolactone takes up to 48 hours for its effects to develop, so it should not be used when the patient needs immediate diuresis. This patient has shortness of breath, crackles, and edema and needs a short-acting diuretic, such as furosemide. Asking the patient about the use of salt substitutes is not indicated. The patient does not need assessment of serum electrolytes.

A
Mannitol is an osmotic diuretic that is used to reduce intracranial pressure by relieving cerebral edema. The presence of mannitol in blood vessels in the brain creates an osmotic force that draws edematous fluid from the brain into the blood. Mannitol can also be used to increase renal perfusion. It can cause peripheral edema and is not used to restore extracellular fluid.

C
Patients taking furosemide should be advised that the risk of furosemide-induced hearing loss can be increased when other ototoxic drugs, such as gentamicin, are also taken. Patients should be told to report tinnitus, dizziness, or hearing loss. Nocturia may be an expected effect of furosemide. Headaches are not likely to occur with concomitant use of gentamicin and furosemide. Urinary retention is not an expected side effect.

A
Hydrochlorothiazide should not be given to patients with severe renal impairment; therefore, an elevated creatinine clearance would cause the most concern. Thiazide diuretics are potassium-wasting drugs and thus may actually improve the patient's potassium level. Thiazides may elevate the serum glucose level in diabetic patients. Thiazides increase LDL cholesterol; however, this patient's levels are low, so this is not a risk.

B
Spironolactone is a potassium-sparing diuretic used to counter the potassium-wasting effects of hydrochlorothiazides. Patients taking potassium supplements are at risk for hyperkalemia when taking this medication, so they should be advised to stop the supplements. Spironolactone takes up to 48 hours to have effects. Salt substitutes contain high levels of potassium and are contraindicated. Spironolactone is a weak diuretic, so the risk of dehydration is not increased.

A, B, E
Thiazide diuretics have the paradoxical effect of reducing urine output in patients with diabetes insipidus. They can also be used to mobilize edema associated with liver disease. They promote tubular reabsorption of calcium, which may reduce the risk of osteoporosis in postmenopausal women. Mannitol is used to treat edema that causes increased intracranial pressure and intraocular pressure.

C
This patient has hypomagnesemia and should be given magnesium sulfate intravenously. The percent of magnesium in solution is correct; however, magnesium should not be infused faster than 1.5 mL/min, so the nurse is correct to question the rate of infusion. Calcium gluconate should be available when magnesium is given, but the nurse needs to clarify the rate of infusion first. Mechanical ventilation is necessary with excessive magnesium. Renal function tests are not indicated.

A
The patient is at risk for respiratory alkalosis as a result of hyperventilation, and giving the patient a gas mixture containing CO2 will help correct the alkalosis. Administering oxygen would worsen the problem. Sodium bicarbonate is given to correct metabolic acidosis. Sedatives may be necessary if initial measures fail.

A
Metabolic acidosis can result from the ingestion of aspirin. The body responds by hyperventilating to reduce CO2, which represents volatile carbonic acid, and raise pH. This child has a rapid respiratory rate in response to metabolic acidosis. In patients with metabolic alkalosis, the body responds with hypoventilation in an effort to increase the CO2 level. Patients with respiratory acidosis usually have retention of CO2 secondary to hypoventilation, and compensation is the result of retention of bicarbonate by the kidneys, which is a slow process. Respiratory alkalosis is caused by hyperventilation; treatment involves having the patient rebreathe CO2 or administering sedatives.

B
Potassium depletion is common with thiazide diuretics, and hypokalemia is especially dangerous for patients receiving digoxin, because the drug can precipitate a fatal dysrhythmia and digoxin toxicity. The provider should be notified of the serum potassium level so that it can be corrected before the digoxin is administered. Giving the digoxin could produce a fatal adverse effect, so this is not an appropriate course of action. Holding the thiazide diuretic will not correct the potassium deficiency. An ECG is not the initial priority.

A patient collapses after running a marathon on a hot day and is brought to the emergency department to be treated for dehydration. The nurse will expect to provide which therapy?
a. Intravenous hypertonic fluids given slowly over several hours
b. Intravenous hypotonic fluids administered in stages
c. Intravenous isotonic fluids given as a rapid bolus
d. Oral electrolyte replacement fluids with potassium

C
Respiratory acidosis results from retention of CO2 secondary to hypoventilation caused either by depression of the medullary respiratory center in the central nervous system (CNS) or by a pathologic lung condition, such as asthma. This child has shallow respirations with evidence of airway obstruction and poor ventilation. Metabolic acidosis occurs in chronic renal failure, loss of bicarbonate with severe diarrhea, metabolic disorders, and ingestion of acids such as salicylates; hyperventilation is a compensatory mechanism. Metabolic alkalosis is usually caused by excessive loss of gastric acid or by ingestion of alkalinizing salts; hypoventilation is a compensatory mechanism. Respiratory alkalosis is produced by hyperventilation and can occur in any condition that increases the respiratory rate and depth.

B
Metabolic alkalosis occurs with excessive loss of acid, such as gastric acid, or an excessive increase in alkalinizing salts. The body compensates for metabolic alkalosis by hypoventilating in an attempt to retain CO2. Metabolic acidosis is usually caused by ingestion of acids or excessive loss of bicarbonate and is compensated by hyperventilation. Respiratory acidosis results from hypoventilation. Respiratory alkalosis is the result of hyperventilation.

A
This patient is taking a potassium-sparing diuretic and is ingesting dietary potassium in salt substitutes. The patient shows signs of hyperkalemia: confusion, shortness of breath, and tingling of the hands and feet. The cardiac effects can be fatal, especially if a patient also is taking digoxin. The most appropriate first action would be to obtain an ECG and serum electrolyte levels to evaluate the extent of the patient's hyperkalemia. The patient does not need increased potassium. Furosemide is a potassium-wasting diuretic and would be helpful. Magnesium sulfate is not indicated. Until the patient's status has been assessed further, intravenous insulin is not indicated.

A
Hypermagnesemia can occur when patients are taking magnesium-containing antacids. Symptoms include muscle weakness, sedation, hypotension, and ECG changes. Aspirin would cause metabolic acidosis. Laxatives can contribute to hypokalemia. Potassium supplements would cause hyperkalemia.

B
Isotonic dehydration should be treated with an isotonic solution of 0.9% NaCl in sterile water. A 0.45% solution or 5% dextrose is used to treat hypertonic dehydration. A 3% NaCl solution is used to treat hypotonic dehydration.

A, C, E
Patients receiving potassium should be monitored for cardiovascular toxicity; an ECG before and during administration can help monitor for this adverse effect. Serum electrolyte levels should be reviewed to make sure the patient is not already hyperkalemic. Because potassium is excreted via the kidneys, it is important to determine that renal function is intact. Intravenous potassium should never be given if the patient has not voided. Patients who are hyperkalemic can be treated with sodium bicarbonate to increase pH and insulin to promote uptake of potassium by cells, but it is not necessary to evaluate the blood gas or glucose levels before administering potassium.

B, C, E
Patients receiving potassium should not receive potassium in solution diluted at more than 40 mEq/L. Diabetic ketoacidosis causes decreased cellular uptake of potassium, and patients in whom acidosis is present should also receive sodium bicarbonate if they need potassium. IV potassium should not be infused faster than 10 mEq/hr. NS with 20 mEq KCl is an appropriate solution for a patient with intact renal function. Oral potassium should be given with a full glass of water to minimize gastrointestinal (GI) effects.

ANS: D
Humoral immunity refers to immunity mediated by antibodies, which are produced by B lymphocytes. Helper T cells have an essential role in antibody production by B cells. The antibody immunoglobulin E plays a role in hypersensitivity reactions. Cytolytic T cells do not produce antibodies; they are key players in cellular immunity

NS: D
The skin is a physical barrier that confers natural immunity. It is not a factor in specific acquired immunity. Cell-mediated and humoral immunity are both types of specific acquired immunity. In specific acquired immunity, each exposure to an antigen evokes a more intense response more quickly. Specific acquired immunity occurs only after initial exposure to an antigen.

ANS: D
The nurse understands that this patient may be vulnerable to opportunistic infections, especially if there were an indication of the HIV conversion to acquired immunodeficiency syndrome (AIDS). A very low helper T lymphocyte count would most concern the nurse, because the helper T cells are essential to the immune system, and people with AIDS have a low or deficient count. A high level of macrophages could indicate an inflammatory response. A low RBC count may indicate anemia. A low neutrophil count can be caused by multiple conditions, but a high count most likely indicates an infection.

ANS: C
Helper T cells have highly specific cell surface receptors that recognize individual antigens. Helper T cells play an essential role in several functions of the immune response. They have an essential role in the production of antibodies by B cells. They carry CD4 molecules on their surface and are also referred to as CD4 cells.

ANS: D
The MHC molecules from one individual are recognized as foreign by the immune system of another individual; therefore, when an attempt is made to transplant organs between individuals who are not identical twins, immune rejection of the transplant is likely. Immunosuppressants are given to counter this response. Antibiotics are used to destroy bacteria. Antihistamines block hypersensitivity reactions. Immune globulins are given to confer passive immunity when specific acquired immunity has not yet developed a response.

ANS: C
When antigens bind to antibodies on mast cells and basophils, chemical mediators of hypersensitivity reactions are released. Although hypersensitivity is an acquired response, mast cells and basophils do not play a role in other acquired responses. An autoimmune response occurs when the immune system fails to discriminate between self and nonself. Transplant rejection occurs when the MHC molecules of the donor are different from those of the patient.

ANS: A
IgD serves as a receptor for antigen recognition on B cells, which is the only place it is found. IgE is involved in hypersensitivity responses and responses to parasites. IgG and IgM are involved in complement responses. IgG crosses the placenta and confers passive immunity on the fetus.

ANS: C
IgA crosses breast milk and, in the GI tract, where it is not absorbed, provides passive immunity to microbes. Infants do not receive protection from hypersensitivity reactions through breast milk. Phagocytes are not transmitted through breast milk. Infants are not protected from respiratory microbes via breast milk.

ANS: C
Lysis of target cells that have been tagged with antibodies is the most dramatic effect of the complement system. Antibodies activate the complement cascade by turning on the classical pathway. C1 cannot bind with free antibodies. Antibody receptors are specific to antigen determinants.

ANS: D
The object of Type IV hypersensitivity (delayed-type hypersensitivity) is to rid the body of bacteria that replicate within macrophages. The macrophage activates the CD4 cell, which in turn activates the macrophage. The other cells listed are not a part of this response.

ANS: B, C, E
The autoimmune response causes the immune system to attack the body's own cells. The hypersensitivity response, mediated by IgE, causes the release of harmful chemical mediators. Recognition of MHC molecules as nonself in a transplanted organ can cause organ rejection. Activation of the complement system causes a cascade of reactions that assist in the immune response. Opsonization is a process that assists with phagocytosis.

ANS: D
The varicella vaccine should be avoided by individuals who are immunocompromised, which includes those infected with the human immunodeficiency virus (HIV) and those who have a congenital immunodeficiency. The DTaP vaccine, Hib vaccine, and polio injection may be administered to immunocompromised individuals, because these are not live vaccines.

ANS: D
Giving analgesic/antipyretic medications before or shortly after vaccines can reduce the immune response, so giving them to prevent pain or fever is not recommended. Children do remember pain, and it is important to provide other comfort measures and to give the injections rapidly. Small needles cause less discomfort, and it is important to reassure the parents about this; however, it is more important to explain why acetaminophen is not recommended. Topical anesthetics are useful before giving the injections, not afterwards.

ANS: C
The rotavirus vaccine product RotaShield was withdrawn because of the high rate of intussusception associated with it. The two products currently on the market—RotaTeq and Rotarix—do not carry a risk for intussusception. Intussusception can be life threatening, so telling parents it is less serious than the disease is incorrect. Intussusception was not merely a coincidental reaction. Herd immunity is not guaranteed.

ANS: B
Children who are immunocompromised should not receive live virus vaccines, including the MMR vaccine and Varivax. Children taking high-dose systemic glucocorticoids are immunocompromised and should not receive the vaccine until therapy is stopped and normal glucocorticoid production returns. The oral polio vaccine (OPV) contains live virus and is contraindicated. Immunoglobulins are not indicated unless children are exposed to the diseases themselves.

ANS: A
Because of concerns about mercury levels, most U.S.-made vaccines contain either zero or very low amounts of mercury. Some multidose vials of flu vaccine still contain thimerosal, but even that is a very low amount. Telling parents that other vaccines contain mercury will increase their suspicion about vaccines and further reduce their trust. Thimerosal is a mercury-based preservative and thus has the same toxicity as mercury. Although it is true that mercury is found in breast milk and other foods, telling parents this belittles their concerns about the vaccines.

ANS: A
Mild reactions to the first dose of the DTaP vaccine are common and most often are manifested by a low-grade fever, fretfulness, drowsiness, and local reactions of swelling and redness. At least 50% of children experience reactions. Seizures are not common. Itchy vesicles do not appear with the DTaP vaccine.

ANS: C
The MMR vaccine can have several adverse effects, including fever up to 103°F; this is not considered a serious effect and does not warrant filing an adverse event report with VAERS. Thrombocytopenia is a rare but serious side effect of the MMR vaccine but is not associated with fever. There is no need to have the parent take the child to the emergency department.

ANS: D
Varicella tends to cause more severe symptoms in adults than in children; adults have a 10-fold greater likelihood of hospitalization and a 20-fold increase in deaths. Chickenpox is highly contagious. Even with herd immunity, because of the degree of contagiousness, spread is likely. Varicella can be serious, even in children.

ANS: A
This infant may have pertussis, for which the primary symptoms are low-grade fever, persistent cough, and runny nose. Infants who have not received the first set of immunizations, including the DTaP vaccine, are especially vulnerable to this disease. The hepatitis B vaccine does not protect against these symptoms. Asking about day care may be important for evaluating exposure, but differentiating between the cough of pertussis and other coughs is best done by determining immunization status. A family history of respiratory disorders may indicate whether the symptoms are related to a chronic lung disease, but these do not usually manifest at 2 months of age.

ANS: B
The HepB vaccine should be administered in the anterolateral thigh in infants and children. The vaccine should be administered in the deltoid of adults and adolescents. The vaccine should not be administered in the deltoid of toddlers, because they have little muscle in that location.

ANS: C
At age 11, both males and females should receive a booster of diphtheria, tetanus, and pertussis (Tdap); the Menactra vaccine against meningitis (MCV4); and the human papilloma virus (HPV) vaccine. A Varivax booster is not recommended at this age. The PCV-23 vaccine is indicated only in high-risk patients. The Td can be given, but a vaccine with a pertussis component is preferred. The MMR is not given at this age. The hepatitis B vaccine is not given at this age.

ANS: D
The MMR vaccine should be postponed in children who have received immunoglobulins, because the immunoglobulin contains antibodies against the viruses in the vaccine. Thrombocytopenia is not a contraindication to the MMR vaccine. A low-grade temperature is not a contraindication. There is no link between receiving the MMR vaccine and the development of autism.

ANS: A
Children who receive the varicella vaccine may sometimes develop a mild, local varicella-like rash within a month of receiving the vaccine. This rash does not indicate that the vaccine was ineffective, and it is not a serious side effect. Because of the association with Reye's syndrome, children should not take aspirin or other salicylates for 6 weeks after receiving the vaccine.

ANS: B
The PCV13 should be given to all children under the age of 2 years and to all healthy children between ages 2 and 5 years, especially those who have conditions such as chronic lung disease that put them at high risk of serious pneumococcal disease. The Hib vaccine is only given up to age 15 months. The Rotavirus vaccine is not given after 32 weeks of age.

ANS: A, D, E
To reduce the risk of transmission, vaccine recipients should temporarily avoid close contact with susceptible high-risk individuals (e.g., neonates, pregnant women, and immunocompromised people).

ANS: B, C, E
Topical anesthetics and tactile stimulation are helpful for minimizing pain associated with vaccine administration, as is giving IM injections rapidly without aspirating. Acetaminophen and ibuprofen are not recommended, because they can inhibit the immune response to the vaccine. Allowing the child to sit up helps minimize pain.

A
Sirolimus is given to prevent rejection in renal transplantation; it has no proof of efficacy in patients with heart, lung, or liver transplants. A serum glucose level is not indicated; patients taking repaglinide for diabetes should be monitored closely while taking cyclosporine. Although antibiotic prophylaxis may be necessary, macrolide antibiotics increase the level of cyclosporine. Tacrolimus is more toxic than cyclosporine.

D
An elevation of BUN and serum creatinine is an indication of nephrotoxicity, which occurs in 75% of patients taking cyclosporine. Hepatotoxicity would cause elevations in liver enzymes, not the BUN and creatinine. Infection would be associated with fever. Organ rejection of a renal transplant would cause elevation in the BUN and creatinine but also would cause tenderness at the graft site and fever.

C
Immunosuppressant drugs increase the risk of infections, especially the BK virus, which can cause renal damage, and other organisms that cause lung infections. Patients taking these drugs must take antibiotics for the first 12 months to help prevent infection. Sirolimus and cyclosporine should be taken 4 hours apart. Patients with diabetes may have trouble with glucose tolerance and require monitoring. Taking cyclosporine and sirolimus increases the risk of renal damage.

A
Macrolide antibiotics, such as azithromycin, can inhibit cyclosporine metabolism, leading to increased levels of the drug. This patient needs either a reduced dose of cyclosporine or a different antibiotic. There is no indication for discontinuing the prednisone during treatment. The dose of cyclosporine would need to be reduced, because azithromycin leads to increased drug levels. There is no contraindication to using acetaminophen.

B
The patient is showing signs of acute organ rejection, which include pain at the graft site, fever, and elevated BUN and creatinine; therefore, intravenous methylprednisolone is indicated. Because the patient is having pain on the right side, along with fever and elevated renal function test results, there is no reason to suspect that the left kidney is failing or that an infection is present. The cyclosporine level is within normal limits.

B
Azathioprine can cause bone marrow suppression, resulting in neutropenia and thrombocytopenia; therefore, a CBC must be evaluated at baseline and periodically thereafter. Patients who have low platelet counts bruise easily, so this symptom should be reported. Alopecia occurs with azathioprine but is not a life-threatening side effect. Fatigue is not a common adverse effect. GI side effects occur but are not life threatening.

B
To prevent toxicity from high drug levels or organ rejection from low levels, blood levels of immunosuppressants should be checked periodically. Immunosuppressants do not prevent infection; they increase the risk of infection. Patients must take immunosuppressants for life. Immunosuppressants do not prevent organ rejection; they help minimize the risk.

B
Cyclosporine and tacrolimus are the most effective immunosuppressants available.

A
Antibodies can be directed against components of the immune system to suppress the immune response and block T-cell function. They inhibit rather than boost immune responses. They do not reduce the proliferation of B cells or suppress interferon production.

C
Basiliximab is used to prevent acute rejection and is administered intravenously.

C
Sirolimus should be used in conjunction with cyclosporine and glucocorticoids to reduce the risk of transplant rejection. Rifampin can reduce and ketoconazole can increase therapeutic levels of sirolimus and cyclosporine; therefore, they are not indicated for transplant patients. Carbamazepine and phenobarbital are not indicated, because they can reduce the therapeutic levels of sirolimus and cyclosporine. Amphotericin B and erythromycin are not indicated, because they can increase the therapeutic levels of sirolimus and cyclosporine.

C
Concurrent use of ketoconazole would warrant a reduction in the dosage of cyclosporine. Ketoconazole often is given concurrently with cyclosporine so that the patient's dosage of cyclosporine, which is costly, can be reduced. Phenytoin would cause a decrease in cyclosporine levels. Prednisone often is given concurrently with cyclosporine to suppress the immune response. Trimethoprim/sulfamethoxazole reduces levels of cyclosporine in the body.

B
Everolimus is not approved in patients younger than 18 years of age. Ketoconazole can decrease the metabolism of cyclosporine and is often given concurrently to allow lower dosing and lower cost. Prednisone and tacrolimus are commonly used, and these doses are correct.

B
Allopurinol delays conversion of mercaptopurine to inactive products and increases the risk of azathioprine toxicity. Patients taking the two concurrently should have an approximate 70% reduction in the azathioprine dose. Altering the allopurinol dose is not indicated.

A
Antihistamines are pregnancy Category C, with debate currently occurring regarding degree of effects on the fetus. They should be avoided unless absolutely necessary. All antihistamines have adverse effects on the fetus. Antihistamines can be excreted in breast milk. The margin of safety of antihistamines in pregnancy is not clear, so these agents should be avoided unless a clear benefit of treatment outweighs any risks

B
Some antihistamines, including dimenhydrinate and promethazine, are labeled for use in motion sickness. Promethazine, however, is contraindicated in children under age 2 years and should be used with caution in children older than 2 years because of the risks for severe respiratory depression. Desloratadine and hydroxyzine are not used for motion sickness.

A
Antihistamines block H1 receptors to prevent the actions of histamine. They do not block the release of histamine. H1 antagonists do not bind to H2 receptors; they do bind to muscarinic receptors. Second-generation antihistamines are more selective than first-generation antihistamines.

A
Severe allergic reactions with symptoms of anaphylaxis are caused by mediators other than histamine, so the benefits of antihistamines are limited. H1 blockers do not block the release of histamine, but this is not why they are not effective in anaphylaxis. Second-generation agents are as effective as first-generation agents in allergic reactions mediated by histamine; neither is effective for treating anaphylaxis

B
Histamine does not mediate cold symptoms, so antihistamines do not provide relief through H1 blockade. Their anticholinergic effects at muscarinic receptor sites can moderately reduce rhinorrhea, so some patients may experience some relief of this symptom. H1-receptor sites do not play a role in cold symptoms. H2-receptor sites do not play a role in cold symptoms. Sedative side effects do not alleviate cold symptoms.

B
Fexofenadine may be given 60 mg twice daily or 180 mg once daily. Fexofenadine does not need to be given with food. Sedation is not a common side effect of fexofenadine. There is no caution to reduce the dosage or increase the dosing interval in patients with renal impairment who take fexofenadine.

C
Promethazine can cause severe respiratory depression, especially in very young patients; it is contraindicated in children younger than 2 years. The medication should not be given as ordered. It is not safe to give the drug and then monitor for bronchoconstriction. The drug is not safe in this age group when given orally.

C
In acute toxicity, patients present with agitation, a flushed face, tachycardia, and uncoordinated movements. There is no specific antidote, so drug removal is the focus of treatment, starting with activated charcoal to absorb the drug, followed by a cathartic to enhance excretion. Atropine would cause an increase in the heart rate. Application of ice packs is recommended for hyperthermia and not for flushing. The child's temperature is normal. Mechanical ventilation is not indicated with this presentation of symptoms, although cardiovascular collapse may eventually develop.

C
Promethazine can cause severe local tissue injury if it extravasates into tissues, so the medication should be administered in an IV that is flowing freely through a large-bore needle. The drug should be administered at a rate of 25 mg/min or less. Dimenhydrinate is indicated for motion sickness, not postoperative N/V. Cardiac dysrhythmias were a concern with two antihistamines no longer on the market, astemizole and terfenadine.

C
Hydroxyzine is a first-generation antihistamine and has sedative effects, so patients should be cautioned not to consume alcohol while taking the drug. In capillary beds, antihistamines reduce edema, itching, and redness. This antihistamine causes sedation. It is not associated with respiratory depression at therapeutic doses.

B
Fexofenadine is the least sedating of the second-generation antihistamines and so is the least likely to have synergistic effects with alcohol. Cetirizine, levocetirizine, and loratadine all have sedative side effects to some extent and thus would be less safe.

A
The child is receiving a low dose of cetirizine and can receive up to 5 mg per day in either a single dose or two divided doses. Cetirizine is available in a chewable tablet, which this child may tolerate better, so the parents should be encouraged to explore this option with their provider. The loratadine 10-mg chewable tablet is approved for children 6 years and older. Fexofenadine would be safe for this child, but it is unlikely that the syrup would be any better than the cetirizine syrup. Desloratadine is not approved for children under the age of 12 years.

A, B, D
The patient is showing signs of acute antihistamine toxicity. Activated charcoal and cathartics are given to absorb the drug and increase excretion. Atropine is not indicated. Lorazepam may be administered for seizures. Second-generation antihistamines are not indicated.

C, D, E
Desloratadine, fexofenadine, and loratadine all have sedative effects classified as low to none. Cetirizine and clemastine have moderate sedative effects.

B
COX-1 inhibitors have beneficial effects of reducing platelet aggregation and thus reducing the risk of myocardial infarction and stroke. COX-2 inhibitors protect against colorectal cancer, reduce inflammation, and reduce fever.

C
Aspirin must be withdrawn at least 1 week before surgery. Aspirin cannot be continued as scheduled, because the risk for bleeding is too great. An interval of 3 days is not long enough for the bleeding effects of aspirin to be reversed. Cutting the dose in half would not reduce the effects of bleeding associated with aspirin use.

B
The differences between the effects of acetaminophen and aspirin are thought to result from selective inhibition of cyclooxygenase; acetaminophen has only minimal effects on cyclooxygenase at peripheral sites, which may explain why acetaminophen does not have adverse GI, renal, and antiplatelet effects. Acetaminophen is a selective COX inhibitor. It is not more similar to opioids than NSAIDs. It is not selective for COX-2.

C
Aspirin (ASA) has analgesic effects for joint pain, muscle pain, and headache, but it is relatively ineffective against visceral pain, including uterine smooth muscle pain, for which NSAIDs are indicated. The risk of Reye's syndrome is associated with the use of ASA in children to treat fever. Increasing the ASA dose to anti-inflammatory levels is useful for rheumatic fever, tendonitis, and bursitis. Acetaminophen is not effective for dysmenorrhea.

D
This patient shows signs of salicylism, which occurs when ASA levels climb just slightly above the therapeutic level. Salicylism is characterized by tinnitus, sweating, headache, and dizziness. Tinnitus is an indication that the maximum acceptable dose has been achieved. Toxicity occurs at a salicylate level of 400 mcg/mL or higher. ASA should be withheld until the symptoms subside and then should be resumed at a lower dose. Increasing the dose would only increase the risk of toxicity. Signs of renal impairment include oliguria and weight gain, which are not present in this patient. This patient has salicylism, not salicylate toxicity, so respiratory support measures are not indicated.

A
The nurse should anticipate giving acetylcysteine, because it is the specific antidote for acetaminophen overdose. It is 100% effective when given within 8 to 10 hours after ingestion and may still have some benefit after this interval. Activated charcoal is effective only if given before the medication is absorbed, so it must be given much sooner. Hemodialysis is not indicated. Respiratory support is used for ASA overdose.

D
This patient shows signs of renal impairment, as evidenced by weight gain despite the use of diuretics, decreased urine output, hypertension, and elevated serum creatinine and BUN. ASA can cause acute, reversible renal impairment and should be withdrawn. Hypertensive medications do not treat the underlying cause. Serum electrolytes are not indicated. Addition of a potassium-sparing diuretic is not indicated.

B
Aspirin poses risks to the pregnant patient and her fetus, including premature closure of the ductus arteriosus. ASA is not safe, especially in the third trimester, because it can cause anemia and can contribute to postpartum hemorrhage. ASA does not induce labor but can prolong labor by inhibiting prostaglandin synthesis. NSAIDs have similar effects and also should be avoided.

A
Aspirin can cause a hypersensitivity reaction in some patients. This may start with profuse watery rhinorrhea and progress to generalized urticaria, bronchospasm, laryngeal edema, and shock. It is not a true anaphylactic reaction, because it is not mediated by the immune system. Epinephrine is the treatment of choice. Patients with sensitivity to ASA often also have sensitivity to NSAIDs; the first indication with this patient is to treat the potential life-threatening effect, not to change the medication. Reduction of the dose of ASA is not indicated, because this reaction is not dose dependent. Antihistamines are not effective, because this is not an allergic reaction.

C
Nonaspirin first-generation NSAIDs carry a risk of hypersensitivity reactions similar to the risk posed by ASA. These agents cause reversible COX inhibition, whereas ASA causes irreversible COX inhibition. NSAIDs do not provide protective benefits for myocardial infarction or stroke, as does ASA. Nonaspirin first-generation NSAIDs do cause suppression of platelet aggregation, but the suppression is reversible.

A
NSAIDs do not cause salicylism and therefore do not cause tinnitus with higher doses. The maximum dose for adults is 3200 mg/day, or 800 mg 4 times/day. Patients taking NSAIDs should be cautioned to limit alcohol intake. Taking NSAIDs with meals helps prevent GI upset.

A
NSAIDs are safe and may be taken while breast-feeding. It is not necessary to use a COX-2 inhibitor while breast-feeding. Narcotics cross breast milk and should be used cautiously while breast-feeding.

B
Diclofenac is available in topical and oral preparations. Patients should be warned to protect treated areas from sunlight. Side effects occur, such as liver toxicity, even with topical dosing. Patients should apply smaller amounts to the upper extremities. Systemic toxicity is lower with topical formulations.

A
Ketorolac is not indicated for chronic or minor pain and should not be used longer than 5 days. Patients discharged home will be instructed to use other NSAIDs for pain. A fixed-dose opioid/NSAID is not indicated. Low-dose ketorolac would not be used, because 5 days would have passed. The intranasal therapy would not be indicated after 5 days.

A
Acetaminophen poses a risk of liver toxicity when taken chronically or in larger doses, especially when combined with alcohol. Patients who drink regularly should be advised to take acetaminophen in low doses and not to exceed 2 gm per day.

A
Glucocorticoids have applications for both endocrine and nonendocrine disorders. Adrenocortical insufficiency requires physiologic, or low-dose, treatment. Pharmacologic doses are used when large doses are required, such as to suppress inflammation. Physiologic doses are used to treat endocrine disorders.

C
When taken in pharmacologic doses, as for inflammatory disorders, glucocorticoids can cause an array of serious adverse effects. When glucocorticoids are given in pharmacologic doses, side effects can occur even when the drugs are taken as prescribed. Interruption of the inflammatory process causes some of the adverse effects. The negative feedback loop does not inhibit side effects.

C
Because of their adrenal suppression, patients taking glucocorticoids long term require increased doses at times of stress and even for a time after stopping the drug until adrenal function returns. This patient's lower blood pressure is an indication that glucocorticoid levels may be depleted. Reducing the dose would only exacerbate the patient's problems. Every other day dosing is used early in glucocorticoid therapy to reduce adrenal suppression, but it would not be useful now. Tapering of doses is used to allow adrenal function to recover as the drug is discontinued.

B
Glucocorticoids have many side effects. They are used because of their multiple mechanisms of action, including their ability to limit tissue damage caused by the inflammatory process and suppression of the immune component of inflammation.

B
Glucocorticoids are used as adjunctive therapy to treat acute exacerbations of rheumatoid arthritis. Glucocorticoids reduce pain and inflammation but do not alter the course of the disease. Oral glucocorticoids produce side effects similar to those of all glucocorticoids, but they are absorbed more rapidly and completely than intra-articular injections. Patients should be warned against overactivity even though their pain has been reduced, because they can further injure their joints.

A
To allow the adrenals to recover, the hydrocortisone dose should be administered before 9:00 AM. The other times are incorrect for oral administration of daily hydrocortisone.

D
Glucocorticoids are contraindicated in patients with a history of systemic fungal infections. Glucocorticoids are used to treat asthma, allergic rhinitis, gout, and seborrheic dermatitis.

B
Calcium and vitamin D supplements can help minimize the patient's risk of developing osteoporosis. A baseline vitamin D level is not recommended. Estrogen therapy can help in postmenopausal women, but its risks outweigh its benefits. Patients should undergo evaluation of the bone mineral density of the lower spine, not skeletal x-rays.

A
High-dose glucocorticoid therapy can cause myopathy, manifesting as weakness. If muscle weakness occurs, the dose should be reduced. Reducing the sodium intake is recommended to minimize sodium and water retention. Muscle weakness is not an expected side effect, because it indicates myopathy. It is incorrect to tell the patient to stop taking the drug, because a glucocorticoid must be withdrawn slowly to allow time for recovery of adrenal function.

A
Because of their mineralocorticoid activity, glucocorticoids can cause sodium and water retention and potassium loss. Asking about the sodium intake can help the nurse evaluate this patient. Although glucocorticoids can affect glucose tolerance, this patient does not have signs of hyperglycemia. Patients with sodium and water retention should be encouraged to increase their potassium intake. Telling a patient to stop taking the drug is incorrect, because a glucocorticoid must be withdrawn slowly to allow time for recovery of adrenal function.

B
Growth retardation can be minimized with alternate day dosing of glucocorticoids. Giving smaller doses does not prevent this effect with long-term therapy. Long-acting glucocorticoids do not prevent this effect. Oral glucocorticoids have the same side effects.

B
This patient shows signs of iatrogenic Cushing's syndrome, which may include serum electrolyte disturbances; therefore, the electrolyte levels should be monitored. Liver function tests, tuberculin skin testing, and vitamin D levels are not indicated.

A
Glucocorticoid therapy can suppress adrenal function, so withdrawal should be done slowly to allow recovery of adrenal function. Reducing the dose of a glucocorticoid by half each day is not recommended. Patients should have their cortisol levels monitored to determine when therapy can be stopped. The withdrawal schedule may take several months. Patients who have stopped the drug may still experience adrenal insufficiency in times of physiologic stress, such as surgery.

A
Glucocorticoid therapy, especially when combined with NSAIDs, can increase the risk of gastric ulcer and possibly GI bleeding. Treatment with antiulcer medications is indicated, but not with OTC antacids, since the provider needs to be aware of this adverse effect. Gastric pain is usually decreased because of the glucocorticoids, so absence of gastric pain is not reassuring. The glucocorticoid should be withdrawn slowly, not immediately.

A
Women who are nursing may take physiologic or low pharmacologic doses of glucocorticoids without achieving concentrations in breast milk that affect the nursing infant. It is not necessary to lower the dose. Since there are negligible levels, there are no effects on the infant. Large pharmacologic doses can cause growth retardation and other adverse effects in the infant.

A, D, E
Glucocorticoids are used topically for allergic rhinitis and are given systemically for gout and ulcerative colitis. They are not useful in anaphylactic reactions, for which epinephrine is the drug of choice, or in bronchiolitis, which generally is induced by a virus, not by an immune response.