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Books on the topic 'Hypothalmic diseases'

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Published: 27 July 2024
Last updated: 29 July 2024

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1

Casanueva, Felipe F., and Ezio Ghigo, eds. Hypothalamic-Pituitary Diseases. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-44444-4.

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2

Casanueva, Felipe F., and Ezio Ghigo, eds. Hypothalamic-Pituitary Diseases. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-38681-2.

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3

Dina, Nerozzi, Goodwin Frederick K. 1936-, Costa Erminio, and International Congress on "Hypothalamic Dysfunction in Neuropsychiatric Disorders" (1986 : Rome, Italy), eds. Hypothalamic dysfunction in neuropsychiatric disorders. New York: Raven Press, 1987.

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4

Geer, Eliza B., ed. The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45950-9.

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5

Kurup, Ravikumar. Hypothalamic digoxin, cerebral dominance and brain function in health and diseases. New York: Nova Science Publishers, Inc., 2003.

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6

C, Gaillard Rolf, ed. The ACTH axis: Pathogenesis, diagnosis, and treatment. Boston: Kluwer Academic Publishers, 2003.

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7

Martin, Joseph B. Clinical neuroendocrinology. 2nd ed. Philadelphia: Davis, 1987.

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8

Ghigo, Ezio, and Felipe F. Casanueva. Hypothalamic-Pituitary Diseases. Springer International Publishing AG, 2018.

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9

Hypothalamic-Pituitary Diseases. Springer, 2018.

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10

Young, Allan H., and Mario F. Juruena. Hypothalamic–pituitary–adrenal axis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0006.

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Increased adrenocortical secretion of hormones, primarily cortisol in depression, is one of the most consistent findings in neuropsychiatry. The maintenance of the internal homeostatic state of an individual is facilitated by the ability to circulate glucocorticoids to exert negative feedback on the secretion of hypothalamic–pituitary–adrenal (HPA) hormones through binding to mineralocorticoid and glucocorticoid receptors, thus limiting the vulnerability to diseases related to psychological stress in genetically predisposed individuals. The HPA axis response to stress can be thought of as a crucial part of the organism’s response to stress: acute responses are generally adaptive, but excessive or prolonged responses can lead to deleterious effects. A spectrum of conditions may be associated with increased and prolonged activation of the HPA axis, including depression, poorly controlled diabetes mellitus, and metabolic syndrome. HPA axis dysregulation and hypercortisolaemia may further contribute to a hyperglycaemic or poorly controlled diabetic state.
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11

Shaw, Robert W. Hypothalamic Pituitary Dysfunction (Advances in Reproductive Endocrinology, Vol 6). Taylor & Francis Group, 1995.

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12

Kurup, Ravikumar. Hypothalamic Digoxin, Cerebral Dominance and Brain Function in Health and Diseases. Nova Science Publishers, Incorporated, 2009.

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13

Kurup, Ravikumar, and Parameswaran Achutha Kurup. Hypothalamic Digoxin, Cerebral Dominance and Brain Function in Health and Diseases. Nova Science Publishers, 2008.

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14

Geer, Eliza B. Hypothalamic-Pituitary-Adrenal Axis in Health and Disease: Cushing's Syndrome and Beyond. Springer, 2016.

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15

Geer, Eliza B. The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease: Cushing’s Syndrome and Beyond. Springer, 2018.

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16

Geer, Eliza B. The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease: Cushing’s Syndrome and Beyond. Springer, 2016.

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17

Newell-Price, John, Alia Munir, and Miguel Debono. Adrenal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0188.

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This chapter reviews the clinical features, diagnosis, and treatment of three adrenal diseases: adrenal insufficiency, primary aldosteronism (hyperaldosteronism), and phaeochromocytoma. Adrenal insufficiency is a disorder characterized by impaired adrenocortical function. In primary adrenal insufficiency, destruction of the adrenal cortex results in a decreased production of glucocorticoids, mineralocorticoids, and/or androgens. Secondary adrenal insufficiency is due to disordered pituitary and hypothalamic function resulting in decreased secretion of adrenocorticotropic hormone or corticotrophin-releasing hormone, with consequent reduction in glucocorticoid and/or androgen secretion. Aldosterone is produced in the zona glomerulosa of the adrenal cortex. Abnormal overproduction of aldosterone results in autonomous primary hyperaldosteronism, leading to hypertension and hypokalaemia. Phaeochromocytomas are rare tumours of the adrenal medulla, arising from chromaffin cells, and produce catecholamines. Tumours arising from extra-adrenal ganglia, both sympathetic and parasympathetic, are called paragangliomas. As the majority of sympathetic paragangliomas secrete catecholamines, they are also called extra-adrenal phaeochromocytomas.
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18

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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19

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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20

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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21

Gaillard, Rolf C. Acth Axis: Pathogenesis, Diagnosis and Treatment. Springer, 2013.

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22

Gaillard, Rolf C. Acth Axis: Pathogenesis, Diagnosis and Treatment. Springer London, Limited, 2012.

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23

Lightman, Stafford. Can neurobiology explain the relationship between stress and disease? Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780198530343.003.0006.

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This chapter explores if neurobiology can explain the relationship between stress and disease. It considers if events that occurred early in life, perhaps during a period of prolonged stress, may affect biological processes, sometimes permanently, through changes in the midbrain neurotransmitter concentrations, the hypothalamic-pituitary-adrenal (HPA) axis, and the central nervous system (CNS). Animal models of stress are used to demonstrate these changes.
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24

Human Hypothalamus: Basic and Clinical Aspects, Part 2: Handbook of Clinical Neurology (Series Editors: Aminoff, Boller and Swaab). Elsevier, 2003.

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25

Reading, Paul J. Neurological diseases and their effects on the sleep–wake cycle. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0035.

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This chapter addresses current neurobiological knowledge of how wake- and sleep-promoting systems interact to produce the daily circadian rhythm of wake and sleep and how this may be adversely affected by a variety of neurological diseases. The crucial importance of sleep quality for optimal brain function is stressed and the potential hazards of prolonged wakefulness highlighted. Insomnia relating to either sleep onset or maintenance is common and increases with normal aging. Many neurodegenerative diseases such as Alzheimer disease appear to enhance the effects of aging on the sleep–wake cycle, with increased fragmentation and reduced deep sleep. Focal pathology in the thalamus or sometimes the hypothalamus may produce striking insomnia, as may several autoimmune encephalitides. Hypersomnia is most often secondary to poor-quality nocturnal sleep, but may also relate to discrete hypothalamic pathology or traumatic head injury. The effects of epilepsy and its treatment on sleep can be significant and are discussed.
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26

Mason, Peggy. Homeostatic Systems. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0027.

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The roles of the hypothalamus in regulating fluid balance and supporting the calm affective state needed for maternal care are described. Hypothalamic control of hormone release is reviewed and related disorders such as Addison’s disease and acromegaly are introduced. Basic thermoregulatory principles are presented and the biological danger of ambient heat is emphasized. The concept of set point is explained in the context of fever, antipyresis and hyperthermia. Neural regulation of blood pressure and orthostatic hypotension are briefly described. The patterns and neural circuits involved in breathing during rest or while exercising or sleeping are detailed. A description of neural control of micturition is used to explain detrusor-sphincter dyssenergia secondary to spinal cord injury. The enteric nervous system is briefly described and Hirschsprung disease is introduced. Finally, the neural control of sleep, disorders of sleep-wake control, and von Economo’s discovery of encephalitis lethargica are detailed.
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27

Neyrinck, Arne P., Patrick Ferdinande, Dirk Van Raemdonck, and Marc Van de Velde. Donor organ management. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0034.

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Organ transplantation is the standard treatment modality for end-stage organ disease in selected cases. Two types of potential organ donors can be identified: the brain-dead ‘heart-beating donors’, referred to as DBD (donation after brain death), and the warm ischaemic ‘non-heart-beating donors’, referred to as DCD (donation after circulatory death). Brain death induces several physiological changes in the DBD donor. An autonomic storm is characterized by massive catecholamine release, followed by autonomic depletion during a vasoplegic phase. This is associated with several hormonal changes (suppression of vasopressin, the hypothalamic-pituitary-adrenal axis, and the hypothalamic-pituitary-thyroid axis) and an inflammatory response. These physiological changes form the basis of organ donor management, including cardiovascular stabilization and hormonal therapy (including vasopressin and analogues, thyroid hormone, and cortisol). Donor management is the continuation of critical care, with a shift towards individual organ stabilization. An aggressive approach to maximize organ yield is recommended; however, many treatment strategies need further investigation in large randomized trials. DCD donors have now evolved as a valid alternative to increase the potential donor pool and challenge the clinician with new questions. Optimal donor comfort therapy and end-of-life care are important to minimize the agonal phase. A strict approach towards the determination of death, based on cardiorespiratory criteria, is prerequisite. Novel strategies have been developed, using ex situ organ perfusion as a tool, to evaluate and recondition donor organs. They might become more important in the future to further optimize organ quality.
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28

Soffer, Jocelyn, and Harold W. Goforth. Endocrine Comorbidities in Persons with HIV. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0045.

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A wide range of endocrine abnormalities commonly accompany and complicate HIV infection, many of which have implications for psychiatrists and other mental health professionals working with this population. Such abnormalities include adrenal insufficiency, hypercortisolism, hyperthyroidism, hypothyroidism, hypogonadism, decreased bone mineral density, and bone disease. Endocrinopathies are great mimickers of psychiatric disorders, manifesting in some cases as disturbances of mood, sleep, appetite, thought process, energy level, or general sense of well-being. Understanding the intricate and complex relationships between immunological, endocrinological, and psychological systems is important to improve recognition and treatment of reversible endocrinopathies, diminish suffering, and enhance quality of life and longevity in persons with HIV and AIDS. This chapter will present an overview of HIV-associated changes in the function of the hypothalamic–pituitary axes, adrenal glands, thyroid gland, gonads, and bone and mineral metabolism, and consider the psychosocial implications of such endocrinopathies.
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29

Yang, James. Endocrine Disorders: Integrative Treatments of Hypothyroidism, Diabetes, and Adrenal Dysfunction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0014.

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Thyroid function, glucose metabolism, and an adaptive hypothalamic–pituitary–adrenal (HPA) axis are critical determinants of health and wellness. This chapter highlights the integrative physiology and interactions between these three systems and an integrative medicine approach to these conditions. Integrative medicine expands the evaluation of endocrine dysfunction through a person-centered approach. Patients’ overall symptoms and physiological function should be taken into account in evaluating thyroid function and planning treatment. Our approach to diabetes focuses on the importance of lifestyle changes and nutrition. Our perspective of the effects of chronic stress has been informed by current perspectives on neurobiology and neuroplasticity; chronic stress leaves its mark on the brain through changes in structure as well as its function in adapting to further stress. We present an integrative approach to manage and improve these three endocrine systems to address disease and improve patients’ energy and health.
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30

Mystakidou, Kyriaki, Irene Panagiotou, Efi Parpa, and Eleni Tsilika. Sleep disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0086.

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Sleep disturbances represent frequent distressing symptoms in the palliative care setting. The more common disorders include insomnia, excessive daytime sleepiness, and circadian rhythm sleep disorders. The most prevalent sleep disorder, insomnia, includes difficulty initiating and/or maintaining sleep, waking up too early, and non-restorative or poor quality sleep. Primary sleep disturbances are thought to be a disorder of hyperarousal, while a hypothalamic-pituitary-adrenal axis dysfunction has also been confirmed. Secondary sleep disorders have been associated with a large number of potential causes, both physical and psychological. Sleep disturbances in palliative care can be due to either the advanced disease and/or its treatment. Chronic medication use, neurological or psychiatric disorders, as well as environmental factors, can also present contributing factors. This chapter discusses the diagnosis and treatment of sleep disturbances, both pharmacological and non-pharmacological, including cognitive behavioural therapy, the cornerstone of non-pharmacological interventions.
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31

Lockley, Steven W. Principles of sleep–wake regulation. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198778240.003.0002.

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The 24-hour sleep–wake cycle is generated by two oscillatory processes: an endogenous hypothalamic circadian pacemaker and a sleep- and wake-dependent homeostat. These processes combine to maintain a consolidated bout of sleep at night and relatively stable waking function across the day. They also combine to determine ‘diurnal preference’—whether one is a ‘lark’ or an ‘owl’—a reflection of the phase relationship between the circadian and homeostatic processes. These processes are affected directly by light, either through resetting of the circadian pacemaker or its direct alerting effects. Sleep deficiency and circadian disruption have been associated with a higher risk of chronic disease, although the methodology for assessing these exposures is not optimal. Both sleep and the circadian system also have myriad influences on other aspects of our physiology, behaviour, and metabolism; therefore, steps should be taken to reduce their potential confounding effects in epidemiological studies.
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32

Bassi, Gabriele, and Roberto Fumagalli. Pathophysiology and management of fever. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0352.

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Core body temperature is strictly regulated by autonomic and behavioural compensatory adaptations and an increase may represent a physiological stereotypical controlled response to septic and inflammatory conditions, or an uncontrolled drop in the hypothalamic thermoregulatory threshold. Fever has been demonstrated to be a potential mechanism of intrinsic resistance against infectious disease playing a pivotal role in the human evolution. High temperature may be detrimental during oxygen delivery-dependent conditions and in a neurological population. Despite this evidence, a definitive conclusion, between the association of fever and the outcome in critically-ill patients, is still lacking. The decision-making strategy in the context of fever management in critical care must be supported by single case assessment. This chapter summarizes the main physiological mechanisms of temperature control that physicians should consider when dealing with fever or deliberate hypothermia and analyses the main evidence in the role of fever in the critically ill in order to help bedside clinical strategy.
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