SUBMITTED BY: MUSTAPHA, NAJIEFAH P. SUBMITTED TO: PLAZA, CHARLIE C.

RN, MN,MAN

INTRODUCTION What is Cushing Syndrome? >Cushings syndrome is a hormonal disorder caused by prolonged exposure of the bodys tissues to high levels of the hormone cortisol. Sometimes called hypercortisolism, Cushings syndrome is relatively rare and most commonly affects adults aged 20 to 50. People who are obese and have type 2 diabetes, along with poorly controlled blood glucose and high blood pressure, have an increased risk of developing the disorder. >result from excessive rather than deficient, adrenocortical activity ANATOMY AND PHYSIOLOGY Each person has 2 adrenal glands, one attached to the upper portion of the kidney. Each adrenal gland is in reality, two endocrine glands with separate, independent functions. ADRENAL MEDULLA >Located at the centre of the glands secretes catecholamines >fxn as part of the autonomic nervous system. Stimulation of paraganglionic sympathetic nerve fibers, which travels directly to the cells of the adrenal medulla, causes release of catecholamine hormones (epinephrine and norepinephrine). 90% of epinephrine is secreted. >catecholamine regulates metabolic pathways to promote catabolism of stored fuels to meet caloric needs from endogenous sources. >the major effects of epinephrine is for fight or flight response. secretion of epinephrine causes decreased blood flow to tissues that are not needed in emergency situations, and increases blood flow to tissues that are important for effective fight or flight, such as cardiac and skeletal muscle.

>catecholamines also induce the release of free fatty acid, increased the basal metabolic rate and elevate the blood glucose level. ADRENAL CORTEX >adrenocortical secretions make it possible for the body to adapt to stress at all kinds. THREE TYPES OF STEROID HORMONES PRODUCED BY ADRENAL CORTEX 1. GLUCOCORTICOID >prototype of which is hydrocortisone secretion results in elevated blood glucose level >secreted in response to the release of adrenocorticotropic hormone from the anterior lobe of the pituitary gland. 2. MINERALOCORTICOID >exert a major effect in electrolyte metabolism. Act principally in renal tubular and gastrointestinal epithelium to cause increased sodium ion absorption in exchange for secretion of potassium ions or hydrogen ions. >ACTH only minimally influences aldosterone secretion, is primarily secreted in response to the presence of angiotensin II in the blood stream.

3. ADRENAL SEX HORMONE >or androgens is the third major type of steroid hormone secreted by the adrenal cortex, exerts effect similar to those of male sex hormones. May also secretes small amount of estrogen.

PATHOPHYSIOLGY OF CUSHIING SYMDROME ETIOLOGY >use of corticosteroid medication >hyperplasia of adrenal cortex >tumor of the pituitary gland >ectopic production of ACTH by malignancies (bronchogenic carcinoma) cause production of ACTH that stimulates the adrenal cortex to increased its hormone secretion

mineralocorticoid sodium retention potassium

glucocorticoids cortisol BUFFALO HUMP- due to steroid level

Fluid retentionEdema/anasarca

glucose/ hyperglycemia moonface- due to cortisol level Tronchal obesity supraclavicular area due to fat deposit

Hypertension

CHF

heavy trunk & relatively thin extremitiesDue to massive protein catabolism

Sex hormone

immune pattern susceptibility to infection

skeletal problem

dematologic problem

Virilism- characterized By appearance of Masculine traits & Recession of feminine traits

osteoporosis

thin fragile, easily traumatized ecchymosis, strea develops

impaired wound healing

muscle wasting

psychiatric problem

hirsutism

kyphosis backache psychoses

breast atrophy constipation clitoris enlargement` libido depression/distress, mood alteration

Menstrual cease

Voice deepen

ASSESSMENT AND DIAGNOSTIC FINDINGS No single lab test is perfect and usually several are needed. The three most common tests used to diagnose Cushings syndrome are the 24-hour urinary free cortisol test, measurement of midnight plasma cortisol or late-night salivary cortisol, and the low-dose dexamethasone suppression test. Another test, the dexamethasone-corticotropin-releasing hormone test, may be needed to distinguish Cushings syndrome from other causes of excess cortisol.

24-hour urinary free cortisol level. In this test, a persons urine is collected several times over a 24-hour period and tested for cortisol. Levels higher than 50 to 100 micrograms a day for an adult suggest Cushings syndrome. The normal upper limit varies in different laboratories, depending on which measurement technique is used. Midnight plasma cortisol and late-night salivary cortisol measurements. The midnight plasma cortisol test measures cortisol concentrations in the blood. Cortisol production is normally suppressed at night, but in Cushings syndrome, this suppression doesnt occur. If the cortisol level is more than 50 nanomoles per liter (nmol/L), Cushings syndrome is suspected. The test generally requires a 48-hour hospital stay to avoid falsely elevated cortisol levels due to stress. However, a late-night or bedtime saliva sample can be obtained at home, then tested to determine the cortisol level. Diagnostic ranges vary, depending on the measurement technique used.

Low-dose dexamethasone suppression test (LDDST). In the LDDST, a person is given a low dose of dexamethasone, a synthetic glucocorticoid, by mouth every 6 hours for 2 days. Urine is collected before dexamethasone is administered and several times on each day of the test. A modified LDDST uses a onetime overnight dose. Cortisol and other glucocorticoids signal the pituitary to release less ACTH, so the normal response after taking dexamethasone is a drop in blood and urine cortisol levels. If cortisol levels do not drop, Cushings syndrome is suspected. The LDDST may not show a drop in cortisol levels in people with depression, alcoholism, high estrogen levels, acute illness, or stress, falsely indicating Cushings syndrome. On the other hand, drugs such as phenytoin and phenobarbital may cause cortisol levels to drop, falsely indicating that Cushings is not present in people who actually have the syndrome. For this reason, physicians usually advise their patients to stop taking these drugs at least 1 week before the test.

Dexamethasone-corticotropin-releasing hormone (CRH) test. Some people have high cortisol levels but do not develop the progressive effects of Cushings syndrome, such as muscle weakness, fractures, and thinning of the skin. These people may have pseudo-Cushings syndrome, a condition sometimes found in people who have depression or anxiety disorders, drink excess alcohol, have poorly controlled diabetes, or are severely obese. Pseudo-Cushings does not have the same long-term effects on health as Cushings syndrome and does not require treatment directed at the endocrine glands. The dexamethasone-CRH test rapidly distinguishes pseudo-Cushings from mild cases of Cushings. This test combines the LDDST and a CRH stimulation test. In the CRH stimulation test, an injection of CRH causes the pituitary to secrete ACTH. Pretreatment with dexamethasone prevents CRH from causing an increase in cortisol in people with pseudo-Cushings. Elevations of cortisol during this test suggest Cushings syndrome.

TREATMENT When Cushing's syndrome results from an ACTH-producing tumor of the pituitary gland (Cushing's disease), treatment may include surgery, radiation, or medication to lower cortisol levels. Surgical removal of a small, well-defined pituitary adenoma is called transsphenoidal adenomectomy. The pituitary is located at the base of the brain. It is possible to access this area through the gums above the upper front teeth or the nose. Using special instruments, the surgeon makes an incision in one of these areas . The incision is extended through the sphenoid sinus, allowing the surgeon to see and remove the adenoma with an endoscope (a thin, lighted tube with a camera). This type of surgery permanently cures Cushing's syndrome in 60 to 70 percent of people. Sometimes a tumor cannot be identified; in these cases, half of the pituitary gland may be removed (hemihypophysectomy) or 85 to 90 percent of the pituitary gland may be removed (subtotal hypophysectomy) to be certain that the tumor has been removed. Surgical removal of half or more of the pituitary gland can reduce pituitary function and interfere with ovulation (in women) and sperm production (in men). Lifelong hormone replacement is often necessary after surgery. Radiation Radiation can be a useful treatment when pituitary tumors cannot be completely removed by surgery. Radiation of pituitary tumors reduces cortisol levels in about half of adults and most children with Cushing's disease. Because this cortisol-lowering effect takes time (3 to 12 months), medications that lower adrenal cortisol production may

be given while waiting for the effects of radiation. These medications include ketoconazole, metyrapone, and aminoglutethimide. Adrenalectomy Surgical removal of the adrenal glands (adrenalectomy) is a final measure that may be recommended if other treatments are not successful. Adrenalectomy stops excess cortisol production but requires that you begin lifelong daily glucocorticoid and mineralocorticoid replacement therapy.

NURSING DIAGNOSIS Risk for infection related to altered protein metabolism and inflammatory response

PLANNING >decreased risk of infection >improved skin integrity

INTERVENTION RATIONALE >tell the pt. to avoid >the nurse frequent unnecessary exposure assess the pt. for to infection. subtle signs of infection, because he anti-inflammatory effects of corticosteroids may mask the common signs of inflammation and infection. >stress proper hand washing by all care giver bet. Therapies of the pt >monitor clients visitor >to prevent cross contamination of the pt.

>to prevent any transmission of any respiratory illness >To prevent any occurrence of infection >to prevent the risk for any nosocomial infection

>promote reverse isolation >instruct client to have daily mouth care, include use of aseptic mouth wash >maintain sterile technique for all

>to prevent associated infection

NURSING DIAGNOSIS Risk for injury related to weakness

PLANNING >decreased risk for injury >demonstrate behaviours, lifestyle changes to reduce risk factor and protect self for injury

INTERVENTION >note client age, gender, developmental stage, decision making, ability, level of cognition/competence. >assess mood, coping abilities, and personality style >assess clients muscle strength, gross and fine motor coordination >provide environment of safety

RATIONALE >affects client ability to protect self from harm

>may result in careless/increased risktaking without consideration of consequences >to identify risk for falls

>To prevent any unusual accident

NURSING DIAGNOSIS Self-care deficit related to weakness, fatigue, muscle wasting

PLANNING >identify individual areas of weakness / needs. >perform self-care activities within level of own ability.

INTERVENTION >determine age/developmental issues >determine individual strengths and skills of the client >assisting client with ADL >provide privacy and equipment within easy reach during personal care >collaboration with physical therapist in rehabilitation >identify energy saving activities

RATIONALE >affecting individual ability to participate in own care.

>to have an idea of what the client can do >to prevent further fatigue >to prevent any complication that may arise

>to identify the pt. improvement >to prevent any further weakness and fatigue