Talk:Endocrine System Development: Difference between revisions

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==Introduction==
{{Talk Page}}
[[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.


==Lecture Objectives==
==Human Endocrine - Embryonic==
* Understanding of hormone types
* Understanding of endocrine gland development
* Understanding of endocrine developmental functions
* Brief understanding of endocrine abnormalities


== Textbooks ==
Based on data from {{Ref-O'Rahilly1983a}}
In general, not dealt with as a system in many textbooks, so various chapters: nervous system, head, gastrointestinal tract, reproductive organs, etc.
<ref name=O'Rahilly1983a>{{Ref-O'Rahilly1983a}}</ref>


* '''Human Embryology '''(3rd ed.) Larson Chapter  9 Gastrointestinal, Chapter 10 Gonad, Kidney Chapter 12 Head
===By Stage===
* '''The Developing Human: Clinically Oriented Embryology '''(6th ed.) Moore and Persaud Chapters 10: p230-233; Ch12: p280-282; Ch13: p319-347
* '''Lectures''' -  [http://embryology.med.unsw.edu.au/Science/ANAT2341lecture21.htm 2008] | [http://embryology.med.unsw.edu.au/Medicine/BGDlectureEndocrine.htm Medicine Lecture - Endocrine Development]
* {{Template:Endocrine Links}} | [http://embryology.med.unsw.edu.au/Notes/endocrine.htm original Endocrine page]


==Endocrine Origins==
[[Endocrine - Pineal Development‎|Pineal]] | [[Endocrine - Hypothalamus Development|Hypothalamus‎]] | [[Endocrine - Pituitary Development‎|Pituitary]] | [[Endocrine - Thyroid Development‎|Thyroid]] | [[Endocrine - Parathyroid Development|Parathyroid]] | [[Endocrine - Thymus Development|Thymus‎]] | [[Endocrine - Pancreas Development|Pancreas‎]] | [[Endocrine - Adrenal Development|Adrenal‎]] | [[Endocrine - Gonad Development|Gonad‎]] |


* Derived from epithelia - covering embryo, lining gastrointestinal tract, lining coelomic cavity
Stage 13
* Also mesenchymal contribution


==Pineal Gland==
[[Endocrine - Pituitary Development‎|Hypophysis]] -  basement membranes of the craniopharyngeal pouch and the brain are clearly in contact (O'Rahilly 1973).
[[File:pineal-body.jpg|thumb|Adult pineal body]]
* Thymus - Weller (1933)<ref name=Weller1933>{{Ref-Weller1933}}</ref> recognized already a thymic primordium "of considerable size" on the ventral part of the third pharyngeal pouch, whereas Norris (1938) considered this stage to be "preprimordial"
[[File:Pineal gland position.jpg|thumb|Pineal gland position]]
[[Endocrine - Thyroid Development‎|Thyroid]] - median thyroid is now bilobed and is connected to the pharynx by a hollow pedicle.<ref name=Weller1933>{{Ref-Weller1933}}</ref> The telopharyngeal body has been regarded as a "lateral thyroid component" by some workers.<ref name=Weller1933>{{Ref-Weller1933}}</ref>
* Pancreas - ventral pancreas may perhaps be distinguishable (Politzer 1952).


* part of epithalmus - neurons, glia and pinealocytes
Stage 14
* 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===
*  [[Endocrine - Pituitary Development‎|Hypophysis]] - craniopharyngeal pouch is prominent (Streeter 1945) and the notochord appears to be inserted into its dorsal wall. The craniopharyngeal pouch has become elongated and blood vessels are beginning to grow in between the basement membranes of the pouch and brain (O'Rahilly 1973a).
* Neuroectoderm - prosenecephalon then diencephalon
*  [[Endocrine - Pineal Development‎|Epiphysis]] - a slight irregularity in the surface outline of the intact head corresponds to the future pineal body (O'Rahilly et al. 1982). Thymus. Weller's (1933)<ref name=Weller1933>{{Ref-Weller1933}}</ref> "thymus" (the third pharyngeal pouch) becomes elongated.
* caudal roof, median diverticulum, epiphysis
*  [[Endocrine - Parathyroid Development|Parathyroids]] - "Parathyrogenic zones" (Politzer and Hann 1935) are recognizable (Streeter 1945). The parathyroid 4 primordium has been illustrated at this stage by Weller (1933, Fig. 16).
* Initially a hollow diverticulum, cell proliferation to solid, pinealocytes (neuroglia), cone-shaped gland innervated by epithalmus
*  [[Endocrine - Thyroid Development‎|Thyroid]] - thyroid pedicle shows further elongation but is still connected to the epithelium of the pharynx.<ref name=Weller1933>{{Ref-Weller1933}}</ref> Right and left lobes and an isthmus may perhaps be presaged (ibid.).
* Adrenal Cortex - A change in the characteristics of the cells of the coelomic epithelium appears between the mesogastrium and the lateral end of the mesonephros.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>
* Adrenal Medulla - paravertebral sympathetic ganglia increase in size as a result of cell division and the addition of nerve fibres from the rami communicantes. The ganglia contain three types of cells: MI, M2, and M3. The M3 cells are the" parasympathetic cells" of Zuckerkandl.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>
* Pancreas - ventral pancreas (which may perhaps be distinguishable as early as stage 13) appears as an evagination from the bile duct at stages 14 (Blechschmidt 1973) and 15 (Streeter 1948). It is generally described as unpaired but, at least in some cases, may perhaps be bilobed<ref name=Odgers1930>{{Ref-Odgers1930}}</ref>  or even multiple (Delmas 1939).


'''Links:''' [[Endocrine - Pineal Development]]
Stage 15


==Hypothalamus==
*  [[Endocrine - Pineal Development‎|Epiphysis]] - pineal body is detectable in the roof of the diencephalon (Stadium I of Turkewitsch 1933) (O'Rahilly 1968).
*  [[Endocrine - Thyroid Development‎|Thyroid]] - thyroid primordium may be detached from the pharyngeal epithelium in some instances. "At about the time" when the thyroglossal duct "becomes broken it loses its lumen" (Grosser 1912).
* Adrenal Cortex - primordium is first recognizable. A new type of cell (C1) from the coelomic epithelium is found in the subjacent mesenchyme. New cells (C2) appear in the medial wall of mesonephric glomeruli and begin to migrate into the suprarenal primordium.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref> Jirfisek (1980) denies a mesonephric contribution to the suprarenal.
* Adrenal Medulla - all types of cells (M1, M2, and M3) increase in number. From stage 15 to stage 18, the suprarenal primordium is cigar-shaped and extends from segment T6 to segment L1, lateral to the aorta and mesogastrium.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>


'''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
Stage 16


===Hypothalamus Development===
*  [[Endocrine - Pituitary Development‎|Hypophysis]] - slight indication of the infundibular recess may be seen in some embryos (O'Rahilly 1973 a).
* Neuroectoderm - prosenecephalon then diencephalon
*  [[Endocrine - Pineal Development‎|Epiphysis]] - cellular migration in an external direction occurs in the pineal body during stages 16 and 17 (Stadium 2 of Turkewitsch 1933) (O'Rahilly 1968).
* ventro-lateral wall intermediate zone proliferation
* Thymus - according to Norris (1938), "not until the primordium of the parathyroid [3] has been outlined can the remaining portion of the third pouch be recognized, by exclusion, as the primordium of the endodermal thymus".
* Mamillary bodies - form pea-sized swellings ventral wall of hypothalamus
*  [[Endocrine - Parathyroid Development|Parathyroids]] - parathyrogenic zones are closely related to the third and fourth aortic arches at 9 mm (Politzer and Hann 1935, unstaged embryo). Parathyroid 3 is identifiable on the anterior wall of the third pharyngeal pouch (Weller 1933, Fig. 17) and "does not arise from a dorsal lobule" of the pouch (Norris 1937). The "sudden appearance of well-differentiated clear chief cells in the early primordia of the parathyroids" at 9 mm was emphasized by Norris (1937).
*  [[Endocrine - Thyroid Development‎|Thyroid]] - has lost its continuity with the pharynx and it consists of two lobes, an isthmus, and a remnant of the pedicle.<ref name=Weller1933>{{Ref-Weller1933}}</ref>
* Adrenal Cortex. Another type of cell (C3) arises from the coelomic epithe- lium. Both C1 and C3 cells enter the suprarenal primordium. An "enormous immigration" of C2 cells occurs.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>
* Adrenal Medulla - cells of neural origin are migrating into the gland, separating the cortical cells into islands. Nerve fibres from the ganglia ac- company the M1 and M3 cells. The M2 cells remain in the ganglia and become sympathetic ganglion cells.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>
* Pancreas - dorsal pancreas and the ventral pancreas are contiguous.<ref name=Blechschmidt1973>{{Ref-Blechschmidt1973}}</ref>


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


==Pituitary==
Stage 17
[[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)
*  [[Endocrine - Pituitary Development‎|Hypophysis]] - juxtacerebral wall of the craniopharyngeal pouch is the thicker. The lateral lobes (future infundibular, or tuberal, part) and the anterior chamber (Vorraum) are clearly visible (O'Rahilly 1973 a). The infundibular recess displays a characteristically folded wall, namely the neurohypophysis (O'Rahilly 1973 a).
* Thymus - connection of the thymus with the pharynx has been severed (Weller 1933). The thymus is intimately approximated to the cervical duct (ibid.) According to Norris (1937), both third and fourth pouches make contact with the ectoderm, although only the third "receives an increment from the ectoderm".
*  [[Endocrine - Parathyroid Development|Parathyroids]] -parathyroid 4 is attached to the lateral surface of what Weller (1933)<ref name=Weller1933>{{Ref-Weller1933}}</ref> termed the "lateral thyroid component"
*  [[Endocrine - Thyroid Development‎|Thyroid]]. The lobes of the thyroid curve around the carotid arteries and are connected by a delicate isthmus. Lacunae "should not be confused with lumina of follicles".<ref name=Weller1933>{{Ref-Weller1933}}</ref>
* Adrenal Cortex - dorsal part of the whole suprarenal primordium is disorganized by the invasion of sympathetic nerves and cells, while the band of C2 cells and the coelomic epithelium remain intact (Crowder 1957).
* Adrenal Medulla - first neural migration is at its height. Growth of the para-aortic complex is extensive. The plexiform complex is derived from paravertebral sympathetic ganglia T6-12 and usually L 1. Included in it are the primordia of the suprarenal medulla and of the celiac, superior mesenteric, and renal plexuses. Nerve fibres and "paraganglion" (M3) cells enter.
* Pancreas - ventral pancreas has now fused with dorsal (Streeter 1948). Perhaps the ventral and dorsal ducts have begun to blend (Russu and Vaida 1959).


'''Posterior pituitary hormones''' - Oxytocin, Arginine vasopressin
Stage 18


===Pituitary Development===
[[Endocrine - Pineal Development‎|Epiphysis]] - cellular migration in the pineal body forms a distinct "anterior lobe" in which follicles appear (Stadium 3 of Turkewitsch 1933) (O'Rahilly 1973 a).
[[File:Pituitary rabbit development.jpg|thumb|Pituitary rabbit development]]
* Thymus- thymus makes contact with the thyroid gland and contains a series of canals internally (Weller 1933).
{|
[[Endocrine - Thyroid Development‎|Thyroid]] - median thyroid is in contact with "lateral thyroid components"<ref name=Weller1933>{{Ref-Weller1933}}</ref>but others have maintained that the telopharyngeal body should not be regarded as a thyroid component (Bejdl and Politzer 1953). The lobes of the thyroid are "composed of series of continuously communicating solid annectent bars" this is "the earliest stage of the definitive thyroid".<ref name=Weller1933>{{Ref-Weller1933}}</ref>  First differentiation occurs in Weller's (1933) "lateral thyroid component," which is beginning to "blend into uniformly constituted thyroid tissue". Weller (1933) illustrated (Fig. 11) a thyroid gland that still showed continuity between its pedicle and the epithelium of the pharynx.
| [[File:Pituitary development animation.gif]]
* Adrenal Cortex - gland becomes reorganized. The C1, 2, and 3 cells form cords as sinusoids develop. Cells divide at or near the surface, where new cells are added.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>  
| <font color=deepskyblue>'''Blue''' - neural tube ectoderm</font>


Stage 19


*  [[Endocrine - Pituitary Development‎|Hypophysis]] - the caudal part of the craniopharyngeal pouch is reduced to a closed epithelial stem (Andersen et al. 1971).
*  [[Endocrine - Pineal Development‎|Epiphysis]] - the "anterior lobe" of the pineal body shows a characteristic step and wedge appearance (Stadium 4 of Turkewitsch 1933) (O'Rahilly 1968).
*  [[Endocrine - Parathyroid Development|Parathyroids]] - 3 become detached from the pharyngeal endo- derm (Jirfisek 1980).
* Adrenal Cortex - C2 cells lie on the surface of the gland and form a "capsule".<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>
* Adrenal Medulla - Sympathicoblasts penetrate the cortex at stages 19 and 20, and form scattered islets of medullary tissue throughout the cortex (Jirfisek 1980).


<font color=darksalmon>'''Red''' - surface ectoderm</font>
Stage 20
|}


* Dual ectoderm origins
* [[Endocrine - Pituitary Development‎|Hypophysis]] - the adenohypophysial epithelium adjacent to the neurohy- pophysis constitutes the beginning pars intermedia (O'Rahilly 1973 a). The walls of the craniopharyngeal pouch bud into the mesenchyme (Andersen et al. 1971 ; Jirfisek 1980).
** Ectoderm - ectoderm roof of stomodeum, Rathke's pouch, adenohypophysis
* Thymus - the right and left components are in contact with each other<ref name=Weller1933>{{Ref-Weller1933}}</ref>  but are "never completely fused" (Norris 1938, Siegler 1969). Thymic cortex appears (in stages 20-22) as a result, according to Norris
** Neuroectoderm - prosenecephalon then diencephalon, neurohypophysis
(1938), of migration of and covering by "cells derived from the cervical sinus".
* [[Endocrine - Parathyroid Development|Parathyroids]] - the parathyroid glands are attached to the lateral lobes of the thyroid (Weller 1933).
Weller (1933, Fig. 23) showed parathyroid 3 still rostral to parathyroid 4 at 23 mm, whereas (presumably due to variation in the "descent" of the thymus) Norris (1937, Fig. 4) showed parathyroid 3 rostral to, level with, and caudal to parathyroid 4 in embryos of 16-17 mm.
* [[Endocrine - Thyroid Development‎|Thyroid]] - the "annectent bars" of the thyroid are more compact then previously.<ref name=Weller1933>{{Ref-Weller1933}}</ref>  The thyroid now exhibits its definitive external form.


'''Adenohypophysis'''
Stage 21
* Anterior wall proliferates - pars distalis
* Posterior wall little growth – pars intermedia
* Rostral growth around infundibular stem – pars tuberalis


'''Neurohypophysis'''
*  [[Endocrine - Pituitary Development‎|Hypophysis]] - the pharyngeal stalk becomes fragmented (Jirfisek 1980).
* Infundibulum – median eminence, infundibulum, pars nervosa
* Adrenal Cortex - the cellular "capsule" becomes covered by a layer of fibrous tissue.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>


===Pituitary Timeline===
Stage 22
* Week 4 - hypophysial pouch, Rathke’s pouch, diverticulum from roof
* Week 5 - elongation, contacts infundibulum, diverticulum of diencephalon
* Week 6 - connecting stalk between pouch and oral cavity degenerates
* Week 10 - growth hormone and ACTH detectable
* Week 16 - adenohypophysis fully differentiated
* Week 20 to 24 - growth hormone levels peak, then decline


'''Links:''' [[Endocrine - Pituitary Development]] | [http://www.med.unc.edu/embryo_images/unit-nervous/nerv_htms/nerv016.htm Embryo Images - Pituitary]
[[Endocrine - Parathyroid Development|Parathyroids]] - Parathyroids 4 become detached from the pharyngeal endoderm (Jirfisek 1980).
* Adrenal Cortex - the C2 cells have changed and resemble fibrocytes.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>


==Thyroid==
Stage 23
* 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)
* Pituitary - adenohypophysis loss of the stalk and lobules of epithelium project into the mesodermal component of the gland, and oriented epithelial follicles are present (Streeter, 1951, plate 2). Abundant angioblasts and capillaries are found.
*  [[Endocrine - Pineal Development‎|Epiphysis]] - The pineal body has reached Stadium 5 of Turkewitsch (1933).<ref name=O'Rahilly1968>{{Ref-O'Rahilly1968}}</ref>
* Thymus - The cortex is well-developed, "true lobulation" has begun with the appearance of" fine superficial scallops," lymphocytes are present sparsely in the subcortical zone, and vessels are found within the thymus (Norris 1938).
* Adrenal Cortex - It appears that C2 cells first enter the body of the gland at this stage. The pattern of the arterial supply is established. The cellular "capsule" is penetrated by arterial capillaries which join the sinusoids. Their points of entry give the surface of the gland an appearance of cobblestones. The zona glomerulosa is formed of CI and C3 cells. Cells from this zone and from the "capsule" migrate centrally into the cords.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>
* Adrenal Medulla - Nerve fibres and neuroblasts are first seen in the body of the gland. The paragangtion (M3) cells are beginning to multiply rapidly and, from 30 mm (stage 23) until birth, some are differentiating into chromaffin cells.<ref name=Crowder1957>{{Ref-Crowder1957}}</ref>


===Thyroid Development===
===Table===
[[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===
{{Endocrine embryo table}}
* 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===
* Initial secreted biologically inactivated by modification, late fetal secretion develops brown fat
* Iodine deficiency- during this period, leads to neurological defects (cretinism)
* Birth - TSH levels increase, thyroxine (T3) and T4 levels increase to 24 h, then 5-7 days postnatal decline to normal levels


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


==Parathyroid==
==Endocrinology - An Integrated Approach==
[[File:Parathyroid adult.jpg|thumb|Parathyroid adult]]
{| class="wikitable collapsible collapsed"
! Thyroid
|-
| [[File:Endocrinology - An Integrated Approach.png|80px]]  
| '''Endocrinology - An Integrated Approach''' Stephen Nussey and Saffron Whitehead


* Parathyroid Hormone - Increase calcium ions [Ca2+], stimulates osteoclasts, increase Ca GIT absorption (opposite effect to calcitonin)
St. George's Hospital Medical School, London, UK Oxford: BIOS Scientific Publishers; 2001. ISBN-10: 1-85996-252-1
* Adult Calcium and Phosphate - Daily turnover in human with dietary intake of 1000 mg/day
* secreted by chief cells
Principal cells cords of cells
===Parathyroid Development===
[[File:Pharyngeal pouches.jpg|thumb|Pharyngeal pouches]]
* Endoderm - third and fourth pharyngeal pouches, could also have ectoderm and neural crest
** 3rd Pharyngeal Pouch - inferior parathyroid, initially descends with thymus
** 4th Pharyngeal Pouch - superior parathyroid
* Week 6 - diverticulum elongate, hollow then solid, dorsal cell proliferation
* Fetal parathyroids - respond to calcium levels, fetal calcium levels higher than maternal


'''Links:''' [[Endocrine - Parathyroid Development]]
Copyright © 2001, BIOS Scientific Publishers Limited. [http://www.ncbi.nlm.nih.gov/books/NBK22 Bookshelf]
|-
| colspan=2|[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/ Chapter 3. The thyroid gland]


==Thymus==
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A246 Iodine intake]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A248 Anatomical features of the thyroid gland]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A249 Iodine trapping and thyroid function]
* [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]


* Thymus - bone-marrow lymphocyte precursors become thymocytes, and subsequently mature into T lymphocytes (T cells)
|}
* Thymus hormones - thymosins stimulate the development and differentiation of T lymphocytes


===Thymus Development===


* Endoderm - third pharyngeal pouch
{|
* Week 6 - diverticulum elongates, hollow then solid, ventral cell proliferation
| [[File:Endocrinology - An Integrated Approach.png]]
* Thymic primordia - surrounded by neural crest mesenchyme, epithelia/mesenchyme interaction
| Stephen Nussey and Saffron Whitehead.


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


==Pancreas==
Copyright © 2001, BIOS Scientific Publishers Limited.
[[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/NBK22/
* 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/A2/ Preface]
[[File:Pancreatic_duct_developing.jpg|thumb|Pancreatic buds and duct developing]]
[[File:Stage22_pancreas_a.jpg|thumb|Stage22 pancreas]]
* Pancreatic buds -  duodenal level endoderm, splanchnic mesoderm forms dorsal and ventral mesentery, dorsal bud (larger, first), ventral bud (smaller, later)
* Pancreas Endoderm - pancreas may be opposite of liver
** Heart cells promote/notochord prevents liver formation
** Notochord may promote pancreas formation
** Heart may block pancreas formation


* Duodenum growth/rotation - brings ventral and dorsal buds together, fusion of buds
===Chapter 1. Principles of 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/A3/ Chapter 1. Principles of 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/A3/#A10 Functions of hormones and their regulation]
* Week 7 to 20 - pancreatic hormones secretion increases, small amount maternal insulin
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A14 Chemical signalling - endocrine, paracrine, autocrine and intracrine mechanisms]
* Week 10 - glucagon (alpha) differentiate first, somatostatin (delta), insulin (beta) cells differentiate, insulin secretion begins
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A16 Chemical classification of hormones and their synthesis]
* Week 15 - glucagon detectable in fetal plasma
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A18 Hormone synthesis]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A22 Transport of hormones in the circulation and their half-lives]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A3/#A23 Hormone receptors - cell surface]
* [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 - Pancreas Development]] | [[Gastrointestinal Tract - Pancreas Development]]
===Chapter 2. The endocrine pancreas===


==Adrenal==
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/ Chapter 2. The endocrine pancreas]


* Richly vascularized - arterioles passing through cortex, capillaries from cortex to medulla, portal-like circulation
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A52 Glucose turnover]
* Fetal Cortex - produces a steroid precursor (DEA), converted by placenta into estrogen
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A58 Anabolic and catabolic phases of glucose metabolism]
* Adult Medulla - produces adrenalin (epinephrine), noradrenaline (norepinephrine)
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A43/#A60 Actions of insulin and glucagon]
* Fetal adrenal hormones - influence lung maturation
* [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]


'''Adrenal cortical hormones''' - (steroids) Cortisol, Aldosterone, Dehydroepiandrosterone
===Chapter 3. The thyroid gland===
* 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.


[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/ Chapter 3. The thyroid gland]


'''Adrenal medullary hormones''' - (amino acid derivatives) Epinephrine, Norepinephrine
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A246 Iodine intake]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A248 Anatomical features of the thyroid gland]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A235/#A249 Iodine trapping and thyroid function]
* [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]


===Adrenal Development===
===Chapter 4. The adrenal gland===
[[File:Adrenal_medulla.jpg|300px|right|link=http://php.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'''
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/ Chapter 4. The adrenal gland]
* 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]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A460 Specificity of the biological effects of adrenal steroid hormones]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A461 Cholesterol and steroid synthesis in the adrenal cortex]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A442/#A464 Anatomical and functional zonation in the adrenal cortex]
* [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/#A518 Pituitary control of adrenocortical steroids - ACTH]
* [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]


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


'''Links:''' [[Endocrine - Adrenal Development]]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A742/#A769 Calcium and phosphate in serum and its measurement]
* [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]


==Gonad==
===Chapter 6. The 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]
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A972/ Chapter 6. The gonad]


===Gonad 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]


* mesoderm - mesothelium and underlying mesenchyme, primordial germ cells
===Chapter 7. The pituitary gland===
* Gonadal ridge - mesothelium thickening, medial mesonephros
* Primordial Germ cells - yolk sac, to mesentery of hindgut, to genital ridge of developing kidney


Differentiation
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/ Chapter 7. The pituitary gland]
* testis-determining factor (TDF) from Y chromosome: presence (testes), absence (ovaries)


Testis
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1267 Anatomical and functional connections of the hypothalamo-pituitary axis]
* 8 Weeks, mesenchyme, interstitial cells (of Leydig) secrete testosterone, androstenedione
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1273 Embryology of the pituitary gland]
* 8 to 12 Weeks - hCG stimulates testosterone production
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1257/#A1295 Craniopharyngioma]
* Sustentacular cells - produce anti-mullerian hormone to puberty
* [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]


Ovary
===Chapter 8. Cardiovascular and renal endocrinology===
* X chromosome genes regulate ovary development


'''Links:''' [[Endocrine - Gonad Development]]
[http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/ Chapter 8. Cardiovascular and renal endocrinology]


==Placenta==
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1537 Endocrinology of heart failure]
[[File:Trophoblast hCG function.jpg|thumb|Trophoblast hCG function]]
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1542 Paracrine and autocrine regulation of blood pressure: the endocrinology of sepsis]
* Human chorionic gonadotrophin (hCG) - like leutenizing hormone, supports corpus luteum in ovary, pregnant state rather than menstrual, maternal urine in some pregnancy testing
* [http://www.ncbi.nlm.nih.gov/books/n/endocrin/A1527/#A1547 Hormones and blood cell production - erythropoietin]
* [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]


* Human chorionic somatommotropin (hCS) - or placental lactogen stimulate (maternal) mammary development
==References==
* 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
===Effects of environmental endocrine disruptors on pubertal development===
* Endocrine function - maternal and fetal precursors, synthesis and secretion
J Clin Res Pediatr Endocrinol. 2011 Mar;3(1):1-6. Epub 2011 Feb 23.
** 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]]
Ozen S, Darcan S.


==Other Endocrine==
Pediatric Endocrinology Unit, Mersin Children Hospital, Mersin, Turkey.
===Endocrine Heart===
Abstract
* Atrial natriuretic peptide (ANP) -  Increase Filtration rate / decrease Na+ reabsorption
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.
* Endothelins - ET-1, ET-2, ET-3, Vasoconstriction / Increase NO
* Nitric oxide (NO) - Vasodilatation


===Endocrine Kidney===
PMID 21448326
* 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===
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065309
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===
==2012==
===Neurobehavioral risk is associated with gestational exposure to stress hormones===
Expert Rev Endocrinol Metab. 2012 Jul;7(4):445-459.


* Leptin - polypeptide hormone produced in adipose and many other tissues with also many different roles
Sandman CA, Davis EP.
* Adiponectin - regulation of energy homeostasis and glucose and lipid metabolism, as well as acting as an anti-inflammatory on the cellular vascular wall
Source
* 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
Department of Psychiatry & Human Behavior, Women and Children's Health and Well-Being Project, University of California, Irvine, Orange, CA, USA.


'''Links:''' [[Endocrine - Other Tissues]]
Abstract


==Endocrine Functional Changes==
The developmental origins of disease or fetal programming model predict that early exposures to threat or adverse conditions have lifelong consequences that result in harmful outcomes for health. The maternal endocrine 'fight or flight' system is a source of programming information for the human fetus to detect threats and adjust their developmental trajectory for survival. Fetal exposures to intrauterine conditions including elevated stress hormones increase the risk for a spectrum of health outcomes depending on the timing of exposure, the timetable of organogenesis and the developmental milestones assessed. Recent prospective studies, reviewed here, have documented the neurodevelopmental consequences of fetal exposures to the trajectory of stress hormones over the course of gestation. These studies have shown that fetal exposures to biological markers of adversity have significant and largely negative consequences for fetal, infant and child emotional and cognitive regulation and reduced volume in specific brain structures.
* 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==
PMID 23144647
'''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/>


* 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]
==External Links==
* 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]
{{External Links}}
===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]
* [http://www.endotext.org/ Endotext.org]
* '''Pubmed''' [http://www.ncbi.nlm.nih.gov/sites/gquery?itool=toolbar&cmd=search&term=endocrine_development endocrine development]


==Histology==
==Histology==

Latest revision as of 13:29, 1 November 2016

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Cite this page: Hill, M.A. (2024, April 19) Embryology Endocrine System Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Endocrine_System_Development


Human Endocrine - Embryonic

Based on data from O'Rahilly R. The timing and sequence of events in the development of the human endocrine system during the embryonic period proper. (1983) Anat. Embryol., 166: 439-451. PMID 6869855 [1]

By Stage

Pineal | Hypothalamus‎ | Pituitary | Thyroid | Parathyroid | Thymus‎ | Pancreas‎ | Adrenal‎ | Gonad‎ |

Stage 13

  • Hypophysis - basement membranes of the craniopharyngeal pouch and the brain are clearly in contact (O'Rahilly 1973).
  • Thymus - Weller (1933)[2] recognized already a thymic primordium "of considerable size" on the ventral part of the third pharyngeal pouch, whereas Norris (1938) considered this stage to be "preprimordial"
  • Thyroid - median thyroid is now bilobed and is connected to the pharynx by a hollow pedicle.[2] The telopharyngeal body has been regarded as a "lateral thyroid component" by some workers.[2]
  • Pancreas - ventral pancreas may perhaps be distinguishable (Politzer 1952).

Stage 14

  • Hypophysis - craniopharyngeal pouch is prominent (Streeter 1945) and the notochord appears to be inserted into its dorsal wall. The craniopharyngeal pouch has become elongated and blood vessels are beginning to grow in between the basement membranes of the pouch and brain (O'Rahilly 1973a).
  • Epiphysis - a slight irregularity in the surface outline of the intact head corresponds to the future pineal body (O'Rahilly et al. 1982). Thymus. Weller's (1933)[2] "thymus" (the third pharyngeal pouch) becomes elongated.
  • Parathyroids - "Parathyrogenic zones" (Politzer and Hann 1935) are recognizable (Streeter 1945). The parathyroid 4 primordium has been illustrated at this stage by Weller (1933, Fig. 16).
  • Thyroid - thyroid pedicle shows further elongation but is still connected to the epithelium of the pharynx.[2] Right and left lobes and an isthmus may perhaps be presaged (ibid.).
  • Adrenal Cortex - A change in the characteristics of the cells of the coelomic epithelium appears between the mesogastrium and the lateral end of the mesonephros.[3]
  • Adrenal Medulla - paravertebral sympathetic ganglia increase in size as a result of cell division and the addition of nerve fibres from the rami communicantes. The ganglia contain three types of cells: MI, M2, and M3. The M3 cells are the" parasympathetic cells" of Zuckerkandl.[3]
  • Pancreas - ventral pancreas (which may perhaps be distinguishable as early as stage 13) appears as an evagination from the bile duct at stages 14 (Blechschmidt 1973) and 15 (Streeter 1948). It is generally described as unpaired but, at least in some cases, may perhaps be bilobed[4] or even multiple (Delmas 1939).

Stage 15

  • Epiphysis - pineal body is detectable in the roof of the diencephalon (Stadium I of Turkewitsch 1933) (O'Rahilly 1968).
  • Thyroid - thyroid primordium may be detached from the pharyngeal epithelium in some instances. "At about the time" when the thyroglossal duct "becomes broken it loses its lumen" (Grosser 1912).
  • Adrenal Cortex - primordium is first recognizable. A new type of cell (C1) from the coelomic epithelium is found in the subjacent mesenchyme. New cells (C2) appear in the medial wall of mesonephric glomeruli and begin to migrate into the suprarenal primordium.[3] Jirfisek (1980) denies a mesonephric contribution to the suprarenal.
  • Adrenal Medulla - all types of cells (M1, M2, and M3) increase in number. From stage 15 to stage 18, the suprarenal primordium is cigar-shaped and extends from segment T6 to segment L1, lateral to the aorta and mesogastrium.[3]

Stage 16

  • Hypophysis - slight indication of the infundibular recess may be seen in some embryos (O'Rahilly 1973 a).
  • Epiphysis - cellular migration in an external direction occurs in the pineal body during stages 16 and 17 (Stadium 2 of Turkewitsch 1933) (O'Rahilly 1968).
  • Thymus - according to Norris (1938), "not until the primordium of the parathyroid [3] has been outlined can the remaining portion of the third pouch be recognized, by exclusion, as the primordium of the endodermal thymus".
  • Parathyroids - parathyrogenic zones are closely related to the third and fourth aortic arches at 9 mm (Politzer and Hann 1935, unstaged embryo). Parathyroid 3 is identifiable on the anterior wall of the third pharyngeal pouch (Weller 1933, Fig. 17) and "does not arise from a dorsal lobule" of the pouch (Norris 1937). The "sudden appearance of well-differentiated clear chief cells in the early primordia of the parathyroids" at 9 mm was emphasized by Norris (1937).
  • Thyroid - has lost its continuity with the pharynx and it consists of two lobes, an isthmus, and a remnant of the pedicle.[2]
  • Adrenal Cortex. Another type of cell (C3) arises from the coelomic epithe- lium. Both C1 and C3 cells enter the suprarenal primordium. An "enormous immigration" of C2 cells occurs.[3]
  • Adrenal Medulla - cells of neural origin are migrating into the gland, separating the cortical cells into islands. Nerve fibres from the ganglia ac- company the M1 and M3 cells. The M2 cells remain in the ganglia and become sympathetic ganglion cells.[3]
  • Pancreas - dorsal pancreas and the ventral pancreas are contiguous.[5]


Stage 17

  • Hypophysis - juxtacerebral wall of the craniopharyngeal pouch is the thicker. The lateral lobes (future infundibular, or tuberal, part) and the anterior chamber (Vorraum) are clearly visible (O'Rahilly 1973 a). The infundibular recess displays a characteristically folded wall, namely the neurohypophysis (O'Rahilly 1973 a).
  • Thymus - connection of the thymus with the pharynx has been severed (Weller 1933). The thymus is intimately approximated to the cervical duct (ibid.) According to Norris (1937), both third and fourth pouches make contact with the ectoderm, although only the third "receives an increment from the ectoderm".
  • Parathyroids -parathyroid 4 is attached to the lateral surface of what Weller (1933)[2] termed the "lateral thyroid component"
  • Thyroid. The lobes of the thyroid curve around the carotid arteries and are connected by a delicate isthmus. Lacunae "should not be confused with lumina of follicles".[2]
  • Adrenal Cortex - dorsal part of the whole suprarenal primordium is disorganized by the invasion of sympathetic nerves and cells, while the band of C2 cells and the coelomic epithelium remain intact (Crowder 1957).
  • Adrenal Medulla - first neural migration is at its height. Growth of the para-aortic complex is extensive. The plexiform complex is derived from paravertebral sympathetic ganglia T6-12 and usually L 1. Included in it are the primordia of the suprarenal medulla and of the celiac, superior mesenteric, and renal plexuses. Nerve fibres and "paraganglion" (M3) cells enter.
  • Pancreas - ventral pancreas has now fused with dorsal (Streeter 1948). Perhaps the ventral and dorsal ducts have begun to blend (Russu and Vaida 1959).

Stage 18

  • Epiphysis - cellular migration in the pineal body forms a distinct "anterior lobe" in which follicles appear (Stadium 3 of Turkewitsch 1933) (O'Rahilly 1973 a).
  • Thymus- thymus makes contact with the thyroid gland and contains a series of canals internally (Weller 1933).
  • Thyroid - median thyroid is in contact with "lateral thyroid components"[2]but others have maintained that the telopharyngeal body should not be regarded as a thyroid component (Bejdl and Politzer 1953). The lobes of the thyroid are "composed of series of continuously communicating solid annectent bars" this is "the earliest stage of the definitive thyroid".[2] First differentiation occurs in Weller's (1933) "lateral thyroid component," which is beginning to "blend into uniformly constituted thyroid tissue". Weller (1933) illustrated (Fig. 11) a thyroid gland that still showed continuity between its pedicle and the epithelium of the pharynx.
  • Adrenal Cortex - gland becomes reorganized. The C1, 2, and 3 cells form cords as sinusoids develop. Cells divide at or near the surface, where new cells are added.[3]

Stage 19

  • Hypophysis - the caudal part of the craniopharyngeal pouch is reduced to a closed epithelial stem (Andersen et al. 1971).
  • Epiphysis - the "anterior lobe" of the pineal body shows a characteristic step and wedge appearance (Stadium 4 of Turkewitsch 1933) (O'Rahilly 1968).
  • Parathyroids - 3 become detached from the pharyngeal endo- derm (Jirfisek 1980).
  • Adrenal Cortex - C2 cells lie on the surface of the gland and form a "capsule".[3]
  • Adrenal Medulla - Sympathicoblasts penetrate the cortex at stages 19 and 20, and form scattered islets of medullary tissue throughout the cortex (Jirfisek 1980).

Stage 20

  • Hypophysis - the adenohypophysial epithelium adjacent to the neurohy- pophysis constitutes the beginning pars intermedia (O'Rahilly 1973 a). The walls of the craniopharyngeal pouch bud into the mesenchyme (Andersen et al. 1971 ; Jirfisek 1980).
  • Thymus - the right and left components are in contact with each other[2] but are "never completely fused" (Norris 1938, Siegler 1969). Thymic cortex appears (in stages 20-22) as a result, according to Norris

(1938), of migration of and covering by "cells derived from the cervical sinus".

  • Parathyroids - the parathyroid glands are attached to the lateral lobes of the thyroid (Weller 1933).

Weller (1933, Fig. 23) showed parathyroid 3 still rostral to parathyroid 4 at 23 mm, whereas (presumably due to variation in the "descent" of the thymus) Norris (1937, Fig. 4) showed parathyroid 3 rostral to, level with, and caudal to parathyroid 4 in embryos of 16-17 mm.

  • Thyroid - the "annectent bars" of the thyroid are more compact then previously.[2] The thyroid now exhibits its definitive external form.

Stage 21

  • Hypophysis - the pharyngeal stalk becomes fragmented (Jirfisek 1980).
  • Adrenal Cortex - the cellular "capsule" becomes covered by a layer of fibrous tissue.[3]

Stage 22

  • Parathyroids - Parathyroids 4 become detached from the pharyngeal endoderm (Jirfisek 1980).
  • Adrenal Cortex - the C2 cells have changed and resemble fibrocytes.[3]

Stage 23

  • Pituitary - adenohypophysis loss of the stalk and lobules of epithelium project into the mesodermal component of the gland, and oriented epithelial follicles are present (Streeter, 1951, plate 2). Abundant angioblasts and capillaries are found.
  • Epiphysis - The pineal body has reached Stadium 5 of Turkewitsch (1933).[6]
  • Thymus - The cortex is well-developed, "true lobulation" has begun with the appearance of" fine superficial scallops," lymphocytes are present sparsely in the subcortical zone, and vessels are found within the thymus (Norris 1938).
  • Adrenal Cortex - It appears that C2 cells first enter the body of the gland at this stage. The pattern of the arterial supply is established. The cellular "capsule" is penetrated by arterial capillaries which join the sinusoids. Their points of entry give the surface of the gland an appearance of cobblestones. The zona glomerulosa is formed of CI and C3 cells. Cells from this zone and from the "capsule" migrate centrally into the cords.[3]
  • Adrenal Medulla - Nerve fibres and neuroblasts are first seen in the body of the gland. The paragangtion (M3) cells are beginning to multiply rapidly and, from 30 mm (stage 23) until birth, some are differentiating into chromaffin cells.[3]

Table

Human Embryonic Endocrine Timeline
Stage 13 (week 4)
  • Pituitary - basement membranes of the craniopharyngeal pouch and the brain are clearly in contact.[7]
  • Thymus‎ - Weller (1933)[2] recognized already a thymic primordium "of considerable size" on the ventral part of the third pharyngeal pouch, whereas Norris (1938)[8] considered this stage to be "preprimordial"
  • Thyroid - median thyroid is now bilobed and is connected to the pharynx by a hollow pedicle.[2] The telopharyngeal body has been regarded as a "lateral thyroid component" by some workers.[2]
  • Pancreas - ventral pancreas may perhaps be distinguishable.[9]
Stage 14 (week 5)
  • Pineal - a slight irregularity in the surface outline of the intact head corresponds to the future pineal body (O'Rahilly et al. 1982).
  • Pituitary - craniopharyngeal pouch is prominent[10] and the notochord appears to be inserted into its dorsal wall. The craniopharyngeal pouch has become elongated and blood vessels are beginning to grow in between the basement membranes of the pouch and brain.[11]
  • Thyroid - thyroid pedicle shows further elongation but is still connected to the epithelium of the pharynx.[2] Right and left lobes and an isthmus may perhaps be presaged (ibid.).
  • Parathyroids - "Parathyrogenic zones" [12] are recognizable.[10] The parathyroid 4 primordium has been illustrated at this stage by Weller (1933, Fig. 16).
  • Thymus‎ - Weller's (1933)[2] "thymus" (the third pharyngeal pouch) becomes elongated.
  • Pancreas - ventral pancreas (which may perhaps be distinguishable as early as stage 13) appears as an evagination from the bile duct at stages 14[5] and 15.[13] It is generally described as unpaired but, at least in some cases, may perhaps be bilobed[4] or even multiple (Delmas 1939).
  • Adrenal‎
    • Adrenal Cortex - A change in the characteristics of the cells of the coelomic epithelium appears between the mesogastrium and the lateral end of the mesonephros.[3]
    • Adrenal Medulla - paravertebral sympathetic ganglia increase in size as a result of cell division and the addition of nerve fibres from the rami communicantes. The ganglia contain three types of cells: MI, M2, and M3. The M3 cells are the" parasympathetic cells" of Zuckerkandl.[3]
Stage 15
  • Pineal - pineal body is detectable in the roof of the diencephalon (Stadium I of Turkewitsch)[14][6]
  • Thyroid - thyroid primordium may be detached from the pharyngeal epithelium in some instances. "At about the time" when the thyroglossal duct "becomes broken it loses its lumen".[15]
  • Adrenal‎
    • Adrenal Cortex - primordium is first recognizable. A new type of cell (C1) from the coelomic epithelium is found in the subjacent mesenchyme. New cells (C2) appear in the medial wall of mesonephric glomeruli and begin to migrate into the suprarenal primordium.[3][16] denies a mesonephric contribution to the suprarenal.
    • Adrenal Medulla - all types of cells (M1, M2, and M3) increase in number. From stage 15 to stage 18, the suprarenal primordium is cigar-shaped and extends from segment T6 to segment L1, lateral to the aorta and mesogastrium.[3]
Stage 16 (week 6)
  • Pituitary - slight indication of the infundibular recess may be seen in some embryos.[11]
  • Pineal - cellular migration in an external direction occurs in the pineal body during stages 16 and 17 (Stadium 2 of Turkewitsch)[14][6]
  • Thymus - according to Norris (1938)[8] , "not until the primordium of the parathyroid [3] has been outlined can the remaining portion of the third pouch be recognized, by exclusion, as the primordium of the endodermal thymus".
  • Parathyroids - parathyrogenic zones are closely related to the third and fourth aortic arches at 9 mm unstaged embryo). [12] Parathyroid 3 is identifiable on the anterior wall of the third pharyngeal pouch (Weller 1933, Fig. 17) and "does not arise from a dorsal lobule" of the pouch.[17] The "sudden appearance of well-differentiated clear chief cells in the early primordia of the parathyroids" at 9 mm was emphasized by Norris (1937).[17]
  • Thyroid - has lost its continuity with the pharynx and it consists of two lobes, an isthmus, and a remnant of the pedicle.[2]
  • Adrenal‎
    • Adrenal Cortex - Another type of cell (C3) arises from the coelomic epithelium. Both C1 and C3 cells enter the suprarenal primordium. An "enormous immigration" of C2 cells occurs.[3]
    • Adrenal Medulla - cells of neural origin are migrating into the gland, separating the cortical cells into islands. Nerve fibres from the ganglia ac- company the M1 and M3 cells. The M2 cells remain in the ganglia and become sympathetic ganglion cells.[3]
  • Pancreas - dorsal pancreas and the ventral pancreas are contiguous.[5]
Stage 17
  • Pituitary - juxtacerebral wall of the craniopharyngeal pouch is the thicker. The lateral lobes (future infundibular, or tuberal, part) and the anterior chamber (Vorraum) are clearly visible.[11]The infundibular recess displays a characteristically folded wall, namely the neurohypophysis.[11]
  • Thymus - connection of the thymus with the pharynx has been severed.[2] The thymus is intimately approximated to the cervical duct (ibid.) According to Norris (1937), both third and fourth pouches make contact with the ectoderm, although only the third "receives an increment from the ectoderm".
  • Parathyroids -parathyroid 4 is attached to the lateral surface of what Weller (1933)[2] termed the "lateral thyroid component"
  • Thyroid. The lobes of the thyroid curve around the carotid arteries and are connected by a delicate isthmus. Lacunae "should not be confused with lumina of follicles".[2]
  • Adrenal‎
    • Adrenal Cortex - dorsal part of the whole suprarenal primordium is disorganized by the invasion of sympathetic nerves and cells, while the band of C2 cells and the coelomic epithelium remain intact.[3]
    • Adrenal Medulla - first neural migration is at its height. Growth of the para-aortic complex is extensive. The plexiform complex is derived from paravertebral sympathetic ganglia T6-12 and usually L 1. Included in it are the primordia of the suprarenal medulla and of the celiac, superior mesenteric, and renal plexuses. Nerve fibres and "paraganglion" (M3) cells enter.
  • Pancreas - ventral pancreas has now fused with dorsal.[13] Perhaps the ventral and dorsal ducts have begun to blend.[18]
Stage 18 (week 7)
  • Pineal - cellular migration in the pineal body forms a distinct "anterior lobe" in which follicles appear (Stadium 3 of Turkewitsch)[14])[11]
  • Thymus- thymus makes contact with the thyroid gland and contains a series of canals internally (Weller 1933).
  • Thyroid - median thyroid is in contact with "lateral thyroid components"[2]but others have maintained that the telopharyngeal body should not be regarded as a thyroid component (Bejdl and Politzer 1953). The lobes of the thyroid are "composed of series of continuously communicating solid annectent bars" this is "the earliest stage of the definitive thyroid".[2] First differentiation occurs in Weller's (1933) "lateral thyroid component," which is beginning to "blend into uniformly constituted thyroid tissue". Weller (1933) illustrated (Fig. 11) a thyroid gland that still showed continuity between its pedicle and the epithelium of the pharynx.
  • Adrenal‎
    • Adrenal Cortex - gland becomes reorganized. The C1, 2, and 3 cells form cords as sinusoids develop. Cells divide at or near the surface, where new cells are added.[3]
Stage 19
  • Pituitary - the caudal part of the craniopharyngeal pouch is reduced to a closed epithelial stem.[19]
  • Epiphysis - the "anterior lobe" of the pineal body shows a characteristic step and wedge appearance (Stadium 4 of Turkewitsch)[14])[6]
  • Parathyroids - 3 become detached from the pharyngeal endoderm.[16]
  • Adrenal Cortex - C2 cells lie on the surface of the gland and form a "capsule".[3]
  • Adrenal Medulla - Sympathicoblasts penetrate the cortex at stages 19 and 20, and form scattered islets of medullary tissue throughout the cortex.[16]
Stage 20 (week 8)
  • Pituitary - the adenohypophysial epithelium adjacent to the neurohy- pophysis constitutes the beginning pars intermedia.[11] The walls of the craniopharyngeal pouch bud into the mesenchyme.[19][16]
  • Thymus - the right and left components are in contact with each other[2] but are "never completely fused"[8] [20]). Thymic cortex appears (in stages 20-22) as a result, according to Norris

(1938), of migration of and covering by "cells derived from the cervical sinus".

  • Parathyroids - the parathyroid glands are attached to the lateral lobes of the thyroid (Weller 1933).

Weller (1933, Fig. 23) showed parathyroid 3 still rostral to parathyroid 4 at 23 mm, whereas (presumably due to variation in the "descent" of the thymus) (Norris 1937, Fig. 4[17]) showed parathyroid 3 rostral to, level with, and caudal to parathyroid 4 in embryos of 16-17 mm.

  • Thyroid - the "annectent bars" of the thyroid are more compact then previously.[2] The thyroid now exhibits its definitive external form.
Stage 21
  • Hypophysis - the pharyngeal stalk becomes fragmented.[16]
  • Adrenal‎
    • Adrenal Cortex - the cellular "capsule" becomes covered by a layer of fibrous tissue.[3]
Stage 22
  • Parathyroids - Parathyroids 4 become detached from the pharyngeal endoderm.[16]
  • Adrenal‎
    • Adrenal Cortex - the C2 cells have changed and resemble fibrocytes.[3]
Stage 23
  • Pituitary - adenohypophysis loss of the stalk and lobules of epithelium project into the mesodermal component of the gland, and oriented epithelial follicles are present (Streeter, 1951, plate 2). Abundant angioblasts and capillaries are found.
  • Epiphysis - The pineal body has reached Stadium 5 of Turkewitsch[14][6]
  • Thymus - The cortex is well-developed, "true lobulation" has begun with the appearance of" fine superficial scallops," lymphocytes are present sparsely in the subcortical zone, and vessels are found within the thymus.[8]
  • Adrenal‎
    • Adrenal Cortex - It appears that C2 cells first enter the body of the gland at this stage. The pattern of the arterial supply is established. The cellular "capsule" is penetrated by arterial capillaries which join the sinusoids. Their points of entry give the surface of the gland an appearance of cobblestones. The zona glomerulosa is formed of CI and C3 cells. Cells from this zone and from the "capsule" migrate centrally into the cords.[3]
    • Adrenal Medulla - Nerve fibres and neuroblasts are first seen in the body of the gland. The paragangtion (M3) cells are beginning to multiply rapidly and, from 30 mm (stage 23) until birth, some are differentiating into chromaffin cells.[3]
Table Data[1]
Links: pineal (epiphysis cerebri) | pituitary (hypophysis) | thyroid | parathyroid | thymus | pancreas | adrenal (suprarenal)
References
  1. 1.0 1.1 O'Rahilly R. The timing and sequence of events in the development of the human endocrine system during the embryonic period proper. (1983) Anat. Embryol., 166: 439-451. PMID 6869855
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 Weller GL. Development of the thyroid, parathyroid and thymus glands in man. (1933) Contrib. Embryol., Carnegie Inst. Wash. 24: 93-139.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 Crowder RE. The development of the adrenal gland in man, with special reference to origin and ultimate location of cell types and evidence in favor of the "cell migration" theory. (1957) Contrib. Embryol., Carnegie Inst. Wash. 36, 193-210.
  4. 4.0 4.1 Odgers PN. Some observations on the development of the ventral pancreas in man. (1930) J. Anat., 65(1): 1-7. PMID 17104298
  5. 5.0 5.1 5.2 Blechschmidt E. Die prdnatalen Organsysteme des Menschen. (1973) Hippokrates, Stuttgart.
  6. 6.0 6.1 6.2 6.3 6.4 O'Rahilly R. The development of the epiphysis cerebri and the subcommissural complex in staged human embryos. (1968) Anat. Rec., 160: 488-489.
  7. O'Rahilly R. Developmental Stages in Human Embryos, Including a Survey of the Carnegie Collection. Part A: Embryos of the First Three Weeks (Stages 1 to 9). (1973) Carnegie Instn. Wash. Publ. 631. Washington, D.C.
  8. 8.0 8.1 8.2 8.3 Norris EH. The morphogenesis and histogenesis of the thymus gland in man: in which the origin of the Hassal's corpuscles of the human thymus is discovered. (1938) Contrib Embryol Carneg Instn 27: 191-207.
  9. Politzer G. Zur Abgrenzung des Anlagebegriffes, er6rtert an der Friihentwicklung von Parathyreoidea, Pancreas und Thyreoidea (Delineation of the development of the parathyroids, the pancreas, and the thyroid gland). (1952) Acta Anat 15:68-84.
  10. 10.0 10.1 Streeter GL. Developmental horizons in human embryos. Description of age group XIII, embryos about 4 or 5 millimeters long, and age group XIV, period of indentation of the lens vesicle. (1945) Carnegie Instn. Wash. Publ. 557, Contrib. Embryol., Carnegie Inst. Wash., 31: 27-63.
  11. 11.0 11.1 11.2 11.3 11.4 11.5 O'Rahilly R. The early development of the hypophysis cerebri in staged human embryos. (1973) Anat Rec 175:511.
  12. 12.0 12.1 Politzer G, Hann F. Uber die Emwicklung der branchiogenen Organe beim Menschen (On the development of the branchiogenic organs in humans). (1935) Z Anat Entw Gesctl 104: 671-708.
  13. 13.0 13.1 Streeter GL. Developmental horizons in human embryos. Description of age groups XV, XVI, XVII, and XVIII, being the third issue of a survey of the Carnegie collection. (1948) Contrib. Embryol., Carnegie Inst. Wash. 575, 32: 133-203.
  14. 14.0 14.1 14.2 14.3 14.4 Turketwitsch N. Die Entwicklung der Zirbeldrüse des Menschen (The development of the pineal gland in humans). (1933) Morphol Jb 72: 379-445.
  15. Grosser O. The development of the pharynx and of the organs of respiration. In: F. Keibel, F.P. Mall (ed) Manual of human embryology. (1912) Philadelphia, Lippincott, pp 446-497.
  16. 16.0 16.1 16.2 16.3 16.4 16.5 Jirásek JE. Human fetal endocrines. (1980) Martinus Nijhoff Publishers BV, The Hague. Springer
  17. 17.0 17.1 17.2 Norris EH. The parathyroid glands and the lateral thyroid in man: their morphogenesis, histogenesis, topographic anatomy and prenatal growth. (1937) Contrib Embryol Carneg Instn 26: 247-294
  18. Russu IG and Vaida A. Neue Befunde zur Entwicklung der Bauchspeicheldriise (New findings on the development of pancreatic disease). (1959) Acta Anat 38: 114-125.
  19. 19.0 19.1 <pubmed>5117462</pubmed>
  20. Siegler R. The thymus and the unicorn-two great myths of gross anatomy. (1969) Anat Rec. 163: 264.


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

2012

Neurobehavioral risk is associated with gestational exposure to stress hormones

Expert Rev Endocrinol Metab. 2012 Jul;7(4):445-459.

Sandman CA, Davis EP. Source Department of Psychiatry & Human Behavior, Women and Children's Health and Well-Being Project, University of California, Irvine, Orange, CA, USA.

Abstract

The developmental origins of disease or fetal programming model predict that early exposures to threat or adverse conditions have lifelong consequences that result in harmful outcomes for health. The maternal endocrine 'fight or flight' system is a source of programming information for the human fetus to detect threats and adjust their developmental trajectory for survival. Fetal exposures to intrauterine conditions including elevated stress hormones increase the risk for a spectrum of health outcomes depending on the timing of exposure, the timetable of organogenesis and the developmental milestones assessed. Recent prospective studies, reviewed here, have documented the neurodevelopmental consequences of fetal exposures to the trajectory of stress hormones over the course of gestation. These studies have shown that fetal exposures to biological markers of adversity have significant and largely negative consequences for fetal, infant and child emotional and cognitive regulation and reduced volume in specific brain structures.

PMID 23144647


External Links

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Histology

Adult

Embryonic

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). PMID: 19171054

lutenizing hormone - (LH) pituitary, protein hormone

melaocyte stimulating hormone - (MSH) pituitary, peptide hormone

prolactin - (PRL) pituitary, peptide hormone

parathyroid hormone - (PTH) parathyroid, peptide hormone

thyroid hormone - (TH) thyroid,amino acid derivative

thyroid stimulating hormone - (TSH) pituitary, protein hormone