Causes, Symptoms, And Management Of Cushing Syndrome

Causes of Cushing Syndrome

Discuss about the Acute Nursing for Corticotropin-Releasing Hormone.

Hormone cortisol in excessive amount is mainly responsible for the occurrence of Cushing syndrome. Oral consumption of corticosteroid medication at high doses are also responsible for its occurrence. It is caused due to the overproduction of cortisol by one or both the adrenal glands or excessive production by adrenocorticotropic hormone (ACTH). A noncancerous pituitary gland tumor leads to excessive secretion of ACTH which stimulates adrenal glands to produce more amount of cortisol. An ectopic ACTH-secreting tumor which occurs in the non-ACTH producing organs is responsible for producing excess amount of ACTH which results in the Cushing syndrome (Duan et al., 2015). Adrenal adenoma which is a non-cancerous tumor of adrenal cortex is also responsible for cushing syndrome. This type of cushing syndrome is mainly due to the primary adrenal gland disease and it is due to excess cortisol production which is not dependent on stimulation of ACTH. Tumors on one or more endocrine glands is also responsible for Cushing syndrome which is termed as familial cushing syndrome (Raff et al., 2014).

Adrenal gland secrets cortisol and other steroid hormones on stimulation with ACTH. Pituitary gland is responsible for the secretion of ACTH which is stimulated by corticotropin-releasing hormone (CRH) from the hypothalamus. At the hypothalamic and pituitary levels, both ACTH and CRH levels maintained by negative feedback mechanism. Neuronal input at the hypothalamic level is also responsible for the stimulation of CRH level. Raised levels of cortisol are responsible for the negative feedback on the CRH in the hypothalamus which results in the decreased amount of ACTH release from the anterior pituitary gland. On the other hand adenoma of the cortex of adrenal gland are responsible for the high secretion of ACTH. There is increased production of ACTH because tumor is not responsive to the negative feedback mechanism (Nieman, 2015). In Cushing syndrome, there is conversion of negative feedback mechanism to the positive mechanism however, there is no change in the integral mechanism. Brain centres superior than the hypophysiotropic area of the hypothalamus plays role in the pathophysiology of cushing syndrome. Cortisol exhibits mineralocorticoid action through activation of renin angiotensin system which results in the hypertension in Susan. Cortisol exhibits its mineralocorticoid action by acting on enzyme 11-betahydroxysteroid dehydrogenase (II-β HSD). In obese patients, aldosterone increases salt sensitivity to blood pressure (Kawarazaki and Fujita, 2016). In case of obesity patients, more amount of aldosterone is being secreted by visceral cells as compared to the subcutaneous cells. Hence, visceral obesity is more in patients with Cushing syndrome. It is evident that adipocytes produce aldosterone through calcineurin-dependent signaling pathways (Briones et al., 2012). Leptin is responsible for the production of aldosterone from the adipose tissue (Vecchiola et al., 2016). Aldosterone induced mineralocorticoid receptor activation results in the impairment of insulin sensitivity in the adipocytes and skeletal muscles (Sharma and Nieman, 2011). 

How Cushing Syndrome is Diagnosed

Adrenalectomy can lead to inability of adrenal axis to recover. There can be increased bleeding which can result in adrenal haemorrhage. Hyponatremia can occur in patients with adrenalectomy mainly due to deficiency of glucocorticoid. Reduced levels of glucocorticoid also result in the hypotension which can result in decreased stretching of arterial baroreceptors of carotid sinus and aortic arch. Removal of tonic vagal and  glossopharyngeal inhibition cause release of high levels of ADH. This increase in ADH lead to increase in water retention and hyponatremia (Harris and Bouloux, 2014).

Due to sudden change in the adrenocorticoid or catecholamine levels or both, there would be dramatic change in the blood pressure in Susan. Adrenolactomy can result in reduced cardiac output, stroke volume and ventricular stroke. In acute stage, there would be reduced peripheral resistance while in chronic stage there would be increased peripheral resistance. There might be sustained growth of pituitary tumour. This might be due to removal of inhibitory effect of cortisol. There might be enlargement of sella turcica, rise in the plasma ACTH level and appearance of Addisonian pigmentation

Adrenolactomy can negatively impact major organs like liver, heart, stomach and kidneys. There would be decreased hepatic glucose output from the liver, reduced levels of digestive enzymes from the stomach, increased loss of sodium and water and retention of potassium from the kidneys and arrhythmias and reduced cardiac output from the heart. Dysfunction of these major organs can lead to deterioration of Susan (Harris and Bouloux, 2014).

Susan should be sent to critical care unit after surgery. In the first 48 hours there should be assessment and recording of vital signs, intake and output and monitoring of electrolyte balance in frequent schedule. Continuous monitoring should be there for Susan because there might be impeding shock which can be reflected in hypotension, weak pulse, reduced urinary output and alteration in consciousness. Pulse and BP might be unstable for first 24 to 48 post surgery and based on the fluctuations vasopressors need to be administered to Susan. Nurse should monitor and maintain normal blood pressure in Susan because stress due to risk of injury might lead to increase in blood pressure in Susan in the initial phase and in the later phase it might change to hypotension. Nurse need to monitor signs and symptoms related to adrenal insufficiency in Susan. These signs and symptoms include vomiting, weakness, hypotension, joint pain, pruritis and emotional disturbance. Early monitoring of these signs and symptoms can be helpful in preventing deterioration of Susan and maintaining her wellbeing (Carpenito, 2013).

Symptoms of Cushing Syndrome

Cortisol need to be given on the day of surgery because removal of adrenal gland can lead to adrenal insufficiency. It can lead to Addisonian crisis and hypovolemic shock. Administration of cortisol can be helpful in the management of adrenal insufficiency. To manage hypovolemic shock, intravenous fluid need to be administered. Dose of the cortisol need to be adjusted based on the BP, blood glucose, serum electrolytes and serum cortisol levels. In the later stage, oral glucocorticoids need to be administered. Body temperature and WBC count need to be assessed. Due to stress of surgery, there might be increase in body temperature and WBC count can be helpful in assessing occurrence of infection. Due to surgical procedure, Susan might be at the risk of infection. Risk of infection, can lead  to pulmonary complications like stagnant secretions and pneumonia. These complications can be effectively managed by encouraging Susan to turn, deep breathing and using spirometer (Gulanick and Myers, 2016).

After surgery, wound drainage need to be carried out in Susan. It would be helpful in removing accumulated fluid in the wound. In Susan, fluid drain can be carried out using rubber tube. Accumulation of fluid in the wound might lead to infection. Wound drainage procedure would be helpful in the removing fluid from the wound. Nurse need to assess, risk of injury in Susan because Addisonian crisis due to drastic decrease in adrenal hormone can lead risk of injury. Pain due to injury need to be assessed in case of Susan and accordingly opioid analgesics need to be administered. In Susan, surgical dressing need to be remove using aseptic technique. Impaired wound healing might lead to occurrence of infection. Nurse should order for the rest period for Susan. It would be helpful in the relieving stress due to surgery and maintenance of vital signs because stressful condition can negatively impact vital signs in Susan (Dewit et al., 2016).

Care managers, pharmacist and diagnostic test technician can play significant role in care of Susan. Care managers can perform multiple functions like planning, directing and coordinating other health practitioners. Care managers can act as link between patient and healthcare providers. Care managers help in solving problems of patients and assist them in decision making. Healthcare managers are responsible for the patient quality care, treatment and rehabilitation of patient.  Care managers establish external links with social groups to provide care after discharge. Care managers play significant role in the discharge planning of patient. They educate the patients about hospital policies and insurance policies. They help patients by reducing their wait time and also by reducing their hospital bills. Care mangers enables person-centred care to the patient by considering their needs and requirements and improving patient and families contribution in decision making. Care managers remove all the barriers for the patient in the hospital. In consultation with the physician, care manager perform the function of preparing report for the patient at the time of discharge. They perform function of arrangement of all the resources required to provide to the patient (Mcconnell, 2012). Pharmacist plays important role in the patient care. These include dispensing medications according to dose and dosage, monitoring patient health, assess progress of patient health condition with respect to administration of medication and optimize patient response to medication and alter the medication based on the therapeutic response. Pharmacist educate other healthcare professionals like physician and nurse in decision making for medication administration. Pharmacist can educate healthcare professionals and patient about storage of drug, adverse effects of drug and interactions of drug with other drugs and food. Pharmacist help patient to eliminate or reduce symptoms in the patient (McHugh, 2013). Medical diagnostic technician operate all the instruments required for the exact diagnosis of Susan and to identify potential complications after surgery. Medical diagnostic technician help patient to get ready for diagnostic test. This technician educate patient abut the test and assist the patient to get ready for test. These technician keep accurate record of the collected data and submit the data to the physician. They compile data obtained during diagnostic tests and compare it with the standard normal values. They prepare report for the data obtained during diagnostic tests. They help and assist physician in analysing the data and for diagnosis of the disease (Laws Jr and Pace, 2016).

References :

Briones, A.M., Nguyen Dinh Cat, A., Callera, G.E., ……Touyz, R.M. (202). Adipocytes produce aldosterone through calcineurin-dependent signaling pathways: implications in diabetes mellitus-associated obesity and vascular dysfunction. Hypertension, 59, 1069–78.

Carpenito, L. J. (2013). Nursing Care Plans: Transitional Patient & Family Centered Care. Lippincott Williams & Wilkins.

Dewit, S. C., Stromberg, H., and Dallred, C. (2016). Medical-surgical Nursing: Concepts & Practice. Elsevier Health Sciences.

Duan, K., Hernandez, K.G., and Mete, O. (2015). Clinicopathological correlates of adrenal Cushing’s syndrome. Postgraduate Medical Journal,  91(1076), 331-42.

Gulanick, M., and Myers, J.L. (2016). Nursing Care Plans – E-Book: Nursing Diagnosis and Intervention. Elsevier Health Sciences.

Harris, P. E., Bouloux, P. G. (2014). Endocrinology in Clinical Practice, Second Edition. CRC Press.

Kawarazaki, W., and Fujita, T. (2016). The Role of Aldosterone in Obesity-Related Hypertension. American Journal of Hypertension, 29(4), 415-23.

Laws Jr, E. R., and Pace, L. (2016). Cushing’s Disease: An Often Misdiagnosed and Not So Rare Disorder. Academic Press.

Mcconnell. (2012). The Health Care Manager’s Human Resources Handbook. Jones & Bartlett Publishers.

McHugh, M. B. (2013). Workbook for the Manual for Pharmacy Technicians. ASHP.

Nieman, L.K. (2015). Cushing’s syndrome: update on signs, symptoms and biochemical screening. European Journal of Endocrinology, 173(4), M33-8.

Raff, H., Sharma, S.T., and Nieman, L.K. (2014). Physiological basis for the etiology, diagnosis, and treatment of adrenal disorders: Cushing’s syndrome, adrenal insufficiency, and congenital adrenal hyperplasia. Comprehensive Physiology, 4(2), 739-69.

Sharma, S.T., and Nieman, L.K. (2011). Cushing’s syndrome: all variants, detection, and treatment. Endocrinology Metabolism Clinics of North America, 40(2), 379-91.

Vecchiola, A., Lagos, C.F., Carvajal, C.A., Baudrand, R., Fardella, C.E. (2016). Aldosterone Production and Signaling Dysregulation in Obesity. Current Hypertension Reports, 18(3), 20. doi: 10.1007/s11906-016-0626-9.