Patient’s Impressions On Assessments Exhibits Cushing’s Syndrome

Causes of Cushing’s syndrome

Discuss about the Patient’s Impression On Assessments Exhibits Cushing’s Syndrome.

The case study review entails a female Patient, Smith Moureen aged 24 years.  She is experiencing gastrointestinal bleeding, abdominal pain and fatigue which are worsening. The patient has a history of rheumatoid arthritis and is currently under corticosteroids medication. Further, she has type II diabetes and she is on metformin medication for the same. On admission various vital information have been undertaken and the patient’s impression on assessments exhibits Cushing’s syndrome.

Cushing syndrome is a collection of various signs and symptoms caused by prolonged exposure of cortisol drug. Accompanying symptoms include high blood pressure, abdominal obesity characterised by slender arms and legs, fat lumps observed on the shoulders and skin which is fragile which is occasioned by poor healing process. Women have been observed to have more hair growth and abnormal menstruation periods. There can also be occasioned headaches and feeling of tiredness, (Bertagna et al, 2009).

Cushing syndrome is caused by excessive cortisol related drugs like prednisone or tissue growth which leads to excessive production of cortisol in the adrenal glands.  The functions of cortisol in the body include regulation of blood pressure, reducing the immune system response on inflammatory system, conversion of carbohydrates, proteins and fats into energy form, regulation of insulin effects and stress response, (Melmed et al, 2011).

The body can be induced to produce elevated levels of cortisol based on factors such as stress levels, alcoholism, malnutrition and depression. Thus the most common causes of Cushing disease is the excessive use of corticosteroid and maintenance of high doses for longer durations, (Jeffcoate et al, 1979).

The incidences of Cushing syndrome have been imprecise and are likely to be under estimated. Pituitary ACTH Cushing syndrome is approximately 5-6 times common than other forms caused by benign or malignant tumours, (Govindan et al, 2006). The epidemiologic reports indicate that there are approximately 5-25 per million cases per year, however with this statistics, the reported cases are much lower at 1.2-2.4 per million in any given year, (James et al, 2016).

The associative prevalence of hypercortisolinism has been estimated to be around 2%-5% among patients with poor control and management of diabetes and hypertension. The female gender has high prevalence to the male gender in the ratio of 3:1, (Melmed et al, 2011). Cushing syndrome is a rare disease among children. the disease is fatal as it can cause death and increased morbidity and mortality rate which is characterised by cardiovascular complications,(Steffensen et al, 2010).

Incidences of Cushing syndrome

In US, studies have estimated that the incidence was higher than those reported form European based studies. The results indicated that it affected an estimate of 6.2 to 7.6 per million persons- years, (Broder et al, 2015).

Cushing syndrome risks factors are well established; however epidemiological studies have diagnosed more females than males. Further it is common among the age group of 25 years to 40 years. The common risks factors for the disease are;

• Type diabetes, obesity and fluctuating blood glucose levels
• Long term usage of corticosteroid drugs
• Pituitary gland tumours
• Adrenal gland disease and
• Ectopic ACTH forms of secreting tumours

Cushing disease has tremendous effects on the patients and the family. Weight management of the patients is affected and further it deteriorates the health status of the patients through increased mortality and morbidity.

The patients often experience sudden increase in weight, poor wound management, prolong fatigue, anxiety disorders, emotional disturbances, sleep disorders, experiencing menstrual irregularities.

These impacts have enormous effects on psychological and emotional disturbance on the patients and their families. The patients often feel increasing signs of sickness but symptoms seem like depression or hypochondriac lacking diet and exercise fitness. Further often the family; don’t understand the situation the patient is undergoing and support your getting is just to advise you to change the lifestyle, further deteriorating the impact on the patient.

The role of medication is to decrease the secretion of cortisol and blockage of receptors of glucocorticoids and inhibition of ACTH. The various classes of these drugs are;

1. Steroid genesis inhibitors

• Op’DDD drugs are aimed at reducing the cleavage around cholesterol. It inhibits cortisol secretion among patients with Cushing syndrome. It is effective in half of the patients and has been shown to induce adrenal atrophy, (Castinetti et al., 2008).
• Another drug inhibitor drug is Ketaconazole which inhibits production of cytochrome p450 enzymes. It normalizes the levels of cortisols, (Castinetti et al., 2008).
• Metyrapone drug blocks the synthesis of cortisol through inhibiting beta hydroxylase. It is effective in more than 50% of the patients, it further induces low production of potassium and hyperandrogenism, (Obinata et al, 2008).

1. Glucocorticoid receptor antagonist drugs

• Mifepristone drug is a receptor antagonist drug under this class. It is effective clinical signs control in hypercortisolism, (Castinetti et al., 2009).
• ACTH lowering drugs
• The drugs under this class are effective anti secretory and anti tumoral in prolactinomas disease.

Monitoring and management of associative complications

In the first 24 hours, there is need for management of adrenal hypofunction, which calls for close monitoring for weak pulse, respiratory rates and body weakness. There is need for administration of IV fluids to the patient and management of electrolytes and presence of corticosteroids, before and after treatment. Further close monitoring of lab results to check statuses of electrolytes is key for the patient. Further since the patient is diabetic, there is need for close monitoring of blood glucose levels and taking appropriate actions towards increase in blood sugar levels. Further there is need for close monitoring for acute adrenal condition, which is a life threatening condition characterised by low levels of cortisol hormone from adrenal glands.

Monitoring the intake and output of the patient is key in ensuring daily weights and glucose levels and accurate assessment of electrolytes. Urine sample tests will be initiated at 24 hours before medication. Blood samples assessment ensures there is regular management of the hormone levels for the patient. Normal levels cortisol in both urine and blood needs to drop after initiation of medication, since the drug initiates signal on pituitary gland to lower levels of Adrenocorticotropic hormone.

Risks factors

Assessment of late night corticosol in saliva is key in ensuring there is sufficient production. The level of cortisols at night normally drops and this might be an indicator for corticosol production management which may require further diagnosis.

Decreasing risk of injury

As a nurse there is need for providing protective environment for the patient to prevent any fall, fracture and other injuries which are linked to bones and body tissues. Further there is need to assist the patient, as he is weak in ambulation and to ensure that there is prevention of falls.

Reduction of risk of infection

There is need to ensure that the patient is kept in an unexposed environment which might lead to infections. As a nurse, there is need to assess subtle infections. In case the patient has been scheduled for surgery in the first 24 hours, there is need to monitor frequently the blood sugar levels and managing it and stool assessments for diabetes mellitus and peptic ulcers which are predominant problems associated with.

References

Assié, G., Bahurel, H., Coste, J., Silvera, S., Kujas, M., Dugué, M. A., … & Bertagna, X. (2007). Corticotroph tumor progression after adrenalectomy in Cushing’s disease: a reappraisal of Nelson’s syndrome. The Journal of Clinical Endocrinology & Metabolism, 92(1), 172-179.

Bertagna, X., Guignat, L., Groussin, L., & Bertherat, J. (2009). Cushing’s disease. Best Practice & Research Clinical Endocrinology & Metabolism, 23(5), 607-623.

Broder, M. S., Neary, M. P., Chang, E., Cherepanov, D., & Ludlam, W. H. (2015). Incidence of Cushing’s syndrome and Cushing’s disease in commercially-insured patients< 65 years old in the United States. Pituitary, 18(3), 283-289.

Castinetti, F., Fassnacht, M., Johanssen, S., Terzolo, M., Bouchard, P., Chanson, P., … & Young, J. (2009). Merits and pitfalls of mifepristone in Cushing’s syndrome. European journal of endocrinology, 160(6), 1003-1010.

Castinetti, F., Morange, I., Jaquet, P., Conte-Devolx, B., & Brue, T. (2008). Ketoconazole revisited: a preoperative or postoperative treatment in Cushing’s disease. European Journal of Endocrinology, 158(1), 91-99.

Cavagnini, F., & Pecori, F. G. (2001, April). Epidemiology and follow-up of Cushing’s disease. In Annales d’endocrinologie (Vol. 62, No. 2, pp. 168-172).

Clayton, R. N., Raskauskiene, D., Reulen, R. C., & Jones, P. W. (2011). Mortality and morbidity in Cushing’s disease over 50 years in Stoke-on-Trent, UK: audit and meta-analysis of literature. The Journal of Clinical Endocrinology & Metabolism, 96(3), 632-642.

Govindan, R., Page, N., Morgensztern, D., Read, W., Tierney, R., Vlahiotis, A., … & Piccirillo, J. (2006). Changing epidemiology of small-cell lung cancer in the United States over the last 30 years: analysis of the surveillance, epidemiologic, and end results database. Journal of clinical oncology, 24(28), 4539-4544.

James, B. C., Aschebrook-Kilfoy, B., Cipriani, N., Kaplan, E. L., Angelos, P., & Grogan, R. H. (2016). The incidence and survival of rare cancers of the Thyroid, Parathyroid, adrenal, and Pancreas. Annals of surgical oncology, 23(2), 424-433.

 Jeffcoate, W. J., Silverstone, J. T., Edwards, C. R. W., & Besser, G. M. (1979). Psychiatric manifestations of Cushing’s syndrome: response to lowering of plasma cortisol. QJM: An International Journal of Medicine, 48(3), 465-472.

Melmed, S., Polonsky, K. S., Larsen, P. R., & Kronenberg, H. M. (1897). Williams Textbook of Endocrinology, 2011. Saunders Elsevier, Philadelphia.

Melmed, S., Polonsky, K. S., Larsen, P. R., & Kronenberg, H. M. (1897). Williams Textbook of Endocrinology, 2011. Saunders Elsevier, Philadelphia.

Obinata, D., Yamaguchi, K., Hirano, D., Yoshida, T., Soma, M., & Takahashi, S. (2008). Preoperative management of Cushing’s syndrome with metyrapone for severe psychiatric disturbances. International journal of urology, 15(4), 361-362.

Steffensen C, Bak AM, Rubeck KZ, Jorgensen JO: Epidemiology of Cushing’s syndrome. Neuroendocrinology. 2010, 92 (Suppl 1): 1-5.

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