Hormones

Anterior Pituitary Disorders

Acromegaly

Excessive growth hormone (GH)

Risk factors

None Anterior Pituitary adenoma; abnormal hypothalamic function (rare) May demonstrate hyperglycemia; in acromegaly, GH level remains increased.

Etiology

Diagnostic Procedures X-ray

x-ray of the skull may show thickening of the bones and enlargement of the nasal sinuses x-rays of the hands show thickening of the bones under the fingertips and swelling of the tissue around the bones The diagnosis is confirmed by blood tests, which usually show high levels of both growth hormone and insulin-like growth factor

Blood Test

CT Scan

usually done to look for abnormal growths in the pituitary gland Because acromegaly is usually present for some years before being diagnosed, a tumor is seen on these scans in most people.

Clinical Manifestations

excessive production of growth hormone begins between the ages of 30 and 50, long after the growth plates of the bones have closed Bones become deformed rather than elongated Facial features become coarse, and the hands and feet swell Overgrowth of the jawbone (mandible) can cause the jaw to protrude (prognathism). Cartilage in the voice box (larynx) may thicken, making the voice deep and husky. The ribs may thicken, creating a barrel chest. Joint pain The tongue may enlarge and become more furrowed Coarse body hair, which typically darkens, increases as the skin thickens

The sebaceous and sweat glands in the skin enlarge, producing excessive perspiration and often an offensive body odor The heart usually enlarges, and its function may be so severely impaired that heart failure occurs Sometimes a person feels disturbing sensations and weakness in the arms and legs as enlarging tissues compress the nerves Nerves that carry messages from the eyes to the brain may also be compressed, causing loss of vision, particularly in the outer visual fields The pressure on the brain may also cause severe headaches. irregular menstrual cycles Production of breast milk even though not breastfeeding (galactorrhea) because of either too much growth hormone or a related increase in prolactin About one third of men who have acromegaly develop erectile dysfunction Life expectancy is reduced in people with untreated acromegaly

Radiation therapy

involves the use of supervoltage irradiation This treatment may take several years to have its full effect, however, and often results in later deficiencies of other pituitary hormones, as normal tissue is often also affected

Drug therapy
Also used to lower growth hormone levels bromocriptine (Parlodel) and other drugs that act like dopamine somatostatin, the hormone that normally blocks growth hormone production and secretion

octreotide (Sandostatin) which only have to be given about once a month These drugs are effective in controlling acromegaly in many people as long as they continue to be taken (they do not provide a cure)

Gigantism

excessive secretion of growth hormone during childhood, before the closure of the bone growth plates excess growth hormone causes overgrowth of the long bones and very tall stature.

Causes

benign pituitary gland tumor If excessive secretion of growth hormone occurs after normal bone growth has stopped, the condition is known as acromegaly The vertical growth in height that marks this condition is also accompanied by growth in muscles and organs, which makes the child extremely large for his or her age. The disorder can also delay puberty Gigantism is very rare

Manifestations:

Excessive growth during childhood Frontal bossing and a prominent jaw Thickening of the facial features Disproportionately large hands and feet with thick fingers and toes Increased perspiration Weakness Secretion of breast milk Irregular menstruation Headache Delayed onset of puberty Double vision or difficulty with peripheral vision

Exams and Tests

increase in insulin growth factor-I (IGF-I) levels failure to suppress serum growth hormone (GH) levels after an oral glucose challenge (maximum 75g) CT or MRI scan of the head showing pituitary tumor High prolactin levels Other hormone levels may be low due to damage to the pituitary, including thyroid hormone, testosterone (boys), stradiol (girls), or cortisol.

Treatment

In pituitary tumors with well-defined borders, surgery is the treatment of choice and is curative is about 80% of cases. For situations in which surgery cannot completely remove the tumor, medication is the treatment of choice. The most effective medications are somatostatin analogs (such as octreotide or long-acting lanreotide), which reduce growth hormone secretion. Dopamine agonists (bromocriptine mesylate, cabergoline) have also been used to reduce growth hormone secretion, but these are generally less effective. Radiation therapy has also been used to normalize growth hormone levels. However, it can take 5-10 years for the full effects to be seen and is almost always associated with deficiencies in other pituitary hormones. In addition, radiation has been associated with learning disabilities, obesity, and emotional changes in children. Most experts will use radiation only if surgery and medication fail.

Possible Complications

The development of secondary sexual characteristics may be delayed. Surgery and radiation can both lead to deficiencies in other pituitary hormones, causing hypothyroidism, adrenal insufficiency, hypogonadism, and (rarely) diabetes insipidus.

Dwarfism the result of the disproportionate growth of the skeleton. In most cases, dwarfism is genetically determined. We refer to those affected as "Little People." A dwarf is a person of short stature - under 4 10 as an adult. More than 200 different conditions can cause dwarfism. A single type, called achondroplasia, causes about 70 percent of all dwarfism. Achondroplasia is a genetic condition that affects about 1 in 25,000 people. It makes arms and legs short in comparison to the head and trunk. Other genetic conditions, kidney disease and problems with metabolism or hormones can also cause short stature. Dwarfism itself is not a disease. However, there is a greater risk of some health problems. With proper medical care, most people with dwarfism have active lives and live as long as other people

Etiology

Family history and parent's stature are usually not relevant to the child's dwarfism. genetic mutations at the moment of conception random combination of two recessive genes that may have been dormant for generations

Signs and Symptoms

In general, the disorders are divided into two broad categories. Disproportionare dwarfism Proportionate dwarfism

Disproportionate dwarfism If body size is disproportionate, some parts of the body are small and others are of average size or above-average size. Disorders causing disproportionate dwarfism inhibit the development of bones. Characteristics:

The person has an average-size trunk and very short limbs, but some people may have a very short trunk and shortened (but disproportionately large) limbs. The other common characteristic of these disorders is the head being disproportionately larger than the body.

Almost all people with disproportionate dwarfism have normal intellectual capacities. Rare exceptions are usually the result of a secondary factor, such as excess fluid in the brain (hydrocephalus). About 70 percent of all people with dwarfism have a disorder called chondroplasia, which causes disproportionately short stature. This disorder usually results in:

An adult height of approximately 4 feet An average-size trunk Short arms and legs, with particularly short upper arms and legs Short fingers, often with a wide separation between the middle and ring fingers Limited mobility at the elbows A disproportionately large head, with a prominent forehead and flattened bridge of the nose Progressive development of bowed legs (genuvarum) Progressive development of swayed lower back (lordosis)

Proportionate dwarfism

A body is proportionately small if all parts of the body are small to the same degree and appear to be proportioned like a body of average stature. Proportionate dwarfism results from medical conditions present at birth or during early childhood that limit overall growth and development. Therefore, the head, trunk and limbs are all small but of average proportions relative to each other. Most of these disorders are uncommon, and signs and symptoms of the disorders vary greatly. A few disorders causing proportionate dwarfism result in mental retardation.

Growth hormone deficiency is a relatively common cause of proportionate dwarfism. It occurs when the pituitary gland fails to produce an adequate supply of growth hormone, which is essential for regular childhood growth. Signs and symptoms include:
Height below the fifth percentile on standard pediatric growth charts Slowed growth before age 5 Periods of little or no change in height Adult height usually less than 5 feet Delayed or no sexual development during adolescence

Intervention

The orthopaedic effects of dwarfism require complex reconstructive surgery and extensive physical therapy. Much like the severe accident victim, surgery on Little People involves bone grafts, fusions, steel screws, pins and plates, then months of physical therapy to regain even the most basic function like walking.

Nursing Management

Families of Little People sacrifice greatly to improve the quality of their children's lives. Medical bills, transportation, multiple hospitalizations and operations, and months spent in casts can take their toll emotionally, economically, and physically on the entire family provide the family with the support they need to endure these trying times, knowing that their goals are attainable and worthwhile

Hypergonadism

A clinical state resulting from enhanced secretion of gonadal hormones. A condition of increased hormone production before puberty, which produces precocious sexual development in both sexes.

Causes

Male: Unknown causes, testicular tumors, and pituitary tumors. Female: primarily due to idiopathic causes. Uncommon causes include ovarian and adrenal tumors. Confirmed by positive clinical history blood testing for evidence of elevated sex hormones.

Diagnosis

Male

Onset of puberty usually occurs around age 13 with Hypergonadism, this development occurs before age 10 Signs of precocious sexual development include:
growth of a beard and pubic hair enlargement of the penis and the testes Rapid growth of muscle and bone leads to early uniting of the epiphyses and a premature stoppage of growth in the long bones.

Female

In the female, onset of puberty, usually occurs around the age of 10 with hypergonadism, this development occurs before age 8. Signs of precocious sexual development include:
onset of menarche appearance of pubic and underarm hair breast enlargement Ovarian development renders the individual fertile, making pregnancy possible.

Hypogonadism

condition more prevalent in males in which the production of sex hormones and germ cells are inadequate.

Boys:

Hypogonadism most often shows up as an abnormality in boys during puberty Kallmann's syndrome is a birth defect in the brain that prevents release of hormones and appears as failure of male puberty. The childhood disease- Mumps, if acquired after puberty, can infect and destroy the testiclesa disease called viral orchitis

Ionizing radiation and chemotherapy, trauma, several drugs (spironolactone, a diuretic and ketoconazole, an antifungal agent), alcohol, marijuana, heroin, methadone, and environmental toxins can all damage testicles and decrease their hormone production.

Females:

Female problems in puberty are not caused by too little estrogen. Even female reproductive problems are rarely related to a simple lack of hormones, but rather to complex cycling rhythms gone wrong. All the problems with too little hormone happen during menopause, which is a normal hypogonadism.

Manifestations

The penis may be small, the testicles undescended (cryptorchidism) or various degrees of "feminization" of the genitals may be present. Besides the tissue changes generated by hormone stimulation, the only other symptoms relate to sexual desire and function. Libido is enhanced by testosterone, and male sexual performance requires androgens. The role of female hormones in female sexual activity is less clear, although hormones strengthen tissues and promote healthy secretions, facilitating sexual activity.

Treatment:

Replacement of missing body chemicals. Estrogen replacement is recommended for nearly all women after menopause for its many beneficial effects. Estrogen can be taken by mouth, injection, or skin patch. It is strongly recommended that the other female hormone, progesterone, be taken as well, because it prevents overgrowth of uterine lining and uterine cancer. Testosterone replacement is available for males who are deficient

Posterior Pituitary Disorders

Posterior pituitary dysfunction include specific disorders involving oversecretion or undersecretion of ADH.
Diabetes Insipidus, caused by undersecretion of ADH, results in excessive dilute urine production. Syndrome of Inappropriate ADH (SIADH), involving oversecretion of ADH, results in excessive water conservation.

Etiology Diabetes Insipidus

Posterior pituitary destruction of tumors Vascular accidents Surgery or hypothalamic damage Certain drugs that interfere with ADH secretion or action (e.g., phenytoin, alcohol, lithium carbonate) Nephrologenic diabetes insipidus, familial or arising from various renal disorders

SIADH

Central nervous system disorders Stimulation due to hypoxia or decreased left atrial filling pressure Overuse of vasopressin therapy Ectopic ADH production associated with some cancers Nausea or narcotic use, which can stimulate ADH secretion

Pathophysiology

Diabetes Insipidus occurs when injury to the posterior pituitary gland causes a decrease in vasopressin, also known as ADH, secretion or an inability of the kidney tubules to respond to ADH. In SIADH, the basic pathologic disturbances are excessive ADH activity, with water retention and dilutional hyponatremia, and inappropriate urinary excretion of sodium in the presence of hyponatremia.

Assessment Findings
Clinical Manifestations Diabetes Insipidus Profoundly increased output (5-20 L/day) Nocturia Extreme thrist Weight loss Possible tachycardia, hypotension, and weakness

SIADH

Decreased urine output Weight gain Altered mental status (e.g. headache, confusion, lethargy, seizures, and coma in severe hyponatremia) Delayed deep tendon reflex

Laboratory and diagnostic study findings

Diabetes Insipidus
Plasma osmolality and serum sodium levels are elevated Water (fluid) deprivation test demonstrates inability of the kidneys to concentrate urine despite increased plasma osmolality and low plasma vasopressin level. Vasopressin test demonstrates that the kidneys can concentrate urine after administration of ADH; this differentiates central (pituitary or hypothalamic) from nephrogenic diabetes insipidus.

SIADH
Plasma osmolality and serum sodium levels are decreased. Urinalysis detects elevated urine sodium and osmolality. Serum ADH level is elevated.

Nursing Management

Provide general nursing care for diabetes insipidus and SIADH.

Assess dehydration, skin turgor, and mucous membranes. Provide meticulous skin and mouth care. Monitor serum electrolyte levels, including sodium and potassium.

Provide specific nursing care for diabetes insipidus.

Administer prescribed medications, which may include ADH replacements. Replace fluids as indicated. Assess for and report any illness, injury, or other problem that could prevent adequate fluid intake. Encourage the client to drink fluids in response to thirst. For some unknown reason, the client craves ice cold water.

Provide specific nursing care for SIADH.

Administer prescribed medications, which may include Furosemide (Lasix), to prevent concentration of urine Regularly assess mental status.

Thyroid Gland Disorders

Hypothyroidism
state of insufficient serum thyroid hormone prevalent in persons between 40 and 50 years old at least twice as common in women as it is in men.

Cretinism Congenital hypothyroidism

results from inadequate secretion of thyroid hormones during fetal life or early infancy brain and skeleton fail to develop properly, resulting in mental retardation and dwarfism

Manifestations

prolonged jaundice after birth, or dry wrinkled skin, a swollen face and tongue that causes noisy respiration and an open mouth that drools fingers may be broad, and a small hernia at the belly button is quite common baby is usually listless, slow-moving, constipated, and a slow feeder older children who develop hypothyroidism suddenly stop growing

Risk Factor

Age, weight, and medical history Women are more likely to develop the disease after age 50; men, after age 60 Obesity family history history of high cholesterol levels autoimmune diseases as lupus, rheumatoid arthritis, or diabetes mellitus

Etiology Primary Hypothyroidism results from pathologic changes in the thyroid gland caused by:

Autoimmune thyroids Thyroidectomy Radioactive iodine therapy Antithyroid medication therapy

Secondary Hypothyroidism results from failure of the pituitary gland to secrete adequate TSH, possibly because of a tumor, surgical removal, or irradiation.

Laboratory and diagnostic study findings

Thyroid function tests reveal decreased T4 and T3 levels Serum TSH test reveal increased TSH (primary). Serum antibody tests detects presence of antithyroid antibodies (autoimmune) Blood studies reveal elevated cholesterol and creatine phosphokinase

Pathophysiology

Inability of the thyroid gland to secrete sufficient amounts of thyroid hormone, (thyroxine regulates such essential functions as heart rate, digestion, physical growth, and mental development, an insufficient supply of this hormone)
1. leads to decreased cellular metabolic activities 2. decreased oxygen consumption 3. decreased heat production

these actions produce mild to marked effects in all organ systems, can slow life-sustaining processes, damage organs and tissues in every part of the body, and lead to life-threatening complications.

Assessment
Clinical Manifestations Sluggishness, lethargy, depression, apathy, fatigue, and exercise intolerance Memory impairment Muscle aches, numbness and tingling of hands Cold intolerance Constipation Weight gain and decreased appetite Menstrual irregularities, infertility, and decreased libido Dry skin, brittle nails and dry hair Possible goiter Delay in muscle contraction and relaxation of tendon reflexes Bradycardia

Myxedema coma

extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration refers to the swelling of the skin and soft tissue that occurs in patients who are hypothyroid Myxedema coma occurs when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection. The cardinal manifestation of myxedema coma is a deterioration of the patient's mental status.

Myedema coma
Hypotension Hypoventilation Hypothermia Stupor, possibly progressing to coma

Nursing Management Provide Pharmacotherapy

Administer prescribed medications, which may include T4 Keep in mind that a client with hypothyroidism is very sensitive to narcotics, anesthetics, and sedatives; drug degradation is delayed, and respiratory depression can develop. Instruct the client and family members or significant others in the prescribed medication regimen, including purpose dosage schedule, and signs of overreplacement and underreplacement.

Administer fluids cautiously, because the client may not be able to excrete a heavy water load. If the client has hypoglycemia, infuse a concentrated source of glucose Provide relief of constipation, as indicated. Prevent vascular collapse in a hypothermic client. Refrain from aggressive rewarming. Institute respiratory assistance when necessary. Implement infection-prevention measures.

Hyperthyroidism

metabolic imbalance resulting from excessive thyroid hormone production Graves disease- most common form The incidence of Graves disease is greatest between the ages of 30-40 and is higher among women than men.

Etiology

Autoimmune dysfunction is the most common cause of Graves disease; autoantibodies apparently mimic TSH, leading to hypersecretion of thyroid hormones. Genetic factors seem to play a role. Other possible causes include:
Toxic nodular goiter Exposure to iodine TSH-secreting pituitary tumor (rare) Thyroiditis, which may be acute, subacute, or chronic (ie, Hashimoto disease)

Pathophysiology

Excessive secretion of thyroid hormone- leads to:

increased metabolic rate excessive heat production increased responsiveness to catecholamines

these actions lead to profound changes in many organ systems.

Assessment Findings Clinical Manifestations

Nervousness, irritability, hyperactivity, emotional excitability, and decreased attention span Weakness, easy fatigability, and exercise intolerance Heat intolerance Weight change (loss or gain) and increased appetite Insomnia and interrupted sleep Frequent stools and diarrhea

Menstrual irregularities and decreased libido Warm, sweaty, flushed skin with a velvety-smooth texture and spider telangiectasias Tremor, hyperkinesias, and Hyperreflexia Exophthalmos, retracted eyelids, and staring gaze Hair loss Goiter Bruits over the thyroid gland

Thyroid storm:

Hyperthermia, Hypertension, Delirium, Vomiting and abdominal pain, Tachyarrhythmias

Laboratory and Diagnostic Study Findings Serum thyroid function test reveal increased T4 and T3 levels. Radioactive iodine uptake test shows an increased uptake. Serum TSH assay reveals a nondetectable TSH level. Thyroid scan reveals increased function (i.e., hot areas) in the thyroid gland.

Nursing Management

Administer prescribed medications Assist the client and family members or significant others in exploring treatment options. Include family members or significant others because the clients attention span deficit may impair retention of information. Options include:
Pharmacotherapy with drugs that interfere with thyroid hormone synthesis of release Radioactive iodine therapy permanently limits thyroid hormone secretion by destroying thyroid tissue. Hypothyroidism, requiring lifelong replacement therapy usually develops at some point after this treatment. Surgery (subtotal or total thyroidectomy). The thyroid levels must be lowered preoperatively to prevent thyroid storm; lifelong replacement therapy may be necessary.

Promote adequate rest. Promote adequate nutrition

Prevent Injury Maintain Normothermia

Provide post-operative care, if appropriate. Support the head and avoid tension on sutures. Monitor for complications and intervene as indicated.

Hemorrhage requires the nurse to assess the surgical dressing and sides and back of neck for bleeding.

Parathyroid Gland Disorders

Hyperparathyroidism

overproduction of PTH, resulting in high blood calcium levels and bone demineralization may be primary or secondary Primary hyperparathyroidism is a common condition, usually occurring after age 60 and affecting women more often than men.

Etiology Primary Hyperparathyroidism

About 80% of cases are linked to a single adenoma of the parathyroid gland; the remaining cases are caused by parathyroid hyperplasia. Secondary hyperparathyroidism results from an adaptive increase in PTH secretion associated with problems involving chronic hypocalcemia.

Assessment Findings Clinical Manifestations

Although hyperparathyroidism may be asymptomatic, it may produce the following signs and symptoms:
Fatigue, muscular weakness, and listlessness Height loss and frequent fractures Renal calculi Anorexia, nausea, abdominal discomfort, and constipation Memory impairment Polyuria and polydipsia Back and joint pain Hypertension

Laboratory and Diagnostic Study Findings

Total and ionized serum calcium levels are elevated Serum and phosphate levels are decreased Urinalysis identifies hypercalciuria and hyperphosphaturia Radiograph or bone densitometry detects bone demineralization PTH levels are elevated Parathyroid scan possibly detects abnormal findings

Nursing Management
Provide preoperative care. Prepare the client for surgical treatment of primary hyperparathyroidism, which ,may include adenoma removal and hyperplastic gland resection. Force fluids to prevent dehydration, constipation, and kidney stone formation. Reduce added calcium by eliminating over-thecounter antacids, which may contain calcium; thiazide diuretics, which interfere with renal calcium excretion; and excessive intake of dairy products.

Provide postoperative care, which is similar to that for thyroidectomy. As indicated, provide aggressive calcium supplementation after surgery to compensate for hungry bone syndrome. Observe the client for symptoms of hypercalcemia (e.g., nausea, vomiting, headache, mental confusion, anorexia). Assess for renal calculi; report hematuria or flank pain as necessary.

Take measures to protect the client from injury.

Assist with the activities of daily living and ambulation as necessary. Encourage weight bearing to reduce calcium loss from the bones. Teach strategies to minimize falls, which may lead to fractures.

Provide relief of constipation as indicated; prune juice, stool softeners, physical activity, and increased fluids help prevent constipation. Monitor nutritional status, and intervene as necessary. Advise the client to avoid a diet with restricted or excess calcium. Reinforce the health care follow-up scheduled.

Hypoparathyroidism

PTH deficiency characterized by hypocalcemia, hyperphosphatemia, and neuromuscular hyperexcitability.

Etiology

iatrogenic, caused by accidental removal of or trauma to parathyroid glands during thyroidectomy, parathyroidectomy, or radical head or neck surgery. autoimmune genetic dysfunction (affects more women than men). A reversible form may be associated with hypomagnesemia, which interferes with PTH secretion.

Assessment Findings
Clinical Manifestations

Anxiety and irritability Numbness, tingling, and cramps in extremities Dysphagia Photophobia Evidence of neuromuscular hyoerexcitability, such as positive Chvostek and Trousseau signs, carpopedal spasms, bronchospasms, laryngeal spasms, arrhythmias, and convulsion

Laboratory and diagnostic study findings

Total and ionized serum calcium levels are low. Serum phosphate level is elevated. Serum PTH level is low.

Nursing Management

Administer prescribed medications, which include calcium and vitamin D supplements. Intervene for lie-threatening tetany as indicated. Administer intravenous calcium gluconate to prevent calcium depletion. Be alert for possible laryngeal spasm and resulting respiratory obstructions; keep a tracheostomy set available. Institute seizure precautions. Provide padded side rails and bite block at bedside. Minimize environmental stimuli. After the crisis resolves, closely monitor calcium levels. Keep intravenous calcium gluconate in the clients room.

Provide care in chronic hypoparathyroidism. high calcium and low phosphorus diet Milk, milk products, and egg yolks must be avoided because they are high in phosphorus. Administer vitamin D and magnesium supplementation, as indicated. In clients receiving magnesium, observe for symptoms of hypermagnesemia (i.e., hypotension, respiratory depression, muscle weakness, and confusion.) Administer oral calcium preparations to supplement the diet.

Provide client and family teaching about the medication regimen, including purpose, dosage schedule, and signs and symptoms of hypocalcemia and hypercalcemia. Inform the client that the dosage will be adjusted periodically based on the laboratory findings.

Adrenal Glands Disorders

Cushing Syndrome

involves excessive production of adrenocortical hormones, primarily cortisol but also androgens and mineralocorticoids. The incident is higher in women than in men.

Etiology The most common cause of Cushing Syndrome is bilateral adrenal hyperplasia (i.e., Cushing disease). Other causes include: Adrenal adenomas and carcinoma Ectopic ACTH production by tumors in other organs, such as the lungs and pancreas. Glucocorticoid therapy

Assessment Findings Clinical Manifestations depend on the adrenocortical hormones involved and may include:

Weight gain and altered fat distribution (e.g., central obesity with round [moon] face and buffalo hump. Muscle weakness, proximal muscle wasting, and fatigue Frequent infections and poor wound healing Symptoms of hyperglycemia Mental status changes and mood swings Menstrual disturbances, such as amenorrhea Diminished libido Skin changes, such as striae, bruises, acne, and thinning of scalp hair Hypertension Hirsutism Susceptibility to compression fractures Edema

Laboratory Findings

Serum potassium level is decreased. Serum glucose level is elevated. WBC count reveals depressed eosinophil and lymphocyte counts. Diurnal variation plasma levels reveal elevated plasma cortisol and 24-hour urine cortisol results.

Results for the 24-hour urinary free cortisol level and 24-hour urine collection for 17hydrocorticosteriods and 17-ketosteroids are elevated. Selected radiographic and axial CT studies may determine the site if ectopic ACTH production

Nursing Management Administer prescribed medications, which may include adrenocortical steroid inhibitors. Take measures to protect the client from injury and infection.

Assess skin integrity regularly. Avoid agents that can damage skin (e.g., tape, strong soaps) Promote good hygiene. Modify the environment to remove or minimize hazards.

Prepare the client for surgery, if indicated. Keep in mind that any treatment modality can cause temporary adrenal insufficiency. Procedures may include: Adrenalectomy, if the cause is adrenal adenoma Transsphenoidal hypophysectomy, if the cause is pituitary adenoma Tumor resection Encourage the client and family to ask questions and verbalize concerns about disease pathology, body image, treatment, and mental status.

Addison disease a primary adrenal hypofunction due to hyposecretion of adrenal cortex hormones.

Etiology Addison Disease can result from:

An autoimmune process Hemorrhage into the adrenal gland Adrenalectomy Neoplasm Fungal infection Tuberculosis

Assessment Findings Clinical Manifestations

Addison disease
Gastrointestinal complaints such as anorexia, nausea, vomiting, abdominal pain, and diarrhea Fatigue, muscle weakness, and arthralgias Decreased alertness and confusion Weight loss Dry skin, decreased body hair, and possible increased pigmentation with excessive ACTH stimulation

Addisonian (adrenal) Crisis

Hypotension Rapid, weak pulse Rapid respiratory rate Pallor and extreme weakness Hyperthermia

Laboratory and Diagnostic Study Findings Suggestive Findings Serum blood glucose is decreased. Serum sodium level is decreased. Serum potassium level is increased. WBC cell count is increased. Definitive Findings Serum cortisol levels are decreased. ACTH stimulation test reveals a low to normal cortisol response.

Nursing Management

Administer prescribed medications, which may include glucocorticosteroids and mineralocorticosteroids. Provide immediate treatment for an addisonian crisis. Treatment includes intravenous fluid, glucose, and electrolytes. Corticosteroid replacement and vasopressors may be administered. The client must avoid exertion.

Help prevent adrenal crisis.

Instruct the client to take precautions to avoid unnecessary activity and events that may be stressful. Ensure that hospitalized, acutely ill clients on a long-term glucocorticoid therapy receive additional doses to compensate for stress.

Provide client and family teaching.

Discuss hormone therapy, including its purpose, side effects, duration, symptoms of abnormalities to report to health care manager, and the need to inform all health care providers about the steroid replacement therapy. If overreplacement of glucocorticoids is indicated, inform the client about the purpose of therapy and possible side effects, such as cushingoid appearance, weight gain, acne, hirsutism, peptic ulcer, diabetes mellitus, osteoporosis, infection, muscular weakness, mood swings, cataracts, and hypertension.

Pheochromocytoma

a tumor that is usually benign and originiates from the chromaffin cells of the adrenal medulla.

peak incidence is ages 20-50 years 10% of the tumors are bilateral; 10% are malignant stimulates hypersecretion of catecholamines (epinephrine and norepinephrine) SNS overactivity causing the five Hs: hypertension, headache, hyperhidrosis, hypermetabolism, hyperglyclemia

Diagnostic Exams
Total Plasma Catecholamine Concentration

the client should lie supine and rest for 30 minutes butterfly needle is inserted 30 minutes before blood specimen is collected (to prevent elevation of catecholamine levels by the stress of venipuncture) normal values:
Epinephrine: 100 pinogram/ml (590 pmol/L) Epinephrine: 100 to 550 pinogram/ml (590-3240 pmol/L)

Clonidine Suppression Test

Clonidine (Catapress) a centrally acting adrenergic blocker suppresess the release of catocholamines. in pheochromocytoma, clonidine does not suppress the release of catecholamines Normal response: 2-3 hours after a single oral dose of clonidine, the total plasma catecholamine value decreases at least 40% from the clients baseline.

CT scan, MRI, and Ultrasound

to localize the pheochromacytoma

Collaborative Management Medical Management

Bed rest, head of bed elevated during episode of hypertension, tachycardia, and anxiety to provide orthostatic decrease in BP. Pharmacologic therapy
Phentolamine (Regitine) Sodium Nitroprusside (Nipride) to lower BP quickly

Surgery

Adrenalectomy Removal of single glands requires corticosteroid therapy for the first few days or weeks postoperatively Bilateral removal requires lifetime corticosteroid therapy

Nursing Management

Teaching the Client Self-Care

Emphasize the importance of periodic follow-up care. Provide instructions on corticosteroid therapy. Teach the client and family on how to measure the clients BP.

End of Chapter!