Nursing management CUSHING'S SYNDROME.pptx

546 views 26 slides Apr 19, 2024
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About This Presentation

Notes on Cushing's syndrome


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CUSHING’S SYNDROME NABIRYE MIRIA 2017/U/NSM/005/P

CUSHING’S SYNDROME C ushing’s syndrome (Cushing's disease, hypercortisolism, adrenal hyper function) is a cluster of clinical abnormalities caused by excessive levels of adrenocortical hormones (particularly cortisol) or related corticosteroids and, to a lesser extent, androgens and aldosterone. The prognosis depends on the underlying cause; it’s poor in untreated people and in those with untreatable ectopic  corticotrophin-producing carcinoma. Cushing’s syndrome results from excessive, rather than deficient, adrenocortical activity. The syndrome may result from excessive administration of corticosteroids or ACTH or from hyperplasia of the adrenal cortex.

Functions of cortisol hormone R egulate your blood pressure Reduces inflammation. Cortisol helps your body respond to stress. It also regulates the metabolism of proteins, carbohydrates and fats in your diet into usable energy.

Statistics and Incidences Incidences of Cushing syndrome are already common worldwide. Cushing’s syndrome affects 13 of every 1 million people. It is more common in  women  than in men and occurs primarily between ages 25 and 40.

Causes (endogenous and exogenous) Excess of cortisol hormone  In approximately 70% of patients, Cushing’s syndrome results from excessive production of corticotropin and consequent hyperplasia of the adrenal cortex. Tumor. In the remaining 30% of the patients, Cushing’s syndrome results from a cortisol-secreting adrenal tumor, which is usually benign .(ACTH tumors) A primary adrenal gland disease . Familial Cushing syndrome. Rarely, people inherit a tendency to develop tumors on one or more of their endocrine glands, affecting cortisol levels and causing Cushing syndrome.

PATHOPHYSIOLOGY Cushing’s syndrome is commonly caused by use of corticosteroid medications and is infrequently due to excessive corticosteroid production by the adrenal cortex (Tierney et al., 2001 ). However, overproduction of endogenous corticosteroids may be caused by several mechanisms, including a tumor of the pituitary gland that produces ACTH and stimulates the adrenal cortex to increase its hormone secretion despite adequate amounts being produced.

CONT. Primary hyperplasia of the adrenal glands in the absence of a pituitary tumor is less common . Another less common cause of Cushing’s syndrome is the ectopic production of ACTH by malignancies; bronchogenic carcinoma is the most common type of these malignancies. Regardless of the cause, the normal feedback mechanisms that control the function of the adrenal cortex become ineffective, and the usual diurnal pattern of cortisol is lost.

Clinical manifestations Muscle weakness. Muscle weakness is due to hypokalemia or a loss of muscle mass from increased catabolism. Buffalo hump. Buffalo hump is one of the symptoms included in the Cushing’s triad, and these are fat pads over the upper back. Moon face. Moon face is a symptom included in the Cushing’s triad and are recognized as excess fats over the face. Truncal obesity. Fat pads throughout the trunk refers to truncal obesity, one of the symptoms in Cushing’ triad

cont. Peptic ulcer results from increased gastric production and pepsin secretion, and decreased gastric mucus. Irritability and emotional lability ranges from euphoric behavior to  depression  and psychosis. Hypertension  occurs due to sodium and water retention. Compromised immune system. Increased susceptibility to infection due to decreased lymphocyte production and suppressed antibody formation Abdominal striae hirtusim

Endocrine/Metabolic Truncal obesity, Moon face, Buffalo hump, Sodium retention, Hypokalemia, Metabolic alkalosis, Hyperglycemia, Menstrual irregularities, Impotence, Negative nitrogen balance, Altered calcium metabolism, Adrenal suppression Immune Function Decreased inflammatory responses Impaired wound healing Increased susceptibility to infections Cardiovascular Hypertension Heart failure Clinical manifestations per system

Skeletal Osteoporosis, Spontaneous fractures, Aseptic necrosis of femur, Vertebral compression, fractures Gastrointestinal Peptic ulcer, Pancreatitis Muscular Myopathy, Muscle weakness Dermatologic Thinning of skin, Petechiae, Ecchymoses, Striae, Acne Psychiatric Mood alterations, Psychoses Clinical manifestations per system

Clinical Manifestations The classic picture of Cushing’s syndrome I n the adults there is that of central-type obesity, with a fatty “buffalo hump” in the neck and supraclavicular areas, a heavy trunk , and relatively thin extremities. The skin is thin, fragile, and easily traumatized; ecchymoses (bruises) and striae develop Sleep is disturbed because of altered diurnal secretion of cortisol.

Cont. Signs and symptoms women with Cushing syndrome may experience Thicker or more visible body and facial hair (hirsutism) Irregular or absent menstrual periods Signs and symptoms men with Cushing syndrome may experience Decreased libido Decreased fertility Erectile dysfunction

Complications Addisonian crisis.  The patient with Cushing’s syndrome whose symptoms are treated by withdrawal of corticosteroids, by adrenalectomy, or by removal of a pituitary tumor is at risk for adrenal hypofunction and addisonian crisis. Bone loss (osteoporosis), which can result in unusual bone fractures, such as rib fractures and fractures of the bones in the feet High blood pressure (hypertension) Type 2 diabetes Frequent or unusual infections Loss of muscle mass and strength

Patients at risk Patients going for organ transplant Patients with neurological conditions

Diagnosis Low-dose dexamethasone suppression test. Dexamethasone (1 mg) is administered orally at 11pm, and a plasma cortisol level is obtained at 8am the next morning, and this usually confirms the diagnosis of Cushing’s syndrome . Suppression of cortisol to less than 5 mg/ dL indicates that the hypothalamic-pituitary-adrenal axis is functioning properly Stimulation test. In a stimulation test, administration of metyrapone, which blocks cortisol production by the adrenal glands, tests the ability of the pituitary gland and hypothalamus to detect and correct low levels of plasma cortisol by increasing corticotropin production.

CONT. Imaging studies. Ultrasound, CT scan, or angiography localizes adrenal tumors and may identify pituitary tumors. Electrolyte levels. A patient with Cushing’s syndrome include an increase in serum sodium and a decrease in potassium levels. Blood studies. Indicators of Cushing’s syndrome include an increase in the blood glucose levels, a reduction in the number of eosinophils, and disappearance of lymphoid tissue.

management Pituitary irradiation. Patients with pituitary-dependent Cushing’s syndrome with adrenal hyperplasia and severe cushingoid symptoms (such as psychosis, poorly controlled diabetes mellitus, osteoporosis, and severe pathologic fractures) may require pituitary irradiation. Adrenal enzyme inhibitors. Metyrapone, aminoglutethimide, mitotane, and ketoconazole may be used to reduce hyperadrenalism if the syndrome is caused by ectopic ACTH secretion by a tumor that cannot be eradicated. Cortisol therapy. Cortisol therapy is essential during and after surgery, to help the patient tolerate the physiologic stress imposed by the removal of the pituitary or adrenals.

CONT. Transsphenoidal hypophysectomy. Surgical removal of the tumor by transsphenoidal hypophysectomy is the treatment of choice if Cushing’s syndrome is caused by pituitary tumors and has an 80% success rate. Adrenalectomy. Adrenalectomy is the treatment of choice in patients with primary adrenal hypertrophy.

Nursing concerns Body image Body weakness Reduced immunity

ASSESSMENT Health history.  The history includes information about the patient’s level of activity and ability to carry out routine and self-care activities. Physical exam. The skin is observed and assessed for trauma, infection, breakdown, bruising, and edema. Mental function. The nurse assesses the patient’s mental function including mood, responses to questions, awareness of environment, and level of depression .

NUURSING DIAGNOSIS Risk for injury related to weakness. Risk for infection related to altered protein metabolism and inflammatory response. Self-care deficit  related to weakness, fatigue, muscle wasting, and altered sleep patterns. Impaired skin integrity related to edema , weight gain, impaired healing, and thin and fragile skin. Disturbed body image related to altered physical appearance, impaired sexual functioning, and decreased activity level. Disturbed thought processes related to mood swings, irritability, and depression.

NURSING DIAGNOSIS Disturbed body image related to altered physical appearance, impaired sexual functioning, and decreased activity level. GOAL Patient will have an improved body image INTERVENTIONS Discuss the impact that changes have had on patient’s self-concept and relationships with others. Major physical changes will disappear in time if the cause of Cushing syndrome can be treated. Weight gain and edema may be modified by a low-carbohydrate, low-sodium diet; a high-protein intake can reduce some bothersome symptoms. EVALUATION Patient had improved body image

NURSING DIAGNOSIS Risk for injury  related to weakness. GOAL Patient will have no injury INTERVENTIONS Provide a protective environment to prevent falls, fractures, and other injuries to  bones  and soft tissues. Assist the patient who is weak in ambulating to prevent falls or colliding into furniture. Recommend foods high in protein, calcium, and vitamin D to minimize muscle wasting and osteoporosis; refer to dietitian for assistance. EVALUATION Patient had no injury

NUSING DIAGNOSIS Impaired skin integrity  related to edema, impaired healing, and thin and fragile skin. GOAL Patient will maintain skin integrity INTERVENTIONS Avoid adhesive tape, which can tear and irritate the skin. Assess skin and bony prominences frequently. Encourage and assist patient to change positions frequently. EVALUATION Patient maintained skin integrity

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