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Efforts to treat narcotic addiction as a medical problem were limited until the advent of methadone maintenance therapy in the 1960s. Heroin use increased during the Vietnam War, when almost half of the enlisted men experimented with opioids. These programs are generally located in large cities, with the highest concentration in the northeastern United States. In 1995, an estimated 141,000 individuals became new heroin users, an upward trend over the previous 5 years comparable to the increases seen in the epidemic of the late 1960s. New initiates in 1995-1996 were likely to be young (90% younger than 26 years) and non-injecting (77% have never injected but rather smoke, sniff, or snort heroin). Polysubstance abuse is increasingly common, with as many as 50% of male and 25% of female narcotic addicts meeting the criteria for alcohol dependence within the first 5 years of active drug treatment. Concurrent use of alcohol, stimulants, sedatives, and/or marijuana occurs in three quarters of narcotic addicts. Opioids exert their effects on specific receptors for three distinct families of endogenous opioid peptides: enkephalins, endorphins, and dynorphins. In the central nervous system, three major classes of opioid receptors with unique selectivity and pharmacologic profiles have been identified: mu, kappa, and delta. Subtypes of these major classes (mu1, mu2, kappa1, kappa2, kappa3, delta1, delta2) have been elucidated primarily by the use of selective receptor antagonists. It is thought that opioid peptides acting as neurotransmitters or neuromodulators exert their actions at neuronal synapses. Heroin may be injected intravenously or subcutaneously, snorted, smoked, or ingested. The parenteral and inhaled routes of administration result in the most rapid delivery of drug to the brain and are hence the most potentially addicting. As the purity of street heroin has increased from less than 5% in the 1960s to 1980s to varying levels up to 80% in the 1990s, its non-parenteral administration has risen. The initial effects may be perceived as a turning in the stomach with tingling and warmth. The intense euphoria is followed by an intoxicated pleasant feeling referred to as "nodding," with decreased respiration and peristalsis. The depressant effect of heroin on the central nervous system is marked, particularly after parenteral administration. Sedation, mental clouding, decreased visual acuity, heavy feeling in the extremities, light sleep with vivid dreams, and reduction in anxiety are typical, at least until tolerance develops. In addition to these effects on opioid receptors, heroin causes the release of histamine, which may result in itching, scleral injection, and hypotension. High levels of tolerance develop rapidly with regard to respiratory depression, analgesia, sedation, vomiting, and euphoric properties. Little tolerance develops for miosis or constipation, so a heroin addict with an acutely painful medical condition may complain of insufficient analgesia despite pinpoint pupils. The timing of withdrawal symptoms, which are directly related to clearance of the drug, begins 4 to 8 hours after the last dose of heroin. The acute withdrawal syndrome will peak in intensity after 36 to 72 hours and resolve over a period of 5 to 7 days. In addition to the acute abstinence syndrome, a protracted abstinence syndrome occurs and lasts 6 months or more. In contrast to the hyperadrenergic characteristics of the primary withdrawal syndrome (tachycardia, hypertension, elevated temperature, miosis, and diaphoresis), the period afterward can consist of sluggishness, sleep disturbance, and malaise. An understanding of the nature of recovery from heroin use is important for setting appropriate expectations for both the patient and the health care provider. Most opioid-related medical complications occur as a result of the spread of infectious agents by injection drug use among heroin addicts. The manifestations of these medical complications are protean but frequently non-specific, such as fever, malaise, weight loss, pain, or dyspnea. Additionally, specific syndromes have been attributed to direct toxic effects of the opioid itself.

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The high-risk strategy targets individuals in whom disease is judged most likely to develop and who would therefore benefit from intervention. This strategy, which is more compatible with usual medical practice, avoids the inefficiency of the population approach with its need to intervene in many who neither desire such help nor are likely to benefit. Preventive policies that focus on high-risk individuals offer substantial benefits for these individuals, but the potential impact on the total burden of disease is often disappointing. Despite the rationale for emphasizing prevention, studies indicate that major gaps exist in the delivery of preventive health services. The main barriers include the time required, the lack of reimbursement, skepticism toward attempting behavioral change, and a health system geared to illness. Primary prevention is directed toward preventing disease or injury before it develops; secondary prevention deals with early detection and treatment to impede the progress of pre-clinical disease. In contrast, tertiary prevention refers to rehabilitative activities after the onset of disease to minimize complications and disability. Detecting and treating hypertension could be considered secondary prevention of hypertensive disease but primary prevention of congestive heart failure and stroke. In any event, prevention can be perceived along a continuum from modification of predisposing factors, to preventing disease, to avoiding premature death and disability. Homicide and legal intervention *Per 100,000 population, age adjusted to the 1940 U. Therefore, increasing emphasis has been placed on preventing risk factors themselves. Indiscriminate screening without adequate advice and follow-up serves no useful purpose. The periodic health examination (see Chapter 10) has evolved from a broad-based, uniform protocol to an approach that targets the prevention, detection, and treatment of specific diseases or risk factors for pre-determined age, gender, and racial groups. Changes in the health care system and the development of national guidelines will probably draw greater attention to health promotion, disease prevention, and the interface of physician-based medical care with the public health system. Physicians should consider each disorder in terms of the potential for prevention as compared with the possibility of adverse effects from the preventive intervention. Ample evidence connects identifiable and oftentimes preventable factors to the morbidity and mortality associated with major health problems (Table 9-2). About half of all deaths, morbidity, and disability can be attributed to such non-genetic factors, and many lifestyle changes benefit multiple systems and disorders. For example, cigarette smoking has been estimated to contribute to one in five deaths in the United States (see Chapter 13); dietary changes (see Chapter 39) may lower the occurrence of atherosclerosis, diabetes, osteoporosis, and cancer. Other important personal behavior factors affecting health include physical activity, alcohol, illicit drug use, sexual practices, and exposure to environmental toxins. Many believe that diseases with a strong heritable component cannot be altered, but susceptibility to disease often requires the interaction of multiple genes and environmental factors for expression (see Chapter 31). In addition, chronic diseases are multifactorial, so other factors can be changed to compensate for an elevated genetic risk. The notion that prevention is less useful in older persons excludes many who would benefit most from prevention. The elderly have a greater absolute risk of disease and have been shown to adhere and respond favorably to preventive measures. In addition, life expectancy is frequently underestimated in the elderly-those who reach 65 years can now expect to live into their 80s. With a larger aging population, decreasing fatality rates, and improved treatment of many disorders, it is essential that the focus be on primary prevention. Otherwise, the prevalence and associated morbidity of major diseases will increase and further consume available medical resources. It should be clearly understood that the purpose of prevention is not only to postpone illness to a later age but also often to prevent the diseases themselves and the resultant disability. The leading causes of disability-adjusted loss of years of life in developed countries over the next 25 years will probably continue to be atherosclerotic diseases, but the impact of depression, smoking-related disease, accidents, alcohol, and degenerative neurologic and rheumatologic diseases will also be substantial (Table 9-3). One of a four-part series by the authors on the Global Burden of Disease Study, which predicts worldwide trends in mortality and morbidity.

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