Oxford Medicine Online
You are looking at 11-20 of 27 items for: psychiatry AND evidence MED00250
Obesity John Wass, Katharine Owen, and Helen Turner Print Publication Year: 2014 Published Online: Mar 2014 ISBN: 9780199644438 eISBN: 9780191742859 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199644438.003.0015
Definition of obesity - Epidemiology of obesity - Aetiology of obesity - Pathophysiology of obesity - Consequences of obesity - Management of an obese patient - Bariatric surgery - -
Psychological problems David Levy Print Publication Year: 2016 Published Online: Sep 2016 ISBN: 9780198766452 eISBN: 9780191820960 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780198766452.003.0011
Psychological disturbances occur throughout Type1 diabetes, from diagnosis to the experience of late tissue complications. Serious life events may precipitate diabetes onset. All parents of newly diagnosed children report stress. Poor glycaemic control is associated with suboptimal school performance, but children do not consider their own quality of life to be poor. Depression during adolescence is no more common than in the background population. Single parenthood and minority ethnicity are associated with worse glycaemic outcomes. Poor glycaemia associated with poor family functioning can be helped by family-based interventions. Eating disorders are not more frequent in diabetes, but disordered eating and insulin omission are prevalent, the last associated with increased mortality. Depression is common, often severe, undiagnosed, and associated with maternal depression. Non-pharmacological treatment is more effective than antidepressants. Diabetic complications increase the risk of depression 2- to 3-fold, and all depressive disorders may increase mortality in people with foot ulceration.
Thyroid function tests and the effects of drugs Jim Stockigt Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.3031
The assessment of thyroid function by laboratory testing began in about 1934 with the measurement of oxygen consumption or basal metabolic rate. Twenty years later Page 1 of 6 PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy). Subscriber: null; date: 15 January 2017
measurement of protein-bound iodine became the standard technique and after a further 20 years this assay was superseded by radioimmunoassays of thyroxine (T4) and triiodothyronine (T3). Radioimmunoassays for thyroid-stimulating hormone (TSH) were reported from 1965, but early techniques could not distinguish normal values from the suppressed levels found in thyrotoxicosis. Until about 1990 this distinction was made by the administration of intravenous thyrotropin-releasing hormone (TRH), which fails to increase TSH to measurable levels in thyrotoxicosis, while producing a clear 5- to 15-fold increase in serum TSH in euthyroid subjects with normal pituitary function. Immunometric TSH assays now allow the suppressed serum TSH levels of thyrotoxicosis to be clearly distinguished from normal. This fundamental advance has coincided with the development of ingenious techniques to estimate the minute fraction of total serum T4 that circulates in the unbound state, but even the best free T4 methods offer only a marginal diagnostic advantage over the measurement of total T4, e.g. when the concentration of thyroxine-binding globulin (TBG) is abnormal. Current enthusiasm for free T4 and T3 estimation needs to be tempered by an understanding of the method-dependent limitations of these techniques, particularly in situations where assessment of thyroid function is most difficult (see below).
Causes and laboratory investigation of hypothyroidism Ferruccio Santini and Aldo Pinchera Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.3243
Hypothyroidism is the clinical state that develops as a result of the lack of action of thyroid hormones on target tissues (1). Hypothyroidism is usually due to impaired hormone secretion by the thyroid, resulting in reduced concentrations of serum thyroxine (T4) and triiodothyronine (T3). The term primary hypothyroidism is applied to define the thyroid failure deriving from inherited or acquired causes that act directly on the thyroid gland by reducing the amount of functioning thyroid tissue or by inhibiting thyroid hormone production. The term central hypothyroidism is used when pituitary or hypothalamic abnormalities result in an insufficient stimulation of an otherwise normal thyroid gland. Both primary and central hypothyroidism may be transient, depending on the nature and the extent of the causal agent. Hypothyroidism following a minor loss of thyroid tissue can be recovered by compensatory hyperplasia of the residual gland. Similarly, hypothyroidism subsides when an exogenous inhibitor of thyroid function is removed. Peripheral hypothyroidism may also arise as a consequence of tissue resistance to thyroid hormones due to a mutation in the thyroid hormone receptor. Resistance to thyroid hormones is a heterogeneous clinical entity with most patients appearing to be clinically euthyroid while some of them have symptoms of thyrotoxicosis and others display selected signs of hypothyroidism. The common feature is represented by pituitary resistance to thyroid hormones, leading to increased secretion of thyrotropin that in turn stimulates thyroid growth and function. The variability in clinical manifestations depends on the severity of the hormonal resistance, the relative degree of tissue hyposensitivity, and the coexistence of associated genetic defects (see Chapter 3.4.8).
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Sequelae of extratesticular disease David J. Handelsman Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.9087
Systemic disease has major effects on male reproductive health, although these are not always recognised. Management of any medical disorder should include careful consideration of the effects of illness and its treatment on androgen secretion, fertility, and sexuality. A functional reproductive system is a profoundly valued aspect of a healthy life and it is an important, albeit often unstated, expectation of medical care that reproductive function is preserved and protected. Hence, recognition of this important but easily overlooked aspect of medical care should form a part of optimal management of chronic medical illness (1).
Hypothalamic dysfunction (hypothalamic syndromes) M. Guftar Shaikh Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.2181
The hypothalamus is a complex area of the brain and is important in co-coordinating signals between the nervous system and the endocrine system, primarily via the pituitary gland. Various processes throughout life, such as birth, puberty, and pregnancy, as well as neurological and psychiatric disorders are regulated by the hypothalamus (1). It influences many hormonal and behavioural circadian rhythms, as well as being involved in the control of body temperature, hunger, and thirst. Damage to the hypothalamus whether it is congenital or acquired will lead to significant clinical morbidity (Box 2.4.1.1). Recent advances in molecular techniques and improved neuroimaging, particularly MRI and positron emission tomography (PET) have given us a better understanding of hypothalamic syndromes and their clinical manifestations. It may be very difficult to differentiate between hypothalamic and pituitary disease as the endocrine abnormalities are often similar. As the hypothalamus regulates both endocrine and autonomic function, there is usually a combination of endocrine and neurological disturbance in hypothalamic damage. This includes abnormal behaviour, eating disorders, and thermoregulation. The hypothalamus consists of a number of different nuclei which have very specific functions and also secretion of hypothalamic hormones and neuropeptides (1). The clinical syndrome will depend on the location and extent of the underlying lesion. The lesion may be very small and only affect specific hypothalamic nuclei which will result in discrete symptoms; however larger lesions, which are more likely, will present with a variety of problems (Fig. 2.4.1.1). The endocrine abnormalities seen in hypothalamic syndromes usually result in pituitary hyposecretion; however due to loss of inhibitory factors hypersecretion can also occur.
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Children and adolescents usually present with growth failure and disorders of puberty, which can be both delayed and precious. Adults with hypothalamic dysfunction can present with dementia, disturbances in appetite and sleep, as well as hormonal deficiencies. Causes of hypothalamic damage, particularly the anterior hypothalamus, include tumours such as craniopharyngiomas, optic nerve gliomas, and inflammatory conditions such as histiocytosis and sarcoidosis.
Management of differences and disorders of sex development in the newborn S. Faisal Ahmed, Paula Midgley, and Martina Rodie Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.7022
The birth of a new baby is one of the greatest wonders of nature. The first question that is usually posed by the new parent is 'is it a boy or a girl?'; without this information the parents cannot even formulate the second question, which is usually 'is he/she alright?'. It is no wonder that the birth of a child with an abnormality of genital development where the sex of rearing is uncertain at birth, presents difficult clinical and ethical issues. However, the recognition of genital ambiguity may depend on the expertise of the observer. The prevalence of genital anomalies at birth may be as high as 1 in 300 births (1), the prevalence of complex anomalies that may lead to true genital ambiguity may be as low as 1 in 5000 births (2). Rather than treating every affected child as a medical emergency, it is paramount that such a child is first assessed by an expert with adequate knowledge about the range of variation in the physical appearance of genitalia, the underlying pathophysiology of disorders of sex development, and the strengths and weaknesses of the tests that can be performed in early infancy. This expert should be able to ensure that the parents’ needs for information are comprehensively addressed, while appropriate investigations are performed in a timely fashion. This expert also needs to have immediate access to the multidisciplinary team that is essential for the management of such a child. Finally, in the field of rare conditions, it is imperative that the clinician shares the experience with others through national and international clinical and research collaboration.
Pituitary radiotherapy Thankamma Ajithkumar and Michael Brada Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.2109
External beam radiotherapy remains an important component of management of patients with pituitary adenoma and a considerable proportion of patients receive it during the course of their illness. Traditional policy had been to use radiotherapy for all patients with residual nonfunctioning pituitary adenoma after surgery as the majority were considered to progress (1). With improvement in surgical techniques and access to MRI, postoperative radiotherapy is no longer routinely employed even in the presence of residual tumour. The Page 4 of 6 PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy). Subscriber: null; date: 15 January 2017
use of radiotherapy is based on relative risk assessment, generally withholding further treatment until progression unless there is a perceived threat to function, particularly vision, if the tumour was to progress. Currently radiotherapy is used in patients with progressive nonfunctioning adenoma demonstrated on interval imaging and achieves tumour control in over 90% of patients at 10 years and 85–92% in 20 years (1–9). Radiotherapy remains an integral component of treatment of patients with secreting adenoma who fail to achieve biochemical cure following surgery and medical treatment and in patients with progressive/ recurrent tumour mass regardless of the status of hypersecretion. The slow rate of decline in hormone levels means that normalization takes months to years and the delay is primarily related to pretreatment hormone levels. Nevertheless radiotherapy leads to normalization of excess hormone secretion in the majority of patients. The past two decades have seen developments in radiotherapy, which can largely be considered as refinement of existing technology. The principal aim of modern highprecision, localized radiotherapy is to treat less normal tissue to significant radiation doses therefore minimizing the risk of late normal tissue injury. The higher precision relies on increased accuracy of tumour delineation using modern imaging. The overall success of modern high-precision treatment is more likely to be related to the treatment centre infrastructure and expertise and the accuracy in identifying the tumour than the exact equipment used.
Clinical assessment and systemic manifestations of hypothyroidism Massimo Tonacchera, Luca Chiovato, and Aldo Pinchera Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.3233
Hypothyroidism may affect people of both sexes and all ages. The clinical expression of thyroid hormone deficiency varies considerably between individuals. It is influenced mainly by the age of the patient and the rate at which hypothyroidism develops although being largely independent of its cause. Most adult patients complain of a slowing of physical and mental activity. Hypothyroidism is a graded phenomenon, ranging from very mild cases, in which biochemical abnormalities (subclinical hypothyroidism; see Chapter 3.4.4) are present but the individual hardly notices symptoms and signs of thyroid hormone deficiency, to very severe cases in which the danger exists of sliding down into a life-threatening myxoedema coma.
Clinically nonfunctioning pituitary tumours and gonadotropinomas W. W. de Herder, R. A. Feelders, and A. J. van der Lely Print Publication Year: Published Online: Jul 2011 ISBN: 9780199235292 eISBN: 9780199608232 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199235292.003.2158
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The significant progress that has been made in the past years in the medical treatment of all pituitary adenomas is in stark contrast with the lack of progress in the medical treatment of clinically nonfunctioning pituitary tumours, or adenomas. In fact, only secreting, or functioning, tumours can be treated by medical therapy with at least modest to very impressive effect. Clinically nonfunctioning pituitary adenomas do not produce clinical signs of hormonal hypersecretion. Therefore, signs and symptoms will depend on the mass effect of these adenomas over the central nervous system (1–3). Due to the lack of hypersecretion of hormones, nonfunctioning pituitary adenomas present themselves because of their mass effect and compression or destruction of surrounding tissues. This could also lead to hypopituitarism, which can be the presenting symptom as well (1–3). Despite their histologically benign nature, giant and ‘invasive’ nonfunctioning pituitary adenomas are one of the most complex neurosurgical challenges. Large nonfunctioning pituitary tumours are usually confined inferiorly by the sellar dura, superiorly by the elevated sellar diaphragm, and laterally by an intact medial wall of the cavernous sinus. If the anatomical extensions of the tumour are understood and a radical tumour resection is achieved, the visual and long-term outcome can be very rewarding. The goals of surgery are twofold: first to make a pathological diagnosis, and second, because these tumours are endocrinologically silent, to decompress the neural tissue (4). The vast majority of nonfunctioning pituitary adenomas are gonadotroph cell adenomas, as demonstrated by immunocytochemistry. However, they are rarely associated with increased levels of dimeric luteinizing hormone or follicle-stimulating hormone. Increased levels of subunits (free #-subunit mainly, LH-B subunit more rarely), however, are more frequently encountered, but are generally modest (5). In this chapter the term ‘clinically nonfunctioning pituitary adenomas’ is used to describe pituitary tumours, which in most instances produce low quantities of hormones causing no clinically recognizable symptomatology. In the few instances, in which such tumours produce intact gonadotropins that activate testicular or ovarian activity, the term ‘gonadotropinomas’ is used.
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