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group_5_presentation_1_-_glucocorticoid_hyperfunction_cushing_s_syndrome [2017/10/01 12:24] mohamesb [Introduction] |
group_5_presentation_1_-_glucocorticoid_hyperfunction_cushing_s_syndrome [2018/01/25 15:18] (current) |
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{{youtube>J6-KRmqimIQ?medium}} | {{youtube>J6-KRmqimIQ?medium}} | ||
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+ | ==== Adrenal Glucocorticoid Hyperfunction: Cushing's Syndrome PowerPoint ==== | ||
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+ | {{:cushing_s_presentation.pptx|}} | ||
===== Introduction ===== | ===== Introduction ===== | ||
- | <box 30% round right | > {{:hpa_.jpg?nolink&350|}} </box| Figure 1: The HPA (stress response) Axis > | + | <box 32% round right | > {{ ::screen_shot_2017-10-01_at_12.42.47_pm.png?345 |}} </box| Figure 1: The HPA (stress response) Axis > |
- | Cushing’s syndrome results from excessive, long-term exposure to endogenous or exogenous forms of glucocorticoids (Orth, 1995). Glucocorticoids are a class of steroids, with cortisol being the most important. Glucocorticoids are particularly important in mediating the stress response of the body, and they are also involved in anti-inflammatory actions (Marshall, Bangert & Lapsley, 2012). Normally, the hypothalamic-pituitary-adrenal axis (HPA Axis) releases cortisol from the adrenal glands in response to a stressor (Figure 1). The hypothalamus releases corticotropin-releasing hormone (CRH), stimulating the pituitary gland to release adrenocorticotropic hormone (ACTH), which acts on the adrenal glands to release cortisol. | + | Cushing’s syndrome results from excessive, long-term exposure to endogenous or exogenous forms of glucocorticoids (Orth, 1995). Glucocorticoids are a class of steroids, with cortisol being the most important. Glucocorticoids are particularly important in mediating the stress response of the body, and they are also involved in anti-inflammatory actions (Marshall, Bangert & Lapsley, 2012). Normally, the hypothalamic-pituitary-adrenal axis (HPA Axis) releases cortisol from the adrenal glands in response to a stressor (Figure 1). Activation of the HPA axis initiates a cortisol cascade. Various stressors will result in the secretion of corticotropin-releasing hormone (CRH) from the hypothalamus, which then stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH). Circulating ACTH acts on the adrenal cortex to release cortisol and exert negative feedback control to restore homeostasis. |
- | However, in Cushing's Disease (the most prevalent endogenous subtype of this syndrome), a tumour in the pituitary causes excessive release of ACTH, therefore acting on the adrenal glands to produce abnormally high levels of cortisol(Orth, 1995). Other endogenous causes of Cushing’s syndrome include an adrenal adenoma over-secreting glucocorticoids, or an ectopic non-pituitary ACTH-producing tumour. Potential sources of an ectopic tumour include the lungs, pancreas, or thymus (Marshall, Bangert & Lapsley, 2012). | + | However, in Cushing's Disease (the most prevalent endogenous subtype of this syndrome), a tumour in the pituitary causes excessive release of ACTH, therefore acting on the adrenal cortex to produce abnormally high levels of cortisol (Orth, 1995). The excess release of glucocorticoids present life-threatening conditions and a host of clinical manifestations. Other endogenous causes of Cushing’s syndrome include a tumour of the adrenal cortex over-secreting cortisol, an ectopic non-pituitary ACTH-secreting tumour, or a tumour of the hypothalamus secreting excessive CRH leading to activation of the cortisol cascade. Potential sources of an ectopic tumour include the lungs, pancreas, or thymus (Marshall, Bangert & Lapsley, 2012). |
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====Pasireotide (Signifor)==== | ====Pasireotide (Signifor)==== | ||
- | Pasireotide acts as an analog to somatostatin, which is known as a growth hormone-inhibiting hormone. The drug inhibits corticotropin secretion from the hypothalamus, a hormone that leads to the secretion of ACTH and eventually the secretion of cortisol (McKeage, 2013). | + | Pasireotide acts as an analog to somatostatin, which is known as a growth hormone-inhibiting hormone. The drug inhibits adrenocorticotropin (ACTH) secretion from the pituitary gland, a hormone that eventually leads to the secretion of cortisol (McKeage, 2013). |
A study done by researchers looked at patients with Cushing’s disease and prescribed them with pasireotide for 6 months. At the end of the trials, 25% of all patients have normalized UFC levels and a significant decrease in the mean UFC levels of all patients. Patients that saw a reduction in their UFC levels also saw improvements in clinical symptoms as well, such as blood pressure and body weight. The drug, however, has shown to cause hyperglycemia in patients and is still under further testing (McKeage, 2013). | A study done by researchers looked at patients with Cushing’s disease and prescribed them with pasireotide for 6 months. At the end of the trials, 25% of all patients have normalized UFC levels and a significant decrease in the mean UFC levels of all patients. Patients that saw a reduction in their UFC levels also saw improvements in clinical symptoms as well, such as blood pressure and body weight. The drug, however, has shown to cause hyperglycemia in patients and is still under further testing (McKeage, 2013). |