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With basiliximab and daclizumab generic 50 mg toprol xl amex, observe for gastro- GI symptoms were often reported in clinical trials order toprol xl 100mg with visa. Although intestinal (GI) disorders (nausea order toprol xl 25mg on-line, vomiting buy generic toprol xl 100 mg on line, diarrhea generic 50 mg toprol xl overnight delivery, heartburn, adverse effects involving all body systems were reported, the abdominal distention) number and type were similar for basiliximab, daclizumab, and placebo groups. With cyclosporine, observe for: (1) Nephrotoxicity (increased serum creatinine and blood This is a major adverse effect, and it may produce signs and symp- urea nitrogen [BUN], decreased urine output, edema, hyper- toms that are difficult to distinguish from those caused by renal graft kalemia) rejection. If it occurs, dosage must be reduced and the patient observed for improved renal function. Also, note that graft rejection and drug-induced nephrotoxicity may be present simultaneously. Nephrotoxicity often occurs 2–3 mo after transplantation and results in a stable but decreased level of renal function (BUN of 35–45 mg/dL and serum creatinine of 2. It usually occurs during the first month, when high doses are used, and decreases with dosage reduction. Do not give a potassium- sparing diuretic as part of the antihypertensive regimen because of increased risk of hyperkalemia. The allergen is thought to be the poly- tension or shock, respiratory distress) oxyethylated castor oil because people who had allergic reac- tions with the IV drug have later taken oral doses without allergic reactions. During IV administration, observe the client continu- ously for the first 30 min and often thereafter. Stop the infusion if a reaction occurs, and give emergency care (eg, epinephrine 1:1000). With infliximab, observe for: (1) Infusion reactions (fever, chills, pruritus, urticaria, chest pain) (2) GI upset (nausea, vomiting, abdominal pain) (3) Respiratory symptoms (bronchitis, chest pain, coughing, dyspnea) f. With leflunomide, observe for: The drug was, in general, well tolerated in clinical trials, with the number and type of most adverse effects similar to those occurring (1) GI upset (nausea, diarrhea) with placebo. With lymphocyte immune globulin, antithymocyte globulin, observe for: (1) Anaphylaxis (chest pain, respiratory distress, hypo- An uncommon but serious allergic reaction to the animal protein tension, or shock) in the drug that may occur anytime during therapy. With methotrexate, observe for: (1) GI disorders (nausea, vomiting, diarrhea, ulcerations, bleeding) (2) Bone marrow depression (anemia, neutropenia, thrombo- Monitor complete blood count (CBC) regularly. Bone marrow cytopenia) depression is less likely to occur with the small doses used for inflammatory disorders than with doses used in cancer chemo- therapy. With muromonab-CD3, observe for: (1) An acute reaction called the cytokine release syndrome This reaction is attributed to the release of cytokines by activated (high fever, chills, chest pain, dyspnea, hypertension, nausea, lymphocytes or monocytes. Symptoms may range from flu-like vomiting, diarrhea) to a less frequent but severe, shock-like reaction that may include serious cardiovascular and CNS disorders. The re- action usually subsides with later doses, but may recur with dosage increases or restarting after a period without the drug. With mycophenolate, observe for: (1) GI effects (nausea, vomiting, diarrhea) GI effects are more likely when mycophenolate is started and may subside if dosage is reduced. The neutropenia may be related to mycophenolate, concomitant medications, viral infec- tions, or a combination of these causes. If a client has neutropenia, interrupt drug administration or reduce the dose and initiate appro- priate treatment as soon as possible. With sirolimus, observe for: Most reactions were common (ie, occurred in >10% of recipients). However, patients were also receiving cyclosporine and a cortico- (1) GI effects—abdominal pain, nausea, vomiting, consti- steroid. With tacrolimus, observe for; (1) Nephrotoxicity—increased serum creatinine, decreased Nephrotoxicity has occurred in one third or more of liver trans- urine output plant recipients who received tacrolimus. Observe for drug interactions Drug interactions have not been reported with the newer bio- logic immunosuppressants (basiliximab, daclizumab, etanercept, infliximab). Drugs that increase effects of azathioprine: (1) Allopurinol Inhibits hepatic metabolism, thereby increasing pharmacologic effects. If the two drugs are given concomitantly, the dose of azathioprine should be reduced drastically to 25%–35% of the usual dose. Drugs that increase effects of cyclosporine: (1) Aminoglycoside antibiotics (eg, gentamicin), antifungals Increased risk of nephrotoxicity. Drugs that decrease effects of cyclosporine: (1) Enzyme inducers, including anticonvulsants (carbamaze- Enzyme-inducing drugs stimulate hepatic metabolism of cyclo- pine, phenytoin), rifampin, trimethoprim-sulfamethoxazole sporine, thereby reducing blood levels.

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Modified from Katz & Pierrot-Deseilligny (1982)((b) buy 50 mg toprol xl mastercard, (c)) and (1998)((d)–(f )) purchase toprol xl 25mg overnight delivery, with permission purchase toprol xl 100mg amex. In addi- possibly due to complete loss of recurrent inhibition tion buy toprol xl 100mg lowest price, Renshaw cells have been shown to receive coupled with other mechanisms generic 50mg toprol xl free shipping, such as extended noradrenergic inhibition from the locus coeruleus susceptibility of motoneurones to Ia excitatory (Fung, Pompeiano & Barnes, 1987), and supraspinal effects (Mazzocchio et al. In the remaining tonic inhibition via serotonergic pathways (Sastry & patients,thesoleusH responsewasreducedbyacute Sinclair, 1976). In any case, increased recurrent inhi- injection of L-Ac (Mazzocchio et al. This change is the opposite of that that observed in normal subjects except that, due to required for abnormal recurrent inhibition to play a the hyperexcitability of the monosynaptic reflex arc, role in the stretch reflex exaggeration of spasticity. In these patients, the chronic intake of Hereditary spastic paraparesis L-Ac reduced the size of H and H , and recurrent max In hereditary spastic paraparesis, the pathology sug- inhibition at rest was then considered to be normal. It is therefore likely that the resulting of L-Ac, the absence of a decay phase in H is unlikely lesion spares more the descending inhibitory path- tobeduetoadecreaseintheAHP,andthisgroupwas ways than the descending facilitatory pathways to considered to have a reduced recurrent inhibition at Renshaw cells and shifts the balance in favour of the rest. Conclusions Amyotrophic lateral sclerosis Only in those patients with slowly progressive para- In amyotrophic lateral sclerosis, the increase in paresis is there evidence for decreased recurrent recurrent inhibition probably reflects pathology inhibition at rest. However, as will be seen below, within the spinal cord rather than the loss of cor- even when recurrent inhibition appears normal ticospinal inputs due to the upper motoneurone at rest, its control during voluntary movements is lesion. In normal subjects, an increase ease with a deficient glycinergic inhibitory system in recurrent inhibition during weak contractions is (see Chapter 5,p. Renshaw cells release bition of H , and a decrease in recurrent inhibi- bothGABAandglycine(Schneider&Fyffe,1992),and tion during strong contractions is inferred from it is possible that the release of GABA is sufficient to greater facilitation of H than of reference H (p. These abnormalities are probably a consequence Conclusions of the lesion interrupting the corticospinal path- way conveying the coordinates for the execution of Changes in recurrent inhibition in normal the movement to Renshaw cells. It is probable that motor control the control of Renshaw cells mediating heterony- mous recurrent inhibition is similarly impaired, no Recurrent inhibition is not a simple negative feed- longer able to oppose unwanted Ia connections. If back to motoneurones and, when its functional role so this would render muscle synergies less flexible, isconsidered,projectionstobothmotoneuronesand and could contribute to the involuntary synkinetic Ia interneurones must be taken into account. During strong flexion–extension movements, Patients with other movement disorders homonymous recurrent inhibition to active moto- neurones is depressed by a descending (probably Patients with a form of cerebral palsy corticospinal) inhibitory control. This: (i) ensures a Recurrent inhibition has been tested in patients high input–output gain for the motoneurone pool, whohadsufferedperinatalbraindamage,producing and (ii) favours a potent depression of antagonis- mental retardation, rigidity and inflexible voluntary tic motoneurones through reciprocal Ia inhibition, and/or postural movements, but without pyramidal, thereby preventing unwanted stretch reflex activa- extrapyramidal or cerebellar signs. It was sug- thelowerlimb,recurrentinhibitionisfacilitatedorat gested that the absence of adaptive changes in least not inhibited. Again, this could serve two roles: recurrent inhibition could partly account for motor (i) to ensure the depression of reciprocal Ia inhi- difficulties experienced by these patients (Rossi, bition necessary to allow parallel activation of the Decchi & Vecchione, 1992). They also monosynaptic Ia excitation in the lower limb, recur- inhibit other Renshaw cells and motoneurones. Thus, the descending control of heterony- mous recurrent inhibition allows the selection of the Methodology appropriate Ia synergism for various postural tasks, by opposing Ia connections that are not required for Useofantidromic motor volleys to activate the chosen task. In most spastic patients with inhibition, and a complex late afferent discharge corticospinal lesions (after stroke or spinal cord in response to the muscle twitch due to the motor injury) homonymous recurrent inhibition is normal volley. However, the ability to modulate recurrent inhibition appropriately for the task being The paired H reflex technique to investigate undertaken is lost. The recurrent IPSP in rones that discharge in the first (H1) reflex will have motoneurones has the short central latency of a theirexcitabilityassessedbythesubsequenttestvol- disynaptic pathway but a long duration (∼40 ms). The test stimulus (SM) is supramaximal for Recurrent collaterals have been found for axons of motoraxonsandproducesanantidromicmotorvol- motoneurones innervating proximal muscles but ley in all motor axons. The H1 conditioning reflex not for axons of motoneurones of distal muscles. They are inhibited by cutaneous ronesthatdischargeinH willbeaffectedbythepost- and group II afferents and by corticospinal vol- spike AHP because these motoneurones discharged leys. There is a striking overlap between the dis- in the H1 conditioning reflex. At conditioning- tribution of heteronymous Renshaw inhibition and test intervals ≥10 ms, Ib inhibition evoked by the Resume´ ´ 189 conditioning volley cannot contaminate recurrent and probably when plateau potentials develop in inhibition. Evidence for recurrent inhibition Comparison with a reference H reflex At low conditioning reflex amplitudes H remains The amplitude of the H test reflex also depends equal to H1, but further increases in H1 result in on any changes in motoneurone excitability in the aprogressive decrease in H , which is related to tested situation. The excitability of the motoneu- the size of the conditioning reflex discharge. This rone pool should be monitored using a control H strongly suggests that, in addition to the AHP, the reflex (reference H) of the same size as H in the con- reflex depression is caused by recurrent inhibition trolsituation. Becauseofchangesinmembranecon- set up by the larger conditioning reflex discharge. Thus, there will have been evidence for a change in recurrent inhibition when there is greater change in the H test reflex than in the reference Pharmacological validation Hreflex: greater facilitation of H reflects decreased Intravenous injection of a cholinergic agonist (L- recurrent inhibition, and greater inhibition of H acetylcarnitine, L-Ac), that does not alter the size increased recurrent inhibition.

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If using information to plan and provide individualized client so toprol xl 25 mg without prescription, what signs and symptoms occurred? It involves both tion is necessary because many people describe minor cognitive and psychomotor skills generic 50mg toprol xl with visa. Unless the nursing process are required for drug therapy proven toprol xl 50 mg, as in the reaction is further explored 25 mg toprol xl with amex, the client may have other aspects of client care buy 100mg toprol xl amex. Try to tablishing goals for nursing care, interventions, and evalu- obtain information to help assess whether the client ation. One might say that assessment and interventions are takes drugs freely or reluctantly, is likely to comply the action phases whereas analysis of assessment data with a prescribed drug regimen, or is likely to abuse and establishing nursing diagnoses and goals are thinking drugs. However, knowledge and informed, rational think- • If long-term drug therapy is likely, can the client afford ing should underlie all data collection, decision-making, to buy medications? Assessment involves collecting data about client characteris- • Are any other conditions present that influence drug tics known to affect drug therapy. For example, all seriously ill clients should be ing and interviewing the client, interviewing family members assessed for risk factors and manifestations of impaired or others involved in client care, completing a physical assess- function of vital organs. Early recognition and treatment ment, reviewing medical records for pertinent laboratory and diagnostic test reports, and other methods. If so, ask for names, how much and how to be especially thorough because the information gained often taken, for how long, their reason for use, and per- may guide the care provided by oneself, other nurses, and ceived benefits or adverse effects. All • In addition to nursing assessment data, use progress available sources of assessment data should be used (eg, client, notes, laboratory reports, and other sources as available family members, medical records). Laboratory tests of liver, kidney, and bone marrow • On initial contact with a client, before drug therapy is function are often helpful because some drugs may started, assess age, weight, health status, pathologic con- damage these organs. Also, if liver or kidney damage ditions, and ability to function in usual activities of daily exists, drug metabolism or excretion may be altered. The effects of these client-related factors on drug Some specific laboratory tests include serum potassium therapy are discussed in Chapter 2. Other data that may CHAPTER 4 NURSING PROCESS IN DRUG THERAPY 49 BOX 4–1 MEDICATION HISTORY Name___________________________________________________________________________ Age_________________________ Health problems, acute and chronic Are you allergic to any medications? Have you had any symptoms or problems that you think are caused by your medicines? Name Dose Frequency Reason How long taken Part 2: Nonprescription Medications Do you take over-the-counter medications? Medication Problem Yes/No Name Amount Frequency Pain Headache Sleep Cold Indigestion Heartburn Diarrhea Constipation Other Part 3: Social Drugs Yes/No Amount/day Coffee Tea Cola drinks Alcohol Tobacco Part 4: Herbal or Dietary Supplements Do you take any herbal or dietary supplements (eg, gingko, glucosamine/chondroitin, kava,)? If so, ask for names, how much and how often taken, reason for use, perceived effectiveness, any adverse effects. In general, nurses must provide care based on available information while knowing that assess- These statements, as developed by the North American Nurs- ment data are always relatively incomplete. As a result, con- ing Diagnosis Association, describe client problems or needs tinued assessment is needed. For example, weigh- text emphasizes those diagnoses that generally apply to any ing seriously ill clients helps in calculating dosages of course of drug therapy. Client teaching as a nursing intervention is presented separately to emphasize its importance. Teaching about Planning/Goals drug therapy is essential because most medications are self- administered and clients need information and assistance to use This step involves stating the expected outcomes of the pre- therapeutic drugs safely and effectively. As a general rule, goals should be stated are given by another caregiver, rather than self-administered, in terms of client behavior, not nurse behavior. Teaching aids to assist the nurse in • Experience relief of signs and symptoms this endeavor include Box 4–2: Preparing to teach a client or • Avoid preventable adverse drug effects caregiver; Client Teaching Guidelines: Safe and effective use • Avoid unnecessary drug ingestion of prescription medications; and Client Teaching Guidelines: • Self-administer drugs safely and accurately Safe and effective use of over-the-counter (OTC) medica- • Verbalize essential drug information tions. Later drug-related chapters contain client teaching • Keep appointments for monitoring and follow-up guidelines for the drugs discussed in particular chapters. These are pre- sented under the heading of Nursing Actions, and rationales Interventions for the interventions are included. Areas of nursing intervention may include assessment, drug ad- vidualizing care.

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With epoetin purchase toprol xl 25 mg without prescription, it takes 2–6 wk for the hematocrit to change after a dosage change buy toprol xl 50mg without prescription. With oprelvekin cheap toprol xl 100mg without prescription, observe for maintenance of a normal or Platelet counts usually increase in approximately 1 wk and con- near-normal platelet count when used to prevent thrombocy- tinue to increase for approximately 1 wk after the drug is stopped cheap 25mg toprol xl visa. With aldesleukin discount toprol xl 100mg line, observe for tumor regression (improve- Tumor regression may occur as early as 4 wk after the first course ment in signs and symptoms). With parenteral interferons, observe for improvement in With hairy cell leukemia, hematologic tests may improve within signs and symptoms. With chronic hepatitis, liver function tests may improve within a few weeks. With intralesional interferon, observe for disappearance of Lesions usually disappear after several weeks of treatment. With darbepoetin alfa and epoetin alfa, observe for nausea, The drugs are usually well tolerated, with adverse effects similar vomiting, diarrhea, arthralgias, and hypertension. With oprelvekin, observe for atrial fibrillation or flutter, In clinical trials, most adverse events were mild or moderate in dyspnea, edema, fever, mucositis, nausea, neutropenia, tachy- severity and reversible after stopping drug administration. Atrial cardia, vomiting arrhythmias are more likely to occur in older adults. With filgrastim, observe for bone pain, erythema at SC in- Bone pain reportedly occurs in 20% to 25% of patients and can be jection sites, and increased serum lactate dehydrogenase, alka- treated with acetaminophen or a nonsteroidal anti-inflammatory line phosphatase, and uric acid levels. With sargramostim, observe for bone pain, fever, head- Pleural and pericardial effusions are more likely at doses greater ache, muscle aches, generalized maculopapular skin rash, and than 20 mcg/kg/d. Adverse effects occur more often with sar- fluid retention (peripheral edema, pleural effusion, pericardial gramostim than filgrastim. With interferons, observe for acute flu-like symptoms Acute effects occur in most patients, increasing with higher doses (eg, fever, chills, fatigue, muscle aches, headache), chronic and decreasing with continued drug administration. Most symp- fatigue, depression, leukopenia, and increased liver enzymes. Fatigue and depression Anemia and depressed platelet and WBC counts may also occur with long-term administration and are dose-limiting effects. With aldesleukin, observe for capillary leak syndrome Adverse effects are frequent, often serious, and sometimes fatal. Capillary leak edema, respiratory distress, gastrointestinal bleeding, renal in- syndrome, which may begin soon after treatment starts, is charac- sufficiency, mental status changes). Other effects may involve terized by a loss of plasma proteins and fluids into extravascular most body systems, such as chills and fever, blood (anemia, space. Signs and symptoms result from decreased organ perfusion, thrombocytopenia, eosinophilia), central nervous system (CNS) and most patients can be treated with vasopressor drugs, cautious (seizures, psychiatric symptoms), skin (erythema, burning, fluid replacement, diuretics, and supplemental oxygen. In addition, drug-induced tumor breakdown may cause hypocalcemia, hyperkalemia, hyper- phosphatemia, hyperuricemia, renal failure, and electro- cardiogram changes. With intravesical BCG, assess for symptoms of bladder These effects occur in more than 50% of patients, usually starting irritation (eg, frequency, urgency, dysuria, hematuria) and sys- a few hours after administration and lasting 2 to 3 d. Drugs that increase effects of sargramostim: (1) Corticosteroids, lithium These drugs have myeloproliferative (bone marrow stimulating) effects of their own, which may add to those of sargramostim. Drugs that increase effects of aldesleukin: All of the listed drug groups may potentiate adverse effects of aldesleukin. Aldesleukin otrexate) is usually given as a single antineoplastic agent; its use in combina- tion with other antineoplastic drugs is being evaluated. What are the hematopoietic, colony-stimulating cytokines, and how do they function in the body? Answer: G-CSF is given to decrease the length and severity of bone marrow suppression after chemotherapy. What are adverse effects of filgrastim and sargramostim, ues (white blood cell count and differential) evaluate the degree and how may they be prevented or minimized? What are the clinical uses of pharmaceutical interleukins In this situation, the nadir (lowest neutrophil count) should be and interferons? What are the adverse effects of interleukins and interferons, bone marrow suppression can affect red blood cells and platelets, and how can they be prevented or minimized? Describe the clinical uses of hematopoietic and immuno- low neutrophil count increases infection risk. Infection in a neu- stimulant drugs in the treatment of anemia, neutropenia, tropenic patient can be life-threatening. Assist clients and family members to identify ders and organ transplantation. Discuss nursing interventions to decrease adverse effects of immunosuppressant drugs.

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