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Acromegaly - Bio Presentation

Negative Feedback Loop - Someone suffers from Acromegaly

Srishti H

on 1 June 2011

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Transcript of Acromegaly - Bio Presentation

Acromegaly stimulus receptor regulator Effector Response Feedback Acromegaly Caused by:
Excess production of GH from a benign adenoma tumour in the anterior pituitary IGF-I = "Insulin Like Growth Factors", which are
Secreted by the liver cells (in response to GH) into the blood to act on the bones
Stimulate cell division in the growth plates, causing the elongation of the skeleton (long bones) Somatostatin injected into the patient is carried
by the blood to the anterior pituitary, inhibiting the secretion of the growth hormone, which in turn inhibits the secretion of IGF-1 by the liver cells. Decrease in Growth Hormone levels, which decreases IGF-1 levels. In normal conditions:
High levels of GH are recognized by GHRH secreting cells.
High levels of GH also results in high levels of IGF-1. Thus, GH is also recognized by IGF-1 secreting cells in the liver. Too much of GH levels
in the blood, resulting in an increase in IGF-1 levels. Growth Hormone Insulin-Like Growth Factor GHRH & IGF-I Secreting Cell Growth Hormone-Releasing Hormone Under normal conditions:
High levels of GH would have inhibited GHRH, resulting in a decrease in the secretion of GH.
High levels of IGF-1 would have aslo inhibited the secretion of growth hormone & also stimulated the secreation of somatostatin.
Thus, in normal conditions GHRH, IGF-1 and somatostatin would've played the role of a Regulator. Once the somatostatin injected into the blood gets used up to control the growth hormone levels. Somatostatin Analogue (SSA) medication Pituitary Gland Amplifier GHRH and IGF-1 secreting cells are the receptors under normal conditions
They must also play the role of receptors under abnormal conditions & recognize the high levels of GH in the bloodstream. Somatostatin acts as the main regulator amongst these three regulators as its main function is to inhibit the secretion of GH by the anterior lobe of the pituitary. However, in abnormal conditions:
GH secretion cannot be inhibitted by GHRH or byIGF-I because the GH is produced by the adenoma tumour
The somatostatin produced by the hypothalamus is not enough to inhibit GH secretion An external regulator has to be injected; a somatostatin analogue (SSA) medication
(drugs include: Octreotide & Lanreotide)
Are synthetic versions of the brain hormone somatostain
compounds that bind to one or more somtostatin receptors suppressing GH production Attempts to act like Somatostatin which is a growth hormone release-inhibiting hormone secreted by the hypothalamus This causes the whole cycle to repeat itself. The somatostantin analog injection needs to be taken by the patient at regular intervals to keep the growth hormone levels under control. The inhibition on the secretion of the growth hormone gets lifted & the anterior lobe of the pituitary once again begins to produce too much of somatotropin as a result of the benign tumor. The receptor (IGF-1 secreting cells in the liver), regulator (somatostatin analogue) and the connecting pathways require only small amounts of energy supplied by ATP to operate. The effector (anterior lobe of the pituitary gland) amplifies the energy by using large amounts of energy from ATP in order to act on the appropriate target cells to reduce the levels of somatotropin and in turn the IGF-1. A serious condition of abnormal growth of the hands, feet, and face, caused by a tumor of the pituitary gland (an adenoma), which overproduce and secrete an excessive amount of Growth Hormone (GH). In a normal body:
Fusion of growth plates of the long bones occurs after puberty so that development of excessive GH production in adults does not result in increased height. In a body infected with acromegaly:
Prolonged exposure to excess GH before fusion of the growth plates causes increased growth of the long bones and increased height.
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