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Clinical Director, Des Moines University College of Osteopathic Medicine

Given that a high proportion of criminal acts are committed against young people, this represents a serious bias. There are a number of studies that have explored aspects of fear of crime among young people and its implications (Anderson et al. Using evidence from the British Crime Survey, Maung (1995) found that the possibility of sexual pestering or assault by a stranger were the chief concerns of female 12- to 15-year-olds: 56 per cent said that they were very worried about the chances of sexual pestering while 48 per cent were very worried about assault by a stranger. A number also expressed concerns about mugging or burglary (35 per cent and 22 per cent respectively). Boys in the Crime and insecurity 117 same age range were somewhat less concerned about the possibility of crime: 31 per cent were very worried about sexual pestering, 28 per cent about assault by a stranger, 24 per cent about mugging and 15 per cent about burglary. For each of these crimes, African Caribbean and Asian youth were significantly more likely to express concern about becoming a victim, as were those living in urban areas and areas in which levels of recorded crime were high. These concerns affected the ways in which young people spent their time and the places they visited. In particular, young women are much more likely than young men to feel unsafe when out alone and often felt the need to take precautions against crime, such as making special transport arrangements or going out with friends (Hough 1995). Young people may avoid visiting places they perceive as risky, or may defend themselves against possible attack. Statistics on victims of crime compiled for 17 industrialized countries by van Kesteren and colleagues (2001) show that overall weapons were used (as a threat or otherwise) in just less than one in four recoded cases of assault or threat (rising to more than four in ten where the victim was a male). In cases where the offender could be identified, less than half were under the age of 16: 10 per cent of offences against boys and 17 per cent of offences against girls were committed by people over the age of 21 (Anderson et al. Indeed, two-thirds of the girls reported having been harassed by adults, sometimes being followed by people either in cars or on foot. Other factors associated with a significant increase in risk include being single, unemployed, living in an area characterized by high levels of disorder and visiting a pub more than three times a week (Nicholas et al. A study of criminal victimization in 17 industrialized countries (van Kesteren et al. While crimes committed against young people are a common occurrence, relatively few incidents are reported to the police. Whereas more than a third of adults will tend to report offences such as assaults, robberies, personal threats and thefts, among 16- to 19-year-olds just 14 per cent would make a formal complaint (Maung 1995). Similarly, Anderson and colleagues (1994) showed that 14 per cent of 11- to 15-year-olds would report an assault to the police. Asian and African Caribbean youths are less likely than white youths to report crimes committed against them, although Maung (1995) argues that ethnic differences are not significant once characteristics of areas are taken into consideration. In many respects, the concentration on young people as the perpetrators of crimes has left us blind to the extent to which young people are victims; they frequently have crimes committed against them and their fears have an impact on their day-to-day behaviour. In particular, young women frequently experience harassment which they are reluctant to report and which restricts their freedom to go out alone. Conclusion Although many young people engage in criminal activities and while significant numbers will be the victims of crime, it would be wrong to suggest that the patterns of criminality which we have described in this chapter represent a breakdown in the social fabric of society. Young people have always indulged in risky behaviour and in activities which are illegal. The youth of previous generations engaged in similar types of activities and also found themselves to be the focus of police attention and the source of anguish to adults (Pearson 1983). There is, however, little evidence that the numbers of serious crimes committed by young people are rising, although criminal careers are perhaps becoming longer. The media focus on abnormal youth crimes has perhaps led to an increased perception of a lawless younger generation and to calls for tougher sanctions against offenders. However, the increased fear of crime has implications for everyone, as Box and colleagues (1988) suggest, the fear of crime can fracture communities as people move away from the cities and restrict their movements: it can also promote the introduction of measures that curtail the feedoms of young people who are not engaged in criminal acts. In this context, Giddens (1991) is wrong to suggest that place loses its significance in the age of high modernity: both the fear of crime, the chances of becoming a victim of crime and the risks of apprehension for involvement in crime continue to reflect social geographies. While Giddens would argue that through the mass media we are all exposed to the consequences of crime and develop a heightened sense of insecurity and mistrust, perceptions of risk are differentially distributed. Viewers contextualize television violence and are more concerned when the risks highlighted by the media are shown to affect their own locality or areas with similar characteristics (Gunter 1987). As such, those who live in deprived inner city areas with visible signs of decay are more frightened to go out alone than those living in non-urban areas (Hough 1995).

Conventional or low-flux dialyzers are relatively impermeable to drugs with a molecular weight greater than 1000 daltons (Da). High-flux hemodialyzers allow the passage of most drugs that have a molecular weight of 10,000 Da or less. The determination of drug concentrations at the start and end of dialysis, with subsequent calculation of the halflife during dialysis, has historically been used as an index of drug removal by dialysis. These approaches may save time in the ambulatory dialysis setting but will increase drug cost because more drug will have to be given to compensate for the increased dialysis removal. This information serves only as initial dosing guidance; measurement of predialysis serum concentrations is recommended to guide subsequent drug dosing. The impact of hemodialysis on drug therapy must not be viewed as a "generic procedure" that will result in removal of a fixed percentage of the drug from the body with each dialysis session; neither should simple "yes/no" answers on the dialyzability of drug compounds be considered sufficient information for therapeutic decisions. Compounds considered nondialyzable with low-flux dialyzers may in fact be significantly removed by high-flux hemodialyzers. Variables that influence drug removal in peritoneal dialysis include drugspecific characteristics such as molecular weight, solubility, degree of ionization, protein binding, and volume of distribution. Patient-specific factors include peritoneal membrane characteristics such as splanchnic blood flow, surface area, and permeability. The contribution of peritoneal dialysis to total body clearance is often low and, for most drugs, markedly less than the contribution of this clearance calculation accurately reflects dialysis drug clearance only if drug does not penetrate or bind to formed blood elements. For patients receiving hemodialysis, the usual objective is to restore the amount of drug in the body at the end of dialysis to the value that would have been present if the patient had not been dialyzed. Antiinfective agents are the most commonly studied drugs because of their primary role in the treatment of peritonitis, and the dosing recommendations for peritonitis, which are regularly updated, should be consulted as necessary. Most other drugs can generally be dosed according to the residual kidney function of the patient because clearance by peritoneal dialysis is small. If there is a significant relationship between the desired peak (Cpeak) or trough (Ctrough) concentration of a drug for a given patient with reduced kidney function and the potential clinical response. Over-the-counter and herbal products, as well as prescription medications, should be assessed to ensure that they are indicated. If a drug interaction is suspected and the clinical implication is significant, alternative medications should be used. The dosage of drugs that are more than 30% renally eliminated unchanged should be verified to ensure that appropriate initial dosage adjustments are implemented. Maintenance dosage regimens should be adjusted based on patient response and serum drug concentration determinations when indicated and available. This estimation method assumes that the drug is administered by intermittent intravenous infusion and its disposition is adequately characterized by a one-compartment linear model. Subsequent individualization of therapy should be undertaken whenever clinical therapeutic monitoring tools, such as plasma drug concentrations, are available. Numerous other resources are available for renal drug dosing information, including online sources, as well as portable handheld databases such as Epocrates, Lexicomp, and Micromedex. Scheinman the coming of age of clinical chemistry in the latter half of the twentieth century, bringing with it the routine measurement of electrolytes and minerals in patient samples, produced descriptions of distinct inherited syndromes of abnormal renal tubular transport. Clinical investigation led to speculation, often ingenious and sometimes controversial, regarding the underlying causes of these syndromes. More recently, the tools of molecular biology made possible the cloning of mutated genes found in patients with monogenic disorders of renal tubular transport. These diseases represent experiments of nature, and for the renal physiologist the insights they have revealed are exciting. Some have provided gratifying confirmation of our existing knowledge of transport mechanisms along the nephron. Examples include mutations in diureticsensitive transporters in the Bartter and Gitelman syndromes. In other cases, positional cloning led to the discovery of previously unknown proteins, often surprising ones that appear to play important roles in epithelial transport. The diseases listed are explained by abnormalities in the corresponding gene product. This is reflected in fewer units of the sodium-dependent phosphate transporter type 2 (NaPi2) in the apical membrane of proximal tubular cells. Autosomal recessive conditions of impaired transepithelial transport of glucose and dibasic amino acids have been shown to be caused by mutations in sodium-dependent transporters that are expressed in both kidney and intestine, resulting in urinary losses and intestinal malabsorption of these solutes.

The diabetes control and complications trial research group: the effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus, N Engl J Med 329:977-986, 1993. As outlined in this section, various novel treatment options are in development that may offer additional renoprotection and have the potential to reduce the high morbidity and mortality rates typically seen in patients with diabetes. Sanders 26 Paraproteinemic kidney diseases are typically the result of deposition of immunoglobulin fragments (heavy chains and light chains) (Fig. Patterns of tubular injury include a proximal tubulopathy and cast nephropathy (also known as "myeloma kidney"). In addition to these paraproteinemic kidney lesions, this chapter includes a discussion of Waldenstrцm macroglobulinemia. In one large study of multiple myeloma, kidney dysfunction was present in approximately 2% of patients who did not exhibit significant urinary free light-chain levels, whereas increasing urinary free light-chain levels were strongly associated with kidney failure, with 48% of myeloma patients who had high urinary monoclonal free light chains having kidney failure and associated poor survival. The type of kidney lesion induced by light chains depends on the physicochemical properties of these proteins. He was the first to report these unique proteins, which now bear his name, and correlate this early urinary biomarker with the disease known as multiple myeloma. More than a century later, Edelman and Gally demonstrated that Bence Jones proteins were immunoglobulin light chains. Plasma cells synthesize light chains that become part of the immunoglobulin molecule (see Fig. In normal states, a slight excess production of light, compared to heavy, chains appears to be required for efficient immunoglobulin synthesis, but this excess results in the release of polyclonal free light chains into the circulation. After entering the bloodstream, light chains are handled similarly to other lowmolecular-weight proteins, which are usually removed from the circulation by glomerular filtration. Unlike albumin, these monomers (molecular weight ~22 kDa) and dimers (~44 kDa) are readily filtered through the glomerulus and are reabsorbed by the proximal tubule. Endocytosis of light chains into the proximal tubule occurs through a single class of heterodimeric, multiligand receptor that is composed of megalin and cubilin. After endocytosis, lysosomal enzymes hydrolyze the proteins, and the amino-acid components are returned to the circulation. The uptake and catabolism of these proteins are very efficient, with the kidney readily handling approximately 500 mg of free light chains that are produced daily by the normal lymphoid system. However, in the setting of a monoclonal gammopathy, production of monoclonal light chains increases, and binding of light chains to the megalin-cubilin complex can become saturated, allowing light chains to be delivered to the distal nephron and to appear in the urine as Bence Jones proteins. Light chains can be isotyped as kappa () or lambda () based on sequence variations in the constant region of the protein. Thus, although possessing similar structures and biochemical properties, no two light chains are identical; however, there are enough sequence similarities among light chains to permit categorizing them into subgroups. Free light chains, particularly the isotype, often homodimerize before secretion into the circulation. The multiple kidney lesions from monoclonal light-chain deposition affect virtually every compartment of the kidney (see Box 26. A classic kidney presentation of multiple myeloma is Fanconi syndrome, which is produced almost exclusively by members of the I subfamily. The qualitative urine dipstick test for protein also has a low sensitivity for detection of light chains. Although some Bence Jones proteins react with the chemical impregnated onto the strip, other light chains cannot be detected; the net charge of the protein may be an important determinant of this interaction. Because of the relative insensitivity of routine serum protein electrophoresis and urinary protein electrophoresis for free light chains, these tests are not recommended as screening tools in the diagnostic evaluation of the underlying etiology of renal disease. Highly sensitive and reliable immunoassays are available to detect the presence of monoclonal light chains in the urine and serum and are adequate tests for screening when both urine and serum are examined. When a clone of plasma cells exists, significant amounts of monoclonal light chains appear in the circulation and the urine. In healthy adults, the urinary concentration of polyclonal light-chain proteins is about 2.

In such cases, the concentration of Na+ per liter of serum water is unchanged, but the concentration of Na+ per liter of serum is artifactually decreased because of the increased relative proportion occupied by lipid or protein. Although measurement of serum or plasma [Na+] by ion-specific electrodes, currently used by most clinical laboratories, is less influenced by high concentrations of lipids or proteins than is measurement of serum [Na+] by flame photometry, such errors nonetheless still occur. However, because direct measurement of Posm is based on the colligative properties of only the solute particles in solution, increased lipids or proteins will not affect the measured Posm. Second, high concentrations of effective solutes other than Na+ can cause relative decreases in serum [Na+] despite an unchanged Posm; this commonly occurs with hyperglycemia. Misdiagnosis can be avoided again by direct measurement of Posm or by correcting the serum [Na+] by 1. The incidence of hyponatremia depends on the patient population screened and the criteria used to define the disorder. Hospital incidences of 15% to 22% are common if hyponatremia is defined as any serum sodium concentration ([Na+]) of less than 135 mEq/L, but in most studies only 1% to 4% of patients have a serum [Na+] lower than 130 mEq/L, and fewer than 1% have a value lower than 120 mEq/L. Recent studies have confirmed prevalences from 7% in ambulatory populations up to 38% in acutely hospitalized patients. The elderly are particularly susceptible to hyponatremia, with reported incidences as high as 53% among institutionalized geriatric patients. Although most cases are mild, hyponatremia is important clinically because (1) acute severe hyponatremia can cause substantial morbidity and mortality; (2) mild hyponatremia can progress to more dangerous levels during management of other disorders; (3) general mortality is higher in hyponatremic patients across a wide range of underlying diseases; and (4) overly rapid correction of chronic hyponatremia can produce severe neurologic complications and death. Plasma osmolality (Posm) can be measured directly by osmometry, and is expressed as milliosmoles per kilogram of water (mOsm/ kg H2O). Imbalances between water and solute can be generated initially either by depletion of body solute more than body water or by dilution of body solute because of increases in body water more than body solute (Box 7. However, this distinction represents an oversimplification, as most hypoosmolar states include variable contributions of both solute depletion and water retention. Nonetheless, this concept has proved useful because it provides a framework for understanding the diagnosis and treatment of hypoosmolar disorders. However, total osmolality is not always equivalent to effective osmolality, which is sometimes referred to as the tonicity of the plasma. Although prevalences vary according to the population being studied, a sequential analysis of hyponatremic patients who were admitted to a large university teaching hospital showed that approximately 20% were hypovolemic, 20% had edema-forming states, 33% were euvolemic, 15% had hyperglycemia-induced hyponatremia, and 10% had kidney failure. Consequently, euvolemic hyponatremia generally constitutes the largest single group of hyponatremic patients found in this setting. Even isotonic or hypotonic volume losses can lead to hypoosmolality if water or hypotonic fluids are ingested or infused as replacement. Diuretic use is the most common cause of hypovolemic hypoosmolality, and thiazides are more commonly associated with severe hyponatremia than are loop diuretics such as furosemide. Although diuretics represent a prime example of solute depletion, the pathophysiologic mechanisms underlying diuretic-associated hypoosmolality are complex and have multiple components, including free water retention. Consequently, any suspicion of diuretic use mandates careful consideration of this diagnosis. A low serum [K+] is an important clue to diuretic use, as few other disorders that cause hyponatremia and hypoosmolality also produce appreciable hypokalemia. Whenever the possibility of diuretic use is suspected in the absence of a positive history, a urine screen for diuretics should be performed. Most other causes of renal or nonrenal solute losses resulting in hypovolemic hypoosmolality will be clinically apparent, although some cases of salt-wasting nephropathies. The red arrow in the center emphasizes that the presence of central nervous system dysfunction resulting from hyponatremia should always be assessed immediately, so that appropriate therapy can be started as soon as possible in significantly symptomatic patients, even while the outlined diagnostic evaluation is proceeding. Values for osmolality are in mOsm/kg H2O, and those referring to serum Na+ concentration are in mEq/L. First, true hypoosmolality must be present, and hyponatremia secondary to pseudohyponatremia or hyperglycemia must be excluded. This does not require that the Uosm be greater than Posm, but merely that the urine not be maximally dilute. Uosm need not be inappropriately elevated at all levels of Posm, but simply at some level of Posm less than 275 mOsm/ kg H2O.

Studies in molecular genetics have not yet identified the particular genes responsible for schizophrenia, but it is evident from research using family, twin, and adoption studies that genetics are important (Walker & Tessner, 2008). Neuroimaging studies have found some differences in brain structure between schizophrenic and normal patients. In some people with schizophrenia, the cerebral ventricles (fluid-filled spaces in the brain) are enlarged (Suddath, Christison, Torrey, Casanova, & Weinberger, 1990). People with schizophrenia also frequently show an overall loss of neurons in the cerebral cortex, and some show less activity in the frontal and temporal lobes, which are the areas of the brain involved in language, attention, and memory. This would explain the deterioration of functioning in language and thought processing that is commonly experienced by schizophrenic patients (Galderisi et al. Woods (1998) indicated that this loss of brain volume occurs suddenly and rapidly. According to Carlson (2011) this loss coincides with a smaller decrease noted with nonschizophrenic young adults and may be due to an increase in synaptic pruning that occurs during this time. Many researchers believe that schizophrenia is caused in part by excess dopamine, and this theory is supported by the fact that most of the drugs useful in treating schizophrenia inhibit dopamine activity in the brain (Javitt & Laruelle, 2006). However, recent evidence suggests that the role of neurotransmitters in schizophrenia is more complicated than was once believed. It also remains unclear whether 354 observed differences in the neurotransmitter systems of people with schizophrenia cause the disease, or if they are the result of the disease itself or its treatment (Csernansky & Grace, 1998). A genetic predisposition to developing schizophrenia does not always develop into the actual disorder. Even if a person has an identical twin with schizophrenia, he still has less than a 50% chance of getting it himself, and over 60% of all schizophrenic people have no first- or seconddegree relatives with schizophrenia (Gottesman & Erlenmeyer-Kimling, 2001; Riley & Kendler, 2005). One hypothesis is that schizophrenia is caused in part by disruptions to normal brain development in infancy that may be caused by poverty, malnutrition, and disease (Brown et al. Stress also increases the likelihood that a person will develop schizophrenic symptoms; onset and relapse of schizophrenia typically occur during periods of increased stress (Walker, Mittal, & Tessner, 2008). However, it may be that people who develop schizophrenia are more vulnerable to stress than others and not necessarily that they experience more stress than others (Walker, Mittal, & Tessner, 2008). For example, many homeless people are likely to be suffering from undiagnosed schizophrenia. Hooley and Hiller (1998) found that schizophrenic patients who ended a stay in a hospital and returned to a family with high expressed emotion were three times more likely to relapse than patients who returned to a family with low expressed emotion. It may be that the families with high expressed emotion are a source of stress to the patient. Key Takeaways · · · · · · Schizophrenia is a serious psychological disorder marked by delusions, hallucinations, and loss of contact with reality. Schizophrenia is accompanied by a variety of symptoms, but not all patients have all of them. Because the schizophrenic patient has lost contact with reality, he or she is experiencing psychosis. Positive symptoms of schizophrenia include hallucinations, delusions, derailment, disorganized behavior, inappropriate affect, and catatonia. Negative symptoms of schizophrenia include social withdrawal, poor hygiene and grooming, poor problem-solving abilities, and a distorted sense of time. Cognitive symptoms of schizophrenia include difficulty comprehending and using information, problems maintaining focus, and problems with working memory. Rather, there are a variety of biological and environmental risk factors that interact in a complex way to increase the likelihood that someone might develop schizophrenia. Is it better to keep patients in psychiatric facilities against their will, but where they can be observed and supported, or to allow them to live in the community, where they may get worse and have problems functioning. Describe the different types of personality disorders and differentiate antisocial personality disorder from borderline personality disorder. Outline the biological and environmental factors that may contribute to a person developing a personality disorder. A personality disorder is a disorder characterized by inflexible patterns of thinking, feeling, or relating to others that cause problems in personal, social, and work situations. Personality disorders tend to emerge during late childhood or adolescence and usually continue throughout adulthood (Widiger, 2006). The disorders can be problematic for the people who have them, but they are less likely to bring people to a therapist for treatment. They are categorized into three types: · Characterized by odd or eccentric behavior · Characterized by dramatic or erratic behavior · Characterized by anxious or inhibited behavior.