Cushing’s Syndrome is a condition that results from chronic exposure to excessive amounts of glucocorticoids circulating in the blood stream for an extended period of time. The disease was first reported by Harvey Cushing over one hundred years ago, yet the condition still plagues endocrinologists today. Reasons for this difficulty include the vast amount of often vague symptoms that the syndrome presents, most of which are found in a plethora of other conditions as well, combined with the multiple forms that the condition can manifest itself. Symptoms of Cushings Syndrome include, but are not limited to, weight gain, hirutism, easy bruising, hypertension, acne, facial plethora, muscle weakness, striae, depression, slender extremities, prominent superclavicular and dorsal cervical fat pads (buffalo hump), and osteoporosis. Glucocorticoids have various effects on target cells that can help give reason to the symptoms that occur in Cushings syndrome. Glucocorticoids speed up the rates of glucose synthesis and glycogen formation, cause adipose tissue to release fatty acids into the blood, and cause other tissues to break down fatty acids acids and proteins. An anti-inflammatory response also occurs due to cortisol’s inhibition of white blood cells and other components of the immune system. The majority of cases of Cushings Syndrome are related to malfunctioning in the hypothalamo-pituitary-adrenal axis but there are a few cases in which the problem of origination is elsewhere in the body.
In a healthy individual, the hyptothalamus releases corticotropin- releasing hormone (CRH), which in turn signals the anterior lobe of the pituitary gland to release adrenocoricotropin hormone (ACTH). ACTH then stimulates the release of glucocorticoid cortisol from the zona fasciculata/reticularis of the adrenal gland. The release of cortisol exerts negative feedback on the hypothalamus as well as on ACTH release from the pituitary gland. Additionally, ACTH...
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