POSTERIOR PITUITARY

SWETHHA V K
MDS - I YEAR
 PITUITARY GLAND
The pituitary gland also called as hypophysis is the master of endocrine glands (ductless glands) located at the
base of the brain extending from the hypothalamus. It rests on the hypophyseal fossa of the sphenoid bone in
the middle cranial fossa.
CORONAL SECTION
RELATIONS :

DIAPHRAGMA CAVERNOUS POSTERIOR OPTIC

WALL OF CHIASM
SELLA SINUS
SPHENOID
SINUS

SUPERIORL LATERALLY ANTERO- ANTERO-

INFERIORLY SUPERIORLY
Y
 STRUCTURE : DIVISIONS
OF PITUITARY
The pea-sized gland is enclosed in a bony enclosure
called sella turcica. It is mainly composed of two lobes.
They are :

● Anterior lobe / Adenohypophysis (epithelial tissue)

● Posterior lobe/ Neurohypophysis (nervous tissue)

They both are connected by an intermediate lobe which is

avascular and almost absent in human beings.
ANTERIOR PITUITARY
SOMATOTROPES : Releases growth hormone/ somatotropin by stimulation from hypothalamic
hypothalamic somatotropin.

CORTICOTROPHS : Adrenocorticotropic hormone (ACTH), melanin-stimulating hormone, beta endorphins

Are released by stimulation from hypothalamic corticotropin releasing hormone.

THYROTROPES : Thyroid stimulating hormone is released by stimulation from thyrotropin releasing

hormone and inhibited by somatostatin.

GONADOTROPINS : Luteinizing hormone and follicle stimulating hormone by gonadotropin releasing

hormone from hypothalamus.

LACTOTROPES : Prolactin stimulated by various factors and inhibited by hypothalamic dopamine.

THE HYPOPHYSEAL PORTAL SYSTEM

The main function of the microcirculation is the transport and exchange between hypothalamus
arcuate nucleus and anterior pituitary gland.
3 TYPES OF CELLS : ANTERIOR PITUITARY
POSTERIOR PITUITARY /
NEUROHYPOPHYSIS

The neurohypophysis is
divided into two regions;
the pars nervosa and the
infundibular stalk.
Sometimes the pars
intermedia and the
median eminence are
included.
PARTS OF POSTERIOR PITUITARY
POSTERIOR PITUITARY : organogenesis
● It is also called as pars posterior or pars nervosa.

● The neurohypophysis consists of axons arising from groups of

hypothalamic neurons from magnocellular neurons of supraoptic and
paraventricular nuclei.

● During embryogenesis neuroepithelial cells of the lining of the third ventricle

mature into magnocellular neurons while migrating laterally to and above the
optic chiasm to form the supraoptic nuclei and to the walls of the third
ventricle to form the paraventricular nuclei.

● The neurosecretory granules mostly contain oxytocin or vasopressin

and form axonal beads close to termini.
BLOOD SUPPLY

The posterior pituitary is supplied directly from the inferior hypophyseal arteries, which are
branches of the posterior communicating and internal carotid arteries. The drainage is into the
cavernous sinus and internal jugular vein.
● The neurohypophysis does not contain
neurosecretory cell bodies instead it is
composed of specialised glial cells
(pituicytes) that in the human brain express
the TTF-1 (thyroid transcription factor 1)
protein in their nuclei.
● The neurohypophysis contains the nerve
endings of the oxytocin and vasopressin
producing cells of the hypothalamus.
● Their large distended nerve endings can be
identified on routine stains as so-called
Herring-bodies, named after Percy Theodore
Herring (University of Edinburgh) who
described them in 1908 as the
‘physiologically active principle’ of the
posterior gland.
 POSTERIOR PITUITARY HORMONES

ANTIDIURETIC HORMONE OXYTOCIN

MAMMARY
KIDNEY GLAND UTERUS

Increases
milk letdown Increases uterine
conserves water;
constricts blood vessels from mammary glands contractions
GENERAL PHYSIOLOGY

● The hormones are stored at the herring bodies of the neurohypophysis, which are the terminal
end of the axons. For their release from the herring bodies, action potentials are produced, which
activates voltage-gated channels allowing calcium to enter and trigger the release of the hormone
into the neurohypophyseal capillaries, which then transport the hormones into the systemic
circulation.
● Predominantly, the paraventricular nucleus is related to oxytocin secretion, while the supraoptic
nucleus is concerned with vasopressin secretion. Small amounts of each hormone are also
produced at the other nuclei.
● The release of these hormones is triggered in response to afferent stimuli coming from outside
neurons projecting to the magnocellular neurons of the hypothalamus.
● The neurohypophysis receives its blood supply from the inferior hypophyseal artery, which is a
branch from the cavernous internal carotid (ICA) artery. The cavernous ICA has a dorsal trunk
called the meningohypophyseal trunk, which gives three terminal branches; inferior hypophyseal
artery. Venous drainage of the posterior pituitary gland is by the short portal and hypophyseal
veins into the cavernous sinus.
PITUICYTOMA
A tumor formed from the pituicytes is called pituicytoma.

The histology varies from streaming bundles of cells to a somewhat storiform pattern
Strong staining for glial fibrillary acidic protein is seen .
OXYTOCIN
OXYTOCIN
OXYTOCIN
Labor stimulation with oxytocin: effects on obstetrical and neonatal outcomes :

● In general, the use of oxytocin during labor may be related to adverse effects on the mother and the
newborn.
● The perfusion of oxytocin for labor stimulation was significantly associated with an increase in the
rates of cesarean sections, a higher percentage of intrapartum fever, lower pH of umbilical cord and
greater need for advanced neonatal resuscitation.
● It seems coherent that the main differences have been found among primiparous women (single birth),
because for them childbirth is usually longer, more difficult and may present more complications.
● In this context, some authors have reported that parity was a factor influencing the type of delivery
and concluded that the normal or spontaneous labor is more common in multiparous than primiparous.
● In another study carried out in 2012, it was found that high temperature was associated with a high
body mass index and with the time elapsed from the rupture of the amniotic sac until delivery, whereas
epidural analgesia did not influence on the temperature increase. In our study, no significant
association between elevated maternal temperature and epidural administration was found.
● The dilation stage proved to be longer in the group of primiparous women non-submitted to
stimulation with oxytocin, so this result is consistent with those of other authors, which showed that
the duration of this first stage of labor was significantly shorter when the dose of oxytocin was
increased.
● Interventions with oxytocin, particularly at high doses, may have potential adverse effects on the
mother and the fetus, such as uterine tachysystole and impairment of fetal heart rates.

● This occurs due to the reduction or interruption of the blood flow to the intervillous space during
contractions.

● Contractions in normal deliveries are well tolerated by the majority of fetuses; however, there is a risk
of fetal hypoxemia and acidemia if the contractions are very frequent and/or prolonged.
BONE EFFECTS :
METABOLIC EFFECTS OF OXYTOCIN
ANTIDIURETIC HORMONE (ADH) / VASOPRESSIN
VASOPRESSIN

➔ Vasopressin or antidiuretic hormone (ADH) or arginine vasopressin (AVP) is a nonapeptide

synthesized in the hypothalamus. It plays an essential role in the control of the body’s
osmotic balance, blood pressure regulation, sodium homeostasis, and kidney functioning.
➔ ADH primarily affects the ability of the kidney to reabsorb water; ADH induces expression of
water transport proteins in the late distal tubule and collecting duct to increase water
reabsorption. Several disease states arise when the body loses control of ADH secretion or
responds to its presence.
➔ In states of hypovolemia or hypernatremia, ADH is released from the posterior pituitary
gland and binds to the type-2 receptor in principal cells of the collecting duct. Binding to the
receptor triggers an intracellular cyclic adenosine monophosphate (cAMP) pathway, which
causes phosphorylation of the aquaporin-2 (AQP2).
➔ After achieving water homeostasis, the ADH levels decrease, and AQP2 is internalized from
the plasma membrane, leaving the plasma membrane watertight again.
 There is evidence that prostaglandins (PGE2 and PGI2)
stimulate renin release in response to reduced NaCl transport
across the macula densa. When afferent arteriole pressure is
reduced, glomerular filtration decreases, and this reduces
NaCl in the distal tubule.

This serves as an important mechanism contributing to the

release of renin when there is afferent arteriole hypotension,
which can be caused by systemic hypotension or narrowing
(stenosis) of the renal artery that supplies blood flow to the
kidney.

When renin is released into the blood, it acts upon a

circulating substrate, angiotensinogen, that undergoes
proteolytic cleavage to form the decapeptide angiotensin I.
Vascular endothelium, particularly in the lungs, has an
enzyme, angiotensin converting enzyme (ACE), that
cleaves off two amino acids to form the octapeptide,
angiotensin II (AII), although many other tissues in the body
(heart, brain, vascular) also can form AII.

This stimulates the release of ADH from the posterior

pituitary, which increases fluid retention by the kidneys.
● ADH is the primary hormone responsible for tonicity homeostasis. Hyperosmolar states most strongly
trigger its release. These neurons express osmoreceptors that are exquisitely responsive to blood osmolarity
and respond to changes as little as two mOsm/L. ADH then acts primarily in the kidneys to increase water
reabsorption, thus returning the osmolarity to baseline.
● ADH secretion also occurs during states of hypovolemia or volume depletion. In these states, decreased
baroreceptors sense arterial blood volume in the left atrium, carotid artery, and aortic arch. Information about
low blood pressure sensed by these receptors is transmitted to the vagus nerve, which directly stimulates the
release of ADH.
● ADH then promotes water reabsorption in the kidneys and, at high concentrations, will also cause
vasoconstriction. These two mechanisms together serve to increase effective arterial blood volume and
increase blood pressure to maintain tissue perfusion. It is also important to note that in states of
hypovolemia, ADH will be secreted even in hypoosmotic states.
● Conversely, hypervolemia inhibits ADH secretion; therefore, in hyperosmotic hypervolemic states, ADH
secretion will be reduced.
● Osmolarity and volume status are the two greatest factors that affect ADH secretion. a variety of other
factors promote ADH secretion such as angiotensin II, pain, nausea, hypoglycemia, nicotine, opiates,
and certain medications. Levels of inappropriate ADH (SIADH) occurs when ADH is released in
excessive unregulated quantities. SIADH results in excess water reabsorption and thus creates
dilutional hyponatremia. Diabetes insipidus is an important cause of hypernatremia.
● ADH secretion is also negatively affected by ethanol, alpha-adrenergic agonists, and atrial natriuretic
peptide.
● Ethanol’s inhibitory effect helps to explain the increased diuresis experienced during intoxicated states
as well as increased free water loss; without appropriate ADH secretion, the kidneys excrete more
water.

● Aside from its role in homeostasis and its part in a variety of pathologies, ADH has also served as a

medication to treat two important bleeding disorders: von Willebrand disease and hemophilia A.
 GENERAL PATHOPHYSIOLOGY
● Sheehan syndrome can develop diabetes insipidus (DI) and hypernatremia due to ischemic necrosis
damage to the posterior gland causing impaired vasopressin secretion.
● Hyponatremia can also occur due to an increased ADH secretion as a response to hypotension and
reduced cardiac output owing to glucocorticoid deficiency. Also, the cortisol deficit stimulated the
secretion of corticotropin-releasing hormone, which further stimulates the ADH secretion.
● During septic shock, vasopressin secretion undergoes a biphasic pattern. Initially, there is an
increased secretion to maintain homeostasis, but later, when hypotension is pronounced, there is an
unexpected significant decrease in the secretion.
● This decrease is thought to occur due to depletion of the vasopressin stores in the neurohypophysis,
from autonomic dysfunction, and from nitric oxide inhibition of secretion at the hypothalamus.
● In TBI, DI is caused by direct damage to the neurohypophysis, pituitary stalk, hypothalamic nuclei,
the vascular supply, traumatic edema in the neurohypophysis, or hypothalamus. These changes are
usually reversible, but irreversible changes with gliosis can cause permanent DI.
CAUSES OF NEUROHYPOPHYSIS DYSFUNCTION
Tumors Infectious Hydrocephalus
Anorexia
● Pituitary adenoma ● Meningitis
● Hypothalamic glioma ● Encephalitis Aneurysm (anterior
● Craniopharyngioma ● Acquired communicating
● Pituicytoma immunodeficiency artery)
● Granular cell tumors syndrome Congenital
● Germ cell tumors ● Abscess
● Septic shock
Pituitary stalk
Traumatic brain injury (TBI) interruption syndrome
Subarachnoid hemorrhage
Brain surgery
Hypoxia Genetic
Metabolic
Inflammatory ● Sheehan syndrome ● Prader–Willi
● Pituitary apoplexy syndrome
● Sarcoidosis ● Cardiac arrest ● Multiple
● Multiple sclerosis endocrine
● Pituitary hypophysitis neoplasia-1
 DRUGS

● Phenothiazines ● Morphine

● Carbamazepine ● Ecstasy drug

● Valproic acid (3,4-methylenedioxym

ethamphetamine)
● Omeprazole
● Vincristine
● Selective serotonin
● Amitriptyline
reuptake inhibitors
TREATMENT :

➔ Diabetes insipidus is treated with a man-made form of the

vasopressin hormone called desmopressin.
➔ Felypressin is a short acting vasoconstrictor.
➔ Oxytocin is available in a variety of forms such as nasal
sprays, topical creams, oral tablets, sublingual tablets, and
troches (lozenges).
➔ Pituitary adenomas is treated with surgery. Radiation
therapy if required.
 REFERENCES:
➔ https://slidetodoc.com/pituitary-gland-pituitary-development-the-master-gland-n/

➔ https://pubmed.ncbi.nlm.nih.gov/32809568/

➔ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982443/#:~:text=Interventions%20with%20oxytocin%2C
%20particularly%20at,intervillous%20space%20during%20contractions%207%20.

➔ https://pubmed.ncbi.nlm.nih.gov/30334138/

➔ https://www.ncbi.nlm.nih.gov/books/NBK560733/

➔ https://www.researchgate.net/publication/281393923_Two_Birds_with_One_Stone_Possible_Dual-Role_
of_Oxytocin_in_the_Treatment_of_Diabetes_and_Osteoporosis/download

➔ https://www.ncbi.nlm.nih.gov/books/NBK425703/

➔ https://docs.google.com/presentation/d/1LIYJFHkLc-8zwj-qHw9M2StucgNuhFl3j1Xhp-Uqf38/edit#slide=id.g10b
56580163_0_19

➔ https://eksaval.com/knowledge-base/structure-and-functions-of-pituitary-gland/
➔
https://pubmed.ncbi.nlm.nih.gov/22926246/#:~:text=The%20kidney%20plays%20a%20central,arterial%20circulation%20an
d%20blood%20pressure.
T H A N K YO U