Pituitary gland

The pea-sized pituitary gland (hypophysis) is one of the most powerful glands in the body. It has been called the “master gland” because, through the negative feedback system, it controls the other endocrine glands. It works closely with the hypothalamus of the brain and is located in the cranial cavity in a small saddlelike depression in the sphenoid bone. It is divided into two segments, the anterior pituitary (adenohypophysis) and the posterior pituitary (neurohypophysis). Each segment has specialized hormones. The hypothalamus actually produces the hormones of the posterior pituitary and releases them for storage in the posterior pituitary gland; they are released from here as a result of nerve impulses received from the hypothalamus.

Thyroid gland

The thyroid gland secretes the hormones thyroxine (T₄) and triiodothyronine (T₃). Adequate oral intake of iodine is necessary for the formation of thyroid hormones. These hormones regulate three main functions: (1) growth and development, (2) metabolism, and (3) activity of the nervous system. Their function is controlled by the release of thyroid-stimulating hormone (TSH) from the pituitary gland.

Calcitonin is a hormone also released by the thyroid gland. It decreases blood calcium levels by causing calcium to be stored in the bones.

Parathyroid glands

Adrenal glands

Pancreas

The pancreas is an elongated gland that lies posterior to the stomach. It is an active organ, composed of both exocrine and endocrine tissue. The endocrine tissue of the pancreas contains more than a million tiny clusters of cells known collectively as the islets of Langerhans. These cells secrete two major hormones. The first, insulin, is secreted by the beta cells in response to increased levels of glucose in the blood. Insulin’s secretion pattern is a physiologic example of negative feedback between insulin and glucose. Elevated blood glucose levels stimulate the pancreas to secrete insulin. The stimulus for insulin secretion decreases as blood glucose levels decrease. The homeostatic mechanism is considered negative feedback because it reverses the change in blood glucose level. The second pancreatic hormone is glucagon, which is secreted by the alpha cells in response to decreased levels of glucose in the blood. Insulin and glucagon play a major role in carbohydrate, fat, and protein metabolism.

Female sex glands

Male sex glands

Suspended outside the body in the scrotum, a saclike structure, are the two oval sex glands called the testes. They release the hormone testosterone, which is responsible for the development of the male secondary sex characteristics, including axillary, pubic, and facial hair; maturation of the reproductive organs; deepening of the voice; and development of muscle and bone mass. Testosterone is necessary for sperm formation.

Thymus gland

Pineal gland

Etiology and pathophysiology

An overproduction of somatotropin (growth hormone [GH]) in the adult causes acromegaly, a condition that affects an estimated 250 people in the United States each year. The cause may be either (1) idiopathic hyperplasia (an increase in number of cells without a known cause) of the anterior lobe of the pituitary gland or (2) tumor growth. Unfortunately, growth changes that occur in acromegaly are irreversible, even with adequate medical or surgical intervention.

Clinical manifestations

Assessment

Subjective data include headaches or visual disturbances and painful, stiff joints. Evaluate muscle weakness and its effect on the patient’s ability to perform activities. Encourage patients to share their emotional responses to sexual problems (such as impotence in men and masculinization in women).

Collection of objective data includes ongoing assessment of bone enlargement and joint involvement, evidenced by gait changes and decreasing ability to perform activities. Changes in vital signs that may herald the onset of early heart failure include dyspnea, tachycardia, weak pulse, and hypotension.

Diagnostic tests

Diagnosis of acromegaly is based on the history and the clinical manifestations, computed tomography (CT) scan, magnetic resonance imaging (MRI), and cranial radiographic evaluation. A complete ophthalmologic examination, including visual fields, is usually performed because a large tumor of the pituitary gland potentially causes pressure on the optic chiasm or optic nerves. Laboratory tests confirm the elevated levels of serum GH and plasma insulin-like growth factor–1. The definitive test for acromegaly is the oral glucose challenge test. Normally GH concentration falls during an oral glucose challenge test, but in acromegaly these levels do not fall (Lewis et al., 2007). Restrict the patient’s oral intake for 8 hours before this test.

Medical management

Nursing interventions and patient teaching

Nursing interventions are mainly supportive. Muscle weakness, joint pain, or stiffness warrant assessment of the ability to perform activities of daily living (ADLs). Headache may impair the patient’s ability to socialize and may also impede education. Worsening headaches may indicate tumor progression. The diet should be soft and easy to chew, since jaw muscles and the temporomandibular joint may be involved. Encourage the patient to chew thoroughly, and allow adequate time during meals, assisting when necessary. Encourage frequent fluid intake. Nonopioid analgesics may be given for pain relief. Visual impairment may increase the risk of injury for these patients, so take care to prevent them from stumbling into furniture or dropping objects.

As the body changes, the patient may develop problems with self-esteem and may feel physically unattractive. He or she may have difficulty communicating with significant others, which can disrupt individual or family coping methods. Other complications of acromegaly are related to enlargement of the liver, the spleen, and the heart. Cardiac dysrhythmias may develop, and the patient may experience heart failure. Abdominal girth may increase as a result of weight gain and inactivity, and respiratory difficulty may occur.

Nursing diagnoses and interventions for the patient with acromegaly include but are not limited to the following:

The patient should remain under the supervision of a physician so that any complications can be promptly diagnosed and adequately treated. Teach the patient exercises that can be performed at home, such as active range-of-motion of joints of the extremities and of the neck, to help prevent muscle atrophy and loss of movement.

Prognosis

Even with adequate medical or surgical treatment, the physical changes are irreversible, and the patient is prone to developing complications.

Etiology and pathophysiology

Gigantism usually results from an oversecretion of GH as a result of hyperplasia of the anterior pituitary; this hyperplastic tissue may develop into a tumor. Another possible cause is a defect in the hypothalamus, which directs the anterior pituitary to release excess amounts of GH.

Clinical manifestations

When overproduction of GH occurs in a child before closure of the epiphyses, there is an overgrowth of the long bones. This results in the attainment of great height, accompanied by increased muscle and visceral development. Weight increases, but body proportions are usually normal. Despite their size, these patients are usually weak. Other kinds of gigantism may be caused by certain genetic disorders or by disturbances in sex hormone production. Once identified, these children should be referred for further medical evaluation and follow-up.

Assessment

Collection of subjective data includes assessment of the patient’s understanding of the disease process and his or her ability to verbalize emotional responses.

Collection of objective data requires frequent measurement of height. Assess the patient’s use of adaptive coping measures and family interactions.

Diagnostic tests

The GH-suppression test (also called the glucose-loading test) may be done to evaluate GH levels. In the patient with gigantism, baseline levels of GH are high.

Medical management

Medical management of children with gigantism may include surgical removal of tumor tissue or irradiation of the anterior pituitary gland, with subsequent replacement of pituitary hormones as indicated. The physician then observes the child for the development of related complications, such as hypertension, heart failure, osteoporosis, thickened bones, and delayed sexual development.

Nursing interventions and patient teaching

Nursing interventions primarily include early identification of children who are experiencing increased growth rates compared with other children their age. The condition causes potential problems with self-image, especially if the child is a preteen who is a great deal taller than peers. Girls usually suffer more emotional trauma in this situation than boys do. Be understanding and compassionate and accentuate the positive aspects of being tall.

Early diagnosis of these patients is essential, since proper medical management can retard the height a child will reach. Stress to the parents the importance of regular visits to the pediatrician or pediatric endocrinologist (a physician who specializes in endocrinology).

Prognosis

With new medical and surgical advances, the expected life span of these patients is longer than it was previously. However, their life expectancy is still shorter than that of the average individual.

Etiology and pathophysiology

Hypopituitary dwarfism is a condition caused by deficiency in GH. Most cases are idiopathic, but a small number can be attributed to an autosomal recessive trait. In some cases the patients also lack adrenocorticotropic hormone (ACTH), TSH, and the gonadotropins.

Clinical manifestations

The most common clinical manifestation of dwarfism is that the child is a great deal shorter than his or her peers. These patients usually appear well proportioned and well nourished but appear younger than their chronologic age. They may have problems with dentition as the permanent teeth erupt, since the jaws are underdeveloped. Sexual development is usually normal but delayed. Many people with hypopituitary dwarfism are able to reproduce normal offspring, unless there is an accompanying deficiency in gonadotropins. Because only a small number of children who experience short stature or delayed growth suffer from dwarfism, a thorough diagnostic workup is crucial.

Assessment

Subjective data include the patient’s understanding of the disease process and emotional responses to it. A family history of dwarfism may reveal previously successful coping strategies. Encourage the patient to verbalize feelings. Most of these children display normal intelligence. The child’s history usually reveals a normal birth weight. It is important to determine when the child’s growth retardation was first noted.

Collection of objective data includes regular measurement of height and weight to determine responses to GH and other hormones that may be administered. Compare current height and weight with standard growth charts, and compare the child’s growth pattern with that of siblings and other relatives at comparable age periods.

Diagnostic tests

Diagnostic tests include radiographic evaluation of the wrist for bone age and an MRI or a CT scan to rule out a pituitary tumor. Definitive diagnosis is based on decreased plasma levels of GH. Restrict the patient’s oral intake after midnight for this test.

Medical management

Medical treatment involves replacement of GH by injection and the addition of other hormones as needed to correct deficiencies. If a tumor is the cause of dwarfism, surgery is usually indicated.

Nursing interventions and patient teaching

Exercise particular care to identify children with growth problems. The physician correlates the onset of growth retardation with symptoms of headache, visual disturbances, or behavior changes that might indicate tumor, so be alert for these symptoms. Be careful not to make the parents feel guilty about any delay in seeking medical attention for their child.

Encourage the child to wear age-appropriate clothing and engage in activities with peers, since major problems with self-esteem can occur in dwarfism. Emphasize the child’s abilities and strengths instead of his or her physical size.

Prognosis

Most of these patients lead fairly normal lives, and many become parents of normal children. Complications experienced are often of the musculoskeletal and cardiovascular systems.

Etiology and pathophysiology

Diabetes insipidus (diabetes, “like a sieve or siphon”; and insipidus, “tasteless”) is a transient or permanent metabolic disorder of the posterior pituitary in which ADH is deficient. The condition may be either primary or secondary to other conditions, such as head injury, intracranial tumor, intracranial aneurysm, or infarct. Infections such as encephalitis or meningitis have been known to cause diabetes insipidus. Diabetes insipidus occurs when either the secretion or action of ADH goes awry. A decrease in ADH results in electrolyte and fluid imbalances. The imbalances are caused by increased plasma osmolality and increased urinary output.

Clinical manifestations

Diabetes insipidus is characterized by marked polyuria and intense polydipsia. The urine is very dilute, looking much like water, with a low specific gravity (1.001 to 1.005; the normal range is 1.003 to 1.030). Urinary output may exceed 5 to 20 L/24 hr, whereas the average is 1.5 L/24 hr. Patients typically lose as much as 200 mL of urine an hour for more than 2 consecutive hours. The patient craves cold or iced water and may drink 4 to 20 L of fluid daily, yet may become severely dehydrated and have increased levels of sodium in the blood (hypernatremia). Even when unconscious after surgery or head trauma, these patients continue to produce copious quantities of urine. If untreated, diabetes insipidus can lead to signs and symptoms of hypovolemic shock, including changes in level of consciousness, tachycardia, tachypnea, and hypotension. However, unlike hypovolemic shock, diabetes insipidus causes an increase in urinary output rather than a decrease.

Assessment

Subjective data include the patient’s understanding of the relationship of symptoms (such as thirst and polyuria) to the underlying cause. The patient should be able to state the importance of not restricting oral fluids. Assess the severity of thirst. The patient may be embarrassed about the constant need to drink and then empty the bladder and may voluntarily restrict social contacts and work activities. The patient is weak, tired, and lethargic.

Diagnostic tests

Diagnosis is based on clinical manifestations, urine specific gravity, and urine ADH measurement. The urine specific gravity often drops below 1.003, and the serum sodium level increases to more than 145 mEq/L (normal serum sodium level is 135 to 145 mEq/L). The serum osmolality may be greater than 300 mOsm/kg (normal is 280 to 300 mOsm/kg). The fluid deprivation (water deprivation) test may be ordered to determine how well the pituitary is producing ADH and to help rule out other causes. A CT scan and radiographic evaluation of the sella turcica (the “Turkish saddle”–shaped depression in the sphenoid bone that houses the pituitary gland) may be done.

Medical management

Medical treatment involves intravenous (IV), subcutaneous, intranasal, or oral administration of ADH preparations in the form of desmopressin acetate (DDAVP). Several other drugs are available for ADH replacement, including aqueous vasopressin (Pitressin intramuscular [IM] or intranasal), vasopressin tannate IM, and lypressin (Diapid intranasal). Coffee, tea, and other beverages containing caffeine are usually eliminated from the diet because of their possible diuretic effect. If the patient cannot match the urinary losses through oral intake, he or she is at risk for dehydration and severe hypernatremia. IV fluids of hypotonic saline or dextrose 5% in water are needed.

Nursing interventions and patient teaching

Because of the potential for fluid volume deficiency, carefully monitor the urinary output of pediatric and unconscious patients. Assess skin turgor frequently, along with the condition of oral mucous membranes. Weigh the patient and record I&O daily. Do not limit oral fluids in an effort to reduce urinary output.

Nursing diagnoses and interventions for the patient with diabetes insipidus include but are not limited to the following:

Nursing Diagnoses

Nursing Interventions

Deficient fluid volume, risk for, related to excessive urine production

Assess for signs and symptoms of dehydration (dry oral mucous membranes, poor skin turgor, soft eyeballs, lowered blood pressure, rapid pulse). Monitor electrolyte status carefully. Measure I&O. Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: 6. Care of the patient with a gallbladder, liver, biliary tract, or exocrine pancreatic disorder 9. Care of the patient with a respiratory disorder 12. Care of the patient with a reproductive disorder 2. Care of the surgical patient Stay updated, free articles. Join our Telegram channel Join Tags: Adult Health Nursing Oct 19, 2016 | Posted by admin in NURSING | Comments Off on 11. Care of the patient with an endocrine disorder Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access