Cushing's Syndrome

Cushing’s syndrome is a rare endocrine disorder that occurs when your body is exposed to an overabundance of the hormone cortisol.3 Cortisol is known as the stress hormone. The interruption of cortisol secretion can cause weight gain and can ultimately determine where you put the weight on.8 There are many underlying causes such as Pituitary Adenomas, Ectopic ACTH Syndrome, Adrenal Tumors, and Familial Cushing’s Syndrome.2 The majority of these people affected by this hormonal disorder experience weak muscles, increase fat, high blood pressure, etc.1 Although thousands are affected in various ways, there are currently several channels of treatment administered by medical professionals. Through the use of improving technology, medical professionals are better understanding the disorder, allowing them to develop better treatment practices.

According to http://www.webmd.com/, “the adrenal glands don't make enough of a hormone called cortisol, or less often, a related hormone called aldosterone.” That's why doctors sometimes call the illness ''chronic adrenal insufficiency,'' or hypocortisolism. “most important function is to help the body respond to stress. It also helps regulate your body's use of protein, carbohydrates, and fat; helps maintain blood pressure and cardiovascular function; and controls inflammation.” Aldosterone helps your kidneys regulate the amount of salt and water in your body -- the main way you regulate blood volume and keep your blood pressure under control. When aldosterone levels drop too low, your kidneys cannot keep your salt and water levels in balance. This makes your blood pressure drop. “There are two forms of Addison's disease. If the problem is with the adrenal glands themselves, it's called primary adrenal insufficiency. If the adrenal glands are affected by a problem starting somewhere else -- such as the pituitary gland -- it's called secondary adrenal

     Addison’s disease is a disorder of the endocrine system. It is a hormonal disorder that can strike anyone, any gender at any age. Addison’s disease has also been called Adrenal Insufficiency (hypocortisolism) because the root of the disease is in the adrenal gland not producing enough of the hormone cortisol, or sometimes not enough of the hormone aldosterone to satisfy the body’s needs.

Cushing 's syndrome (CS) is characterized by pathologically elevated free glucocorticoid levels. Endogenous hypercortisolism is usually due to ACTH-secreting pituitary corticotropic adenomas and less often due to ectopic ACTH-secreting neuroendocrine neoplasms or ACTH-independent adrenal cortisol hypersecretion (Yaneva, 2010). Cushing 's disease occurs infrequently in an inherited setting in both of these conditions (Yaneva, 2010).

Another diagnostic method to diagnose adrenal tumors is cortisol saliva testing. In this test, the amount of cortisol in the saliva at or near midnight is normally very low. Multiple repeats of the test to confirm elevated cortisol levels can diagnose Cushing's syndrome. Cushing's syndrome is excess cortisol levels, possibly due to the body secreting too much

1. Cushing's disease is a hormonal disorder which is caused by prolonged exposure of the body's tissues to high levels of the hormone cortisol. It is sometimes referred to as hypercortisolism, it is fairly rare and it most commonly affects adults between the ages of 20 to 50. There is an estimated 10 to 15 of every million people who are affected every year.

themselves are malfunctioning that is called primary adrenal insufficiency. Another reason that cortisol production is lacking might be because not enough ACTH is being generated by the pituitary gland. The second order effect of inadequate levels of ACTH being secreted results in cortisol not being produced. When this is the case it is called secondary adrenal insufficiency (MedlinePlus, 2011).

“In 1855, Thomas Addison first described adrenal insufficiency, which was subsequently named after him. The basis of Addison disease has dramatically changed since its initial description. Originally, the disease usually resulted from

The two most common are Cushing Syndrome and Amenorrhea. “Cushing syndrome occurs when your body is expose to high levels of the hormone cortisol for a long time.” (Mayo Staff Clinic, 2016, p.1) There are several symptoms that Cushing Syndrome shares with Polycystic Ovarian Syndrome. Some of the symptoms are: weight gain, acne, hirsutism and/or irregular or absent menstrual periods. Evidently, the two diseases share similar symptoms. Another disease that shares similarities with PCOS is Amenorrhea. It is when one or more menstrual cycles are missed or the absence of menstruations. Some of the symptoms are: hair loss, excess facial hair and acne. Amenorrhea, also,

The basic cause for Equine Cushing's Disease is the lack of dopaminergic control within the intermediate lobe. As a result peptide hormones are overly secreted into the body. Melanotrophs of the intermediate lobe release pro-opiomelanocortin (POMC) into the body. This is then split to form three hormones: α-melanocyte–stimulating hormone (α-MSH), β-endorphin (β-END)–related peptides and corticotropin-like intermediate peptide (CLIP). Normally, dopamine binds to 2 inhibitory receptors on the melanotrophs, stoping the production of hormones. This function is lacking in individuals with Equine Cushing's Disease. Consequentially hypertrophy, hyperplasia, and over production of POMC peptides occur in the intermediate lobe of the pituitary gland.

Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder diagnosed in women of reproductive age. The disease manifests itself with varying symptoms and has long term consequences of heart disease, diabetes, and infertility. PCOS has no clear etiology or pathophysiology, and as new information is being contributed, the mechanism and components of the disease is being updated. Presented here are the most understood and accepted components of PCOS, and its pathology as a reproductive disorder along with its endocrine and metabolic relationships. PCOS pathophysiology exhibits itself mainly through increased androgen synthesis through ovaries and adrenal glands causing follicle growth to halt in the antral stage. Its etiology has been determined to be multifactorial with both genetic and environmental factors causing or increasing effects. Genetics of PCOS have shown its transmission to be in autosomal dominant fashion while environmental factors such as obesity, insulin resistance, and intrauterine environment contributes to its phenotype. Relationships between the factors are discussed and how they contribute to the overall phenotype.

Cushing’s syndrome (CS) is an endocrine affection that is characterized by chronic excess of cortisol in the bloodstream, which results in a large number of clinical conditions. It has been reported that these conditions are associated with high rates of mortality in comparison to the general population (1). If not correctly treated, CS patients have a percentage of survival of 50% at five years (1). Nowadays, the treatment of CS primarily consists in promoting the reduction of cortisol levels in order to avoid its damages by resecting the tumour that secretes cortisol (2). In addition to this invasive management, pharmacological therapy acts considerably as an adjuvant factor (1,2). In spite of not being the treatment of first choice, the function of pharmacological therapy in patients with CS is supplementary and may be helpful to improve the

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,

This is consistent with the idea that typical point estimates provided by plasma or saliva measurement are driven at least in part by the same underlying constitutive differences and pituitary adrenocortical activity that contribute to the values obtained from hair sampling. Another likely factor in the relationship is that hair, like saliva, is thought to incorporate only free unbound fractional cortisol from the bloodstream. Davenport et al 2006 These authors have found the correlation between hair cortisol and salivary cortisol in monkeys. Meyer & Novak 2012 This approach should be thought of as complementary to measurements of salivary and or plasma court not as replacement cost of such markers. Meyer et al 2014 An increasing body of evidence has shown that hair cortisol levels reflect systemic plasma levels of the hormone over time, allow- ing estimation of chronic stress, both psychological and physio-logical, as well as disorders of the hypothalamic-pituitary- adrenal axis, including Cushing syndrom and Addison’s disease

Etomidate is an imidazole derivative similar to Ketoconazole that inhibits both 11α-hydroxylase as well as an inhibitor of 17α-hydroxylase. According to Wells and DiPiro, it is only available in a parenteral formulation and thus its use is limited to patients with acute hypercortisolemia requiring emergency treatment. In addition, in the treating of Cushing’s syndrome Etomidate serves as an intravenous alternative to Ketoconazole. According to Chandler and Batjer, Most investigators to date have analyzed its use in hospitalized patients with neoplasms secreting ACTH. In one study in which the authors used it at a nonsedating dose of 0.3 mg/kg/hour, it normalized serum cortisol levels within 12 hours in six patients with Cushing disease. The