1. Chapter 52
Care of Patients with Pituitary, Thyroid, Parathyroid, and Adrenal Disorders
Med-Surg II

2. Pituitary Tumors Etiology and pathophysiology Signs and symptoms
Benign pituitary adenoma-Tumor secretes growth hormone (GH), leading to continued growth of bones & soft tissues. May cause optic nerve damage & acts against insulin, resulting in an increase in blood glucose & glucose intolerance.
Signs and symptoms
Local symptoms-HA, visual disturbances (possible blindness).
Systemic symptoms-May be vague & progress slowly. Personality changes, weakness, fatigue, & abdominal pain may be present for years before diagnosis.

3. Pituitary Tumors (cont.)
Excessive growth hormone may result in gigantism in children, leading to excessively tall stature, as the bone growth plates have not yet closed. In adults the result is acromegaly, and the adults facial features change: the lips thicken, the nose enlarges, and the forehead develops a bulge. Also, the adult’s hands & feet become enlarged; the 1st sign may be that the patient's shoes no longer fit. Muscle weakness may occur and osteoporosis & joint pain are common.

4. Progression of Acromegaly
See Figure 37-1 on p. 834.

5. Pituitary Tumors Diagnosis Treatment
Complete history and physical examination
Magnetic resonance imaging (MRI)
High-resolution computed tomography (CT) with contrast media
Treatment
Hormone therapy
Irradiation
Surgery—hypophysectomy (removal of pituitary gland). Usual route is transsphenoidal (through the nose)

6. Transsphenoidal Surgical Approach for Hypophysectomy
See Figure 37-2 on p. 834.

7. Postoperative Nursing Care
Semi-Fowler’s position
Note any change in vision, mental status, level of consciousness, or strength
Diabetes insipidus
Nasal packing
Patient teaching

8. Hypofunction of the Pituitary Gland
Etiology and pathophysiology
Autoimmune disorders, infections, or destruction of the pituitary gland
Sheehan syndrome (a rare, but serious postpartum complication; involves infarction of the gland secondary to postpartum hemorrhage)
Decrease in GH (in children, results in short stature; in adults, results in increased bone fragility) and gonadotropins (may lead to testicular failure in a man, and ovarian failure in women)

9. Diagnosis History and physical examination
Levels of pituitary hormones
MRI and CT

10. Treatment and Nursing Management
Hormone replacement
Surgery and radiation
Patient teaching

11. Diabetes Insipidus Etiology and pathophysiology
Central DI, associated with brain tumors, head injury, neurosurgery, or central nervous system (CNS) infections
Nephrogenic DI, caused by drug therapy (lithium) or kidney disease
Dispogenic DI, caused by excessive water intake (sometimes associated with schizophrenia)

12. Signs and Symptoms Diuresis
Thirst, weakness, and fatigue, often from nocturia (urination at night)
Deficient fluid volume
Signs of shock and CNS manifestations

13. Diagnosis Complete history and physical examination
Urine and plasma osmolality and urine specific gravity
Water deprivation test

14. Treatment and Nursing Management
Replacement of fluid and electrolytes
Hormone therapy
Early detection, maintenance of fluid and electrolyte balance, and patient education

15. Syndrome of Inappropriate Antidiuretic Hormone
Signs and symptoms
Confusion, seizure, loss of consciousness, weight gain, and edema
Hyponatremia, muscle cramps, and weakness
Diminished urine output

16. Pathophysiology
See Concept Map 37-2 on p. 837.

17. Diagnosis Urine and serum osmolality tests
Blood urea nitrogen (BUN), hemoglobin, hematocrit, and creatinine clearance

18. Treatment and Nursing Management
Correct underlying cause
Restrict fluids to 500 to 1000 mL/day
Administer sodium chloride, diuretics, and demeclocycline

19. Regulation of Thyroid Hormone Secretion
See Concept Map 37-3 on p. 838.

20. Goiter
Etiology and pathophysiology: Greatly enlarged thyroid gland. One type is caused by iodine deficiency.
Signs, symptoms, and diagnosis: First sign is usually enlargement in front of neck. Later, as it grows larger, it may press against the esophagus and cause difficulty swallowing. It may also press against the trachea, causing dyspnea.
Treatment: Iodine will stop the growth, but will not cure it. If it becomes very large, may require surgical removal.

21. Goiter (cont.)
See Figure 37-3 on p. 839.

22. Goiter (cont.)
Nursing management: If giving iodine preparations, use a straw as iodine can stain the teeth. Also, be aware of side effects of iodine: stomach upset, metallic taste, skin rashes, allergic reactions, and epigastric pain.

23. Hyperthyroidism Etiology and pathophysiology
Women are at greatest risk.
Primary hyperthyroidism—Graves’ disease or toxic goiter results from problem with gland itself.
Secondary hyperthyroidism-Usually results from abnormality in another gland, such as pituitary.
Signs and symptoms
Earliest symptoms: Weight loss (in spite of a good appetite) and nervousness. Later symptoms include weakness, insomnia, agitation, tachycardia, diarrhea, ankle edema, exertional dyspnea, decreased libido, scanty menstruation, and infertility.

24. Hyperthyroidism (cont.)
The condition is sometimes not diagnosed in early stages because of the vagueness of symptoms. In some cases, hyperthyroidism is misdiagnosed as a cardiovascular disease, as symptoms are similar.
If not diagnosed correctly & continues to be untreated, may result in true heart disease & MI. Emotional upheaval may occur as a result of the action of thyroid hormones on the nervous system. Uncontrollable crying & depression followed by intense physical activity & euphoria are common.

25. Exophthalmos of Graves’ Disease
See Figure 37-4 on p. 840.

26. Hyperthyroidism Diagnosis Treatment and nursing management
Clinical manifestations
Heart rate while sleeping (rate consistently >80)
EKG, CT, or MRI
Treatment and nursing management
Radioactive iodine and antithyroid drugs
Mild sedatives, and beta-adrenergic blocking agents

27. Treatment of Hyperthyroidism
Thyroid crisis (thyroid storm)
Antithyroid drugs
Thyroidectomy
Preoperative nursing care including thyroid crisis
Postoperative nursing care
Thyroid storm (also known as thyroid crisis or thyrotoxicosis) is caused by a sudden increase in the output of thyroxine caused by manipulation of the thyroid as it is being removed.
Another cause of TS may be improper reduction of thyroid secretions before surgery.
In a patient with hyperthyroidism, TS also can be triggered by other factors unrelated to surgery; TS can also be caused by a patient with hypothyroidism who consumes an overdose of levothyroxine.
The symptoms of TS are produced by a sudden and extreme elevation of all body processes. The temperature may rise to 106° F (41.1° C) or more, the pulse increases to as much as 200 beats per minute, respirations become rapid, and the patient exhibits marked apprehension and restlessness. Unless the condition is relieved, the patient quickly passes from delirium to coma to death from heart failure.

28. Thyroid Storm
Thyroid storm (also known as thyroid crisis or thyrotoxicosis) is caused by a sudden increase in the output of thyroxine caused by manipulation of the thyroid as it is being removed.
Another cause of TS may be improper reduction of thyroid secretions before surgery.
In a patient with hyperthyroidism, TS also can be triggered by other factors unrelated to surgery; TS can also be caused by a patient with hypothyroidism who consumes an overdose of levothyroxine.
The symptoms of TS are produced by a sudden and extreme elevation of all body processes. The temperature may rise to 106° F (41.1° C) or more, the pulse increases to as much as 200 beats per minute, respirations become rapid, and the patient exhibits marked apprehension and restlessness. Unless the condition is relieved, the patient quickly passes from delirium to coma to death from heart failure.

29. Common Causes of Thyroid Storm
Administration of drugs or dyes containing iodine
Childbirth (immediately postpartum)
Congestive heart failure
Diabetic ketoacidosis
Inadequate hormone replacement
Infection
Pulmonary embolism
Severe emotional distress
Stroke
Trauma or surgery
See Box 37-1 on p. 843.

30. Treatment of Thyroid Storm
Reduce the temperature
Cardiac drugs to slow the heart rate
Sedatives such as a barbiturates to reduce restlessness and anxiety

31. Hypothyroidism
Etiology and pathophysiology: Can be caused by inflammation of thyroid, decreased TSH secretion hypothalamus dysfunction, atrophy of thyroid gland, or by treatment of hyperthyroidism which may destroy thyroid cells.
Congenital hypothyroidism—cretinism
Signs and symptoms
Myxedema (very low thyroid production) is characterized by a decrease in appetite but increase in weight due to very slow metabolism

32. Hypothyroidism (cont.)
Other s/s are tiredness, low energy, lethargy, facial swelling, bags under eyes, slurred speech, cold intolerance, constipation, flatulence, impaired memory, depression, husky voice, hair loss, brittle nails, easy bruising, muscle cramps, dry skin, and non- pitting edema.
Diagnosis and treatment: Clinical s/s and lab tests
Clinical signs and symptoms
Serum levels of thyroid hormones and TSH

33. Nursing Management Managing hypothyroidism
Nurses should increase awareness of look-alike, sound-alike products and help patients to recognize the exact name and purpose of their medications
Myxedema coma—cause, signs and symptoms, and treatment
Myxedema coma is life-threatening. It can be precipitated by abrupt withdrawal of thyroid therapy, acute illness, anesthesia, use of sedatives or narcotics, surgery, or hypothermia in the hypothyroid patient. Signs and symptoms are loss of consciousness along with hypotension, hypothermia, respiratory failure, hyponatremia, and hypoglycemia. Treatment is administration of levothyroxine sodium IV, fluid replacement, maintenance of an airway and respiration, IV glucose administration, corticosteroids, and provision of warmth.

34. Myxedema Coma
Myxedema coma is life-threatening. It can be precipitated by abrupt withdrawal of thyroid therapy, acute illness, anesthesia, use of sedatives or narcotics, surgery, or hypothermia in the hypothyroid patient. Signs and symptoms are loss of consciousness along with hypotension, hypothermia, respiratory failure, hyponatremia, and hypoglycemia. Treatment is administration of levothyroxine sodium IV, fluid replacement, maintenance of an airway and respiration, IV glucose administration, corticosteroids, and provision of warmth.

35. Thyroiditis Etiology and pathophysiology
Inflammation of the thyroid gland
Acute (infection related), subacute (related to upper respiratory viral infection, for example), or chronic (most common type)
Autoimmune thyroiditis (Hashimoto’s thyroiditis) is a chronic form usually affecting women age The body produces antibodies against the thyroid, which destroys the gland. Cause is unknown, but seems to be genetic as people who have this disease usually have other autoimmune disorders, such as RA.

36. Thyroiditis (cont.)
Signs and symptoms: Painless enlargement of thyroid gland which may cause dysphagia.
Diagnosis: Lab tests, including thyroid hormone levels, TSH levels and radioactive iodine uptake. Needle biopsy may be performed.
Treatment: Thyroid hormone to prevent hypothyroidism and decrease the size of the thyroid (sometimes with surgery).
Nursing management: Patient teaching; providing comfort.

37. Thyroid Cancer
Etiology and pathophysiology: More common in recent years. Most common form is papillary carcinoma, which occurs most often in younger women. Slow growing tumor can be present for years before diagnosis. Cause is unknown.
Signs and symptoms: First sign is a nodule found on routine physical examination. Only 5%-10% of nodules are found to be cancerous. Fatigue, weight changes, or depression may also be present.

38. Thyroid Cancer (cont.)
Diagnosis: US used to assess thyroid size and locate nodules; Iodine uptake studies may also be used. The definitive test is fine-needle aspiration, in which a specimen of tissue is taken & analyzed.
Treatment & Nursing Management: TX is thyroidectomy. In some cases, radioactive iodine (ablation) therapy may be used in lieu of surgery to disable the gland. A new drug, vandetanib, has been approved in 2011 which inhibits tumor growth in symptomatic thyroid cancer.

39. Hypoparathyroidism
Etiology and pathophysiology: Most often caused by atrophy or traumatic injury to the parathyroid glands. This can occur as a result of accidental removal or destruction of parathyroid tissue during a thyroidectomy.
Hypoparathyroidism will result in a drop in serum calcium levels and an increase in phosphorus levels.

40. Hypoparathyroidism (cont.)
Signs and symptoms of low calcium include mild tingling, numbness, muscle cramps, and mental changes, such as irritability.
Chvostek sign manifests as muscle irritability when the facial nerve is gently tapped.
Trousseau sign manifests as a carpal spasm, elicited by inflating a BP cuff above the systolic blood pressure.
Tetany is a serious sign resulting from low calcium. Muscular twitching & spasms occur because of extreme irritability of neuromuscular tissue.
Convulsions, cardiac dysrhythmias, and spasms of the larynx will occur if calcium levels continue to fall.

41. Hypoparathyroidism (cont.)
Diagnosis is established by clinical signs & lab tests. ECG may show abnormalities which return to normal when calcium level is corrected. CT scan may show calcifications in the brain if hypocalcemia is chronic.
Treatment and nursing management: Acute hypoparathyroidism with tetany is treated with IV calcium gluconate. Oral calcium salts may be used simultaneously. In chronic hypoparathyroidism, treatment is aimed at restoring & maintaining blood calcium levels. This is accomplished by hormone replacement therapy, vitamin D in massive doses, & oral administration of calcium salts. Nursing care revolves around education & electrolyte replacement. Remind Pt. it is lifelong therapy & to wear a medical alert bracelet.

42. Hyperparathyroidism (Von Recklinghausen’s Disease)
Etiology and pathophysiology: Common endocrine disorder that most often occurs in postmenopausal women. Hypercalcemia occurs with this disease.
Signs and symptoms: More than 50% are asymptomatic. S/S may be mild or severe and include: dehydration, confusion, lethargy, arrhythmias, anorexia, n/v, weight loss, constipation, thirst, frequent urination, & HTN. May be skeletal changes, including thinning of the bone & bone cysts. A bone fracture may cause the pt. To seek medical attention.

43. Hyperparathyroidism (Von Recklinghausen’s Disease)
Diagnosis: Labs
Serum calcium elevated and phosphate levels low
Serum parathyroid hormone is the best test for initial confirmation
Serum albumin is also measured because serum calcium needs to be corrected for low albumin levels
Treatment: Depends on the severity. Infusions of isotonic sodium chloride and administration of diuretic agents promotes excretion of excess calcium in the urine. Phosphate therapy is given to correct the deficit; mithramycin binds calcium & enhances secretion from body; calcitonin decreases the rate of skeletal calcium release. Surgical removal of portion of gland may be necessary.
Nursing management: I&O; daily weight; electrolytes; cardiac monitoring.

44. Causes of Hyperparathyroidism
Parathyroid tumor (benign or malignant)
Congenital enlargement
Neck trauma or irradiation
Vitamin D deficiency
Chronic renal failure with hypocalcemia
Lung, kidney, or GI tract cancers
See Box 37-2 on p. 846.

45. Comparison of Hyperparathyroidism and Hypoparathyroidism
Serum calcium levels
Serum phosphate levels
Bone resorption
Calcium and phosphate in urine
Neuromuscular irritability
SEE TABLE 37-2 ON P. 846!
See Table 37-2 on p. 846.

46. Pheochromocytoma
Etiology and pathophysiology: Rare tumor of the adrenal medulla that secretes catecholamines (epinephrine & norepinephrine). It often causes severe HTN and if left untreated it can lead to death.
Signs, symptoms, and diagnosis: Tachycardia, severe HTN, profuse sweating, severe HA, and palpitations. Diagnosis is made by measuring serum catecholamines and 24-hour urine measurement. CT & MRI may be used to locate tumor.

47. Pheochromocytoma Treatment Surgical removal Nursing management
Hypertensive crisis

48. Adrenocortical Insufficiency (Addison’s Disease)
Etiology and pathophysiology: Characterized by decreased function of adrenal cortex resulting in a deficit of all three hormones secreted by the adrenal cortex. Major problems related to insufficiencies of mineralcorticoids & glucocorticoids. Insufficiency of androgenic hormones can be compensated for by the ovaries & testes.
Primary insufficiency: Disorder in the cortex itself.
Secondary insufficiency: Disorder in pituitary gland which stimulates adrenal secretion.

49. Adrenocortical Insufficiency (Addison’s Disease) (cont.)
Signs and symptoms: Early symptoms are so vague, most patients don’t seek tx. Later, severe symptoms associated with fluid & electrolyte imbalance & hypoglycemia. A major problem is depletion of sodium (hyponatremia) which in turn causes depletion of extracellular fluid & potassium retention (hyperkalemia). Generalized malaise, muscle weakness, muscle pain, orthostatic hypotension, and cardiac dysrhythmias may also be present. GI symptoms, such as flatulence, N/V, and diarrhea may also be present.

50. Adrenocortical Insufficiency (Addison’s Disease) (cont.)
Diagnosis of Addison’s is made by examining blood and urine electrolytes. ACTH stimulation test may determine if the problem lies in the adrenal gland or the pituitary. CT & MRI may be used to locate tumor. Abnormal serum electrolytes (hyponatremia & hyperkalemia), decreased glucose tolerance, elevated WBC’s and abnormally low levels of free cortisol are among the criteria used to diagnose Addison’s disease.
Treatment: Replacement therapy providing the missing hormones usually brings about a rapid recovery, but lifelong therapy is required.

51. Adrenocortical Insufficiency (Addison’s Disease) (cont.)
Intensive care and support and Addisonian crisis
Prevent problems related to fatigue and orthostatic hypotension
Alleviate gastrointestinal problems
Patient teaching

52. Acute Adrenal Insufficiency or Addisonian Crisis
Etiology: Physical stress from the flu or other infection, or from surgery, can send the patient with Addison’s disease into addisonian crisis.
Treatment and nursing management
Monitor vital signs, glucose, and potassium
Fluid replacement
Kayexalate, diuretics, insulin, and glucagon
Hormone replacement

53. Excess Adrenocortical Hormone (Cushing Syndrome)
Causes
Excessive secretion of ACTH by the pituitary, which may result from faulty release of corticotropin- releasing factor (CRF) from the hypothalamus
A secreting tumor of the adrenal cortex
Ectopic production of ACTH by tumors outside the pituitary, such as lung cancer
Iatrogenic Cushing syndrome from prolonged use of steroid therapy

54. Excess Adrenocortical Hormone (Cushing Syndrome) (cont.)
Signs and symptoms: Buffalo hump, moon face, enlarged abdomen with thin extremities, bruising following even minor traumas, impotence, amenorrhea, HTN, and weakness.
Diagnosis
Plasma cortisol
24-hour urine test
Dexamethasone suppression test
Treatment: Surgery, using steroids cautiously.
Nursing management: Assist w/psychosocial concerns.

55. Common Characteristics of Cushing Syndrome
See Figure 37-5 on p. 852.