Exogenous Cushing Syndrome And Its Effects On Maureen

Signs and Symptoms

The major disease that Maureen is infected with is the Exogenous Cushing Syndrome. The disease is a disorder in which the Cushing syndrome occurs due to the higher level of cortisol hormone than normal.

Exogenous Cushing syndrome occurs to a person when he/she uses synthetic glucocorticoid medicines to treat a disease. Exogenous means something from outside the body, such that the exogenous Cushing syndrome will occur when a person uses human-made glucocorticoid medicines to treat an illness. Some of the diseases that are mostly treated with glucocorticoids medicines are inflammatory bowel disease, joints disease like rheumatoid arthritis, type 2 diabetes and brain tumors (Sharma, Nieman &Feelders, 2015).

According to the case study two, the patient, Maureen was diagnosed with two diseases; rheumatoid arthritis (RA) and type two diabetes. Maureen was diagnosed with RA at an early age when she was 15 years. After multiple exacerbations of rheumatoid arthritis, she was advised by her general practitioner (GP) to start using a high dose of corticosteroids. For type two diabetes, Maureen uses metformin for control. The two diseases that Maureen has been diagnosed with are the major incidences that have led to the occurrence of the exogenous Cushing syndrome due to the synthetic medicines she has been using to treat those diseases.

A person with exogenous Cushing syndrome may develop some of the health complications which are as follows; a person with a low immune system may have frequent cases of infections. An exogenous Cushing syndrome patient is at risk of developing diabetes complication as Maureen has developed type 2 diabetes. Risk of blood clots is high to a person with exogenous Cushing syndrome. A person with this disease develops complications like osteoporosis (weak bones) and increased risk of fractures.

The clinical complications of the exogenous Cushing’s syndrome negatively do impact the quality of life of the patient due to the increased morbidity due to other infective diseases and cardiovascular complications. The patient with Cushing’s syndrome is advised to visit a neurocognitive specialist and psychiatrist due to patient’s mental disorders like mania, depression and anxiety. This is because most patient suffering from Cushing syndrome frequently do complain of changes in the physical appearance like where Maureen’s face started to become round, her fats mainly concentrated at her abdominal area and a hump between her shoulders. Other complain that Maureen’s husband noticed were fatigue and emotional instability as it interferes with the family life and workplace performance.

Pathophysiology

The disease has a lot of impact on the family in terms of daily activities and medical cost. Also, there are a lot of duties that are affected in the family that could be done by the patient. After the patient is discharged from the hospital due some of the required exacerbations like in Maureen’s case, her husband has a burden of duties and daily activities to perform while taking care of her to ensure a quick recovery. The family member as in Maureen’s husbands also suffers depression due to the observable changes that occur to her wife both physical and emotional (Wagner-Bartaket al, 2017).

Signs and Symptoms	Pathophysiology
Abdominal pain. Maureen had a body mass index of 28kg/m2,and fat accumulation was mainly contributed around her abdominal area and a high level of low lipoprotein cholesterol density. The patient had increased weight gain due to the accumulation of fat around the abdomen, but fat lacked in the arms, legs, and buttocks which are commonly known as central obesity (Dumesicet al, 2015).	This is induced by the visceral nociceptors stimulation. Pathological events such as for ischemia and inflammation are required for the activation of the nociceptors. It is evidenced that pain states are associated with profound alterations of the sensory input. The Abdominal pain can occur due to the pathology of the visceral structure which only explains the pain complains as there are no objective signs of the visceral lesions (Dumesicet al, 2015).
Gastrointestinal (GI) bleeding. There is perforation of the gastrointestinal when a patient has exogenous Cushing syndrome. Maureen may have developed gastrointestinal bleeding as a result of multiple exacerbations of rheumatoid arthritis which led her to use a high dosage of corticosteroids. Some of the signs of GI bleeding include; tarry stool, dizziness, paleness, abdominal cramps, tiredness and stool mixed with bright red blood.	The pathophysiology of gastrointestinal bleeding is as a result of elevated portal pressure conveyed to the gastric varices and the esophageal leading to gastropathy. The common cause of gastrointestinal bleeding is peptic ulcers which are open sores that develop on the lining of the duodenum. As a symptom of Cushing disease gastrointestinal bleeding is associated with hypercortisolism the patient because of elevated levels of cortisol serum due to clinical signs of perforations (Nieman, 2015).
Fatigue. Maureen’s fatigue has been worsening.  Her blood pressure was 154/106 mmHg, PR of 88bpm and RR of 18bpm on assessment. When a person has fatigue, he/she experiences a vast range of physical emotional and mental symptoms. These signs include; dizziness, moodiness, chronic tiredness, and aching muscles	It is caused by a poor supply of blood to the body tissues. Poor supply of blood can be due to some inflammation diseases as a result of the accumulation of fat in a certain part of the body. The pathophysiology of fatigue can be described as a disorder of the immune response to an antigenic challenge or a precipitating infection (Lacroix, Feelders, Stratakis &Nieman, 2015).

Taking oral corticosteroids drugs in high doses for a long period can to a patient developing exogenous Cushing syndrome. The corticosteroids are also useful in minimizing surgical risk and improve signs and symptoms before and after the surgery. They are useful also in control of cortisol production. These medications include prednisone of which Maureen is currently using which have a similar consequence in the body as cortisol produced in the body. For example, the cobicistat and ritonavir are potent inhibitors of P450 3A4 (CYP3A4) cytochrome activity (Wood, Lacy, Johnston,Weigle & Dhanireddy, 2015).

The corticosteroids are used as sub-therapeutic doses in combination with other drugs like Cushing syndrome protease inhibitors and prednisolone so that to increase their concentrations and lower their dosing. Maureen’s blood test shown low cortisol and ACTH levels due to continuous usage of corticosteroids medicines. These drugs after combinations with protease inhibitors, the pharmacokinetic manipulation as a result of interactions with CYP3A4 substrate leads to the observed body effects (Elliot et al, 2016). The increase of the exogenous corticosteroids plasma concentrations and their half-life may lead to exogenous Cushing syndrome and at supraphysiological levels to suppress adrenocorticotropic hormone (ACTH)and secretion of the endogenous corticosteroids which result to the insufficiency of secondary adrenal.

Maureen has been using metformin to manage type diabetes mellitus which have contributed to the immune suppression due to the glucocorticoids leading to side effects like fluid shift, brain changes and psychological changes. The pharmacokinetic mechanism of the glucocorticoids affects the body as the initial steroids bind to the intracellular glucocorticoid receptors then translocation to the nucleus and changes in the transcription of the gene. In the unbound state the intracellular glucocorticoids receptors are bound to the stable proteins such as immunophilin and shock protein 90 (Morgan, Hassan-Smith &Lavery, 2016).

Assessment goals and information	Nursing diagnosis	Outcome criteria	Interventions	Rationale for the interventions	Outcome evaluation
-Abdominal pain due to exacerbations. – Several tests which include; blood pressure BP 150/106 mmHg, blood glucose level which was 14.0mmol/L. Temperatures 36.90C, the bpm PR 88, bpm RR 18 and body mass index (BMI) which was 28kg/m2 – fatigue and abdominal pain which has been worsening – bone mineral density test and urine test for measuring the cortisol level.	(a). Maureen’s body shape is much influenced by the disease as it has affected her physical body shape. (b). the patient has excess fat concentrated at her abdomen and excess fluid associated with a hump that is between her shoulders (Wilkes et al, 2016). (c). the risk to secondary injury due to fatigue and body weakness. (d). The risk of secondary infections due to the impaired immune system caused by the RA and type 2 diabetes (Van Leeuwen&Bladh, 2017).	(a). The patient experience’s normal body fluid balance and minimal or have no gastrointestinal bleeding. (b). The client will be free from secondary infections. (c). The client will remain free from both internal and external injuries. (d). The client understands the physical effects of the illness and regains her self-esteem in the realization of her desired shape and appearance. (e). The patient regains her normal shape of the face and equal fat’s distribution in the body.	(a). Monitoring of the signs of blood pressure and RR (Garber et al,2017). (b). Weighing of the client’s body mass index by use of the weighing scale. (c). encouraging the patient to elevate her feet when she is sitting. (d). ensuring the room is well lit for the client to be able to dress properly while going out. (e). Provide confidential and privacy environment for the patient and give her a conducive environment to explain herself and restrict visitors without the client permission. (f). While giving care to the client ensure strict surgical sepsis (Nieman et al, 2015).	(a). Elevation of feet while sitting down minimizes the accumulation of fluid within the lower extremities. (b). The accumulation and expansion of the fluid may lead to an increase in sodium pressure and water retention. (c). Excessive cortisol increases the blood pressure which may cause fatigue (Kumar & Kelly, 2017, February).	(a). The abdominal pain reduces, and there are no further signs of infections (Woods et al, 2015). (b). there is no bleeding of the gastrointestinal tract. (c). the decrease in blood pressure. (d). there is no hump within the patient’s shoulders and uniformity in the distribution of fats in the body. (e). The face of the client regains its original shape (Papoianet al, 2015).

 References

Assessment goals and information

Dumesic, D. A., Oberfield, S. E., Stener-Victorin, E., Marshall, J. C., Laven, J. S., &Legro, R. S. (2015). Scientific statement on the diagnostic criteria, epidemiology, pathophysiology, and molecular genetics of polycystic ovary syndrome. Endocrine reviews, 36(5), 487-525.

Elliot, E. R., Theodoraki, A., Jain, L. R., Marshall, N. J., Boffito, M., Baldeweg, S. E., & Waters, L. J. (2016). Iatrogenic Cushing’s syndrome due to drug interaction between glucocorticoids and the ritonavir or cobicistat containing HIV therapies. Clinical Medicine, 16(5), 412-418.

Garber, A. J., Abrahamson, M. J., Barzilay, J. I., Blonde, L., Bloomgarden, Z. T., Bush, M. A., … & Garber, J. R. (2017). Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm–2017 executive summary. Endocrine Practice, 23(2), 207-238.

Kumar, S., & Kelly, A. S. (2017, February). Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. In Mayo Clinic Proceedings (Vol. 92, No. 2, pp. 251-265). Elsevier.

Lacroix, A., Feelders, R. A., Stratakis, C. A., &Nieman, L. K. (2015). Cushing’s syndrome. The lancet, 386(9996), 913-927.

Morgan, S. A., Hassan-Smith, Z. K., &Lavery, G. G. (2016). Mechanisms in endocrinology: tissue-specific activation of cortisol in Cushing’s syndrome. European journal of endocrinology, 175(2), R81-R87.

Nieman, L. K. (2015). Cushing’s syndrome: update on signs, symptoms and biochemical screening. European Journal of Endocrinology, 173(4), M33-M38. 

Nieman, L. K., Biller, B. M., Findling, J. W., Murad, M. H., Newell-Price, J., Savage, M. O., &Tabarin, A. (2015). Treatment of Cushing’s syndrome: an endocrine society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 100(8), 2807-2831.creening. European Journal of Endocrinology, 173(4), M33-M38.

Papoian, V., Biller, B. M., Webb, S. M., Campbell, K. K., Hodin, R. A., &Phitayakorn, R. (2015). PATIENTS’PERCEPTION ON CLINICAL OUTCOME AND QUALITY OF LIFE AFTER A DIAGNOSIS OF CUSHING SYNDROME. Endocrine Practice, 22(1), 51-67. 

Sharma, S. T., Nieman, L. K., &Feelders, R. A. (2015). Cushing’s syndrome: epidemiology and developments in disease management. Clinical epidemiology, 7, 281.

Van Leeuwen, A. M., &Bladh, M. L. (2017). Davis’s comprehensive handbook of laboratory & diagnostic tests with nursing implications. FA Davis.

Wagner-Bartak, N. A., Baiomy, A., Habra, M. A., Mukhi, S. V., Morani, A. C., Korivi, B. R., … &Elsayes, K. M. (2017). Cushing syndrome: diagnostic workup and imaging features, with clinical and pathologic correlation. American Journal of Roentgenology, 209(1), 19-32.

Wilkes, G. M., & Barton-Burke, M. (2016). 2017 Oncology Nursing Drug Handbook. Jones & Bartlett Learning.

Wood, B. R., Lacy, J. M., Johnston, C., Weigle, D. S., &Dhanireddy, S. (2015). Adrenal insufficiency as a result of ritonavir and exogenous steroid exposure: report of 6 cases and recommendation for management. Journal of the International Association of Providers of AIDS Care (JIAPAC), 14(4), 300-305.

Woods, C. P., Argese, N., Chapman, M., Boot, C., Webster, R., Dabhi, V., … & Crowley, R. K. (2015). Adrenal suppression in patients taking inhaled glucocorticoids is highly prevalent and management can be guided by morning cortisol. European journal of endocrinology, 173(5), 633-642.