Hyper and Hypopituitarism

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  • Topic: Hypothalamus, Hypopituitarism, Pituitary gland
  • Pages : 9 (2129 words )
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  • Published : October 5, 2012
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Hyper & Hypopituitarism
Hyperpituitarism is the result of excess secretion of adenohypophyseal trophic hormones. Hypopituitarism is the decreased secretion of one or more of the pituitary hormones. If there is decreased secretion of most pituitary hormones, this condition is called panhypopituitarism (pan meaning "all").

Historical Background
The pituitary was known by Galen, and various theories were proposed about its role in the body. In the late 19th century, acromegaly is caused by pituitary tumors was described. In 1914, Simmonds reported pituitary necrosis in a woman with severe puerperal sepsis caused hypopituitarism. In 1932, Cushing documented the presence of small pituitary adenomas with clinical features of adrenocortical hyperfunction. Most of the classic causes of hypopituitarism were described in the 20th century.

Anatomy of the pituitary gland
Pituitary gland has two distant parts such as anterior and posterior lobes. Between there is a small, relatively avasacular zone called the pars intermedia. This intermediate lobe is absent in human beings. Pituitary gland lies in the sella turcica at the base of the brain and is connected to the hypothalamus by the pituitary stalk.

Hormones of pituitary gland (Hypophysis)
Anterior pituitary (adenohypophysis) secretes thyroid stimulating hormone (TSH, thyrotropin), adrenocorticotropic hormone (ACTH, corticotropin), lutenizing hormone (LH), follicle stimulating hormone (FSH), prolactin and growth hormone (hGH).

Posterior pituitary (neurohypophysis) secretes arginine vasopressin (AVP) and oxytocin.
Intermediate lobe cells, corticotropes of the anterior pituitary, the hypothalamus and some other tissues synthesize pro-opio melano cortin (POMC). In the intermediate lobe, POMC is further hydrolysed into β-endohin, α - melanocyte stimulating hormone, corticotropin like intermediate lobe peptide and γ – LPH.

Hyperpituitarism is the result of excess secretion of adenohypophyseal trophic hormones. Causes
1.Pituitary adenoma (most common)
-Prolactinoma (60% of primary pituitary tumors)
-Growth hormone secreting adenoma (20 %)
-ACTH-secreting adenoma (10%)
-Thyrotropin – secreting pituitary adenoma (rare)
-Gonadotropin-secreting pituitary adenoma (rare)
2.Hyperplasia of adenohypophysis
3.Carcinoma of adenohypophysis
4.Secretion by non-pituitary tumours and
5.Some hypothalamic disorders

Anterior Pituitary Hyperfunction
Growth Hormone Excess
hGH excess produces gigantism (before epiphyseal closure) and acromegaly (after epiphyseal closure).

Gigantism and Acromegaly
Acromegaly and gigantism are virtually always secondary to pituitary adenoma. In some cases, it could be secondary to abnormal hypothalamic function. As a consequence, all body tissues grow rapidly including bones. If the condition occurs before epiphyseal closure (before puberty), height increases so that the person become a giant as tall as 8 feet.

In adults, growth hormone excess leads to acromegaly. It is characterized by local overgrowth of bone, particularly of the skull and mandible. Linear growth does not occur because of epiphyseal closure of long bones.

In acromegaly, hGH secretion is increased and its dynamic control is abnormal. Secretion remains episodic. But the number, duration and amplitude of secretory episodes are increased and they occur randomly throughout the 24 hour period. The characteristic nocturnal surge is absent and there are abnormal responses to suppresion and stimulation. Thus glucose suppressibility is lost and hGH stimulation by hypoglycaemia is usually absent. TRH and GnRH may cause hGH release, whereas they do not normally stimulate hGH secretion. Dopamine and dopamine agonists such as brompcriptine normally stimulate hGH secretion. But in 70 – 80 % of acromegalic patient, they suppress hGH secretion.

Most of the deleterious effects of chronic hGH...
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