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Cushing's Disease



Cushing Syndrome Research

This paper explains the etiology and pathophysiology of Cushing's disease, the knowledge of which is useful in the diagnosis of the disease. It describes the various glands affected by the pathology to be recognized. The different causes of the disease are explained depending on the organ affected. For instance, the abnormalities of the pituitary, hypothalamus, and adrenal glands are explained by how they cause Cushing's disease. The symptoms of the disease have been dissected to indicate the progression of the disease.

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The pathophysiology of the illness is described, starting from the common physiology of how the glands function and how they regulate the secretion of different hormones. In line with normal physiology, abnormalities leading to Cushing's disease are described to understand the pathology by using the hypothalamus-pituitary-adrenal gland axis. Differential diagnosis of illness is used to distinguish it from other disorders with similar characteristics. Following the description of Cushing's disease, the etiology, pathophysiology, and the ways the disease manifests itself, one can easily diagnose it when making a differential diagnosis. Therefore, the paper explains Cushing's disease in its entirety.

Cushing's disease is a health condition, during which the pituitary gland, an endocrine organ, produces too many adrenocorticotropic hormones (ACTH). It is a form of Cushing's syndrome that causes the body to produce high levels of cortisol hormone. According to Swearingen and Biller (2011), the discovery of Cushing's disease dates back to the discovery of medicine by Hippocrates. Cushing's disease, as described by Thomas Sydenham, has become identified as a clinical description, consisting of a complex of signs and symptoms that had been recognized as a new entity different from other diseases and syndromes (Swearingen & Biller, 2011).

The clinical description occurred in three periods - the description of the disease as a clinical syndrome, the explanation of the syndrome as elevated cortisol levels, and the delineation of the three causes of hypercortisolism vital in bridging the gap between the initial theories and actual pathophysiology. Cushing later advanced Syndehams studies to describe the disease in its entirety. Understanding the etiology, symptoms, and pathophysiology is essential for the diagnosis and explanation of Cushing's disease.

Etiology of Cushing's Disease

According to Ignatavicious and Workman (2015), Cushing's disease is caused by the excess secretion of cortisol from various origins. Cortisol may come from the adrenal cortex itself; it may be a problem from the anterior pituitary gland or a defect in the hypothalamus. In addition, the disease can be caused by the use of glucocorticoid therapy that may lead to the elevation of cortisol hormone in the blood (Ignatavicious & Workman, 2015).

Often, the anterior pituitary gland may cause an increase in cortisol due to abnormalities such as macroadenomas. The tumors produce the hormone adrenocorticotropic that stimulates the adrenal glands to make the hormone cortisol in the absence of a feedback system (Mayo Clinic Staff, 2016). The anterior pituitary tumors may affect the functioning of the hypothalamus. Subsequently, there may be an injury to the hypothalamus through concussion, which may influence the proper operation of the hypothalamus.

Furthermore, the presence of tumors in the hypothalamus may cause it to hyper-secrete corticotrophin release hormone. The tumors include a glioma - a type of brain tumor that causes the hypothalamus gland to grow abnormally. The judicious use of glucocorticoid therapy can result in the increased production of cortisol (Ignatavicious & Workman, 2015). Glucocorticoid therapy is a mimic of the cortisol hormone.

Pathophysiology of Cushing's Disease

Typically, the body homeostasis and endocrine system work at equilibrium. According to Hurley and Piras (2012), in response to the body hormone fluctuations, the hypothalamus, which is a region in the brain, secretes a hormone called corticotropin-releasing hormone (CRH). The hormone released affects the anterior pituitary. The corticotropin-releasing hormone stimulates the anterior pituitary gland to secrete adrenocorticotropic hormone (ACTH), which is a well-coordinated function of the hypothalamus (Hurley & Piras, 2012).

The adrenocorticotropic hormone is released through the petrosal venous sinus. The ACTH stimulates the adrenal-cortical part to secrete a stress hormone called cortisol. Usually, the peak release occurs just before waking up in the morning, and the ACTH levels decline throughout the day (Hurley & Piras, 2012).

The body produces cortisol from cholesterol, a component found in fatty foods (Hurley & Piras, 2012). Usually, after its secretion, it inhibits the hypothalamus that relays signals to the pituitary, altering more cortisol release of corticotropin-releasing hormone and adrenocorticotropic hormone respectively. The response is a negative loop system of the three organs that are vital for the proper functioning of the endocrine system. The path followed by the ACTH activates the adrenal-cortical glands of the kidneys to secrete three steroid hormones, and among them is cortisol (Hurley & Piras, 2012). Thus, the primary effect of ACTH is cortisol.

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Hurley and Piras (2012) argue that in the case of an abnormality, the entire hypothalamus-pituitary axis is affected. For instance, a problem in the adrenal cortex or the anterior pituitary gland, or the hypothalamus results in abnormal functioning of the glands with an inappropriate feedback system (Ignatavicious & Workman, 2015).

Cushing's disease is marked by a pituitary microadenoma that is less than 10mm in size. The benign basophilic tumor produces adrenocorticotropic hormone (ACTH) composed of corticotroph cells that cause the hyperplasia of the adrenal glands and end up in the excess secretion of cortisol (Hurley & Piras, 2012). Hurley and Piras (2012) state that the overproduction coupled with a lack of suppressive effects from the negative feedback mechanism of the hypothalamic-pituitary-adrenal (HPA) axis marks the pathology of Cushing's disease.

Clinical Symptoms of Cushing's Disease

The signs of Cushing's disease that differentiate it from other hormonal disorders arise from the extreme cortisol levels. The symptoms increase over time (Hurley & Piras, 2012). According to the University of Maryland Medical Centre (2016), Cushing's disease causes massive weight gain. The weight gain changes are due to the wide distribution of fat all over the body, resulting in a puffy face resembling the moon, a dorsocervical hump on the upper part of the back, and a large abdomen that is characteristic of centripetal obesity (Hurley & Piras, 2012).

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Furthermore, according to Hurley and Piras (2012), peripheral extremities show the emaciation of muscles. The arms and legs often appear weak as a result of body protein losses, which is a common reason for most individuals complaining of malaise. The energy breakdown effect of the hormone has a counteractive effect on the bone density due to osteoporosis coupled with the decreased absorption in the gastrointestinal tract (Hurley & Piras, 2012).

In addition to muscle wasting, the skin changes due to the cortisol increase that affects collagen formation in the skin. The continuous decrease in collagen makes the skin thin and fragile, with purple-like marks of the skin on the abdomen different from the striae seen during pregnancy (Hurley & Piras, 2012).

Excess cortisol levels often affect the sex hormones in men and women (Wisse, 2015). For instance, women become susceptible to the growth of hair on their faces and chest with the changes in reproductive cycles. At the same time, men often report a decreased desire for sex and impotence (Hurley & Piras, 2012). Other symptoms include mental changes such as reports of insomnia, anxiety, depression, and change in moods. Other individuals report hypertension due to heart muscle hypertrophy, which is a consequence of increased cortisol (Hurley & Piras, 2012). Moreover, diabetes may set in due to the suppressive modality of excess cortisol.

Differential Diagnoses of Cushing's Disease

Diagnosis of Cushing's disease follows some diagnostic tests that are critical in identifying the actual condition. The tests used in the diagnosis include the Low-dose and High- dose dexamethasone suppression testing (Wisse, 2015). The diagnostic gold standard is a day's analysis of urine to determine the concentration of unbound cortisol. The extremely low and variable high dexamethasone suppression tests are classic diagnostic tests. Often, it yields to the absence of cortisol in the urine (Hurley & Piras, 2012).

Moreover, the imaging studies display the tumors of the pituitary and hypertrophy of the kidney glands. Once one receives the laboratory findings, it is easy to distinguish Cushing's disease and other Cushing's syndrome disorders such as ectopic ACTH, adrenal carcinoma, adrenal adenoma, macronodular adrenal hyperplasia, and McCune-Albright syndrome.

The differential diagnosis is made by measuring the plasma ACTH. If the findings are low, the doctors should suspect ACTH-independent Cushing's syndrome. If normal, a CRH stimulation test should be performed to ascertain the ectopic ACTH source. If the plasma ACTH is high, a pituitary MRI is to be suggested. The positive results are is indicative of Cushing's disease. With normal results, doctors are to suggest performing a bilateral inferior sinus sampling. If the test turns positive, it is indicative of Cushing's disease; however, if it turns to be negative, then one can suspect an ectopic ACTH source. Thus, it is the standard differential diagnosis of Cushing's disease.

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Cushing's disease is a condition that causes the pituitary gland to release the excessive adrenocorticotropic hormone, (ACTH). This disease is traced back to the evolution of medicine, with Cushing spearheading its description entirely. Cushing's disease is a type of Cushing syndrome with dependency on the production of ACTH. The disease is caused by abnormalities in the adrenal cortex due to tumors, abnormalities, or injuries of the hypothalamus that cause hyper-secretion of corticotropin-releasing hormone, abnormalities of the anterior pituitary gland, and the use of glucocorticoid medication.

Often, these defects result in the excessive secretion of stimulating or actual hormones that lead to the excessive secretion of cortisol. Moreover, the negative feedback mechanism regulating the secretion of hormones is disrupted from functioning normally. A change in the normal physiological system of the hypothalamus, pituitary, and adrenal gland leads to the development of Cushing's disease. The symptoms of Cushing's disease range from a skin change, muscle wasting, and bone fragility, trunk obesity, changes in sexuality due to altered hormonal balance, diabetes, and high blood pressure.

The usage of various diagnostic tests ranging from the plasma corticotropin hormone, high and low-dose dexamethasone suppression tests to MRI and Computed tomography distinguishes the Cushings disease from other disorders mimicking it. Therefore, this paper has discussed given aspects of the disease important in making the appropriate diagnosis.

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