2014 Group Project 6 - Revision history

Z8600021: Protected "2014 Group Project 6" ([Edit=Allow only administrators] (indefinite) [Move=Allow only administrators] (indefinite))

2014-10-24T13:20:22Z

Protected "2014 Group Project 6" ([Edit=Allow only administrators] (indefinite) [Move=Allow only administrators] (indefinite))

← Older revision	Revision as of 00:20, 25 October 2014
(No difference)

Z3418698 at 07:22, 24 October 2014

2014-10-24T07:22:55Z

← Older revision		Revision as of 18:22, 24 October 2014
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	*'''Congenital Adrenal Hyperplasia (CAH)'''		*'''Congenital Adrenal Hyperplasia (CAH)'''

	Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. <ref name= PMID25227725><pubmed>25227725</pubmed></ref>.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. <ref><pubmed>10748766</pubmed></ref> CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.~~[[File:Cushing's syndrome.jpg\|150px\|right\|thumb\|This image shows a 3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]]~~ Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. <ref><pubmed>15838095</pubmed></ref> Males tend to appear asymptomatic but can exhibit oligozoospermia. <ref name= PMID25227725><pubmed>25227725</pubmed></ref>		Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. <ref name= PMID25227725><pubmed>25227725</pubmed></ref>.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. <ref><pubmed>10748766</pubmed></ref> CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more. Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. <ref><pubmed>15838095</pubmed></ref> Males tend to appear asymptomatic but can exhibit oligozoospermia. <ref name= PMID25227725><pubmed>25227725</pubmed></ref>


	*'''Cushing's Syndrome'''		*'''Cushing's Syndrome'''
			[[File:Cushing's syndrome.jpg\|150px\|right\|thumb\|This image shows a 3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]]
	Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH <ref><pubmed>24656295</pubmed></ref>. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. <ref name= PMID24365350><pubmed>24365350</pubmed></ref> The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. <ref name= PMID24365350><pubmed>24365350</pubmed></ref>		Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH <ref><pubmed>24656295</pubmed></ref>. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. <ref name= PMID24365350><pubmed>24365350</pubmed></ref> The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. <ref name= PMID24365350><pubmed>24365350</pubmed></ref>

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	*PGCs migrate through the primitive streak in gastrulation and then reside at the junctional region of the hindgut yolk sac. Migration of the PGCs to the gonadal ridge along the hindgut’s dorsal mesentery <ref name= PMID>17237341<pubmed>17237341</pubmed></ref>		*PGCs migrate through the primitive streak in gastrulation and then reside at the junctional region of the hindgut yolk sac. Migration of the PGCs to the gonadal ridge along the hindgut’s dorsal mesentery <ref name= PMID>17237341<pubmed>17237341</pubmed></ref>
	*Week 6- PGCs incorporated into the gonadal cords and are called oogonia, having entered underlying mesenchyme.		*Week 6- PGCs incorporated into the gonadal cords and are called oogonia, having entered underlying mesenchyme.
			[[File:Fetal ovary morphogenesis (mouse).jpg\|300px\|right\|thumb\|Diagramatic representation of fetal mouse ovary morphogenesis]]
	'''Fetal stage of ovarian development - from week 8 of gestation onwards:'''		'''Fetal stage of ovarian development - from week 8 of gestation onwards:'''

	~~[[File:Fetal ovary morphogenesis (mouse).jpg\|300px\|right\|thumb\|Diagramatic representation of fetal mouse ovary morphogenesis]]~~
	*Weeks 8 to 9- Gonad is identifiable as an ovary now due to change in internal structure. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. Inner ovary; disintegrating blastema surrounded by a thick blastemal layer. Tissue has a cortical region (encloses PGCs) and a central medullary region (reticulum of somatic cells) <ref name= PMID>7158813<pubmed>7158813</pubmed></ref>		*Weeks 8 to 9- Gonad is identifiable as an ovary now due to change in internal structure. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. Inner ovary; disintegrating blastema surrounded by a thick blastemal layer. Tissue has a cortical region (encloses PGCs) and a central medullary region (reticulum of somatic cells) <ref name= PMID>7158813<pubmed>7158813</pubmed></ref>
	*Weeks 10 to 12- Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue <ref name= PMID>22106406<pubmed>22106406</pubmed></ref>		*Weeks 10 to 12- Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue <ref name= PMID>22106406<pubmed>22106406</pubmed></ref>

Z3418837: /* Thymus */

2014-10-24T07:11:36Z

Thymus

← Older revision		Revision as of 18:11, 24 October 2014
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	The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.		The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.
	In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs. Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.		In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs. Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.
	[[File:Stage 22 image 168.jpg\|~~200px~~\|thumb\|right\|This image shows the 54 - 56th week of thymus development]]		[[File:Stage 22 image 168.jpg\|350px\|thumb\|right\|This image shows the 54 - 56th week of thymus development]]

	'''How far has the thymus gland developed by week 8 of gestation?'''		'''How far has the thymus gland developed by week 8 of gestation?'''

Z3418698 at 06:29, 24 October 2014

2014-10-24T06:29:48Z

← Older revision		Revision as of 17:29, 24 October 2014
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	The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour<ref name= PMID7643957><pubmed>7643957</pubmed></ref>. The hypothalamus is involved in two main signalling pathways, the Hyothalamus-Pituitary-Adrenal (HPA) and the Hypothalamus-Pituitary-Gonad (HPG) and exerts most of it's influence on the body through these two axes.		The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour<ref name= PMID7643957><pubmed>7643957</pubmed></ref>. The hypothalamus is involved in two main signalling pathways, the Hyothalamus-Pituitary-Adrenal (HPA) and the Hypothalamus-Pituitary-Gonad (HPG) and exerts most of it's influence on the body through these two axes.
	[[File:Adult human hypothalamus 04.jpg\|250x\|thumb\|~~Figure 1.~~ illustrates the location of nuclei in the hypothalamus]]		[[File:Adult human hypothalamus 04.jpg\|250x\|thumb\|This image illustrates the location of nuclei in the hypothalamus]]

	The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex<ref name= PMID11954031><pubmed>11954031</pubmed></ref>.		The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex<ref name= PMID11954031><pubmed>11954031</pubmed></ref>.

	Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in fetal development up till and including the birth process<ref name= PMID7643957><pubmed>7643957</pubmed></ref>. Fetal oxytocin may initiate or accelerate the course of labor whereas vasopressin plays a role in the adaptation to stress caused by the birth process by redistribution of fetal blood flow.		Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in fetal development up till and including the birth process<ref name= PMID7643957><pubmed>7643957</pubmed></ref>. Fetal oxytocin may initiate or accelerate the course of labor whereas vasopressin plays a role in the adaptation to stress caused by the birth process by redistribution of fetal blood flow.

	~~[[File:Development of hypothalamus.jpg\|900px\|right\|thumb\|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]]~~


	'''How far has the hypothalamus gland developed by week 8 of gestation?'''		'''How far has the hypothalamus gland developed by week 8 of gestation?'''
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	'''Fetal Stage of hypothalamus development - from week 8 of gestation onwards:'''		'''Fetal Stage of hypothalamus development - from week 8 of gestation onwards:'''
			[[File:Hypothalamus histology 001.jpg\|250x\|thumb\|right\|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]
			* Week 9- The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.
			* Week 18- By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumen.
			[[File:Stage 22 image 057.jpg\|200x\|thumb\|Histological cross-section of stage 22 embryo]]
			* Weeks 19-27- Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus <ref name=Rizzoti>K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html</ref>
			* Week 28- Sexual differentiation of hypothalamus is complete

	* Week 9- The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).		[[File:Development of hypothalamus.jpg\|900px\|centre\|thumb\|Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]]
	* Week 18- By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c).
	[[File:~~Stage 22 image 057~~.jpg\|~~200x~~\|thumb\|~~Image 1. Histological cross-section~~ of ~~stage 22 embryo]]~~
	* Weeks 19-27- Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus~~. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.~~d)~~<ref name=Rizzoti>K. Rizzoti, R. Lovell~~-~~Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html</ref>~~
	* Week 28~~- Sexual differentiation of hypothalamus is complete~~

	''Table 2. Summarises the hormones released by the human hypothalamus and their role in embryonic and fetal development''		''Table 2. Summarises the hormones released by the human hypothalamus and their role in embryonic and fetal development''
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	\| Somatostatin (growth hormone-inhibiting hormone) \|\| SS, GHIH, or SRIF \|\| Neuroendocrine cells of the Periventricular nucleus \|\| Stimulates release of growth hormone (GH) from anterior pituitary and also has inhibitory effect on release of thyroid-stimulating hormone (TSH) from the anterior pituitary		\| Somatostatin (growth hormone-inhibiting hormone) \|\| SS, GHIH, or SRIF \|\| Neuroendocrine cells of the Periventricular nucleus \|\| Stimulates release of growth hormone (GH) from anterior pituitary and also has inhibitory effect on release of thyroid-stimulating hormone (TSH) from the anterior pituitary
	\|}		\|}
	~~[[File:Hypothalamus histology 001.jpg\|250x\|thumb\|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]~~

	===Abnormalities===		===Abnormalities===

Z3418698: /* Pineal gland */

2014-10-24T06:20:58Z

Pineal gland

← Older revision		Revision as of 17:20, 24 October 2014
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	===Fetal development===		===Fetal development===

	[[File:Keith1902 fig167.jpg\|200px\|thumb\|right\| ~~Image 1: schematic~~ of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg\|170px\|thumb\|right\|~~Image 2: Shows the location~~ of the pineal gland in the adult brain.]]		[[File:Keith1902 fig167.jpg\|200px\|thumb\|right\|Schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg\|170px\|thumb\|right\|Location of the pineal gland in the adult brain.]]

	The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier<ref name=Bruce>J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview</ref>.		The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier<ref name=Bruce>J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview</ref>.
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	{\| align="center" style="text-align:centre"		{\| align="center" style="text-align:centre"
	\|-		\|-
	\| [[File:Primary brain vesicles.jpg\|frame\|right\|middle\|180x150px\|Primary brain vesicles]]\|\|[[File:~~Week 6 embryonic development of CNS~~.jpg\|frame\|right\|middle\|180x150px\|~~Week 6 embryonic~~ development ~~of CNS~~]]\|\| [[File:Week ~~11 fetal~~ development of CNS.jpg\|frame\|right\|middle\|180x150px\|Week ~~11 fetal~~ development of CNS]] \|\| [[File:~~Fetal pineal gland 01~~.jpg\|frame\|right\|middle\|180x150px\| ~~(d)~~ Week ~~19-21]]\|\| [[Image:Fetal Hair Follicle Development - Week 23-28 .JPG\|frame\|right\|middle\|180x150px\|~~fetal ~~pineal gland at the end~~ of ~~the first trimester of development.~~]]		\| [[File:Primary brain vesicles.jpg\|frame\|right\|middle\|180x150px\|Primary brain vesicles]]\|\|[[File:Fetal pineal gland 01.jpg\|frame\|right\|middle\|180x150px\|Fetal pineal gland at the end of the first trimester of development.]]\|\|[[File:Week 6 embryonic development of CNS.jpg\|frame\|right\|middle\|180x150px\|Week 6 embryonic development of CNS]]\|\|[[File:Week 11 fetal development of CNS.jpg\|frame\|right\|middle\|180x150px\|Week 11 fetal development of CNS]]
	\|}		\|}

Z3418698 at 06:10, 24 October 2014

2014-10-24T06:10:39Z

← Older revision		Revision as of 17:10, 24 October 2014
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	Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth.		Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth.

	~~[[File:Primary brain vesicles.jpg\|150px\|left\|thumb\|Image 3: Primary brain vesicles]]~~'''How far has the pineal gland developed by week 8 of gestation?'''		'''How far has the pineal gland developed by week 8 of gestation?'''
	*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).<ref name=Bruce>J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview</ref>		*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).<ref name=Bruce>J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview</ref>
	~~[[File:Week 6 embryonic development of CNS.jpg\|150px\|left\|thumb\|Image 4: Week 6 embryonic development of CNS]]~~
	~~[[File:Week 11 fetal development of CNS.jpg\|150px\|right\|thumb\|Image 5: Week 11 fetal development of CNS]]~~
	*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4).		*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4).

	~~[[File:Fetal pineal gland 01.jpg\|150px\|thumb\|right\|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]~~

	'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:'''		'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:'''
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	*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)		*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)
	*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.<ref name=Bruce>J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview</ref>		*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.<ref name=Bruce>J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview</ref>

			{\| align="center" style="text-align:centre"
			\|-
			\| [[File:Primary brain vesicles.jpg\|frame\|right\|middle\|180x150px\|Primary brain vesicles]]\|\|[[File:Week 6 embryonic development of CNS.jpg\|frame\|right\|middle\|180x150px\|Week 6 embryonic development of CNS]]\|\| [[File:Week 11 fetal development of CNS.jpg\|frame\|right\|middle\|180x150px\|Week 11 fetal development of CNS]] \|\| [[File:Fetal pineal gland 01.jpg\|frame\|right\|middle\|180x150px\| (d) Week 19-21]]\|\| [[Image:Fetal Hair Follicle Development - Week 23-28 .JPG\|frame\|right\|middle\|180x150px\|fetal pineal gland at the end of the first trimester of development.]]
			\|}

	''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development''		''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development''

Z3418837: /* Abnormalities */

2014-10-24T05:46:09Z

Abnormalities

← Older revision		Revision as of 16:46, 24 October 2014
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	*'''Ectopic Posterior Pituitary:'''		*'''Ectopic Posterior Pituitary:'''
	This is an abnormal pituitary development disorder that results from improper migration of the posterior pituitary from the neural tissue that initially forms an invagination at the floor of the third ventricle. This results in the posterior pituitary lobe developing and maturing at the level of the median eminence or in line with the pituitary stalk rather than sitting further down in the cella turcica. <ref name =di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M> di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M, 2009, Developmental Abnormalities of the Posterior Pituitary Gland, Endocrine Involvement in Developmental Syndromes: 14(2009); 83-94, http://www.karger.com/Article/FullText/207479></ref>		This is an abnormal pituitary development disorder that results from improper migration of the posterior pituitary from the neural tissue that initially forms an invagination at the floor of the third ventricle. This results in the posterior pituitary lobe developing and maturing at the level of the median eminence or in line with the pituitary stalk rather than sitting further down in the cella turcica. Consequently, the releasing factors secreted from the hypothalamus that normally migrate down the portal circulation towards the anterior pituitary can only target their destination using the general vasculature. This leads to growth hormone deficiency and in some cases panhypopituitarism.<ref name =di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M> di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M, 2009, Developmental Abnormalities of the Posterior Pituitary Gland, Endocrine Involvement in Developmental Syndromes: 14(2009); 83-94, http://www.karger.com/Article/FullText/207479></ref>

	*'''Hypopituitarism:'''		*'''Hypopituitarism:'''

Z3418698: /* The Endocrine System */

2014-10-24T05:18:06Z

The Endocrine System

Show changes

Z3418698: /* Pituitary gland */

2014-10-24T04:49:26Z

Pituitary gland

← Older revision		Revision as of 15:49, 24 October 2014
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	[[File:Pituitary Development.jpg\|300px\|right\|thumb\|Anatomy of Human Pituitary Gland]]		[[File:Pituitary Development.jpg\|300px\|right\|thumb\|Anatomy of Human Pituitary Gland]]
	=== Fetal development ===		=== Fetal development ===
	~~Pre-fetal stage of~~ pituitary gland ~~development:~~
			<small>'''How far has the pituitary gland developed by week 8 of gestation?'''</small>

	*Formation of Rathke's Pouch by week 4-5 of gestation		*Formation of Rathke's Pouch by week 4-5 of gestation
	** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe		** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe
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			'''Fetal stage of pituitary development - from week 8 of gestation and onwards:'''<small>Small text</small>

	By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control ~~centre~~ for release of hormones that are vital for subsequent organ development.		* Week 8 - By week 8 embryological development, the pituitary gland is fully formed and begins functioning as a control center for release of hormones that are vital for subsequent organ development.

	* Week 10 - Growth Hormone and ACTH detectable		* Week 10 - Growth Hormone and ACTH detectable
	* Week 21 - Vasopressin hormone synthesis established		* Week 21 - Vasopressin hormone synthesis established
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	{\| class="wikitable"		{\| class="wikitable"
	\|-		\|-
	! Hormone ~~!! Abbreviation~~ !! Neuronal Origin !! Function		! Hormone !! Neuronal Origin !! Function
	\|-		\|-
	\| Oxytocin ~~\|\| Example~~ \|\| Hypothalamic paraventricular and supraoptic nuclei \|\|		\| Oxytocin \|\| Hypothalamic paraventricular and supraoptic nuclei \|\|
	* Cardiomyogenesis		* Cardiomyogenesis
	* Protective action of fetal neurons during brain development		* Protective action of fetal neurons during brain development
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	oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#></ref>		oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#></ref>
	\|-		\|-
	\| Vasopressin ~~\|\| Example~~ \|\| Hypothalamic paraventricular and supraoptic nuclei \|\|		\| Vasopressin \|\| Hypothalamic paraventricular and supraoptic nuclei \|\|
	* Regulates fetal renal function		* Regulates fetal renal function
	* Regulates amniotic fluid content and concentration		* Regulates amniotic fluid content and concentration
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	===Abnormalities===		===Abnormalities===

	'''*Ectopic Posterior Pituitary:		*'''Ectopic Posterior Pituitary:'''
	'''
	This is an abnormal pituitary development disorder that results from improper migration of the posterior pituitary from the neural tissue that initially forms an invagination at the floor of the third ventricle. This results in the posterior pituitary lobe developing and maturing at the level of the median eminence or in line with the pituitary stalk rather than sitting further down in the cella turcica. <ref name =di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M> di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M, 2009, Developmental Abnormalities of the Posterior Pituitary Gland, Endocrine Involvement in Developmental Syndromes: 14(2009); 83-94, http://www.karger.com/Article/FullText/207479></ref>		This is an abnormal pituitary development disorder that results from improper migration of the posterior pituitary from the neural tissue that initially forms an invagination at the floor of the third ventricle. This results in the posterior pituitary lobe developing and maturing at the level of the median eminence or in line with the pituitary stalk rather than sitting further down in the cella turcica. <ref name =di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M> di Iorgi N. • Secco A. • Napoli F. • Calandra E. • Rossi A. • Maghnie M, 2009, Developmental Abnormalities of the Posterior Pituitary Gland, Endocrine Involvement in Developmental Syndromes: 14(2009); 83-94, http://www.karger.com/Article/FullText/207479></ref>



	'''*Hypopituitarism:		*'''Hypopituitarism:'''
	'''
	This is a disorder that results from abnormal production of pituitary hormones like growth hormone, luteinizing hormone, vasopressin and oxytocin. If there are insufficient levels of fetal production of these hormones, there are many postnatal effects. The infant would have irregularities in bone growth, urinary system development and brain growth and would show retinal dysfunction. This is because the pituitary gland plays a pivotal role in the hypothalamic-pituitary axis in maintaining proper body balance and organ growth. <ref name =Webb EA1, AlMutair A, Kelberman D, Bacchelli C, Chanudet E, Lescai F, Andoniadou CL, Banyan A, Alsawaid A, Alrifai MT, Alahmesh MA, Balwi M, Mousavy-Gharavy SN, Lukovic B, Burke D, McCabe MJ, Kasia T, Kleta R, Stupka E, Beales PL, Thompson DA, Chong WK, Alkuraya FS, Martinez-Barbera JP, Sowden JC, Dattani MT> Webb EA1, AlMutair A, Kelberman D, Bacchelli C, Chanudet E, Lescai F, Andoniadou CL, Banyan A, Alsawaid A, Alrifai MT, Alahmesh MA, Balwi M, Mousavy-Gharavy SN, Lukovic B, Burke D, McCabe MJ, Kasia T, Kleta R, Stupka E, Beales PL, Thompson DA, Chong WK, Alkuraya FS, Martinez-Barbera JP, Sowden JC, Dattani MT. (2013). ARNT2 mutation causes hypopituitarism, post-natal microcephaly, visual and renal anomalies. Brain, 136(10), 3096-3105, http://www.ncbi.nlm.nih.gov/pubmed/24022475></ref>		This is a disorder that results from abnormal production of pituitary hormones like growth hormone, luteinizing hormone, vasopressin and oxytocin. If there are insufficient levels of fetal production of these hormones, there are many postnatal effects. The infant would have irregularities in bone growth, urinary system development and brain growth and would show retinal dysfunction. This is because the pituitary gland plays a pivotal role in the hypothalamic-pituitary axis in maintaining proper body balance and organ growth. <ref name =Webb EA1, AlMutair A, Kelberman D, Bacchelli C, Chanudet E, Lescai F, Andoniadou CL, Banyan A, Alsawaid A, Alrifai MT, Alahmesh MA, Balwi M, Mousavy-Gharavy SN, Lukovic B, Burke D, McCabe MJ, Kasia T, Kleta R, Stupka E, Beales PL, Thompson DA, Chong WK, Alkuraya FS, Martinez-Barbera JP, Sowden JC, Dattani MT> Webb EA1, AlMutair A, Kelberman D, Bacchelli C, Chanudet E, Lescai F, Andoniadou CL, Banyan A, Alsawaid A, Alrifai MT, Alahmesh MA, Balwi M, Mousavy-Gharavy SN, Lukovic B, Burke D, McCabe MJ, Kasia T, Kleta R, Stupka E, Beales PL, Thompson DA, Chong WK, Alkuraya FS, Martinez-Barbera JP, Sowden JC, Dattani MT. (2013). ARNT2 mutation causes hypopituitarism, post-natal microcephaly, visual and renal anomalies. Brain, 136(10), 3096-3105, http://www.ncbi.nlm.nih.gov/pubmed/24022475></ref>

Z3418837: /* Fetal development */

2014-10-24T04:43:34Z

Fetal development

← Older revision		Revision as of 15:43, 24 October 2014
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	The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.		The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.
	In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs. Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.		In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs. Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.
			[[File:Stage 22 image 168.jpg\|200px\|thumb\|right\|This image shows the 54 - 56th week of thymus development]]
	'''Timeline'''		'''Timeline'''