Talk:Lecture - Endocrine Development: Difference between revisions

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==Introduction==
==2015==
[[File:Pharynx_cartoon.jpg |thumb|Head and Neck]]
[[File:Historic-pituitary.jpg|thumb|Pituitary]]
The endocrine system resides within specific endocrine organs and both organs and tissues with other specific functions. Epithelia (ectoderm and endoderm) form the majority of the “ductless” endocrine glands like gastrointestinal and skin associated “ducted” glands. Differentiation of several also organs involves a epithelial/mesenchye interaction, seen in repeated in many differentiation of many different tissues. The endocrine glands produce hormones, which are distributed by the vascular system to the many body tissues, subsequently these organs are richly vascularized.


Hormones “orchestrate” responses in other tissues, including other endocrine organs, and these overall effects can be similar or different in different tissues. These signaling pathways are often described as "axes" the two major types are the: '''HPA''' ('''H'''yothalamus-'''P'''ituitary-'''A'''drenal) and  '''HPG''' ('''H'''ypothalamus-'''P'''ituitary-'''G'''onad). These hormone effects (like music) can be rapid, slow, brief, diurnal, or long-term. Hormone effects can be mimicked, stimulated, and blocked by therapeutic drugs, nutritional and environmental chemicals. Importantly, fetal endocrine development is required for normal fetal growth and differentiation.
{| class="wikitable mw-collapsible mw-collapsed"
! ECHO360 Recording
|-
| [[File:ECHO360_icon.gif|right|link=https://lectures.unsw.edu.au/ess/portal/section/691ba9a0-7c35-4ad2-8fd0-846db7771557]]
Links only work with currently enrolled UNSW students.


==Lecture Objectives==
[[Lecture - Endocrine Development|Lecture 11]] - 
* Understanding of hormone types
|}
* Understanding of endocrine gland development
* Understanding of endocrine developmental functions
* Brief understanding of endocrine abnormalities


==Hormones==
[[File:Steroid hormone receptor signaling.jpg|thumb|Steroid hormone receptor signaling<ref><pubmed>17464358</pubmed>| [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1853070 PMC1853070] | [http://www.nursa.org/article.cfm?doi=10.1621/nrs.05003 Nucl Recept Signal.]</ref>]]
===Hormone Types===
[[File:Steroid biosynthesis pathway.png|thumb|Steroid biosynthesis pathway]]
* '''Amino acid derivatives''' - noradrenaline (norepinepherine), adrenalin (epinepherine) , thyroid hormone
* '''Proteins, peptides''' - thyroid stimulating hormone, leutenising hormone, follicle stimulating hormone
* '''Steroids''' - androgens, glucocorticoids, mineralocorticoids


===Hormone Actions===
* Autocrine - acts on self (extracellular fluid)
* Paracrine - acts locally (extracellular fluid)
* Endocrine - acts by secretion into blood stream (endocrine organs are richly vascularized)


===Hormone Receptors===
==Introduction==
Hormones are recognised by either cell surface receptors (modified amino acids, peptides, proteins) or cytoplasmic/nuclear receptors (steroids).


--[[User:S8600021|Mark Hill]] 06:17, 26 September 2011 (EST) Interested in hormone history? Listen to ABC Radio Ockham's Razor 2005-07-31 [[:File:Audio_-_centenary_of_hormone.mp3|Centenary of the word "hormone"]], by Sydney medical scientist (from SOMS) and writer Dr John Carmody commemorates the centenary of the entry of the word 'hormone' into the English language.
* [[Media:Endocrine Development.pdf‎‎| 2013 lecture PDF]] Lecture Date: 2013-10-08  Lecture Time: 12:00 Venue: Wallace Wurth LG02 Speaker: Steve Palmer


==Endocrine Origins==
* 2009 Lecture Audio Lecture Date: 06-10-2009 Lecture Time: 12:00 Venue: BioMed E Speaker: Mark Hill [http://lectopia.elearning.unsw.edu.au/ilectures/ilectures.lasso?ut=153&id=48844 Endocrine]


* Derived from epithelia - covering embryo, lining gastrointestinal tract, lining coelomic cavity
* Also mesenchymal contribution


==Pineal Gland==
'''2013:''' [[Lecture - Endocrine Development|Current lecture]]
[[File:pineal-body.jpg|thumb|Adult pineal body]]
[[File:Pineal gland position.jpg|thumb|Pineal gland position]]


* part of epithalmus - neurons, glia and pinealocytes
'''2009:''' [http://embryology.med.unsw.edu.au/Medicine/BGDlectureEndocrine.htm Medicine Lecture - Endocrine Development] | [http://embryology.med.unsw.edu.au/Medicine/BGD09Endocrines1.pdf lecture 1 slide/page PDF]
* pinealocytes secrete melatonin - cyclic nature of activity, melatonin lowest during daylight
** inhibit hypothalamic secretion of GnRH until puberty, pineal gland then rapidly regresses.
* other activities - possibly gamete maturation, antioxidant effect, protect neurons?


===Pineal Development===
'''2008:''' [http://embryology.med.unsw.edu.au/Science/ANAT2341lecture21.htm Lecture - Endocrine Development] | [http://embryology.med.unsw.edu.au/pdf/ANAT2341L21Endocrines1.pdf lecture 1 slide/page PDF] | [http://embryology.med.unsw.edu.au/pdf/ANAT2341L21Endocrines4.pdf lecture 4 slides/page PDF] |
* Neuroectoderm - prosenecephalon then diencephalon
* caudal roof, median diverticulum, epiphysis
* Initially a hollow diverticulum, cell proliferation to solid, pinealocytes (neuroglia), cone-shaped gland innervated by epithalmus


'''Links:''' [[Endocrine - Pineal Development]]


==Hypothalamus==
{{Template:Endocrine Links}} | [http://embryology.med.unsw.edu.au/Notes/endocrine.htm original Endocrine page]


'''Hormones''' - Thyrotrophin releasing hormone (TRH), Corticotrophin releasing hormone (CRH), Arginine vasopressin (AVP), Gonadotrophin releasing hormone (GnRH), Growth hormone releasing hormone (GHRH), Somatostatin, Prolactin relasing factor (PRF), Dopamine
==Endocrinology - An Integrated Approach==


===Hypothalamus Development===
* Neuroectoderm - prosenecephalon then diencephalon
* ventro-lateral wall intermediate zone proliferation
* Mamillary bodies - form pea-sized swellings ventral wall of hypothalamus
'''Links:''' [[Endocrine - Hypothalamus Development]]
==Pituitary==
[[File:Embryonic_and_fetal_pituitary.jpg]]
[[File:Historic-pituitary.jpg|thumb|Adult pituitary]]
'''Anterior pituitary hormones''' - Thyroid-stimulating hormone (TSH), Adrenocorticotrophic hormone (ACTH), Luteinizing hormone (LH), Follicle-stimulating hormone (FSH), Somatotrophin/growth hormone (GH), Prolactin (PRL), Melanocyte-stimulating hormone (MSH)
'''Posterior pituitary hormones''' - Oxytocin, Arginine vasopressin
===Pituitary Development===
[[File:Pituitary rabbit development.jpg|thumb|Pituitary rabbit development]]
{|
{|
| [[File:Pituitary development animation.gif]]
| [[File:Endocrinology - An Integrated Approach.png]]
| <font color=deepskyblue>'''Blue''' - neural tube ectoderm</font>
| 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.


<font color=darksalmon>'''Red''' - surface ectoderm</font>
http://www.ncbi.nlm.nih.gov/books/NBK22/
|}
|}


* Dual ectoderm origins
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A2/ Preface]
** Ectoderm - ectoderm roof of stomodeum, Rathke's pouch, adenohypophysis
** Neuroectoderm - prosenecephalon then diencephalon, neurohypophysis


'''Adenohypophysis'''
===Chapter 1. Principles of endocrinology===
* Anterior wall proliferates - pars distalis
* Posterior wall little growth – pars intermedia
* Rostral growth around infundibular stem – pars tuberalis


'''Neurohypophysis'''
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/ Chapter 1. Principles of endocrinology]
* Infundibulum – median eminence, infundibulum, pars nervosa


===Pituitary Timeline===
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A10 Functions of hormones and their regulation]
* Week 4 - hypophysial pouch, Rathke’s pouch, diverticulum from roof
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A14 Chemical signalling - endocrine, paracrine, autocrine and intracrine mechanisms]
* Week 5 - elongation, contacts infundibulum, diverticulum of diencephalon
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A16 Chemical classification of hormones and their synthesis]
* Week 6 - connecting stalk between pouch and oral cavity degenerates
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A18 Hormone synthesis]
* Week 10 - growth hormone and ACTH detectable
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A22 Transport of hormones in the circulation and their half-lives]
* Week 16 - adenohypophysis fully differentiated
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A23 Hormone receptors - cell surface]
* Week 20 to 24 - growth hormone levels peak, then decline
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A29 Hormone receptors - intracellular]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A32 Hormones and gene transcription]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A33 Hormone receptor regulation]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A35 Neuroendocrine interactions]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A36 Hormones and the immune system]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A40 Hormones, growth promotion and malignancy]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A41 Genes, mutations and endocrine function]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A42 Clinical evaluation of endocrine disorders]


'''Links:''' [[Endocrine - Pituitary Development]] | [http://www.med.unc.edu/embryo_images/unit-nervous/nerv_htms/nerv016.htm Embryo Images - Pituitary]
===Chapter 2. The endocrine pancreas===


==Thyroid==
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/ Chapter 2. The endocrine pancreas]
* Functions from wk10, required for neural development, stimulates metabolism (protein, carbohydrate, lipid), reduced/absence = cretinism (see abnormalities)


'''Hormones''' - (amino acid derivatives) Thyroxine (T4), Triiodothyronine (T3)
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A52 Glucose turnover]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A58 Anabolic and catabolic phases of glucose metabolism]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A60 Actions of insulin and glucagon]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A63 Lipid metabolism - insulinopenia and diabetic ketosis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A81 Protein metabolism and the anabolic actions of insulin]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A89 Definition and diagnosis of diabetes mellitus]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A101 Etiology of type 1 DM]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A113 Prevention of type 1 DM]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A114 Structure, synthesis and metabolism of insulin and glucagon]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A117 Anatomical features of pancreatic islets in relation to hormone secretion and its control]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A121 Control of insulin and glucagon secretion]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A126 Type 2 DM]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A134 Causes of DM]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A146 Genetic disorders of β-cell function]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A147 Counter-regulatory hormones and DM]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A150 Complications of DM]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A159 Macrovascular circulatory changes]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A161 Microvascular changes - diabetic retinopathy, nephropathy and neuropathy]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A168 Diabetes and the neuropathic foot]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A169 Diabetes and insulin resistance of pregnancy]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A170 Development of the pancreas: effects of DM on organogenesis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A172 Treatment of DM - rationale and practical considerations]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A183 Hypoglycemia]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A211 Physiological responses to hypoglycemia and its treatment]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A214 Hypoglycemia and insulinoma]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A217 Hypoglycemia in infancy]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A228 Disorders of the α, γ and PP cells of the islets]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A229 Clinical case questions]


===Thyroid Development===
===Chapter 3. The thyroid gland===
[[File:Stage13 and 22 thyroid development a.jpg|thumb|Stage 13 and Stage 22 thyroid development]]
[[File:Tongue1.png|thumb|foramen caecum]]
* thyroid median endodermal thickening in the floor of pharynx, outpouch – thyroid diverticulum
* tongue grows, cells descend in neck
* thyroglossal duct - proximal end at the foramen cecum of tongue [http://www.upstate.edu/cdb/grossanat/imgs/tgdfig2.jpg thyroglossal duct]
* thyroid diverticulum - hollow then solid, right and left lobes, central isthmus


===Thyroid Timeline===
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/ Chapter 3. The thyroid gland]
* 24 days - thyroid median endodermal thickening in the floor of pharynx, outpouch – thyroid diverticulum
* Week 11 - colloid appearance in thyroid follicles, iodine and thyroid hormone (TH) synthesis
growth factors (insulin-like, epidermal) stimulates follicular growth


===Fetal Thyroid Hormone===
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A246 Iodine intake]
* Initial secreted biologically inactivated by modification, late fetal secretion develops brown fat
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A248 Anatomical features of the thyroid gland]
* Iodine deficiency- during this period, leads to neurological defects (cretinism)
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A249 Iodine trapping and thyroid function]
* Birth - TSH levels increase, thyroxine (T3) and T4 levels increase to 24 h, then 5-7 days postnatal decline to normal levels
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A278 Synthesis of thyroid hormones]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A280 Actions of thyroid hormones]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A289 Control of thyroid hormone synthesis and secretion]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A292 Hyperthyroidism — Graves' disease]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A329 Surgical anatomy and embryology of the thyroid gland]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A332 Primary hypothyroidism — Hashimoto's disease and myxedema]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A362 Secondary hypothyroidism]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A364 Hypothyroidism in infancy and childhood]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A375 Thyroid hormone resistance]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A376 Non-thyroid illness (‘sick euthyroid’ syndrome)]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A393 Transport and metabolism of thyroid hormones]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A394 Biochemical measurements of thyroid hormone status]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A399 Thyroid growth]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A400 Nodular thyroid disease]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A402 Thyroid cancer]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A435 Clinical case questions]


'''Links:''' [[Endocrine - Thyroid Development]]
===Chapter 4. The adrenal gland===


==Parathyroid==
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/ Chapter 4. The adrenal gland]
[[File:Parathyroid adult.jpg|thumb|Parathyroid adult]]


* Parathyroid Hormone - Increase calcium ions [Ca2+], stimulates osteoclasts, increase Ca GIT absorption (opposite effect to calcitonin)
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A460 Specificity of the biological effects of adrenal steroid hormones]
* Adult Calcium and Phosphate - Daily turnover in human with dietary intake of 1000 mg/day
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A461 Cholesterol and steroid synthesis in the adrenal cortex]
* secreted by chief cells
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A464 Anatomical and functional zonation in the adrenal cortex]
Principal cells cords of cells
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A468 Glucocorticoid receptors]
===Parathyroid Development===
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A470 Actions of glucocorticoids and clinical features of Cushing's syndrome]
[[File:Pharyngeal pouches.jpg|thumb|Pharyngeal pouches]]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A508 Adrenal cortical androgens]
* Endoderm - third and fourth pharyngeal pouches, could also have ectoderm and neural crest
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A516 Hypothalamic control of adrenocortical steroid synthesis - CRH and vasopressin]
** 3rd Pharyngeal Pouch - inferior parathyroid, initially descends with thymus
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A518 Pituitary control of adrenocortical steroids - ACTH]
** 4th Pharyngeal Pouch - superior parathyroid
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A526 Feedback control of glucocorticoids]
* Week 6 - diverticulum elongate, hollow then solid, dorsal cell proliferation
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A527 Excess glucocorticoids: biochemical investigation of Cushing's syndrome]
* Fetal parathyroids - respond to calcium levels, fetal calcium levels higher than maternal
* [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]


'''Links:''' [[Endocrine - Parathyroid Development]]
===Chapter 5. The parathyroid glands and vitamin D===


==Thymus==
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/ Chapter 5. The parathyroid glands and vitamin D]


* Thymus - bone-marrow lymphocyte precursors become thymocytes, and subsequently mature into T lymphocytes (T cells)
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A769 Calcium and phosphate in serum and its measurement]
* Thymus hormones - thymosins stimulate the development and differentiation of T lymphocytes
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A770 Intracellular calcium concentration]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A772 Calcium and phosphate balance]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A774 Hormonal control of serum Ca<sup>2+</sup> and P<sub>i</sub> concentrations]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A776 Sources, metabolism and transport of vitamin D]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A788 Classical actions of vitamin D on intestine and bone]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A792 Parathyroid glands and PTH synthesis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A796 Control of PTH secretion]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A819 Actions of PTH]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A823 Hypercalcemia and primary hyperparathyroidism]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A827 Hyperparathyroidism and multiple endocrine neoplasia (MEN)]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A828 Hypercalcemia and vitamin D excess]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A829 Hypercalcemia and malignancy]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A831 Parathyroid hormone-related peptide (PTHrp)]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A832 Treatment of hypercalcemia]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A843 Mutations of the Ca<sup>2+</sup> or PTH receptors]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A857 Hypocalcemia and its treatment]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A897 Pseudohypoparathyroidism]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A898 Vitamin D deficiency]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A916 Non-classical actions of vitamin D]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A930 Vitamin D resistance and rickets]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A932 Hormones and the skeleton]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A933 Structure, formation and function of bone]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A934 Osteoporosis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A946 Paget's disease (osteitis deformans)]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A948 Calcitonin and calcitonin gene-related peptide]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A966 Clinical case questions]


===Thymus Development===
===Chapter 6. The gonad===


* Endoderm - third pharyngeal pouch
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/ Chapter 6. The gonad]
* Week 6 - diverticulum elongates, hollow then solid, ventral cell proliferation
* Thymic primordia - surrounded by neural crest mesenchyme, epithelia/mesenchyme interaction


'''Links:''' [[Endocrine - Thymus Development]]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A982 Genetic determination of sexual differentiation]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1022 Sexual differentiation of the gonads and internal reproductive tracts]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1024 Sexual differentiation of the external genitalia]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1056 Control of steroid production in the fetal gonads]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1058 Puberty]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1061 GnRH and the control of gonadotrophin synthesis and secretion]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1095 The gonadotrophins - LH and FSH - and their actions]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1098 Endocrine changes in puberty]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1101 Precocious sexual development]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1104 Delayed puberty]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1144 Premature adrenarche]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1145 Acne, hair growth and hirsutism]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1148 The breast - premature development, hypoplasia and gynecomastia]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1172 Testicular function]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1175 Control of testicular function]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1180 Transport, metabolism and actions of androgens]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1185 Spermatogenesis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1208 Erection and ejaculation]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1223 Ovarian control and the menstrual cycle]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1228 Transport, metabolism and actions of ovarian steroids]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1229 The ovary - folliculogenesis and oogenesis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1231 Non-steroidal factors in the control of the hypothalamic-pituitary-gonadal axis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1232 Ovulation, menstruation and its problems]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1240 Polycystic ovary syndrome (PCOS)]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1245 Contraception]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1247 Infertility]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1248 Ovulation induction and assisted conception]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1251 Ovarian failure, the menopause and andropause]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1252 Hormonal replacement therapy (HRT) and selective estrogen receptor modulators (SERMS)]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/#A1253 Clinical case questions]


==Pancreas==
===Chapter 7. The pituitary gland===
[[File:Pancreas adult.jpg|thumb|Pancreas adult]]
[[File:Pancreas cartoon.jpg|thumb|pancreas structure]]


* Functions - exocrine (amylase, alpha-fetoprotein), 99% by volume; endocrine (pancreatic islets) 1% by volume
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/ Chapter 7. The pituitary gland]
* Exocrine function - begins after birth
* Endocrine function -  from 10 to 15 weeks onward hormone release
** exact roles of hormones in regulating fetal growth?


===Pancreas Development===
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1267 Anatomical and functional connections of the hypothalamo-pituitary axis]
[[File:Pancreatic_duct_developing.jpg|thumb|Pancreatic buds and duct developing]]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1273 Embryology of the pituitary gland]
[[File:Stage22_pancreas_a.jpg|thumb|Stage22 pancreas]]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1295 Craniopharyngioma]
* Pancreatic buds - duodenal level endoderm, splanchnic mesoderm forms dorsal and ventral mesentery, dorsal bud (larger, first), ventral bud (smaller, later)
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1297 Blood supply of the hypothalamo-pituitary axis]
* Pancreas Endoderm - pancreas may be opposite of liver
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1299 Sheehan's syndrome]
** Heart cells promote/notochord prevents liver formation
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1312 Growth and somatotrophin deficiency]
** Notochord may promote pancreas formation
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1348 Growth hormone - secretory patterns and control]
** Heart may block pancreas formation
* [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]


* Duodenum growth/rotation - brings ventral and dorsal buds together, fusion of buds
===Chapter 8. Cardiovascular and renal endocrinology===
* Pancreatic duct - ventral bud duct and distal part of dorsal bud, exocrine function
* Islet cells - cords of endodermal cells form ducts, from which cells bud off to form islets


===Pancreatic Islets===
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/ Chapter 8. Cardiovascular and renal endocrinology]
* Islets of Langerhans - 4 endocrine cell types
* '''Alpha''' - glucagon, mobilizes lipid
* '''Beta''' - insulin, increase glucose uptake
** Beta cells, stimulate fetal growth, continue to proliferate to postnatal, in infancy most abundant
* '''Delta''' - somatostatin, inhibits glucagon, insulin secretion
* '''F-cells''' - pancreatic polypeptide


===Pancreas Timeline===
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1537 Endocrinology of heart failure]
* Week 7 to 20 - pancreatic hormones secretion increases, small amount maternal insulin
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1542 Paracrine and autocrine regulation of blood pressure: the endocrinology of sepsis]
* Week 10 - glucagon (alpha) differentiate first, somatostatin (delta), insulin (beta) cells differentiate, insulin secretion begins
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1547 Hormones and blood cell production - erythropoietin]
* Week 15 - glucagon detectable in fetal plasma
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1557 Carcinoid]
 
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1564 Clinical case questions]
'''Links:''' [[Endocrine - Pancreas Development]] | [[Gastrointestinal Tract - Pancreas Development]]
 
==Adrenal==
 
* Richly vascularized - arterioles passing through cortex, capillaries from cortex to medulla, portal-like circulation
* Fetal Cortex - produces a steroid precursor (DEA), converted by placenta into estrogen
* Adult Medulla - produces adrenalin (epinephrine), noradrenaline (norepinephrine)
* Fetal adrenal hormones - influence lung maturation
 
'''Adrenal cortical hormones''' - (steroids) Cortisol, Aldosterone, Dehydroepiandrosterone
* zona glomerulosa - regulated by renin-angiotensin-aldosterone system controlled by the juxtaglomerular apparatus of the kidney.
* zona fasciculata - regulated by hypothalamo-pituitary axis with the release of CRH and ACTH respectively.
 
 
'''Adrenal medullary hormones''' - (amino acid derivatives) Epinephrine, Norepinephrine
 
===Adrenal Development===
[[File:Adrenal_medulla.jpg|300px|right|link=http://embryology.med.unsw.edu.au/embryology/images/a/a4/Adrenal_medulla.mov]]
[[File:Week10 adrenal.jpg|thumb|Week 10 adrenal gland]]
* Fetal Adrenals - fetal cortex later replaced by adult cortex
* Week 6 - fetal cortex, from mesothelium adjacent to dorsal mesentery; Medulla, neural crest cells from adjacent sympathetic ganglia
* Adult cortex - mesothelium mesenchyme encloses fetal cortex
 
'''Adrenal Cortex'''
* Late Fetal Period - differentiates to form cortical zones
* Birth - zona glomerulosa, zona fasiculata present
* Year 3 - zona reticularis present
 
[http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&part=A442&rendertype=box&id=A466 Endocrinology - Adrenal Cortex Development]
 
'''Adrenal Medulla'''
* neural crest origin, migrate adjacent to coelomic cavity, initially uncapsulated and not surrounded by fetal cortex, cells have neuron-like morphology
* 2 cell types - secrete epinepherine (adrenaline) 80%; secrete norepinepherine (noradrenaline* 20%
 
[[Media:Adrenal_medulla.mov]]
 
'''Links:''' [[Endocrine - Adrenal Development]]
 
==Gonad==
[[File:XXhpgaxis.gif|thumb|Female HPG axis]]
 
HPG Axis - [http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&part=A972&rendertype=box&id=A1057 Endocrinology - Simplified diagram of the actions of gonadotrophins]
 
===Gonad Development===
 
* mesoderm - mesothelium and underlying mesenchyme, primordial germ cells
* Gonadal ridge - mesothelium thickening, medial mesonephros
* Primordial Germ cells - yolk sac, to mesentery of hindgut, to genital ridge of developing kidney
 
Differentiation
* testis-determining factor (TDF) from Y chromosome: presence (testes), absence (ovaries)
 
Testis
* 8 Weeks, mesenchyme, interstitial cells (of Leydig) secrete testosterone, androstenedione
* 8 to 12 Weeks - hCG stimulates testosterone production
* Sustentacular cells - produce anti-mullerian hormone to puberty
 
Ovary
* X chromosome genes regulate ovary development
 
'''Links:''' [[Endocrine - Gonad Development]]
 
==Placenta==
[[File:Trophoblast hCG function.jpg|thumb|Trophoblast hCG function]]
* Human chorionic gonadotrophin (hCG) - like leutenizing hormone, supports corpus luteum in ovary, pregnant state rather than menstrual, maternal urine in some pregnancy testing
 
* Human chorionic somatommotropin (hCS) - or placental lactogen stimulate (maternal) mammary development
* Human chorionic thyrotropin (hCT)
* Human chorionic corticotropin (hCACTH)
* progesterone and estrogens - support maternal endometrium
* Relaxin
 
* Placenta - Maternal (decidua) and Fetal (trophoblastic cells, extraembryonic mesoderm) components
* Endocrine function - maternal and fetal precursors, synthesis and secretion
** Protein Hormones - chorionic gonadotropin (hCG), chorionic somatomammotropin (hCS) or placental lactogen (hPL), chorionic thyrotropin (hCT), chorionic corticotropin (hCACTH)
*** hCG - up to 20 weeks, fetal adrenal cortex growth and maintenance
*** hCS – rise through pregnancy, stimulates maternal metabolic processes, breast growth
** Steroid Hormones - progesterone (maintains pregnancy), estrogens (fetal adrenal/placenta)
 
'''Links:''' [[Endocrine - Placenta Development]]
 
==Other Endocrine==
===Endocrine Heart===
* Atrial natriuretic peptide (ANP) -  Increase Filtration rate / decrease Na+ reabsorption
* Endothelins - ET-1, ET-2, ET-3, Vasoconstriction / Increase NO
* Nitric oxide (NO) - Vasodilatation
 
===Endocrine Kidney===
* Renin - Increase Angiotensin-aldosterone system
* Prostaglandins - decrease Na+ reabsorption
* Erythropoietin - Increase Erythrocyte (rbc) production
* 1,25 (OH)2 vitamin D - calcium homeostasis
* Prekallikreins - Increase Kinin production
 
===GIT Endocrine===
Enteric control of digestive function
* Gastrin - Secreted from stomach (G cells), role in control of gastric acid secretion
* Cholecystokinin - small intestine hormone, stimulates secretion of pancreatic enzymes and bile
* Secretin - small intestine hormone (epithelial cells), stimulates secretion of bicarbonate-rich fluids from pancreas and liver
 
===Adipose Tissue===
 
* Leptin - polypeptide hormone produced in adipose and many other tissues with also many different roles
* Adiponectin - regulation of energy homeostasis and glucose and lipid metabolism, as well as acting as an anti-inflammatory on the cellular vascular wall
* Resistin - (for resistance to insulin, RETN) a 108 amino acid polypeptide and the related resistin-like protein-beta (Resistin-like molecule-beta, RELMbeta) stimulate endogenous glucose production
 
'''Links:''' [[Endocrine - Other Tissues]]
 
==Endocrine Functional Changes==
* Puberty- Increased activity
* Menopause- Decreased activity
* Disease (diabetes, thyroid, kidney) suggested trends that genetics, health, nutrition, lifestyle may influence time that these events occur
* Pharmaceutical impact - birth control, steroids, Hormone Replacement Therapy (HRT)
 
==Abnormalities==
'''NIH Genes & Disease''' [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=gnd.chapter.41 Chapter 41 - Glands and Hormones]
===Pineal===
* hypoplasia - associated with retinal disease.
* tumours - in children are associated with abnormal puberty development.
 
===Pituitary===
* craniopharyngeal canal - Rathke's pouch abnormality, from the anterior part of the fossa hypophyseos of the sphenoid bone to the under surface of the skull.
* pituitary tumours (adenomas) - several abnormalities associated with abnormal levels of the hormonal output of the pituitary.
** Growth hormone (GH) adenomas - benign pituitary tumors lead to chronic high GH output levels, that may lead to acromegaly.
* Cushing's disease - caused either by a pituitary adenoma produces excess adrenocorticotropic hormone (ACTH, corticotropin) or due to ectopic tumors secreting ACTH or corticotropin-releasing hormone (CRH).
 
=== Thyroid ===
[[File:Thyroid_pyramidal_lobe.jpg|thumb|Thyroid pyramidal lobe]]
[[File:Thyroid uptake scans .jpg|thumb|Thyroid uptake scans]]
* Pyramidal lobe - from isthmus (50% of people) attached to hyoid bone distal end of thryoglossal duct.
* Congenital hypothyroidism - approximately 1 in 3000 births, associated with neurological abnormalities.
* Lingual thyroid gland - failure of thyroid descent.
* Thyroglossal cyst - persistance of thyroglossal duct. [http://www.upstate.edu/cdb/grossanat/imgs/tgdfig2.jpg Image - thyroglossal duct]
* Thyroglossal fistula - partial degeneration of the thyroglossal duct.
* Abnormal development of the thyroid - incomplete or excessive descent.
* Childhood hypothyroidism delays ossification and bone mineralization.
 
Iodine Deficiency
* A teaspoon of iodine, total lifetime requirement, cannot be stored for long periods by our body,  tiny amounts are needed regularly
* Areas of endemic iodine deficiency, where soil and therefore crops and grazing animals do not provide sufficient dietary iodine to the populace
* food fortification and supplementation - Iodized salt programs and iodized oil supplements are the most common tools in fight against IDD
 
===Parathyroid===
* Usually four glands are present (2 on each side), but three to six glands have been found in human.
* Lower parathyroid glands arise from the third pharyngeal pouch and descend with the thymus. Variable descent can lead to a range of adult locations, from just beneath the mandible to the anterior mediastinum.
 
===Pancreas===
* Type 1 Diabetes - juvenile onset diabetes, more severe form of illness, increases risk of blindness, heart disease, kidney failure, neurological disease, T-lymphocyte-dependent autoimmune disease, infiltration and destruction of the islets of Langerhans, Approx 16 million Americans
* Type 2 Diabetes - loosely defined as "adult onset" diabetes, becoming more common cases of type 2 diabetes seen in younger people
* Risk of developing diabetes - environmental factors (food intake and exercise play an important role, either overweight or obese),  Inherited factors (genes involved remain poorly defined)
 
===Adrenal===
* Congenital Adrenal Hyperplasia (CAH) - family of inherited disorders of adrenal steroidogenesis enzymes which impairs cortisol production by the adrenal cortex. Androgen excess leads newborn females with external genital ambiguity and postnatal progressive virilization in both sexes.
** Enzymes most commonly affected: 21-hydroxylase (21-OH), 11beta-hydroxylase, 3beta-hydroxysteroid dehydrogenase.
** Enzymes less commonly affected: 17alpha-hydroxylase/17,20-lyase and cholesterol desmolase.
 
* Pheochromocytomas (PCC) - Catecholamine-producing (neuro)endocrine tumor located in the adrenal medulla. Similar catecholamine-producing tumors outside the adrenal gland are called paragangliomas (PGL).
 
===Endocrine Disruptors===
Exogenous chemicals that interfere with the function of hormones. There are 3 main mechanisms: mimic, block or interfere.
 
'''Mimic''' - effects of natural hormones by binding receptors
* Diethylstilbestrol - (DES or diethylstilbetrol) a drug prescribed to women from 1938-1971 to prevent miscarriage in high-risk pregnancies. Acts as a potent estrogen (mimics natural hormone) and therefore a potential endocrine disruptor. Female fetus, increased risk abnormal reproductive tract and cancer. Male fetus, abnormal genitalia. Banned by USA FDA in 1979 as a teratogen, previously used as livestock growth promoter.
 
'''Block''' - binding of a hormone to receptor or hormone synthesis
* Finasteride - chemical used to prevent male pattern baldness and enlargement of prostate glands. An anti-androgen (blocks synthesis of dihydrotestosterone) and therefore a potential endocrine disruptor, exposed pregnant women can impact on male fetus genetial development.
* Vinclozolin - a dicarboximide fungicide, perinatal exposure in rats inhibits morphological sex differentiation. In adult rats, shown to cause gonad tumours (Leydig cell) and atrophy. Chemical has androgen-antagonist (antiandrogenic) activity, metabolies compete with natural androgen
 
'''Interfere''' - with hormone transport or elimination
 
*  Polychlorinated biphenyl pollutants - (PCBs) Rats exposed to PCBs have low levels of thyroid hormone. Compete for binding sites of thyroid hormone transport protein. Without being bound to this protein, thyroid hormones are excreted from the body (McKinney et al. 1985; Morse et al. 1996)


==References==
==References==
<references/>
* Endocrinology: An Integrated Approach Nussey, S.S. and Whitehead, S.A. London:Taylor & Francis; c2001 [http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&part=A3&rendertype=box&id=A11 Major hormone types]
* Genes and Disease, Bethesda (MD): National Library of Medicine (US), NCBI [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=gnd.chapter.41 Chapter 41 - Glands and Hormones]
===Search ===
* '''Bookshelf'''  [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=endocrine endocrine] | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=pineal_gland pineal gland] | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=hypothalmus hypothalamus] | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=pituitary_gland pituitary gland] | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=thyroid_gland thyroid gland] | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=parathyroid_gland parathyroid gland] | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=thymus_gland thymus gland] | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=endocrine_pancreas endocrine pancreas]  | [http://www.ncbi.nlm.nih.gov/sites/entrez?db=Books&cmd=search&term=adrenal_gland adrenal gland]
* '''Pubmed''' [http://www.ncbi.nlm.nih.gov/sites/gquery?itool=toolbar&cmd=search&term=endocrine_development endocrine development]
==Histology==
===Adult===
<gallery>
File:Pineal_histology_001.jpg|Pineal (high power)
File:Thyroid_histology_001.jpg|Thyroid (low power)
File:Thyroid_histology_002.jpg|Thyroid (high power)
File:Parathyroid_histology_001.jpg|Parathyroid (low power)
File:Parathyroid_histology_002.jpg|Parathyroid (high power)
File:Pituitary histology 001.jpg|Pituitary - adenohypophysis
File:Pituitary histology 002.jpg|Pituitary - adenohypophysis
File:Pituitary histology 003.jpg|Pituitary - neurohypophysis
File:Adrenal histology 001.jpg|Adrenal - Cortex and Medulla
File:Adrenal histology 002.jpg|Adrenal - Cortical Zones
File:Adrenal histology 003.jpg|Adrenal - Zona Reticularis and Medulla
File:Pancreatic islet.png|Pancreatic islet
</gallery>
===Embryonic===
<gallery>
File:Stage22_pancreas_b.jpg|Stage 22 - Pancreatic duct
File:Stage22 adrenal.jpg|Stage 22 - Adrenal gland
File:Week10 adrenal.jpg|Week 10 - Adrenal gland
</gallery>
==Terms==
'''adrenocorticotropin''' - (ACTH  or corticotropin) anterior pituitary, peptide hormone
'''antidiuretic hormone''' - (ADH) hypothalamus, peptide hormone
'''atrial natriuretic factor''' - (ANP) heart, , peptide hormone
'''calcitonin''' - (CT) C cells of thyroid, peptide hormone
'''follicle stimulating hormone''' - (FSH)  pituitary, protein hormone
'''growth hormone''' - (GH) pituitary, peptide hormone
'''human chorionic gonadotropin''' -  (hCG) pancreas glycoprotein hormone with 2 subunits (alpha and beta joined non covalently). Similar in structure to luteinizing hormone (LH), hCG exists in multiple hormonal and non-endocrine agents (regular hCG, hyperglycosylated hCG and the free beta-subunit of hyperglycosylated hCG). [http://www.ncbi.nlm.nih.gov/pubmed/19171054 PMID: 19171054]


'''lutenizing hormone''' - (LH) pituitary, protein hormone
===Effects of environmental endocrine disruptors on pubertal development===
J Clin Res Pediatr Endocrinol. 2011 Mar;3(1):1-6. Epub 2011 Feb 23.


'''melaocyte stimulating hormone''' - (MSH) pituitary, peptide hormone
Ozen S, Darcan S.


'''prolactin''' - (PRL) pituitary, peptide hormone
Pediatric Endocrinology Unit, Mersin Children Hospital, Mersin, Turkey.
Abstract
The onset and course of puberty are under the control of the neuroendocrine system. Factors affecting the timing and regulation of the functions of this system may alter the onset and course of puberty. Several environmental endocrine disruptors (EDs) with significant influences on the normal course of puberty have been identified. Numerous animal and human studies concerning EDs have been conducted showing that these substances may extensively affect human health; nevertheless, there are still several issues that remain to be clarified. In this paper, the available evidence from animal and human studies on the effects of environmental EDs with the potential to cause precocious or delayed puberty was reviewed.Conflict of interest:None declared.


'''parathyroid hormone''' - (PTH) parathyroid, peptide hormone
PMID 21448326


'''thyroid hormone''' - (TH) thyroid,amino acid derivative
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065309


'''thyroid stimulating hormone''' - (TSH) pituitary, protein hormone
==External Links==


[[Category:Endocrine]] [[Category:Adrenal]] [[Category:Thyroid]] [[Category:Parathyroid]] [[Category:Pituitary]] [[Category:Pancreas]] [[Category:Genital]]
* [http://www.endotext.org/ Endotext.org]

Latest revision as of 15:39, 21 September 2016

2015

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Links only work with currently enrolled UNSW students.

Lecture 11 -


Introduction

  • 2013 lecture PDF Lecture Date: 2013-10-08 Lecture Time: 12:00 Venue: Wallace Wurth LG02 Speaker: Steve Palmer
  • 2009 Lecture Audio Lecture Date: 06-10-2009 Lecture Time: 12:00 Venue: BioMed E Speaker: Mark Hill Endocrine


2013: Current lecture

2009: Medicine Lecture - Endocrine Development | lecture 1 slide/page PDF

2008: Lecture - Endocrine Development | lecture 1 slide/page PDF | lecture 4 slides/page PDF |


Endocrine Links: Introduction | BGD Lecture | Science Lecture | Lecture Movie | pineal | hypothalamus‎ | pituitary | thyroid | parathyroid | thymus | pancreas | adrenal | endocrine gonad‎ | endocrine placenta | other tissues | Stage 22 | endocrine abnormalities | Hormones | Category:Endocrine
Historic Embryology - Endocrine  
1903 Islets of Langerhans | 1903 Pig Adrenal | 1904 interstitial Cells | 1908 Pancreas Different Species | 1908 Pituitary | 1908 Pituitary histology | 1911 Rathke's pouch | 1912 Suprarenal Bodies | 1914 Suprarenal Organs | 1915 Pharynx | 1916 Thyroid | 1918 Rabbit Hypophysis | 1920 Adrenal | 1935 Mammalian Hypophysis | 1926 Human Hypophysis | 1927 Adrenal | 1927 Hypophyseal fossa | 1930 Adrenal | 1932 Pineal Gland and Cysts | 1935 Hypophysis | 1935 Pineal | 1937 Pineal | 1935 Parathyroid | 1940 Adrenal | 1941 Thyroid | 1950 Thyroid Parathyroid Thymus | 1957 Adrenal

| original Endocrine page

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/

Preface

Chapter 1. Principles of endocrinology

Chapter 1. Principles of endocrinology

Chapter 2. The endocrine pancreas

Chapter 2. The endocrine pancreas

Chapter 3. The thyroid gland

Chapter 3. The thyroid gland

Chapter 4. The adrenal gland

Chapter 4. The adrenal gland

Chapter 5. The parathyroid glands and vitamin D

Chapter 5. The parathyroid glands and vitamin D

Chapter 6. The gonad

Chapter 6. The gonad

Chapter 7. The pituitary gland

Chapter 7. The pituitary gland

Chapter 8. Cardiovascular and renal endocrinology

Chapter 8. Cardiovascular and renal endocrinology

References

Effects of environmental endocrine disruptors on pubertal development

J Clin Res Pediatr Endocrinol. 2011 Mar;3(1):1-6. Epub 2011 Feb 23.

Ozen S, Darcan S.

Pediatric Endocrinology Unit, Mersin Children Hospital, Mersin, Turkey. Abstract The onset and course of puberty are under the control of the neuroendocrine system. Factors affecting the timing and regulation of the functions of this system may alter the onset and course of puberty. Several environmental endocrine disruptors (EDs) with significant influences on the normal course of puberty have been identified. Numerous animal and human studies concerning EDs have been conducted showing that these substances may extensively affect human health; nevertheless, there are still several issues that remain to be clarified. In this paper, the available evidence from animal and human studies on the effects of environmental EDs with the potential to cause precocious or delayed puberty was reviewed.Conflict of interest:None declared.

PMID 21448326

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065309

External Links

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