Talk:BGD Lecture - Endocrine Histology: Difference between revisions

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===Chapter 7. The pituitary gland===
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/ Chapter 7. The pituitary gland]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1267 Anatomical and functional connections of the hypothalamo-pituitary axis]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1269 Box 7.3 Anatomy of the functional connections between the hypothalamus and pituitary gland]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1270 Box 7.4 Hormone secretions of the anterior lobe of the pituitary gland and their control]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1272 Box 7.5 Diagram of the anatomy of the hypothalamo-pituitary axis showing the major hypothalamic nuclei]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1297 Blood supply of the hypothalamo-pituitary axis]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1298 Box 7.8 Diagrammatic representation of the blood supply and venous drainage of the median eminence and pituitary gland]


===Chapter 4. The adrenal gland===
===Chapter 4. The adrenal gland===
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** [http://www.ncbi.nlm.nih.gov/books/NBK26/box/A465 Box 4.6 Histology and blood supply of the adrenal gland]
** [http://www.ncbi.nlm.nih.gov/books/NBK26/box/A465 Box 4.6 Histology and blood supply of the adrenal gland]
** [http://www.ncbi.nlm.nih.gov/books/NBK26/box/A467 Box 4.39 Biosynthesis and control of catecholamines secreted by the adrenal medulla]
** [http://www.ncbi.nlm.nih.gov/books/NBK26/box/A467 Box 4.39 Biosynthesis and control of catecholamines secreted by the adrenal medulla]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A468 Glucocorticoid receptors]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A470 Actions of glucocorticoids and clinical features of Cushing's syndrome]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A508 Adrenal cortical androgens]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A516 Hypothalamic control of adrenocortical steroid synthesis - CRH and vasopressin]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A516 Hypothalamic control of adrenocortical steroid synthesis - CRH and vasopressin]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A518 Pituitary control of adrenocortical steroids - ACTH]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A518 Pituitary control of adrenocortical steroids - ACTH]
** [http://www.ncbi.nlm.nih.gov/books/NBK26/box/A517 Box 4.14 Control of cortisol and androgens from the adrenal cortex]
** [http://www.ncbi.nlm.nih.gov/books/NBK26/box/A517 Box 4.14 Control of cortisol and androgens from the adrenal cortex]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A526 Feedback control of glucocorticoids]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A526 Feedback control of glucocorticoids]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A527 Excess glucocorticoids: biochemical investigation of Cushing's syndrome]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A540 Measurements of cortisol in blood, urine and saliva]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A559 Dynamic tests of endocrine function]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A567 Imaging the adrenal gland]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A577 Treatment of Cushing's syndrome]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A591 Nelson's syndrome]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A592 Excess adrenal androgens - congenital adrenal hyperplasia (CAH)]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A602 Deficiency of adrenocortical secretions - Addison's disease]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A635 Aldosterone and the control of salt and water balance]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A657 Transport and metabolism of adrenocortical steroids]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A672 Selective mineralocorticoid excess and deficiency]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A697 The adrenal medulla and pheochromocytoma]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A698 Catecholamine synthesis and secretion]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A720 Diagnosis and treatment of pheochromocytomas]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A737 Clinical case questions]
===Chapter 7. The pituitary gland===


[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/ Chapter 7. The pituitary gland]


* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1267 Anatomical and functional connections of the hypothalamo-pituitary axis]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1269 Box 7.3 Anatomy of the functional connections between the hypothalamus and pituitary gland]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1270 Box 7.4 Hormone secretions of the anterior lobe of the pituitary gland and their control]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1272 Box 7.5 Diagram of the anatomy of the hypothalamo-pituitary axis showing the major hypothalamic nuclei]
** [http://www.ncbi.nlm.nih.gov/books/NBK27/box/A1298 Box 7.8 Diagrammatic representation of the blood supply and venous drainage of the median eminence and pituitary gland]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1273 Embryology of the pituitary gland]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1295 Craniopharyngioma]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1297 Blood supply of the hypothalamo-pituitary axis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1299 Sheehan's syndrome]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1312 Growth and somatotrophin deficiency]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1348 Growth hormone - secretory patterns and control]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1377 Actions of growth hormone and insulin-like growth factors]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1398 GH replacement therapy]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1421 GH excess - gigantism and acromegaly]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1426 Pituitary adenomas - incidence and treatment]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1427 Prolactinomas]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1429 Prolactin and its control]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1453 Circadian rhythms and the suprachiasmatic nucleus]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1456 The pineal gland and melatonin]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1457 Autonomic functions of the hypothalamus]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1458 Obesity]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1489 The neural lobe of the pituitary gland - AVP and oxytocin]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1523 Clinical case questions]


===Ghrelin immunoexpression in the human hypophysis===
===Ghrelin immunoexpression in the human hypophysis===

Revision as of 15:02, 13 Mayıs 2012

Endocrinology - An Integrated Approach

Endocrinology - An Integrated Approach.png Stephen Nussey and Saffron Whitehead.

St. George's Hospital Medical School, London, UK Oxford: BIOS Scientific Publishers; 2001. ISBN-10: 1-85996-252-1

Copyright © 2001, BIOS Scientific Publishers Limited.

http://www.ncbi.nlm.nih.gov/books/NBK22/


Chapter 7. The pituitary gland

Chapter 7. The pituitary gland


Chapter 4. The adrenal gland

Chapter 4. The adrenal gland


Ghrelin immunoexpression in the human hypophysis

Appl Immunohistochem Mol Morphol. 2012 Jan;20(1):77-81.

Rotondo F, Rotondo A, Scheithauer BW, Cusimano M, Latta E, Syro LV, Kovacs K. Source Division of Pathology, Department of Laboratory Medicine, St. Michael's Hospital, University of Toronto, Toronto, Canada. rotondof@smh.ca Abstract The aim of this study was to immunohistochemically localize ghrelin in autopsy-obtained, nontumoral human pituitaries. Double immunostaining was also undertaken to determine the pituitary cell type expressing both adenohypophysial hormones and ghrelin. Results showed that ghrelin is present in the adenohypophysis, its immunoexpression being cytoplasmic, weak-to-moderate, and localized to a subset of cells. Double immunostaining showed that ghrelin is present in 51% to 90% of growth hormone-producing, luteinizing-producing, and α-subunit-producing cells. Ghrelin immunoexpression was less frequently observed in other adenohypophysial cell types, being seen in 30% of adrenocorticotropin and follicle-stimulating hormones, 15% of thyrotropin, and 10% of prolactin-immunoreactive cells. Ghrelin immunopositivity was also seen in nerve fibers and Herring bodies of the neurohypophysis and pituitary stalk. More work is needed to elucidate the role of ghrelin in adenohypophysial and neurohypophysial endocrine activity. It may well be that ghrelin exerts an autocrine/paracrine effect and can modulate hormone synthesis and release.

PMID 22157058


The role of lipotropins as hematopoietic factors and their potential therapeutic use

Exp Hematol. 2008 Jun;36(6):752-4. Epub 2008 Mar 20.

Halabe Bucay A. Source Department of Pediatrics, Hospital Angeles Lomas, Huixquilucan, Mexico. doctorhalabe@hotmail.com Abstract Lipotropins are peptides that act as hormones that are released from a common precursor together with other physiologically important peptides; their function is to mobilize the lipids that are stored in adipocytes as an energy reserve. This review will explain the existing scientific evidence on the action of lipotropins in adipocytes and, specifically, when these lipotropins activate bone marrow adipocytes to function as hematopoietic factors and suggest the potential therapeutic use of lipotropins based on these effects.

PMID 18358591


Anorexia nervosa: a unified neurological perspective

Int J Med Sci. 2011;8(8):679-703. Epub 2011 Oct 22.

Hasan TF, Hasan H. Source Mahatma Gandhi Mission's Medical College, Aurangabad, Maharashtra, India. zainabhasan52@hotmail.com

Abstract

The roles of corticotrophin-releasing factor (CRF), opioid peptides, leptin and ghrelin in anorexia nervosa (AN) were discussed in this paper. CRF is the key mediator of the hypothalamo-pituitary-adrenal (HPA) axis and also acts at various other parts of the brain, such as the limbic system and the peripheral nervous system. CRF action is mediated through the CRF1 and CRF2 receptors, with both HPA axis-dependent and HPA axis-independent actions, where the latter shows nil involvement of the autonomic nervous system. CRF1 receptors mediate both the HPA axis-dependent and independent pathways through CRF, while the CRF2 receptors exclusively mediate the HPA axis-independent pathways through urocortin. Opioid peptides are involved in the adaptation and regulation of energy intake and utilization through reward-related behavior. Opioids play a role in the addictive component of AN, as described by the "auto-addiction opioids theory". Their interactions have demonstrated the psychological aspect of AN and have shown to prevent the functioning of the physiological homeostasis. Important opioids involved are β-lipotropin, β-endorphin and dynorphin, which interact with both µ and κ opioids receptors to regulate reward-mediated behavior and describe the higher incidence of AN seen in females. Moreover, ghrelin is known as the "hunger" hormone and helps stimulate growth hormone (GH) and hepatic insulin-like-growth-factor-1(IGF-1), maintaining anabolism and preserving a lean body mass. In AN, high levels of GH due to GH resistance along with low levels of IGF-1 are observed. Leptin plays a role in suppressing appetite through the inhibition of neuropeptide Y gene. Moreover, the CRF, opioid, leptin and ghrelin mechanisms operate collectively at the HPA axis and express the physiological and psychological components of AN. Fear conditioning is an intricate learning process occurring at the level of the hippocampus, amygdala, lateral septum and the dorsal raphe by involving three distinct pathways, the HPA axis-independent pathway, hypercortisolemia and ghrelin. Opioids mediate CRF through noradrenergic stimulation in association with the locus coeruleus. Furthermore, CRF's inhibitory effect on gonadotropin releasing hormone can be further explained by the direct relationship seen between CRF and opioids. Low levels of gonadotropin have been demonstrated in AN where only estrogen has shown to mediate energy intake. In addition, estrogen is involved in regulating µ receptor concentrations, but in turn both CRF and opioids regulate estrogen. Moreover, opioids and leptin are both an effect of AN, while many studies have demonstrated a causal relationship between CRF and anorexic behavior. Moreover, leptin, estrogen and ghrelin play a role as predictors of survival in starvation. Since both leptin and estrogen are associated with higher levels of bone marrow fat they represent a longer survival than those who favor the ghrelin pathway. Future studies should consider cohort studies involving prepubertal males and females with high CRF. This would help prevent the extrapolation of results from studies on mice and draw more meaningful conclusions in humans. Studies should also consider these mechanisms in post-AN patients, as well as look into what predisposes certain individuals to develop AN. Finally, due to its complex pathogenesis the treatment of AN should focus on both the pharmacological and behavioral perspectives.

PMID 22135615


In search of HPA axis dysregulation in child and adolescent depression

Clin Child Fam Psychol Rev. 2011 Jun;14(2):135-60.

Guerry JD, Hastings PD. Source University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. jguerry@email.unc.edu

Abstract

Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis in adults with major depressive disorder is among the most consistent and robust biological findings in psychiatry. Given the importance of the adolescent transition to the development and recurrence of depressive phenomena over the lifespan, it is important to have an integrative perspective on research investigating the various components of HPA axis functioning among depressed young people. The present narrative review synthesizes evidence from the following five categories of studies conducted with children and adolescents: (1) those examining the HPA system's response to the dexamethasone suppression test (DST); (2) those assessing basal HPA axis functioning; (3) those administering corticotropin-releasing hormone (CRH) challenge; (4) those incorporating psychological probes of the HPA axis; and (5) those examining HPA axis functioning in children of depressed mothers. Evidence is generally consistent with models of developmental psychopathology that hypothesize that atypical HPA axis functioning precedes the emergence of clinical levels of depression and that the HPA axis becomes increasingly dysregulated from child to adult manifestations of depression. Multidisciplinary approaches and longitudinal research designs that extend across development are needed to more clearly and usefully elucidate the role of the HPA axis in depression.

PMID 21290178