Case Study Cushing Syndrome 1

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Case Study

Cushing Syndrome
Patient Profile:
T.H. is a 34-year old male elementary school teacher. He seeks the advice of his
HCP because of changes in his appearance over the past year.

Subjective Data:
Reports weight gain (particularly through his midsection), easy bruising, and
edema of his feet, lower legs and hands. He has been having increasing weakness

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and insomnia.

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Objective Data:
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Physical Exam:
B/P 150/110; 2+ edema of lower extremities; purplish striae on abdomen; thin
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extremities with thin, friable skin; severe acne of the face and neck
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Blood analysis:
Glucose 167 mg/dL; white blood cell count (WBC) 13,600 /µL; lymphocytes 12%
( norm 25%-40%); red blood cells count (RBC) 6.0 x 10 ⁶/ µL (low); K+ 3.2 mEq/L
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Discussion Questions:
1. Discuss the probable causes of the alterations in T.H.’ s
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laboratory results
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Manifestations of hyperglycemia, hypokalemia related to hypersecretion of glucocorticoids.


Decreased inflammatory and immune response results in high levels of cortisol which destroys
lymphocytes.
Laboratory findings:
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o increased blood glucose level


o decreased lymphocyte count
o decreased RBC count
o decreased K+
o increased sodium level

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o decreased calcium level
2. Explain the pathophysiology of Cushing syndrome
o The adrenal cortex secretes and excess of glucocorticoids or the
pituitary gland an excess of ACTH as a result of either a pituitary
tumor, pituitary hyperplasia, adrenal tumor or from ongoing
glucocorticoid therapy. An excess of ACTH stimulates the release of
cortisol.

3. What diagnostic testing would identify the cause of T.H.’s


Cushing syndrome?
Diagnosis of Cushing's syndrome is based on a review of your medical history, physical examination
and laboratory tests, which help to determine the presence of excess levels of cortisol.
 Pituitary adenoma is the most common cause of Cushing’s disease, and magnetic resonance
imaging (MRI) would visualize such a tumor. The other imaging to identify lesions: X-rays, CT

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scans, Arteriography.

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 Diagnosis of Hypercortisolism

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o Diagnostic evaluation of hypercortisolism includes assessment of

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 cortisol levels

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 results of suppression tests
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 serum electrolytes.
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o Blood, salivary and urine cortisol test will be high
o Plasma ACTH levels vary, depending on the cause of the problem
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 pituitary Cushing’s: high level


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 adrenal Cushing’s: low level


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o Measurement of urinary free cortisol is used as an initial screening tool because it


measures urine cortisol over a 24-hour period.
 Dexamethasone suppression testing:
 Takes place overnight or over a 3 day period.
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 When cortisol levels are suppressed by dexamethasone,


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Cushing’s disease is not present


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4. What is the usual treatment of Cushing syndrome?


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○ Drug therapy Involves the use of drugs that interfere with:


■ adrenocorticotropic hormone (ACTH) production
■ adrenal hormone synthesis for temporary relief
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○ Metyrapone (Metopirone); aminoglutethimide (Elipten, Cytadren) & ketoconazole use


different pathways to decrease cortisol production.
○ Cyproheptadine (Periactin): used in patients with hypercortisolism resulting from ACTH
production. ( It interferes with ACTH production)
○ Mitotane (Lysodren) is an adrenal cytotoxic agent used for inoperable tumors causing
hypercortisolism.

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○ Mifepristone (Korlym) is a synthetic steroid that blocks glucocorticoid receptors. Used in
patients with type 2 diabetes who have increased ACTH production and have not
responded to other drug therapies. Cannot be used during pregnancy. It blocks
progesterone receptors and would cause termination of a pregnancy.
o Pasireotide (Signifor)
o Surgical Management
■ Surgical treatment of adrenocortical hypersecretion depends on the cause of the
disease

5. What is meant by a “medical adrenalectomy”


○ Adrenalectomy
■ May be unilateral or bilateral
■ Usually minimally invasive: laparoscopic adrenalectomy

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● If needed, an open surgery through the abdomen or lateral flank may be

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done.

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■ Patient is usually in the ICU postoperatively
■ Lifelong glucocorticoid & mineralocorticoid replacement is needed after a

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bilateral adrenalectomy
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■ In unilateral adrenalectomy, hormone replacement continues until the remaining
adrenal gland increases hormone production (may take 2 years)
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6. What are the priority nursing responsibilities in the care of T.H.?


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○ The basis of medical management for hypercortisolism and fluid overload include:
■ Patient safety
■ Drug therapy
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■ Nutrition therapy
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■ Monitoring
○ Management
■ Focuses on preventing complications associated with:
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● Fluid overload
● Immune status
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● Skin integrity
● Body structure
■ Prevent fluid overload- monitor for indicators:
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● bounding pulse
● increasing neck vein distention
● lung crackles
● increasing peripheral edema
● reduced urine output

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■ Monitor for and prevent any skin breakdown
■ Nutrition therapy may involve restrictions of fluid and sodium intake.
● Monitor intake and educate patient.
■ Monitor intake and output and weight:
● Can indicate therapy effectiveness.
○ Ensure that these measurements are accurate.
○ Weigh patient daily (same time, same scale, similar clothing)
■ Administer medications as ordered & monitor response
■ Emotional support

7. Based on the assessment data presented, what are the priority nursing
diagnoses?
1. Disturbed body imagine related to acne on face and neck.
2. Risk for infection related to abnormal lab values.

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3. Risk for injury related to potential diminished bone density.

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8. What are the complications of this disorder?

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o Complications of Hypercortisolism

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○ Osteoporosis:
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■ may develop relative to the effects of cortisol on bone density
■ Increase the risk of pathological fractures
○ Acute adrenal crisis
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■ may occur in patients with hypercortisolism secondary to exogenous


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corticosteroid therapy if the medication is abruptly withdrawn


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○ Elevated serum glucose


■ may complicate the management of diabetes mellitus in patients with this
disorder
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○ Gastrointestinal bleeding:
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■ May develop as a result of:


● decreased mucus production in the GI tract
● decreased blood flow
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● release of hydrochloric acid secondary to the effects of cortisol.


○ Infection:
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■ Increased risk
■ Glucocorticoids reduce both the inflammation and he immune responses.
o Risk for impaired skin integrity
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o Risk for thromboembolism


o Cardiac dysrhythmias
o HTN
o Kidney stones

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