NCLEX: Endocrine disorders

Endocrine disorders: Nursing diagnoses

Focus topic: Endocrine disorders

When caring for patients with endocrine disorders, you’ll typically use several nursing diagnoses. These appear below, along with appropriate nursing interventions and rationales.

Endocrine disorders: Imbalanced nutrition: More than body requirements

Focus topic: Endocrine disorders

Related to increased appetite, high calorie intake, inability to use nutrients, and inactivity, Imbalanced nutrition: More than body requirements is associated with many disorders, including Cushing’s syndrome and diabetes mellitus.

Expected outcomes
• Patient expresses feelings about weight.
• Patient plans menus appropriate to prescribed diet.
• Patient adheres to prescribed diet.

Nursing interventions and rationales
• Obtain the patient’s dietary history. Permanent weight change begins with examination of contributing factors. Provide the patient with a written copy of a calorie-based meal plan. Obtain dietary consultation as needed. Evaluate the patient’s eating habits and include preferred foods in his meal plan.
• Provide support and encouragement as the patient attempts to change his calorie intake. Encouragement provides positive reinforcement and reduces frustration.
• Encourage activity and exercise based on the patient’s physical ability and limitations. Exercise not only helps the patient lose weight, it also reduces stress and helps curb stress-related eating.
• Refer the patient to community resources as needed and available.

Endocrine disorders: Insomnia

Focus topic: Endocrine disorders

Related to anxiety or hormone imbalance, Insomnia is associated with such disorders as hyperthyroidism, diabetes insipidus, and diabetes mellitus.

Expected outcomes
• Patient identifies factors that prevent or disrupt sleep.
• Patient sleeps ___ hours per night.
• Patient expresses a feeling of being well rested.

Nursing interventions and rationales
• Promote usual sleep and rest practices. Decrease environmental stimuli. Provide a quiet, darkened, private room.
• Encourage frequent, short periods of ambulation.
• Administer antihormone medications as ordered and sedatives as needed.
• Instruct the patient and his family to eliminate caffeine-containing foods — such as coffee, tea, cola, and chocolate — from his diet.
• Provide and encourage quiet diversionary activities to promote rest and sleep.

Endocrine disorders: Common endocrine disorders

Focus topic: Endocrine disorders

Endocrine dysfunction takes one of two forms: hyperfunction, which results in excessive hormone production or response, or hypofunction, which results from a relative or absolute hormone deficiency. Hormonal imbalance can also be classified according to the disease site. Disease within an endocrine gland causes primary dysfunction. Disease caused by dysfunction outside a particular endocrine gland, but affecting that gland or its hormone or hormones, is termed secondary dysfunction.

Endocrine disorders: Addison’s disease

Focus topic: Endocrine disorders

The most common form of adrenal hypofunction, Addison’s disease occurs when more than 90% of the adrenal gland is destroyed. With early diagnosis and adequate replacement therapy, the prognosis for adrenal hypofunction is good. Acute adrenalinsufficiency, or adrenal crisis (addisonian crisis), is a medical emergency requiring immediate, rigorous treatment.

What causes it
Although autoimmune causes are the most common causes of
Addison’s disease, it can also result from:
• tuberculosis
• bilateral adrenalectomy
• hemorrhage into the adrenal gland
• neoplasms
• fungal infections.
Secondary adrenal hypofunction can be caused by:
• hypopituitarism
• abrupt withdrawal of long-term corticosteroid therapy
• removal of a nonendocrine, corticotropin-secreting tumor.

Pathophysiology
In the autoimmune process of Addison’s disease, circulating antibodies react specifically against the adrenal tissue, leading to decreased secretion of androgens, glucocorticoids, and mineralocorticoids. Adrenal hypofunction may also result from a disorder outside the gland, in which case aldosterone secretion commonly continues. In a patient with adrenal hypofunction, adrenal crisis occurs when the body’s stores of glucocorticoids are exhausted by trauma, infection, surgery, or other physiologic stressors.

What to look for
When trying to determine the presence of Addison’s disease, look for:
• weakness or fatigue
• anorexia and weight loss
• nausea and vomiting
• chronic constipation or diarrhea
• conspicuous bronze skin coloration, especially in hand creases and over the metacarpophalangeal joints, elbows, and knees
• darkening of scars and areas of vitiligo (absence of pigmentation)
• increased pigmentation of the mucous membranes, especially the buccal mucosa
• cardiovascular abnormalities, such as orthostatic hypotension, decreased heart size and cardiac output, and a weak, irregular pulse
• decreased tolerance for even minor stress
• poor coordination
• fasting hypoglycemia
• a craving for salty food
• amenorrhea.
The clinical effects of secondary adrenal hypofunction resemble those of Addison’s disease but without hyperpigmentation, hypotension, and electrolyte abnormalities. Adrenal crisis is characterized by profound weakness and fatigue, shock, severe nausea and vomiting, hypotension, dehydration and, occasionally, high fever.

What tests tell you
• Decreased plasma cortisol and serum sodium levels and increased corticotropin, serum potassium, and blood urea nitrogen (BUN) levels confirm adrenal hypofunction.
• Metyrapone and corticotropin stimulation tests are special provocative studies that determine whether adrenal hypo function is primary or secondary.

How it’s treated
Corticosteroid replacement, usually with cortisone or hydrocortisone (both also have a mineralocorticoid effect), is the primary lifelong treatment for patients with primary or secondary adrenal hypofunction. Drug therapy may also include fludrocortisone, which acts as a mineralocorticoid to prevent dehydration and hypotension.
Adrenal crisis requires prompt administration of dexamethasone, hydrocortisone, or both. The patient receives later doses of hydrocortisone I.V. until his condition stabilizes. With proper treatment, the crisis usually subsides quickly, blood pressure stabilizes, and fluid and sodium levels return to normal. Subsequent oral maintenance doses of hydrocortisone preserve stability.

What to do
• In an adrenal crisis, monitor vital signs carefully for hypotension, volume depletion, and other signs of shock (decreased LOC and urine output). Watch for hyperkalemia before treatment and for hypokalemia after treatment (from excessive mineralocorticoid effect).
• If the patient also has diabetes, check blood glucose levels frequently because steroid replacement may necessitate changing the insulin dosage. Carefully record weight and intake and output, because the patient may have volume depletion. Force fluids to replace excessive fluid loss until the onset of mineralocorticoid effects.

The dish on diet

Focus topic: Endocrine disorders

• Arrange for a diet that maintains sodium and potassium balance. If the patient is anorectic, suggest six small meals per day to increase calorie intake. Ask the dietitian to provide a diet high in protein and carbohydrates.
• Observe the patient receiving steroids for cushingoid signs such as fluid retention around the eyes and face. Watch for fluid and electrolyte imbalance, especially if the patient receives mineralocorticoids.
• Evaluate the patient’s understanding of his condition and treatment. He should maintain a proper diet; maintain normal serum sodium, potassium, and plasma cortisol levels; understand the need to take his medication routinely; and make necessary adjustments in times of stress.

Endocrine disorders

Endocrine disorders: Cushing’s syndrome

Focus topic: Endocrine disorders

A disorder of adrenal hyperfunction, Cushing’s syndrome results from excessive levels of adrenocortical hormones (particularly cortisol) or related corticosteroids and, to a lesser extent, androgens and aldosterone. Its unmistakable signs include adiposity of the face (moon face), neck, and trunk and purple striae on the skin, especially the abdomen. Cushing’s syndrome is more common in females than males by a 5:1 margin. Prognosis depends on the underlying cause; it’s poor in untreated persons and in those with untreatable ectopic corticotropin-secreting carcinoma or metastatic adrenal carci noma.

What causes it
Cushing’s syndrome can stem from:
• pituitary hypersecretion of corticotropin (Cushing’s disease)
• corticotropin-secreting tumor in another organ (particularly bronchogenic or pancreatic carcinoma)
• administration of synthetic glucocorticoids
• adrenal tumor, which is usually benign in adults (less common cause).

Pathophysiology
A loss of normal feedback inhibition by cortisol occurs in Cushing’s syndrome. Elevated levels of cortisol don’t suppress hypothalamic and anterior pituitary secretion of corticotropin-releasing hormone and corticotropin. The result is excessive levels of circulating cortisol.

What to look for
The patient who has some or all of these signs and symptoms might have Cushing’s syndrome:
• weight gain
• muscle weakness
• fatigue
• buffalo hump
• thinning extremities with muscle wasting and fat mobilization
• thin, fragile skin
• moon face and ruddy complexion
• hirsutism
• truncal obesity
• broad purple striae
• bruising
• impaired wound healing.

What tests tell you
• A low-dose (overnight) dexamethasone suppression test, elevated 24-hour urinary free cortisol levels, and high night time cortisol levels (indicating loss of circadian rhythm) confirm the diagnosis of Cushing’s syndrome.
• A plasma corticotropin test and high-dose dexamethasone suppression test can determine the cause of Cushing’s syndrome.
• With an adrenal tumor, corticotropin levels aren’t detectable and steroid levels aren’t suppressed. Ectopic corticotropin syndrome shows elevated corticotropin or unsuppressed steroid levels. Normal to elevated corticotropin with steroid suppressed to less than 50% of baseline indicates Cushing’s disease.
• Ultrasonography, CT scan, or angiography localizes adrenal tumors.
• CT scan or MRI of the head helps localize pituitary tumors.

How it’s treated
The patient may require radiation, drug therapy, or surgery to restore hormone balance and reverse Cushing’s syndrome. For example:
• Transsphenoidal resection of the corticotropin-secreting pituitary microadenoma is the therapy of choice for pituitary tumors that cause Cushing’s disease.
• Adrenal tumor is treated by unilateral adrenalectomy with good prognosis, but the patient will require glucocorticoid therapy perioperatively and postoperatively.
• Nonendocrine corticotropin-secreting tumors require excision. Drug therapy with etomidate (Amidate), ketoconazole (Nizoral), metyrapone (Demser), or mitotane (Lysodren) decreases cortisol levels if signs and symptoms persist or the tumor is inoperable.
• Before surgery, the patient with cushingoid signs and symptoms needs special management to control hypertension, edema, diabetes, and cardiovascular manifestations and to prevent infection. Glucocorticoid administration on the morning of surgery can help prevent acute adrenal insufficiency during surgery.

What to do
• Provide painstaking assessment and supportive care to the patient with Cushing’s syndrome. Implement these measures: – Frequently monitor vital signs, especially blood pressure. Carefully observe the hypertensive patient who also has cardiac disease.– Check laboratory reports for hypernatremia, hypokalemia, hyperglycemia, and glycosuria.
– Because the cushingoid patient is likely to retain sodium and water, check for edema and carefully monitor daily weight, intake, and output. To minimize weight gain, edema, and hypertension, ask the dietitian to provide a diet high in protein and potassium but low in calories, carbohydrates, and sodium.
– Watch for infection — a significant problem in Cushing’s syndrome.
– Carefully perform passive range-of-motion exercises for the patient who has osteoporosis and is bedridden.
– Cushing’s syndrome produces emotional lability. Record incidents that upset the patient, and try to prevent such situations if possible. Help the patient get the necessary physical and mental rest — by sedation if necessary. Offer emotional support throughout the difficult testing period.
– Evaluate the patient. After successful therapy, the patient will take medication as prescribed, recognize signs and symptoms of steroid underdose and overdose, and carry medical identification. Fluid, electrolyte, and plasma cortisol levels will be within normal limits and the patient will seek counseling for stress as needed.

Endocrine disorders

Endocrine disorders: Diabetes insipidus

Focus topic: Endocrine disorders

Diabetes insipidus results from a deficiency of circulating ADH, or vasopressin. It’s an uncommon condition but occurs equally in men and women. The prognosis is good with uncomplicated diabetes insipidus and, with adequate water replacement, patients usually lead normal lives. The prognosis varies in cases complicated by an underlying disorder such as metastatic cancer.

What causes it
Diabetes insipidus may be familial, acquired, or idiopathic. It can be acquired as the result of intracranial neoplastic or metastatic lesions. Other causes may include:
• hypophysectomy or other neurosurgery
• head trauma, which damages the neurohypophyseal structures
• infection
• granulomatous disease
• vascular lesions
• autoimmune disorders.

Pathophysiology
Normally, ADH is synthesized in the hypothalamus and then stored by the posterior pituitary gland. When it’s released into the general circulation, ADH increases the water permeability of the distal and collecting tubules of the kidneys, causing water reabsorption. If ADH is absent, the filtered water is excreted in the urine instead of being reabsorbed, and the patient excretes large quantities of dilute urine.

What to look for
The cardinal sign of diabetes insipidus is extreme polyuria —usually 4 to 16 L/day of dilute urine but sometimes as much as 30 L/day, with a low specific gravity (less than 1.005). Other symptoms i nclude:
• polydipsia, particularly for cold, iced drinks
• nocturia
• fatigue (in severe cases)
• dehydration, characterized by weight loss, poor tissue turgor, dry mucous membranes, constipation, muscle weakness, dizziness, tachycardia, and hypotension.

What tests tell you
• Urinalysis reveals almost colorless urine of low osmolality (less than 200 mOsm/kg) and low specific gravity (less than 1.005).
• A water deprivation test confirms the diagnosis by demonstrating renal inability to concentrate urine (evidence of ADH deficiency).
• Subcutaneous injection of 5 units of vasopressin produces decreased urine output with increased specific gravity if the patient has central diabetes insipidus.

How it’s treated
Until the cause of diabetes insipidus can be identified and eliminated, administering various forms of vasopressin or a vasopressin stimulant controls fluid balance and prevents dehydration. Thiazide diuretics may be prescribed to reduce urine volume by creating mild salt depletion.

What to do
• Record fluid intake and output carefully. Maintain the patient’s fluid intake to prevent severe dehydration.
• Watch for signs of hypovolemic shock, and monitor blood pressure and heart and respiratory rates regularly, especially during the water deprivation test.
• Check weight daily.
• Remember to keep the bed’s side rails up and assist with walking if the patient is dizzy or has muscle weakness.
• Monitor urine specific gravity between doses. Watch for decreased specific gravity with increased urine output, indicating an inability to concentrate urine and the need for the next dose or a dosage increase.

Bulking up

Focus topic: Endocrine disorders

• Add more bulk foods and fruit juices to the diet if constipation develops. If necessary, obtain an order for a mild laxative such as milk of magnesia.
• Provide meticulous skin and mouth care, and apply a lubricant to cracked or sore lips.
• Make sure caloric intake is adequate and the meal plan is low in sodium.
• Watch for decreased urine output and increased specific gravity between doses of medication.
• Monitor electrolyte levels and watch for hyponatremia.
• Evaluate the patient. He should maintain an adequate fluid volume and electrolyte balance and resume his normal elimination pattern. If diabetes insipidus hasn’t been eliminated, the patient should also know how to administer his medication correctly and how to record his intake and output; preferably he’ll self-medicate while still an inpatient. He should wear medication identification jewelry, carry a wallet identification card, and schedule regular follow-up appointments.

Endocrine disorders

Endocrine disorders: Diabetes mellitus

Focus topic: Endocrine disorders

Diabetes mellitus is characterized by disturbances in carbohydrate, protein, and fat metabolism. A leading cause of death in North America, diabetes is a major risk factor for myocardial infarction (MI), stroke, renal failure, and peripheral vascular disease. It’s also the leading cause of blindness in adults.

Taking form

Focus topic: Endocrine disorders

Two forms exist: type 1 and the more prevalent type 2 diabetes mellitus. Type 1 diabetes usually occurs before age 30 (although it may occur at any age); the patient is usually thin and will require exogenous insulin and dietary management to achieve control. Conversely, type 2 most commonly occurs in obese adults after age 40; it’s usually treated with exercise, meal planning, and antidiabetic drugs. Treatment may include insulin therapy. An increasing number of adolescents and young people are being diagnosed with type 2 diabetes.

Shocking results

Focus topic: Endocrine disorders

In hyperosmolar hyperglycemic nonketotic syndrome (HHNS), dehydration may cause hypovolemia and shock. Long-term diabetes may lead to retinopathy, nephropathy, atherosclerosis, and peripheral and autonomic neuropathy. Peripheral neuropathy usually affects the legs and may cause numbness.

What causes it
Type 1 is an autoimmune disease strongly associated with human leukocyte antigens DR 3 and 4. It may also be associated with certain viral infections.
Type 2 may result from:
• impaired insulin secretion
• peripheral insulin resistance
• increased basal hepatic glucose production.
Other associated factors include:
• obesity
• insulin antagonists (such as excess counter-regulatory hormones and phenytoin)
• hormonal contraceptives
• pregnancy.

Pathophysiology
The effects of diabetes mellitus result from insulin deficiency or resistance to endogenous insulin. Normally, insulin allows glucose transport into the cells for use as energy or storage as glycogen. Insulin also stimulates protein synthesis and free fatty acid storage in adipose tissue. Insulin deficiency compromises the body tissues’ access to essential nutrients for fuel and storage.

What to look for
Assess the patient for:
• fatigue
• polyuria related to hyperglycemia
• polydipsia
• nocturia
• dry mucous membranes

• poor skin turgor
• weight loss
• blurred vision
• polyphagia.

What tests tell you
• Two fasting plasma glucose tests above 126 mg/dl or, with normal fasting glucose, two blood glucose levels above 200 mg/dl during a 2-hour glucose tolerance test confirm the diagnosis.
• Ophthalmologic examination may show diabetic retinopathy.
• Other tests include plasma insulin level determination, urine testing for glucose and acetone, and glycosylated hemoglobin (hemoglobin A1C [Hb A1C]) determination.

How it’s treated
Meal planning, exercise and, sometimes, insulin or oral antidiabetic agents are prescribed to normalize carbohydrate, fat, and protein metabolism and avert long-term complications while avoiding hypoglycemia.

All about food

Focus topic: Endocrine disorders

All types of diabetes require strict adherence to carefully planned meals to meet nutritional needs, control blood glucose levels, and reach and maintain appropriate body weight. The American Diabetes Association recommends an individualized nutritional assessment and medical nutrition therapy to achieve therapeutic goals. Therapy works best when the patient consistently follows the meal plan. Aerobic exercise is also generally prescribed at least three times per week for a minimum of 45 to 60 minutes. Patients are asked to exercise five or six times per week when weight loss is a therapeutic goal.

Insulin deficiency? Absolutely!

Focus topic: Endocrine disorders

Patients with type 1 diabetes must take insulin daily because of their absolute insulin deficiency. Patients with type 2 diabetes may require insulin to control blood glucose levels unresponsive to diet and oral antidiabetic agents, or during periods of acute stress. Patients with other types of diabetes commonly require daily insulin therapy to achieve blood glucose control.

Endocrine disorders

Adding drugs to the mix

Focus topic: Endocrine disorders

Patients with type 2 diabetes who can’t achieve their target blood glucose levels with meal planning and exercise may require antidiabetic medications. Used in combination with one another or with insulin, these medications help patients with type 2 diabetes maintain normal glucose levels. Several types of medications are used to treat type 2 diabetes.
• Insulin secretagogues enhance pancreatic insulin secretion and include:
– first generation — the sulfonylureas, tol azamide, tolbutamide
– second generation — glyburide (DiaBeta), glipizide (Gluco trol), and glimepiride (Amaryl). In addition, repaglinide (Prandin) enhances insulin secretion but acts more quickly.
• Biguanides (metformin [Glucophage] is the only one currently available) prevent inappropriate hepatic gluconeogenesis.
• Alpha-glucosidase inhibitors acarbose (Precose) and miglitol (Glyset) delay the intestinal absorption of carbohydrates.

Endocrine disorders

Endocrine disorders

Endocrine disorders

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What to do
• Emphasize that adherence to the treatment plan is essential. It’s crucial to bring the patient’s blood glucose level within an acceptable range (usually less than 120 mg/dl before a meal and 180 mg/dl between meals) and alleviate or prevent diabetic ketoacidosis (DKA) or hypoglycemia.
• For the patient with unstable diabetes who isn’t experiencing DKA or HHNS, monitor blood glucose levels several times per day as prescribed until they stabilize.
• Administer insulin as prescribed, and keep the practitioner informed until blood glucose levels are under control. Then expect to begin the patient on an insulin regimen.

• If the patient has type 2 diabetes, he may need an oral antidiabetic or a trial period with diet therapy.

Dinner is at 6 sharp!

Focus topic: Endocrine disorders

• Make sure meals are on time for the patient receiving insulin or an insulin secretagogue.
• Monitor the patient closely for signs and symptoms of DKA or HHNS as well as for hypoglycemia (caused by too rapid reduction in blood glucose level). Suspect DKA or HHNS if your patient begins to exhibit Kussmaul’s respirations, develops a fruity odor to his breath, and shows signs and symptoms of severe dehydration. If these indications occur, immediately notify the practitioner.
• If the patient has DKA or HHNS, treatment may include fluid and electrolyte replacement, increased insulin therapy, and therapy to reduce acidosis. Administer doses of I.V. insulin as prescribed. Monitor the patient’s blood glucose levels frequently during insulin infusion. Alert the practitioner when the glucose level reaches 250 to 300 mg/dl so that the insulin dosage can be decreased to prevent hypoglycemia. Typically, insulin decreases blood glucose levels by about 75 to 100 mg/dl each hour. Patients with HHNS have a greater insulin sensitivity than patients with DKA, so expect to give less insulin.
• After the crisis, expect to resume the patient’s usual insulin regimen. Infuse I.V. fluids rapidly at the prescribed rate. Hypotonic or isotonic saline solution will be administered, depending on the patient’s condition. When the glucose level is slightly above normal, the practitioner may switch to a glucose solution to prevent hypoglycemia and reduce the risk of cerebral edema.

Preserving potassium

Focus topic: Endocrine disorders

• Monitor an elderly patient closely for evidence of fluid overload. Monitor the patient’s electrolyte levels closely and administer potassium replacement therapy as ordered. Patients with an extremely low pH level may require bicarbonate therapy to treat acidosis, but fluid and insulin replacement alone usually correct metabolic acidosis.
• The meal plan is the cornerstone of diabetes care because it directly controls the body’s major glucose source. Your patient can prevent widely fluctuating blood glucose levels by controlling his food intake. If he takes insulin or sulfonylureas, he’ll need to adhere to his meal plan even more carefully to avoid hypoglycemia.
• Monitor the patient for complications related to insulin therapy, which include hypoglycemia, the dawn phenomenon (early morning rise in blood glucose), insulin lipodystrophy (usually caused by continually using the same injection site), insulin allergy, and insulin resistance.

• Administer oral antidiabetics as prescribed. Check the patient’s history for conditions — such as pregnancy, breast-feeding, stressful situations, or illnesses — that increase insulin requirements, as well as for known allergies to sulfa agents. Monitor the patient for adverse reactions.

Keying in on ketones

Focus topic: Endocrine disorders

• If necessary, check your patient’s urine for ketones. Urine testing is sometimes used to monitor blood glucose control, but it’s rapidly being replaced with blood glucose monitoring. Despite their convenience, urine tests don’t always reflect blood glucose levels accurately. However, only urine testing can detect ketone bodies — particularly important for the ketosis-prone patient with type 1 diabetes.
• Demonstrate to the patient how to check his blood glucose. Because blood glucose changes may cause misleading signs and symptoms — or none at all — the patient with diabetes must measure his glucose level often. Capillary blood glucose monitoring allows the patient (and the nurse) to determine metabolic status quickly, receive feedback on problems with the diet or medication regimen, and make immediate adjustments. It’s especially useful for the patient on a tightly controlled regimen. Recent research shows that good glycemic control (Hb A1C level less than 7%) reduces the risk of long-term complications from diabetes.
• Blood glucose monitoring equipment varies greatly, so it’s important to carefully follow the manufacturer’s instructions. The health care provider may order blood glucose testing before meals, after meals, and at bedtime, or less frequently for a patient who has established stable control.
• Monitor the patient’s Hb A1C as ordered to assess long-term diabetes control. The amount of glycosylation directly correlates with blood glucose levels. Ideally, the patient’s Hb A1C should measure no more than 11/2 times the normal level, which ranges from 3% to 6%. A high Hb A1C value with any blood glucose level suggests hyperglycemia over several weeks; a low value coupled with a high blood glucose level suggests recent onset of hyperglycemia.

Vital records

Focus topic: Endocrine disorders

• Keep accurate records of vital signs, weight, fluid intake, urine output, and caloric intake in addition to monitoring serum glucose and urine ketone levels.
• Monitor the patient closely for signs and symptoms of hyperglycemia and hypoglycemia. If a hypoglycemic reaction occurs, obtain a blood glucose level and immediately give carbohydrates in the form of fruit juice, hard candy, or honey. Give glucagon or I.V. dextrose if the patient is unconscious. Notify the practitioner of a significant change in the patient’s blood glucose levels.
• Provide meticulous skin care, especially to the feet and legs, to avert problems associated with peripheral vascular disease and neuropathy. Even a tiny skin break can produce complications that lead to amputation. Avoid constricting hose, slippers, or bed linens. Refer the patient to a podiatrist if indicated.
• Evaluate the patient. He should have normal blood glucose levels, maintain an adequate nutritional intake, understand his drug regimen, monitor himself for complications of the disease, and obtain medical identification jewelry and a wallet identification card.

Endocrine disorders

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