Adrenalectomy Pathophysiology and Nursing Care

Running head: NURSING ASSIGNMENT
NURSING ASSIGNMENT
Name of the Student
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Author’s note

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Adrenalectomy pathophysiology and nursing care
Susan Summer is a 40 year old female having 3 children and has been diagnosed with
type 2 diabetes. Susan has been admitted in to the hospital due to some changes in her
appearance due to Cushing syndrome, caused due to benign tumor on the right adrenal gland.
Susan has been admitted to the ED for a laparoscopic right adrenalectomy. This analysis will
help to identify the aetiology and the pathophysiology of the patient’s condition. This will also
help to provide the underlying pathophysiology of the underlying condition of the patient in the
post operative period. The paper also aims to discuss about the specific priorities of care for
Susan and the possible referrals.
According to the case study Susan was suffering from Cushing syndrome. Discussing
about the pathophysiology of Cushing syndrome is a disorder that is caused when the body has
got higher level of cortisol hormone. Cortisols are released by adrenal tumors (Aksakal et al.,
2013). Non cancerous tumors such as Adrenal adenomas and macronodular hyperplasia that
causes enlargement of the adrenal gland and the over production of the cortisol. Excess
glucocorticoid production can be because of primary adrenal lesions or ACTH producing
pituitary adenoma (Allolio, 2015). The production of the cortisol occurs by a precise chain of
events. At first the hypothalamus of the brain sends corticotropin releasing hormone to the
pituitary gland (de La Villéon et al., 2015). The CRH helps the pituitary to release the
adrenocorticotropin hormone which in turn stimulates the adrenal glands. The adrenal glands
respond by secreting cortisol (Lacroix et al., 2015). The Cushing syndrome can be ACTH
dependant or ACTH independent. If it is ACTH independent then it can be caused by the

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overproduction of the glucocorticoids due to the adrenal adenoma (de La Villéon et al., 2015).
The ACTH level in the ACTH dependant Cushing syndrome is less because of the negative
feedback control to the corticotrophin cells of the pituitary from high level of serum cortisol
(Lacroix et al., 2015). The most common signs and symptoms involve moon faces, supraclavial
fat pads, truncal obesity which is clearly seen in Susan, purple striae and facial plethora. Other
features are weight gain, excess hair growth in women, fatigue and hypertension (Lacroix et al.,
2015).
The clinical manifestations of Susan can be linked to the pathophysiology of the clinical
condition in many ways. Some of the risk factors related to Cushing syndrome are obesity and
the case study reveals that the BMI of Susan is quite high. Obesity in Susan can be linked with
excess adrenocorticotrophic hormone, cortisol or the CRH levels (Husebye et al., 2012).
Normally cortisol accumulates in the body and replaces the consumed fats and the carbohydrates,
and this is how it maintains the BMI (Lacroix et al., 2015). But in case of Susan the cortisol level
is high in the body which would require more carbohydrates. Hence excess cortisol metabolizes
the food even there is no requirement (Iacobone et al., 2015). Hence excess fats get accumulated
in different parts of the body. One of the symptoms of Cushing syndrome is the high blood sugar
level. DM in CS is caused due to the insulin resistance and impaired insulin secretion by the
excess of glucocorticoids (Husebye et al., 2012). Insulin resistance is brought about the excess of
GC by interfering with the insulin signaling cascade, which ultimately results in low uptake and
synthesis of glycogen. Excess GC also leads to excess lipolysis. The augmentation in the level of
the amino acids further impairs the insulin signaling pathway, this ultimately diabetes (Mazziotti
et al., 2013).