PITUITARY

GLAND
(HYPOPHYSIS) -I
Mohamed Elsadig
 Small gland about 1 centimeter in diameter and 0.5 to 1 gram in weight.

 It lies in the sella turcica (latin word for Turkish seat ) which is saddle-
shaped depression present in the sphenoid bone at the base of skull.
 It is connected to the hypothalamus by the pituitary stalk (hypothalamic-
hypophysial) .
 Pituitary gland consists of two loops:

1. The anterior pituitary (adenohypophysis):

 It originates from Rathke's pouch from pharyngeal epithelium.

 It synthesizes and releases hormones.

2. The posterior pituitary (neurohypophysis):

 It originates from the hypothalamus.

 It does not synthesize hormones it stores hormones.

HYPOTHALAMIC-HYPOPHYSIAL TRACT
(STALK)
 It is neuro-endocrine connection between hypothalamus and pituitary
gland.
 Through this connection, the hypothalamus controls the pituitary by
releasing hormones and inhibitory hormones.
 There are two connections:

1. Neural connection: between the hypothalamus and the posterior

pituitary.
2. Vascular (portal) connection: between the hypothalamus and anterior
pituitary.
VASCULAR CONNECTION
NEURAL CONNECTION
 Anterior pituitary has two types of cells which have different staining
properties:
A. Chromophobe cells.

B. Chromophil cells.

A) Chromophobe cells:
 They do not have granules and stain poorly.

 These are precursors of chromophil cells.

 It constitutes 50% of total cells in anterior pituitary.

B. Chromophil cells:
1. Acidophilic cells or alpha cells, constitute 35% which include:
i. Somatotropes, which secrete growth hormone(GH).
ii. Lactotropes, which secrete prolactin(PRL).
2. Basophilic cells or beta cells, constitute 15%which include:
i. Corticotropes, which secrete adrenocorticotropic hormone(ACTH).
ii. Thyrotropes, which secrete thyroid-stimulating hormone (TSH)
iii. Gonadotropes, which secrete follicle-stimulating hormone (FSH) and
luteinizing hormone (LH).
HYPOTHALAMUS HORMONES
A. Releasing hormones:
1. Corticotropin releasing hormone (CRH).
2. Gonadotropin releasing hormone (GnRH).
3. Thyroid releasing hormone (TRH).
4. Growth hormone releasing hormone (GHRH).
5. Prolactin releasing hormone (PRLRH).
B. Inhibitory hormones:
1. Growth hormone inhibitory hormone (GHIH) also called somatostatine.
2. Prolactin inhibitory hormone (PRLIH), also known as dopamine.
 Hypothalamus

GnRH GHRH GHIH/SS TRH PRIH PRH CRH

+ + - - + + - + +
FSH & LH GH TSH Prolactin ACTH
Anterior Pituitary
THE ANTERIOR PITUITARY
HORMONES
 These are six peptide hormones.

1. Growth hormone (somatotropin)(GH):

 It promotes growth of the entire body.

2. Adrenocorticotropin (corticotropin) (ACTH):

 It controls the secretion of some of the adrenocortical hormones.

3. Thyroid-stimulating hormone (thyrotropin) (TSH):

 It controls the rate of secretion of thyroxine and triiodothyronine.
4. Prolactin (PRL):
 It promotes mammary gland development and milk production.

5. Follicle-stimulating hormone (FSH).

6. luteinizing hormone (LH).
 FSH and LH control gonadal growth and hormones, so they are
collectively called gonadotropin hormones.
 Anterior Pituitary

FSH & LH GH TSH Prolactin ACTH

+ + + + +
Thyroid Mammary Adrenal
Gonads Most tissues
gland glands cortex

 estrogen;
 protein synthesis; + T4; + milk;  glucocorticoids
progeterone;
 Lipolysis; & + T3 + breast
 testosterone development
 blood glucose +thyroid
+ gametes; growth
+ ovulation;
+ corpus Lut.
THE POSTERIOR PITUITARY
HORMONES
 These are two peptide hormones.

 They are synthesized in the supraoptic and paraventricular nuclei of the

hypothalamus.
 These hormones are:

1. Antidiuretic hormone (ADH):

 For water reabsorption.

2. Oxytocin(OTC):
 For milk ejection.
GROWTH HORMONE (GH)
 Characteristics of GH:

 It also called somatotropic hormone or somatotropin.

 Is polypeptide hormone.

 The half-life is 6–20 min.

 Secreted in a pulsatile pattern with bursts of secretion occurring

approximately every 2 hours.
 It’s secretion decreases slowly after adolescence.
CONTROL OF GH SECRETION
Stimulate Growth Hormone
Secretion
 Decreased blood glucose
 Decreased blood free fatty acids
 Increased blood amino acids
 Starvation or fasting, protein deficiency
 Stress.
 α-Adrenergic agonists
 Testosterone, estrogen, GABA
 Deep sleep (Non REM)
 GHRH
 Ghrelin
Inhibit Growth Hormone
Secretion
 Increased blood glucose
 Increased blood free fatty acids
 GHIH (somatostatin)
 Growth hormone (exogenous)
 Somatomedins (insulin-like growth factors)
 Aging
 Obesity
 β-Adrenergic agonists
GROWTH HORMONE ACTION(FUNCTION)
1. Promotion of growth of many body tissues directly and indirectly.
a. Direct growth:
 Occurs in most tissues by increasing the sizes of the cells and increased
mitosis.
b. Indirect growth:
 Occurs in bone and cartilage through somatomedin C (insulin like growth
factor-1(IGF-1) which produces mainly by liver under the effect of GH as
follow:
i. Before puberty:
 The long bones grow in length at the epiphyseal cartilages by deposition
of new chondrocytes, followed by its conversion into osteogenic cells
(new bone).
ii. Within and after puberty:
 Deposition of osteoblasts on bone periosteum with the same time action of
osteoclast.
2. Metabolism:
a. Metabolism of CHO:
 It has diabetogenic effect, it decreases carbohydrate utilization by:

i. Decreases glucose uptake in muscles and adipose tissues.

ii. Increases glucose production by the liver (gluconeogenesis and
glycogenolysis).
 NB:

 Growth hormone stimulates insulin secretion indirectly because it

decreases glucose uptake in the muscles and adipose tissues which leads
to hyperglycemia, hyperglycemia is the main stimulus of insulin.
 Growth hormone also stimulate insulin secretion directly.
b. Metabolism of protein:
 It stimulates protein synthesis (anabolic effect)by:

i. Enhancement of amino acid transport through the cell membranes to

inside.
ii. Stimulating transcription and translation.
iii. Decreased catabolism of protein and amino acids.
 NB:

 Stimulation of protein synthesis exerts +ve nitrogen balance, so, it decreases the
level of blood urea and amino acids.
c. Metabolism of fat:
i. Release of fatty acids from adipose tissue (lipolysis).
ii. Enhances the conversion of fatty acids to acetyl coenzyme A (acetyl-CoA)
for energy utilization(ketogenic effect).
 NB:

 GH increases both glucose and FFAs in plasma, but, it prevents utilization of

glucose by antagonizing the effects of insulin, so, it shifts the metabolism
towards utilization of FFAs and sparing glucose as a source of energy for the
brain.
3. Effect on electrolytes:
a. GH increases absorption of calcium and phosphate in the intestine
(through activation of vitamin D).
b. Decreases excretion of sodium and potassium by the kidney.
4. Lactogenic effect:
 It produces milk (similar in chemical structure to prolactin).

NB:
 Insulin and carbohydrate are necessary for the growth-promoting action of
growth hormone.
 Excessive secretion of GH lead to excessive fatty acids formation and in this
lead to:
 Formation of acetoacetic acid by the liver which is ketone body.

 Fatty liver.
ABNORMALITIES OF GROWTH
HORMONE SECRETION
1. GH excesses:
a. Before puberty:
 It causes gigantism with this features:

i. Tall stature.
ii. Large viscera.
iii. Hyperglycemia.
iv. Constant head ache.
GIGANTISM
b. After puberty:
 It causes acromegaly with these features:

i. Increase in size of frontal bone, lower jaw, hands and feet(acral).

ii. Kyphosis (extreme curvature of upper back –thoracic spine).
iii. Large viscera.
iv. Hyperglycemia.
v. Hypertension.
vi. Headache.
vii. Visual disturbance (bitemporal hemianopia).
ACROMEGALY
2. GH deficiency:
a. Before puberty:
 It is caused by pituitary tumor or defect in GH receptors.

 It causes dwarfism (short stature) with intact mental function.

b. After puberty:
 It causes acromicria which is characterized by:

i. Atrophy of the extremities of the body.

ii. Lethargy.
iii. Obesity.
iv. Loss of sexual functions.
DWARFISM
Thanks