Running head: MILESTONE ONE 1
MILESTONE ONE 4
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
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).
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.
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 cases, victims have diarrhea, vomiting, and nausea (Bancos et al., 2015). The patient’s blood pressure falls drastically when standing, causing dizziness or fainting. Skin discoloration is part of Addison’s disease with a spot of dark tainting or hyperpigmentation covering naked body parts. In most cases, these dark skin spots are visible in pressure points, elbows, or scars such as mucous membranes, lips, toes, knuckles, knees, and elbows. Patients can develop depression and irritability as a result of Addison’s disease. This is due to increased craving of foods with salt leading to salt loss. In children, hypoglycemia is more prevalent than in adults. There are irregular menstrual cycles in women.
Since the manifestations progress gradually, they are typically disregarded until an unpleasant event like an ailment or a mishap makes them worse. This is called an Addisonian crisis or intense adrenal deficiency. In many patients, side effects are severe enough to look for treatment before an emergency happens. Nonetheless, in around 25% of patients, manifestations initially show up during an Addisonian crisis (Bancos et al., 2015).
Bancos, I., Hahner, S., Tomlinson, J., & Arlt, W. (2015). Diagnosis and management of adrenal insufficiency. The Lancet Diabetes & endocrinology, 3(3), 216-226.
White, K. G. (2009). Jane Austen and Addison’s disease: an unconvincing diagnosis. Medical humanities, 35(2), 98.