2. Pituitary gland or
hypophysis cerebri
is an
neuroglandular
body suspended
from floor of 3 rd
ventricle by a stalk
infundibulam.
It is called master
gland since it
controls the other
endocrine gland.
3. Location
Situated in the
hypophysial fossa
a bony depression
in the sella tunica
of body of
sphenoid bone.
Lined by the dura
matar and
covered by a
portion of the
dura mater
,diaphragm sellae.
4. Measurement
The gland measures approximately 1cm times 1 to
1.5cm
Weight:0.5 gm in men and slightly more in women
Parts
Adenohypophysis(Anterior pituitary)
-Pars distalis
-Pars intermedia
-Pars tuberalis
Neurohypophysis
-Median eminence
-Infundibulam
-Pars nervosa
5. Relations
Superior
-Optic chiasma
-Diaphragm sella
-Anterior communicating artery
-Floor of 3rd ventricle
Inferior
-Hypophyseal fossa
-Sphenoidal air sinus
Anterior-Anterior intercavernous sinus
Posterior-Posterior intercavernous sinus
Lateral-Cavernous sinus and its related structure
6. Arterial supply
Two pairs of arteries
from the internal
carotid artery
Superior hypophyseal
artery supplies pars
tuberalis &
infundibulum and form
primary capillary plexus
in median eminence
Inferior hypophyseal
artery supplies
posterior lobe
8. REGULATION OF SECRETION
Hypothalamo-hypophyseal Relationship
• The relationship between hypothalamus and pituitary
gland is called hypothalamo-hypophyseal relationship.
• Hormones secreted by hypothalamus are transported to
anterior pituitary and posterior pituitary.
• But the mode of transport of these hormones is different.
• Hormones from hypothalamus are transported to anterior
pituitary through hypothalamo-hypophysial portal blood
vessels.
• Hormones from hypothalamus to posterior pituitary are
transported by nerve fibers of hypothalamo-hypophyseal
tract
9. HORMONES SECRETED BY
ANTERIOR PITUITARY
1. Growth hormone (GH) or somatotropic hormone
(STH)
2. Thyroid-stimulating hormone (TSH) or
thyrotropic hormone
3. Adrenocorticotropic hormone (ACTH)
4. Follicle-stimulating hormone (FSH)
5. Luteinizing hormone (LH) in females or
interstitialcell-stimulating hormone (ICSH) in males
6. Prolactin
10. 1. Growth hormone (GH) or
somatotropic hormone (STH)
• Function-GH is responsible for the general
growth of the body.
• GH also acts on the metabolism of all the three
major types of foodstuffs in the body, viz.
proteins, lipids and carbohydrates.
• On bones-In embryonic stage, GH is responsible
for the differentiation and development of bone
cells. In later stages, GH increases the growth of
the skeleton. It increases both the length as well
as the thickness of the bones.
• Mode of Action of GH – Somatomedin
11. 2.Actions of Thyroid-stimulating
Hormone
Thyroid-stimulating hormone increases:
1. The number of follicular cells of thyroid
2. The conversion of cuboidal cells in thyroid gland into
columnar cells and thereby it causes the development of
thyroid follicles
3. Size and secretory activity of follicular cells
4. Iodide pump and iodide trapping in follicular cells
5. Thyroglobulin secretion into follicles
6. Iodination of tyrosine and coupling to form the hormones
7. Proteolysis of the thyroglobulin, by which release of
hormone is enhanced and colloidal substance is decreased.
12. • TSH triggers the release of thyroid
hormones by thyroid glands
• Function of thyroid hormone-
I. To increase basal metabolic rate
II. To stimulate growth in children.
13. 3.Actions of ACTH on adrenal cortex
(Adrenal actions)
Actions of ACTH on adrenal cortex (Adrenal actions)
1. Maintenance of structural integrity and vascularization of zona
fasciculata and zona reticularis of adrenal cortex.
2. Conversion of cholesterol into pregnenolone, which is the precursor of
glucocorticoids. Thus, adrenocorticotropic hormone is responsible for the
synthesis of glucocorticoids
3. Release of glucocorticoids
4. Prolongation of glucocorticoid action on various cells.
Other (Nonadrenal) actions of ACTH
1. Mobilization of fats from tissues
2. Melanocyte-stimulating effect. Because of structural similarity with
melanocyte-stimulating hormone(MSH), ACTH shows melanocyte-
stimulating effect. It causes darkening of skin by acting on melanophores,
which are the cutaneous pigment cells containing melanin.
14. 4. Actions of Follicle-stimulating
hormone (FSH)
In males FSH:
1. Initiation of spermatogenesis. It binds with Sertoli cells and
spermatogonia and induces the proliferation of spermatogonia.
2. It also stimulates the formation of estrogen and androgen-binding
protein from Sertoli cells
In females FSH:
1. Causes the development of graafian follicle from primordial follicle
2. Stimulates the theca cells of graafian follicle and causes secretion of
estrogen
3. Promotes the aromatase activity in granulosa cells, resulting in
conversion of androgens into estrogen
15. 5.Action of Luteinizing Hormone (LH)
In males,
• LH is known as interstitial cell-stimulating hormone (ICSH) because
it stimulates the interstitial cells of Leydig in testes. This hormone is
essential for the secretion of testosterone from Leydig cells
In females, LH:
1. Causes maturation of vesicular follicle into graafian follicle along
with follicle-stimulating hormone
2. Induces synthesis of androgens from theca cells of growing follicle
3. Is responsible for ovulation
4. Is necessary for the formation of corpus luteum
5. Activates the secretory functions of corpus luteum
16. 6.Prolactin
• Prolactin is necessary for the final preparation
of mammary glands for the production and
secretion of milk.
• Prolactin acts directly on the epithelial cells of
mammary glands and causes localized
alveolar hyperplasia.
18. 1. Antidiuretic hormone (ADH) or
vasopressin
1. Retention of water-Major function of ADH is
retention of water by acting on kidneys. It increases
the facultative reabsorption of water from distal
convoluted tubule and collecting duct in the kidneys
• 2. Vasopressor action-In large amount, ADH
shows vasoconstrictor action. Particularly, causes
constriction of the arteries in all parts of the
body. Due to vasoconstriction, the blood pressure
increases. ADH acts on blood vessels through V1A
receptors.
19. 2. Oxytocin
• In females, oxytocin acts on mammary glands
and uterus.
• Stimulate contraction of smooth muscle cells
of uterus during childbirth
• Stimulates myoepithelial cells in mammary
gland to cause milk ejection.
28. Possible extent of
tumor
Clinical features
Headache
• Suprasellar
extension
visual loss(mech?)
• intrasellar mass Pituitary stalk compression
→“stalk section” phenomenon
-early hyperprolactinemia and later
concurrent loss of other pituitary hormones
• Lateral mass
invasion
impinge on the cavernous sinus and compress its
neural contents
-cranial nerve III, IV, and VI palsies
as well as effects on the ophthalmic and maxillary
branches of CNV
• invade the palate
roof
nasopharyngeal obstruction, infection, and CSF
leakage
• Temporal and uncinate seizures, personality disorders, and
31. Clinical Physical Examination
Growth hormone deficiency
• Reduced lean body mass
• Increased fat mass (deposition intra-abd
viscera fat)
• Increase waist-to-hip ratio
• Muscle & bone weakness
• Fatigue
• Hyperlipidemia
32. Clinical Physical Examination
Reproductive system: Secondary hypogonadism
• Loss of axillary/pubic hair
• Gynaecomastia
• Testis atrophy
• Muscle loss
• Incomplete sexual development
**Examination of external genitalia**
33. Clinical Physical Examination
Adrenal function: Secondary hypoadrenalism
• Loss axillary/pubic hair (lack glucocorticoids)
• Weight loss
• Palpitation (weak and rapid pulse -
hyperkalemia)
• Weak clammy pale skin (shock)
• Confusion (hyponatremia & shock)
35. Clinical Physical Examination
Ophthalmic examination:
1) Visual acuity test:
• Measure near and distant vision for both eyes
• Distant: Read a snellen chart from 6m, record visual acuity (6/6 -
normal)
• Near: Standard Jaeger card (read until smallest print)
• If pt unable to read anything at 6m, move closer 3m, then 1m, assess by
counting number of fingers, assess ability to detect a moving hand, if
unable, assess light perception.
** If refractive error suspected, read through a pin-hole**
2) Visual field test (temporal field & sensory inattention) + colour vision
test (ishihara chart)
3) Pupillary reflex (size, shape, symmetry then direct & consensual &
accomodation reflex)
4) Assess ocular muscle movement (CN III, IV, VI) *report diplopia*
5) Fundoscopy
36.
37. 1 Post-fixed Post-fixed chiasm is located over the dorsum sellae
2 Central Normal chiasm located directly over optic chiasm (80%)
4 Pre-fixed Pre-fixed chiasm is located anterior to its normal position over
the tuberculum sellae
Optic chiasm compression
38.
39. Cavernous sinus invasion
• Some macroadenomas demonstrate invasive
growth, extension into the cavernous sinuses.
• Compress cranial nerves resulting in deficits
• Oculomotor nerve (CN III) commonly involved,
followed by the abducens nerve (CN VI).
• Difficult to completely resect the cavernous
sinuses.
42. ACTH deficiency
Measure level of: after ACTH stimulation test
• Serum cortisol
• Serum ACTH
TSH deficiency
Measure level of:
• Serum TSH
• Serum Thyroxine (free T4)
Prolactin deficiency
Measure level of:
• Serum prolactin
Normal range at morning:
ACTH: 10 – 50 pg/ml
Cortisol: 10-20 pg/ml
Free Thyroxine: 0.7-1.9 ng/dl
Serum TSH: 0.5-6 uiU/ml
Normal prolactin:
Males: <20 ng/dL Nonpregnant
females: 5 to 40 ng/dL
43. Basic Investigation
Imaging:
• CT scan – pituitary mass (macroadenoma:
>10mm) in sella turcica or hypothalamic mass
• MRI (hyperdense)
Diagnosis:
Presence of clinical or biochemical evidence of
hypopituitarism and visualization of pituitary mass
or hypothalamic mass.
46. • Management consists of treating the underlying
cause (e.g., transsphenoidal resection in cases
of pituitary macroadenomas) and hormone
replacement therapy.
• Growth hormone deficiency
– Children: GH hormone replacement;
– Adults: GH hormone replacement is usually not
required
• TSH deficiency: administration
of levothyroxine (see hypothyroidism)
• Patients with TSH deficiency should not be
treated with levothyroxine until ACTH deficiency
has been ruled out and/or treated
because levothyroxine increases
the clearance of cortisol and may precipitate
an adrenal crisis!
47. • CTH deficiency: glucocorticoid replacement therapy
with increased dosage during periods of
stress (adrenal insufficiency)
• Immediate treatment with glucocorticoids, without
waiting for diagnostic confirmation, is required
when acute ACTH deficiency is suspected (e.g.,
following pituitary apoplexy) to prevent an adrenal
crisis!
• GnRH deficiency
– Males
• If fertility is desired: exogenous gonadotropins (e.g., HCG)
should be administered
• If fertility is not desired: testosterone replacement therapy
– Females: estrogen replacement therapy
with/without progesterone
• Prolactin deficiency: no treatment is required
• Central diabetes insipidus: desmopressin
Editor's Notes
Apoplexy is an endocrine emergency that may result in severe hypoglycemia, hypotension and shock, (CNS)
hemorrhage, and death
In addition to hormone replacement therapy, the underlying cause of hypopituitarism should be treated, e.g., via transsphenoidal resection in the case of pituitary macroadenomas
