UNIT 3

Intensive Insulin Therapy.

A second approach is to use a more complex insulin regimen to achieve levels of blood glucose that are as close to normal as is safe and practical. An intensive insulin therapy regimen involves three to four injections of insulin a day using both long-acting and short-acting insulin or using insulin pump therapy. Although intensive treatment is beneficial in reducing the risk of complications, not all people with diabetes are candidates for this approach to diabetes management.

Alpha-Glucosidase Inhibitors.

Acarbose (Precose) and miglitol (Glyset) are alpha-glucosidase inhibitors. They work by delaying the absorption of glucose in the intestines, which results in a lower level of postprandial blood glucose. Reduction in plasma glucose results in improved diabetes control and lower A1c levels. The advantage of alpha-glucosidase inhibitors is that they are not systemically absorbed, making them safer to use. Side effects include diarrhea and flatulence. These effects may be minimized by starting at a very low dose and increasing the dose gradually. Because acarbose and miglitol affect food absorption, they must be taken immediately before a meal, making therapeutic adherence a potential problem.

Aplastic anemia

An immune response mediated by cytotoxic T cells; targets the cells in the bone marrow, causing cell death and bone marrow failure Hereditary or acquired (exposure to benzene, pesticides) Decreased reticulocyte count Decreased white blood cells, Hgb, Hct, and platelets Immunosuppressive therapy (e.g., cyclosporine, corticosteroids, antithymocyte globulin) Stem cell transplant

Bleeding

Bleeding from gastrointestinal tract, menorrhagia (excessive menstrual flow), epistaxis (nosebleed), trauma results in decrease in circulating blood volume and decreased Hgb and Hct Increased reticulocyte level Normal Hgb and Hct if measured soon after bleeding starts, but levels decrease thereafter Normal MCV initially but later decreases Decreased ferritin and iron levels (later) Packed RBC transfusions Identify and control source of blood loss

Impaired glucose tolerance

Borderline diabetes Latent diabetes Chemical diabetes Subclinical diabetes Asymptomatic diabetes Oral glucose tolerance test value between 140 mg/dL (7.7 mmol/L) and 200 mg/dL (11 mmol/L) Impaired fasting glucose is defined as a fasting plasma glucose between 110 mg/dL (6 mmol/L) and 126 mg/dL (7 mmol/L) 29% eventually develop diabetes Above-normal susceptibility to atherosclerotic disease Renal and retinal complications usually not significant May be obese or nonobese Should be screened for diabetes periodically

Autoimmune hemolytic anemia Acquired; caused by extrinsic insults such as infection, medications, venom, trauma

Both inherited and acquired forms result in hemolysis within blood vessels and/or lymphoid tissue Presence of schistocytes Increased spherocyte level Increased reticulocytes Immunosuppressive therapy (i.e., corticosteroids) Acquired: remove insult, treat underlying disorder

Iron deficiency

Chronic blood loss, failure to recapture iron from recycled RBCs Demands for iron exceed iron intake. Decreased iron intake results in use and depletion of iron stores, resulting in decreased Hgb production Decreased reticulocytes, iron, ferritin, iron saturation, MCV Increased TIBC Iron replacement therapy: ferrous sulfate 325 mg PO t.i.d. Parenteral iron therapy reserved for those who cannot take oral replacement due to intolerance, poor enteral absorption, or continued blood loss IV iron therapy requires careful monitoring for signs of hypersensitivity

Type 1 (5-10% of all diabetes)

Juvenile diabetes Juvenile-onset diabetes Ketosis-prone diabetes Brittle diabetes Insulin-dependent diabetes mellitus (IDDM) Onset any age, but usually young (under 30 years of age) Usually thin at diagnosis; recent weight loss Etiology includes genetic, immunologic, and environmental factors (e.g., virus) Often have positive islet cell or GAD (glutamic acid decarboxylase) antibodies Little or no endogenous insulin Need insulin to preserve life Ketosis-prone when insulin absent Acute complication of hyperglycemia: diabetic ketoacidosis

Decreased erythropoietin production

Kidney disease can impair erythropoietin production (due to renal disease, malignancy), which, in turn, decreases RBC production Decreased erythropoietin level; normal MCV and MCH; increased creatinine level Erythropoietin replacement

Type 2

(90-95% of all diabetes: obese—80% of type 2; nonobese—20% of type 2) Adult-onset diabetes Maturity-onset diabetes Ketosis-resistant diabetes Stable diabetes Non-insulin-dependent diabetes (NIDDM) Onset any age, usually over 30 years of age Usually obese at diagnosis Causes include obesity, heredity, and environmental factors No islet cell antibodies Decrease in endogenous insulin, or increased with insulin resistance Most patients can improve blood glucose through weight loss if obese Oral antidiabetic agents may improve blood glucose levels if dietary modification and exercise are unsuccessful May need insulin on a short- or long-term basis to prevent hyperglycemia Ketosis uncommon, except in stress or infection Acute complication: hyperglycemic hyperosmolar nonketotic syndrome

Normocytic

(MCV 80-100 fL), normochromic Cells of normal size with normal Hgb content Aplastic anemia Acute blood loss Hemolytic anemia Anemia of chronic disease Sickle cell anemia Normal MCV Normal MCHC ↓ Hgb ↓ Hct

Macrocytic

(MCV greater than 100 fL), normochromic Large in size, thickness, and volume Folic acid deficiency Vitamin B12 deficiency Alcohol abuse Medications (e.g., hydroxyurea) ↑ MCV Normal MCHC ↓ Hgb ↓ Hct

Microcytic

(MCV less than 80 fL), hypochromic Small, reduced amount of Hgb Iron deficiency anemia Sideroblastic anemia Thalassemia ↓ MCV ↓ MCHC ↓ Hgb ↓ Hct

Hypoglycemia

(low blood glucose) occurs when the blood glucose falls below the range of 50 to 60 mg/dL. Clinical Manifestations and Assessment hunger diaphoresis, tremor, tachycardia, palpitation, anxiety, Hunger. inability to concentrate, headache, lightheadedness, confusion, memory lapses, numbness of the lips and tongue, slurred speech, impaired coordination, emotional changes, irrational or combative behavior, diplopia (double vision), d drowsiness. disoriented behavior, seizures, difficulty arousing from sleep, loss of consciousness. Medical and Nursing Management Giving Carbohydrates The usual recommendation is that 15 to 20 g of a fast-acting concentrated source of glucose be taken orally. Sources of glucose for the treatment of hypoglycemia include: Three or four commercially prepared glucose tablets 4 to 6 oz of fruit juice or regular soda 6 to 10 hard candies 2 to 3 teaspoons of sugar or honey The blood glucose level should be retested in 15 minutes and retreated with another 15 g of carbohydrate if the patient is still hypoglycemic. If the symptoms persist for longer than 15 minutes after initial treatment, the treatment is repeated even if blood glucose testing is not possible. Once the blood glucose has returned to normal, a snack or meal containing protein and starch (e.g., milk or cheese and crackers) is recommended to prevent recurrent hypoglycemia Initiating Emergency Measures For adult patients experiencing hypoglycemia who are unconscious or unable to swallow safely, an injection of glucagon 1 mg can be administered either subcutaneously or intramuscularly. Glucagon is a hormone produced by the alpha cells of the pancreas that stimulates the liver to convert glycogen to glucose. Because of glycogen's short duration of action, the patient should be given both a concentrated source of carbohydrate followed by a snack once he or she regains consciousness. This will prevent recurrence of hypoglycemia and help replenish the glucose stored in the liver.

MEGALOBLASTIC ANEMIAS

In the anemias caused by deficiencies of either vitamin B12 or folic acid, identical bone marrow and peripheral blood changes occur because both vitamins are essential for normal DNA synthesis. In either anemia, the erythrocytes that are produced are abnormally large and are called megaloblastic red cells; therefore, the MCV is elevated. Other cells derived from the myeloid stem cell (nonlymphoid leukocytes, platelets) are also abnormal, resulting in low leukocyte and platelet counts in advanced stages of disease. A bone marrow analysis reveals hyperplasia (abnormal increase in the number of cells), and the precursor erythroid and myeloid cells are large and bizarre in appearance.

Ketones

(or ketone bodies) are by-products of fat breakdown that accumulate in the blood and urine. Ketones in the urine signal that control of type 1 diabetes is deteriorating and that the risk of DKA is high. When there is little or no effective insulin available, the body starts to break down stored fat for energy. Urine testing is the most common method used for self-testing of ketone bodies by patients. A urine dipstick (Ketostix or Chemstrip uK) is used to detect ketonuria. Other strips are available for measuring both urine glucose and ketones (Keto-Diastix or Chemstrip uGK). Urine ketone testing should be performed whenever patients with type 1 diabetes have glycosuria, persistently elevated blood glucose levels, or are symptomatic for DKA, as well as during illness and pregnancy.

Anemia of chronic disease

(seen in AIDS, malignancy, SLE, chronic kidney disease, chronic liver disease, rheumatoid arthritis) Marked by three defects: Decreased erythrocyte lifespan, ineffective bone marrow response to erythropoietin, altered iron metabolism Normal MCV and MCHC Low serum iron Low or normal TIBC Normal or high ferritin Primary treatment is to treat the underlying cause

Rapid-acting

Lispro (Humalog) Aspart (Novolog) Glulisine (Apidra) 15 minutes 15 minutes 15 minutes 1 h 40-50 minutes 1 hour 3-5 hours 3-5 hours Used for rapid reduction of glucose level, to treat postprandial hyperglycemia, and/or to prevent nocturnal hypoglycemia "Meal-time insulin"

Gestational diabetes mellitus (GDM

) is any degree of glucose intolerance with onset occurring during pregnancy. Hyperglycemia can develop during pregnancy because of the secretion of placental hormones, which causes insulin resistance. It also can develop when the physiologic stress of pregnancy reveals glucose tolerance abnormalities that were not apparent prior to pregnancy. Gestational diabetes occurs in around 9% of pregnant women (DeSisto, 2014). Having hyperglycemia increases the risk for congenital anomalies and other complications during pregnancy Those at high risk should have their blood glucose tested as soon as possible in the first trimester and retested between 24 and 28 weeks of gestation, if initial glucose was normal. Women at low to moderate risk for gestational diabetes should be tested between 24 and 28 weeks of pregnancy (ADA, 2017b). Initial management of gestational diabetes includes diet and exercise changes as well as blood glucose monitoring. If hyperglycemia persists despite lifestyle changes, then medication is prescribed. Goals for blood glucose levels during pregnancy are 95 mg/dL or less before meals, less than or equal to 140 mg/dL 1 hour after meals, and less than or equal to 120 mg/dL 2 hours after meals

Sickle cell disease

Inherited disorder in which abnormal hemoglobin (HbS) polymerizes when deoxygenated, creating a semisolid gel that makes an RBC rigid with a distorted shape (sickle cell) that leads to hemolytic anemia, pain (stasis of RBCs in capillaries) and organ failure Anemia (resulting from chronic hemolysis), reticulocytosis, leukocytosis, and thrombocytosis are common. Elevations of bilirubin and lactate dehydrogenase are also common. Peripheral blood smear may reveal sickle cells Transfusion therapy with PRBCs Monitor ferritin regularly to assess for iron overload Hydroxyurea

Vitamin B12 Deficiency

A deficiency of vitamin B12 can occur in several ways. Inadequate dietary intake is rare but can develop in strict vegans (who consume no meat or dairy products). Faulty absorption from the GI tract is a more common cause. This occurs in conditions such as Crohn disease, or after ileal resection, bariatric gastric bypass surgery, or gastrectomy. Even if adequate vitamin B12 and intrinsic factor are present, a deficiency may occur if disease involving the ileum or pancreas impairs absorption. Another cause is the absence of intrinsic factor, as in pernicious anemia. Intrinsic factor is normally secreted by cells within the gastric mucosa; normally, it binds with the dietary vitamin B12 and travels with it to the ileum, where the vitamin is absorbed. Without intrinsic factor, orally consumed vitamin B12 cannot be absorbed, and eventually erythrocyte production is diminished. Pernicious anemia, which tends to run in families, is primarily a disorder of adults, particularly the elderly. Pernicious anemia is an autoimmune disorder involving autoantibodies to intrinsic factor and parietal cells resulting in poor absorption of B12 (Rojas Hernandez & Oo, 2015). For unknown reasons, patients with pernicious anemia have a higher incidence of gastric cancer, adenocarcinomas, and other cancers compared to the general population (Murphy et al., 2015). Though routine screening for this population has not yet been recommended, these patients should understand their risks and be educated on reporting any new symptoms promptly to health care providers. It is recommended that patients with newly diagnosed pernicious anemia or any patient with pernicious anemia and GI symptoms undergo screening endoscopy (Evans et al., 2015). The body normally has large stores of vitamin B12 so years may pass before the deficiency results in anemia. Because the body compensates so well, the anemia can be severe before the patient becomes symptomatic. Clinical Manifestations and Assessment fatigue, mood changes, memory difficulty, weakness (Lolin, 2014). Mild jaundice may be apparent and is best seen in the sclera without using fluorescent lights. Vitiligo (patchy loss of skin pigmentation) and premature graying of the hair are often seen in patients with pernicious anemia. The tongue is smooth, red, and sore (referred to as glossitis). the neurologic manifestations of vitamin B12 deficiency do not occur with folic acid deficiency, and they persist if vitamin B12 is not replaced. Medical Management Underlying causes for vitamin B12 and folate deficiency should be investigated and treated. Vitamin B12 deficiency is treated by vitamin B12 replacement. Vegetarians can prevent or treat deficiency with oral supplements, vitamins, or fortified soy milk. When the deficiency is due to the more common defect in absorption or the absence of intrinsic factor, replacement by IM injections of vitamin B12 is necessary. The replacement schedule includes daily or every other day administration of 1 mg (1,000 µg) of cyanocobalamin IM for 1 week, followed by weekly administration for 1 to 2 months and then monthly through the remainder of the patient's life

Thalassemias

A group of inherited forms of autoimmune hemolytic anemia Caused by cellular abnormalities of the Hgb structure, marked by an imbalance between the beta chain and alpha chain of Hgb, resulting in RBC membrane damage, ineffective RBC production, and hemolysis Decreased MCV; fragmented RBCs Increased reticulocyte level Transfusion therapy with PRBCs Monitor ferritin regularly to assess for iron overload

Peripheral Neuropathy

Clinical Manifestations and Assessment Initial symptoms of neuropathy may include paresthesias (numbness or tingling) and aching or burning sensations, especially at night. A decrease in proprioception (awareness of posture and movement of the body and of position and weight of objects in relation to the body) and a decreased sensation of light touch may lead to an unsteady gait. Decreased sensations of pain and temperature place patients with neuropathy at increased risk for injury and undetected foot infections. Joint deformities may result from abnormal weight distribution on joints, resulting from lack of proprioception. Sensation can be assessed using a monofilament device On physical examination, there may be a decrease in deep tendon reflexes and vibratory sensation. For patients who have few or no symptoms of neuropathy, these physical findings may be the only indication of neuropathic changes.

Local Allergic Reactions. Systemic Allergic Reactions. Insulin Lipodystrophy. Resistance to Injected Insulin. Fasting Hyperglycemia.

Complications of Insulin Therapy

Folate deficiency

Decreased folic acid intake; impaired absorption; alcohol impairs folate metabolism in the liver, causing a significant depletion in folate reserves Decreases in folate impair DNA synthesis and increase erythroblast cell deaths Decreased folate levels Increased MCV Oral folic acid 1-5 mg/day PO

Folic Acid Deficiency

Folic acid is stored as compounds referred to as folates. The folate stores in the body are much smaller than those of vitamin B12, and they are quickly depleted when the dietary intake of folate is deficient (within 4 months). Folate is found in green leafy vegetables, legumes, egg yolks, fortified foods like cereal, and liver (Lolin, 2014). Folate deficiency occurs in people who rarely eat uncooked vegetables. Alcohol increases folic acid requirements; patients with alcoholism usually have a diet that is deficient in the vitamin. Folic acid requirements are also increased in patients with chronic hemolytic anemias and in women who are pregnant because the need for erythrocyte production is increased in these conditions. Folate is absorbed in the upper small intestine; therefore, some patients with malabsorptive diseases of the small bowel, such as celiac sprue, may not absorb folic acid normally Clinical Manifestations and Assessment fatigue, mood changes, memory difficulty, weakness (Lolin, 2014). Mild jaundice may be apparent and is best seen in the sclera without using fluorescent lights. Vitiligo (patchy loss of skin pigmentation) and premature graying of the hair are often seen in patients with pernicious anemia. The tongue is smooth, red, and sore (referred to as glossitis). the neurologic manifestations of vitamin B12 deficiency do not occur with folic acid deficiency, and they persist if vitamin B12 is not replaced. Medical Management Supplemental oral folic acid should be administered at a dosage of 1 to 5 mg daily until recovery (Lolin, 2014). Patients with malabsorption will need to continue folic acid supplements over the long term. Pregnant patients should take folic acid (0.4 to 0.8 mg daily) when planning for pregnancy as well as throughout the course of pregnancy (Antony, 2016).

Take care of your diabetes: Work with your health care team to keep your blood glucose level within a normal range. Inspect your feet every day: Look at your bare feet every day for cuts, blisters, red spots, and swelling. Use a mirror to check the bottoms of your feet, or ask a family member for help if you have trouble seeing. Check for changes in temperature. Wash your feet every day: Wash your feet in warm, not hot, water. Dry your feet well. Be sure to dry between the toes. Do not soak your feet. Do not check water temperature with your feet; use a thermometer or your elbow. Keep the skin soft and smooth: Rub a thin coat of skin lotion over the tops and bottoms of your feet but not between your toes. Have corns and calluses trimmed by a podiatrist. Inspect toenails. All diabetic individuals should seek a qualified podiatrist for maintenance of feet and nails. Wear shoes and socks at all times: Never walk barefoot. Wear comfortable closed-toe shoes that fit well and protect your feet. Stockings should fit well (without folds, wrinkles, or seams), be comfortable, and be changed daily. Feel inside your shoes before putting them on each time to make sure the lining is smooth and there are no objects inside. Wear sandals in public showers. Protect your feet from hot and cold: Wear shoes at the beach or on hot pavement. Wear socks at night if your feet get cold. Keep the blood flowing to your feet: Put your feet up when sitting. Wiggle your toes and move your ankles up and down for 5 minutes, two or three times a day. Do not cross your legs for long periods of time. Do not smoke. Check with your health care provider: Have your health care provider check your bare feet and find out whether you are likely to have serious foot problems. Remember that you may not feel the pain of an injury. Call your health care provider right away if there is a cut, sore, blister, or bruise on your foot that does not begin to heal after 1 day. Follow your health care provider's advice about foot care. Do not self-medicate or use home remedies or over-the-counter agents to treat foot problems.

Foot Care Tips

Long-acting

Glargine (Lantus, Basaglar) Glargine U-300 (Toujeo) Detemir (Levemir) 2 hours Continuous (no defined onset or peak) 24 hours Used for basal dose

Biguanides.

Metformin, the most commonly used biguanide, produces its antidiabetic effects by decreasing hepatic production of glucose and facilitating the action of insulin on peripheral receptor sites. Biguanides have no effect on pancreatic beta cells. Metformin is contraindicated in patients with kidney impairment and in those at risk for acute kidney dysfunction. Metformin-induced lactic acidosis is a serious complication of biguanide therapy in patients with kidney failure. Metformin should not be administered for 2 days before any diagnostic testing that may require use of a contrast agent, and normal kidney function should be confirmed before the medication is restarted after the procedure.

Intermediate-acting

NPH (Humulin N, Novolin N) 2-4 hours 6-8 hours 12-16 hours Usually taken after food

Autonomic Neuropathies

Neuropathy of the ANS can result in a broad range of dysfunctions affecting many organ systems. Three manifestations of autonomic neuropathy are related to the cardiac, GI, and urogenital systems. Cardiovascular symptoms may range from resting tachycardia, exercise intolerance, and orthostatic hypotension to silent, or painless, myocardial ischemia and infarction. GI symptoms of early satiety, bloating, nausea, vomiting, and constipation or diarrhea may occur as a result of delayed gastric emptying. Decreased gastric motility may result in poor control of blood glucose caused by delayed absorption of glucose from ingested foods, which leads to increased variability in blood glucose levels and increased risk of hypoglycemia. Urinary retention, a decreased sensation of bladder fullness, and other urinary symptoms of neurogenic bladder may result from autonomic neuropathy. The patient with a neurogenic bladder is predisposed to development of urinary tract infections because of the inability to empty the bladder completely. This is especially true of patients with poorly controlled diabetes because hyperglycemia impairs resistance to infection. Sexual dysfunction, especially erectile dysfunction and ejaculatory changes in men, is a complication of diabetes. Impotence occurs with greater frequency in men with diabetes. Some men with autonomic neuropathy have normal erectile function and can experience orgasm but do not ejaculate normally. The effects of autonomic neuropathy on female sexual functioning include reduced vaginal lubrication, decreased libido, and lack of orgasm. Vaginal infection, which is more common in women with diabetes, may be associated with decreased lubrication, itching, and tenderness.

Somogyi Effect

Normal or elevated blood glucose at bedtime, a decrease at 2-3 AM to hypoglycemic levels, and a subsequent increase caused by the production of counterregulatory hormones Decrease evening (predinner or bedtime) dose of intermediate-acting insulin, or increase bedtime snack.

Conventional Insulin Therapy.

One approach to insulin use is to simplify the regimen as much as possible, with the goal of avoiding acute complications of diabetes (hypoglycemia and symptomatic hyperglycemia). Conventional insulin therapy typically involves one injection per day of long-acting insulin, but other insulins, such as short-acting or mixed insulins, can be used depending on the patient's blood glucose pattern.

Gestational diabetes

Onset during pregnancy, usually in the second or third trimester Due to hormones secreted by the placenta, which inhibit the action of insulin Above-normal risk for perinatal complications, especially macrosomia (abnormally large babies) Treated with diet and, if needed, insulin to strictly maintain normal blood glucose levels Occurs in about 2-5% of all pregnancies Glucose intolerance transitory but may recur: In subsequent pregnancies 30-40% will develop overt diabetes (usually type 2) within 10 years (especially if obese) Risk factors include obesity, over 30 years of age, family history of diabetes, previous macrosomia (over 9 lb) All pregnant women between 24 and 28 weeks of gestation should be screened with oral glucose tolerance test

PITUITARY TUMORSPITUITARY TUMORS

Pathophysiology are usually benign, although their location and effects on hormone production by target organs can cause life-threatening effects. Although local symptoms, such as headache and visual changes, may be seen as the tumor causes pressure within the brain, systemic effects are varied depending on the over/undersecretion of particular hormones. Prolactinomas are the most common form of pituitary tumor, causing a hypersecretion of prolactin that may lead to amenorrhea (loss of menstruation), galactorrhea (spontaneous, inappropriate flow of milk from male or female breasts in the absence of pregnancy/breastfeeding), and infertility in females. In males, these tumors can cause hypogonadism, decreased libido, and impotence. Because the disorder is not diagnosed early, generally the tumor is large; therefore, visual complaints from pressure on the optic chiasm (Fig. 31-1) and headaches are common findings. Risk Factors Multiple endocrine neoplasia, type 1 (MEN1), also known as Wermer syndrome, is an autosomal dominant hereditary condition that is strongly associated with developing pituitary tumors (National Cancer Institute, 2015). Clinical Manifestations and Assessment The affected person may be more than 7 ft tall and large in all proportions, but the person may be so weak and lethargic that he or she can hardly stand. If the disorder begins during adult life, the excessive skeletal growth occurs only in the feet, the hands, and the superciliary ridge (bony ridge located above the eye sockets); facial features (nose, lips, ears, and forehead) become broader and larger, the tongue enlarges, the space between the teeth increases, and the lower jaw grows, resulting in an underbite and extended lower jaw severe headaches and visual disturbance loss of color discrimination, diplopia (double vision), temporal hemianopia (loss of vision of one half of the visual field). These tumors promote protein synthesis, which stimulates the growth of all organs; liver gluconeogenesis, causing hyperglycemia; decalcification of the skeleton; muscular weakness; endocrine disturbances. Skeletal changes that occur with acromegaly are not reversible, whereas soft tissue changes may be. . Because the pituitary gland releases growth hormone, thyroid-releasing hormone (TRH), ACTH, luteinizing hormone, follicle-stimulating hormone, and prolactin, signs and symptoms vary depending on the specific hormones that are deficient but may include weight loss; somnolence; fine, scant hair; dry, soft skin; a pasty complexion; short stature; and small bones. Patients also experience headaches, loss of libido, and visual defects progressing to blindness. Other signs and symptoms include polyuria, polyphagia, a lowering of the basal metabolic rate, and a subnormal body temperature.

THYROID TUMOR AND CANCER

Pathophysiology The most common type of goiter, a simple or colloid goiter, often is encountered in geographic regions where there is lack of iodine (e.g., the Great Lakes areas of the United States). If too little iodine exists, the level of T4 will decrease, causing the stimulation of TSH from the anterior pituitary. This stimulation causes the enlargement of the thyroid. Simple goiter also may be caused by an intake of large quantities of goitrogenic substances in patients with unusually susceptible glands. These substances include excessive amounts of iodine or lithium, often used in the treatment of bipolar disorders. Too much iodine can cause enlargement of the thyroid, resulting in the development of excess secretion of thyroid hormone. Keep in mind that many patients receive IV iodine in the hospital as a result of diagnostic studies that require contrast, such as cardiac catheterization and CT scans. Simple goiter represents a compensatory hypertrophy of the thyroid gland, caused by stimulation by the pituitary gland. Such goiters usually cause no symptoms, except for the swelling in the neck, which may result in tracheal compression when excessive. Many goiters of this type recede after the iodine imbalance is corrected. Supplementary iodine, such as SSKI, is prescribed to suppress the pituitary's thyroid-stimulating activity. Some thyroid glands are nodular because of areas of hyperplasia (overgrowth). No symptoms may arise unless these nodules increase in size and descend into the thorax, where symptoms of local pressure may manifest. Some nodules become malignant, and some are associated with a hyperthyroid state. The patient with many thyroid nodules eventually may require surgery. Clinical Manifestations and Assessment pressure in the neck. On assessment, the patient may present with a soft, diffusely enlarged nodule over the neck. As the goiter progresses, the patient may experience symptoms, such as difficulty breathing and swallowing. Patients usually present in euthyroid state with normal levels of TSH and T4. lesions that are single, hard, and fixed on palpation or associated with cervical lymphadenopathy suggest malignancy. Fine-needle biopsy (FNB) of the thyroid gland often is used to establish the diagnosis of thyroid cancer. The purpose of the biopsy is to differentiate cancerous thyroid nodules from noncancerous nodules and to stage the cancer if detected. The procedure is safe and usually requires only a local anesthetic. Another type of aspiration or biopsy uses a large-bore needle rather than the fine needle. This method often is used to detect rapid-growing tumors or when the results of the FNB are inconclusive. Other diagnostic studies include ultrasound, MRI, CT, thyroid scans, radioactive iodine uptake studies, and thyroid suppression tests. Medical Management Most patients with small, simple goiters and euthyroid states do not require treatment. Patients with large goiters generally receive exogenous thyroid hormones and iodine to reduce thyroid growth. Surgery is not required unless the goiter continues to grow (1) despite pharmacologic treatment, (2) causing airway difficulties, and (3) leading to suspected malignancy. Surgical removal, however, is the treatment of choice for thyroid cancers. Total or near-total thyroidectomy is performed if possible.

DKA

Patients most commonly affected Can occur in type 1 or type 2 diabetes; more common in type 1 diabetes Precipitating event Omission of insulin; physiologic stress (infection, surgery, stroke, MI) Onset Rapid (less than 24 hours) Blood glucose levels Usually over 250 mg/dL (over 13.9 mmol/L) Arterial pH level Below 7.3 Serum and urine ketones Present Serum osmolality 300-350 mOsm/L Plasma bicarbonate level Less than 15 mEq/L BUN and creatinine levels Elevated Mortality rate Less than 5%

Thiazolidinediones (TZDs).

Pioglitazone (Actos) is an oral antidiabetic medication categorized as a thiazolidinedione (TZD). This class of medication enhances insulin action at receptor sites without increasing insulin secretion from the beta cells of the pancreas. These medications can be used alone or in combination with other antidiabetic agents. These medications may impair liver function and also may increase the risk of myocardial infarction and congestive heart failure. Liver function studies must be performed at baseline and at frequent intervals throughout treatment.

Prediabetes

Potential abnormality of glucose tolerance (PotAGT) No history of glucose intolerance Increased risk of diabetes if: Positive family history Obesity Mother of babies over 9 lb at birth Member of certain Native American tribes (e.g., Pima) with high prevalence of diabetes Screening and weight advice as in PrevAGT

Prediabetes

Previous abnormality of glucose tolerance (PrevAGT) Current normal glucose metabolism Previous history of hyperglycemia (e.g., during pregnancy or illness) Periodic blood glucose screening after age 40 if there is a family history of diabetes or if symptomatic Encourage ideal body weight, because loss of 10-15 lb may improve glycemic control

Insulin Waning

Progressive rise in blood glucose from bedtime to morning Increase evening (predinner or bedtime) dose of intermediate- or long-acting insulin, or institute a dose of insulin before the evening meal if one is not already part of the treatment regimen.

Short-acting

Regular (Humulin-R, Novolin-R) ½-1 hour 2-3 hours 4-6 hours Usually administered 20-30 minutes before a meal; may be taken alone or in combination with longer-acting insulin

Dawn Phenomenon

Relatively normal blood glucose until about 3 AM, when the level begins to rise Change time of injection of evening intermediate-acting insulin from dinnertime to bedtime.

Nonsulfonylurea Insulin Secretagogues.

Repaglinide (Prandin) and naglitinide (Starlix) act similarly to sulfonylureas but have a different chemical structure. Both lower the blood glucose level by stimulating insulin release from the pancreatic beta cells. These drugs have a very rapid onset and a short duration and must be taken with meals; they should not be taken if a meal is skipped.

Family history of diabetes (i.e., parents or siblings with diabetes) Obesity (i.e., BMI at least 25 kg/m2) Ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islanders) Age 45 years of age or older Previously identified impaired glucose tolerance or impaired fasting glucose Hypertension (at least 140/90 mm Hg) HDL cholesterol level at least 35 mg/dL (0.90 mmol/L) and/or triglyceride level at least 250 mg/dL (2.82 mmol/L) History of gestational diabetes or delivery of babies over 9 lb

Risk Factors for Diabetes Mellitus

Clinical Manifestations and Assessment polyuria, polydipsia, Polyphagia. dehydration, weight loss, fatigue and weakness, vision changes (the accumulation of glucose on the lens causes refractive error but resolves with glucose control, tingling or numbness in the hands or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections. . There are three ways to diagnose diabetes: fasting plasma glucose (FPG) levels of 126 mg/dL a random plasma glucose level exceeding 200 mg/dL in a patient with classic symptoms of hyperglycemia, A1c level of 6.5% or higher Criteria for the Diagnosis of Diabetes Mellitus A1c of 6.5% or greater or Symptoms of diabetes plus casual plasma glucose concentration equal to or greater than 200 mg/dL (11.1 mmol/L). "Casual" is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss. or Fasting plasma glucose greater than or equal to 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hours. or Two-hour postload glucose equal to or greater than 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

SIGNS AND SYMPTOMS/ DIAGNOSIS OF DIABETES

Diabetes mellitus associated with other conditions or syndromes

Secondary diabetes Accompanied by conditions known or suspected to cause the disease: pancreatic diseases, hormonal abnormalities, medications such as corticosteroids and estrogen-containing preparations Depending on the ability of the pancreas to produce insulin, the patient may require treatment with insulin

All insulin, including spare pens and vials not in use, should be refrigerated. Extremes of temperature should be avoided; insulin should not be allowed to freeze and should not be kept in direct sunlight or in high temperatures. The insulin pen or vial in use should be kept at room temperature to reduce local irritation at the injection site, which may occur if cold insulin is injected. Typically, insulin can be kept at room temperature for 1 month, but the patient should consult the package insert for individual instructions for each type of insulin. Vials of intermediate-acting insulin also should be inspected for flocculation, which is a frosted, whitish coating inside the bottle. If a frosted, adherent coating is present, some of the insulin is bound and should not be used. Pens or vials of insulin that have been open for more than 1 month or those that have passed the expiration date also should be discarded.

Storing Insulin.

1-mL syringes that hold 100 units 0.5-mL syringes that hold 50 units 0.3-mL syringes that hold 30 units Insulin syringes are disposable and have a 31-gauge needle that is 6 mm, 8 mm, or 12.7 mm long. The smaller syringes are marked in 1-unit increments and may make it easier for patients with visual deficits and those taking very small doses of insulin to get a dose that is more accurate. The 1-mL syringes are marked in 1- and 2-unit increments. Preparing the Injection: Mixing Insulins. Regular and NPH insulins can be mixed together in the same syringe. Regular insulin must be inspected for clarity and not used unless it is crystal clear. NPH will be cloudy and should be mixed carefully by rolling the vial gently. The regular insulin is drawn into the syringe first, followed by the NPH. Injecting cloudy insulin into a vial of clear insulin contaminates the entire vial of clear insulin and alters its action. Selecting Insulin Pen Needles. Sizes range from 4 mm/32-gauge to 12.7 mm/29-gauge. For most patients, the smaller needles will allow for equivalent glucose control but less pain on injection compared to the larger needles (Bergenstal et al., 2015).

Syringes must be matched with the insulin concentration (e.g., U-100). Currently, three sizes of U-100 insulin syringes are available:

Anemia,

a condition in which the hemoglobin concentration is lower than normal, reflects the presence of fewer than normal erythrocytes (red blood cells; RBCs) within the circulation. As a result, the amount of oxygen delivered to body tissues is also diminished. Classification of Anemias Morphologic classification includes the cell size, color, Shape. Changes in the size of the RBC are described as normocytic (normal or average size), macrocytic (larger than normal), microcytic (smaller than normal). normochromic (normal in color), hyperchromic (darker cellular contents), hypochromic (pale or lighter cellular contents)

ANEMIA IN KIDNEY DISEASE

The degree of anemia in patients with end-stage kidney disease (ESKD) varies greatly, but in general patients do not become significantly anemic until the serum creatinine level exceeds 3 mg/dL. Pathophysiology This anemia is caused by both a mild shortening of erythrocyte lifespan and a deficiency of erythropoietin (necessary for erythropoiesis). As kidney function decreases, erythropoietin, which is produced by the kidney, also decreases. Because erythropoietin is also produced outside the kidney, some erythropoiesis continues, even in patients whose kidneys have been removed. However, the number of RBCs produced is small and the degree of erythropoiesis is inadequate. Patients undergoing long-term hemodialysis lose blood into the dialyzer and, therefore, may become iron deficient. Folic acid deficiency develops because this vitamin passes into the dialysate. Therefore, patients who receive hemodialysis and who have anemia should be evaluated for iron and folate deficiency and treated appropriately. Clinical Manifestations and Assessment fatigue and decreased activity tolerance, are often the most disturbing. If untreated, the hematocrit may fall to between 20% and 30%, although in rare cases it may fall to less than 15%. The erythrocytes appear normal in shape, size, and color on the peripheral smear. Medical and Nursing Management The availability of recombinant erythropoietin (also referred to as erythropoiesis stimulating agents or ESAs) (epoetin alfa [Epogen, Procrit]; darbepoetin alfa [Aranesp]) has dramatically altered the management of anemia in ESKD by decreasing the need for RBC transfusion, with its associated risks. Erythropoietin, in combination with oral iron supplements, can raise and maintain hematocrit levels to between 33% and 38%.

IRON DEFICIENCY ANEMIA

The development of iron deficiency anemia occurs when the body's iron stores are depleted and there is no iron available for hemoglobin synthesis. The volume of individual iron stores is dependent upon sex, age, rate of growth, and the balance between dietary iron absorption and losses. Iron is stored primarily in the liver, spleen, and bone marrow. The remainder of iron exists as hemoglobin and proteins. Iron deficiency anemia is diagnosed based on the presence of a microcytic anemia, transferrin saturation below 20%, and ferritin below 30 ng/mL The most common cause of iron deficiency anemia in men and postmenopausal women is bleeding (from ulcers, gastritis, inflammatory bowel disease, or GI tumors). The most common cause of iron deficiency anemia in premenopausal women is menorrhagia (excessive menstrual bleeding) and pregnancy with inadequate iron supplementation. Patients with chronic alcoholism often have chronic blood loss from the GI tract, which causes iron loss and eventual anemia. Other causes include iron malabsorption, as is seen after gastrectomy or with celiac disease. Medical Management DIAGNOSTICS Stool specimens should be tested for occult blood and H. pylori infection. Blood samples should be sent for celiac serology and antiparietal cell antibodies (to rule out pernicious anemia). In the presence of iron deficiency, patients over 50 years of age, those with a family history of GI disorders, those with GI symptoms, men with Hgb below 13 g/dL or women with Hgb below 10 g/dL should undergo endoscopy and colonoscopy to rule out GI blood loss TREATMENT Iron preparations—ferrous sulfate, ferrous succinate, ferrous gluconate, and ferrous fumarate—are available for treating iron deficiency anemia. Ferrous sulfate, fumarate, and gluconate each contain 50 to 65 mg of elemental iron per tablet with recommended dosing of one tab three times/day Despite the development of a number of orally effective iron-containing compounds, the original salt, ferrous sulfate (325 mg three times daily), remains the most useful. Food can decrease iron absorption by as much as 50% although vitamin C facilitates the absorption of iron. Therefore, oral iron should be taken with a glass of orange juice or a vitamin C tablet on an empty stomach to maximize absorption.

hypoglycemia, DKA, HHNS, also called hyperglycemic hyperosmolar syndrome (HHS).

The three major acute complications of diabetes are caused by short-term imbalances in blood glucose levels. They are

Type 2 Diabetes

The two main problems related to insulin in type 2 diabetes are insulin resistance and impaired insulin secretion. Insulin resistance refers to decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism. In type 2 diabetes, these intracellular reactions are diminished, making insulin less effective in stimulating glucose uptake by the cells and at regulating glucose release by the liver (Fig. 30-1). The exact mechanisms that lead to insulin resistance and impaired insulin secretion in type 2 diabetes are unknown, although increasing age, obesity, and lack of physical exercise as well as genetic factors are thought to play a role (ADA, 2017b). To overcome insulin resistance and prevent the buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose level. However, if the beta cells cannot keep up with the increased demand for insulin, the glucose level rises, and type 2 diabetes develops. If the patient experiences symptoms, they are frequently mild and may include fatigue, irritability, increased urination, increased thirst, poor wound healing, frequent infections, or changes in vision. Many patients with type 2 diabetes are diagnosed as a result of routine laboratory tests or during ophthalmoscopic examinations. One consequence of undetected diabetes is that long-term microvascular (diabetic retinopathy, neuropathy, and nephropathy) and macrovascular complications (peripheral vascular, coronary disease, and stroke) may have developed before the actual diagnosis of diabetes is made (

Pernicious, megaloblastic

Vitamin B12 deficiency; lack of intrinsic factor required for B12 absorption Decreased vitamin B12 level; increased MCV Elevated methylmalonic acid and homocysteine levels Low reticulocyte count B12 replacement Cyanocobalamin 1,000 μg IM monthly

Sodium glucose co-transporter-2 (SGLT-2) inhibitors

are oral medications that work primarily by inhibiting reabsorption of glucose in the proximal renal tubules, which promotes loss of glucose through the urine, thereby reducing blood glucose levels. Weight loss and improved blood pressure also are seen with these medications. Common side effects include increased urinary frequency and genital mycotic infections, and some patients have developed DKA while taking the medication.

Primary aldosteronism,

also known as Conn syndrome, is a condition in which the adrenal cortex produces too much aldosterone because of hyperplasia or tumor. The principal action of aldosterone is to conserve body sodium, thus excessive aldosterone will result in increased renal reabsorption of sodium and an increase in extracellular fluids and blood pressure. Clinical Manifestations and Assessment Patients with hyperaldosteronism exhibit a profound decline in the serum levels of potassium (hypokalemia) and hydrogen ions (alkalosis, leading to tetany) as demonstrated by an increase in pH and serum bicarbonate concentration. The serum sodium level is normal or typically elevated depending on the amount of water reabsorbed with the sodium or water loss in the urine. Hypertension is the most prominent and almost universal sign of aldosteronism and accounts for 10% of cases of hypertension (Piaditis, Markou, Papanastasiou, Androulakis, & Kaltsas, 2015). Hypokalemia leads to muscle weakness, cramping, and fatigue as well as an inability on the part of the kidneys to acidify or concentrate the urine, leading to polyuria. Serum sodium becomes abnormally concentrated, contributing to excessive thirst (polydipsia) and arterial hypertension. A secondary increase in blood volume and possible direct effects of aldosterone on nerve receptors, such as the carotid sinus, result in hypertension. Hypokalemic alkalosis may decrease the level of ionized serum calcium and predispose the patient to tetany and paresthesia. Glucose intolerance may occur because hypokalemia interferes with insulin secretion from the pancreas. In addition to a high or normal serum sodium level and a low serum potassium level, diagnostic studies indicate high serum aldosterone and low serum renin levels. The measurement of the aldosterone excretion rate after salt loading is a useful diagnostic test for hyperaldosteronism. The renin-aldosterone stimulation test and bilateral adrenal venous sampling are useful in differentiating the cause of primary aldosteronism. Antihypertensive medication may be discontinued up to 2 weeks before testing. Medical Management Treatment of primary aldosteronism usually involves surgical removal of the adrenal tumor through adrenalectomy. Adrenalectomy is performed through an incision in the flank or the abdomen using laparoscopic techniques. In general, postoperative care resembles that for other abdominal surgeries. The patient is susceptible to fluctuations in adrenocortical hormones and requires administration of corticosteroids, fluids, and other agents to maintain blood pressure and prevent acute complications. If the adrenalectomy is bilateral, lifetime replacement of corticosteroids will be necessary. If one adrenal gland is removed, the replacement therapy may be only temporary because of the suppression of the remaining adrenal gland by high levels of adrenal hormones. A normal level of serum glucose is maintained with insulin, IV fluids, and dietary modifications. Hypokalemia resolves for all patients after surgery, but hypertension may persist. Spironolactone (potassium-sparing diuretic) and Eplerenone may be prescribed to control hypertension and minimize hypokalemia.

GLP-1 agonists

are a class of medications that work to increase insulin secretion, delay gastric emptying, promote satiety, and suppress glucagon secretion. All GLP-1 medications are injected once daily or once weekly depending on the preparation. Whereas most other non-insulin antidiabetic agents are weight neutral or cause weight gain, GLP-1 agonists promote weight loss. They also are glucose dependent and generally do not cause hypoglycemia unless combined with other medications or insulin. Usually side effects are mild but can include

The thalassemias

are a group of hereditary anemias characterized by hypochromia (an abnormal decrease in the hemoglobin content of erythrocytes), extreme microcytosis (smaller-than-normal erythrocytes), destruction of blood elements (hemolysis), and variable degrees of anemia due to impaired hemoglobin production and ineffective RBC production (Tubman et al., 2015). The thalassemias occur worldwide, but the highest prevalence is found in people of Mediterranean, African, and Southeast Asian ancestry. Thalassemias are classified into two major groups according to which hemoglobin chain is diminished: alpha or beta. The alpha thalassemias occur mainly in people from Asia and the Middle East, and the beta thalassemias are most prevalent in people from Mediterranean regions but also occur in those from the Middle East or Asia. The alpha thalassemias are milder than the beta forms and often occur without symptoms; the erythrocytes are extremely microcytic, but the anemia, if present, is mild. The severity of beta thalassemia varies depending on the extent to which the hemoglobin chains are affected. Patients with mild forms have a microcytosis and mild anemia. If left untreated, severe beta thalassemia (thalassemia major, or Cooley anemia) can be fatal within the first few years of life. Peripheral blood stem cell transplant (PBSCT) offers a chance of cure, but when this is not possible, the disease is usually treated with transfusion of PRBCs. Complications related to lifelong transfusions include the development of anti-RBC antibodies, transfusion-associated infections, and iron overload. Transfusional iron overload is the primary cause of death in patients with thalassemia (90% of deaths). In the 1980s, life expectancy was not expected to exceed the third decade of life. Treatment of iron overload involves the use of chelating agents. Deferoxamine (given IV or SQ), deferasirox (oral), and deferiprone (oral) are used alone or in combination to treat iron overload.

Jet injection devices

deliver insulin through the skin under pressure in an extremely fine stream. These devices are more expensive than other methods of insulin administration and require thorough training and supervision when first used. In addition, patients should be cautioned that absorption rates, peak insulin activity, and insulin levels may be different when using a jet injector.

Myxedema coma

describes the most extreme, severe stage of hypothyroidism, in which the patient is hypothermic and unconscious. Increasing lethargy may progress to stupor and then to coma. Myxedema leads to the accumulation of mucopolysaccharides in subcutaneous and other interstitial tissues; this causes nonpitting edema and doughy skin. The fluid accumulation causes a characteristic puffy appearance to the face and eyes (periorbital edema). The patient's tongue can be enlarged, and his or her voice becomes hoarse and husky. Sometimes myxedematous fluid can cause pericardial and pleural effusions (Porth, 2015). Myxedema coma may also develop with undiagnosed hypothyroidism and may be precipitated by infection, systemic disease, or the use of sedatives or opioid analgesic agents. The patient's respiratory drive is depressed, resulting in alveolar hypoventilation, progressive carbon dioxide retention, narcosis, and coma.

The sulfonylureas

exert their primary action by stimulating the pancreas directly to secrete insulin. Therefore, a functioning pancreas is necessary for these agents to be effective, and they are not indicated in patients with type 1 diabetes. Sulfonylureas improve insulin action at the cellular level and also may directly decrease glucose production by the liver. The most common side effect of sulfonylureas is hypoglycemia. Second-generation sulfonylureas (glipizide, glyburide, glimepiride) have fewer side effects and drug interactions than do first-generation sulfonylureas since they are excreted by both the liver and the kidneys, thus making them safer to use in the elderly. However, if renal or hepatic insufficiency is suspected, patients must be monitored for hypoglycemia. Because the second-generation drugs are a safer option, first-generation sulfonylureas are seldom used today.

ARREST DISORDERS

include secondary arrest of dilation (no progress in cervical dilation in over 2 hours), arrest of descent (fetal head does not descend for more than 1 hour in primiparas and more than 30 minutes in multiparas), and failure of descent (no descent). About 20% of labors involve either protracted or arrest disorders (Ehsanipoor & Satin, 2020).

Continuous subcutaneous insulin infusion (CSII), or insulin pump therapy,

involves the use of small devices worn externally that more closely mimic the functioning of the normal pancreas. Insulin pumps contain a special syringe, called a reservoir, and are connected to a subcutaneous needle by a thin, narrow-lumen tube with a needle or Teflon catheter attached to the end. The patient inserts the needle or catheter into subcutaneous tissue, usually on the abdomen, and secures it with tape or a transparent dressing. The needle or catheter is changed and the reservoir is refilled at least every 2 to 3 days. Figure 30-5 illustrates CSII equipment. In order to more closely approximate the action of a pancreas that is functioning normally, the insulin pump is programmed to deliver rapid-acting insulin in both a basal and bolus manner. The basal rate is infused continuously over 24 hours, though the rate itself can be tailored to the patient's specific needs at specific times of day. For instance, the basal rate is set at a higher rate overnight if the patient has a history of dawn phenomenon (abnormal early-morning increase in blood sugar—usually between 3 and 8 AM) or abnormal nocturnal rise in blood glucose due to release of hormones. Boluses at meals can be calculated by the pump after the patient inputs the blood glucose at the time of the bolus and the amount of carbohydrate that he or she intends to consume. Because the pump is infusing rapid-acting insulin, the patient has increased control over delivery of the insulin and, therefore, has more flexibility regarding meal times, food choices, and exercise timing. The pump can easily be disconnected for limited periods for showering, exercise, or sexual activity. In general, only rapid-acting insulins, such as lispro, aspart, and glulisine, are used in the insulin pump. In rare cases, Humulin R U-500 insulin may be used for patients who have extreme insulin resistance. One disadvantage of insulin pumps is that unexpected disruptions in the flow of insulin from the pump may happen if the tubing or needle becomes occluded, if the supply of insulin runs out, or if the battery is depleted. These occurrences increase the risk of DKA. Another disadvantage is the potential for infection at the sites of needle insertion.

Diabetes insipidus

is a disorder of the posterior lobe of the pituitary gland that is characterized by a deficiency of ADH, also known as vasopressin. In general, this disorder is characterized by excessive thirst (polydipsia) and large volumes of dilute urine. It is helpful to remember the three D's: Diabetes insipidus, Decreased ADH, and Diuresis. There are three types of diabetes insipidus: neurogenic, nephrogenic, and psychogenic polydipsia. Pathophysiology Neurogenic diabetes insipidus is characterized by an acute onset resulting from the destruction of the posterior pituitary gland, resulting in a lack of vasopressin. Nephrogenic diabetes insipidus generally results from drug-related damage to the renal tubules, resulting in the inability to conserve water. Psychogenic diabetes insipidus is caused by excessive water intake. Clinical Manifestations and Assessment Without the action of ADH on the distal nephron of the kidney, a patient with ADH likely will have an enormous daily output of very dilute urine (3 to 20 L) with nocturia, frequency, and a specific gravity of 1.001 to 1.005 occurs. Signs and symptoms of fluid volume deficit that occur as patients are unable to compensate for the massive urinary loss include: Weight loss Poor skin turgor Dry mucous membranes Increased heart rate Hypotension To diagnose diabetes insipidus, an accurate 24-hour urine collection is obtained to measure for volume and creatinine. A urine volume of less than 2 L/24 hours (without hypernatremia) rules out diabetes insipidus. A fluid deprivation test may be considered, but it is contraindicated if the patient's serum sodium is elevated. This test involves withholding fluids for 8 to 12 hours or until 3% to 5% of the body weight is lost, and plasma and urine osmolality studies are performed at the beginning and end of the test. Diabetes insipidus is likely if the patient continues to excrete large volumes of urine with low specific gravity and osmolality or experiences weight loss, increasing serum osmolality, and elevated levels of serum sodium. During the deprivation test, ADH or vasopressin can be given subcutaneously as described previously. However, the patient's condition needs to be monitored frequently due to the risk of severe dehydration. The test will be terminated if the patient develops tachycardia, excessive weight loss, or hypotension.

Thyroid storm (thyrotoxic crisis)

is a form of severe hyperthyroidism, usually of abrupt onset. It is fatal if left untreated, but with proper treatment, the mortality rate is reduced substantially. The patient with thyroid storm or crisis is critically ill and requires astute observation and aggressive and supportive nursing care during and after the acute stage of illness. Usually life-threatening thyroid storm is precipitated by stress, such as injury, infection, thyroid and nonthyroidal surgery, tooth extraction, insulin reaction, diabetic ketoacidosis, pregnancy, digitalis intoxication, abrupt withdrawal of antithyroid medications, extreme emotional stress, or vigorous palpation of the thyroid. These factors can precipitate thyroid storm in a patient whose hyperthyroidism is partially controlled or completely untreated. Current methods of diagnosis and treatment for hyperthyroidism have greatly decreased the incidence of thyroid storm, making it uncommon today. Clinical Manifestations Thyroid storm is characterized by: High fever (hyperpyrexia) above 38.5°C (101.3°F) Extreme tachycardia (more than 130 bpm) Exaggerated symptoms of hyperthyroidism with disturbances of a major system—e.g., GI (weight loss, diarrhea, abdominal pain) or cardiovascular (edema, chest pain, dyspnea, palpitations) Altered neurologic or mental state, which frequently appears as delirium, psychosis, somnolence, or coma Management Immediate objectives are reduction of body temperature and heart rate and prevention of vascular collapse. Measures to accomplish these objectives include: A hypothermia mattress or blanket, ice packs, a cool environment, hydrocortisone, and acetaminophen (Tylenol). Salicylates (e.g., aspirin) are not used because they displace thyroid hormone from binding proteins and worsen the hypermetabolism. Humidified oxygen is administered to improve tissue oxygenation and meet the high metabolic demands. ABG levels or pulse oximetry may be used to monitor respiratory status. IV fluids containing dextrose are administered to replace liver glycogen stores that have been decreased in the hyperthyroid patient. PTU or methimazole is administered to impede formation of thyroid hormone and block conversion of T4 to T3, the more active form of thyroid hormone. Hydrocortisone is prescribed to treat shock or adrenal insufficiency. Iodine is administered to decrease output of T4 from the thyroid gland. For cardiac problems, such as atrial fibrillation, arrhythmias, and heart failure, sympatholytic agents may be administered. Propranolol, combined with digitalis, has been effective in reducing severe cardiac symptoms.

A continuous glucose monitoring system (CGMS)

uses technology capable of monitoring blood glucose continuously. A sensor capable of measuring glucose in the interstitial fluid is inserted subcutaneously, and the information is transmitted to a receiver or blue-tooth enabled device. The glucose is measured approximately every 3 to 5 minutes, providing real-time information regarding glucose level and rate of change in either direction. Information from the CGMS is especially useful for patients using insulin pumps and intensive insulin regimens in that it can warn the patient of hypoglycemia and hyperglycemia, as well as provide information regarding patterns of diabetes control over specific periods of time

Insulin

is a hormone produced by the pancreas that controls blood glucose levels by regulating the production, use, and storage of glucose. It is secreted by beta cells, in the islets of Langerhans of the pancreas. In patients with diabetes, cells may respond inadequately to insulin or the pancreas may decrease insulin secretion or stop insulin production completely. Insulin is an anabolic, or storage hormone. When a person eats a meal, insulin secretion increases and moves glucose from the blood into muscle, liver, and fat cells. Once inside the cells, insulin functions in the following ways: Transports and metabolizes glucose for energy Stimulates storage of glucose as glycogen in the liver and muscle cells Signals liver cells to stop the release of glucose Enhances storage of dietary fat in adipose tissue Accelerates transport of amino acids into cells Facilitates the transport of potassium into the cells Inhibits the breakdown of stored glucose, protein, and fat

anemia of chronic disease"

is a misnomer in that only the chronic diseases of inflammation, infection, and malignancy cause this type of anemia. Many chronic inflammatory diseases are associated with a normochromic, normocytic anemia (i.e., the erythrocytes are normal in color and size). These disorders include rheumatoid arthritis; severe, chronic infections; and many cancers. It is, therefore, imperative that the "chronic disease" be diagnosed when this form of anemia is identified so that it can be managed appropriately. The anemia is usually mild to moderate and nonprogressive. It develops gradually over 6 to 8 weeks and then stabilizes at a hematocrit seldom less than 25%. The hemoglobin level rarely falls below 9 g/dL, and the bone marrow has normal cellularity with increased stores of iron as the iron is diverted from the serum. Most of these patients have few symptoms and do not require treatment for the anemia. With successful treatment of the underlying disorder, the bone marrow iron is used to make erythrocytes and the hemoglobin level rises.

HHNS

is a serious life-threatening condition characterized by hyperosmolality (at least 340 mOsm/L) and hyperglycemia (at least 600 mg/dL) with alterations in level of consciousness. Ketosis is minimal or absent. Persistent hyperglycemia causes osmotic diuresis, which results in losses of water and electrolytes. The higher the serum glucose, the more profound the dehydration, and the greater the risk for renal impairment and mental status changes. Table 30-7 compares DKA and HHNS. Pathophysiology HHNS occurs most often in older people between 50 and 70 years of age who have no known history of diabetes or who have type 2 diabetes. HHNS often can be traced to a precipitating event, such as infection, acute or chronic illness (e.g., pneumonia, stroke), medications that exacerbate hyperglycemia, or therapeutic procedures, such as surgery or dialysis. The history may include days to weeks of polyuria and polydipsia. What distinguishes HHNS from DKA is that ketosis and acidosis generally do not occur in HHNS, partly because of differences in insulin levels. In DKA, no insulin is present, and this promotes the breakdown of stored glucose, protein, and fat, which leads to the production of ketone bodies and ketoacidosis. In HHNS, the insulin level is too low to prevent hyperglycemia and subsequent osmotic diuresis, but it is high enough to prevent fat breakdown. Clinical Manifestations and Assessment hypotension, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, variable neurologic signs (e.g., alteration of sensorium, seizures, hemiparesis). Diagnostic assessment reveals very high blood glucose, usually 600 to 1,200 mg/dL, high serum osmolality, often exceeding 350 mOsm/kg. Levels of electrolytes and blood urea nitrogen (BUN) are consistent with the clinical picture of profound dehydration. Mental status changes and neurologic deficits are common secondary to cerebral dehydration that results from extreme hyperosmolality. Postural hypotension results from the dehydration. Medical Management The overall approach to the treatment of HHNS is similar to that of DKA: replacement of fluids, correction of electrolyte imbalances, and administration of insulin s. Fluid treatment is started with 0.9% or 0.45% NS, depending on the patient's sodium level and the severity of volume depletion. Fluid replacement is guided by central venous or hemodynamic pressure monitoring. Potassium is added to IV fluids when urinary output is adequate and is guided by continuous ECG monitoring and frequent laboratory determinations of potassium. yperglycemia. As in DKA, replacement IV fluids with dextrose are administered after the glucose level has decreased to the range of 250 to 300 mg/dL

SIADH

is a syndrome characterized by excessive secretion of ADH, causing significant retention of water. As a result, the sodium level becomes dilute, and hyponatremia ensues. It is the most frequently cited cause of euvolemic hyponatremia. In patients hospitalized with hyponatremia, over 50% of cases can be attributed to SIADH (Ferri, 2016a). Table 31-3 details the characteristics of DI versus SIADH. TABLE 31-3 Differentiating Features of DI versus SIADH Pathophysiology SIADH is a disorder of impaired water excretion caused by the inability to stop the secretion of ADH. As a result, excessive ADH can be secreted from the pituitary gland directly into the bloodstream, or by abnormal synthesis and secretion of vasopressin by tumors. Patients with this disorder cannot excrete diluted urine. They retain water and develop a subsequent sodium deficiency known as dilutional hyponatremia. With too much H2O in the bloodstream, the kidneys cannot excrete dilute urine, and the water moves from the extracellular compartment to the intracellular region, causing brain cells to swell. This has a significant impact on the CNS (brain and spinal cord) because of brain edema and increased ICP. If the sodium level becomes low enough (approximately 115 mEq/L), seizures may occur. Clinical Manifestations and Assessment The clinical manifestations of SIADH include the following: Hyponatremia (sodium below 134 mEq/L), Decreased serum osmolality (less than 280 mOsm/kg) with inappropriately increased urine osmolality (greater than 100 mOsm/kg—reveals impaired ability of the kidneys to dilute the urine), Urine sodium over 20 mEq/L, Low blood urea nitrogen (BUN) (below 10 mg/dL), and Hypouricemia (uric acid below 4 mg/dL) (Cho, 2015).

Addisonian crisis

is an acute life-threatening event that develops with disease progression. Acute hypotension is characterized by cyanosis and the classic signs of circulatory shock: pallor, apprehension, rapid and weak pulse, rapid respirations, and low blood pressure. In addition, the patient may complain of headache, nausea, abdominal pain, and diarrhea and may show signs of confusion and restlessness. Even slight overexertion, exposure to cold, acute infection, or a decrease in salt intake may lead to circulatory collapse, shock, and death if untreated. The stress of surgery or dehydration resulting from preparation for diagnostic tests may precipitate an addisonian or hypotensive crisis. Medical Management Immediate treatment is directed toward combating circulatory shock: restoring blood circulation, administering fluids and corticosteroids, monitoring vital signs, and placing the patient in a recumbent position with the legs elevated. Corticosteroid use is discussed in Box 31-12 and Table 31-8. Hydrocortisone (Solu-Cortef) is administered intravenously, followed by 5% dextrose in normal saline. Oral hydrocortisone replacement is resumed once intravenous infusion is discontinued. Vasopressor amines may be required if hypotension persists. Broad-spectrum antibiotics may be administered if infection has precipitated adrenal crisis in a patient with chronic adrenal insufficiency. In addition, the patient is assessed closely to identify other factors, stressors, or illnesses that led to the acute episode. Monitoring and Managing Addisonian Crisis Physical and psychological stressors must be avoided since the patient with Addison disease is at risk for an addisonian crisis, which presents as complete circulatory collapse and shock. Triggers include exposure to cold, overexertion, infection, and emotional distress. The patient with an addisonian crisis requires immediate treatment with IV administration of fluid, glucose, and electrolytes, especially sodium; replacement of missing steroid hormones; and vasopressors. Additionally, the patient must avoid exertion; therefore, the nurse must anticipate the patient's needs and take measures to meet them

DKA

is caused by an absence or markedly inadequate amount of insulin. This deficit of insulin results in disorders in the metabolism of carbohydrates, proteins, and fats. The primary clinical features of DKA are hyperglycemia, ketosis, dehydration, electrolyte loss, and metabolic acidosis. Pathophysiology Without insulin, the amount of glucose entering the cells is reduced, and production and release of glucose by the liver is increased. Both factors lead to hyperglycemia. In an attempt to rid the body of the excess glucose, the kidneys excrete excess glucose, causing an osmotic diuresis, leading to dehydration and marked loss of electrolytes. The hyperosmolality of the extracellular fluid leads to the stimulation of thirst, resulting in polydipsia and fluid shifting from intracellular to extracellular space. This fluid shifting causes low or normal levels of serum sodium despite water losses with polyuria. This low serum sodium level is referred to as pseudohyponatremia. Another effect of insulin deficiency is the breakdown of fat (lipolysis) into free fatty acids and glycerol. The free fatty acids are converted into ketone bodies by the liver. In DKA, the excessive production of ketone bodies leads to the development of metabolic acidosis. A characteristic response to this acidemia is for the respiratory center to blow off its respiratory acid, leading to rapid deep respirations known as Kussmaul respirations. Causes of DKA include insufficient or missed doses of insulin, physical or emotional stress, and illness or infection. An insulin deficit may result from an insufficient dosage of insulin prescribed or from insufficient insulin being administered by the patient. Physical and emotional stress increases the level of the counter regulatory ("stress") hormones—glucagon, epinephrine, norepinephrine, and cortisol—all of which cause an increase in blood glucose. Finally, illness and infection are associated with insulin resistance, which puts the patient at risk for hyperglycemia. If insulin is not increased during times of stress, illness, and infection, hyperglycemia may progress to DKA. For some patients with undiagnosed or untreated type 1 diabetes, DKA is the initial manifestation of diabetes. Clinical Manifestations and Assessment Hyperglycemia leads to polyuria, polydipsia, weakness, Malaise. The ketosis and acidosis of DKA lead to gastrointestinal (GI) symptoms, such as anorexia, nausea, vomiting, and abdominal pain. The patient may have acetone breath (a fruity odor) as well as Kussmaul respirations representing the body's attempt to decrease the acidosis, counteracting the effect of ketone accumulation. Mental status changes in DKA vary widely; the patient may be alert, lethargic, or comatose, usually depending on the severity of the abnormality of plasma osmolality. Diagnostic findings include: Blood glucose levels greater than 250 mg/dL Low serum pH (6.8 to 7.3) Low serum bicarbonate (0 to 15 mEq/L) Accumulation of serum and urine ketones Presence of glucose in the urine Abnormal levels of serum electrolytes (sodium, potassium, and chloride) Rehydration Initially, 0.9% sodium chloride (normal saline) is the IV solution selected for patients admitted with DKA. Many protocols call for administration of 1 to 2 L in the first 1 to 2 hours and then 1 L/hour for 3 to 4 hours, depending on the patient's response. Restoring Electrolytes Potassium is the major electrolyte of concern during treatment of DKA. The initial plasma concentration of potassium may be low because of renal loss due to osmotic diuresis. Conversely, it may be normal or high because of the shifting of potassium out of the cell to accompany the movement of hydrogen into the cells because of acidemia. If the potassium level is elevated, potassium replacement is withheld until serum levels fall to normal; this prevents the possibility of cardiac arrest from hyperkalemia. The serum level of potassium will decrease with insulin administration as insulin facilitates the movement of potassium intracellularly. Additionally, rehydration leads to increased plasma volume and subsequent decreases in the concentration of serum potassium as well as increased urinary excretion of potassium. It is critical that serum potassium levels be monitored carefully during treatment for DKA. Reversing Acidosis Accumulation of ketone (acetone) bodies occurs as a result of fat breakdown. The acidosis that occurs in DKA is reversed with insulin, which inhibits fat breakdown. Regular insulin is added to a saline solution and infused intravenously at a slow, continuous rate (e.g., 0.1 U/kg/hr) To avoid a rapid drop in the level of blood glucose during treatment, normal saline (NS) solutions with higher concentrations of glucose (e.g., D5NS, D5.45NS) are administered when blood glucose levels reach 250 mg/dL.

Diabetic retinopathy

is caused by changes in the small blood vessels in the retina, the area of the eye that receives images and sends information about the images to the brain. The retina is richly supplied with blood vessels of all kinds: small arteries and veins, arterioles, venules, and capillaries. Figure 30-8 shows the difference between a healthy retina and a retina affected by diabetes. Changes in the microvasculature include microaneurysms, intraretinal hemorrhage, hard exudates, and focal capillary closure. Retinopathy has three stages: nonproliferative, preproliferative, and proliferative. Stage I: Nonproliferative retinopathy is characterized by macular edema and occurs in approximately 10% of people with type 1 or type 2 diabetes. It may lead to visual distortion and loss of central vision. Stage II: Preproliferative retinopathy involves more widespread vascular changes and loss of nerve fibers. Approximately 10% to 50% of patients with preproliferative retinopathy develop proliferative retinopathy in a short time, some within a year. Stage III: Proliferative retinopathy is characterized by production of new blood vessels and formation of scar tissue. The new vessels are prone to bleeding. Fibrous scar tissue places traction on the retina that may cause hemorrhage or retinal detachment, with subsequent loss of vision. Clinical Manifestations and Assessment Retinopathy is a painless process. In nonproliferative and preproliferative retinopathy, blurry vision secondary to macular edema occurs in some patients, although many patients are asymptomatic. Even patients with a significant degree of proliferative retinopathy and some hemorrhaging may not experience major visual changes. Symptoms indicative of hemorrhaging include floaters or cobwebs in the visual field, sudden visual changes including spotty or hazy vision, or complete loss of vision.

Type 1 diabetes

is characterized by destruction of the pancreatic beta cells. The diagnosis is further defined as type 1a, or immune-mediated diabetes, and type 1b, or idiopathic (Porth, 2015). The etiology of type 1a diabetes is primarily autoimmune. Autoimmune diseases are caused by abnormal immune responses in which antibodies are directed against normal tissues of the body, responding to those tissues as if they were foreign. Immune destruction of the beta cells, caused by autoantibodies against islet cells and insulin, is associated with certain types of human leukocyte antigen (HLA). It is believed that destruction by the immune system of the beta cells is initiated by a combination of genetic, immunologic, and environmental factors, such as viruses or toxins. The risk of developing type 1 diabetes is three to five times higher in people with certain types of HLA. People do not inherit type 1 diabetes itself, but rather they may have a genetic predisposition, or tendency, toward development of the disease. Type 1b diabetes represents beta cell failure without an immune-mediated etiology. Whereas there is genetic susceptibility in type 1a diabetes, those with type 1b diabetes have a very strong hereditary component (Porth, 2015). Regardless of the specific cause, beta cell destruction results in decreased insulin production, unchecked glucose production by the liver, and hyperglycemia. In addition, glucose derived from food cannot be stored in the liver but instead remains in the blood and contributes to postprandial (after meals) hyperglycemia. If the concentration of glucose in the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dL, the kidneys cannot reabsorb all of the filtered glucose; glucose then appears in the urine (glycosuria). Glucose is an osmotic agent; water follows it. As the glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes. This is termed osmotic diuresis. In addition, fat breakdown occurs, resulting in an increased production of ketones, which are organic acids. If excessive amounts of ketones are present in the blood, ketoacidosis develops.

Hyperparathyroidism

is characterized by having excess parathormone (PTH), leading to a markedly increased level of serum calcium that can present as a potentially life-threatening situation The actions of PTH are increased by the presence of vitamin D. The serum level of ionized calcium regulates the output of parathormone (Fig. 31-5). Increased serum calcium leads to a decreased secretion of parathormone, thus creating a negative feedback system. When the product of serum calcium and serum phosphorus rises, calcium phosphate may precipitate and calcify in various organs of the body, such as the kidneys. Clinical Manifestations and Assessment Hypercalcemia Be alert for the following signs and symptoms: Stones: Kidney Bones: Bone pain, osteoporosis, pathologic fractures Abdominal Moans: Nausea, vomiting, and abdominal pains (hypercalcemia can lead to development of peptic ulcer and acute pancreatitis) Psychic Groans: Mental irritability, neurosis, confusion Primary hyperparathyroidism is diagnosed by persistent elevation of serum calcium levels and an elevated concentration of PTH. Radioimmunoassay for PTH is sensitive and differentiates primary hyperparathyroidism from other causes of hypercalcemia in more than 90% of patients with elevated serum calcium levels. An elevated serum calcium level alone is a nonspecific finding because serum levels may be altered by diet, medications, and kidney disease and bone changes. Bone changes on x-ray or bone scans indicates advanced disease. The double-antibody parathyroid hormone test distinguishes between primary hyperparathyroidism and malignancy as a cause of hypercalcemia. Ultrasound, MRI, thallium scan, and FNB evaluate the parathyroid functions and localize parathyroid cysts, adenomas, or hyperplasia. Medical and Nursing Management surgical removal of abnormal parathyroid tissue (parathyroidectomy). In some patients who are without symptoms and have serum calcium concentrations that are only mildly elevated and normal kidney function, surgery may be delayed, and the patient is monitored closely for worsening of hypercalcemia, bone deterioration, renal impairment, or the development of kidney stones. Nursing management involves providing hydration, encouraging mobility, administering nutrition and medications, providing emotional support, and observing for and managing hypercalcemic crisis.

Diabetic microvascular disease (microangiopathy)

is characterized by thickening of the membrane of the capillary basement. The basement membrane surrounds the endothelial cells of the capillary. Increased blood glucose levels react through a series of biochemical responses to thicken the basement membrane to several times its normal thickness. Two areas affected by these changes are the retina and the kidneys.

Precipitate labor

is labor that is completed in less than 3 hours from the start of contractions to birth. Not only can labor be too slow, but it can be abnormally rapid. The prevailing opinion has been that too rapid a labor can result in maternal injury and place the fetus at risk for traumatic or asphyxia insults (Borhart & Voss, 2019). Women experiencing precipitate labor typically have soft perineal tissues that stretch readily, permitting the fetus to pass through the pelvis quickly, or abnormally strong uterine contractions. Maternal complications are rare if the maternal pelvis is adequate and the soft tissues yield to a fast fetal descent. However, if the fetus delivers too fast, it does not allow the cervix to dilate and efface, which leads to cervical lacerations and the potential for uterine rupture. Potential fetal complications may include head trauma, such as intracranial hemorrhage or nerve damage, and hypoxia due to the rapid progression of labor (Cunningham et al., 2018). Precipitate labor is an anxiety-producing situation and frequently very painful with little rest between contractions. Continuous monitoring, frequent updates on labor progress, pain management, and reassurance about the mother's condition can assist her anxiety. Management includes readiness of the health care team for this rapid birth.

Dystocia

is the abnormal progression of labor. It can be influenced by a number of maternal and fetal factors. Dystocia is characterized by a slow and abnormal progression of labor. It occurs in approximately 10% of all labors and is the leading indicator for primary cesarean birth in the United States (Ehsanipoor & Satin, 2020). It is a fatiguing factor for both the mother and fetus and is associated with an increase in postpartum hemorrhage, infections, and perineal lacerations; it frequently requires medical or surgical interventions, which increases risk It is usually during the active phase that dystocia becomes apparent. Because dystocia cannot be predicted or diagnosed with certainty, the term "failure to progress" is often used. This term includes lack of progressive cervical dilation, lack of descent of the fetal head, or both. An adequate trial of labor is needed to declare with confidence that dystocia or failure to progress exists. risk for dystocia include epidural analgesia, excessive analgesia, multiple pregnancy, hydramnios, maternal exhaustion, ineffective maternal pushing technique, occiput posterior position, longer first stage of labor, nulliparity, short maternal stature (less than 5 ft tall), fetal birth weight (more than 8.8 lb), shoulder dystocia, abnormal fetal presentation or position (breech), fetal anomalies (hydrocephalus), maternal age older than 34 years, high caffeine intake, overweight, gestational age more than 41 weeks, chorioamnionitis, ineffective uterine contractions, and high fetal station at complete cervical dilation

Persistent occiput posterior

is the most common malposition, occurring in up to 5% of laboring women (Havelkova et al., 2019). The reasons for this malposition are often unclear. This position presents slightly larger diameters to the maternal pelvis, thus slowing fetal descent. A fetal head that is poorly flexed may be responsible. In addition, poor uterine contractions may not push the fetal head down into the pelvic floor to the extent that the fetal occiput sinks into it rather than being pushed to rotate in an anterior direction

Hyperthyroidism

occurs as a result of the overproduction of T3, T4, or both from the thyroid gland. Oversecretion of thyroid hormones (hyperthyroidism) is manifested by a greatly increased metabolic rate. Other characteristics of hyperthyroidism result from the increased response to circulating catecholamines (epinephrine and norepinephrine). Refer to Box 31-4. Usually oversecretion of thyroid hormones is associated with an enlarged thyroid gland (goiter). Graves disease is a common cause of hyperthyroidism. It is an autoimmune disease of the thyroid gland that results in the binding of antibodies to TSH, which causes the overproduction of thyroid hormones T3 and T4. Symptoms may appear after an emotional shock, stress, or an infection, but the exact significance of these relationships is not understood. Other less common causes of hyperthyroidism include thyroiditis (inflammation of the thyroid), overmedication with synthetic thyroid hormone, and thyroid nodules. Symptoms of hyperthyroidism also may occur with the release of excessive amounts of thyroid hormone as a result of inflammation after irradiation of the thyroid or destruction of thyroid tissue by tumor. . When untreated, the disease may progress relentlessly, leading to emaciation, nervousness, delirium, disorientation, and heart failure. The term thyrotoxicosis refers to symptomatic hyperthyroxinemia. While hyperthyroidism is a type of thyrotoxicosis, they are not the same. Although thyrotoxicosis can be caused by hyperthyroidism, other examples of thyrotoxicosis are associated with inflammation of the thyroid gland or ingestion of thyroid hormone. In these circumstances, there is an increased in either release of stored thyroid hormone or ingestion of exogenous hormone but not accelerated synthesis. Finally, a life-threatening complication of hyperthyroidism, in which profound hypermetabolism involves multiple systems, is called thyrotoxic crisis or thyroid storm. Clinical Manifestations and Assessment symptoms of nervousness. emotionally hyperexcitable, irritable, Apprehensive. Palpitations. Rapid resting pulse rates typically range between 90 and 160 beats per minute. The systolic blood pressure is elevated; electrocardiogram (ECG) findings may reveal sinus tachycardia or atrial fibrillation. Patients tolerate heat poorly and perspire unusually freely (hyperhydrosis-excessive sweating). The skin appears flushed and feels warm, soft, and moist. A fine tremor of the hands and tongue may be observed. exophthalmos (bulging eyes associated with abnormal fluid accumulation behind the eyes), which produces a startled facial expression. increased dietary intake, progressive weight loss, abnormal muscular fatigability, weakness (e.g., difficulty climbing stairs and rising from a chair), amenorrhea, decreased fertility, changes in bowel patterns (increased peristalsis). osteoporosis and fracture are associated with hyperthyroidism because of increased loss of bone minerals. thyroid gland is enlarged, feels soft, and may pulsate; often a thrill can be palpated, and a bruit is heard over the thyroid arteries. T Medical Management . Treatment of hyperthyroidism aims to reduce thyroid hyperactivity, relieve symptoms, and prevent complications. The use of radioactive iodine (131I) is the most common form of treatment for Graves disease due to the small risk of developing thyrotoxic crisis (thyroid storm) that can be minimized with 1 month's dosing of antithyroid drugs before radioiodine treatment (Jameson & Weetman, 2015).

Hypotonic uterine dysfunction

occurs during active labor (dilation more than 5 to 6 cm) when contractions become poor in quality and lack sufficient intensity to dilate and efface the cervix. Factors associated with this abnormal labor pattern include overstretching of the uterus, a large fetus, multiple fetuses, hydramnios, multiple parity, bowel or bladder distention preventing descent, and excessive use of analgesia. Clinical manifestations of hypotonic uterine dysfunction include weak contractions that become milder, a uterine fundus that can be easily indented with fingertip pressure at the peak of each contraction, and contractions that become more infrequent and briefer

Hypertonic uterine dysfunction

occurs when the uterus never fully relaxes between contractions. Subsequently, contractions are ineffectual, erratic, and poorly coordinated because they involve only a portion of the uterus and because more than one uterine pacemaker is sending signals for contraction. Women in this situation experience a prolonged latent phase, stay at 2 to 3 cm, and do not dilate as they should. Placental perfusion becomes compromised, thereby reducing oxygen to the fetus. These hypertonic contractions exhaust the mother, who is experiencing frequent, intense, and painful contractions with little progression. This dysfunctional pattern occurs in early labor and affects nulliparous women more often than multiparous women (Ehsanipoor & Satin, 2020).

Cushing syndrome,

or hypercortisolism, is a disorder characterized by high levels of serum cortisol—too much ACTH is at work in the body. Three important causes of Cushing syndrome are: A pituitary tumor that overproduces ACTH, termed Cushing disease An adrenal tumor that overproduces ACTH, termed Cushing syndrome Long-term glucocorticoid pharmacologic therapy, termed iatrogenic Pathophysiology Cushing syndrome is commonly caused by chronic use of synthetic corticosteroid medications and infrequently is due to excessive production of corticosteroid secondary to hyperplasia or tumor of the adrenal cortex. Overproduction of endogenous corticosteroids may be caused by several mechanisms, including a tumor of the pituitary gland that produces ACTH and stimulates the adrenal cortex to increase its hormone secretion despite production of adequate amounts (as noted earlier, technically termed Cushing disease). Primary hyperplasia of the adrenal glands in the absence of a pituitary tumor is less common. Another less common cause of Cushing syndrome is the ectopic production of ACTH by malignancies; bronchogenic carcinoma is the most common type of these malignancies. Regardless of the cause, the normal feedback mechanisms that control the function of the adrenal cortex become ineffective, and the usual diurnal pattern of cortisol is lost. Clinical Manifestations and Assessment arrest of height, obesity, musculoskeletal changes, glucose intolerance. central-type obesity, a protruding abdomen, fatty "buffalo hump" in the neck and supraclavicular areas, round "moon-faced" appearance (Fig. 31-8). The skin is thin, fragile, and easily traumatized; ecchymoses (bruises) and purple striae develop (secondary to stretching of the weakened skin). The patient complains of weakness and lassitude. Sleep is disturbed due to altered diurnal secretion of cortisol. Muscle weakness, wasting, and thin extremities are caused by protein wasting. Excessive catabolism of bone protein can result in osteoporosis. Kyphosis, backache, and compression fractures of the vertebrae may result. Retention of sodium and water occurs as a result of increased mineralocorticoid activity, producing hypertension, hypokalemia, and heart failure. Hyperglycemia or overt diabetes may develop. The patient may report weight gain, increased susceptibility to infection, and slow healing of minor cuts. In females of all ages, virilization may occur as a result of excess androgens. Virilization is characterized by the appearance of masculine traits and the recession of feminine traits. There is an excessive growth of hair on the face (hirsutism), the breasts atrophy, menses cease, the clitoris enlarges, and the voice deepens. Libido is lost in men and women. The initial diagnostic assessment involves: urine free cortisol (2 measurements), late night salivary cortisol (2 measurements), and dexamethasone suppression test: 1 mg overnight or 2 mg over 2 days (Nieman et al., 2008). The 1 mg overnight dexamethasone suppression test is widely used and the most sensitive screening for the diagnosis of pituitary and adrenal causes of Cushing disease (Porth, 2015). In general, 1 mg of dexamethasone is administered orally at 11:00 PM, and a plasma cortisol level is obtained at 8:00 AM the next morning. Suppression of cortisol to less than 5 mg/dL indicates that the hypothalamic-pituitary-adrenal axis is functioning properly. salivary cortisol concentrations are shown to be reflective of active free cortisol in plasma. Usually a saliva sample is collected on two separate evenings either by passive drooling into a plastic tube or by chewing a piece of cotton salivette for 1 to 2 minutes (Nieman et al., 2008). Saliva samples can be obtained easily in a nonstressful environment (e.g., at home); the test is relatively safe and easy to administer, with a sensitivity of 92% to 100% and a specificity of 93% to 100% Medical Management Treatment is directed at the pituitary gland if Cushing's is caused by pituitary tumors rather than tumors of the adrenal cortex. Successful surgical removal of the tumor by transsphenoidal hypophysectomy is the treatment of choice, . Adrenalectomy is the treatment of choice in patients with primary adrenal hypertrophy or when other therapies have failed. Adrenal enzyme inhibitors, such as metyrapone, aminoglutethimide, mitotane, and ketoconazole, are used to reduce hyperadrenalism if the syndrome is caused by ectopic ACTH secretion by a tumor that cannot be eradicated. Close monitoring is necessary because symptoms of inadequate adrenal function may result due to possible side effects of these medications. If Cushing syndrome is a result of the administration of corticosteroids, an attempt is made to reduce or taper the medication to the minimum dosage needed to treat the underlying disease process (e.g., autoimmune, allergic disease, or rejection of transplanted organ). Frequently, alternate-day therapy decreases the symptoms of Cushing syndrome and allows recovery of the adrenal glands' responsiveness to ACTH.

Addison disease,

or primary adrenocortical insufficiency, occurs when adrenal cortex function is inadequate to meet the patient's need for cortical hormones. The three adrenal corticosteroids are glucocorticoids (primarily cortisol, which decreases inflammatory reaction, decreases WBC migration to inflamed area, increases fat metabolism, and raises serum glucose), mineralocorticoids (primarily aldosterone, which causes sodium reabsorption and, with it, water, along with renal excretion of potassium), and androgens (sex hormones). Pathophysiology A primary adrenal insufficiency originates in the adrenal glands themselves and is likely associated with autoimmune or idiopathic atrophy of the adrenal cortex when cell-mediated immune mechanisms result in decreased production of adrenocortical hormones (e.g. cortisol and aldosterone). While primary adrenal insufficiency is an uncommon disorder, autoimmunity is responsible for about 80% of spontaneous cases in the United States (Fitzgerald, 2015). In contrast, secondary adrenal insufficiency can be due to either a lack of pituitary ACTH secretion, or Hypothalamic corticotropin-releasing hormone (CRH) dysfunction. This causes a resultant decrease production of cortisol but not aldosterone. ACTH only minimally influences aldosterone secretion, as it is secreted primarily in response to the presence of angiotensin II in the bloodstream. Risk Factors The risk factors for Addison disease include surgical removal of both adrenal glands and infection of the adrenal glands. Tuberculosis, cytomegalovirus, and bacterial infections (such as Neisseria meningitidis) are common infections that destroy adrenal gland tissue (National Institute of Diabetes and Digestive and Kidney Disease [NIDDK], 2014). Although autoimmune destruction has replaced tuberculosis as the principal cause of Addison disease, tuberculosis should be considered in the diagnostic workup because of its increasing incidence. Clinical Manifestations and Assessment muscle weakness, anorexia, GI symptoms, fatigue, emaciation, skin pigmentation changes hypotension low blood glucose, low serum sodium, high serum potassium levels. Depression, emotional lability, apathy, confusion are present in 60% to 80% of patients. With decreased glucocorticoids, mineralocorticoids, and androgens, there is a stimulation of the anterior pituitary to increase ACTH. This releases the melanocyte hormone, which results in a bronze-pigmented rash (Fig. 31-7). Figure 31-7 details the clinical manifestations of Addison disease and diagram specifies the relationship of signs and symptoms to specific hormone deficiency.

Diabetic nephropathy,

or renal disease secondary to microvascular changes in the kidney occurs in 20% to 40% of patients with diabetes and is the single leading cause of End Stage Kidney Disease (ESKD) (ADA 2017f). It is characterized by albuminuria (albumin in the urine), hypertension, and progressive renal insufficiency. Some patients eventually require dialysis or kidney transplantation. Patients with type 1 diabetes frequently show initial signs of renal disease after 10 to 15 years, while patients with type 2 diabetes may develop renal disease within 10 years after diagnosis. However, because many patients with type 2 diabetes have had diabetes for many years before diagnosis, there can be evidence of nephropathy at the time of diagnosis. Pathophysiology If blood glucose levels are elevated consistently for a significant period of time, the kidney's filtration mechanism is stressed, allowing blood proteins to leak into the urine. As a result, the pressure in the blood vessels of the kidney increases. It is thought that this elevated pressure serves as the stimulus for the development of nephropathy. Clinical Manifestations and Assessment Albuminuria of ≥30 mg/g is abnormal and signals early nephropathy. People with diabetes should have their urine checked at least annually for the presence of albumin

Diabetic neuropathy

refers to a group of diseases that affect all types of nerves, including peripheral (sensorimotor) and autonomic nerves. The disorders are clinically diverse and depend on the location of the affected nerve cells. They may be focal or diffuse (ADA, 2017f). The etiology of neuropathy appears to be related to elevated levels of blood glucose over a period of years. The pathogenesis of neuropathy may be attributed to either vascular or metabolic mechanisms, or both. Thickening of the membrane of the capillary basement and closure of capillaries disrupt blood supply to nerves. Also, demyelinization of nerves, which is thought to be related to hyperglycemia, and accumulation of sorbitol in nerve cells slow nerve conduction. The two most common types of diabetic neuropathy are sensorimotor polyneuropathy and autonomic neuropathy. Sensorimotor polyneuropathy, also called peripheral neuropathy, most commonly affects the distal portions of the nerves, especially the nerves of the lower extremities. Mononeuropathies (e.g., cranial neuropathies affecting the oculomotor nerve) affect a single nerve. Autonomic neuropathies cause a variety of clinical manifestations, depending on the area involved.

External cephalic version

refers to a procedure in which the fetus is rotated from the breech to the cephalic presentation by manipulation through the mother's abdominal wall at or near term. Several national organizations (ACOG, WHO, American Academy of Family Physicians [AAFP]), recommend that this maneuver be offered to women between 36 and 38 weeks' gestation. It is performed only in hospital settings under direct ultrasound guidance and continuous fetal monitoring. External cephalic version is successful in approximately 50% of cases. Women with breech presentations are now often advised to have surgical births with no attempt to rotate the fetal position (ACOG, 2018).

protracted disordersprotracted disorders

refers to a series of events including protracted active phase dilation (slower-than-normal rate of cervical dilation) and protracted descent (delayed descent of the fetal head in the active phase). A laboring woman with a slower-than-normal rate of cervical dilation is said to have a protracted labor pattern disorder. Slow progress may be the result of cephalopelvic disproportion. Most women, however, benefit greatly from adequate hydration and some nutrition, emotional reassurance, and position changes; these women may go on and give birth vaginally.

Thyroiditis

refers to the inflammation of the thyroid gland that may result in abnormalities in its functioning. The clinical classification of thyroiditis is based on the onset and duration of the disease, resulting from causes that are acute, subacute, or chronic. Thyroiditis can result in the swelling of the thyroid gland, manifesting symptoms in the form of acute and subacute thyroiditis. The chronic form of thyroiditis often presents with painless enlargement of the thyroid gland. Pathophysiology Acute thyroiditis is a rare disorder caused by infection of the thyroid gland by bacteria, fungi, mycobacteria, or parasites. The most common cause of acute thyroiditis is Staphylococcus aureus and other staphylococci. Chronic thyroiditis occurs frequently in women between 30 and 50 years of age. It has been termed as Hashimoto disease or chronic lymphocytic thyroiditis. The diagnosis is based on the histologic appearance of the inflamed gland. Cell-mediated immunity may play a significant role in the pathogenesis of chronic thyroiditis, and there may be a genetic predisposition to it. If left untreated, the disease runs a slow, progressive course, eventually leading to hypothyroidism. Clinical Manifestations and Assessment pharyngitis or pharyngeal pain is present. Physical examination may reveal warmth, erythema (redness), and tenderness over the thyroid gland. The condition manifests as a painful swelling in the anterior neck that lasts between 1 and 2 months and then disappears spontaneously without residual effect. It often follows a respiratory infection. The thyroid enlarges symmetrically and may be painful. The overlying skin is often red and warm. Swallowing may be difficult and uncomfortable. Irritability, nervousness, insomnia, weight loss, chills, fever, and manifestations of hyperthyroidism are common. In contrast to acute thyroiditis, the chronic forms are not accompanied by pain, pressure symptoms, or fever, and thyroid activity is normal or low rather than increased. The most common presentation in a patient suspected to have chronic thyroiditis is a palpable, enlarged, and painless firm mass over the thyroid gland. In addition, patients are likely to present with symptoms of hypothyroidism (Fitzgerald, 2015). Medical Management The medical management of acute thyroiditis includes antimicrobial agents and fluid replacement. Surgical incision and drainage may be needed if an abscess is present. In subacute thyroiditis, the treatment aims to control the inflammation. Nonsteroidal anti-inflammatory drugs are commonly used to relieve neck pain. e. Beta-adrenergic blocking agents (e.g., propranolol) may be used to control symptoms of hyperthyroidism. Antithyroid agents that block the synthesis of T3 and T4 are not effective in thyroiditis because the associated thyrotoxicosis results from the release of stored thyroid hormones rather than from their increased synthesis.

Diabetic macrovascular (macroangiopathy) complications

result from changes in medium to large blood vessels. Blood vessel walls thicken, sclerose, and become occluded by plaque that adheres to the vessel walls. Eventually, blood flow is blocked. These atherosclerotic changes tend to occur more often and at an earlier age in patients whose diabetes is poorly controlled. Coronary artery disease, cerebrovascular disease, and peripheral vascular disease are the three main types of macrovascular complications that occur frequently in the diabetic population. Cardiovascular disease is the major cause of illness and death for people with diabetes iscussed in detail in Chapter 14. Cerebral blood vessels are affected similarly by accelerated atherosclerosis. Occlusive changes or an embolus elsewhere in the vasculature that lodges in a cerebral blood vessel can lead to transient ischemic attacks and strokes.

Hypoparathyroidism

results from hyposecretion of the parathyroid glands, leading to low levels of PTH that eventually results in hypocalcemia and hyperphosphatemia. In the absence of PTH, there is increased blood phosphate (hyperphosphatemia) and a resultant decreased level of blood calcium (hypocalcemia) due to the inverse relationship between serum phosphorus and calcium described in Box 31-8. Without PTH, there is also decreased intestinal absorption of dietary calcium as well as decreased resorption of calcium from bone and through the renal tubules, causing hypocalcemia. The most common cause of hypoparathyroidism is from surgical removal of parathyroid gland tissue during thyroidectomy, parathyroidectomy, or radical neck dissection. These small glands are easily overlooked and can be removed inadvertently during thyroid surgery. Hypoparathyroidism also may occur in patients who have undergone a subtotal resection or total parathyroidectomy with parathyroid autotransplantation. Other risk factors include genetic predisposition, exposure to radiation, and magnesium depletion (hypomagnesemia: less than 0.4 mmol/L; less than 0.8 mEq/L) (Jameson & Weetman, 2015). Clinical Manifestations and Assessment Hypocalcemia causes irritability of the neuromuscular system and contributes to the chief symptom of hypoparathyroidism, tetany. Tetany is a general muscle hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with or without efforts to make voluntary movements. Symptoms of latent tetany are numbness, tingling, and cramps in the extremities, and the patient complains of stiffness in the hands and feet. In overt tetany, the signs include bronchospasm, laryngeal spasm, carpopedal spasm (flexion of the elbows and wrists and extension of the carpophalangeal joints and dorsiflexion of the feet), dysphagia, photophobia, cardiac arrhythmias, and seizures. Other symptoms include anxiety, irritability, depression, and even delirium. ECG changes, such as prolonged QT intervals, and hypotension also may occur. A positive Trousseau sign or a positive Chvostek sign on physical assessment suggests latent tetany (Fig. 31-6). Trousseau sign is positive when carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes with a blood pressure cuff. Chvostek sign is positive when a sharp tapping over the facial nerve just in front of the parotid gland and anterior to the ear causes spasm or twitching of the mouth, nose, and eye. The diagnosis of hypoparathyroidism often is difficult because of the vague symptoms, such as aches and pains. Therefore, laboratory studies are especially helpful. Tetany develops at serum calcium levels of 5 to 6 mg/dL (1.2 to 1.5 mmol/L) or lower. Serum phosphate levels are increased, and x-rays of bone show increased density. Calcification is detected on x-rays of the subcutaneous or paraspinal basal ganglia of the brain. Medical Management The goal is to increase the serum calcium level to 8 to 9 mg/dL (2.0 to 2.25 mmol/L) and to eliminate the symptoms of hypoparathyroidism and hypocalcemia. When hypocalcemia and tetany occur after a thyroidectomy, the immediate treatment is administration of IV 10% calcium gluconate. If this does not decrease neuromuscular irritability and seizure activity immediately, sedative agents, such as pentobarbital, may be administered. Parenteral PTH can be administered to treat acute hypoparathyroidism with tetany. The patient receiving PTH is monitored closely for allergic reactions and changes in serum calcium levels. Treatment for chronic hypoparathyroidism is determined after serum calcium levels are obtained. A diet high in calcium and low in phosphorus is prescribed (Box 31-10). Oral calcium salts, such as calcium gluconate, may be used to supplement the diet. Aluminum hydroxide gel or aluminum carbonate (Gelusil, Amphojel) may be used after meals to bind phosphate and promote its excretion through the GI tract. Other variable dosages of a vitamin D preparation—dihydrotachysterol (AT 10 or Hytakerol), ergocalciferol (vitamin D), or cholecalciferol (vitamin D)—are usually required and enhance calcium absorption from the GI tract.

The DPP-4 inhibitor

s act by reducing the activity of the DPP-4 enzyme, whose primary action is to degrade glucagon-like peptide 1 (GLP-1). This prolongs the availability of GLP-1, whose actions are to stimulate insulin production, slow gastric emptying, and suppress glucagon secretion.

Be alert for the following signs and symptoms: General: Weakness, fatigue Dizziness Pica (craving unusual items including: ice, starch, or dirt) Neurologic: Numbness and tingling (paresthesias), irritability Weakness Headache Poor coordination, confusion Gait disturbances Reflex abnormalities Loss of position (proprioception) and vibration sense Spasticity Roaring, rushing, ringing, or pounding sensation in the ears Integumentary: Pallor of the skin and mucous membranes Jaundice (hemolytic anemia) Brittle, ridged, concave nails Impaired wound healing Loss of elasticity Early thinning and graying of hair Dry skin Painful mouth sores Beefy red, sore tongue (megaloblastic anemia) Smooth and red tongue (iron deficiency anemia) Ulcerated corners of the mouth (angular cheilitis) Cardiovascular: Palpitations Chest pain Tachycardia Hypotension Peripheral edema Murmurs Respiratory: Dyspnea Orthopnea Tachypnea Gastrointestinal: Anorexia, nausea, vomiting Dysphagia Abdominal pain Flatulence Diarrhea Hepatomegaly Splenomegaly Musculoskeletal: Muscle pain (claudication) Complications General complications of severe anemia include heart failure, paresthesias (abnormal sensation of pricking, tingling, numbness, burning, etc.), and confusion.

signs and symptoms/ complications of anemia

hemolytic anemias,

the erythrocytes have a shortened lifespan; thus, their number in the circulation is reduced. Fewer erythrocytes result in decreased available oxygen, causing hypoxia, which, in turn, stimulates an increase in erythropoietin release from the kidney. The erythropoietin stimulates the bone marrow to compensate by producing new erythrocytes and releasing some of them into the circulation somewhat prematurely as reticulocytes. If the red cell destruction persists, the hemoglobin is broken down excessively; about 80% of the heme is converted to bilirubin, conjugated in the liver, and excreted in the bile. The mechanism of erythrocyte destruction varies, but all types of hemolytic anemia share certain laboratory features: the reticulocyte count is elevated, the fraction of indirect (unconjugated) bilirubin is increased, and the supply of haptoglobin (a binding protein for free hemoglobin) is depleted as more hemoglobin is released. As a result, the plasma haptoglobin level is low. The severity of anemia will increase if the marrow does not compensate by replacing the hemolyzed erythrocytes (poor response indicated by a decreased reticulocyte count). Causes of hemolytic anemia are discussed in Box 20-3.

Medical Management . In asymptomatic patients, fluid restriction is the treatment of choice (less than 1 L water per day), whereas in acutely symptomatic patients (profound hyponatremia is present with Na below 120 mEq/L), an IV of 3% sodium chloride (hypertonic saline) will be infused slowly via a central line and IV pump. Diuretics, such as furosemide (Lasix) IV, will prevent extracellular fluid volume expansion by causing diuresis.

treatment of SIADH

Medical Management The objectives of medical therapy are to replace ADH (which is usually a long-term therapeutic program), to ensure adequate fluid replacement, and to identify and correct the underlying intracranial pathology. Desmopressin/DDAVP, a synthetic vasopressin, is used to control fluid balance and prevent dehydration. Desmopressin does not have the vascular effects of natural ADH. Thus, it is particularly valuable due to its longer duration of action and fewer adverse effects compared to other preparations previously used to treat the disease. Desmopressin can be administered orally as tablets or intranasally using a spray or a flexible calibrated plastic tube. Usually one or two administrations daily (every 12 to 24 hours) are needed to control the symptoms. However, sometimes nasal decompression can cause rhinitis or conjunctivitis (Fitzgerald, 2015). Other medications used to treat patients with diabetes insipidus include intramuscular administration of vasopressin, chlorpropamide (Diabinese), thiazide diuretics (potentiate the action of vasopressin), and/or prostaglandin inhibitors (e.g., ibuprofen, indomethacin, and aspirin).

treatment of diabetes insidious

Medical Management Hypophysectomy using a transsphenoidal approach is the treatment of choice for patients with a pituitary tumor, as the approach offers direct access to the sella turcica with minimal risk of trauma and hemorrhage. Tumors within the sella turcica and small adenomas of the pituitary can be removed through a transsphenoidal approach: an incision is made beneath the upper lip (sublabial) or via an endonasal approach, in which entry is gained successively into the nasal cavity, sphenoidal sinus, and sella turcica with minimal risk of trauma and hemorrhage. Microsurgical techniques used in the transsphenoidal approach provide improved illumination, magnification, and visualization so that nearby vital structures can be avoided. The transsphenoidal approach also avoids the risks of craniotomy, and the postoperative discomfort is similar to that of other transnasal surgical procedures. Corticosteroids may be administered before and after surgery because the pituitary is the source of ACTH. In addition, the absence of the pituitary gland can alter the function of many body systems. Nursing Management Preoperative nursing care of patients undergoing transsphenoidal removal of the pituitary tumor includes teaching deep-breathing exercises before surgery and instructing the patient to avoid vigorous coughing, blowing the nose, sucking through a straw, or sneezing because these actions may place increased pressure at the surgical site and cause a leak of cerebrospinal fluid (CSF) Therefore, the nurse assesses for signs of meningeal irritation, such as nuchal rigidity, temperature elevation, and changes in mental status (see Chapter 46). The nurse teaches patients to avoid activities, such as bending over or straining during urination or defecation, because they can raise intracranial pressure (ICP).

treatment of pituitary tumors