Changes

==Anatomy==

==Anatomy==

The pituitary gland, or ''hypophysis'' is an elongated appendage of the brain lying within a bony cavity of the [[Skull and Facial Muscles - Anatomy & Physiology#Sphenoid Bone (os sphenoidale)|sphenoid bone]] in the base of the skull - the '''Sella Turcica'''. The hypophysis is suspended from the hypothalamus by a thin stalk. It lies between the more rostral '''optic chiasma''', and the more caudal '''mammillary bodies'''.

The pituitary gland, or ''hypophysis'' is an elongated appendage of the brain lying within a bony cavity of the [[Skull and Facial Muscles - Anatomy & Physiology#Sphenoid Bone (os sphenoidale)|sphenoid bone]] in the base of the skull - the '''Sella Turcica'''. The hypophysis is suspended from the hypothalamus by a thin stalk. It lies between the more rostral '''optic chiasma''', and the more caudal '''mammillary bodies'''.

==Blood Supply==

==Blood Supply==

The adenohypophysis and the neurohypophysis are separatley vascularised. The '''neurohypophysis''' is supplied by small branches of the ''internal carotid'' (inferior hypophyseal artery) and the ''arterial circle'' of the brain (Circle of Willis). The '''adenohypophysis'''  is supplied  by the ''superior hypohyseal artery''. Drainage is via the ''cavernous sinus''.

The adenohypophysis and the neurohypophysis are separatly vascularised. The '''neurohypophysis''' is supplied by small branches of the ''internal carotid'' (inferior hypophyseal artery) and the ''arterial circle'' of the brain (Circle of Willis). The '''adenohypophysis'''  is supplied  by the ''superior hypophyseal artery''. Drainage is via the ''cavernous sinus''.

==Histology==

==Histology==

<center><gallery>

<center><gallery>

Image:PituitaryGlandlowpower.jpg|<p>'''Pituitary Gland Low Power 1'''</P>^{©RVC 2008}

Image:PituitaryGlandlowpower.jpg|<p>'''Pituitary Gland Low Power 1'''</P>^{©RVC 2008}

Image:Pituitary Gland Histology 2.jpg|<p>'''Pituitary Gland Low Power 2'''</P>^{©RVC 2008}

Image:Pituitary Gland Histology 2.jpg|<p>'''Pituitary Gland Low Power 2'''</P>^{©RVC 2008}

Image:PituitaryGland-Pars Distalis.jpg|<p>'''Pars Distalis'''</P>^{©RVC 2008}

Image:PituitaryGland-Pars Distalis.jpg|<p>'''Pars Distalis'''</P>^{©RVC 2008}

Image:Pituitary Gland-Pars Intermedia.jpg|<p>'''Pars Intermedia'''</P> ^{©RVC 2008}

Image:Pituitary Gland-Pars Intermedia.jpg|<p>'''Pars Intermedia'''</P> ^{©RVC 2008}

Image:Pituitary Gland-Pars Nervosa.jpg|<p>'''Pars Nervosa</P> ^{©RVC 2008}

Image:Pituitary Gland-Pars Nervosa.jpg|<p>'''Pars Nervosa</P> ^{©RVC 2008}

</gallery></center>

</gallery></center>

The anterior pituitary contains the '''pars distalis''', and the '''pars tuberalis'''. This part of the pituitary gland is controlled by ''releasing factors'' from the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]. These factors reach the anterior pituitary via the '''hypophyseal portal system''', venous channels allowing direct passage between the hypothalamus and the pituitary gland. The anterior pituitary gland secretes two types of hormone:

The anterior pituitary contains the '''pars distalis''', and the '''pars tuberalis'''. This part of the pituitary gland is controlled by ''releasing factors'' from the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]. These factors reach the anterior pituitary via the '''hypophyseal portal system''', venous channels allowing direct passage between the hypothalamus and the pituitary gland. The anterior pituitary gland secretes two types of hormone:

1.'''Trophic hormones''': Stimulate a further endocrine gland E.g. TSH, ACTH, FSH, LH. These are then controlled by [[Negative Feedback - Anatomy & Physiology|negative feedback]], whereby the product of the downstream endocrine gland limits the release of the orginial stimulating hormone.

1.'''Trophic hormones''': Stimulate a further endocrine gland e.g. TSH, ACTH, FSH, LH. These are then controlled by [[Negative Feedback - Anatomy & Physiology|negative feedback]], whereby the product of the downstream endocrine gland limits the release of the orginal stimulating hormone.

2.'''Direct-action hormones''': Act directly on non-endocrine tissues E.g. GH. There is no target gland, so release of these hormones is controlled by a balance of releasing and inhibitory factors from the hypothalamus. For example; GH is controlled by stimulatory '''somatocrinin''' (aka Growth Hormone Releasing Hormone) and inhibitory '''somatostatin'''.

2.'''Direct-action hormones''': Act directly on non-endocrine tissues e.g. GH. There is no target gland, so release of these hormones is controlled by a balance of releasing and inhibitory factors from the hypothalamus. For example; GH is controlled by stimulatory '''somatocrinin''' (aka Growth Hormone Releasing Hormone) and inhibitory '''somatostatin'''.

===Pars Distalis===

===Pars Distalis===

The '''pars distalis''' contains 5 cell types which produce 6 hormones. '''Somatotropes''' and '''lactotropes''' are ''acidophillic''. '''Corticotropes, thyrotropes''' and '''gonadotropes''' are ''basophillic''.

The '''pars distalis''' contains five cell types which produce six hormones. '''Somatotropes''' and '''lactotropes''' are ''acidophillic''. '''Corticotropes, thyrotropes''' and '''gonadotropes''' are ''basophillic''.

[[Image:Pituitary Gland - Pars Distalis - Acidophils and Basophils.jpg|center|thumb|350px|'''Pars Distalis''' ©RVC 2008]]

[[Image:Pituitary Gland - Pars Distalis - Acidophils and Basophils.jpg|center|thumb|350px|'''Pars Distalis''' ©RVC 2008]]

|50%

|50%

|[[Pituitary Growth Hormone - Anatomy & Physiology|Growth Hormone]] - '''GH'''  

|[[Pituitary Growth Hormone - Anatomy & Physiology|Growth Hormone]] - '''GH'''  

|Growth, [[IGF-1 - Anatomy & Physiology|IGF-1]] Secretion by [[Liver - Anatomy & Physiology|liver]], Protein Synthesis, lipolysis, insulin inhibition. Also casues increased fibroblast differentiation leading to chondrocyte, osteoblast and adipocyte formation

|Growth, [[IGF-1 - Anatomy & Physiology|IGF-1]] Secretion by [[Liver - Anatomy & Physiology|liver]], Protein Synthesis, lipolysis, insulin inhibition. Also causes increased fibroblast differentiation leading to chondrocyte, osteoblast and adipocyte formation

|-

|-

!Lactotropes

!Lactotropes

==Pars Intermedia==

==Pars Intermedia==

This is the residual lumen of '''Rathke's Pouch''' and consists of of a series of small cystic cavities (follicles filled with colloid), with both basophillic and chromatophobic (poorly staining) cell types. These extend into the '''pars nervosa'''. In horses, '''melanotropes''' convert the [[Prohormones - Anatomy & Physiology|prohormone]] ''proopiomelanocorticotropin'' (POMC) to ''melanocyte Stimulating Hormone'' (a-MSH) and ''corticotropin-like intermediate lobe peptide'' (CLIP):

This is the residual lumen of '''Rathke's Pouch''' and consists of a series of small cystic cavities (follicles filled with colloid), with both basophillic and chromatophobic (poorly staining) cell types. These extend into the '''pars nervosa'''. In horses, '''melanotropes''' convert the [[Prohormones - Anatomy & Physiology|prohormone]] ''proopiomelanocorticotropin'' (POMC) to ''melanocyte stimulating hormone'' (a-MSH) and ''corticotropin-like intermediate lobe peptide'' (CLIP):

'''POMC --> ACTH --> a-MSH + CLIP'''

'''POMC --> ACTH --> a-MSH + CLIP'''

==Posterior Pituitary Gland==

==Posterior Pituitary Gland==

Also known as the '''Neurohypophysis''', the posterior pituitary gland releases '''Antidiuretic Hormone - ADH''' and '''Oxytocin''' both of which act directly on non-endocrine tissue. The  cell bodies of the neurons of the posterior pituitary are located in the [[Hypothalamus - Anatomy & Physiology|hypothalamus]].

Also known as the '''neurohypophysis''', the posterior pituitary gland releases '''Antidiuretic Hormone - ADH''' and '''Oxytocin''' both of which act directly on non-endocrine tissue. The  cell bodies of the neurons of the posterior pituitary are located in the [[Hypothalamus - Anatomy & Physiology|hypothalamus]].

===Antidiuretic Hormone===

===Antidiuretic Hormone===

ADH, also called ''arginine vasopressin (AVP)'' is a peptide [[Hormones - Anatomy & Physiology|hormone]] produced by cell bodies in the ''Paraventricular and Supraoptic nuclei'' of the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]. It is transported down axons into the posterior pituitary for storage, prior to release. It is derived from a preprohormone which is converted to the active form enroute to the posterior pituitary gland. It acts on the [[:Category:Nephron|renal tubules]] and blood vessels.

ADH, also called ''arginine vasopressin (AVP)'' is a peptide [[Hormones - Anatomy & Physiology|hormone]] produced by cell bodies in the ''paraventricular and supraoptic nuclei'' of the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]. It is transported down axons into the posterior pituitary for storage, prior to release. It is derived from a preprohormone which is converted to the active form en route to the posterior pituitary gland. It acts on the [[:Category:Nephron|renal tubules]] and blood vessels.

====Action on the Renal Tubules====

====Action on the Renal Tubules====

ADH is released in response to reduction in plasma volume, a decrease in blood pressure (detected by baroreceptors in the left atrium, pulmonary vessels, aortic arch and carotid sinus), high levels of angiotensin 2 (part of the [[Renin Angiotensin Aldosterone System| RAAS]]), increased sympathetic activation or an increase in the osmolarity of the extracellular fluid (ECF)(detected by osmoreceptors within the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]). If the osmolarity is high or the volume is low, ADH will be released. This acts on the renal tubules, decreasing water loss into the urine by the following mechanisms:

ADH is released in response to reduction in plasma volume, a decrease in blood pressure (detected by baroreceptors in the left atrium, pulmonary vessels, aortic arch and carotid sinus), high levels of angiotensin 2 (part of the [[Renin Angiotensin Aldosterone System| RAAS]]), increased sympathetic activation or an increase in the osmolarity of the extracellular fluid (ECF)(detected by osmoreceptors within the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]). If the osmolarity is high or the volume is low, ADH will be released. This acts on the renal tubules, decreasing water loss into the urine by the following mechanisms:

It acts on V2 receptors on the peritubular surface of the collecting ducts in the kidney. The permeability to water in the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Distal Tubule|distal tubule]] and [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology|collecting duct]] is increased via insertion of [[Aquaporins of the Kidney and Water Homeostasis - Anatomy & Physiology| aquaporins]] into the apical membrane of principal cells (aquaporins are always present in the basolateral membranes). More water therefore, moves out of the tubule and into the intracellular space. Urine volume decreases and urine concentration increases. It is also released in response to '''cholecystokinin''' from the small intestine.

It acts on V2 receptors on the peritubular surface of the collecting ducts in the kidney. The permeability to water in the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Distal Tubule|distal tubule]] and [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology|collecting duct]] is increased via insertion of [[Aquaporins of the Kidney and Water Homeostasis - Anatomy & Physiology| aquaporins]] into the apical membrane of principal cells (aquaporins are always present in the basolateral membranes). More water therefore, moves out of the tubule and into the intracellular space. Urine volume decreases and urine concentration increases. It is also released in response to '''cholecystokinin''' from the small intestine.

====Action on the Blood Vessels====

====Action on the Blood Vessels====

It causes vasoconstriction of blood vessels as a secondary function. It binds to V1 receptors on vascular smooth muscle and acts via the '''IP3 signal transduction pathway'''. It increases the arterial pressure. Normal physiological concentrations do not cause vasoconstriction, if severe hypovolaemic shock is suffered, lots of ADH is released due to decreased plasma volume - the amount of ADH released is relative to the degree of hypovoleamia. These very high levels are what is called ''vasoactive'' and help with a compensatory mechanism of increased vascular resistance. This increased vascular resistance increases arterial blood pressure. Stretch, or volume receptors in the veins and atria can detect a decrease in volume of the blood. This causes nervous impulses to be sent to the hypothalamus, resulting in an increase in ADH production, conserving water at the kidneys. This mechanism is only triggered by a large loss of volume, but results in a large amount of ADH being produced. It should be noted that thirst stimulation is the main method of correcting a dehydration status.

It causes vasoconstriction of blood vessels as a secondary function. It binds to V1 receptors on vascular smooth muscle and acts via the '''IP3 signal transduction pathway'''. It increases the arterial pressure. Normal physiological concentrations do not cause vasoconstriction, if severe hypovolaemic shock is suffered, lots of ADH is released due to decreased plasma volume - the amount of ADH released is relative to the degree of hypovoleamia. These very high levels are what is called ''vasoactive'' and help with a compensatory mechanism of increased vascular resistance. This increased vascular resistance increases arterial blood pressure. Stretch, or volume receptors in the veins and atria can detect a decrease in volume of the blood. This causes nervous impulses to be sent to the hypothalamus, resulting in an increase in ADH production, conserving water at the kidneys. This mechanism is only triggered by a large loss of volume, but results in a large amount of ADH being produced. It should be noted that thirst stimulation is the main method of correcting a dehydration status.

===Oxytocin===

===Oxytocin===

Oxytocin is produced by cell bodies in the '''Paraventricular and Supraoptic nuclei''' of the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]. Oxytocin is transported down axons into the posterior pituitary where they are stored prior to release. Release is controlled by neural activity in the nerve cells; '''Neurosecretion'''. It acts on the smooth muscle of the [[Mammary Gland - Anatomy & Physiology|mammary gland]] and [[Uterus - Anatomy & Physiology|uterus.]]

Oxytocin is produced by cell bodies in the '''paraventricular and supraoptic nuclei''' of the [[Hypothalamus - Anatomy & Physiology|hypothalamus]]. Oxytocin is transported down axons into the posterior pituitary where they are stored prior to release. Release is controlled by neural activity in the nerve cells; '''neurosecretion'''. It acts on the smooth muscle of the [[Mammary Gland - Anatomy & Physiology|mammary gland]] and [[Uterus - Anatomy & Physiology|uterus.]]

See Also: [[Lactation - Endocrine Control - Anatomy & Physiology|Lactation - Endocrine Control]].

See Also: [[Lactation - Endocrine Control - Anatomy & Physiology|Endocrine Control of Lactation]].

====Action====

====Action====

=====Milk Let-Down=====

=====Milk Let-Down=====

Oxytocin stimulates milk let down via contraction of the mammary alveoli. It does NOT stimulate milk ''synthesis'' ([[Pituitary Gland - Anatomy & Physiology#Hormones of the Anterior Pituitary Gland|Prolactin]] has this role). Oxytocin release occurs via neural activity. The teats have a high density of sensory nerve fibres, and these detect suckling, or preparation for milking. Other sensory inputs such as sight, smell, sounds of calf can add to the process:

Oxytocin stimulates milk let down via contraction of the mammary alveoli. It does NOT stimulate milk ''synthesis'' ([[Pituitary Gland - Anatomy & Physiology#Hormones of the Anterior Pituitary Gland|prolactin]] has this role). Oxytocin release occurs via neural activity. The teats have a high density of sensory nerve fibres, and these detect suckling, or preparation for milking. Other sensory inputs such as sight, smell, sounds of calf can add to the process:

Impulses travel via superfical [[Sensory Pathways - Anatomy & Physiology|sensory pathways]] and the inguinal nerve. Afferent sensory neurons enter the lumbar part of the spinal cord to the thalmus. They reach the cell bodies of neuroendocrine cells. Oxytocin is released from the nerve endings in the posterior pituitary gland and enters capillaries and the systemic circulation. Mammillary capillaries contract and the pressure within the alveoli increases. Resistance in the excretory ducts and teat canal is reduced, resulting in an increased milk outflow. This process takes 45-60 seconds to act.

Impulses travel via superficial [[Sensory Pathways - Anatomy & Physiology|sensory pathways]] and the inguinal nerve. Afferent sensory neurons enter the lumbar part of the spinal cord to the thalmus. They reach the cell bodies of neuroendocrine cells. Oxytocin is released from the nerve endings in the posterior pituitary gland and enters capillaries and the systemic circulation. Mammillary capillaries contract and the pressure within the alveoli increases. Resistance in the excretory ducts and teat canal is reduced, resulting in an increased milk outflow. This process takes 45-60 seconds to act.

=====Parturition=====

=====Parturition=====

During Stage 2 of parturition, the foetus engages the cervix. This initiates a neuroendocrine reflex, '''The Fergusson reflex'''. This is an example of a [[Positive Feedback - Anatomy & Physiology|positive feedback mechanism]], which occurs when stretch receptors in the [[Cervix - Anatomy & Physiology|cervix]] are stimulated. Sensory nerve endings in cervix are stimulated causing afferent nerve impulses to be sent to the hypothalamus. Neuroendocrine cells of the paraventricular and supraoptic nuclei depolarise and Oxytocin is secreted from the pars nervosa. Oxytocin enters the blood circulation and acts on the oxytocin receptors in the myometrium. Uterine contractions therefore, increase in strength and frequency.

During Stage 2 of parturition, the foetus engages the cervix. This initiates a neuroendocrine reflex, '''the Fergusson reflex'''. This is an example of a [[Positive Feedback - Anatomy & Physiology|positive feedback mechanism]], which occurs when stretch receptors in the [[Cervix - Anatomy & Physiology|cervix]] are stimulated. Sensory nerve endings in the cervix are stimulated causing afferent nerve impulses to be sent to the hypothalamus. Neuroendocrine cells of the paraventricular and supraoptic nuclei depolarise and oxytocin is secreted from the pars nervosa. Oxytocin enters the blood circulation and acts on the oxytocin receptors in the myometrium. Uterine contractions therefore, increase in strength and frequency.

==Links==

==Links==

[[Category:Endocrine System - Anatomy & Physiology]]

[[Category:Endocrine System - Anatomy & Physiology]]

[[Category:Image Review]]

[[Category:A&P Done]]

[[Category:To Do - AimeeHicks]][[Category:To Do - Review]]