Brief Introduction:
Pituitary Gland:
It is located in the center of the skull just behind the bridge of the nose. It is an important link between the nervous system and the endocrine system and releases many hormones which affect growth, sexual development, metabolism and the reproductive system. It has two distinct parts, the Anterior and the Posterior lobes, each of which releases different hormones which affect bone growth and regulate activity in other glands.
The Anterior lobe of the pituitary gland is the larger of the two glands. Blood supply to the anterior pituitary comes from the superior hypophyseal arteries, which are branches of the internal carotid arteries. These hypophyseal arteries supply the primary capillary plexuses of the hypothalamohypophyseal portal vessels, which travel down the pituitary stalk.
On the other hand, the Posterior pituitary develops from the neural tube of the embryo, it has the same embryogenic origin as the nervous system- hence the same neurohypophysis. It has direct nerve tract connections with the hypothalamus, mainly with the supraoptic nucleus and the paraventricular nuclei.
Hormones secreted by the Anterior Pituitary:
[Thyriod Stimulating Hormone] TSH
[Adrenocorticotrophic Hormone] ACTH
[Follicle Stimulating Hormone] FSH
[Lutenizing Hormone] LH
[Growth Hormone] GH
[Prolactine] PRL
Hormones secreted by the Posterior Pituitary:
[Antidiuretic Hormone] ADH
[Oxytocin]
Growth Hormone (GH)
Growth hormone (GH) is secreted through life. The name growth hormone is misleading, as it implies its secretion during the growth periods. It is a single-chain peptide of 191 amino acids, was first used therapeutically for treatment of pituitary dwarfism in 1958. GH is a part of the hypophyseal-pituitary axis. It is synthesized in somatotroph cells in response to binding of Growth-Hormone Releasing Hormone (GHRH) to its receptor, activating gene transcription by cyclic adenosine monophosphate- dependent mechanisms.
Its release from somatotroph cells is also regulated by both central and peripheral mechanisms. Centrally, its synthesis and release are promoted by GHRH and inhibited by somatostadin. Stress, excercise, malnutrition and anorexia also stimulate its secretion during the day. The release is counter-regulated by three negative feedback loops.
GH inhibits its own secretion by 3 mechanisms:
1- Acting on somatotroph cell generating IGF-1 locally that in turn inhibits the cell.
2- Inhibiting GHRH mRNA synthesis and GHRH release at the hypothalamic level.
3- Stimulating both mRNA levels and release of somatostatin.
GH Secretion:
The secretion of GH takes place in discrete pulses, so that basal levels are usually very low. The pattern of its secretion is found to occur as follows:
1. GH is released under conditions of lack of glucose.
2. Muscular exercise in the postabsorptive state results in GH secretion.
3. GH appears in postabsorptive phase following glucose intake.
4. Intake of protein or amino acids results in the secretion of GH.
5. During sleep GH is found to be released several times. The levels of these peaks are higher and occur with greater frequency in children than in adults.
6.Stress conditions, e.g. Due to trauma.
7.Glucagon, lysine-vasopressin and L-dopa have also been found to stimulate the release of GH. On the other hand, cortisol, Free Fatty Acids (FFAs), GH and glucose are found to inhibit its secretion.
Effects of the Hormone:
Aside from its general effect in causing growth, GH has many specific effects, including:
1. Increased rate of protein synthesis in all cells of the body.
2. Increased mobilization of Fatty Acids from adipose tissue causing an increase in the concentration of (FFAs) in blood; and the increased use of Fatty Acids for energy.
3. Decreased rate of glucose utilization throughout body.
The effects of GH on tissue growth are not direct but are believed to be mediated by certain growth factors, Somatomedins, secreted by the liver and possibly other tissues in response to stimulation of GH. Somatomedins promote cell proliferation and protein synthesis in their target cells.
When the Anterior pituitary is removed from a growing animal, it stops growing. Injection of GH into that animal results in the resumption of growth.
Mechanism of Action:
Attached Figure: Gh.
Abnormalities:
I- Deficiency:
Deficiency (Absence or reduced levels) of GH in chilhood results in retardation of somatic growth leading to DWARFISM. Pituitary Dwarf has a small body but normal head size and normally doesn't show mental retardation. As the child reaches adolescence, secondary sexual characteristics and the external genitalia fail to develop. In addition, patients may present with various degrees of adrenal insufficiency and hypothyroidism.
In certain individuals who lack only the gene for GH but have an otherwise normal pituitary, are short in stature. But sexual maturation and pregnancy may still occur. Deficiency in adult life is not fully understood.
Manifistations of GH deficiency may be expressed by unusual sensitivity to insulin and by fasting hypoglycemia.
II- Hypersecretion:
In adults with excessive growth hormone secretion, bone grow in width because it can't grow longer in length due to fusion of the epiphyseal plates. During Childhood and adolescence with pituitary or hypothalamic tumors, hypersecretion of GH leads to GIANTISM. The patient experiences rapid longitudinal growth and becomes a Giant.
Pituitary Giants are more than 8 feet tall. After somatic growth is completed, GH hypersecretion will not cause Giantism but thickening of bones and soft tissues this condition is termed ACROMEGALY.
Acromegaly is the abnormal growth of bones in digits, toes, mandible and back leading to a characteristic bodily deformity. Acromegalic patients exhibit enlargement of hands and feet, also have large visceral organs, particularly the tongue, liver and kidney. Facial features become coarse, and there's enlargment of the paranasal and frontal sinuses. Frontal bossing, prominence of the supraorbital ridges. Patients exhibit high basal GH levels too which can be tested further by the administration of oral glucose.
In Normal subjects the induction of hyperglycemia by oral glucose suppresses GH levels; while in Acromegalic patients or giants the induction of hyperglycemia by oral glucose fail to suppress GH levels.
Although, changes in facial features help diagnose the condition on simple observation.
By... SH.Y.O
References:
1. Concise Human Physiology, By: Sukkar.
2. El-Munshid & Ardawi Pathophysiology.
3. Clinical Concepts of Disease Processes, Fifth edition By: Price Wilson.
4. Internet:
www.science.mcmaster.ca, www.innerbody.com, www.medscape.com, www.fwkc.com
www.adam.com, www.msn.com, www.lprf.org
2. This will lead to 2 further mechanisms:
a- GTH Somatostatin.
b- GIH (-ve) --> Somatostatin.
Both act on the Somatotroph cell of Pituitary Gland.
3. This will lead to releasing GH which act on:
a- Growth Hormone --> Adipose Tissue.
b- Growth Hormone --> Liver.
4. Liver produces Somatomedins in response to the action of GH and the resuls will be:
1. Protein Formation.
2. Cell Proliferation.
3. Skeletal growth.
a- Acromegaly.
b- Dwarfism.
c- Giantism.
5. Adipose Tssue will act by inhancing ATP action on the Muscle cell.