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Hormonal and Para-Neoplastic Syndromes - also Skin Lesions.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
Cushing's syndrome (with excess ACTH production leading to hyperplasia of the adrenal cortex, but usually without the full blown clinical picture) is also fairly common and may lead to skin pigmentation, hypercalcaemia, nocturia, etc. Acromegaly, enteritis, or migratory thromboses may also be seen (Illus. CUSHING'S SYNDROME).
Trauma Physiology and Metabolism
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
In addition to these neurogenic effects the body also compensates in other ways. Selective arteriolar and precapillary sphincter constriction occurs in non-essential organs (for example, skin and gut) helping to maintain vital organ perfusion (especially the brain and the heart). Specialized cells within the juxtaglomerular apparatus of the kidney respond to a reduction in renal blood flow by releasing renin. This leads to the formation of angiotensin II, a vasopressor and stimulator of aldosterone production. Aldosterone, secreted by the adrenal cortex, and antidiuretic hormone (vasopressin), released from the pituitary, increase reabsorption of sodium and water by the kidney, reducing urine output to help maintain the circulating volume.
Adrenocortical Disease
Published in T.M. Craft, P.M. Upton, Key Topics In Anaesthesia, 2021
The adrenal cortex produces glucocorticoid, mineralocorticoid and sex hormones (mainly testosterone). Cortisol, the principal glucocorticoid, modulates stress and inflammatory responses. It is a potent stimulator of gluconeogenesis and antagonizes insulin. Aldosterone is the principal mineralocorticoid. It causes increased sodium reabsorption, and potassium and hydrogen ion loss at the distal renal tubule. Adrenal androgen production increases markedly at puberty, declining with age thereafter. Androstenedione is converted by the liver to testosterone in the male and oestrogen in the female. Cortisol and androgen production are under diurnal pituitary control (adrenocorticotrophic hormone — ACTH). Aldosterone is released in response to angiotensin II, produced following renal renin release and subsequent pulmonary angiotensin I conversion.
Moyamoya syndrome in a male pseudohermaphrodite patient with congenital adrenal hyperplasia – a rare association. Case report and review of literature
Published in British Journal of Neurosurgery, 2023
Remesh Chirayil Vasudevan, Reshma Vachali Madayi, Rohit Ravindranath Nambiar
CAH is a rare disorder that results from defective biosynthesis of steroid hormones in the adrenal cortex. CAH with 17 alpha-hydroxylase and 11 beta-hydroxylase deficiencies is associated with hypertension. Pathogenesis of CAH is due to various genetic mutations in the enzymes involved in steroid synthesis. As a result, cortisol production is reduced and the negative feedback control on adrenocorticotropic hormone (ACTH) is lost. Elevated ACTH level results in overproduction and accumulation of steroids precursors prior to the enzyme defect.6 There is hyperplasia of adrenal cortex. The clinical features depend on the level of enzyme defect. Patients with ambiguous genitalia, hypogonadism, hypertension and associated hypokalemia should be evaluated for possible CAH. In CAH due to 17 alpha-hydroxylase deficiency, both adrenal and gonadal steroid hormones production will be impaired. In male patients, lack of testosterone will impair Wolffian duct development. They will have gonads but no internal genitalia.7 High 11 deoxycorticosterone levels will cause sodium retention, potassium loss and hypertension due to potent mineralocorticoid action.
Recent developments in wearable & non-wearable point-of-care biosensors for cortisol detection
Published in Expert Review of Molecular Diagnostics, 2023
Simran Kaur, Niharika Gupta, Bansi D. Malhotra
Stress can be associated with many biomarkers in a body, out of which cortisol is the most prominent one. Prolonged stress is responsible for activation of brain routes that stimulate the adrenal cortex to release cortisol, hence cortisol is known as the stress hormone. Cortisol, also known as hydrocortisone ((11β)-11,17,21-trihydroxy pregn-4-ene-3,20-dione), is a lipophilic molecule and is transported throughout the body via blood circulation. Physiologically, its role includes the modulation of blood pressure in order to supplement fat and glucose in muscles and brain, which further assist in successfully managing stress. However, the prolonged increase in cortisol has the potential to cause serious ailments like depression, hypertension, etc. [8–10]. It is a glucocorticoid hormone that is significantly involved in the regulation of many physiological processes, including glucose levels, carbohydrate metabolism, blood pressure, etc. It also affects the cognitive abilities like memory, sleep, mood, fatigue, etc. [4]. Abnormalities in cortisol levels may indicate mental health concerns like depression and, hence, its regular monitoring can benefit at-risk individuals significantly.
Circadian rhythms of risk factors and management in atherosclerotic and hypertensive vascular disease: Modern chronobiological perspectives of an ancient disease
Published in Chronobiology International, 2023
Yong-Jian Geng, Michael H. Smolensky, Oliver Sum-Ping, Ramon Hermida, Richard J. Castriotta
The release into circulation of the hormone aldosterone from the adrenal cortex enhances the reabsorption of sodium and water by kidney tubules (Rautureau et al. 2011). Additionally, aldosterone participates in processes that promote vascular inflammation, oxidative stress, fibrosis, endothelial dysfunction and structural remodeling, particularly in the presence of elevated plasma sodium chloride concentration (Park and Schiffrin 2002). In endothelial cells and VSMCs, aldosterone, with the influence of Ang-II, exerts effects via mitogen-activated protein kinase (also termed extracellular signal regulated kinase) and cellular Src kinase (a non-receptor tyrosine kinase), plus it partakes in epidermal growth factor receptor transactivation (Mazak et al. 2004; Min et al. 2007; Nakano et al. 2005). Aldosterone thus increases oxidative stress in VSMCs and negatively impacts endothelial function, most likely through reducing the bioavailability of NO (Nakano et al. 2005), and it induces vascular inflammation in endothelial cells through enhancing expression of intercellular adhesion molecule 1 (ICAM-1) and leukocyte adhesion (Caprio et al. 2008).