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Drugs that alter effects of 5-HT3 receptor antagonists: (1) Atenolol and cimetidine increase effects of dolasetron The drugs decrease dolasetron metabolism and clearance buy 100mg celecoxib with mastercard. Philadelphia: Lippincott Answer: When giving very emetogenic drugs discount celecoxib 200mg with mastercard, it is important to Williams & Wilkins buy 200 mg celecoxib. Springhouse buy cheap celecoxib 100 mg line, PA: Springhouse Cor- antiemetics work in different ways buy 100 mg celecoxib otc, so they can be used in com- poration. Supportive care: Controlling chemotherapy-induced and Review and Application Exercises postoperative nausea and vomiting. Are antiemetics more effective if given before, during, or York: McGraw-Hill. Describe major types of antineoplastic drugs interventions to prevent or minimize adverse in terms of mechanism of action, indications drug effects. Manage or assist clients/caregivers in manag- surgical treatment, and with radiation therapy. Critical Thinking Scenario Georgia Sommers, a 39 year-old mother of 4, is diagnosed with breast cancer that was detected by routine mammography. She is recovering from a modified radical mastectomy when she comes to the clinic to dis- cuss additional treatment with chemotherapy with the oncologist. He explains that she will receive combina- tion therapy with three drugs on a cycle of every 4 weeks. The normal cell cycle is the interval between the birth of a cell and its division into two daughter cells (Fig. Oncology is the study of malignant neoplasms and their treat- The daughter cells may then enter the resting phase (G0) or ment. Drugs used in oncologic disorders include those used to proceed through the reproductive cycle to form more new kill, damage, or slow the growth of cancer cells, and those used cells. Normal cells are also well differentiated in appearance to prevent or treat adverse drug effects. In- ment modality for cancer, along with surgery and radiation stead, they occupy space and take blood and nutrients away therapy. They grow in an uncontrolled fashion characteristics of cancer are described below. They are undifferentiated, which means they have lost the structural and functional character- NORMAL AND MALIGNANT CELLS istics of the cells from which they originated. They are loosely connected, so that cells break off from the primary Normal cells reproduce in response to a need for growth or tumor and invade adjacent tissues. Loose cells also enter tissue repair and stop reproduction when the need has been blood and lymph vessels, by which they circulate through the 913 914 SECTION 11 DRUGS USED IN SPECIAL CONDITIONS mutations of normal growth-regulating genes called proto- G0 oncogenes, which are present in all body cells. Normally, proto-oncogenes are active for a brief period in the cell re- G1 productive cycle. When exposed to carcinogens and genetically altered to oncogenes, however, they may operate continuously and cause abnormal, disordered, and unregulated cell growth. Unregulated cell growth and proliferation increases the prob- ability of neoplastic transformation of the cell. Tumors of the breast, colon, lung, and bone have been linked to activation of oncogenes. M S Tumor suppressor genes (anti-oncogenes) normally func- tion to regulate and inhibit inappropriate cellular growth and proliferation. Abnormal tumor suppressor genes (ie, absent, damaged, mutated, or inactivated) may be inherited or re- sult from exposure to carcinogens. When these genes are in- activated, a block to proliferation is removed and the cells begin unregulated growth. One tumor suppressor gene, p53, G2 is present in virtually all normal tissues. When cellular de- oxyribonucleic acid (DNA) is damaged, the p53 gene allows Figure 64–1 Normal cell cycle. The normal cell cycle (the interval be- time for DNA repair and restricts proliferation of cells with tween the birth of a cell and its division into two daughter cells) in- volves several phases. Mutations of the p53 gene, a common ge- 0 usual functions except replication; that is, they are not dividing but are netic change in cancer, are associated with more than 90% of capable of doing so when stimulated. Different types of cells spend small-cell lung cancers and more than 50% of breast and different lengths of time in this phase, after which they either reenter colon cancers. Mutant p53 proteins can also form complexes the cell cycle and differentiate or die. During the first active phase (G1), with normal p53 proteins and inactivate the function of the ribonucleic acid (RNA) and enzymes required for production of de- oxyribonucleic acid (DNA) are developed.

The answer is not to get rid of all 67 THE A–Z OF MEDICAL WRITING these uncommon words completely buy celecoxib 200mg cheap, but to make sure that we use the right language for our audience cheap celecoxib 100mg without a prescription. Jokes It is difficult to make these work in the unforgiving black and white of the printed word discount 100mg celecoxib with amex. Journalese Doctors often use this word as a general term of abuse for vulgar and sensational writing cheap 100 mg celecoxib with amex. Journalism At its worst the hounder of innocent princesses and enemy of sensible government order celecoxib 200 mg visa. At its best the exposer of unprin- cipled villains and deposers of evil regimes. Whether you love it or loathe it, the practice of journalism provides some useful lessons for those wishing to learn how to communicate effectively (see tabloids). It also provides major opportunities for putting out important public health messages (see press releases). BOOKLIST: journalism • The fight for public health, by Simon Chapman and Deborah Lupton, London: BMJ Books, 1994. Written by two experienced campaigners it shows how the mass media, if understood and used properly, can put across immensely powerful public health messages. This book tries to explain how doctors can learn to write for magazines and newsletters rather than journals. Professional exposition of how to write feature articles for newspapers and magazines. Journals All over the world thousands of journals are published each year, most run by commercial organizations, but some in partnership with professional associations. They contain a blend of material, such as editorials, review articles, letters, obitu- aries and news, but what distinguishes them from magazines is that they include scientific papers sent out for peer review. More recently, through the development of peer review, they have played a key role in validating science (and scientists). In the last few years electronic publishing has challenged a number of assumptions, such as the fact that space to publish is limited and that reviewing can be done only before publication. One of the most likely scenarios seems to be the increasing use of electronic publishing to validate science, and (with luck) the return of journals to their original purpose of communicating exciting advances of knowledge. Whatever happens, the need to understand effective writing will not go away. BOOKLIST: journals • Journal publishing by Gillian Page, Robert Campbell and Jack Meadows, Cambridge: Cambridge University Press, 1997. Unlikely to help anyone with their writing problems, but will delight the fans of peer review. Published to mark the retirement of Stephen Lock as editor of the BMJ, this book has a range of provocative and entertaining articles on all aspects of medical 69 THE A–Z OF MEDICAL WRITING journals. It is particularly interesting to look back at how Richard Smith, the current editor, predicted the development of journals. Journalology The word used to describe the study of matters of interest to editors of learned journals. Key words These are the half dozen or so words that you need to include with an article in order to aid electronic retrieval. Terms from the medical subject head- lines (MeSH) list of Index Medicus should be used. Kill fee If a commissioned article is returned unused authors will sometimes receive a kill fee to compensate them for the time spent (see commissioning). Latin education Not a good preparation for those who want to be able to write effective contemporary English. Finally, Latin is no longer a developing language and therefore can encourage the delusion that language has immutable rules (see pub test). Law of late literals At least one mistake in every piece of writing will be discovered once it is too late to do anything about it. The only consolation is to think of all the things you did get right (see proofreading; spelling). Lawyers It is usually best to avoid their interventions (see copyright; libel) – but beware falling into the trap of defensive writing. Lay person A put-down by those in one group to describe members of another. The difference is usually made to seem greater than it is by the use of jargon.

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Do not give between cancer chemotherapy 14 d before and 24 h after cytotoxic chemotherapy buy cheap celecoxib 100 mg on line. Sargramostim (GM-CSF) After bone marrow transplanta- Bone marrow reconstitution purchase 200 mg celecoxib mastercard, (Leukine) tion to promote bone marrow IV infusion over 2 h order celecoxib 200mg overnight delivery, 250 function or to treat graft fail- mcg/m2/d buy celecoxib 200 mg low price, starting 2–4 h ure or delayed function after bone marrow infusion cheap celecoxib 100 mg with amex, Mobilization of stem cells in and continuing for 21 d peripheral blood so they can Graft failure or delay, IV infusion be collected. Course of treatment may be re- peated after 7 d off therapy if engraftment has not occurred. Mobilization of stem cells, SC or IV over 24 h, 250 mcg/m2/d CHAPTER 44 HEMATOPOIETIC AND IMMUNOSTIMULANT DRUGS 659 Drugs at a Glance: Hematopoietic and Immunostimulant Agents (continued) Generic/Trade Name Indications for Use Routes and Dosage Ranges Comments Interleukins Aldesleukin (interleukin-2) Metastatic renal cell carcinoma IV infusion over 15 min Adverse reactions are common (Proleukin) in adults* 600,000 IU or 0. Oprelvekin (Neumega) Prevention of severe thrombocy- SC, 50 mcg/kg once daily Start 6–24 h after completion of topenia with antineoplastic chemotherapy and continue chemotherapy that depresses until postnadir platelet count bone marrow function in is 50,000 cells/mm3 or clients with nonmyeloid malig- higher, usually 10–21 d. Give all doses three times weekly, with at least 48 h between doses Interferon beta-1b (Betaseron) Same as Interferon beta-1a SC, 0. Repeat once weekly for 6 wk, then give one dose monthly for 6–12 mo (TICE BCG) or one dose at 3, 6, 12, 18, and 24 mo (TheraCys). AIDS, acquired immunodeficiency syndrome; ANC, absolute neutrophil count. These genes are then inserted Some newer formulations (eg, darbepoetin alfa, pegfil- into bacteria (usually Escherichia coli) or yeasts capable grastim, and peginterferon alfa 2b) can be given less of producing the substances exogenously. An additional consideration is that the sub- genes that encode interferons, for example, has made it stances are powerful biologic response modifiers and possible to produce large amounts of these substances they can cause unanticipated adverse effects. Exogenous drug preparations have the same mecha- terferon beta-1b) are synthetic versions of deoxyribonu- nisms of action as the endogenous products described cleic acid (DNA) recombinant products. Despite extensive research efforts, relatively few surfaces of immature blood cells in the bone marrow cytokine-like drugs are available for clinical use. One and increase the number, maturity, and functional abil- of the difficulties in using cytokines is maintaining ef- ity of the cells. Interferons, called alfa, beta, or gamma fective dose levels over treatment periods of weeks or according to specific characteristics, also bind to spe- months. During a natural immune response, inter- cific cell surface receptors and alter intracellular activ- acting body cells produce adequate concentrations of ities. In viral infections, they induce enzymes that cytokines around target cells. However, achieving ad- inhibit protein synthesis and degrade viral ribonucleic equate local concentrations from injected, exogenous acid. CHAPTER 44 HEMATOPOIETIC AND IMMUNOSTIMULANT DRUGS 661 In addition to their antiviral effects, interferons also with chronic renal failure, and peak plasma levels occur in have antiproliferative and immunoregulatory activities. They can increase expression of major histocompatibil- ity complex (MHC) molecules, augment the activity of Colony Stimulating Factors natural killer (NK) cells, increase the effectiveness of antigen presenting cells in inducing the proliferation Filgrastim and sargramostim are drug formulations of gran- of cytotoxic T cells, aid the attachment of cytotoxic ulocyte colony stimulating factor (G-CSF) and granulocyte T cells to target cells, and inhibit angiogenesis. Because macrophage colony stimulating factor (GM-CSF), respec- of these characteristics, the interferons are used mainly tively, produced by recombinant DNA technology. In chronic he- used to stimulate blood cell production by the bone marrow in patitis C, interferon improves liver function in approxi- clients with bone marrow transplantation or chemotherapy- mately 50% of clients, but relapse often occurs when induced neutropenia. The drugs are being in- mote growth of blood vessels (angiogenesis) in clients with vestigated for additional uses. The drug apparently promotes growth are usually well absorbed, widely distributed, and elim- of arterioles around blocked areas in coronary arteries. In cancer, the exact mechanisms by which interferons because arterioles are larger and can carry more blood. However, their immunostimulant effects are thought to enhance activities of immune cells (ie, NK Interleukins cells, T cells, B cells, and macrophages), induce tumor Aldesleukin (Proleukin) is a recombinant DNA version of cell antigens (which make tumor cells more easily rec- interleukin-2 (IL-2). It differs from native IL-2 but has the ognized by immune cells), or alter the expression of same biologic activity (eg, activates cellular immunity; pro- oncogenes (genes that can cause a normal cell to change duces tumor necrosis factor, IL-1, and interferon gamma; and to a cancer cell). It is used to treat metastatic renal cell cancer of the urinary bladder by stimulating the im- carcinoma and melanoma and is being investigated for use in mune system and eliciting a local inflammatory re- other types of cancer. The drug is given by IV infusion, after sponse, but its exact mechanism of action is unknown. They are given by subcutaneous (SC) or intravenous spaces and eliminated by metabolism in the kidneys. Darbe- have had organ transplantation or those with serious cardio- poetin alfa (Aranesp), epoetin alfa (Epogen), filgrastim vascular disease (eg, an abnormal thallium stress test, which (Neupogen), oprelvekin (Neumega), and the interfer- reflects coronary artery disease) or serious pulmonary disease ons are often self- or caregiver-administered to ambu- (eg, abnormal pulmonary function tests). They may produce adverse effects so that clients do not icity during earlier courses, including the following: feel better when taking one of these drugs.

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In general cheap celecoxib 200 mg amex, researchers are interested in assignable variation because they can link—or assign—variation to a single specific cause and act accordingly purchase celecoxib 200 mg. This type of variation is generally easy to measure given the widespread training of healthcare quality researchers in statistical methods purchase celecoxib 200mg with mastercard, breadth of tests and criteria for determining whether variation is assignable or ran- dom buy celecoxib 100mg free shipping, and increasing sensitivity and power of numerical analysis buy cheap celecoxib 100mg on-line. Measurement of assignable variation, however, is subject to potential mis- understanding because of complexity of design and interpretation, partic- ularly in understanding true variation versus artifact or statistical error (Powell, Davies, and Thomson 2003; Samsa et al. Process Variation Our discussion uses three different categories of variation of quality in med- ical practice. The first of these is process variation, which is the difference in procedure throughout an organization. In this case, for example, one might measure the degree to which physicians use various screening meth- ods for colorectal cancer. Some might prefer fecal occult blood testing, others might elect to use sigmoidoscopy or colonoscopy, and yet others might prescribe a combination of these tests. It is essential to distinguish between process and technique, however, the latter being the multitude of ways in which any given procedure can be performed within the realm of acceptable medical practice (Mottur-Pilson, Snow, and Bartlett 2001). Outcome Variation Another category is outcome variation, which is the difference in the results of any single process. This is ultimately what most healthcare quality researchers and medical practitioners want to know: which process yields the optimum results (Samsa et al. In some cases, this is easily deter- mined, as the results of a particular process can be observed in relatively short order or procedural changes can be undertaken in a timely fashion. Unfortunately, genuine outcome variation requires study over an extended period, often years or decades, and many studies labeled as outcome research are largely process research. This threshold, or best practice, is the standard 46 The Healthcare Quality Book against which all other measurements of variation are compared, although some key analytical tools, such as statistical process control, do not directly address performance relative to a gold standard. Without knowing what is optimal, assignable vari- ation is merely descriptive and of little value. Without some concept of a best practice, process variation offers little beyond an enumeration of meth- ods to fulfill some task. Without a threshold value, outcome variation reveals only what happened over time, not the desirability of a particular outcome. Performance variation tells us where we are and how far we are from where want to be, as well as suggests ways to achieve the desired goal. Variation in Medical Practice The language of quality improvement in medical practice suggests a sub- jective and occasionally pejorative view of variation. Standard procedures, operating protocols, flowcharts, prescriptive guidelines, handbooks, and checklists are all intended to reduce or eliminate variation and hence the potential for error or excessive costs (Mottur-Pilson, Snow, and Bartlett 2001). There is also a widespread tendency to assume that variation implies ranking, that measures reflect quality and that variations in the measures reflect variations in quality (Powell, Davies, and Thomson 2003). This interpretation results from the attribution of causality between the processes of care provided and the observed quality measures—high measured per- formance reflects good actual performance, and low measured perform- ance reflects poor actual performance. In many cases, this link between variation and quality is valid, but far too many times the link is tenuous at best, subjective, and not always supportable by research focused on the relation between process and outcome of care. Variation, however, can be a profoundly desirable goal, as a successful procedure that differs from other, less successful procedures is by defini- tion a variation. The objective, then, for quality improvement researchers is not simply to identify variation but to determine its value. If variation reveals a suboptimal process, the task at hand is to identify how the varia- tion can be reduced or eliminated in ways that focus on the variation rather than the people involved. If the variation is good or desirable, it is essen- tial to understand how can it be applied across an organization in an effort to improve quality more broadly. Put plainly, understanding the implica- tions for quality of variation in medical practice is not simply learning how to eliminate variation per se but learning how to improve performance by identifying and accommodating good or suboptimal variation from a pre- defined best practice. V ariation in Medical Practice and Implications for Quality 47 Scope and Use of Variation in Healthcare The origins of quality assessment in healthcare in the United States can be traced to the pioneering work of Ernest A. Codman and the Mayo broth- ers during the early twentieth century (Codman 1984, 1996; Mallon 2000). Over the next ten years, the Joint Commission on Accreditation of Healthcare Organizations (Joint Commission 2003), U. Preventive Services Task Force (2003), National Quality Forum (2002), and Centers for Medicare & Medicaid Services (CMS 2003a) produced explicit indicators for quality measures. Quality researchers use a variety of categories to measure improve- ments and detect variation in quality of care, including fiscal, service, and clinical indicators. Hospital-based clinical indicators, for example, incor- porate those derived from the CMS Seventh Scope of Work measures and other advisory directives and include indicators pertaining to acute myocar- dial infarction (AMI), community-acquired pneumonia, and congestive heart failure (CMS 2003a).

Once the sources of variance have been identified order 100mg celecoxib otc, the next step is to determine how the underlying neuronal population contributes to those variances buy celecoxib 200 mg line. Since a par- ticular component of variance can arise from several di¤erent underlying neuronal firing patterns (Deadwyler et al celecoxib 100 mg without prescription. First buy celecoxib 100mg with mastercard, there will be at least some neurons that encode the input features to the ensemble buy celecoxib 200 mg low cost, especially in cases where the identified source(s) reflect prominent dimensions of the stimulus or task (i. However, other components of the ensemble may reflect interactions between dimensions, such as the occurrence of a particular response at a particular time in a particular direction. Because there could be more than one way in which the popula- tion could encode such information, it is necessary to understand how individual neurons fire with respect to relevant dimensional features of the task. The three-dimensional graph shows individual neurons (horizontal axis at left), versus time during a DNMS trial. The phases of the DNMS trial are SR, response on the sample lever; NR, response on the nonmatch lever. Each neuron responds with an increased firing rate to di¤erent features or events within the trial. No single neuron is capable of encoding the total information in the task, nor does straightfor- ward examination of the ensemble firing rate lead to derivation of the encoded infor- mation, since each neuron does not always fire during all trials. However, by combining statistical extraction methods applied to the total population of recorded neurons with categorization of individual cell types, the nature of the encoding pro- cess is gradually revealed. The 3-D histograms illustrate several neurons with either sample or nonmatch phase selectivity. The trials were divided according to whether the sam- ple response was to the left (left trial) or right lever (right trial), but there was no dis- tinction in phase responses of these neurons with respect to position. The raster diagram at the top right shows a single, nonmatch, cell with elevated firing only at the nonmatch response, irrespective of response position. This encoding of the DNMS phase by single neurons underlies the di¤erential encoding of the task phase by the ensemble, as shown by the discriminant scores at the bottom right. Further allocation of variance revealed a complementary set of neurons that encoded response position irrespective of DNMS phase. Ensembles of 10–16 neurons were recorded from the rat hippocampus and analyzed via canonical discriminant analysis (Deadwyler et al. The greatest percent of variance (42%) was contributed by a discriminant function (DF1) that di¤erentiated the sample from the nonmatch phase. The graph at the bottom right shows the maximum separation of discriminant scores for DF1 at the sample response (SR) and nonmatch response (NR) events, with scores near zero during intertrial interval (ITI), delay, and last nosepoke during the de- lay (LNP). There was no significant di¤erence in firing at left (left trial) or right (right trial) lever positions. The three-dimensional histograms at the left depict the firing of 12 neurons, 6 sample (toward the lower right) and 6 nonmatch (toward the upper left). Note that the same neurons were active during sample or nonmatch phases on both trial types. The rastergrams (top right) show the activity of a single nonmatch cell. The trials are represented by rows, with each dot indicating a single action recorded potential. Note that the same neurons were active during the sample phase of one trial, but also during phase of the other. The single trial rasters at the top right show the firing of a single left posi- tion cell during both sample and nonmatch responses at the left, but not the right, position. The discriminant scores therefore also selectively reflected ensemble encod- ing of response position in the DNMS task. Note that the variance sources contributing to this ensemble activity clearly encoded information consistent with the features or events of the DNMS task. This is not a necessary outcome of the discriminant analysis because there may be sources of variance encoding other sensory, attentional, or motivational features of the task. However, in each case, once a source of variance is identified, it should be possible to identify single neurons that contribute to that variance, and hence demonstrate the same encoding features. The existence of such unexplained components can be a helpful indicator of the task-relevant firing correlates within a particular behavioral paradigm.

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