Analysis of Cushing's Syndrome and Related Studies

The provided document is an assignment that delves into the realm of endocrinology, specifically focusing on Cushing's syndrome. The content encompasses a broad range of topics, from the definition and causes of this condition to its symptoms, diagnosis, and treatment options. Additionally, it includes a systematic review of various studies related to Cushing's syndrome, highlighting key research findings and methodologies. This comprehensive analysis is likely intended for students in medical or health-related programs, serving as a valuable resource for understanding this complex endocrine disorder.

Running head: NURSING
Nursing
Name of the Student
Name of the University
Author note

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Case study-Susan summers
Cushing syndrome results in prolonged Cortisol secretion that leads to several signs and
symptoms. There are various causes of this syndrome including high cholesterol level, side
effects of steroid medications (Lacroix et al., 2015). The essay focuses on the case study of
Susan Summers and discusses the aetiology, pathophysiology of the disease presented and the
post-operative deterioration. Aappropriate nursing management of the patient during this time is
outlined in essay.
The most common cause of the Cushing syndrome is the exogenous corticosteroid
exposure. Endogenous Cushing syndrome in 70-80% cases is caused by adrenocorticotropic
hormone (ACTH). The hormone secretes pituitary adenomas. These adenomas secrete excessive
ACTH only in 10-15% of cases (Seltzer et al., 2015). Endogenous Cushing syndrome in 10% of
the time is caused by the adrenal adenomas that involve secretion of Cortisol in unregulated
manner. Adrenal adenomas 6-9% of the time secrete Cortisol autonomously (Lacroix et al.,
2015). In the endogenous, hypercortisolism, no specific modifiable factors have been identified.
Overall there is a poor understanding of the etiology of the pituitary overproduction of ACTH
(Lacroix et al., 2015). On the other hand the etiology of overproduction of Cortisol due to
adrenal function is also poorly understood. Adrenal carcinoma results in Cushing syndrome in
about 1% cases and in 30-40% of the cases results in adrenal overproduction of Cortisol, which
is known as the ACTH-independent Cushing syndrome (Lacroix et al., 2015). Genetic factors
also play role in the Cushing syndrome. On the aspect of etiology, mutation has been identified
in patients with this syndrome in new gene, ubiquitin-specific protease 8 (Dekkers et al., 2013).

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The literature on aetiology shows that, the patient’s presenting Cushing syndrome can be
due to the endogenous glucocorticoid overproduction. Cushing syndrome is manifested due to
ACTH independent hypercortisolism. It is primarily due to adrenocortical neoplasm that is
adenoma as commonly known. It is rarely called as carcinoma (Lacroix et al., 2015). In this
disease there is an excess secretion of Cortisol. In ACTH independent hypercortisolism, the level
of ACTH is low due to negative feedback. It occurs from high serum Cortisol level that gives
negative feedback to pituitary corticotroph cells (Lacroix et al., 2015). In Cushing syndrome that
is ACTH dependent the level of ACTH is high that stimulates the adrenal gland to secrete excess
Cortisol. It is attributed to the anterior pituitary tumor. However, Cushing syndrome is also
caused by the Nonpituitary ectopic sources of ACTH (Lacroix et al., 2015). It includes
neuroendocrine tumors, resulting in the high ACTH levels. Eventually it results in the
hypercortisolism (Prodam et al., 2013). It is manifested in the form of severe muscle weakness
and weight loss. The clinical manifestation results from excess exposure of the tissues to the
Cortisol. It is the case of Susan Summers, who is diagnosed with Cushing syndrome due to
benign tumour of her right adrenal gland. It is also called as adrenal adenomas (Nieman, 2015).
It is the reason for excess production of Cortisol in the patient as adrenal gland comprises of
Cortisol producing cells. The patient is suffering from ACTH independent Cushing syndrome.
The symptoms associated with the disease are the obesity, diabetes, hypertension,
weakness, moon face, menstrual abnormalities, excess hair growth and problems in bones
(Pivonello et al., 2016). Two of the above symptoms noted in the patient given in case study are
obesity and type 2 diabetes. Excess secretion of Cortisol results in high blood glucose level and
causes weight gain. Patients with this syndrome in 60-70% of the cases have been found to have
impaired glucose tolerance. It results in diabetes eventually and specifically type 2 diabetes if

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there is an insulin resistance and obesity (Karaman et al., 2017). When glucose tolerance is
impaired, the beta cells of pancreas are unable to increase the insulin secretion to compensate for
the insulin resistance (Elliott & Coventry, 2012). Body cells like muscles, liver, and fat cells fail
to respond to insulin. Liver cells fail to store glycogen, triglycerides are broken to fatty acids for
energy in fat cells and muscle cells are deprived of energy (Pivonello et al., 2016). It increases
the glucose level. People like Susan with type 2 diabetes have high likelihood of developing
Cushing syndrome.
Obesity is caused by increase weight gain and fat level. Cortisol alters the metabolism of
carbohydrates, proteins, and fats when secreted in excess level. It is the chief stress hormone of
the body and helps reduce inflammation (Polak et al., 2016). Excess Cortisol increases the
appetitite and therefore enhances fat synthesis and accumulation. It results in weight gain and
obesity (Bizarro et al., 2015). On the other hand active Cortisol is also produced by the Adipose
stromal cells. These cells are not from subcutaneous fat but from the omental fat. This Cortisol is
produced from the inactive cortisone via expression of enzyme 11β-HSD1. This enzyme has
increased expression after exposure to Cortisol. Thus, glucocorticoids are constantly exposed to
the omental adipose tissues (Rodriguez et al., 2015). Excess glucorticoids stimulates
gluconeogenesis in the liver. They increase glucose production and inhibit the insulin sensitivity.
It is eventually manifested as diabetes (Bizarro et al., 2015).
Postoperative patient are regularly assessed to rule out any abnormality and
complications, as they commonly occur after surgery (Brown et al., 2017). It includes
measurement of vital signs and general physical condition. The blood pressure in normal
condition should be 120/80 mmHg, whereas the patient showed higher than the range (160/90
mm Hg) indicating high blood pressure and hypertensiveness. A high pulse rate was observed in

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patient (128bpminstead of 50-80 bpm). A higher respiration rate (more than 20bpm instead of
normal range 16-20) was observed indicating tachypnea. It means more inspiration and
expiration per unit time than usual (Elliott & Coventry, 2012). According to Pivonello et al.,
(2016) high blood pressure is linked to elevated heart rate. It is caused by weight gain and
obesity and are considered a major risk factor. Alcohol consumption also elevates blood pressure
and heart rate and is known to decrease respiratory functions. Susan as per the case history takes
a bottle of wine every night. Respiratory complications are outcome of obesity as per Bizarro et
al., (2015) that increases oxygen demand.
There is also fall in body temperature that is 35°C instead of the normal 36.5 °C. It may
be called hypothermia that results in decreased metabolic rate. Heat generation is lowered and
hormones are stimulated to compensate for loss. This is overall reflected in the vital signs of the
patient. Fall in body temperature is associated with decreased cardiac outpour and oxygen intake.
It may be the cause of irregular heart rhythm (Pasquier et al., 2014). After any surgical
procedure, the urine output is monitored. The normal output is 800-2000 milliliters/day and is
observed to lower after surgical procedure, whcih in case Susan is adrenalectomy. Urine output
is also affected by the pneumoperitoneum that increases abdominal pressure and decrease urine
production (Nieman, 2015). It is clear indication of deterioration after the patient underwent
laparoscopic right adrenalectomy.
The Cushing syndrome is also responsible for the deterioration of the patient after
laparoscopic right adrenalectomy (Jamali, 2017). Excess secretion of Cortisol disturbs the renal
function due to impairment in conversion of Cortisol to cortisone. This condition increases the
level of mineralocorticoids, and ability of renal tubules to reabsorb sodium. Impaired renal
function also results in hypokalemia (Hine, Schwell & Kairys, 2017). Increased Cortisol also

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elevates the glucorticoids in addition to mineralocorticoids. The former result in the high plasma
volume, and worsens the hypertension. It increases the cardiac output through peripheral
vascular resistance. Therefore, it is manifested as high blood pressure and hypertensive effects.
Glucocorticoids increases renovascular resistance and sequentially hypertension (Pivonello et al.,
2016). The deterioration overall indicates need of person centered and evidence based care to
ensure patient’s safety.
The nurse must provide routine post-op care and observe for any hemorrhage and shock.
The nurse must be involved in regular monitoring of vital signs. The physician may administer
IV therapy and order vasopressors (Fleseriu & Petersenn, 2015). To restore normal function of
adrenal gland, steroid therapy may be started. Wound care is mandatory to prevent the infections.
Wound dressing shall be performed in aseptic technique (Fleseriu, 2015). Respiratory infection
can be prevented by asking patient to cough and take deep breaths (Iacobone et al., 21015). The
concerned physician on collaboration with endocrinologist must administer the cortisone or
hydrocortisone to balance the Cortisol (Geiger et al., 2015). Pain medication using NSAIDS such
as ibuprofen should be prescribed. The patient may be administered with laxatives to prevent
constipation due to side effects caused by medication. The care plan also requires nurses to
provide patient with discharge instructions. Patient education shall be based on the importance of
follow up care and self care such as hygiene, and adherence to medication (Fleseriu, 2015).
A multidisciplinary team may be involved in care process of Susan. The nurse may
design effective care and discharge plan for the patient post operation as well advocate for
healthy lifestyle interventions. The nurse plays a vital role in patient’s pain management. An
endocrinologist may develop interventions for restoring the hormonal imbalance that is excess
Cortisol (Melmed, 2016). The nurse may refer the patient to physical therapist. The role of

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therapist is to enhance the mobility after discharge and increase ability to resume activities of
daily living (Australian physiotherapy association, 2016). The patient may be recommended
balanced diet by the nutritionist as well instructions on daily fluid intake. Currently the patient
may be asked by nutritionist to consume protein rich diet to reduce weight (Dietiticians
association of Australia, 2014). This kind of care from the team of health care professionals will
help Susan to improve her clinical conditions and live normally after discharge.
In conclusion, the case of Cushing syndrome has helped to develop the skills required to
design care plan based on evidence. It helped develop patient centered care for Susan’s illness
after surgery. The essay helped to learn the role of nurse in surgical care. The case study helped
improve problem-solving skills and critical thinking. The skills of clinical reasoning are
important to understand the clinical deterioration of the patient and develop appropriate
interventions.

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