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By: R. Faesul, M.B.A., M.B.B.S., M.H.S.

Assistant Professor, Marian University College of Osteopathic Medicine

They are a group of disorders seen quite frequently in unwell patients admitted to medical or surgical wards and are encountered quite commonly by liaison psychiatrists in general hospitals back pain treatment kerala purchase imdur online. Porphyria is included as a rare but striking example of an inborn error of metabolism with important psychiatric features knee pain treatment home remedy buy imdur 40mg with mastercard. The chapter focuses on the clinical psychiatric manifestations of the primary endocrine disorders, discussed together with the results of relevant research literature. Whilst a significant majority of patients with the conditions discussed will present either to a general physician or general practitioner, occasional individuals will present in such a way that psychiatric manifestations dominate the clinical picture and the endocrine disturbance may go unnoticed. Endocrine disorders can be accompanied by prominent abnormalities of the mental state, as for example in hypothyroidism and hyperthyroidism, and epochs of life such as after childbirth that are associated with rapid changes in hormonal levels appear to be associated with special liability to mental disturbance. Conversely, it is now clear that primary emotional disorders are accompanied by changes in neuroendocrine regulatory functions and may even predispose to the development of endocrine disorders such as diabetes mellitus. Historically, treatment by means of hormones has often been viewed as a possibility in psychiatry. Kraepelin (1896) once proposed that dementia praecox was basically an endocrine disorder. More recently, studies of patients treated for hypopituitarism have revealed that hormones such as growth hormone, previously thought to play a role only in childhood and adolescence, continue to be important to mental well-being and metabolic function throughout adult life. On the other hand, exogenous administration of hormones, most notably corticosteroids, may lead to the development of cognitive, psychotic or affective disorder. Recent research has continued to pursue the question of how hormones influence fundamental aspects of brain development and human behaviour during both early childhood development and later adult life. Experimental work in animals has clarified the morphological basis by which lack of thyroxine during early development impairs the maturation of behaviour (Eayers 1968). Prenatal steroid hormones have a decisive influence in animals on sexual differentiation and on a wide range of sexual and social behaviours (McCarthy 1994; Signoret & Balthazart 1994). Diabetes mellitus Diabetes mellitus is a group of metabolic diseases characterized by hyperglycaemia resulting from defects in insulin production, insulin action or both. Recent consensus opinion has advised a change to an aetiopathologically based classificatory system (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus 2003), with the vast majority of cases fitting into one of two broad categories. In type 1 diabetes the associated abnormalities of protein, carbohydrate and fat metabolism are the result of insufficient insulin action on peripheral target tissues as a result of reduced insulin secretion, whereas in type 2 diabetes these metabolic abnormalities are the result of diminished tissue response to insulin with or without an associated deficiency in insulin secretion. Type 1 diabetes is associated with pancreatic islet -cell loss that results in proneness to ketosis. Most cases typically present by age 20 and appear to be the result of an autoimmune reaction, possibly triggered by an environmental insult, on a background of raised genetic susceptibility. Type 2 diabetes likely results from a combination of inadequate insulin secretion and peripheral insulin resistance. Insulin levels may be higher than seen in normals but are insufficient to overcome resistance in liver, muscle and adipose tissue. It is well established that genetic mechanisms contribute to the development of both forms of the disease, and interesting progress has been made in relation to type 1 diabetes (Bennett et al. The insulin gene is flanked upstream by multiple repeats of a 14-bp sequence, variations in length of the sequence correlating with disease susceptibility, perhaps through a direct effect on transcription of the insulin gene. Textbooks of medicine should be consulted for the general clinical associations of the disorder and the principles of management by diet, insulin and oral hypoglycaemic agents. Psychiatric disorders, particularly emotional disorders, are more prevalent in the diabetic population, whilst the development of depression in diabetic patients is associated with poorer glycaemic control, higher prevalence of multiple diabetic complications and greater functional impairment. Furthermore, mood disorder appears to be an independent risk factor for the development of type 2 diabetes. A number of medications commonly used by psychiatrists, including all the antipsychotic drugs, are associated with an increased incidence of diabetes. It is therefore important that all practising psychiatrists should be familiar with current diagnostic criteria for diabetes mellitus, enabling any patient developing diabetes to be rapidly identified and referred for appropriate treatment. Failure to do so will unnecessarily expose patients seen by psychiatrists to increased risk of developing cardiovascular disease and diabetic microvascular complications. These issues are discussed below, along with the question of brain damage in diabetic patients.

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The spatiotemporal information obtained in this manner was displayed as colour-coded maps pain treatment guidelines 2012 cheap imdur 20mg free shipping, interpolated values being calculated for points between electrode placements pain management for my dog buy genuine imdur line. Nowadays the input of many more electrodes is used and the system may be used to detect subtle changes during a cognitive task or at rest. Morihisa (1989) describes the strengths and limitations of such techniques and the findings that have emerged in relation to schizophrenia and developmental dyslexia, and uses have been described in relation to encephalopathies and attention deficit disorder. It aims to measure not the electrical activity directly but the minute magnetic fields which are a by-product of that activity. The fundamentals of the Clinical Assessment 131 technique are described by Reeve et al. The resulting information is fed through appropriate electronics to a data acquisition system. Apart from cost and logistics, there is the problem of developing valid models for localisation deep within the brain in the presence of multiple dipole sources with differing orientations. However, it is likely that the technique will contribute importantly to the understanding of the genesis of signals related to perception, cognition and behavioural responses, and might possibly clarify the site of major electrophysiological disturbances associated with psychiatric disorders. It could ultimately find a valuable place in the clinical investigation of patients with epilepsy (Reite 1990; Parra et al. The principal hazard is in patients with raised intracranial pressure and particularly when an intracranial tumour is present. The abrupt reduction of pressure due to withdrawal of fluid can bring about tentorial herniation or a medullary pressure cone with fatal results. Even when the needle is quickly removed there may be continued leakage from the puncture hole in the dura mater so that complications can follow some time later. Lumbar puncture is therefore strictly contraindicated in the presence of papilloedema or when there are symptoms suggestive of raised intracranial pressure, except under skilled supervision and when neurosurgical help is immediately to hand. In the absence of raised intracranial pressure the risk attached to lumbar puncture is small. In psychiatric practice it will sometimes be indicated in patients who show disturbance of consciousness or unexplained change of behaviour, even in the absence of definite neurological signs. The pressure is raised in the presence of tumour, haematoma, abscess or cerebral oedema. The pressure may also be raised in certain rare disorders such as lead poisoning or hypoparathyroidism. A pleocytosis implies inflammatory changes in the meninges, either primary as in meningitis, or secondary to cerebral infection as in encephalitis or cerebral abscess. Polymorphonuclear leucocytes predominate with pyogenic infections and may number many thousands per cubic millimetre, rendering the fluid turbid. Virus encephalitis shows mainly lymphocytes, though with some varieties there may be polymorphs in the early stages. When present, pleocytosis can be an essential observation for confirming the diagnosis. A slight pleocytosis, nearly always of lymphocytes, may be present in other conditions including primary and secondary cerebral tumours, cerebral infarctions or multiple sclerosis. Xanthochromia in the absence of frank blood is also sometimes found with subdural haematomas. An increased protein content is common to many conditions and can be difficult to interpret. The protein rises with meningitic infections and this can persist for some time after the pleocytosis has resolved. With certain tumours such as meningiomas or acoustic neuromas the level is often considerably higher. The globulin fraction is raised in relation to the albumin in many inflammatory conditions.

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In a few cases pain treatment ulcerative colitis order imdur with amex, blood glucose concentrations may return to normal once the drug is discontinued american pain society treatment guidelines purchase imdur 20 mg without a prescription. In one trial in children, 10% of cases developed hyperglycemia, and all showed glycosuria [156]. Its analog, acipimox, does not have adverse effects on glycemic control in people with diabetes [161]. Yes Continue to monitor No Adjust insulin to achieve fasting and preprandial glucose < 8 mmol/L Continue to monitor Figure 16. The incidence of gatifloxacin-induced hyperglycemia is estimated at around 1%, and reported cases have involved both new-onset diabetes and worsening of glycemic control in patients with existing diabetes. The exact underlying mechanism is unknown, but data from animal studies point towards possible inhibition of insulin secretion [164] or increased secretion of epinephrine [165]. Transient hyperglycemia has been described following treatment or overdose with a number of commonly prescribed drugs such as non-steroidal anti-inflammatory drugs [166] and isoniazid. There are also anecdotal reports of drug-induced hyperglycemia associated with nalidixic acid [167], carbamazepine [168], encainide [169], benzodiazepines [170] and mianserin [171]. Treatment of drug-induced hyperglycemia Clinically relevant hyperglycemia occurs most commonly with high doses of glucocorticoids. If hyperglycemia occurs during thiazide treatment, the need for the drug should be reassessed. If a diuretic is required, then a small dose of furosemide or bumetanide may be substituted. If an antihypertensive agent is needed, it may be possible to reduce the dosage of bendroflumethiazide. Steroid-induced diabetes It may not be possible to withdraw glucocorticoid therapy, although "steroid-sparing" immunosuppressive drugs such as azathioprine can sometimes be introduced for certain indications. Random blood glucose measurements provide only an approximate guide, and therapy should be adjusted by frequent blood glucose monitoring; simple relief of symptoms alone is inadequate. A target fasting blood glucose concentration of <8 mmol/L may be suitable in the short term, and the usual criteria for good control should be applied if long-term glucocorticoid therapy is undertaken (see Chapter 20). This dosage is unlikely to produce hypoglycemia and indeed may need to be increased progressively, as dictated by blood glucose monitoring. Patients with diabetes who are to begin high-dosage glucocorticoid therapy must be warned that their glycemic control will worsen, and treatment for their diabetes should be adjusted prospectively. For patients already taking insulin, the dosage may need to be 273 Part 4 Other Types of Diabetes increased by 50% initially, starting on the same day as steroid therapy. Conclusions Many drugs can cause hyperglycemia and diabetes, or worsen blood glucose control in patients with diabetes. The possible contribution of diabetogenic drugs should be considered in newly diagnosed patients with diabetes, or if hyperglycemia develops in subjects with previously well-controlled diabetes. Drug effects are often reversible and there are often alternative treatments to achieve the same therapeutic goals. Where the prescription of diabetogenic drugs is inevitable, careful monitoring of glycemic control and prudent use of suitable antidiabetic treatment can mitigate their effects. Risk factors for developing noninsulin dependent diabetes: a 10 year follow up of men in Uppsala. The effects of adrenalectomy and hypophysectomy upon experimental diabetes in the cat. The production of glycosuria in the normal rat by means of 17-hydroxy-11-dehydrocorticosterone. Symposium on the influence of adrenal cortical steroids on carbohydrate metabolism in man.

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It seems likely that damage to orbitofrontal or ventromedial frontal cortex is central to both the impairment of higher cognition (social cognition pain treatment with methadone discount imdur 20 mg on-line, decision-making and control of goal-directed behaviour) and the personality uab pain treatment center imdur 20 mg visa. It is proposed that normal social behaviour depends on a somatic marker, linked to the limbic system, guiding social decisions based on experience of the outcome of previous similar situations. Decisions which in Head Injury 209 the past have resulted in poor outcomes are suppressed by the somatic marker. This process is critically dependent on the medial orbitofrontal cortex, where limbic system responses, thought to underpin the somatic marker, are able to influence decisions that depend on cortical processing. Damasio suggests that failure to recognise and understand emotional signals and social cues is not the problem. The problem lies in the ability to decide and act appropriately despite good social understanding. Patients with ventromedial frontal lesions show impaired ability to interpret nonverbal emotional expression. Similarly, impairments of recognition of expressions of emotion have been found in a patient with orbitofrontal injury and acquired sociopathy (Blair & Cipolotti 2000). Others have emphasised the role of ventral frontal cortex in the extinction of previously rewarded behaviour (Rolls et al. Patients with ventral frontal lesions, half of whom had suffered a head injury, were unable to alter their behaviour appropriately despite being aware that the situation had changed. Their scores on a questionnaire rating disinhibition or other socially inappropriate behaviours correlated with failure to switch responses. Tests of gambling behaviour may weakly predict the failure of patients to regulate behaviour according to internal goals (Levine et al. It therefore seems likely that the personality change many describe as the frontal lobe syndrome is due to subtle but disabling impairments of higher cognitive function, particularly as they relate to social understanding and decisionmaking especially in complex unstructured situations to meet internal goals. Aggression the symptom of reduced control over aggression deserves special consideration (see Chapter 2, Disordered control of aggression). This is seen with sufficient frequency after head injury, and often enough in relative isolation, to suggest a particular association with head injury. Three times as many head-injured patients showed significant aggression during the first 6 months post injury as did a control group with multiple trauma but without head injury (33. This difference was not explained by greater alcohol use or depression in the head injured. Indeed relatives tend to report increasing problems with temper outbursts over the years post injury (Brooks et al. Using a fairly conservative estimate of aggressive behaviour, measured using the Overt Aggression Scale (Yudofsky et al. At each time point it was not simply the same patients who displayed aggression; a good proportion of patients moved from being aggressive to not aggressive and vice versa in no particular pattern. It is customary to distinguish verbal aggression from physical aggression towards either objects or people. Though this is important for risk management, there is little evidence that these different behaviours can be teased apart. Agitation, on the other hand, with marked restlessness and distractibility, is usefully considered separately even though aggression may be present. Agitation is particularly likely to be seen in the early post-injury period in the context of the post-traumatic delirium. Sexually aggressive behaviour, often with evidence of other sexually disinhibited behaviour, may be seen in relative isolation from other forms of aggression and is considered in detail later in this chapter (see Sexuality, social adaptation and effects on the family). The authors stressed that the condition was very different from the more common symptom of post-traumatic irritability, especially in its explosive quality. In general the problem was found to follow severe head injury, although in a few cases the blow had been quite mild. Such behaviour has been described as the organic aggression syndrome (Silver et al. The argument that an epileptic disturbance may be involved is difficult to confirm but receives gentle support from the observation that carbamazepine may be effective. However, good empirical evidence that brain injury does result in a specific syndrome of aggressive behaviour is 210 Chapter 4 Box 4.

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