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By: John Alexander Bartlett, MD

  • Professor of Medicine
  • Director of the AIDS Research and Treatment Center
  • Research Professor of Global Health
  • Professor in the School of Nursing
  • Affiliate of the Duke Initiative for Science & Society
  • Member of the Duke Cancer Institute

https://medicine.duke.edu/faculty/john-alexander-bartlett-md

The following clinical problems illustrate the ways in which the dentist can use outcomes information in the treatment planning process and how the patient can use the information to medicine woman dr quinn haldol 1.5 mg online make a treatment decision symptoms 6 days after conception cheap haldol 10 mg amex. Using Outcomes Information in the Treatment Planning Process When Should a Defective Restoration Be Replaced? Research demonstrates that when old restorations are replaced with new ones medicine 3605 purchase haldol 5mg visa, the new restorations tend to treatment multiple sclerosis discount haldol 5 mg with visa be larger and more expensive than their predecessors. Outcomes studies provide some guidance21: · Teeth with obvious recurrent caries should be restored. When faced with the decision as to whether a restoration should be replaced, a review of the relevant outcomes literature provides the practitioner with additional context for the decision, an understanding of the consequences of the available options, and some broad treatment parameters. Such a review will not provide, however, answers to such diagnostic questions as whether active caries exists under an old restoration with open or stained margins. If all the information revealed by careful evaluation and inspection of the tooth fails to resolve that question, then an exploratory repair preparation may be in order. This is a common clinical scenario and it takes on particular importance in the present context because it is also, unfortunately, one of the most common opportunities for overtreatment in dentistry. To be sure, there are compelling reasons for doing a crown on an otherwise heavily restored tooth. A tooth with an obvious fracture line and pain on biting-the classic "cracked tooth syndrome" (see Chapter 6)-is one such example. But in the absence of symptoms, new or recurrent caries, restoration defect, or fracture line in the tooth, is the mere presence of a large direct fill restoration sufficient indication to recommend a crown to a patient? The results that a patient and practitioner anticipate receiving as a result of a course of treatment are outcomes expectations. An outcome expectation is closely linked to both risk assessment and prognosis determination. For example, if the patient remains at risk for new caries and the prognosis for control of the caries is poor, then it follows that the outcomes of treatment can be expected to be unfavorable. Based on sound clinical research, expected outcomes are usually expressed in quantifiable terms, such as the 5-year survival rate for the tooth or the average life expectancy of a restoration. Comprehensive outcome measures for the complete range of dental treatment procedures are not yet available, but some meaningful work has been published and examples of selected findings are discussed later in this chapter. The Role of Outcomes Measures Many treatment decisions are facilitated by knowledge of the likely outcome for each of the proposed treatment alternatives. Such predictions can help the dentist select the best options, refine the list of realistic choices, and serve as an important adjunct to the presentation of the treatment plan to the patient. This information could be even more important to the patient who attempts to weigh the pros and cons of the various treatment options. The most valuable outcomes information for the patient would be the success rate for a specific procedure when performed by the practitioner who is proposing to do the treatment. Unfortunately, these data are usually not formally tracked and therefore are not available. Chapter 2 Evidence-Based Treatment Planning 45 To answer this question, the dentist will need to evaluate several parameters: · What is the stability and viability of the current restoration? Past history of the tooth and restoration in question is most often a good predictor of longevity and future success. In other words, if the current restoration has been in the mouth for many years and there have been no negative outcomes, then it is more likely that there will be a continuing track record of success if the restoration is retained. Severe attrition, loss of vertical dimension, and heavy lateral or incline forces on the tooth all increase the probability of tooth fracture and therefore increase the probable benefit of crowning the tooth. Certainly a patient with a recent history of multiple tooth fractures is at greater risk for future fractures. Ultimately the treat versus no treat decision must be made by the patient following the consent discussion. In most situations, when the patient presents with a diseasefree and asymptomatic tooth that has a large direct fill restoration, there will not be a compelling argument for placing a crown, but the patient should nevertheless be made aware of the treatment options and the benefits and deficits of the options-including any negative sequelae that may arise with either choice-and the probability of those negative sequelae. Here is an instance in which good outcomes data-especially those data that reflect what occurs under similar clinical conditions-can be very helpful to the patient trying to weigh the options and decide whether or not to proceed with a crown at this time. Conventional wisdom has encouraged the replacement of missing teeth when posterior tooth loss has created a space surrounded by remaining teeth.

However given the great uncertainties on the in vivo activity of radiation-associated genomic instability already noted in this chapter medicine bow wyoming discount 1.5mg haldol, the adaptive mechanism suggested by Mitchel and others (2003) is regarded as being highly speculative medications nursing haldol 5mg free shipping. Published genetic catalogs (McKusick 1998; Mulvihill 1999) show that around 6% of recorded human disorders and mutant genes have some degree of association with neoplastic disease symptoms 9 weeks pregnancy generic haldol 10 mg line. The number of such disorders for which the association is unambiguously strong remains small (less than 50) and tends to medications list a-z order haldol 5 mg free shipping be restricted to rare autosomal recessive and autosomal dominant diseases. Highly expressing autosomal dominant diseases usually manifest as familial cancer, often without other major clinical features. Autosomal recessive diseases tend to be more rare, and excess cancer is usually accompanied by other characteristic clinical features. Since their manifestation demands a genetic input from both parents, these disorders do not typically express as familial cancer. In summary, while these more recent data on adaptive responses for radiation-induced tumorigenesis may act as a focus for further research, they do not provide coherent evidence of the generality of this mechanism and its importance for judgments on low-dose cancer risk. Indeed, family pedigrees providing evidence of strongly expressing predisposition, particularly to colon carcinoma, were published in the early part of the 1900s, but it was not until the development of molecular genetic techniques in the 1970s that the whole field of human cancer genetics began its rapid development. Since the 1970s the generality of this crucial association has been much more firmly established by a combination of clinical, epidemiologic, and molecular genetic approaches. The first objectives of this section are to outline the data that relate to (1) cancer-prone human genetic disorders determined by strongly expressing genes, (2) less strongly expressing cancer-associated genes, and (3) the evidence available on radiosensitivity and predisposition to radiation tumorigenesis. The principal conclusions from these reviews will then be applied in the development of judgments on the identification of human subgroups having potentially increased cancer risk after radiation and the likely magnitude of that increased risk. In developing these judgments, particular attention will be given to the uncertainties involved. In considering the examples given in Tables 3-3 and 3-4, a number of general points can be added to the descriptions. Second, there are general clinical and medical genetic features of the cancer-prone disorders of Tables 3-3 and 3-4 that are important for the judgments to be developed. For autosomal dominant human mutations of cancer to be detected readily in the population via family studies, the Copyright National Academy of Sciences. This increased mutational load will tend to increase cancer risk, albeit with differing degrees of expression among tissues. Given that, on average, spontaneous cancer incidence in the general population is around 30%, the information currently available is restricted largely to mutations where the cancer in question is expressed at a high relative frequency in gene carriers. Other features of importance are (1) the organ specificity of many cancer-predisposing mutations, (2) the age of onset of given neoplasms in gene carriers that usually occurs at younger ages than in noncarriers, (3) the frequent occurrence of multiple tumors in gene carriers, and (4) the substantial variation for cancer risk between carriers of a given gene mutation, suggestive of major influences from the genetic background and/or life-style of the host. The crucial point, to be developed later, is that current knowledge of heritable cancer susceptibility in humans is restricted largely to relatively rare mutations of high penetrance. Cancer may be regarded as a multifactorial disorder (see Chapter 4), and genetic views developed from the study of other multifactorial conditions, such as coronary heart disease, suggest strongly that there will be many more variant cancer genes having lower penetrance than those listed in Tables 3-1 and 3-2. The current lack of knowledge about the nature, frequency, and impact of such genes imposes fundamental limitations in respect of the objectives stated earlier. Mechanistic Aspects of Genetically Determined Radiation Response In making judgments on the radiation response of cancer-prone individuals it is valuable to consider first the theoretical expectations that follow from current knowledge of the cellular mechanisms that are likely to be involved in cancer susceptibility. Accordingly there is no expectation of increased genome-wide sensitivity to the mutagenic effects of radiation. In these instances increased radiation cancer risk may be anticipated on the basis of the now well-supported hypothesis of Knudson (1986). In brief, there is good evidence that many tumor-suppressor type genes act as tissue-specific gatekeepers to neoplastic pathways (Kinzler and Vogelstein 1997). Since loss or mutation of both autosomal copies of such genes from single cells is believed to be rate limiting for the initiation of neoplastic development, tumor initiation in normal individuals is expected to be a rare cellular event. A carrier of a germline mutation in a given tumor-suppressor gene will however show loss of function of one such gene copy, thus "unshielding" the second copy in all target somatic cells. The lifetime risk of spontaneous loss or mutation of that second copy from any given population of target cells will be relatively high-hence the often dramatic increase in organ-specific cancer risk. There is also a clear expectation that exposure of the carrier individual to ionizing radiation or indeed other genotoxic carcinogens would, via the same genetic-somatic mechanism, result in a greater-than-normal risk of organ-specific cancer.

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The benign prostatic hyperplasia registry and patient survey: study design symptoms 4-5 weeks pregnant buy haldol 1.5mg online, methods and patient baseline characteristics medications prednisone 10 mg haldol sale. A double-blind placebocontrolled study evaluating the onset of action of doxazosin gastrointestinal therapeutic system in the treatment of benign prostatic hyperplasia symptoms 0f food poisoning discount 10mg haldol with mastercard. Alpha1-adrenergic receptors and their inhibitors in lower urinary tract symptoms and benign prostatic hyperplasia treatment glaucoma generic haldol 1.5 mg. Safety and efficacy of alfuzosin 10 mg once-daily in the treatment of lower urinary tract symptoms and clinical benign prostatic hyperplasia: a pooled analysis of three double-blind, placebo-controlled studies. Diagnostic effect of an improved preembedding method of prostate needle biopsy specimens. Association of cigarette smoking, alcohol consumption and physical activity with lower urinary tract symptoms in older American men: findings from the third National Health And Nutrition Examination Survey. Concordance rates and modifiable risk factors for lower urinary tract symptoms in twins. Re: Body size and serum levels of insulin and leptin in relation to the risk of benign prostatic hyperplasia. Association between serum concentrations of micronutrients and lower urinary tract symptoms in older men in the Third National Health and Nutrition Examination Survey. Associations of obesity with lower urinary tract symptoms and noncancer prostate surgery in the Third National Health and Nutrition Examination Survey. Increased oxidative stress with gene alteration in urinary bladder urothelium after the Chernobyl accident. Acute urinary retention due to benign prostatic hyperplasia in a 23-year-old patient. Inverse expression of uroplakins and inducible nitric oxide synthase in the urothelium of patients with bladder outlet obstruction. Serum sialic acid and prostate-specific antigen in differential diagnosis of benign prostate hyperplasia and prostate cancer. Association between captopril, other antihypertensive drugs and risk of prostate cancer. Durability and cost-effectiveness of transurethral needle ablation of the prostate as an alternative to transurethral resection of the prostate when alpha-adrenergic antagonist therapy fails. Comparative gene and protein expression in primary cultures of epithelial cells from benign prostatic hyperplasia and prostate cancer. Lower urinary tract symptoms and sexual dysfunction: additional evidence of an association. Update on the relationship between sexual dysfunction and lower urinary tract symptoms/benign prostatic hyperplasia. Development and validation of four-item version of Male Sexual Health Questionnaire to assess ejaculatory dysfunction. Effects of alfuzosin 10 mg once daily on sexual function in men treated for symptomatic benign prostatic hyperplasia. Page 201 108840 161540 102460 119050 138260 165330 153230 101630 101470 132030 124000 154220 130720 102950 127850 109070 155500 September 2010 Appendix 3: Master Bibliography American Urological Association, Inc. A practical guide to the evaluation and treatment of male lower urinary tract symptoms in the primary care setting. Curvilinear transurethral ultrasound applicator for selective prostate thermal therapy. Longterm impact of superinfection by hepatitis G virus in hepatitis C virus-positive renal transplant patients. A study on the outcome of percutaneous transluminal renal angioplasty in patients with renal failure. Decision aids for benign prostatic hyperplasia: applicability across race and education. Immunoexpressions of p21, Rb, mcl-1 and bad gene products in normal, hyperplastic and carcinomatous human prostates.

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Subramaniam treatment 3rd nerve palsy discount 1.5 mg haldol amex, Hamsa medicine 1900s spruce cough balsam fir buy discount haldol 10mg, Generose Mulokozi medications similar to vyvanse cheap 1.5 mg haldol amex, Zo Rambeloson treatment improvement protocol discount haldol 5 mg on line, Rolf Klemm, and Christina Nyhus Dhillon. For instance, vitamin A supplementation coverage from Demographic and Health Surveys usually underestimates true coverage, because the timing of the survey in relation to the vitamin A supplementation distribution impact maternal recall (Hodges et al. Discrepancies may be noted between different data sources, based on whether information was collected prior to or following a supplementation campaign. Industrial food fortification refers to adding micronutrients and minerals to industrially processed and widely consumed edible products (Allen et al. Common fortified foods, for example, include salt; wheat and maize flours; edible oils; and sugar, but can also include bouillon cubes or soy sauce. Foods fortified with iron will likely have the highest impact on anemia, although foods fortified with other nutrients, such as vitamin A and folic acid, may also be important. One advantage of industrial food fortification is that it requires limited changes in consumer behavior compared to other micronutrient interventions. You should consider the quality and coverage of industrial food fortification in the population, and whether it is reaching those who need it the most. Young children may not consume sufficient quantities of industrially fortified foods to meet their micronutrient needs and, thus, additional micronutrient interventions may be needed for this population. In addition, industrial food fortification may not reach populations who do not have access to markets; therefore, you should consider the reach of products to communities in rural or hard-to-reach areas. Small-scale fortification-for example, hammer mills to grind small batches of maize in East Africa-may, theoretically, fall under fortification legislation, but feasibility, compliance, and enforcement may be very limited. Depending on the fortification interventions in your country, these indicators may or may not be relevant for all food vehicles. To understand the policy environment for industrially fortified foods, review the legislation governing the fortification of food in the country to determine if it is mandatory, voluntary, or neither. If a law mandates fortification, or if fortification is voluntary, then the industries fortifying foods must ensure that their food meets the fortification standards. Fortification standards establish the levels (or ranges) of micronutrients expected to be found in the final packaged foods. Look for additional data from a governmental regulatory agency on external quality control results to establish, for example, the number of metric tons of adequately fortified wheat flour in the last year. The website or annual reports of the ministry governing the program may post summary data on how adequate the fortification of foods is at the production and retail levels. Qualitative methods add reagents that indicate the presence of micronutrients by forming a colored compound. Quantitative methods use procedures like spectrophotometry for iron in wheat flour; high-performance liquid chromatography for vitamin A in flour, sugar, and oil, and water soluble vitamins (thiamin, riboflavin, niacin and folic acid) in foods; and, microbiological assays for folic acid and vitamin B12 in fortified foods. A fortification rapid assessment tool is often conducted before a fortification program is implemented; it can be used with complementary monitoring data to understand reach and potential dietary impact of implementation. Once a fortification program is underway, you need to quantify the contributions of micronutrients from the different fortified foods to the diets of the population. The tool is used in population-based surveys to assess the coverage of fortifiable and fortified foods purchased or consumed at the household and individual level, and to test household food samples for their nutrient content. Household-level consumption of a particular fortified food may also be found through consumer expenditure surveys, or other nationally or regionally representative datasets. These datasets vary from country to country, but it is often possible to add fortification-relevant questions to existing surveys or survey collection systems to understand the functioning of a food fortification program. Household surveys like Demographic and Health Surveys, Multiple Indicator Cluster Surveys, and household consumption and expenditure surveys may also collect information on the purchase or consumption of fortified and fortifiable foods. The Food Fortification Initiative is a comprehensive source of data on fortification policies, fortification practices, industry information, and nutrient deficiencies across most countries ( These data may only be available directly from the industries fortifying the foods, if at all. Because of market competition, most industries do not share their production data. The quality of the data from these regulatory agencies can vary, based on the resources they have to carry out production-level monitoring.

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