Risk Factors: Risk factors for the development of SIADH include pituitary damage caused by infection, trauma, or neoplasm; secretion of vasopressin-like substances from some types of malignant tumors (particularly pulmonary malignancies); and thoracic pressure changes from compression of pulmonary or cardiac pressure receptors, or both.

Clinical Presentation: Symptoms of SIADH are the clinical opposite of symptoms of DI. They are the result of water retention and the subsequent dilution of sodium in the blood serum and body cells. Neurologic and neuromuscular signs and symptoms predominate and are directly related to the swelling of brain tissue and sodium changes within neuromuscular tissues.

Clinical Presentation: Degenerative arthropathy may be seen in the peripheral joints of a client with acromegaly, most frequently attacking the large joints. On x-ray studies, osteophyte formation may be seen, along with widening of the joint space because of increased cartilage thickness. In late-stage disease, joint spaces become narrowed, and occasionally chondrocalcinosis may be present.

Stiffness of the hand, typically of both hands, is associated with a broad enlargement of the fingers from bony overgrowth and with thickening of the soft tissue. Thickening and widening of the phalangeal tufts are typical x-ray findings in soft tissue. In clients with these x-ray findings, much of the pain and stiffness is believed to be due to premature osteoarthritis.

CTS is seen in up to 50% of people with acromegaly. The CTS that occurs with this growth disorder is thought to be caused by compression of the median nerve at the wrist from soft tissue hypertrophy or bony overgrowth or by hypertrophy of the median nerve itself.

Myopathy in people with acromegaly is commonly reported but poorly understood. Changes in muscle size and strength are associated with acromegaly and are probably multifactorial in origin. Screening individuals with acromegaly for muscle weakness and poor exercise tolerance is now recommended.¹²

About half the individuals with acromegaly have back pain. X-ray studies demonstrate increased intervertebral disk spaces and large osteophytes along the anterior longitudinal ligament (ALL), mimicking diffuse idiopathic skeletal hyperostosis (DISH).

DISH (also known as Forestier’s disease) is characterized by abnormal ossification of the ALL, resulting in an x-ray image of large osteophytes seemingly “flowing” along the anterior border of the spine. DISH is particularly common in the thoracic spine and has been reported to be more prevalent among persons with diabetes than among the nondiabetic population. DISH appears to be an age-related predisposition to ossification of tendon, joint capsule, and ligamentous attachments. Identification of the presence of DISH syndrome prior to surgery is important in the prevention of heterotropic bone formation.¹³

Primary Adrenal Insufficiency: Chronic adrenocortical insufficiency (hyposecretion by the adrenal glands) may be primary or secondary. Primary adrenal insufficiency is also referred to as Addison’s disease (hypofunction), named after the physician who first studied and described the associated symptoms. It can be treated by the administration of exogenous cortisol (one of the adrenocortical hormones).

Primary adrenal insufficiency occurs when a disorder exists within the adrenal gland itself. This adrenal gland disorder results in decreased production of cortisol and aldosterone, two of the primary adrenocortical hormones. The most common cause of primary adrenal insufficiency is an autoimmune process that causes destruction of the adrenal cortex.

The most striking physical finding in the person with primary adrenal insufficiency is the increased pigmentation of the skin and mucous membranes. This discoloration may vary in the white population from a slight tan or a few black freckles to an intense generalized pigmentation, which has resulted in persons being mistakenly considered to be of a darker-skinned race. Members of darker-skinned races may develop a slate-gray color that may be obvious only to family members.

Melanin, the major product of the melanocyte, is largely responsible for the coloring of skin. In primary adrenal insufficiency, the increase in pigmentation is initiated by the excessive secretion of melanocyte-stimulating hormone (MSH) that occurs in association with increased secretion of adrenocorticotropic hormone (ACTH). ACTH is increased in an attempt to stimulate the diseased adrenal glands to produce and release more cortisol.

Most commonly, pigmentation is visible over extensor surfaces such as the backs of the hands; elbows; knees; and creases of the hands, lips, and mouth. Increased pigmentation of scars formed after the onset of the disease is common. However, it is possible for a person with primary adrenal insufficiency to demonstrate no significant increase in pigmentation.

Secondary Adrenal Insufficiency: Secondary adrenal insufficiency refers to a dysfunction of the gland because of insufficient stimulation of the cortex owing to a lack of pituitary ACTH. Causes of secondary disease include tumors of the hypothalamus or pituitary, removal of the pituitary, or rapid withdrawal of corticosteroid drugs. Clinical manifestations of secondary disease do not occur until the adrenals are almost completely nonfunctional and are primarily related to cortisol deficiency only.

Effects of Cortisol on Connective Tissue: Overproduction of cortisol or closely related glucocorticoids by abnormal adrenocortical tissue leads to a protein catabolic state. This overproduction causes liberation of amino acids from muscle tissue. The resultant weakened protein structures (muscle and elastic tissue) cause a protuberant abdomen, poor wound healing, generalized muscle weakness, and marked osteoporosis (demineralization of bone causing reduced bone mass), which is made worse by an excessive loss of calcium in the urine.

Excessive glucose resulting from this protein catabolic state is transformed mainly into fat and appears in characteristic sites, such as the abdomen, supraclavicular fat pads, and facial cheeks. The change in facial appearance may not be readily apparent to the client or to the therapist, but pictures of the client taken over a period of years may provide a visual record of those changes.

The effect of increased circulating levels of cortisol on the muscles of clients varies from slight to very marked. There may be so much muscle wasting that the condition simulates muscular dystrophy. Marked weakness of the quadriceps muscle often prevents affected clients from rising out of a chair unassisted. Those with Cushing’s syndrome of long duration almost always demonstrate demineralization of bone. In severe cases, this condition may lead to pathologic fractures, but it results more commonly in wedging of the vertebrae, kyphosis, bone pain, and back pain

Obesity, diabetes, polycystic ovarian syndrome, and other metabolic/endocrine problems can resemble Cushing’s syndrome. It is important to recognize critical indicators of this particular disorder, such as excessive hair growth, moonface, mood disorders, and increased muscle weakness, as indicators for further endocrine diagnostic testing.¹⁵

The poor wound healing that is characteristic of this syndrome becomes a problem when any surgical procedures are required. Inhibition of collagen formation with corticosteroid therapy is responsible for the frequency of wound breakdown in postsurgical clients.

Clinical Presentation: Excessive thyroid hormone creates a generalized elevation in body metabolism. The effects of thyrotoxicosis occur gradually and are manifested in almost every system (Fig. 11-3 and Table 11-4).

In more than 50% of adults older than 70, three common signs are tachycardia, fatigue, and weight loss. In clients younger than 50, clinical signs and symptoms found most often include tachycardia, hyperactive reflexes, increased sweating, heat intolerance, fatigue, tremor, nervousness, polydipsia, weakness, increased appetite, dyspnea, and weight loss.¹⁸

Chronic periarthritis is also associated with hyperthyroidism. Inflammation that involves the periarticular structures, including the tendons, ligaments, and joint capsule, is termed periarthritis. The syndrome is associated with pain and reduced range of motion. Calcification, whether periarticular or tendinous, may be seen on x-ray studies. Both periarthritis and calcific tendinitis occur most often in the shoulder, and both are common findings in clients who have endocrine disease (Case Example 11-3).

Painful restriction of shoulder motion associated with periarthritis has been widely described among clients of all ages with hyperthyroidism. The involvement can be unilateral or bilateral and can worsen progressively to become adhesive capsulitis (frozen shoulder). Acute calcific tendinitis of the wrist also has been described in such clients. Although antiinflammatory agents may be needed for the acute symptoms, chronic periarthritis usually responds to treatment of the underlying hyperthyroidism.

Proximal muscle weakness (most marked in the pelvic girdle and thigh muscles), accompanied by muscle atrophy known as myopathy, occurs in up to 70% of people with hyperthyroidism. Muscle strength returns to normal in about 2 months after medical treatment, whereas muscle wasting resolves more slowly. In severe cases normal strength may not be restored for months.

The incidence of myasthenia gravis is increased in clients with hyperthyroidism, which in turn can aggravate muscle weakness. If the hyperthyroidism is corrected, improvement of myasthenia gravis follows in about two-thirds of clients.

Thyroid Storm: Life-threatening complications with hyperthyroidism are rare but still important for the therapist to recognize. Unrecognized disease, untreated disease, or incorrect treatment can result in a condition called thyroid storm. In addition, precipitating factors, such as trauma, infection, or surgery, can turn well-controlled hyperthyroidism into a thyroid storm.

Thyroid storm is characterized by signs and symptoms of hypermetabolism including severe tachycardia with heart failure, shock, and hyperthermia (up to 105.3° F [40.7° C]). Restlessness, agitation, chest pain, abdominal pain, nausea and vomiting, and coma can occur. Immediate medical referral is required to return the client to a normal thyroid state and prevent cardiovascular or hyperthermic collapse. Look for a recent history of the precipitating factors mentioned.

Risk Factors: Women are 10 times more likely than men to have hypothyroidism. More than 10% of women over age 65 and 15% over age 70 are diagnosed with this disorder. Risk factors include surgical removal of the thyroid gland, external irradiation, and some medications (e.g., lithium, amiodarone).

Clinical Presentation: As with all disorders affecting the thyroid and parathyroid glands, clinical signs and symptoms affect many systems of the body (Table 11-5). Because the thyroid hormones play such an important role in the body’s metabolism, lack of these hormones seriously upsets the balance of body processes.

Among the primary symptoms associated with hypothyroidism are intolerance to cold, excessive fatigue and drowsiness, headaches, and weight gain. In women, menstrual bleeding may become irregular, and premenstrual syndrome (PMS) may worsen. Physical assessment often reveals dryness of the skin and increasing thinness and brittleness of the hair and nails. There may be nodules or other irregularities of the thyroid palpable during anterior neck examination.

Ichthyosis, or dry scaly skin (resembling fish scales; the word ichthyosis is derived from the Latin word ichthus, which means “fish”), may be an inherited dermatologic condition (Fig. 11-4). It may also be the result of a thyroid condition. It must not be assumed that clients who present with this condition are merely in need of better hydration or regular use of skin lotion. A medical referral is needed to rule out underlying pathology.

Clinical Presentation: Many systems of the body are affected by hyperparathyroidism (Table 11-6). Proximal muscle weakness and fatigability are common findings and may be secondary to a peripheral neuropathic process. Myopathy of respiratory muscles with associated respiratory involvement often goes unnoticed. Striking reversal of muscle weakness and atrophy occur with successful treatment of the underlying hyperparathyroidism.

Other symptoms associated with hyperparathyroidism are muscle weakness, loss of appetite, weight loss, nausea and vomiting, depression, and increased thirst and urination (Case Example 11-5). Hyperparathyroidism can also cause GI problems, pancreatitis, bone decalcification, and psychotic paranoia (Fig. 11-6).

Bone erosion, bone resorption, and subsequent bone destruction from hypercalcemia associated with hyperparathyroidism occurs rarely today. In most cases, hypercalcemia is mild and detected before any significant skeletal disease develops. The classic bone disease osteitis fibrosa cystica affects persons with primary or renal hyperparathyroidism. Bone lesions called Brown tumors appear at the end stages of the cystic osteitis fibrosa. There are increasing reports of this condition in hyperparathyroidism secondary to renal failure because of the increasing survival rates of clients on hemodialysis.

Currently, skeletal manifestations of primary hyperparathyroidism are more likely to include bone pain secondary to osteopenia, especially diffuse osteopenia of the spine with possible vertebral fractures. In addition, a number of articular and periarticular disorders have been recognized in association with primary hyperparathyroidism. The therapist may encounter cases of ruptured tendons caused by bone resorption in clients with hyperparathyroidism.

Inflammatory erosive polyarthritis may be associated with chondrocalcinosis and CPPD deposits in the synovial fluid. This erosion is called osteogenic synovitis. Concurrent illness and surgery (most often parathyroidectomy) are recognized inducers of acute arthritic episodes.

Clinical Presentation: Hypocalcemia occurs when the parathyroids become inactive. The resultant deficiency of calcium in the blood alters the function of many tissues in the body. These altered functions are described by the systemic manifestations of signs and symptoms associated with hypoparathyroidism (Table 11-7).

The most significant clinical consequence of hypocalcemia is neuromuscular irritability. This irritability results in muscle spasms, paresthesias, tetany, and life-threatening cardiac arrhythmias. Muscle weakness and pain have been reported along with hypocalcemia in clients with hypoparathyroidism.

Hypoparathyroidism is primarily treated through pharmacologic management with intravenous calcium gluconate, oral calcium salts, and vitamin D. Acute hypoparathyroidism is a life-threatening emergency and is treated rapidly with calcium replacement, anticonvulsants, and prevention of airway obstruction.

Clinical Presentation: Specific physiologic changes occur when insulin is lacking or ineffective. Normally, the blood glucose level rises after a meal. A large amount of this glucose is taken up by the liver for storage or for use by other tissues such as skeletal muscle and fat. When insulin function is impaired, the glucose in the general circulation is not taken up or removed by these tissues; thus it continues to accumulate in the blood. Because new glucose has not been “deposited” into the liver, the liver synthesizes more glucose and releases it into the general circulation, which increases the already elevated blood glucose level.

Protein synthesis is also impaired because amino acid transport into cells requires insulin. The metabolism of fats and fatty acids is altered, and instead of fat formation, fat breakdown begins in an attempt to liberate more glucose. The oxidation of these fats causes the formation of ketone bodies. Because the formation of these ketones can be rapid, they can build quickly and reach very high levels in the bloodstream. When the renal threshold for ketones is exceeded, the ketones appear in the urine as acetone (ketonuria).

The accumulation of high levels of glucose in the blood creates a hyperosmotic condition in the blood serum. This highly concentrated blood serum then “pulls” fluid from the interstitial areas, and fluid is lost through the kidneys (osmotic diuresis). Because large quantities of urine are excreted (polyuria), serious fluid losses occur, and the conscious individual becomes extremely thirsty and drinks large amounts of water (polydipsia). In addition, the kidney is unable to resorb all the glucose, so glucose begins to be excreted in the urine (glycosuria).

Certain medications can cause or contribute to hyperglycemia. Corticosteroids taken orally have the greatest glucogenic effect. Any person with diabetes taking corticosteroid medications must be monitored for changes in blood glucose levels.

Other hormones produced by the body also affect blood glucose levels and can have a direct influence on the severity of diabetic symptoms. Epinephrine, glucocorticoids, and growth hormone can cause significant elevations in blood glucose levels by mobilizing stored glucose to blood glucose during times of physical or psychologic stress.

When persons with DM are under stress, such as during surgery, trauma, pregnancy, puberty, or infectious states, blood glucose levels can rise and result in the need for increased amounts of insulin. If these insulin needs cannot be met, a hyperglycemic emergency such as diabetic ketoacidosis can result.

It is essential to remember that clients with DM who are under stress will have increased insulin requirements and may become symptomatic even though their disease is usually well controlled in normal circumstances.

Diagnosis: To be diagnosed with diabetes, a person must have fasting plasma glucose (FPG) readings of 126 mg/dL or higher on two different days. The previous cutoff, set in 1979, was 140 mg/dL. This change occurred as a result of research showing that individuals with readings as low as the mid-120s have already started developing tissue damage from diabetes. A value greater than 100 mg/dL is a risk factor for future diabetes and cardiovascular disease. It has been suggested that the term “prediabetes” is no longer used: the person either has diabetes or does not.³⁶

The American Diabetes Association offers consumers a risk test for diabetes (http://www.diabetes.org/risk-test.jsp). All adults should take this risk test; anyone 45 or older should be tested for diabetes every 3 years. Individuals with elevated FPG values as described should be tested every 1 to 2 years. The therapist can offer at-risk clients information on increased activity and exercise as a means of lowering their risk of developing diabetes.³⁷

Physical Complications: At presentation, the client with DM may have a variety of serious physical problems. Infection and atherosclerosis are the two primary long-term complications of this disease and are the usual causes of severe illness and death in the person with diabetes.

Blood vessels and nerves sustain major pathologic changes in the person affected by DM. Atherosclerosis in both large vessels (macrovascular changes) and small vessels (microvascular changes) develops at a much earlier age and progresses much faster in the individual with DM. The blood vessel changes result in decreased blood vessel lumen size, compromised blood flow, and resultant tissue ischemia. The pathologic end-products are cerebrovascular disease (CVD), coronary artery disease (CAD), renal artery stenosis, and peripheral vascular disease (PVD).

Microvascular changes, characterized by the thickening of capillaries and damage to the basement membrane, result in diabetic nephropathy (kidney disease) and diabetic retinopathy (disease of the retina). Diabetes is the leading cause of kidney failure and new cases of blindness in the United States as of 2007.30,38

Poorly controlled DM can lead to various tissue changes that result in impaired wound healing. Decreased circulation to the skin can further delay or diminish healing. Skin eruptions called xanthomas (Fig. 11-7) may appear when high lipid levels (e.g., cholesterol and triglycerides) in the blood cause fat deposits in the skin over extensor surfaces such as the elbows, knees, back of the head and neck, and heels. Yellow patches on the eyelids are another sign of hyperlipidemia. Medical referral is required to normalize lipid levels.

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