Endocrine care



Endocrine care






Diseases


Adrenal hypofunction

Adrenal hypofunction, also called adrenal insufficiency, may be classified as primary or secondary. Primary adrenal hypofunction (Addison’s disease) originates within the adrenal gland and is characterized by decreased mineralocorticoid, glucocorticoid, and androgen secretion. A relatively uncommon disorder, Addison’s disease occurs in people of all ages and both sexes. Adrenal hypofunction may also occur secondary to a disorder outside the gland, such as with a pituitary tumor with corticotropin deficiency, but, unlike the primary form, aldosterone secretion remains unaffected.

With early diagnosis and adequate replacement therapy, the prognosis for both forms of adrenal hypofunction is promising.

Adrenal crisis—also called addisonian crisis—is a critical deficiency of mineralocorticoids and glucocorticoids that generally follows acute stress, sepsis, trauma, surgery, or the discontinuation of steroid therapy. Adrenal crisis is a medical emergency that necessitates immediate, vigorous treatment.


Signs and symptoms



  • Confusion, depression, delirium, and possibly psychosis


  • Bronze coloration of the skin that resembles a deep suntan, especially in the creases of the hands and over the metacarpophalangeal joints, elbows, and knees (Addison’s disease)


  • Cravings for salty food


  • Decreased tolerance for even minor stress


  • Dry skin and mucous membranes


  • Fatigue


  • Hypotension


  • Light-headedness (when rising from a chair or bed)


  • Muscle weakness, myalgia, arthralgia


  • Nausea, vomiting, anorexia, chronic diarrhea, and weight loss


  • Poor coordination


  • Weak, irregular pulse


  • Decreased pubic hair, diminished libido, and amenorrhea in women



Treatment


Primary and secondary adrenal hypofunction



  • Lifelong corticosteroid replacement


  • Fludrocortisone, a synthetic drug that acts as a mineralocorticoid, to
    prevent dangerous dehydration and hypotension (Addison’s disease)




    image


Adrenal crisis



  • I.V. bolus administration of dexamethasone followed by an I.V. bolus of hydrocortisone.


  • To correct hypovolemia: infusion of 3 to 5 L of I.V. normal saline or 5% dextrose solution during the acute stage


  • After the crisis, maintenance doses of hydrocortisone to preserve physiologic stability



Nursing considerations



  • In adrenal crisis, monitor vital signs carefully, especially for hypotension, volume depletion, and other signs of shock. Check for decreased level of consciousness and reduced urine output, which may also signal shock. Monitor for hyperkalemia before treatment and for hypokalemia afterward (from excessive mineralocorticoid effect). Check for cardiac arrhythmias.


  • Check blood glucose levels regularly because steroid replacement may increase levels.


  • Record weight and intake and output carefully because the patient may have volume depletion. Until onset of mineralocorticoid effect, force fluids to replace excessive fluid loss.


Patients on maintenance steroid therapy



  • Control the environment to prevent stress. Encourage the patient to use relaxation techniques.


  • Encourage the patient to dress in layers to retain body heat, and adjust room temperature, as indicated.


  • Provide good skin care. Use alcohol-free skin care products and an emollient lotion after bathing. Turn and reposition the bedridden patient every 2 hours. Avoid pressure over bony prominences.


  • Use protective measures to minimize the risk of infection, if necessary. Limit the patient’s visitors if they have infectious conditions. Use meticulous hand-washing technique.


  • Consult with a dietitian to plan a diet that maintains sodium and potassium balances and provides adequate protein and carbohydrates.


  • Watch for cushingoid signs, such as fluid retention around the eyes and face. Monitor fluid and electrolyte balance, especially if the patient is receiving mineralocorticoids. Monitor weight and check blood pressure to assess body fluid status. Check for petechiae because these patients bruise easily.


  • In women receiving testosterone injections, watch for and report facial hair growth and other signs of masculinization.


  • If the patient is receiving only glucocorticoids, observe for orthostatic hypotension or abnormal serum electrolyte levels, which may indicate a need for mineralocorticoid therapy.




Cushing’s syndrome

Cushing’s syndrome is the clinical manifestation of glucocorticoid (particularly cortisol) excess. Excess secretions of mineralocorticoids and androgens may also cause Cushing’s syndrome. In about 70% of patients, Cushing’s syndrome results from excess production of corticotropin and consequent hyperplasia of the adrenal cortex.

The disorder is classified as primary, secondary, or iatrogenic, depending on its cause, and is most common in females.

The hallmark signs of Cushing’s syndrome include adiposity of the face, neck, and trunk, and purple striae on the skin. The nature of the prognosis depends largely on early diagnosis, identification of the underlying cause, and effective treatment.


Signs and symptoms



  • Fatigue


  • Muscle weakness


  • Sleep disturbances


  • Water retention


  • Amenorrhea


  • Decreased libido


  • Irritability


  • Emotional instability


  • Thin hair


  • Moon-shaped face


  • Hirsutism


  • Acne


  • Buffalo humplike back


  • Thin extremities


  • Petechiae, ecchymoses, and purplish striae


  • Delayed wound healing


  • Swollen ankles


  • Hypertension





Nursing considerations



  • Keep accurate records of vital signs, fluid intake, urine output, and weight. Monitor serum electrolyte levels daily.


  • Consult a dietitian to plan a diet high in protein and potassium and low in calories, carbohydrates, and sodium.


  • Use protective measures to reduce the risk of infection, if necessary. Use meticulous hand-washing technique.


  • Schedule activities around the patient’s rest periods to avoid fatigue. Gradually increase activity, as toler-ated.


  • Institute safety precautions to minimize the risk of injury from falls.


  • Help the bedridden patient turn every 2 hours. Use extreme caution while moving the patient to minimize skin trauma and bone stress. Provide frequent skin care, especially over bony prominences. Provide support with pillows and a convoluted foam mattress.


  • Encourage the patient to verbalize feelings about body image changes and sexual dysfunction. Offer emotional support and a positive, realistic assessment of the patient’s condition. Help the patient to develop coping strategies. Refer to a mental health professional for additional counseling, if necessary.




Diabetes insipidus

A disorder of water metabolism, diabetes insipidus results from a deficiency of circulating vasopressin (also called antidiuretic hormone, or ADH), a resistance to vasopressin at the receptor sites in the kidneys, or an abnormal thirst mechanism. A decrease in ADH levels leads to altered intracellular and extracellular fluid control, causing renal excretion of a large amount of urine. Diabetes insipidus can strike people of all ages, from infancy to adulthood.

In uncomplicated diabetes insipidus and with adequate water replacement, the prognosis is good and patients usually can lead normal lives. However, in cases complicated by an underlying disorder, such as cancer, the prognosis is variable.


Signs and symptoms



  • Extreme polyuria (usually 4 to 16 L/day of dilute urine, but sometimes as much as 30 L/day)


  • Extreme thirst


  • Weight loss


  • Dizziness


  • Weakness


  • Constipation


  • Slight to moderate nocturia


  • Dry skin and mucous membranes


  • Fever


  • Dyspnea


  • Pale and voluminous urine


  • Poor skin turgor


  • Tachycardia


  • Decreased muscle strength


  • Hypotension




Treatment



  • Desmopressin acetate (DDAVP) administered nasally, orally, or by injection; affects prolonged antidiuretic activity and has no pressor effects, depending on dosage


  • Chlorpropamide (Diabinese): a sulfonylurea used in diabetes mellitus; also sometimes used to stimulate endogenous release of antidiuretic hormone and is effective if some pituitary function is intact


  • Carbamazepine to enhance the patient’s response to ADH; clofibrate to increase the release of ADH


  • Low-sodium, low-protein diet and thiazide diuretics to treat nephrogenic diabetes insipidus


Nursing considerations



  • Make sure that you keep accurate records of the patient’s hourly fluid intake and urine output, vital signs, and daily weight. Be sure to administer adequate replacement fluids.


  • Closely monitor the patient’s urine specific gravity. Also monitor serum electrolyte and blood urea nitrogen levels.


  • Watch the patient for signs of hypovolemic shock. Monitor blood pressure, pulse rate, and body weight. Also watch for changes in mental or neurologic status.


  • If the patient has any complaints of dizziness or muscle weakness, institute safety precautions to help prevent injury.


  • Make sure that the patient has easy access to the bathroom or bedpan. Insert an indwelling urinary catheter if the patient is incontinent so output can be monitored.


  • Provide meticulous skin and mouth care. Use a soft toothbrush and mild mouthwash to avoid trauma to the oral mucosa. If the patient has cracked or sore lips, apply petroleum jelly, as needed. Use alcohol-free skin care products, and apply emollient lotion to the patient’s skin after baths.


  • Use caution when administering vasopressin to a patient with coronary artery disease because the drug can cause coronary artery constriction. Therefore, closely monitor the patient’s electrocardiogram, looking for changes and exacerbation of angina.


  • Urge the patient to verbalize feelings. Offer encouragement, and provide a realistic assessment of the situation.


  • Help the patient identify his strengths, and help him see how he can use these strengths to develop effective coping strategies.


  • As necessary, refer the patient to a mental health professional for additional counseling.


  • Advise the patient to wear a medical identification bracelet at all times. Tell him he should always keep his medication with him.




Diabetes mellitus

Diabetes mellitus is a chronic disease of absolute or relative insulin deficiency or resistance. It’s characterized by disturbances in carbohydrate, protein, and fat metabolism. Insulin deficiency compromises the body tissues’ ability to access essential nutrients for fuel and storage.

Diabetes mellitus occurs in two primary forms: type 1, characterized by absolute insufficiency; and the more prevalent type 2, characterized by insulin resistance with varying degrees of insulin secretory defects.

Onset of type 1 usually occurs before age 30, although it may occur at any age. type 2 usually occurs in obese adults after age 40; however, it’s becoming more common in North American youths.

Diabetes mellitus is thought to affect about 7% of the population of the United States (24 million people); about 6 million cases are undiagnosed. Incidence is essentially the same between males and females and increases with age.

In type 1 diabetes, pancreatic beta-cell destruction or primary defect in beta-cell function results in a failure to release insulin and ineffective glucose transport. Type 1 immune-mediated diabetes is caused by cell-mediated destruction of pancreatic beta cells. In type 2 diabetes, beta cells release insulin, but receptors resist insulin, glucose transport is variable and ineffective.




Signs and symptoms



  • Polyuria


  • Polydipsia


  • Polyphagia


  • Nausea and anorexia


  • Weight loss


  • Headaches, fatigue, lethargy, reduced energy levels, impaired school or work performance


  • Muscle cramps, irritability, emotional lability


  • Vision changes such as blurring


  • Numbness and tingling


  • Abdominal discomfort and pain; diarrhea or constipation


  • Recurrent infections


  • Delayed wound healing


Treatment


Type 1 diabetes



  • Exogenous insulin


  • Dietary management


  • Exercise therapy


  • Islet cell or pancreas transplantation


Type 2 diabetes



  • Insulin therapy


  • Oral antidiabetic drugs


  • Exercise therapy


  • Lipase inhibitor (such as orlistat) combined with a low-calorie diet to significantly decrease weight


  • Dietary management


Nursing considerations



  • Keep accurate records of vital signs, weight, fluid intake, urine output, and calorie intake. Monitor serum glucose and urine acetone levels.


  • Monitor for acute complications of diabetic therapy, especially hypoglycemia (vagueness, slow cerebration, dizziness, weakness, pallor, tachycardia, diaphoresis, seizures, and coma); immediately give carbohydrates in the form of fruit juice, hard candy, honey or, if the patient is unconscious, glucagon or I.V. dextrose. Also be alert for signs of hyperosmolar coma (polyuria, thirst, neurologic abnormalities, and stupor). This hyperglycemic crisis requires I.V. fluids and insulin replacement.


  • Monitor diabetic effects on the cardiovascular system, such as cerebrovascular, coronary artery, and peripheral vascular impairment, and on the peripheral and autonomic nervous systems.


  • Provide meticulous skin care, especially to the feet and legs. Treat all injuries, cuts, and blisters. Avoid constricting clothing, slippers, or bed linens. Refer the patient to a podiatrist if indicated.


  • Observe for signs of urinary tract and vaginal infections. Encourage adequate fluid intake.


  • Monitor the patient for signs of diabetic neuropathy (numbness or pain in the hands and feet, footdrop, and neurogenic bladder).


  • Consult a dietitian to plan a diet with the recommended allowances of calories, protein, carbohydrates, and fats, based on the patient’s particular requirements.


  • Encourage the patient to verbalize feelings about diabetes and its effects on lifestyle and life expectancy. Offer emotional support and a realistic assessment of his condition. Stress that with proper treatment, he can lead a relatively normal life. Help the patient to develop coping strategies. Refer him and his family for counseling, if necessary. Encourage them to join a support group.




Hyperthyroidism

Thyroid hormone overproduction results in the metabolic imbalance hyperthyroidism, which is also called thyrotoxicosis.

The most common form is Graves’ disease, which increases thyroxine (T4) production, enlarges the thyroid gland (goiter), and causes multiple systemic changes. Incidence of Graves’ disease is highest between ages 30 and 40, especially in people with family histories of thyroid abnormalities; only 5% of hyperthyroid patients are younger than age 15. With treatment, most patients can lead normal lives.

However, thyrotoxic crisis (or thyroid storm), an acute exacerbation of hyperthyroidism, is a medical emergency that can lead to life-threatening cardiac, hepatic, or renal failure.


Signs and symptoms



  • Enlarged thyroid


  • Nervousness


  • Heat intolerance


  • Weight loss despite increased appetite


  • Sweating


  • Frequent bowel movements


  • Tremor


  • Palpitations


  • Exophthalmos (considered most characteristic but is absent in many patients with thyrotoxicosis)



Jun 5, 2016 | Posted by in NURSING | Comments Off on Endocrine care

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