By D. Lester. New World School of the Arts.
Availability (particularly alongside curiosity) buy luvox 50 mg with mastercard, anticipation of effects 50 mg luvox with amex, youth culture and current fashions regarding substance use each play a role in young people’s experimentation with drugs. For the majority of people, experimentation is confined to those drugs which are socially acceptable. Experimentation with substances does not automatically lead onto recreational drug use or, indeed, dependent use and may cease once the initial motivating factors have been satisfied. The following characteristics of experimental use have been identified: y Curiosity and risk taking are deemed the primary motive y Mood altering effects are secondary to the ‘adventure’ of drug use itself y The young people may try more than one substance but usually not more than a few times. As with any drug use by young people, experimental use can be an enormous source of concern; but Morgan (2000) notes that: “… risk factors are not always negative in nature, especially in the case of experimental drug use. This is illustrated in a longitudinal study by Shedler and Block (1990) who collected information on personality and adjustment from five years upwards. Their results showed that, at least in the American context of the time, those adolescents who engaged in mild experimentation with cannabis were relatively better adjusted (less anxious particularly) than those who had never experimented while frequent users were the least well adjusted. This phase is characterised by: y regular use y group activity y use over a longer period of time 12 Stages of Drug Use The key here is that control is exerted over use, with specific choices being made in relation to what drugs are used, in what amount, where they are used (normally in specific situations) and when. As users become schooled in what drugs give the effect they desire in different situations, their substance use develops a degree of predictability and, generally, is not perceived to be problematic. What is at play here is a combination of personal and social checks and balances which moderate and sanction drug use. However, this does not mean that recreational drug use comes without its own dangers. The predominant experience of recreational drug use in Ireland obviously relates to alcohol given its centrality of place in our culture; but this does not mean that what is socially permissible comes without health risks. Recreational or social use has particular emphasis on the peer group, its influence, its networks and a sense of belonging. The following have been identified as the characteristics of social use: y Social acceptance is the primary motive. Emotional Use – Generative Or Suppressive These two patterns of social drug use centre on the purposeful manipulation of feelings, emotions and behaviour with an aim to elicit or inhibit certain behaviours and feelings. With this type of drug use, the adolescent is now generally seeking the mood swing. The following have been identified as the characteristics of emotional use, which is generative or hedonistic in nature: y To have fun is the primary motive. The following have been identified as the characteristics of emotional use which is suppressive or compensatory in nature: y To cope with stress and uncomfortable feelings is the primary motive. Habitual This next stage of use sees an increasing concentration on the drug use at the expense of other interests which, in turn, can contribute to a range of problems. Dependent Use The definitions given in the preceding section on habitual use cover the factors involved in dependent use. The key factors of dependent use compared to other stages of substance use would be: y Lack of control over substance use y Ongoing use regardless of the awareness of potential or actual problems experienced y Use in hazardous situations y The damage caused in terms of health, relationships, social commitments and legal implications One of the key factors in building up effective, meaningful dialogues with young people about their health behaviours and the decisions they make about drug use is the ability to understand what motivates the different types of drug use and the subjectively positive, desired outcomes as well as the negatives. Responses which ignore the significance of the peer group and the subjective pleasures derived from drug use by young people are unlikely to have any impact in terms of education and prevention. This could be seen to present an obstacle to adults working with young people as their apparent lack of vernacular drug terms may appear to undermine both teachers’ effectiveness and credibility. The challenge is how to capture the meaning, nuance and intonation of words and phrases used by the young people you work with. However, as with all dictionaries of slang, the problem is that once a phrase has been dignified by print, its usage and meaning will often change and be replaced by a new term. You are far less likely to undermine your credibility by asking pupils you teach to explain the phrases and slang-terms they use than if you misuse a slang term appropriated from youth culture by the adult world. Another advantage of adopting this approach is that it affords an opportunity to explore the depth and range of the pupils’ drug knowledge which can assist the teacher in determining the appropriate level of drug education. The following diagram8 shows the three factors at play which im pact on all stages of drug use. Another area to consider when discussing drug use is the inter- relatedness of the wide range of drug-related factors that can influence attem pted or com pleted suicide. So for example, there are very different levels of risk attached to a male adult drinker consuming four bottles of lager in a pub to a 16 year old female consuming the same four bottles of lager at a party. Person Factors – Adolescent Development “[It’s] not that teens are stupid or incapable … it’s sort of unfair to expect them to have adult levels of organisation skills or decision-making before their brain is finished being built. However, equal im portance m ust be attached to looking at adolescence itself and how the developm ent of young people’s autonom y and distinct identities can influence and im pact on a range of behaviours. Bobby Sm ith, Consultant Child and Adolescent Psychiatrist, South Western Area Health Board “Adolescence is one of many stages during the lifecycle. During this period, a person moves from a state of major dependence on the family towards a state of being able to operate as an independent functioning adult in society. The key change that permits this progression is a development in cognitive functioning.
Central to each of these “expanded —Legitimately seen as purely academic question paradigms” is the role for follow-up: deciding when a pa- —Suggests it is not worth time for follow-up tient is acutely ill and required hospitalization order luvox 50mg with mastercard, versus rela- ● High frequency of symptoms for which no deﬁnite tively stable but in need of careful observation cheap luvox 100mg online, watching for diagnosis is ever established complications or response after a diagnosis is made and a —Self-limited nature of many symptoms/diagnoses —Nonspeciﬁc symptoms for which no “organic” etiology treatment started, monitoring for future recurrences, or even ever identiﬁed simply revising the diagnosis as the syndrome evolves. One key un- —Patients busy; inconvenient to return —Cost barriers answered question is, To what extent can we judge the Œ Out-of-pocket costs from ﬁrst visit can inhibit return accuracy of diagnoses based on how patients do over time Œ Perceived lack of “value” for return visit or respond to treatment? In other words, if a patient gets —If improved, seems pointless better and responds to recommended therapy, can we as- —If not improved, may also seem not worthwhile sume the treatment, and hence the diagnosis, was correct? A partial list of ● “Information breakage” despite return to original setting/ such complexities is shown in Table 3. What coproduction of diagnosis really should mean —What follow-up surveillance is required and how to is that the patient is a partner in thinking through and testing interpret results the diagnostic hypothesis and has various important roles to ● Diagnosis of cure or failure to respond play, some of which are described below. Building dialogue into the clinical diagnostic process, Should I, as the physician of each of the actual patients whereby the patient tells the practitioner how he/she is cited above, have “taken a better history” and uncovered doing, represents an important premise. Each level, doing so demonstrates a degree of caring that extends emerged only through subsequent follow-up. It have asked more detailed probing questions during my ﬁrst is impossible to exaggerate the amazement and appreciation encounter with the patient? Shouldn’t I have asked fol- of my patients when I call to ask how they are doing a day low-up questions during the initial encounter that more or a week after an appointment to follow up on a clinical actively explored my differential diagnosis based on (what problem (as opposed to them calling me to complain that ideally should be) my extensive knowledge of various dis- they are not improving! The old tools—ad hoc Carefully reﬁned signals from downstream feedback repre- fortuitous feedback, individual idiosyncratic systems to track sent an important antidote to a well-known cognitive bias, patients, reliance on human memory, and patient adherence to anchoring, i. For experience, an uphill battle at best, lack the power to provide example, upon learning that a patient with a headache that the intelligence needed to inform learning organizations. What was initially dismissed as benign was found to have a brain is needed instead is a systematic approach, one that fully tumor, the physician works up all subsequent headache involves patients and possesses an infrastructure this is hard patients with imaging studies, even those with trivial histo- wired to capture and learn from patient outcomes. Thus, potentially useful feedback on the patient with a than such a linking of disease natural history to learning orga- missed brain tumor is given undue weight, thereby biasing nizations poised to hear and learn from patient experiences and future decisions and failing to properly account for the rarity physician practices will sufﬁce. Edwards Deming came Division of General Medicine into a factory, one of the ﬁrst ways he improved quality was Brigham and Women’s Hospital to stop the well-intentioned workers from “tampering,” i. As he dramatically showed with his classic funnel the sponsor of this supplement article or products discussed experiment, in which subjects dropped marbles through a in this article: funnel over a bull’s-eye target, the more the subject at- Gordon D. By overreacting to this random variation each time the target was missed, the subjects 1. Diagnosing diagnostic errors: If each time a physician’s discovery that his/her diagnos- lessons from a multi-institutional collaborative project. Overconﬁdence as a cause of diagnostic error in diagnosis, he/she vowed never to order so many tests, our medicine. Learning from malpractice claims about negligent, adverse events in diagnostic decision making is perhaps doing more harm primary care in the United States. It suggests a critical need to noses in the ambulatory setting: a study of closed malpractice claims. Judgment under uncertainty: heuristics and emperor’s clothes provide illusory court comfort. The pull system mystery explained: drum, buffer and Presented at: Annual Meeting of the Healthcare Management Di- rope with a computer. From the historical perspective, there is substan- many of these strategies show potential, the pathway to ac- tial good news: medical diagnosis is more accurate and complish their goals is not clear. Advances in the medical sciences enable has been done while in others the results are mixed. Innovation in have easy ways to track diagnostic errors; no organizations are the imaging and laboratory sciences provides reliable new ready or interested to compile the data even if we did. More- tests to identify these entities and distinguish one from over, we are uncertain how to spark improvements and align 1 another. It is perfectly ap- on overconﬁdence as a pivotal issue in an effort to engage propriate to marvel at these accomplishments and be thank- providers to participate in error-reducing strategies, this is just ful for the miracles of medical science. My goal in this commentary is nized discussion of what the goal should be in terms of to survey a range of approaches with the hope of stimulating diagnostic accuracy or timeliness and no established process discussion about their feasibility and likelihood of success. In This requires identifying all of the stakeholders interested in the history of medicine, progress toward improving medical diagnostic errors. Besides the physician, who obviously is at diagnosis seems to have been mostly a passive haphazard the center of the issue, many other entities potentially in- affair. Every day and are healthcare organizations, which bear a clear responsi- in every country, patients are diagnosed with conditions bility for ensuring accurate and timely diagnosis. Further- ful, however, that physicians and their healthcare organiza- more, patients are subjected to tests they don’t need; alter- tions alone can succeed in addressing this problem. Despite our best intentions to make diag- the help of another key stakeholder—the patient, who is nosis accurate and timely, we don’t always succeed. Patients are Our medical profession needs to consider how we can in fact much more than that. Goals that funding agencies, patient safety organizations, over- should be set, performance should be monitored, and sight groups, and the media can play to assist in the overall progress expected. The authors in this supplement to The American these parties, based on our current—albeit incomplete and untested— understanding of diagnostic error (Table 1). Statement of Author Disclosure: Please see the Author Disclosures section at the end of this article.
Activity of ∆6 and ∆5 desaturases has been demonstrated in human fetal tissue from as early as 17 to 18 weeks of gestation (Chambaz et al cheap 100mg luvox with mastercard. Furthermore luvox 50mg overnight delivery, the ability to convert α-linolenic acid appears to be greater in premature infants than in older term infants (Uauy et al. Some have included arachidonic acid or γ-linolenic acid (18:3n-6), the ∆6 desaturase product of linoleic acid. These include a prospective, double-blind design with a sufficient number of infants randomized to control for the multiple genetic, environmental, and dietary factors that influence infant development and to detect meaningful treatment effects (Gore, 1999; Morley, 1998); the amount and balance of linoleic and α-linolenic acid; the duration of supplementation; the age at testing and tests used; and the physiological significance of any statistical differences found. Early studies by Makrides and colleagues (1995) reported better visual evoked potential acuity in infants fed formula with 0. However, this group did not confirm this finding in subsequent studies with formulas containing 0. The effect of low n-6:n-3 ratios (high n-3 fatty acids) on arachidonic acid metabolism is also of concern in growing infants. Additionally, no differ- ences in growth were found among infants fed formulas with 1. In conclusion, randomized clinical studies on growth or neural devel- opment with term infants fed formulas currently yield conflicting results on the requirements for n-3 fatty acids in young infants, but do raise concern over supplementation with long-chain n-3 fatty acids without arachidonic acid. Trans Fatty Acids and Conjugated Linoleic Acid Small amounts of trans fatty acids and conjugated linoleic acid are present in all diets. However, there are no known requirements for trans fatty acids and conju- gated linoleic acid for specific body functions. Pancreatic secretion after initial stimulation with either secretin or pancreozymin is not diminished with age (Bartos and Groh, 1969). The ratio of mean surface area to volume of jejunal mucosa has been reported not to differ between young and old individuals (Corazza et al. Total gastrointestinal transit time appears to be similar between young and elderly individuals (Brauer et al. Documented changes with age may be confounded by the inclu- sion of a subgroup with clinical disorders (e. The presence of bile salt-splitting bacteria normally present in the small intes- tine of humans is of potential significance to fat absorption. In addition, increases in fat malabsorption have not been dem- onstrated in normal elderly compared to younger individuals (Russell, 1992). Exercise Imposed physical activity decreased the magnitude of weight gain in nonobese volunteers given access to high fat diets (60 percent of energy) (Murgatroyd et al. In the exercise group, energy and fat balances (fat intake + fat synthesis – fat utilization) were not different from zero. Thus, high fat diets may cause positive fat balance, and therefore weight gain, only under sedentary conditions. These results are consistent with epidemiological evidence that show interactions between dietary fat, physical activity, and weight gain (Sherwood et al. Higher total fat diets can probably be consumed safely by active individuals while maintaining body weight. Although in longitudinal studies of weight gain, where dietary fat predicts weight gain independent of physical activity, it is important to note that physical activity may account for a greater percentage of the variance in weight gain than does dietary fat (Hill et al. High fat diets (69 percent of energy) do not appear to compromise endurance in trained athletes (Goedecke et al. This effect on training was not observed following long-term adaptation of high fat diets. Genetic Factors Studies of the general population may underestimate the importance of dietary fat in the development of obesity in subsets of individuals. Some data indicate that genetic predisposition may modify the relationship between diet and obesity (Heitmann et al. Additionally, some indi- viduals with relatively high metabolic rates appear to be able to consume high fat diets (44 percent of energy) without obesity (Cooling and Blundell, 1998). Intervention studies have shown that those individuals susceptible to weight gain and obesity appear to have an impaired ability to increase fat oxidation when challenged with high fat meals and diets (Astrup et al. Animal studies show that there are important gene and dietary fat interactions that influence the ten- dency to gain excessive weight on a high fat diet (West and York, 1998). The formation of nicotinamide adenine dinucleotide, resulting from ethanol oxidation, serves as a cofactor for fatty acid biosynthesis (Eisenstein, 1982). Similar to carbohydrate, alcohol consumption creates a shift in postprandial substrate utilization to reduce the oxidation of fatty acids (Schutz, 2000). Significant intake of alcohol (23 percent of energy) can depress fatty acid oxidation to a level equivalent to storing as much as 74 percent as fat (Murgatroyd et al. If the energy derived from alcohol is not utilized, the excess is stored as fat (Suter et al. Interaction of n-6 and n-3 Fatty Acid Metabolism The n-6 and n-3 unsaturated fatty acids are believed to be desaturated and elongated using the same series of desaturase and elongase enzymes (see Figure 8-1).
Thus luvox 50 mg visa, a combination of protein and fat utilization is required to supply the small amount of glucose still required by the brain in a person fully adapted to starvation cheap 50mg luvox visa. Presum- ably this also would be the obligatory glucose requirement in people adapted to a carbohydrate-free diet. Thus, the normal metabolic adapta- tion to a lack of dietary protein, as occurs in a starving person in whom the protein metabolized is in excess of that lost daily, is to provide the glucose required by the brain. Nevertheless, utilization of this amount of glucose by the brain is vitally important. Without it, function deteriorates dramati- cally, at least in the brain of rats (Sokoloff, 1973). The required amount of glucose could be derived easily from ingested protein alone if the individual was ingesting a carbohydrate-free, but energy-adequate diet containing protein sufficient for nitrogen balance. However, ingested amounts of protein greater than 30 to 34 g/d would likely stimulate insulin secretion unless ingested in small amounts through- out a 24-hour period. For example, ingestion of 25 to 50 g of protein at a single time stimulates insulin secretion (Krezowski et al. This rise in insulin would result in a diminution in the release of fatty acids from adipose cells and as a consequence, reduce ketoacid formation and fatty acid oxidation. The ultimate effect would be to increase the requirement for glucose of the brain and other organs. Thus, the minimal amount of glucose irreversibly oxidized to carbon dioxide and water requires utilization of a finely bal- anced ratio of dietary fat and protein. Azar and Bloom (1963) reported that 100 to 150 g/d of protein was necessary for maintenance of nitrogen balance. This amount of protein could typically provide amino acid substrate sufficient for the production of 56 to 84 g of glucose daily. However, daily infusion of 90 g of an amino acid mixture over 6 days to both postoperative and nonsurgical starving adults has been reported to reduce urinary nitrogen loss without a sig- nificant change in glucose or insulin concentration, but with a dramatic increase in ketoacids (Hoover et al. Glucose utilization by the brain has been determined either by mea- suring arteriovenous gradients of glucose, oxygen, lactate, and ketones across the brain and the respiratory quotient (Kety, 1957; Sokoloff, 1973), or with estimates of brain blood flow determined by different methods (e. Using 18F-2-fluoro-2-deoxyglucose and positron emission tomography, the rate of glucose accumulation in the brain also has been determined (Chugani, 1993; Chugani and Phelps, 1986; Chugani et al. This is an indirect method for measuring glucose utilization, and also has limitations (Hatazawa et al. Brain O2 consumption in association with the brain respiratory quotient also has been used as an indirect estimate of glucose utilization (Kalhan and Kiliç, 1999). The glucose consumption by the brain can be used along with informa- tion from Dobbing and Sands (1973) and Dekaban and Sadowsky (1978), which correlated weight of the brain with body weight to calculate glucose utilization. The brain utilizes approximately 60 percent of the infant’s total energy intake (Gibbons, 1998). Therefore, the turnover of glucose per kilogram of body weight can be up to fourfold greater in the infant compared to the adult (Kalhan and Kiliç, 1999). In species in which the mothers’ milk is very high in fat, such as in rats, the circulat- ing ketoacid concentration is very high in the suckling pups, and the ketoacids are an important source of fuel for the developing brain (Edmond et al. In addition, the gluconeogenic pathway is well developed even in premature human infants (Sunehag et al. Indeed, provided that adequate lipid and protein substrates are supplied, gluconeogenesis can account for the majority of glucose turn- over. Whether gluconeogenesis can account for the entire glucose require- ment in infants has not been tested. Fomon and coworkers (1976) provided infants with formulas containing either 34 or 62 percent of energy from carbohydrate for 104 days. There were no significant dif- ferences in the length or weight of the infants fed the two formulas. Inter- estingly, it also did not affect the total food energy consumed over the 6 or 12 months of life. From the limited data available, the lowest intake that has been documented to be adequate is 30 percent of total food energy. However, it is likely that infants also may grow and develop normally on a very low or nearly carbohydrate-free diet since their brains’ enzymatic machinery for oxidizing ketoacids is more efficient than it is in adults (Sokoloff, 1973). The lower limit of dietary carbohydrate compatible with life or for optimal health in infants is unknown. The only source of lactose in the animal kingdom is from the mammary gland and therefore is found only in mammals. The resulting glucose and galactose also readily pass into the portal venous system. They are carried to the liver where the galactose is converted to glucose and either stored as glycogen or released into the general circula- tion and oxidized. The net result is the provision of two glucose molecules for each lactose molecule ingested.
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