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Books on the topic 'Hydrocortisone'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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1

Savage, Edward Bruce. Hydrocortisone induces aortic rupture in inbred blotchy mice: Implications for abdominal aortic aneurysmal disease in humans. [New Haven: s.n.], 1985.

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2

McK, Jefferies William, ed. Safe uses of cortisol. 2nd ed. Springfield, Ill., U.S.A: C.C. Thomas, 1996.

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3

Clarke, Dara. The control of androgen production in human adrenals: Examination of the effects of pro-opiomelanocortin-derived peptides on androgen and cortisol production in isolated human adrenal cells. Dublin: University College Dublin, 1996.

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4

Emotionale Reaktionsmuster und Cortisolveränderungen im Speichel. Frankfurt am Main: P. Lang, 1988.

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5

Cholesterol: Interactions with testosterone and cortisol in cardiovascular diseases. Berlin: Springer-Verlag, 1987.

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6

K, Lüdecke Dieter, Chrousos George P, Tolis George, and International Symposium on Challenges of Hypersecretion: ACTH, Cushing's Syndrome, and Other Hypercortisolemic States (2nd : 1989 : Crete, Greece), eds. ACTH, Cushing's syndrome, and other hypercortisolemic states. New York: Raven Press, 1990.

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7

Yan, Wang, ed. Mu ai de li liang: Mu ai ru he su zao he cu jin ying er de da nao fa yu. Shanghai Shi: Hua dong shi fan da xue chu ban she, 2008.

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8

Why love matters: How affection shapes a baby's brain. Hove, East Sussex: Brunner-Routledge, 2004.

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9

Justin, Lam, and Lam Carrie, eds. Advanced symptoms of adrenal fatigue syndrome: A metabolic perspective. Loma Linda, CA: Adrenal Institute Press, 2016.

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10

Cameron, Stauth, ed. Brain longevity: The breakthrough medical program that improves your mind and memory. New York: Warner Books, 1997.

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11

Cameron, Stauth, ed. Brain longevity: The breakthrough medical programme that regenerates your mental energy, memory and learning abilities. London: Century, 1997.

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12

Khalsa, Dharma Singh. Brain Longevity. New York: Grand Central Publishing, 2001.

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13

Blokdijk, G. J. Hydrocortisone Butyrate; Third Edition. CreateSpace Independent Publishing Platform, 2018.

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14

Blokdijk, G. J. Hydrocortisone Valerate; Second Edition. CreateSpace Independent Publishing Platform, 2018.

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15

Patel, J. J. The degradation of Hydrocortisone and Dexamethasone. 1986.

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16

R, Chandra. The degradation of hydrocortisone and dexamethasone. 1986.

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17

Cortisol: Physiology, Regulation and Health Implications. Nova Science Publishers, Incorporated, 2012.

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18

William McK., M.D. Jefferies. Safe Uses of Cortisol. 3rd ed. Charles C. Thomas Publisher, 2004.

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19

William McK., M.D. Jefferies. Safe Uses of Cortisol. 3rd ed. Charles C. Thomas Publisher, 2004.

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20

Publications, ICON Health. Hydrocortisone - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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21

Torok, Donald J. The salivary cortisol response to maximal exercise in female distance runners. 1989.

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22

Sikes, Carolyn R. Neuropsychological correlates of hypothalamic-pituitary-adrenocortical dysregulation in depression. 1988.

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23

Sharpe, Cameron Saunders. Genetic and environmental variation in stress physiology among steelhead trout (Oncorhynchus mykiss). 1992.

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24

Voller, Bernadette E. Cortisol, pregnene and pregnane profiles in normal and dysmature newborn pony and lighthorse foals. 1993.

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25

(Foreword), Heidi Skolnik, ed. The Cortisol Connection Diet: The Breakthrough Program to Control Stress and Lose Weight. Hunter House, 2004.

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26

The Cortisol Connection: Why Stress Makes You Fat and Ruins Your Health - And What You Can Do About It. Hunter House, 2002.

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27

Talbott, Shawn. Cortisol Connection Diet: The Breakthrough Program to Control Stress and Lose Weight. Turner Publishing Company, 2013.

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28

Glenville, Marilyn. Mastering Cortisol: Stop Your Body's Stress Hormone from Making You Fat Around the Middle. Ulysses Press, 2006.

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29

Cortisol Control and the Beauty Connection: The All-Natural, Inside-Out Approach to Reversing Wrinkles, Preventing Acne and Improving Skin Tone. Hunter House, 2007.

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30

Talbott, Shawn. Cortisol Connection: Why Stress Makes You Fat and Ruins Your Health - and What You Can Do about It. Turner Publishing Company, 2013.

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31

Kraemer, William, and Shawn Talbott. Cortisol Connection: Why Stress Makes You Fat and Ruins Your Health -- and What You Can Do about It. Turner Publishing Company, 2007.

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32

Talbott, Shawn. The Cortisol Connection: Why Stress Makes You Fat and Ruins Your Health - And What You Can Do About It. Hunter House, 2007.

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33

The effect of a circuit weight training program followed by a detraining period on saliva cortisol and testosterone in males. 1989.

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34

The effect of a circuit weight training program followed by a detraining period on saliva cortisol and testosterone in males. 1990.

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35

Soto-Rivera, Carmen L., and Michael S. D. Agus. Endocrine Disorders in Pediatric Critical Care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0016.

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This chapter focuses in pediatric endocrine disorders that can present acutely and warrant intensive care. Because most of the symptoms associated with endocrine diseases are nonspecific, a broad index of suspicion and knowledge of the details of hormonal regulation are essential for accurate diagnosis and timely management. The chapter includes important information on the pathophysiology, clinical manifestations, evaluation, and management of potentially life-threatening endocrine disorders, including diabetes insipidus, syndrome of inappropriate antidiuretic hormone secretion, acute primary and secondary adrenal insufficiency, disorders of calcium homeostatis, thyroid storm, and diabetic ketoacidosis. For treatment of these disorders, the authors discuss the use of vasopressin (aqueous pitressin), desmopressin, hydrocortisone, calcitonin, bisphosphonates, methimazole, iodide therapy, and insulin.
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36

Adrenal Fatigue: The 21st Century Stress Syndrome. Smart Publications, 2002.

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37

Miss Diagnosed: Unraveling Chronic Stress. iUniverse, Inc., 2005.

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38

Serum and salivary cortisol responses during aerobic exercise in children. 1993.

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39

Serum and salivary cortisol responses during aerobic exercise in children. 1993.

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40

Platt, Philip, and Ismael Atchia. Injection therapy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0087.

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Joint and soft tissue injections with glucocorticoids and other agents remain a critical aspect of the management of musculoskeletal conditions. Injection therapy has previously consisted mainly of glucocorticoid and local anaesthetic, but other agents such as hyaluronic acid, radioactive agents, plasma-rich products, and biologics have also been introduced in the practice of musculoskeletal clinicians. Overall glucocorticoid injection remains the most widely performed procedure, and is an effective treatment for an inflamed joint or soft tissue. This procedure has been widely used for at least five decades. Hydrocortisone was the initial steroid used but longer-acting steroid agents are now favoured for large joints. There is evidence of efficacy not only for inflammatory arthritis conditions, but also for osteoarthritis. There are certain contraindications for injection therapy. Hyaluronic acid (viscosupplementation) injection has become part of the management of osteoarthritis. More recently other agents such as disease-modifying anti-rheumatic drugs (DMARDs) and biologics have been injected with varying degree of success. The ability to deliver an injection accurately depends on appropriate knowledge of the anatomy and, as for any procedures, the experience and skill of the clinician. The approach to different joints and soft tissue structures is described in this chapter.
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41

Keh, Didier. Steroids in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0054.

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The benefit of prolonged application of moderate-dose corticosteroids in systemic inflammatory diseases remains controversial. In critical illness, the endogenous cortisol effect may become insufficient due to adrenal dysfunction and corticosteroid resistance to counterbalance an exaggerated and protracted inflammatory response, which has been termed ‘critical illness-related corticosteroid insufficiency’ (CIRCI). There is evidence that moderate-dose hydrocortisone (200–300 mg/day) significantly fastens shock reversal in patients with septic shock, but may improve survival probably only in patients with high risk of death. Thus, therapy should be considered only in refractory shock with poor response to fluid administration and vasopressor therapy. The indication should be based on clinical judgement and not on cortisol measurement. The application prolonged of moderate-dose methylprednisolone (1 mg/kg/day) was found to be most effective in early acute respiratory distress syndrome, and associated with improved lung function, reduction of mechanical ventilation, and faster discharge from the ICU, but a survival benefit was found only in pooled data, including cohort studies. A continuous infusion and weaning of corticosteroids may be preferable to bolus applications and abrupt withdrawal to avoid side effects such as rebound of inflammation and shock, glucose variability, or respiratory failure. There is currently no evidence that prolonged application of moderate-dose corticosteroids increase the risk of secondary infections or muscle weakness, but infection surveillance should be implemented and combination with muscle relaxants be avoided.
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42

Sampson, Brett G., and Andrew D. Bersten. Therapeutic approach to bronchospasm and asthma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0111.

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The optimal management of bronchospasm and acute asthma is reliant upon confirmation of the diagnosis of asthma, detection of life-threatening complications, recognition of β‎2 agonist toxicity, and exclusion of important asthma mimics (such as vocal cord dysfunction and left ventricular failure). β‎2 agonists, anticholinergics, and corticosteroids are the mainstay of treatment. β‎2 agonists should be preferentially administered by metered dose inhaler via a spacer, and corticosteroids by the oral route, reserving nebulized (and intravenous) salbutamol, as well as intravenous hydrocortisone, for situations when these routes are not possible. A single intravenous dose of magnesium may be of benefit in severe asthma, but repeat dosing is likely to cause serious side effects. Parenteral administration of adrenaline may prevent the need for intubation in the patient in extremis. Aminophylline has an unfavourable side effect profile and has not been shown to offer additional benefit in adults. However, it does have a role in paediatric asthma. Unproven medical therapies with potential benefit include ketamine, heliox, inhalational anaesthetics, and leukotriene antagonists. The need for ventilatory support is usually preceded by worsening dynamic hyperinflation, exhaustion, hypoxia, reduced conscious state, or a combination of these. While non-invasive ventilation may have a temporizing role to allow time for response to medical therapy, there is insufficient evidence for its use, and should not delay invasive ventilation. If invasive ventilation is indicated, a strategy of hypoventilation and permissive hypercapnoea, minimizes barotrauma and dynamic hyperinflation. Extracorporeal support may have a role as a rescue therapy.
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43

Paech, Michael J., and Patchareya Nivatpumin. Postdural puncture headache. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0027.

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Postdural puncture headache (PDPH) may follow either deliberate or unintentional (accidental) penetration of the interdigitating meninges, the dura and arachnoid mater. It is one of the most common and clinically important complications of regional anaesthesia and analgesia in the obstetric population. The headache develops as a consequence of cerebrospinal fluid loss, low intracranial pressure and cerebrovascular changes in the upright position and can prove debilitating. The diagnosis is clinical, making thorough assessment and regular review all the more important, to revise treatment plans, exclude rare serious pathology such as subdural haematoma, and avoid misdiagnosis. This chapter reviews the pathophysiology, incidence, risk factors (needle, technical and patient related), features, natural history, diagnosis, and management of PDPH. High level evidence supports prevention by using small gauge, non-cutting spinal needles, but other preventative strategies against either unintentional dural puncture or PDPH are poorly supported. The absent or poor efficacy of measures such as bed rest, hydration, cerebral vasoconstrictor therapy, epidural or intrathecal saline injection, intrathecal catheter placement or prophylactic epidural blood patch, is noted. Validation of better evidence supporting epidural morphine or intravenous cosyntropin is required. Symptomatic treatment of PDPH is also unreliable. Very limited evidence that requires substantiation supports a modest benefit from caffeine, gabapentinoids or intravenous hydrocortisone. The intervention of epidural blood patch is highly likely to relieve post-spinal PDPH, but only completely resolves epidural needle-induced PDPH in 30–50% of cases. Much detail about EBP remains undetermined, but delayed intervention and injection of approximately 20 mL of autologous blood appear appropriate.
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44

Debaveye, Yves, and Greet Van den Berghe. Pathophysiology and management of pituitary disorders in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0262.

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The pituitary gland plays a predominant role in the endocrine system. Consequently, patients with pituitary diseases or after pituitary surgery present unique challenges to the intensivist. Failure of the anterior pituitary gland to secrete one or more pituitary hormones results in a clinical syndrome known as hypopituitarism. While hypopituitarism is mostly encountered in patients in whom the diagnosis has already been made, acute exacerbation of an undiagnosed insufficiency may occasionally occur. Acute decompensated patients with suspected hypopituitarism should be admitted to an intensive care unit for haemodynamic stabilization, replacement of missing hormones, and identification and treatment of the causative stressor. Prompt administration of hydrocortisone is the single most important acute medical intervention in hypopituitaric patients. Failure of the posterior pituitary to secrete antidiuretic hormone results in diabetes insipidus (DI). DI is characterized by excess volumes of severely diluted urine, which can lead to hyperosmolality and hypernatraemia as many critically-ill patients do not have free access to oral fluids due to obtundation or sedation. Management of DI includes the correction of free water deficit and the reduction of polyuria with desmopressin. The post-operative care following pituitary surgery focuses on vigilant observation for neurosurgical complications (visual loss, meningitis, and cerebrospinal fluid leakage) and monitoring of neuroendocrinological perturbations (hypopituitarism and disorders of water balance, such as DI and SIADH). SIADH presents with hyponatremia, hypo-osmolality, and inappropriately concentrated urine in a setting of euvolaemia and can be managed in most cases by fluid restriction. Potential disruption of the pituitary-adrenal function is covered with peri-operative glucocorticoids.
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45

Wright, Sarah E. Redefining Trauma: Understanding and Coping with a Cortisoaked Brain. Taylor & Francis Group, 2020.

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46

Wright, Sarah E. Redefining Trauma: Understanding and Coping with a Cortisoaked Brain. Taylor & Francis Group, 2020.

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47

Gerhardt, Sue. Why Love Matters: How Affection Shapes a Baby's Brain. Brunner-Routledge, 2005.

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48

Brain Longevity: The Breakthrough Medical Program that Improves Your Mind and Memory. Grand Central Publishing, 1999.

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49

Khalsa, Dharma Singh, and Cameron Stauth. Brain Longevity: The Breakthrough Medical Program that Improves Your Mind and Memory. Grand Central Publishing, 2001.

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50

Khalsa, Dharma Singh. Brain Longevity. Random House Audiobooks, 1997.

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