Pituitary gland is also known as hypophysis. It is a small gland that lies at the base of skull.

It is connected with hypothalamus by pituitary stalk or hypophyseal stalk.

Pituitary gland is situated at the base of skull.

It is connected with hypothalamus by the pituitary or hypophyseal stalk.

Pituitary gland is divided into two portions:

1. Anterior pituitary or adenohypophysis.
2. Posterior pituitary or neurohypophysis.

Though anterior pituitary and posterior pituitary are situated in close approximation, both are entirely different in their development, structure and function.

Each division of pituitary gland develops from different sources.

Anterior Pituitary

Anterior pituitary is ectodermal in origin and develops from the pharyngeal epithelium as an upward growth known as Rathke pouch.

Posterior Pituitary

Posterior pituitary is neuroectodermal in origin and arises from hypothalamus as a downward diverticulum.

Rathke pouch and downward diverticulum from hypothalamus grow towards each other and meet in midway between roof of buccal cavity and base of brain. There, both structures lie close together.

Transport of Hypothalamic Hormones

Hormones from hypothalamus are transported to anterior pituitary through hypothalamo-hypophyseal portal blood vessels.

Hormones from hypothalamus are transported to posterior pituitary through nerve fibers of the hypothalamo-hypophyseal tract.

Anterior pituitary is also known as the master gland because it regulates many other endocrine glands by its hormones.

Parts and Functional Histology

Anterior pituitary consists of three divisions:

1. Pars distalis.
2. Pars tuberalis.
3. Pars intermedia.

Functional Histology of Anterior Pituitary

Depending upon staining property, cells of anterior pituitary are classified into two types:

1. Chromophobe cells → cells which do not have granules and stain poorly. Chromophobe cells are not secretory in nature.
2. Chromophil cells → cells which contain large granules and are stained darkly. Chromophil cells are secretory in nature.

Classification of Chromophil Cells

A. Classification Depending Upon Staining Property

Depending upon staining property, chromophil cells are divided into two types:

1. Acidophilic cells or α-cells.
2. Basophilic cells or β-cells.

B. Classification Depending Upon Secretory Function

Depending upon secretory function, chromophil cells are classified into five types:

1. Somatotrophs → secrete growth hormone.
2. Corticotrophs → secrete adrenocorticotropic hormone.
3. Thyrotrophs → secrete thyroid stimulating hormone.
4. Gonadotrophs → secrete follicle stimulating hormone and luteinizing hormone.
5. Lactotrophs → secrete prolactin.

Somatotrophs and lactotrophs are acidophilic whereas other cells are basophilic cells.

Regulation of Secretion of Anterior Pituitary Hormones

Secretion of anterior pituitary hormones is regulated by hypothalamus. Hypothalamus secretes releasing and inhibitory hormones (factors), which are called neurohormones.

Neurohormones are transported from hypothalamus to anterior pituitary through hypothalamo-hypophyseal portal vessels.

Releasing and Inhibitory Hormones Secreted by Hypothalamus

1. Growth hormone-releasing hormone (GHRH) → stimulates the release of GH.
2. Growth hormone-releasing polypeptide (GHRP) → stimulates the release of GHRH and GH.
3. Growth hormone-inhibitory hormone (GHIH) or somatostatin → inhibits GH release.
4. Thyrotropin-releasing hormone (TRH) → stimulates release of TSH.
5. Corticotropin-releasing hormone (CRH) → stimulates release of ACTH.
6. Gonadotropin-releasing hormone (GnRH) → stimulates release of gonadotropins, FSH and LH.
7. Prolactin-inhibitory hormone (PIH) → inhibits prolactin secretion.

Hormones Secreted by Anterior Pituitary

Anterior pituitary secretes six hormones:

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 interstitial cell stimulating hormone (ICSH) in males.
6. Prolactin.

In addition, the hormone β-lipotropin is found to be secreted by anterior pituitary.

Tropic Hormones

First five hormones of anterior pituitary stimulate other endocrine glands. Growth hormone also stimulates the secretory activity of liver and other tissues. Therefore, these five hormones are called tropic hormones.

Prolactin is concerned with milk secretion.

Gonadotropic Hormones

FSH and LH are together called gonadotropic hormones or gonadotropins because of their action on the gonads.

General Information

Source of Secretion

Growth hormone (GH) is secreted by somatotrophs, which are the acidophilic cells in anterior pituitary.

Chemistry, Blood Level and Daily Output

GH is protein in nature, having a single chain polypeptide with 191 amino acids.

Its molecular weight is 21,500.

Basal level of GH concentration in blood of normal adult is up to 300 ng/dL.

In children, it is up to 500 ng/dL.

Daily output of GH in adults is 0.5 to 1.0 mg.

Transport

Growth hormone is transported in blood by growth hormone-binding proteins (GHBPs).

Half-life and Metabolism

Half-life of circulating growth hormone is about 20 minutes.

It is degraded in liver and kidney.

Actions of Growth Hormone

Actions on Growth

Growth hormone is responsible for growth of almost all tissues of the body, which are capable of growing.

It increases size of the cells.

It also increases number of cells by accelerating mitotic division.

GH also causes differentiation of certain types of cells like bone cells and muscle cells.

Actions on Metabolism

GH acts on metabolism of all three major types of foodstuffs in the body, viz. proteins, fats and carbohydrates.

GH increases synthesis of proteins, mobilization of lipids and conservation of carbohydrates.

Action on Protein Metabolism

GH accelerates synthesis of proteins by:

1. Increasing amino acid transport through cell membrane.
2. Increasing ribonucleic acid (RNA) translation. Because of this, ribosomes are activated and more proteins are synthesized.
3. Increasing transcription of DNA to RNA. RNA, in turn, accelerates the synthesis of proteins in the cells.
4. Decreasing catabolism of protein. GH inhibits breakdown of cellular protein and helps in building up of tissues.
5. Promoting anabolism of proteins indirectly by causing release of insulin from β-cells of islets of pancreas, which has anabolic effect on proteins.

Action on Fat Metabolism

GH mobilizes fats from adipose tissue. Because of this action, concentration of fatty acids increases in body fluids. Fatty acids are used for production of energy by the cells. So, proteins are spared.

During utilization of fatty acids for production of energy, a lot of acetyl coenzyme A is produced by liver and released into body fluids, leading to ketosis.

Sometimes excess mobilization of fat from adipose tissue causes accumulation of fat in liver, resulting in fatty liver.

Action on Carbohydrates

Major action of GH on carbohydrates is the conservation of glucose.

Effects of GH on carbohydrate metabolism are:

1. Decrease in peripheral utilization of glucose for production of energy.
2. Increase in formation of glycogen in cells. Since glucose is not utilized for energy production by cells, it is converted into glycogen which is deposited in the cells.
3. Decrease in uptake of glucose by the cells. As deposition of glycogen increases, cells become saturated with glycogen. Because of this, no more glucose can enter the cells. So, blood glucose level increases.

Diabetogenic Effect of GH

Hypersecretion of GH increases blood glucose level enormously. Increased blood sugar stimulates β-cells in the islets of Langerhans in pancreas continuously and increases insulin secretion.

In addition to this, GH also stimulates the β-cells of islets of pancreas directly and causes secretion of insulin.

Because of excess stimulation, β-cells are burnt out at one stage. This causes deficiency of insulin, which leads to true diabetes mellitus of full-blown diabetes mellitus. This effect is called the diabetogenic effect of GH.

Action on Bones

In embryonic stage, GH is responsible for differentiation and development of bone cells.

In later stages, GH increases growth of the skeleton. It increases both length and thickness of the bones.

In bones, GH increases:

1. Protein synthesis by chondrocytes and osteogenic cells.
2. Multiplication of chondrocytes and osteogenic cells.
3. Formation of new bones by converting chondrocytes into osteogenic cells.
4. Calcium absorption from intestine. By this, GH enhances availability of calcium for mineralization of bone matrix.

Effect of GH on Length of Bones

GH increases length of the bones until epiphysis fuses with shaft of bone. Normally, fusion occurs at puberty.

After epiphyseal fusion, length of the bones cannot be increased. However, GH stimulates the osteoblasts strongly. So, the bone continues to grow in thickness throughout life. Particularly the membranous bones such as jaw bone and skull bones become thicker under the influence of GH.

Mode of Action of GH on Bones and Metabolism

GH acts on bones, growth and protein metabolism through a substance called somatomedin, which is secreted by liver. GH stimulates the liver to secrete somatomedin.

Somatomedin

Somatomedin is a polypeptide.

Somatomedin is of two types:

1. Insulin-like growth factor-I (IGF-I), which is also called somatomedin C.
2. Insulin-like growth factor-II.

Among the two somatomedins, somatomedin C (IGF-I) is responsible for the action of GH on bones and metabolism.

Regulation of GH Secretion

Secretion of GH is regulated by hypothalamus and feedback control.

Role of Hypothalamus in the Secretion of GH

Hypothalamus regulates GH secretion by releasing three hormones:

1. Growth hormone releasing hormone (GHRH) → increases secretion of GH by stimulating somatotrophs of anterior pituitary.
2. Growth hormone releasing polypeptide (GHRP) → promotes release of GHRH from hypothalamus and GH from pituitary.
3. Growth hormone inhibitory hormone (GHIH) or somatostatin → inhibits secretion of GH.

Above hormones are transported from hypothalamus to anterior pituitary through hypothalamo-hypophyseal portal blood vessels.

Factors Increasing GH Secretion

1. Hypoglycemia.
2. Fasting.
3. Starvation.
4. Exercise.
5. Stress and trauma.
6. Initial stages of sleep.

Factors Decreasing GH Secretion

1. Hyperglycemia.
2. Increase in free fatty acids in blood.
3. Later stages of sleep.

Feedback Control

GH secretion is under negative feedback control. Hypothalamus releases GHRH and GHRP, which promote release of GH from anterior pituitary.

GH acts on various tissues. It also activates the liver cells to secrete somatomedin C (IGF-I).

Now, somatomedin C acts in three ways:

1. It increases release of GHIH from hypothalamus. GHIH in turn inhibits release of GH from pituitary.
2. Somatomedin also inhibits secretion of GHRP from hypothalamus.
3. It acts on pituitary directly and inhibits secretion of GH.

GH inhibits its own secretion by stimulating the release of GHIH from hypothalamus. This type of feedback is called short-loop feedback control.

Similarly, GHRH inhibits its own release by short-loop feedback control.

Whenever blood level of GH decreases, GHRH is secreted from hypothalamus. It in turn causes secretion of GH from pituitary.

Thyroid-stimulating Hormone (TSH)

TSH is necessary for growth and secretory activity of thyroid gland.

Adrenocorticotropic Hormone (ACTH)

ACTH is necessary for structural integrity and secretory activity of adrenal cortex.

Follicle-stimulating Hormone (FSH)

Actions in Males

In males, FSH acts along with testosterone and accelerates the process of spermatogenesis.

Actions in Females

1. It is responsible for development of graafian follicle from primordial follicle.
2. It stimulates the theca cells of graafian follicle and causes secretion of estrogen.
3. It promotes aromatase activity in granulosa cells resulting in conversion of androgens into estrogen.

Luteinizing Hormone (LH)

Actions in Males

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 secretion of testosterone from Leydig cells.

Actions in Females

1. LH causes maturation of vesicular follicle along with follicle stimulating hormone.
2. It induces synthesis of androgens from theca cells of growing follicle.
3. It is responsible for ovulation.
4. It is necessary for formation of corpus luteum.
5. It stimulates secretory functions of corpus luteum.

Prolactin

Prolactin is necessary for the final preparation of mammary glands for production and secretion of milk.

β-Lipotropin

β-lipotropin mobilizes fat from adipose tissue and promotes lipolysis (breakdown of lipids).

Parts and Functional Histology

Posterior pituitary consists of three divisions:

1. Pars nervosa or infundibular process.
2. Neural stalk or infundibular stem.
3. Median eminence.

Pars tuberalis of anterior pituitary and the neural stalk of posterior pituitary together form the hypophyseal stalk.

Functional Histology

Posterior pituitary is made up of nerve cells called pituicytes and unmyelinated nerve fibers.

Pituicytes act as supporting cells and do not secrete any hormone.

Posterior pituitary also has numerous blood vessels, hyaline bodies, neuroglial cells and mast cells.

Hormones of Posterior Pituitary

Posterior pituitary hormones are:

1. Antidiuretic hormone (ADH) or vasopressin.
2. Oxytocin.

Source of Secretion of Posterior Pituitary Hormones

Posterior pituitary does not secrete any hormone. ADH and oxytocin are synthesized in the hypothalamus.

ADH is synthesized mainly by the supraoptic nucleus of hypothalamus.

Oxytocin is synthesized mainly by the paraventricular nucleus of hypothalamus.

From hypothalamus, both hormones are transported to posterior pituitary through nerve fibers of the hypothalamo-hypophyseal tract by means of axonic flow.

In the posterior pituitary, the hormones are stored at the nerve endings. Whenever impulses from hypothalamus reach the posterior pituitary, the hormones are released from nerve endings into circulation. Hence, ADH and oxytocin are called neurohormones.

General Information

Source of Secretion of ADH

Antidiuretic hormone (ADH) is secreted mainly by supraoptic nucleus of hypothalamus. It is also secreted by paraventricular nucleus in small quantity.

From here, this hormone is transported to posterior pituitary through the nerve fibers of hypothalamo-hypophyseal tract by means of axonic flow.

Chemistry and Half-life of ADH

Antidiuretic hormone is a polypeptide containing 9 amino acids. Its half-life is 18 to 20 minutes.

Actions of ADH

Major function of ADH is retention of water by acting on kidneys.

It increases facultative reabsorption of water from distal convoluted tubule and collecting duct.

ADH increases water reabsorption in the tubular epithelial membrane by regulating water channel proteins called aquaporins through V2 receptors.

Vasopressor Action of ADH

In large amount, ADH shows vasoconstrictor action in all parts of the body.

Due to vasoconstriction, the blood pressure increases.

ADH acts on blood vessels through V1A receptors.

Regulation of Secretion of ADH

Secretion of ADH depends upon volume of body fluid and osmolarity of the body fluids.

Potent Stimuli for ADH Secretion

1. Decrease in ECF volume.
2. Increase in osmolar concentration in ECF.

Role of Osmoreceptors

Osmoreceptors are the receptors which give response to change in osmolar concentration of blood.

Osmoreceptors are situated in the hypothalamus near supraoptic and paraventricular nuclei.

When osmolar concentration of blood increases, the osmoreceptors are activated and stimulate supraoptic and paraventricular nuclei.

Both the nuclei send motor impulses to posterior pituitary through the nerve fibers and cause release of ADH.

ADH causes reabsorption of water from the renal tubules. This increases volume of ECF and restores the normal osmolarity.

General Information

Source of Secretion of Oxytocin

Oxytocin is secreted mainly by paraventricular nucleus of hypothalamus. It is also secreted by supraoptic nucleus in small quantity.

Oxytocin is transported from hypothalamus to posterior pituitary.

In posterior pituitary, oxytocin is stored in nerve endings of hypothalamo-hypophyseal tract.

When suitable stimuli reach posterior pituitary from hypothalamus, oxytocin is released into blood.

Oxytocin is secreted in both males and females.

Chemistry and Half-life of Oxytocin

Oxytocin is a polypeptide having 9 amino acids. It has a half-life of about 6 minutes.

Actions of Oxytocin in Females

In females, oxytocin acts on mammary glands and uterus.

Action of Oxytocin on Mammary Glands

It causes ejection of milk from the mammary glands.

Ducts of the mammary glands are lined by myoepithelial cells. Oxytocin causes contraction of myoepithelial cells and squeezes the milk from alveoli of mammary glands to the exterior through duct system and nipple.

The process by which milk is ejected from the alveoli of mammary glands is called milk ejection reflex or milk let-down reflex.

Milk Ejection Reflex

Plenty of touch receptors are present on the mammary glands, particularly around nipple.

When the infant suckles mother’s nipple, touch receptors are stimulated and impulses are discharged.

Impulses from these receptors are carried by somatic afferent nerve fibers and reach the paraventricular and supraoptic nuclei of hypothalamus.

Hypothalamus sends impulses to posterior pituitary through hypothalamus and causes release of oxytocin into blood.

Oxytocin causes contraction of myoepithelial cells in mammary glands and milk ejection occurs.

Since this reflex is initiated by nervous factors and completed by hormonal action, it is called a neuroendocrine reflex.

During this reflex, a large amount of oxytocin is released by positive feedback mechanism.

Action of Oxytocin on Uterus

Action on Pregnant Uterus

Throughout the period of pregnancy, oxytocin secretion is inhibited by estrogen and progesterone.

At the end of pregnancy, when secretion of these hormones decreases suddenly, secretion of oxytocin commences.

Oxytocin causes contraction of uterus and helps in expulsion of fetus.

During Labor

During labor, large quantity of oxytocin is released by means of positive feedback mechanism.

Oxytocin induces contraction of uterus, which in turn causes release of more amount of oxytocin.

Contraction of uterus during labor is also a neuroendocrine reflex.

Oxytocin also stimulates release of prostaglandins in placenta. Prostaglandins intensify the uterine contraction induced by oxytocin.

Action on Non-pregnant Uterus

Oxytocin causes uterine contraction during sexual intercourse.

Uterine contraction facilitates transport of sperms through female genital tract up to fallopian tube.

During sexual intercourse, receptors in vagina are stimulated. Impulses generated by vaginal receptors are transmitted by somatic afferent nerves to paraventricular and supraoptic nuclei of hypothalamus.

When these two nuclei are stimulated, oxytocin is released and transported by blood.

While reaching the female genital tract, the hormone causes antiperistaltic contractions of uterus towards the fallopian tube, which accelerates transport of sperms.

This is also a neuroendocrine reflex.

Action of Oxytocin in Males

In males, release of oxytocin increases during ejaculation.

It facilitates release of sperm into urethra by causing contraction of smooth muscle fibers in reproductive tract, particularly vas deferens.

Mode of Action of Oxytocin

Oxytocin acts on mammary glands and uterus by activating G-protein coupled oxytocin receptor.

Disorders of pituitary gland include hyperactivity and hypoactivity of anterior pituitary, hyperactivity and hypoactivity of posterior pituitary and hypoactivity of both anterior and posterior pituitary.

Disorders of Pituitary Gland

Hyperactivity of Anterior Pituitary

I. Gigantism

Gigantism is a pituitary disorder characterized by excess growth of the body.

Affected subjects look like giants with average height of about 7 to 8 feet.

Cause of Gigantism

Gigantism is due to hypersecretion of GH in childhood or preadolescence, i.e. before fusion of epiphysis of bone with shaft.

It occurs due to pituitary tumors.

Signs and Symptoms of Gigantism

1. General overgrowth of the person leads to development of a huge stature with a height of more than 7 or 8 feet. Limbs are disproportionately long.
2. Giants are hyperglycemic and they develop glycosuria and pituitary diabetes. Hyperglycemia causes constant stimulation of β-cells of islets of Langerhans in pancreas and release of insulin.
3. Over activity of β-cells of Langerhans leads to degeneration of these cells and deficiency of insulin, ultimately diabetes mellitus develops.
4. Pituitary tumor itself causes constant headache.
5. Pituitary tumor also causes visual disturbances. It compresses the lateral fibers of optic chiasma leading to bitemporal hemianopia.

II. Acromegaly

Acromegaly is the pituitary disorder characterized by enlargement, thickening and broadening of bones, particularly in the extremities of the body.

Cause of Acromegaly

Acromegaly is due to hypersecretion of GH in adults after fusion of epiphysis with shaft of the bone.

Hypersecretion of GH is due to adenomatous tumor of anterior pituitary involving the acidophilic cells.

Signs and Symptoms of Acromegaly

1. Striking facial features such as protrusion of supraorbital ridges, broadening of nose, thickening of lips, thickening and wrinkles formation on forehead, and prognathism (protrusion of lower jaw) are developed.
2. Face with above features is called acromegalic or guerrilla face.
3. Hands and feet are enlarged.
4. Kyphosis (bowing of spine: extreme curvature of upper back; thoracic spine).
5. Scalp is thickened and thrown into folds or wrinkles like bulldog scalp.
6. There is general overgrowth of body hair.
7. Visceral organs such as lungs, heart, liver and spleen are enlarged.
8. Thyroid gland, parathyroid glands and adrenal glands show hyperactivity.
9. Hyperglycemia and glucosuria occur resulting in diabetes mellitus.
10. Hypertension.
11. Headache.
12. Visual disturbance (bitemporal hemianopia) is developed.

III. Acromegalic Gigantism

It is a rare disorder with symptoms of both gigantism and acromegaly.

Hypersecretion of GH in children before fusion of epiphysis of the bones causes gigantism.

If hypersecretion of GH is continued even after fusion of epiphysis, the symptoms of acromegaly also appear.

IV. Cushing’s Disease

This is another rare disease characterized by obesity.

Causes of Cushing’s Disease

Cushing’s disease develops by basophilic adenoma of adenohypophysis. It increases the secretion of adrenocorticotropic hormone, which in turn stimulates the adrenal cortex to release cortisol.

Cushing’s disease also develops by hyperplasia or tumor of adrenal cortex. Usually, the disorder due to pituitary cause is called Cushing’s disease and when due to adrenal cause, it is called Cushing’s syndrome.

Hypoactivity of Anterior Pituitary

I. Dwarfism

It is a pituitary disorder in children characterized by stunted growth.

Causes of Dwarfism

Hyposecretion of GH in infancy or early childhood causes dwarfism.

Hyposecretion of GH occurs in the following conditions:

1. Deficiency of GHRH from hypothalamus.
2. Deficiency of somatomedin C.
3. Atrophy or degeneration of acidophilic cells in anterior pituitary.
4. Tumor of chromophobes: a nonfunctioning tumor which compresses and destroys the normal cells secreting GH.
5. Panhypopituitarism: dwarfism due to this disease is associated with other symptoms which occur due to deficiency of other pituitary hormones.

Signs and Symptoms of Dwarfism

1. Primary symptom of hypopituitarism in children is stunted skeletal growth. Maximum height of anterior pituitary dwarf at the adult age is only about 3 feet.
2. Body proportions of different parts of the body are almost normal. Only head becomes slightly larger in relation to the body.
3. Pituitary dwarfs do not show any deformity and their mental activity is normal with no mental retardation.
4. Reproductive function is not affected if there is only GH deficiency. However, in panhypopituitarism, dwarfs do not obtain puberty due to deficiency of gonadotropic hormones.

Other Types of Dwarfism

II. Acromicria

This is a rare pituitary disorder in adults characterized by atrophy of extremities of the body.

Causes of Acromicria

Hyposecretion of GH in adults causes acromicria.

Hyposecretion of GH occurs in the following conditions:

1. Deficiency of GH releasing hormone from hypothalamus.
2. Atrophy or degeneration of acidophilic cells in anterior pituitary.
3. Tumor of chromophobes: a nonfunctioning tumor which compresses and destroys the normal cells which secrete GH.
4. Panhypopituitarism: acromicria is associated with other symptoms due to deficiency of other pituitary hormones.

Signs and Symptoms of Acromicria

1. Atrophy and thinning of extremities of body (hands and feet) are the major symptoms in acromicria.
2. Acromicria is mostly associated with hypothyroidism and hyposecretion of adrenocortical hormones.
3. Affected person becomes lethargic and obese.
4. Sexual functions are lost.

III. Simmond’s Disease

Simmond’s disease is another rare pituitary disease. It is also called pituitary cachexia.

Cause of Simmond’s Disease

Simmond’s disease occurs mostly in panhypopituitarism.

Symptoms of Simmond’s Disease

1. Major feature is the rapidly developing senile decay. Thus, a 30-years-old person looks like a 60-years-old person.
2. There is loss of hair over the body and loss of teeth.
3. Skin over face becomes dry and wrinkled. So, there is shrunken appearance of facial features. It is the most common feature of this disease.

Hyperactivity of Posterior Pituitary

Syndrome of Inappropriate Hypersecretion of Antidiuretic Hormone (SIADH)

SIADH is a condition characterized by loss of sodium through urine due to hypersecretion of ADH.

Cause of SIADH

SIADH occurs due to cerebral tumors, lung tumors and lung cancers because the tumor cells and cancer cells secrete ADH.

In normal conditions ADH decreases urine output by inducing facultative reabsorption of water from distal convoluted tubule and collecting duct. So, concentrated urine is formed with more sodium and other ions and less water.

This decreases osmolarity of plasma making it hypotonic.

Hypotonic plasma inhibits ADH secretion resulting in restoration of plasma osmolarity.

However, ADH secreted from tumor or cancer cells is not inhibited by hypotonic plasma. So, there is continuous loss of sodium resulting in persistent plasma hypotonicity.

Signs and Symptoms of SIADH

1. Loss of appetite.
2. Weight loss.
3. Nausea and vomiting.
4. Headache.
5. Muscle weakness, spasm and cramps.
6. Fatigue.
7. Restlessness and irritability.
8. Convulsions and coma and death in severe conditions.

Hypoactivity of Posterior Pituitary

Diabetes Insipidus

Diabetes insipidus is a posterior pituitary disorder characterized by excess excretion of water through urine.

Causes of Diabetes Insipidus

This disorder develops due to deficiency of ADH which occurs in the following conditions:

1. Lesion (injury) or degeneration of supraoptic and paraventricular nuclei of hypothalamus.
2. Lesion in hypothalamo-hypophyseal tract.
3. Atrophy of posterior pituitary.
4. Inability of renal tubules to give response to ADH. Such condition is called nephrogenic diabetes insipidus.

Signs and Symptoms of Diabetes Insipidus

1. Polyuria

Polyuria is the increased urinary output with frequent voiding. It is due to water diuresis.

Daily output of urine varies between 4 and 12 liters.

In the absence of ADH, water is not reabsorbed from the renal tubules and collecting duct leading to loss of water through urine.

2. Polydipsia

Polydipsia is intake of excess water. Loss of water due to polyuria stimulates the thirst center of hypothalamus resulting in intake of large quantity of water.

3. Dehydration

In some cases, thirst center in the hypothalamus is also affected by lesion. This decreases thirst sensation in these patients. So, loss of water through urine is not compensated. Thus, dehydration develops which may lead to death.

Hypoactivity of Anterior and Posterior Pituitary

Dystrophia Adiposogenitalis

Dystrophia adiposogenitalis is a disease characterized by obesity and hypogonadism affecting mainly adolescent boys.

It is also called Fröhlich’s syndrome or hypothalamic eunuchism.

Causes of Dystrophia Adiposogenitalis

It is due to hypoactivity of both anterior pituitary and posterior pituitary.

Common cause of this disease is a tumor in pituitary gland and hypothalamic regions that are concerned with food intake and gonadal development.

Symptoms of Dystrophia Adiposogenitalis

Obesity is the common feature of this disorder. Due to abnormal stimulation of feeding center, the person overeats and becomes obese.

Obesity is accompanied by sexual infantilism (failure to develop secondary sexual characters) or eunuchism.

Dwarfism occurs if the disease starts in growing age.

This disease develops in adults also. Major symptoms in adults are obesity and loss of sex organs. Other features are behavioral changes and loss of vision. Some patients develop diabetes insipidus.

Panhypopituitarism

Panhypopituitarism is a condition caused by hyposecretion of all hormones of pituitary gland.

Symptoms of dwarfism and acromicria develop during panhypopituitarism.