Homeostasis is dependent on the precision of the organs and organ system regulations in the body. The nervous system works together with the nervous system to regulate and offer coordination to the activities of almost all other parts of the body. Just like the nervous system, the endocrine system uses chemical known as hormones to communicate with other parts of the body. A hormone molecule is a specific messenger that is synthesized and released by specialized cells known as an endocrine gland. The endocrine glands are ductless with the hormones being released into the blood directly and taken to the target organs where they perform their functions. This is unlike the digestive glands that have ducts and, therefore, release their content in the site of action through their duct. These kinds of glands are known as exocrine glands (Marieb and Hoehn). The glands that release hormones that affect cells that are near their point of release are known as paracrine glands (Princeton).
The shape of each hormone is specifically designed so that it can be recognized by their target cells. Most of the hormones are produced in antagonistic pairs having opposite effects on the organs where they target. For instance, glucagon and insulin result to opposite effects on the control of blood sugar by the liver. Insulin works by lowering the level of sugar in the body while glucagon works to increase the glucose level. Much regulation by hormone is dependent on a feedback loops in order to maintain proper balance and homeostasis (Carter).
Generally, hormones are grouped into three classes based on their chemical structure and not based on their function. These hormones include steroid hormones that include prostaglandins that have important functions in female, amino acid derivatives such as epinephrine, and peptide hormones such as insulin. When the endocrine system is not able to function in a proper manner, there is a chance that conditions will deviate from the normal homeostasis. Some of the disorders that may result from abnormal functioning of the endocrine system include Addison’s disease and insulin-dependent diabetes (Seeley, Stephens and Tate).
Addison’s disease occurs as a result of abnormal low levels of hormones such as aldosterone and cortisol. Although the actual cause is not known, Addison’s disease is suspected to be an autoimmune disease where the defense mechanisms in the body destroy inappropriately the adrenal cortex. Other conditions such as tuberculosis, fungal infections, cancer and adrenal hemorrhage may also result to damage in the adrenal cortex and may thus result in Addison’s disease. Glucocorticoids treatment may also cause the disease. Some of the symptoms that associated with Addison’s disease are weakness, anorexia, fatigue, weight loss, and increased skin pigmentation (Seeley, Stephens and Tate).
Normally, the cortisol that is produced by the adrenals is balanced at a specific level in the body by the hypothalamus in the brain and the pituitary gland. The adrenal glands are made up of an outer cortex and an inner medulla derived from two different embryonic tissues. The adrenal medulla comes from a neural crest cells that are also the source postganglionic neurons belonging to the sympathetic division. The adrenal cortex is made from mesoderm unlike most of the other glands that are derived from the epithelial tissue invaginations (Seeley, Stephens and Tate).
The balance is attained by the corticotropin-releasing hormone from the hypothalamus that triggers the pituitary gland to release releases a trigger hormone called cortiocotropin-releasing hormone (CRH) that signals the pituitary gland. The cortiocotropin-releasing hormone is usually released in response to hypoglycemia or stress through the hypothalamohypophysial portal system. The pituitary responds by sending out adrenocorticotropic hormone, which in turn goes to the adrenal glands causing it to produce cortisol. The binding of adrenocorticotropic hormone to the receptors that are bound on the membrane of the adrenal cortex cells cause a trigger that lead to the secretion of cortisol. To complete the cycle, cortisol that is released by the adrenal glands sends a signal back to the hypothalamus and pituitary causing these gland to reduce the release of their respective hormones (NIH).
The adrenal cortex when in normal conditions has massive functions that are reserved and are normally called upon when the body is under intensive stress. Some of these stressful moments include trauma, surgery, or serious infection. One of the most significant consequences when the body is suffering from Addison’s disease is that the body fails to adapt to the situations that are stressful by releasing the much needed cortisol. Absence of enough steroids during these situations may result lead to a state of shock, which is usually known as an Addisonian crisis. The Addisonian crisis is classified as a medical emergency. Destruction of adrenals may result in the adrenal failing to respond to the increased levels of adrenocorticotropic hormone (Figure 1).
Figure 1: Cortisol release and regulation pathway (Seeley, Stephens and Tate)
Addison's disease is usually treated by replacing or substituting cortisol using hydrocortisone tablets, which are synthetic glucocorticoids. If the disease has also affected aldosterone, it can be replaced using mineralocorticoid known as fludrocortisone acetate (Baker). Those patients who are in acute adrenal crisis need to undergo infusion of an isotonic solution of sodium chloride to restore the reduced body volume and correct the hypotension situation. Other patients may require supplementation of glucose and the precipitating cause need to be corrected whenever possible. Normally, the level of cortisol that is released by the adrenal gland is about 250-300 mg in a day. This amount should be given to a patient of Addison’s disease through continuous infusion. The infusion mode of administering hydrocortisol helps in maintaining the level of cortisol at a steady level. There is also need to monitor blood pressure, which is an indication of improvement and occurs within six hours after the hydrocortisone infusion is started (Griffing).
After 2-3 days, the dose is reduced to 100-150 mg and infused for a whole day without considering the clinical status of the patient. As far as the patient is being given a dose of hydrocortisone that is 100 mg or higher in 24 hours, there is no need to administer mineralocorticoid replacement. This is because the mineralocorticoid activity that is in the hydrocortisone contained in the dosage is enough. However, as the dose of hydrocortisol is being weaned, there is the need to replace the dose with mineralocorticoid at doses that are equal to the output of aldosterone by the adrenal gland. Fludrocortisone is mainly used in treating cerebral salt wasting and works by increasing the levels of sodium ions, which then result into an increase in the volume of blood in the body (Griffing).
Works Cited
Baker, Sarah J. What is Addison's disease? 2002. Online. 21 August 2013. <http://www.addisons.org.uk/info/addisons/page1.html>.
Carter, J. Stein. Endocrine System. 2004. Online. 21 August 2013. <http://biology.clc.uc.edu/courses/bio105/endocrin.htm>.
Griffing, George T. Addison Disease Treatment & Management. 2012. Online. 22 August 2013. <http://emedicine.medscape.com/article/116467-treatment>
Marieb, E. N. and K. Hoehn. Human anatomy and physiology. New York: Pearson Education, 2010. Print.
NIH. Adrenal Insufficiency and Addison's Disease. 2009. Online. 21 August 2013. <http://endocrine.niddk.nih.gov/pubs/addison/addison.aspx>.
Princeton. Exocrine gland. 2013. Online. 21 August 2013. <http://www.princeton.edu/~achaney/tmve/wiki100k/docs/Exocrine_gland.html>.
Seeley, R., T. D. Stephens and P. Tate. Anatomy and Physiology. 6th. New York: The McGraw Hill Companies, 2004. Print.
