fi 7- hp

Milestone Two

Born in 1775, Jane Austen was a novelist from England whose works were founded on the British landed gentry. She had six major novels, including "Pride and Prejudice," "Persuasion," and "Emma," among others. Austen died when she was forty-one years old after manifesting a myriad of diseases that went undiagnosed. However, with advancements in medicine years later, White (2009) asserts that Austen died after succumbing to Addison's sickness, a failure of the adrenal organs. The pathophysiology of Addison’s sickness changes the normal state of the body by affecting the mineralocorticoid and glucocorticoid functions.

Mineralocorticoids facilitate the excretion of potassium and the reabsorption of sodium. Therefore, if mineralocorticoids are not produced, there will be high potassium and sodium content in the body resulting in high urinary salt and water loss. Consequently, one will portray symptoms such as severe hydration, decreased circulatory volume, and plasma hypertonicity, among others (Bancos et al., 2015). On the other hand, a deficiency in glucocorticoids adversely affects the metabolism of protein, carbohydrate, and fats. Also, it leads to insulin sensitivity and hypotension. Symptoms include weakness, which is caused by compromise neuromuscular function, and myocardial weakness, which is caused by circulatory failure.

The clinical manifestations of Addison’s sickness start slowly through things like fatigue, weight loss, and muscle weakness. Other symptoms include vomiting, diarrhea, and low blood pressure that can cause fainting episodes or dizziness. Addison’s sickness is also characterized by skin discoloration where one has dark hyperpigmentation in pressure points such as elbows, knees, and lips. Individuals diagnosed with this sickness may be irritable or depressed since they crave salt-laden foods (Bancos et al., 2015). Considering that these symptoms appear gradually, most cases of Addison’s sickness tend to go untreated until the condition becomes severe.

History

There are two major explanations for variations in pathophysiology. On the one hand, Addison's sickness can occur in the early years of one's life in what is known as the autoimmune polyendocrine syndrome type 1 (APS type 1). This variation happens when the autoimmune suppressor gene in chromosome 21q22.3 is mutated. Eighty percent of individuals with APS type 1 go on to contract Addison’s sickness. On the other hand, Addison’s sickness can occur in the later years of one’s life in what is referred to as APS type 2. This is a more genetically complex variation compared to the APS type 1. APS type 2 is prevalent in the genotypes HLA- DR4/DQ8, and DR3/DQ2 (Leelarathna, Powrie, & Carroll, 2009). Furthermore, Addison’s sickness can develop in an individual who has a mutated allele of a MICA gene that does not rely on the polymorphism of the DQ or DR gene.

There are two physiological stressors that affect the course of Addison’s sickness. First, there is the primary adrenal insufficiency. This relates to the adrenal cortex being gradually destroyed by the immune system of the body. Consequently, the majority of individuals diagnosed with Addison's sickness are caused by autoimmune disorders. The antibodies of an individual's immune system slowly attack and destroy the organs and tissues of the affected person. When the destruction of the adrenal cortex reaches approximately ninety percent, primary adrenal insufficiency occurs. Second, there is the secondary adrenal insufficiency. In this case, the production of cortisol by the adrenal glands drops significantly. Secondary adrenal insufficiency is common when a person stops taking glucocorticoid hormone medication after consuming it for a long time. Also, one can experience secondary adrenal insufficiency when benign ACTH producing tumors are surgically removed.

It follows that the historical impact of patient care technology in the context of Addison’s sickness has been immense. Initially, little was known about Addison’s sickness, which is why Jane Austen died before receiving a proper diagnosis. Thomas Addison, the man credited with identifying the disease, used a monograph to identify the problem with the adrenal glands. This was an isolated incident since little was known about adrenal glands at the time. Nevertheless, the use of the monograph proved to be a technological breakthrough in patient care.

Planning

Two Short-Term Goals

Goal 1 – Accurately diagnose the patient and determine whether he/she has primary or secondary adrenal insufficiency and any other notable aspects that can affect the intervention methods. This goal is achieved within one day. The diagnosis can be achieved through four tests. First, there are blood tests that measure the levels of antibodies that propagate Addison’s sickness. Also, they measure the patient’s ACTH, cortisol, potassium, and sodium levels in the blood, all of which affect the production of hormones in the adrenal cortex. Second, there is the insulin-induced hypoglycemia test, which entails giving the patient an injection of insulin then checking his/her cortisol and blood sugar levels. This will denote if the patient’s condition is due to pituitary disease. Third, there are the ACTH simulation tests that signal the production of cortisol from the adrenal gland. Finally, there are the imaging tests where adrenal glands’’ sizes are checked using a CT scan of the abdomen.

Goal 2 – Effectively deal with cases of patients experiencing an Addisonian crisis. This goal is achieved within two to four hours. It entails the patient receiving intravenous injections of dextrose, saline, and hydrocortisone. The objective of the goal is to ensure the patient’s potassium, blood sugar, and blood pressure levels are normalized.

The accomplishment of these short-term goals should be complete before patients can attain long-term goals. The main objective of these goals is to measure and record the progress of the patients with respect to the long-term goals. More so, the achievement of these short-term goals offers the patients suitable reinforcement that can encourage them to continue working towards fighting the disease. These short-term goals are effective in acute care conditions that require nurses to emphasize on the immediate needs of the patients.

Two Long-Term Goals

Goal 1 – After six weeks of undergoing treatment, the patient is expected to have acceptable levels of steroid hormones to take over the roles played by cortisol and aldosterone in the body. The patient’s body is expected to have better metabolism, mood, tissue function, and response to stress.

Goal 2 – After six weeks of treatment, the patient should be well equipped to effectively live with Addison’s disease and handle emergencies in case of an Addisonian crisis. The patient is expected to have a medical bracelet or card that informs emergency healthcare workers of his/her condition. Also, the patient must have extra medication in case of emergencies.

These two long-term goals define the changes that the patient undergoes over a long period. The goals defined work to restore the normal functioning of the patients' problem areas. In case the restoration of normal functioning is impossible, then these goals will define the maximum functioning level, which is attainable based on the resources and health condition of the patient.

Intervention

An interdependent intervention will be used to handle a case of a patient that has Addison's sickness. This form of intervention entails collaboration between a nurse and other healthcare workers, for instance, physicians, and dietitians. The first part of the intervention will be observation. The nurse will have to carefully observe the patient and note how he/she responds to treatment and whether any complications develop. The nurse must make a note of every issue, including high-risk problems and probable nursing diagnoses. During this stage, the nurse can take note of the common symptoms associated with Addison's sickness, for instance, hyperpigmentation of the skin, muscle weakness, low appetite, changes in mood, craving for salt-laden food, headache, diarrhea, vomiting, and fainting (Neto & de Carvalho, 2014). Also, the nurse will have to take note of things like low blood pressure, severe abdominal or back pains, low sodium levels, and high potassium levels. Observation is crucial in this regard since the quick worsening of symptoms might result in an Addisonian crisis or acute adrenal failure. If such situations go unnoticed, the result might be death.

The second part of the intervention is prevention. This entails implementing the necessary care to ensure complications are prevented, and risk factors are reduced. This part of the intervention is crucial for collaborative challenges and high-risk nursing diagnoses. Nevertheless, they can be utilized for practical nursing diagnoses. One solution in this regard is the use of salt additives in food (Michels & Michels, 2014). Since a patient might be unable to retain sodium naturally, he/she might require his/her food to have salt additives. This is especially handy in periods of salt loss, for instance, high temperatures and sweating.

The third part of the intervention is treatment. It normally entails implementing the necessary care to treat a problem. Often, actual nursing diagnoses require appropriate treatment. There are three major treatments for Addison’s sickness. First, there is the use of hydrocortisone. This refers to a form of synthetic medication that takes the place of the cortisol lost in the body. The doses given to the patient vary from 20 to 50 milligrams, depending on his/her metabolism and weight. Patients with Cushing syndrome might need dosage adjustment. Typically, hydrocortisone is given in two doses. There is the 2/3 dose in the morning, and 1/3 does in the afternoon. Second, there is the use of fludrocortisone. This refers to a synthetic mineralocorticoid, which is necessary for individuals that do not have aldosterone. It is vital for the kidney's potassium excretion and sodium retention. It is crucial to take note of fluid overload and hypertension in the patient that might occur as a result of excessive retention of sodium. Finally, there is the androgen replacement therapy. This therapy is necessary for females who require replacement therapy for the androgen that is produced by the adrenal cortex (Michels & Michels, 2014). However, this form of therapy is only carried out under special circumstances.

The final part of the intervention entails health promotion. In situations where health problems are absent, the nurse will ensure the patient can identify certain improvement areas, to promote better wellness levels. Strategies that propagate the promotion of health are needed to encourage approach behaviors. This way, a patient can prevent the occurrence of negative outcomes and promote the occurrence of positive outcomes. These strategies actualize the health potential of the patient. In this regard, the prevention of the Addisonian crisis is vital. Nurses can aid patients in monitoring their levels of hypotension, hypoglycemia, electrolyte and fluid balance, and appropriate fluid volume.

Throughout the intervention process, technology can be utilized for health promotion and patient safety. For starters, technology facilitates communication between the different healthcare workers that take care of the patient. This reduces any errors or miscommunication that might be fatal for the patient. Also, technology promotes patient-centered care. This is vital to patient safety and satisfaction in the care received.

Evaluation

An evaluation of the plan of care is vital in noting the health status of the patient and the results of the intervention. The evaluation, in this case, will involve a comparison between the patient's initial condition and their present condition. More so, the evaluation will check the response of the patients to the intervention strategies. It is expected that the evaluation process will be ongoing and iterative involving the patient and the healthcare workers to determine the extent of the achievement of the medication and the effectiveness of the intervention plan. The necessary data in this regard will cover the patients’ levels of hypotension, hypoglycemia, electrolyte and fluid balance, and appropriate fluid volume (Neto & de Carvalho, 2014). Others include things like low blood pressure, severe abdominal or back pains, low sodium levels, and high potassium levels. Taking note of such data will enable the nurses and physicians to determine how the patient is responding to the intervention and whether additional strategies are required.

Following the successful intervention, for Addison's sickness, a patient is expected to be no longer dehydrated and have standard blood pressure. Also, it is expected that a patient will be oriented, alert, and ready to cater to his/her needs while at home. Catering to his needs will show that the patient understands his/her dietary requirements and maintains his/her medication doses. Overall, the evaluation is supposed to reveal normal fluid balance and standard peripheral perfusion with normalized blood pressure. Furthermore, symptoms such as fatigue, diarrhea, vomiting, and abdominal pains are expected to go away. If the evaluation does not yield such results, then the healthcare professionals will have to reevaluate their approach and come up with a new plan of intervention.

References

Bancos, I., Hahner, S., Tomlinson, J., & Arlt, W. (2015). Diagnosis and management of adrenal insufficiency. The Lancet Diabetes & Endocrinology, 3(3), 216-226.

Leelarathna, L., Powrie, J. K., & Carroll, P. V. (2009). Thomas Addison's disease after 154 years: modern diagnostic perspectives on an old condition. QJM: An International Journal of Medicine, 102(8), 569-573.

Michels, A., & Michels, N. (2014). Addison disease early detection and treatment principles. Am Fam Physician, 89(07).

Neto, R. A. B., & de Carvalho, J. F. (2014). Diagnosis and classification of Addison's disease (autoimmune adrenalitis). Autoimmunity Reviews, 13(4-5), 408-411.

White, K. G. (2009). Jane Austen and Addison's disease: an unconvincing diagnosis. Medical Humanities, 35(2), 98.