Running head: MILESTONE ONE 1 MILESTONE ONE 4 Milestone One Introduction of Individual In 1816, the author of such beloved books as "Emma" and "Pride and Prejudice" came down with a large group of puzzling diseases including fatigue, back pain, skin discoloration, "bilious attacks" and fever. Only one year later, she was dead at 41 years old. Much theory has been dedicated to Jane Austen's infection in the years since, with the most widely recognized diagnosis being that she had Addison's sickness, a malfunction of the adrenal organs that wasn't known to medicine until quite a while after her demise (White, 2009). Even though delayed in its onset, the confusion is known to cause changes in skin color during its late stages, which may clarify Austen's cases that her complexion had turned "black and white and every wrong color." Identification of Pathophysiology Mineralocorticoid deficiency Sodium reabsorption and excretion of potassium from the body are stimulated by mineralocorticoids, whereby if mineralocorticoids are not produced, it leads to decreased production of potassium and increased excretion of sodium, primarily through sweat, urine, saliva and times in gastrointestinal tract. A high serum concentration of potassium and low sodium concentration may be detected as a result. Symptoms such as but not limited may result where there is high water loss and urinary salt: hypotension, decreased circulatory volume, acidosis, plasma hypertonicity, severe dehydration, and finally, circulatory collapse. Nevertheless, when adrenocorticotropic hormone (ACTH) leads to adrenal inadequacy due to its low production, the circulatory problems are less severe, and the electrolyte levels are somewhat normal or mildly deranged (Bancos et al., 2015). Glucocorticoid deficiency Insufficiency of Glucocorticoid production leads to hypotension and severe insulin sensitivity as well as interferes with protein, fat, and carbohydrate metabolism. From protein, carbohydrates are formed when there is inadequate production of cortisol, and also hypoglycemia and reduced liver glycogen result. As a result of neuromuscular function, the person feels weak. Circulatory failure may result due to myocardial weakness and dehydration because there is reduced cardiac output. Additionally, glucocorticoid deficiency leads to reduced production of cortisol which affects ACTH production to a decreased level and elevated the amount of blood beta-lipotropin, which has melanocyte-stimulating activity and, when combined with ACTH, causes the hyperpigmentation of skin and mucous membranes characteristic of Addison disease (Bancos et al., 2015). Therefore, hyperpigmentation is not caused by the adrenal deficiency secondary to pituitary failure. Clinical Manifestations Addison’s disease manifestation starts gradually. Symptoms such as weight loss, loss of appetite, muscle weakness, fatigue, and chronic are examples of disease characteristics. In about 50% of reported cas ...