2. anatomy
•The pituitary is an endocrine (hormone-
producing) gland that sits just beneath the
base of the brain, behind the bridge of the
nose.
•the gland is located within the sella turcica
of the sphenoid bone. It is very small only
about the size of a pea.
•The hypothalamus is sited at the base of the
brain around the third ventricle and above
the pituitary stalk, which leads down to the
pituitary itself,
3.
4.
5.
6. HYPOTHALAMIC-PITUITARY RELATIONSHIPS
• The hypothalamus and pituitary gland function in a coordinated
fashion to orchestrate many of the endocrine systems.
• The hypothalamic-pituitary unit regulates the functions of the
thyroid, adrenal, and reproductive glands and also controls growth,
milk production and ejection, and osmoregulation.
• It is important to visualize the anatomic relationships between the
hypothalamus and the pituitary because these relationships underlie
the functional connections between the glands.
7. • The pituitary gland, which also is called the hypophysis, consists of a
posterior lobe and an anterior lobe.
• The posterior lobe (or posterior pituitary) is also called the
neurohypophysis.
• The anterior lobe (or anterior pituitary) is also called the
adenohypophysis.
• The hypothalamus is connected to the pituitary gland by a thin stalk
called the infundibulum.
• Functionally, the hypothalamus controls the pituitary gland by both
neural and hormonal mechanisms
8.
9. • posterior pituitary is controlled by nerve signals from the hypothalamus.
• The anterior pituitary is controlled by hormones known as hypothalamic
releasing/inhibitory hormones released from the hypothalamus. These
hormones travel to the pituitary via the hypothalamic-hypophysial portal vessels
where they act on glandular cells to control secretion of pituitary hormones.
Hypothalamus and
Hypothalamic neurons
Hypophyseal artery
Hypothalamic-hypophyseal
Portal veins
Anterior Pituitary
Hypophyseal vein
10. Hypothalamic Releasing Hormones
Hormone Actions on Anterior Pituitary
•Corticotropin-releasing hormone (CRH) Stimulates ACTH secretion by corticotrophs;
•Thyrotropin-releasing hormone (TRH) Stimulates TSH secretion by thyrotrophs;
stimulates PRL synthesis by lactotrophs
•Growth hormone-releasing hormone (GHRH) Stimulates GH secretion by somatotrophs;
•Luteinizing hormone-releasing hormone (LHRH), Stimulates FSH and LH secretion by gonadotrophs
gonadotrophin releasing hormone (GnRH)
•Somatostatin, somatotropin release inhibiting Inhibits GH secretion by somatotrophs;
factor (SRIF) inhibits TSH secretion by thyrotrophs
•Dopamine Inhibits PRL synthesis and secretion by lactotrophs
15. Growth Hormone
In contrast to other anterior pituitary hormones, GH does not function through a target
gland, but exerts its effects directly on all, or almost all, tissues of the body. GH causes
growth of almost all tissues of the body that are capable of growing. It promotes
increased sizes of the cells and increased mitosis. GH promotes differentiation of
certain types of cells such as bone growth cells and early muscle cells
Actions of GH
GH affects the metabolic activity of most of the tissues in the body. GH has a
promoting effect on the uptake of amino acids which are incorporated into proteins in
muscles and bones therefore promoting growth. The release of GH stimulates the
release of IGF-1 (Insulin like growth factor 1) which has strong mitogenic activity,
especially in muscle and bone. GH has effect on carbohydrate and fat metabolism. GH
increases blood glucose by stimulating hepatic gluconeogenesis and inhibiting glucose
16. Acromegaly is a condition characterised by excessive growth hormone secretion from the pituitary. The
condition may be caused by a number of pathways:
A mutation in a regulation gene which causes constitutive activation of growth hormone secretion from
pituitary adenoma cells
Over-expression of the pituitary tumour transforming gene
Release of GHRH from a hypothalamic tumour RARE
Ectopic release of GHRH from other neuroendocrine tumours RARE
Ectopic secretion of GH from non-endocrine tumours RARE
The clinical features of acromegaly are due to excess GH and IGF-1 in the blood. GH and IGF-1 both have
metabolic and somatic effects.
The somatic effects include stimulation of growth of tissues such as the skin, connective tissue, cartilage,
bone and many epithelial tissues.
The metabolic effects include nitrogen retention, insulin antagonism, lipolysis.
If the excess GH is due to a tumour, the local symptoms may include headache and visual field defects.
17.
18. Clinical Manifestations The onset of acromegaly is usually very slow and the diagnosis usually made from a series of photographs.
Overgrowth Patients usually have an enlarged jaw and enlarged swollen hands and feet. This results in increasing show and glove size and patients will
usually say they have had to have a ring enlarged. The facial features become coarse with enlargement of the nose and frontal bones. Joint tissue and
cartilage also enlarge which causes joint pain.
Metabolic In addition to high GH and IGF-1, acromegaly is associated with hyperinsulinism, insulin resistance and diabetes.
Cardiovascular Disease Hypertension, cardiomyopathy and other abnormalities are reported.
Height Adults with acromegaly do not become taller, but if excess GH secretion begins before the epiphysis of the long bones are fused, linear growth
does increase – the result is gigantism.
Pituitary Function Acromegaly can cause disfunction of other pituitary hormones.
Skin and Hair The skin thickens and hair growth increases. Some women have hirsutism.
Soft Tissues Macroglossia leading to sleep apnea, deepening of the voice and paresthesias of the hands.
19. Diagnosis
Acromegaly is usually suspected clinically and is confirmed by a biochemical diagnosis.
The concentration of GH and IGF-1 can be measured in the patients blood.
Normally, GH is secreted in a pulsatile fashion across the day, but in acromegaly there is little
change in GH concentration across the day and has no response to food intake or exercise.
To confirm the diagnosis, the patient undertakes a dynamic function test called an oral
glucose tolerance test. In normal patients, upon ingestion of glucose, the GH should
suppress within 2 hours. In acromegalic patients, the secretion of GH is not regulated by
glucose intake and so is not suppressed when analysed on serial measurements.
20. Treatment
There are three ways acromegaly can be treated:
1) Surgical removal of the tumour (transphenoidal surgery)
2) Radiotherapy to shrink the tumour
3) Medical – several drugs are available to treat acromegaly
(octreotide, bromocriptane, pegvisomant)
Medical treatment aims to block secretion or action of GH.
All treatment aims to lower GH and IGF-1 concentrations to within the normal reference
range. Surgery or radiotherapy will remove the complications caused by the tumour size
(headache, visual field defects).
Acromegaly patients are monitored closely, even after they have been cured. Annual MRI
scans, biochemical testing and investigation of secondary complications are part of the
long-term monitoring of acromegaly.
21. Antidiuretic Hormone
•ADH increases the reabsorption of water by the kidneys and so reduces the excretion
of water from the body.It acts on the distal portions of the mammalian nephrons,
increasing their permeability to water. Water moves passively out of the nephrons
alone as osmotic gradient, and so urine volume is decreased.
•ADH acts of vascular smooth tissue and initiates a pathway which triggers muscle
contraction. Under physiological conditions, ADH does not significantly alter arterial
pressure because it is counter acted by baroreceptor reflexes.
Control of ADH Secretion
There are several factors that increase ADH secretion:
Increasing osmotic pressure detected in the hypothalamus
Changes in blood volume and pressure
Pain, exercise, stress, sleep and drugs (e.g. morphine)
Alcohol is a powerful inhibitor of ADH secretion.
23. Actions of Oxytocin
Oxytocin stimulates the myoepithelial cells of the mammary gland causing milk let-down. It also causes uterine
contraction during child birth and is used clinically to induce labour.
Oxytocin levels rise in both males and females in response to sexual activity and may assist in the passage of sperm in
the male and female genital tracts.
Control of Oxytocin Secretion
Milk let-down is a reflex action in response to suckling at the breast. A neuroendocrine reflex pathway is involved in
which impulses initiated by suckling are relayed to the hypothalamopituitary axis, causing the release of oxytocin which
is then carried to the mammary glands.
Oxytocin is released in response to stretching of the uterus and cervix during labour.
