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pituitary gland
called the "master gland," plays a central role invregulating many endocrine functions. It is located at the base of the brain, just below the hypothalamus, and is connected to it via the pituitary stalk.
anatomical structure
anterior pituitary
posterior pituitary
anterior pituitary
Made up of glandular cells, this section produces and secretes several key hormones in response to signals from the hypothalamus.
posterior pituitary
Composed of neural tissue, it stores and releases hormones that are produced in the hypothalamus
MRI imaging and tumour identification
MRI scans are used to visualise the pituitary gland and detect abnormalities. In
the images:
•A normal pituitary gland appears as a small, well-defined structure.
•A pituitary tumour may appear as an enlarged mass, often pushing
upwards against the optic chiasm, which can be seen displaced in the
scan.
This displacement can lead to visual disturbances, such as blurred vision
or loss of peripheral sight, due to pressure on the optic nerves
pituitary tumours: characteristic and effects
Most pituitary tumours are:
•Benign (non-cancerous)
•Slow-growing, but still clinically significant due to their location and
hormonal impact
They can cause:
•Hormone overproduction (hypersecretion) – leading to
conditions like acromegaly, Cushing’s disease, or hyperprolactinemia
•Hormone underproduction (hyposecretion) – resulting in
deficiencies such as hypothyroidism or adrenal insufficiency
hypothalamus and pituitary gland: hormonal control centre
The hypothalamus and pituitary gland form a central regulatory system that controls many endocrine functions. They work together to coordinate hormone release throughout the body
anterior pituitary
Releasing hormones from the hypothalamus travel through the hypothalamic- hypophyseal portal system to reach the anterior pituitary. These signals
stimulate specific endocrine cells to release hormones into the bloodstream.
endocrine cells in anterior pituitary
somatotrophs
lactotrophs
corticotrophs
thyrotrophs
gonadotrophs
somatotrophs
release growth hormone (GH), which promotes growth
and metabolism.
lactotrophs
release prolactin, which supports milk
production.
corticotrophin
release ACTH, which stimulates cortisol production from
the adrenal glands.
thytrophs
release TSH, which stimulates the thyroid gland.
gonadotrophs
release LH and FSH, which regulate reproductive
functions.
SHypothalamic Releasing Hormones
GnRH (Gonadotropin-releasing hormone) – stimulates release of LH
and FSH.
•GHRH (Growth hormone-releasing hormone) – stimulates GH release.
•TRH (Thyrotropin-releasing hormone) – stimulates TSH and prolactin
release.
•CRH (Corticotropin-releasing hormone) – stimulates ACTH release.
•Dopamine – inhibits prolactin release.
anterior pituitary tropic hormones
In response to hypothalamic signals, the anterior pituitary releases tropic
hormones that act on peripheral glands:
LH and FSH
GH
TSH
prolactin
ACTH
LH and FSH
act on the gonads to stimulate production of sex hormones
(oestrogen, progesterone, testosterone
GH
acts on the liver, which produces IGF-1 to
promote growth.T
TSH
acts on the thyroid gland to
produce thyroid hormones (T3 and T4)
prolactin
acts on breast tissue to support lactation.
ACTH
acts on the adrenal cortex to stimulate cortisol production.
Growth Hormone (GH / Somatotropin): Function and Regulation
Growth hormone (GH), also known as somatotropin, is a key hormone involved
in linear growth and metabolic regulation. It is secreted by acidophilic cells in
the anterior pituitary gland.
GH regulatory pathways
The release of GH is controlled by the hypothalamus, which secretes GHRH (Growth Hormone-Releasing Hormone). This stimulates the anterior pituitary to release GH.
Once released, GH acts as a tropic hormone, primarily targeting the liver. In the liver, GH stimulates the production of somatomedins, also known as insulin-like growth factors (IGFs). IGFs then act on target cells throughout the body to promote growth, especially in bones and tissues.
GH direct and indirect function
Growth hormone (GH) plays a vital role in both metabolism and growth. Its
effects can be divided into direct actions on metabolic processes and indirect
actions mediated through insulin-like growth factors (IGFs), also known
as somatomedins.
direct effects on metabolism
•Increasing blood glucose levels by opposing insulin’s action (anti-insulin
effect).
•Stimulating gluconeogenesis in the liver, which produces glucose from
non-carbohydrate sources.
•Enhancing protein synthesis, contributing to muscle growth and repair.
•Reducing glucose uptake in peripheral tissues, helping preserve glucose
•Promoting lipolysis, which breaks down fat stores to release energy.
These metabolic effects support energy availability during growth and
stress, and they help maintain lean body mass
indirect effects on growth
Hypertrophy – an increase in cell size, supported by enhanced protein
synthesis.
•Hyperplasia – an increase in cell number, driven by cell division.
•Skeletal growth – especially in long bones, contributing to linear height
increase during childhood and adolescence.
These effects also support the enlargement of organs and overall body
development
regulatory pathways
GH release begins in the hypothalamus, which secretes GHRH
GH then acts on the liver, prompting the production of somatomedins, also
known as insulin-like growth factors (IGFs). These IGFs act on target cells to
promote growth, especially in bones and tissues.
influencing factor
GH then acts on the liver, prompting the production of somatomedins, also
known as insulin-like growth factors (IGFs). These IGFs act on target cells to
promote growth, especially in bones and tissues.
causes of GH deficiency
Congenital – due to genetic mutations or structural abnormalities in the
brain present at birth.
•Acquired – resulting from damage to the pituitary gland caused by injury,
infection, or radiation.
•Idiopathic – where the cause is unknown despite clinical evidence of
deficiency.
treatment of growth hormone deficiency
Growth hormone deficiency can significantly affect growth, metabolism, and
quality of life. Treatment involves hormone replacement therapy, most
commonly using Somatropin, a recombinant form of human growth
hormone
Growth Hormone (GH) Excess: Gigantism and Acromegaly
Excessive secretion of growth hormone (GH) can lead to two distinct clinical
conditions depending on the age of onset: gigantism in children
and acromegaly in adults. Both result from prolonged exposure to high GH
levels, often due to a pituitary tumour
Gigantism (in Children)
Gigantism occurs when GH excess begins before the closure of growth
plates in bones. This leads to excessive linear growth and other systemic
effects.
Acromegaly (in Adults)
Acromegaly develops when GH excess begins after growth plates have closed so it does not cause increased height but leads to tissue and bone thickening.
surgical treatment
Surgery is often the first-line treatment, especially when a pituitary adenoma is
the cause of GH excess. If the tumour is small and accessible, surgical removal
can completely cure acromegaly.
However, large adenomas pose a challenge due to their proximity to critical brain
structures. In such cases, surgery may only partially reduce GH levels, requiring
additional therapies.
radiation therapy
When surgery is not fully effective or feasible, radiation therapy may be used.
This includes:
•Stereotactic radiation – a precise, targeted method
•Conventional radiation – broader but less targeted
Radiation requires extreme care, as it can damage surrounding tissues and impair
the function of other pituitary hormones. Patients often need lifelong hormone
replacement therapy to compensate for these losses.
drug therapy
Pharmacological options are available to either reduce GH secretion or block its
effects. These include:
•Somatostatin analogues (e.g., octreotide, lanreotide) – inhibit GH release.
•GH receptor antagonists (e.g., pegvisomant) – block GH action at target tissues.
•Dopamine agonists (e.g., cabergoline) – may help in some cases, especially
when prolactin is also elevated