Cushing Syndrome: Aetiology, Pathophysiology, Post-operative Deterioration and Nursing Management

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Acute Nursing

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Q1.
Aetiology :
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).
Pathophysiology:
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

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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).
Q2.
Post-operative deterioration :
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).
Nursing management :