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By J. Vibald. Pacific States University. 2019.

Measurement of concentrations before steady state is reached results in a falsely low estimate of the steady-state concentration proven glucophage sr 500 mg, and inappropriate dose increases may result20 order glucophage sr 500mg, 21 buy glucophage sr 500mg fast delivery. Rifampicin and liquid antacids may decrease the concentration or effects of digoxin. Digoxin is contraindicated in patients with subaortic obstruction or hypertrophic cardiomyopathy, and in patients with severe electrolyte or acid-base disturbances (hypokalemia, or alkalosis) or metabolic disorders (hypothyroidism) Gastrointestinal: nausea, vomiting, diarrhea, abdominal pain, lack of appetite or intolerance to feeding Metabolic: hyperkalemia in cases of toxicity Central nervous system: fatigue, somnolence, drowsiness, vertigo, disori- entation, asthenia Neuromuscular and skeletal: neuralgia, myalgia Ophthalmological: blurred vision, photophobia, diplopia, flashing lights, aberrations of color vision Other: gynecomastia Contraindications Digoxin is contraindicated in patients with subaortic obstruction or hyper- trophic cardiomyopathy, and in patients with severe electrolyte or acid-base dis- turbances (hypokalemia, alkalosis) or metabolic disorders (hypothyroidism). Inotropic and Vasoactive Drugs 39 Poisoning Information Digoxin therapeutic levels should be monitored in the following circumstances: suspicion of toxicity, therapeutic failure, lack of compliance with the prescribed dosing regimen, renal dysfunction, and concomitant administration of drugs that might modify digoxin concentrations22. Toxicity is usually associated with digoxin serum concentrations levels greater than 2 ng/mL (normal ther- apeutic range, 0. Close monitoring of potassium levels (risk of hypokalemia) and of hemodynamic parameters is recommended. Digoxin serum levels might acutely rise, but the drug will be almost entirely bound to Fab fragments and, thus, unable to react with receptors. Administer Ipecac and charcoal, even several hours after ingestion of oral dig- oxin 2. Consider transvenous pacing and cardioversion, if necessary Compatible Diluents Oral digoxin should ideally be administered 1 hour before or 2 hours after meals to avoid erratic absorption secondary to diets rich in fiber or pec- tin content. Rimensberger Dobutamine Indication Dobutamine is an adrenergic agonist agent (sympathomimetic) with a potent β1 and mild β2 and α1 effect. Thus, it increases myocardial contractility, cardiac out- put and stroke volume (to a lesser extent than dopamine), and blood pressure by its strong inotropic and mild systemic and pulmonary vasodilator action23–27. Mechanisms of Action Dobutamine stimulates β1-adrenergic receptors, causing increased contrac- tility and heart rate. Its action is mediated by a direct β-adrenergic mechanism without associated norepinephrine release. Dobutamine also lowers central venous pressure and wedge pressure, but it has no selective effect on pulmonary vascular resistance28, 29. Dobutamine increases splanchnic blood flow in sepsis, particularly when combined with norepinephrine30, 31. Dosing Dobutamine is to be used as a continuous infusion and should be titrated within the therapeutic range and to the minimal effective dose until the desired response is achieved. Inotropic and Vasoactive Drugs 41 Adverse Effects Cardiovascular: sinus tachycardia, ectopic beats, palpitations, hypertension, chest pain, atrial and ventricular arrhythmias. Particular attention should be paid to patients with hypertrophic subaortic stenosis Gastrointestinal: nausea, vomiting Respiratory: dyspnea Neuromuscular: paresthesia, cramps Central nervous system: headache Cutaneous/peripheral: dermal necrosis (extravasation), inflammatory disorders, phlebitis Poisoning Information Adverse effects caused by excessive doses or altered pharmacokinetics of dobutamine may be observed. In these circumstances, it is recommended to temporarily decrease or even withdraw the drug and treat symptomatically (significant individual variability). In the case of extravasation, local adminis- tration of either phentolamine or papaverine should be considered. Compatible Diluents Dobutamine is a stable product in various solutions, except for alkaline solu- tions, for 24 hours. It is recommended to dilute dobutamine with normal saline or dextrose, with a maximal concentration of 5mg/mL. Dobutamine must be administered into a central vein, except in urgent scenarios (and using lower concentrations), with an infusion device allowing proper and reliable titration. Dobutamine may be administered with other vasoactive drugs, mus- cle relaxants, lidocaine, potassium chloride, and aminoglycosides. Dopamine Indication Dopamine is an adrenergic agonist agent (sympathomimetic) with moderate α1-,α2- andβ1-receptor stimulator effects and a mildβ2 effect. Therefore, dopamine increases car- diac contractility and output and improves blood pressure27–29, 33. In some postoperative cardiac pathologies, such as Fallot’s tetralogy or in patients undergoing a Stage 1 Norwood procedure, high doses of dopamine may exert negative effects35. There is no evidence-based data supporting the use of dopamine as a renal protector, particularly after cardiac surgery36, 37. Rimensberger Mechanisms of Action Dopamine or 3-hydroxy tyramine, a precursor of norepinephrine, stimulates adrenergic and dopaminergic receptors and releases norepinephrine in the heart. Dopamine also increases mesenteric blood flow, although this may be associated with negative hepatic energy balance at high doses30, 31. Dosing Dopamine is to be used as a continuous infusion and should be titrated within the therapeutic range and to the minimal effective dose until the desired response is achieved. Premature babies of younger than 30 weeks gestation may require higher doses to achieve the desired effect. The hemodynamic effects are dose-dependent: 1 to 5mg/kg/min (low dosage): increased renal and mesenteric blood flow, increased urine output 5 to 15mg/kg/min (intermediate dosage): increased renal blood flow, heart rate, inotropic effect with increased cardiac contractility and output More than 15mg/kg/min (high dosage): predominant α-adrenergic effect with systemic vasoconstriction If doses greater than 20mg/kg/min are needed, and depending on the pathophysiological conditions, vasoconstrictors that are more specific (in case of vasoplegia [epinephrine, norepinephrine, vasopressin, or phenylephrine]) or vasodilators when there is a need to reduce ventricular afterload (nitroprusside, nitroglycerine, phentolamine) should be considered to avoid marked, undesirable side-effects Neonates: 1 to 20µg/kg/min; some centers tend to use higher doses as required, up to 50µg/kg/min, in this age-group32–34 Infants/children: 1 to 20µg/kg/min, maximal dose of 50µg/kg/min in spe- cific and exceptional scenarios Adults: 1 to 20µg/kg/min, maximal dose of 50µg/kg/min in specific and exceptional scenarios Pharmacokinetics38, 39 Onset of action: 5 minutes Duration: less than 10 minutes Protein binding: 30% 3. It may have nonlinear kinetics in children and it may be increased by concomi- tant administration of dobutamine. Tricyclic antidepressant drugs, β-adrenergic blocking agents, and α- adrenergic blocking agents may decrease dopamine’s effect. Phenytoin may decrease dopamine’s effect and cause serious hypotension, seizures, and bradycardia. Hydrogenated anesthetics may decrease dopamine’s effect and cause serious cardiac arrhythmias. In these circumstances, it is recommended to decrease temporarily or even withdraw the drug and treat symptomatically (significant individual variability). In the case of extravasation, local adminis- tration of phentolamine or papaverine should be considered. Rimensberger Compatible Diluents Dopamine is to be infused diluted in dextrose with a maximal concentration of 3. It must be administered into a central vein, except in urgent scenarios (using lower concentrations), with an infusion device allowing proper and reliable titration. It may be administered with other vasoactive drugs, muscle relaxants, and lidocaine. Dopex- amine displays beneficial hemodynamic effects in patients with acute heart failure and those requiring hemodynamic support after cardiac surgery, and these effects are substantially maintained during longer-term administra- tion (≤24h). Dopexamine reduces afterload through pronounced arterial vasodilation, increases renal perfusion by selective renal vasodilation, and evokes mild cardiac stimulation through direct and indirect positive inotro- pism. It has also been shown to improve gastrointestinal blood flow and to increase oxygen delivery in high-risk surgical patients40, 41. Dopexamine may be superior to other dopaminergic agents in patients at risk for splanchnic hypoperfusion31, 40, 42, 43. Mechanisms of Action Dopexamine is an inhibitor of neuronal reuptake of norepinephrine. Dopexamine is not an α-adrenergic agonist and, therefore, does not cause vasoconstriction. Dosing Dopexamine is to be used as a continuous infusion and should be titrated within the therapeutic range and to the minimal effective dose until the desired response is achieved. Adverse Effects Cardiovascular:sinus tachycardia, ventricular ectopic beats, arrhythmogenic potential, angina, chest pain, and palpitations. For this reason, it should be used cautiously in patients with ischemic heart disease Central nervous system: tremor Gastrointestinal: nausea, vomiting Metabolic: hyperglycemia, hypokalemia; cautious use in patients with hyperglycemia or hypokalemia Cutaneous: phlebitis (extravasation) Other: reversible reduction in neutrophil and platelet counts Poisoning Information Adverse effects caused by excessive doses or altered pharmacokinetics of dopex- amine may be observed. These effects are likely to be of short duration because of dopexamine’s short half-life.

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Farrell M & Marsden J (2008) Acute risk of drug-related death among newly released prisoners in England and Wales trusted 500mg glucophage sr. Health Protection Agency order 500mg glucophage sr otc, Department of Health purchase glucophage sr 500mg otc, Social Services and Public Safety, National Public Health Service for Wales, Health Protection Scotland (2009) Shooting up. Health Protection Agency Prison Infection Prevention Team (2011) Health protection in prisons report 2009-2010. Strang J, Griffiths P, Powis B et al (1999) Which drugs cause overdose among opiate misusers? Darke S & Hall W (2003) Heroin overdose: research and evidence-based intervention. United Nations Office on Drugs and Crime (2006) Custodial and non-custodial measures. Oliver P, Keen J, Rowse G et al (2010) The effect of time spent in treatment and dropout status on rates of convictions, cautions and imprisonment over 5 years in a primary care-led methadone maintenance service. Hickman M, Vickerman P, Robertson R et al (2011) Promoting recovery and preventing drug-related mortality: competing risks? Granfield R & Cloud W (1999) Coming clean: overcoming addiction without treatment. Royal College of Psychiatrists & Royal College of General Practitioners (2012) Delivering quality care for drug and alcohol users: the roles and competencies of doctors. Barnaby B, Drummond C, McCloud A et al (2003) Substance misuse in psychiatric inpatients: comparison of a screening questionnaire survey with case notes. Intervention Study Group (2003) Attitudes and management of alcohol problems in general practice: descriptive analysis based on findings of a World Health Organization international collaborative survey. Degenhardt L, Knox S, Barker B et al (2005) The management of alcohol, tobacco and illicit drug use problems by general practitioners in Australia. British Medical Association Medical Ethics Department (2012) Medical ethics today. General Medical Council (2008) Good practice in prescribing medicines – guidance for doctors. Strang J, Babor T, Caulkins J et al (2012) Drug policy and the public good: evidence for effective interventions. International Centre for Drug Policy (2007) Substance misuse in the undergraduate medical curriculum. Royal College of Psychiatrists & Royal College of General Practitioners (2005) Roles and responsibilities of doctors in the provision of treatment for drug and alcohol misusers. Glanz A & Taylor C (1986) Findings of a national survey of the role of general practitioners in the treatment of opiate misuse: extent of contact with opiate misusers. Glanz A (1986) Findings of a national survey of the role of general practitioners in the treatment of opiate misuse: dealing with the opiate misuser. National Treatment Agency for Substance Misuse (2011) National and regional estimates of the prevalence of opiate and/or crack cocaine use 2009-10: a summary of key findings. National Treatment Agency for Substance Misuse (2006) Models of care for treatment of adult drug misusers: update 2006. House of Commons Home affairs Select Committee Drugs: breaking the cycle: ninth report of session 2012-2013. No part of this publication may be reproduced or transmitted in any form or by any means, or stored in any retrieval system of any nature without written permission, except for permitted fair dealing under the Copyright, Designs and Patents Act 1988, or in accordance with terms of a licence issued by the Copyright Licensing Agency in respect of photocopying and/or reprographic reproduction. Application for permission for other use of copyright materials including permission to reproduce extracts in another published works shall be made to the publishers. The Board produces numerous reports containing policies for national action by Government and other organisations, with specific recommendations and areas for action affecting the medical and allied professions. We would particularly like to thank: Professor Neil McKeganey Director of the Centre for Drug Misuse Research. It undertakes research in such diverse areas as the impact of parental drug use on children, recovery from dependent drug use, the impact of drug use on prostitution, the effectiveness of drug-treatment services and the nature of preteen drug use. In 2011, the centre moved from the University of Glasgow to operate as an independent research organisation. The centre is currently undertaking work on the effectiveness of Suboxone® (buprenorphine and naloxone), the impact of drug and alcohol problems on doctors and dentists, and the effectiveness of prison- based drug treatment. Professor McKeganey has written widely on the topic of drugs policy and has contributed to the United-Nations-based International Narcotics Control Board. He is the author of over 150 academic papers and his most recent book Controversies in drug policy and practice was published in 2011 by Palgrave Macmillan. Professor Robin Room School of Population Health, University of Melbourne, and Director of the Centre for Alcohol Policy Research at Turning Point Alcohol and Drug Centre, Fitzroy, Victoria, Australia. He is also a professor at and was the founding director of the Centre for Social Research on Alcohol and Drugs at Stockholm University. He had previously directed research at the Addiction Research Foundation of Ontario (1991-1998) and the Alcohol Research Group in Berkeley, California (1977-1991). He is a co-author of a number of books on alcohol and drug policy, including Young men and drugs (National Institute on Drug Abuse, 1975), Alcohol in developing societies (Finnish Foundation for Alcohol Studies, 2002), Drug policy and the public good (Beckley Foundation Press and Oxford University Press, 2010), Cannabis policy – moving beyond stalemate (Oxford University Press, 2010) and Alcohol – no ordinary commodity (Oxford University Press, 2e, 2010). His research interests include historical, cultural and social epidemiological studies of alcohol and other drugs, including comparative research across psychoactive substances. The group comprised senior members of affected professions who have demonstrated experience and interest in relation to the issue of drug use. Declaration of interest Declarations of interest for outside experts have been provided in Appendix 1. Abuse liability The propensity of a particular Psychoactive substance to be susceptible to abuse. It is defined in terms of the relative probability that use of the substance will lead to social, physical or psychological problems for an individual or society. Addiction Repeated use of a Psychoactive substance or substances, to the extent that the user (referred to as an addict) is periodically or chronically intoxicated, shows a compulsion to take the preferred substance (or substances), has great difficulty in voluntarily ceasing or modifying Substance use, and exhibits determination to obtain psychoactive substances by almost any means. Typically, Tolerance is prominent and a Withdrawal syndrome frequently occurs when substance use is interrupted. The life of the addict may be dominated by substance use to the virtual exclusion of all other activities and responsibilities. The term addiction also conveys the sense that such substance use has a detrimental effect on society, as well as on the individual. It is regarded by many as a discrete disease entity, a debilitating disorder rooted in the pharmacological effects of the Drug, which is often progressive. Different Psychoactive drugs have different levels of addictiveness (or Dependence potential); these are outlined in Appendix 2. Participants support each other in recovering from, or maintaining recovery from, their dependence. It uses a 12-step programme based on a non-denominational spiritual approach, with an emphasis on mutual aid and support.

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This pattern of use is usually characterised by moderate levels of consumption and periods when the person stops using the substance without difficulty buy glucophage sr 500mg low price. Harmful cheap 500mg glucophage sr otc, dependent and hazardous use There are clear buy glucophage sr 500mg free shipping, internationally agreed frameworks for describing harmful and dependent patterns of substance use. These frameworks define a hierarchy of physical, psychological and social harm to the individual. Within the chapter on mental and behavioural disorders, a subchapter defines mental and behavioural disorders due to psychoactive substance use. It defines a number of categories including acute intoxication (see Glossary), harmful use, dependence and withdrawal. The level of harm caused by a particular pattern of substance use is defined by the categories ‘harmful’ and ‘dependent’. Psychological dependence involves a need (craving – see Glossary) for repeated doses of the drug to feel good, or avoid feeling bad. Physiological (physical) dependence is associated with tolerance (see Glossary), where increased doses of the drug are required to produce the effects originally produced by lower doses, and development of withdrawal syndrome (see Glossary) when the drug is withdrawn. Withdrawal syndrome is characterised by physiological and psychological symptoms that are specific to a particular drug. The term ‘dependence’ is often used interchangeably with ‘addiction’ (see Glossary). In contrast to harmful use, hazardous use also refers to patterns of use that are of public health significance, despite the absence of any current disorder in the individual user. These terms, and many others that are used throughout the report, are discussed in more detail in the Glossary. Substances have been clearly shown to affect the brain in the short and longer term. Some substances (eg heroin, cannabis) mimic endogenous neurotransmitters, while others (eg cocaine, amphetamine) increase the availability of endogenous neurotransmitter to the brain, by either increasing neurotransmitter release or inhibiting its breakdown. If a person uses substances over a longer period of time, the brain’s structure and function begin to change, prompting behavioural changes in that individual. The prefrontal cortex area of the brain is particularly vulnerable to the effect of substances. This brain area is crucial for decision making, such as weighing up the pros and cons of a certain activity. Research suggests that the prefrontal cortex is one of the last brain areas to mature. It is a naturally occurring, ‘feel good’ neurotransmitter that is important in rewarding positive behaviours (eg eating, drinking). Some psychoactive substances cause dopamine to be released rapidly and in huge quantities when compared to usual brain levels. Raised levels of dopamine in the mesolimbic system lead to intense feelings of pleasure, known to users as a ‘high’ (see Glossary). If substance use persists, the brain responds to the dopamine overstimulation by decreasing the amount of dopamine produced and reducing the number of dopamine receptors (see Glossary) available. This, in turn, can lead to the user feeling emotionally flat and exhausted once the immediate effect of the drug has subsided. The user will often try to stimulate further additional dopamine release by using larger quantities of the substance. The role of dopamine in the effect of psychoactive drugs is considered further in Section 4. Genetics There is strong evidence for a genetic component to dependence, provided by family, twin and adoption studies (see Chapter 4). Although research suggests many genes may be involved,18 there is evidence that a single genetic variant in the aldehyde dehydrogenase 2 gene impacts on patterns of drinking and the risk of dependence. The genetics of dependence is a rapidly developing area but, apart from the studies on the aldehyde dehydrogenase 2 gene, there is little immediate prospect of a breakthrough in genetics leading to improved patient care. As described above, dependence can be considered primarily a brain disorder, but one that interacts with a range of predisposing, precipitating, perpetuating and protective factors. These factors can best be described in a framework in which the biological, psychological and social components are identified. Psychological factors include comorbid mental health problems such as depression, psychosis and personality disorder. Traumatic events, such as childhood sexual abuse, may also increase a person’s vulnerability to subsequent use of psychoactive substances. Social factors include the availability of a particular substance; the nature of, and support provided by, a person’s social network; peer pressure; and environmental factors such as housing and employment. A range of evidence-based treatments are available to help people with harmful/ dependent substance use, and some of these are discussed in Chapters 8 to 10. Each individual is unique, and treatment of harmful/dependent use should be planned with a clear understanding of the predisposing and protective factors. Appendix 2 gives further details about the nature and addictiveness of these drugs, and Appendix 3 gives details of health-related harms associated with illicit drug use. These recommendations are non-binding, and have, on occasion, been ignored or rejected. Mephedrone and related cathinone derivatives, as well as naphthylpyrovalerone analogues, were classified as Class B drugs in 2010. The Drugs Act 2005 amended the Misuse of Drugs Act 1971 and the Police and Criminal Evidence Act 1984, to increase the powers of the police and courts in relation to drug control (see Glossary). It includes stronger measures to allow police to test drug offenders on arrest rather than at the time of charging, and requires those testing positive to undergo treatment. In July 2011, the Government announced a ban on the importation of phenazepam – a harmful drug advertised as producing a ‘legal high’– as well as its intention to control it as a Class C drug in 2012. It is important to emphasise that that the development of new agents will inevitably run ahead of the Government’s ability to amend the legislation. It is worth noting that many provisions in national legislation are not required by these international drug control treaties. Over 100 illicit substances are placed in four schedules, nominally based on their perceived harmfulness. Limited flexibility is allowed in the interpretation and implementation in many areas of the legislation, which has allowed countries to respond to their specific circumstances. Convention on Psychotropic Substances 1971 This convention was developed in response to increasing concern about emerging drugs and related behaviours during the 1960s, such as the use of amphetamine- like stimulants, barbiturates and other sedative-hypnotics/depressants, and hallucinogens. As with the 1961 convention, these drugs are classified into four schedules according to perceived harm and therapeutic value, with a corresponding hierarchy of controls to license medical, scientific or other uses. Market and trade controls and national requirements are less onerous than those under the Single Convention. Convention against Illicit Traffic in Narcotic Drugs and Psychotropic Substances 1988 The 1988 convention strengthened the existing powers for prevention of international drug trafficking (including provisions against money laundering and the diversion (see Glossary) of precursor chemicals). It also included provisions to make the intentional possession, purchase or cultivation of narcotic drugs or psychotropic (see Glossary) substances for personal consumption a criminal offence under domestic law. These factors create a framework within which an individual’s predisposing, precipitating, perpetuating and protective elements can be used to plan the most effective treatments. As a teenager, he had been in a gang and had previous convictions for possession of dangerous weapons (knives), burglaries, street robberies (mainly mobile phones) and assault.

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Senate Majority Leader William Frist described a fctional patient and the overall healthcare system in the year 015 in a manner that succinctly captured a trend in the United States of envisioning a personalized therapeutic approach cheap glucophage sr 500 mg mastercard. Interviewed by the journal Personalized Medicine best 500mg glucophage sr, Dolores Ibarreta of the European Commission Joint Research Center purchase glucophage sr 500mg without a prescription, Institute for Prospective Technological Studies, explained: In the specifc context of personalized medicine, we are looking at barriers for development and clinical implementation in Europe. Frist, “Health Care in the 1st Century,” New England Journal of Medicine 352 (2005), 267-272. Interestingly, the tensions emerging in the United States between making health care responsive to consumers while protecting patients and ensuring they have treatment and care are notably less pronounced in Europe. Conclusion: The Interface of Innovation and Regulation Since 1980 and at a rate that accelerated in the 1990s, the United States became the leading worldwide location for pharmaceutical research, clinical testing, and marketing. The “pharmacy to the world,” once located in Germany, Switzerland, or France, today is found in the United States. Studies of the industry have attributed this sustained competitive advantage to a variety of factors, including U. Government regulation of the pharmaceutical market is revealing a country’s concept of innovation at a specifc historical moment; intriguingly, regulations also shed light on enduring cultural differences between nations. Historically, legislative interventions in the United States were predicated on the notion that patients must be protected by the state from the worst ravages of free-market capitalism. In the 1980s and 1990s, however, patients represented by disease-based organizations agitated for greater access to drugs and speedier approvals. At the same time, critics warned that the country’s competitive standing depended on the pharmaceutical and biotech sectors. Regulation of pharmaceuticals in the United States has followed an overall progression from medical profession to the state to a new consumer/patient oversight model. In Germany, by contrast, the medical profession exercised a near-monopoly over constructions of “the patient” and drug laws codifed existing power-sharing arrangements. Instead of the state claiming authority over pre-market testing, it acted as one member of a network overseeing pharmaceutical drugs. A fexible boundary between testing and market was predicated on informal trial protocols, a structured system for collecting reports of adverse reactions, and compromises among organized interests and government offcials. The drug approval process thus only rarely became a signifcant site for debates over national competitiveness or industry innovation. Nevertheless, Germany too has seen different waves of regulatory style, from physicians to a networked approach that incorporates the state, select disease-based organizations, and the medical profession. The comparative perspectives developed in this chapter suggest that despite recent convergences in government efforts to stimulate and steer innovation, for example through support for small biotech ventures, national regulatory differences infuence the competitive status of the pharmaceutical sector. In contrast to the argument that it is German and European healthcare cost containment that has undermined its domestic pharmaceutical industry, this chapter suggests instead that regulation also plays a role in the success and failure of industry. In fact, the emergence of a consumer/patient regulatory mode in the United States has driven increased use of prescription drugs. While this comes at high fnancial cost and stress on government regulators, it offers the benefts of avoiding painful cost vs. At the same time, the consumer mode that has emerged in the United States has proven easy to manipulate for industry, as in the cases of corporate-fnanced organizations claiming to be self-organized by patients. A combination of public attention to drug prices, health concerns from product withdrawals due to adverse reactions, and criticisms of the failure to deliver medicines to patients in developing countries pose signifcant challenges to industry and regulators. Research on the interplay of pharmaceutical innovation and regulation presented here suggests that signifcant change in the blockbuster model followed by most pharmaceutical companies may not happen as quickly as critics would like. An open question is whether the current “pharmacy to the world” of the United States may soon loose ground to competitors from developing countries. As Indian and Chinese frms that started in the generics business integrate upstream into the invention and testing of new molecules, they may become the next generation of competitors to the current top-ranking frms. Finally, the emergence of a consumer model of regulation poses a number of critical unresolved questions about the longer-term role of government, industry, the medical profession, and citizens. The era of paternalistic medicine has passed, but the notion that patients can act as consumers and make appropriate decisions concerning medical treatment poses countervailing risks of its own. A better accommodation among key players needs to be struck to foster safe use of pharmaceuticals. The precise form of this accommodation will necessarily vary from one country to the next, which holds out the possibility for additional policy learning from future cross-national comparisons. In the biomedical model, medication is defned as a substance that acts on the condition of a living organism. In many other models it is regarded as a mediator of symbolic relationships linking people to their environment. The complexity of these relationships indicates the extent to which – over the course of their interactions – social actors (industry representatives, physicians, pharmacists, patients, and the like) have become the builders of this representational universe. Moreover, by differentiating itself into a variety of social meanings depending on space and time, this plural universe gives rise to different types of social, economic and legal issues that engender ambiguity and make the analyst’s work diffcult. Consequently, in analyzing medications, the tendency is generally to break up the pathway they follow so that it is more accessible. Critics of biomedical models and supporters of the theory of complexity, such as Gatrell,2 Urry,3 Thrift,4 Byrne,5 and Cilliers,6 suggest instead that healthcare and, along with it, the medication pathway, be considered in their complexity and holistically. We would thus avoid the reductionism of the compartmentalization posited by certain academic disciplines in particular. In a way, paradigms are being changed so that we can examine the processes and interactions that occur all along the medication pathway from the biomolecular mechanisms to the socio-institutional ones, without which epidemiological and clinical fndings cannot be placed in context. The medication cycle To meet these paradigmatic demands, our studies in healthcare have led us to develop the notion of “la chaîne des medicaments,” which we have translated as the “medication cycle. Gatrell, Complexity theory and geographies of health: a critical assessment social. We are thus adopting a broader perspective inspired by the systemic visions of Le Moigne7 and Watzlawick8 and the theory of complexity of Byrne,9 Urry10 and Cilliers11. The notion of the cycle thus necessarily becomes a factor in both the different spheres of research and in care-providing settings. Indeed, it effects a radical conceptual transformation by putting medications back into the context of the total dynamic and steering clear of compartmentalization. In terms of interventions, it also allows us to surmount the gaps in multidisciplinarity by building bridges and providing a common language. The notion of the cycle may be said to take a variety of forms in a framework of variable geometry, in which different cycles ft into each other and mix together in a world of interactions. These dynamic interactions are defned by practices, implicit and explicit regulations derived from healthcare policies, and professional and public organizations that provide a framework for medication use. These dynamic interactions are also based on types of knowledge that simultaneously delimit the nature of medications, drug action and the transactions that take place around drugs. In developing this concept, our studies have allowed us to start building a series of models that take into account diversity and complexity. Furthermore – and this is the fundamental argument – this development is part of our theoretical and epistemological approach that refects thinking in a late-twentieth-century sociology of science that Olivier Martin has described as “calmed down. Indeed, in linking together the biological, social and environmental systems that keep people in their condition, our studies are mainly concerned with breaks, with the crises that more and more often rock the medication cycle.

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