ENDOCRINE UNIT TEST STUDY GUIDE

1. CHAPTER 38

A. Know the glands of the endocrine system

i. Anterior Pituitary Gland

1. The anterior pituitary gland secretes its hormones in response to releasing hormones from the hypothalamus.

2. Secretion of growth hormone (GH) is regulated by growth hormone–releasing hormone (GHRH) and by growth hormone–inhibiting hormone (GHIH, or somatostatin), both produced by the hypothalamus.

3. GHRH is produced during hypoglycemia or when there is a high blood level of amino acids.

4. GHIH is secreted during hyperglycemia, when carbohydrates are available for energy production and the mobilization of fat is not needed.

5. Thyroid-stimulating hormone (TSH) stimulates growth and secretions of the thyroid gland.

a. TSH secretion is stimulated by thyrotropin-releasing hormone (TRH).

6. Adrenocorticotropic hormone (ACTH) stimulates secretion of cortisol and related hormones from the adrenal cortex.

7. Corticotropin-releasing hormone (CRH) from the hypothalamus stimulates the release of ACTH.

a. CRH is produced during any type of stress such as injury, disease, exercise, or hypoglycemia.

ii. Posterior Pituitary Gland

1. The posterior pituitary gland stores and releases antidiuretic hormone (ADH; sometimes called vasopressin) and oxytocin.

2. Axon tracts from the hypothalamus transmit the hormones to the posterior pituitary and signal their release.

3. ADH increases water reabsorption by the kidney tubules, which decreases urine output.

a. The water is reabsorbed back into the blood, thereby maintaining normal blood volume and pressure.

b. In cases of great fluid loss, such as severe hemorrhage, the large amount of ADH secreted is especially important because it causes arteriole vasoconstriction, which increases blood pressure to homeostatic levels.

4. Oxytocin causes contractions of the myometrium to bring about delivery of a newborn and placenta.

a. Release of oxytocin operates on a positive feedback loop.

b. During breastfeeding, the subsequent release of oxytocin causes contraction of the smooth muscle cells around the mammary ducts.

i. This release of milk is called milk ejection (or letdown).

iii. Thyroid Gland

1. The thyroid gland consists of two lobes connected by a piece of tissue called the isthmus.

2. Three hormones are produced by the thyroid gland: triiodothyronine (T3), thyroxine (T4), and calcitonin.

a. T3 and T4 increase cellular respiration of glucose and fatty acids, which increases the metabolic rate—that is, energy and heat production.

i. They are essential for normal physical growth, mental development, and reproductive maturation.

ii. Sufficient iodine intake is required for T 3 and T4 production.

b. The direct stimulus for secretion of T3 and T4 is TSH from the anterior pituitary.

c. A decrease in metabolic rate causes the hypothalamus to secrete TRH.

d. TRH stimulates the anterior pituitary to secrete TSH, which stimulates the thyroid to increase secretion of T3 and T4.

i. This then increases energy production and raise the metabolic rate.

e. Negative feedback decreases the secretion of TRH from the hypothalamus until the metabolic rate decreases again.

3. The third thyroid hormone, calcitonin, targets bone tissue and is especially important during childhood when bone growth is accelerated.

a. Resorption of calcium and phosphorous into the blood is inhibited by calcitonin so these minerals are retained in the bones.

i. This one function of calcitonin has two important results: the maintenance of normal blood levels of calcium and

2

phosphate, and the maintenance of a strong, stable bone matrix.

1. The stimulus for secretion of calcitonin is hypercalcemia

iv. Parathyroid Gland

1. There are usually four parathyroid glands, two on the back of each lobe of the thyroid gland.

2. They produce parathyroid hormone (PTH), an antagonist to calcitonin.

a. Besides bone, the target organs of PTH are the small intestine and kidneys.

b. The overall effect of PTH is to raise the blood calcium level and lower the blood phosphate level.

3. Homeostasis of blood calcium level is regulated by calcitonin and PTH.

4. Calcium ion delivery through the blood is essential for normal excitability of neurons and muscle cells and for the process of blood clotting.

v. Adrenal Medulla

1. The catecholamines (epinephrine and norepinephrine), released by the adrenal medulla, are sympathomimetic, meaning they mimic the sympathetic nervous system.

2. During stress, the hypothalamus stimulates their release to prolong the body’s stress (fight or flight) response.

vi. Adrenal Cortex

1. The adrenal cortex secretes three types of steroid hormones: mineralocorticoids, glucocorticoids, and gonadocorticoids (“sex steroids”).

2. Aldosterone is the most abundant of the mineralocorticoids, and its target organs are the kidneys.

a. Aldosterone increases the reabsorption of sodium ions and the excretion of potassium ions by the kidney tubules.

b. As sodium ions are reabsorbed, hydrogen ions may be excreted in exchange.

i. This is one mechanism to prevent the accumulation of hydrogen ions, which would lead to acidosis.

ii. Also, as sodium ions are reabsorbed, water follows; this is important for maintaining normal blood volume and blood pressure.

3. Cortisol is the most abundant of the glucocorticoids and has many target tissues.

a. It stimulates gluconeogenesis in the liver and increases lipolysis and protein catabolism for energy production.

3

b. By providing energy sources to body tissues, cortisol ensures that glucose will be available for the brain (glucose-sparing effect).

c. Cortisol release is increased during response to stress.

4. The hypothalamus causes secretion of ACTH by the anterior pituitary, which increases cortisol secretion by the adrenal cortex.

a. The resultant increase in energy availability is necessary for stress-induced changes. Cortisol also has an anti-inflammatory effect.

b. However, excess cortisol decreases the immune response and can delay healing of damaged tissue.

5. The gonadocorticoids are small amounts of male androgens.

a. In females, they are converted to estrogens.

i. They are the only source of estrogen after menopause.

b. In both genders, they contribute to libido (sexual desire)

vii. Pancreas

1. The pancreas is both an exocrine and endocrine gland.

a. As an endocrine gland, the pancreas secretes insulin and glucagon for blood glucose homeostasis.

i. It also secretes somatostatin, which inhibits both insulin and glucagon.

2. Hypoglycemia stimulates alpha cells to release glucagon.

a. Glucagon raises blood glucose, making it available to cells.

3. Hyperglycemia stimulates beta cells to release insulin.

a. Insulin increases the movement of glucose from the blood into cells.

i. This lowers blood glucose and makes glucose available to cells for energy.

4. Hyperglycemia occurs after meals, especially those high in carbohydrates.

5. Insulin and glucagon function as antagonists; normal secretion of both hormones ensures a blood glucose level that varies within normal limits.

B. Know the function of EACH hormone produced

i. Hormones of the Posterior Pituitary Gland

1. Antidiuretic hormone (ADH, or vasopressin)

a. Increases water reabsorption by the kidney tubules (water returns to the blood)

b. Decreases sweating

c. Causes vasoconstriction (in large amounts)

2. Oxytocin

a. Promotes contraction of myometrium of uterus (during labor)

4

b. Promotes release of milk from mammary glands

ii. Hormones of the Anterior Pituitary Gland

1. Growth hormone (GH)

a. Increases rate of mitosis

b. Increases amino acid transport into cells

c. Increases rate of protein synthesis

d. Increases use of fats for energy

2. Thyroid-stimulating hormone (TSH)

a. Increases secretion of triiodothyronine (T3) and thyroxine (T4) by thyroid gland

3. Adrenocorticotropic hormone (ACTH)

a. Increases secretion of cortisol by the adrenal cortex

4. Prolactin

a. Stimulates milk production by the mammary glands

5. Follicle-stimulating hormone (FSH)

a. In women:

i. Initiates growth of ova in ovarian follicles

ii. Increases secretion of estrogen by follicle cells

b. In men:

i. Initiates sperm production in the testes

6. Luteinizing Hormone (LH)

a. In women:

i. Causes ovulation

ii. Causes the ruptured ovarian follicle to become the corpus luteum

iii. Increases secretion of progesterone by the corpus luteum

b. In men:

i. Increases secretion of testosterone by the interstitial cells of the testes

iii. Hormones of the Thyroid Gland

1. Thyroxine and triiodothyronine (T3 & T4)

a. Increase energy production from all food types

b. Increase rate of protein synthesis

2. Calcitonin

a. Decrease the reabsorption of calcium and phosphate from bones to blood

iv. Hormones of the Parathyroid Gland

1. Parathyroid hormone (PH)

5

a. Increase the reabsorption of calcium and phosphate from bone to blood

b. Increases absorption of calcium and phosphate by the small intestine

c. Increases the reabsorption of calcium and the excretion of phosphate by the kidneys; activates vitamin D

v. Hormones of the Adrenal Medulla

1. Epinephrine, norepinephrine

a. Increases heart rate and force of contraction

b. Dilates bronchioles

c. Decreases peristalsis

d. Increases conversion of glycogen in glucose in the liver

e. Causes vasodilation in skeletal muscles

f. Causes vasoconstriction in skin and viscera

g. Increases use of fats for energy

h. Increases the rate of cell respiration

vi. Hormones of the Intestine

1. Glucagon-like peptide (GLP-1)

2. Gastric inhibitory polypeptide (GIP)

a. Regulate blood sugar by increasing insulin secretion and decreasing glucagon secretion from the pancreas

vii. Hormones of the Pancreas

1. Glucagon (alpha cells)

a. Increases conversion of glycogen to glucose in the liver

b. Increases the use of excess amino acids and fats for energy

2. Insulin (beta cells)

a. Increases glucose transport into cells and the use of glucose for energy production

b. Increases the conversion of excess glucose to glycogen in the liver and muscles

c. Increases amino acid and fatty acid transport into cells, and their use in synthesis reactions

3. Somatostatin (delta cells)

a. Decreases secretion of insulin and glucagon

b. Slows absorption of nutrients

viii. Hormones of the Adrenal Cortex

1. Aldosterone

a. Increases reabsorption of Na+ (sodium) ions by the kidneys to the blood

6

b. Increases excretion of K+ (potassium) ions by the kidneys in urine

2. Cortisol

a. Increases use of fats and excess amino acids for energy

b. Decreases use of glucose for energy (except for the brain)

c. Increases conversion of glucose to glycogen in the liver

d. Anti-inflammatory effect: stabilizes lysosomes and blocks the effects of histamine

C. Know where each hormone is produced (anterior/posterior pituitary)

i. Listed above.

D. How does aging effect the endocrine system

i.

E. Know key terms, learning tips, tables, and charts

i. Affect: emotional tone

ii. Exophthalmos: abnormal protrusion of the eyeball

7

2. CHAPTER 39

A. What are the disorders that effect the pituitary, how do you care for clients with these disorders?

i. Diabetes Insipidus

1. Pathophysiology:

a. DI is unrelated to diabetes mellitus.

i. Diabetes mellitus is caused by insulin-resistant tissue or insufficient insulin production.

1. DI is caused by a deficiency of ADH.

2. If ADH is lacking, adequate reabsorption of water is prevented, leading to diuresis.

ii. Patients can urinate from 3 to 15 L per day.

1. This leads to dehydration and increased serum osmolality (concentrated blood).

b. The increased osmolality and decreased blood pressure normally trigger ADH secretion, which causes water retention and dilutes the blood; in patients with DI, this does not happen.

i. Increased osmolality also leads to extreme thirst, which usually causes the patient to drink enough fluids to maintain fluid balance.

ii. In an unconscious patient or a patient with a defective thirst mechanism, however, dehydration can quickly occur if the problem is not recognized and corrected.

2. Nursing Care

a. When collecting data for a patient with DI, pay special attention to fluid balance.

b. Daily weights are the most reliable method for monitoring the amount of fluid that is being lost.

c. Taking accurate intake and output (I&O) measurements is also helpful.

d. Skin turgor will be poor, and mucous membranes will be dry and sticky if the patient is becoming dehydrated.

e. Monitor skin integrity because dehydration increases risk of breakdown.

f. Monitor vital signs for signs of shock.

g. Use a reagent strip (dipstick) or urinometer to measure urine specific gravities.

h. Monitor serum electrolytes and osmolality as ordered and watch for changes in level of consciousness.

8

i. Assess the patient’s understanding of his or her disease and treatment.

i. Once treatment is initiated, continue to monitor fluid balance, being especially alert to signs of fluid overload.

ii. Syndrome of Inappropriate Antidiuretic Hormone

1. Pathophysiology

a. SIADH results from too much ADH in the body.

i. This causes excess water to be reabsorbed by the kidney tubules and collecting ducts and back into the blood, leading to decreased urine output and fluid overload.

ii. As fluid builds up in the bloodstream, osmolality decreases, and the blood becomes diluted.

iii. Normally, decreased serum osmolality inhibits release of ADH.

iv. In SIADH, however, ADH continues to be released, adding to the fluid overload.

2. Nursing Care

a. Excess fluid volume with hyponatremia is the primary concern for the patient with SIADH.

b. To monitor fluid balance, assess vital signs, daily weight, I&O, urine specific gravity, and skin turgor.

c. Edema and pulmonary crackles are not typically present.

d. Determine the patient’s ability to maintain a fluid restriction.

e. Assess level of consciousness and neuromuscular function.

f. Monitor laboratory tests, including serum sodium level, as ordered by the HCP.

g. Assess the patient’s understanding of the disease process and treatment.

iii. Growth Hormone Deficiency

1. Pathophysiology

a. When GH is deficient in childhood, a condition called short stature occurs.

i. In the past, this was referred to as dwarfism.

b. A deficiency of GH in adults does not affect growth, but in recent years GH has been found to have important functions even during adulthood.

2. Nursing Care

a. Assessment of the adult with GH deficiency includes mental status, ability to cope with the effects of the disorder, and understanding of the treatment plan.

9

b. Assess all patients for signs of cardiovascular disease and other complications of the disorder.

iv. Acromegaly

1. Pathophysiology

a. Acromegaly occurs because of overproduction of GH in an adult.

b. Bones increase in size, leading to enlargement of facial features, hands, and feet.

c. Long bones grow in width but not length because the epiphyseal disks are closed.

d. Subcutaneous connective tissue increases, causing a fleshy appearance.

e. Internal organs and glands enlarge.

f. Impaired tolerance of carbohydrates leads to elevated blood glucose.

B. What are the disorders that effect the thyroid, how do you care for clients with these disorders?

i. Hypothyroidism

1. Pathophysiology

a. Primary hypothyroidism occurs when the thyroid gland fails to produce enough TH even though enough thyroid-stimulating hormone (TSH) is being secreted by the pituitary gland.

b. The pituitary gland responds to the low level of TH by producing more TSH.

c. Secondary hypothyroidism is caused by low levels of TSH, which fail to stimulate release of TH.

d. Tertiary hypothyroidism results from inadequate release of thyrotropin-releasing hormone (TRH), secreted by the hypothalamus.

e. Most cases of hypothyroidism are primary.

f. Because thyroid hormones are responsible for metabolism, low levels of these hormones result in a slowed metabolic rate, which causes many of the characteristic symptoms of hypothyroidism.

ii. Hyperthyroidism

1. Pathophysiology

a. Hyperthyroidism results in excessive amounts of circulating TH (thyrotoxicosis).

b. Primary hyperthyroidism occurs when a problem within the thyroid gland causes excess hormone release.

10

c. Secondary hyperthyroidism occurs because of excess TSH release from the pituitary gland, causing overstimulation of the thyroid gland.

d. Tertiary hyperthyroidism is caused by excess TRH from the hypothalamus.

e. A high level of TH increases the metabolic rate.

i. It also increases the number of beta-adrenergic receptor sites in the body, which enhances the activity of epinephrine and norepinephrine.

ii. The resulting fight-or-flight response is the cause of many of the symptoms of hyperthyroidism.

2. Nursing Care

a. Monitor the patient with hyperthyroidism closely until normal thyroid activity is restored.

b. Assess vital signs and lung sounds, and report changes to the RN or HCP.

c. Assess level of anxiety and ability to cope with symptoms.

d. Monitor weight, bowel function, and ability to sleep.

e. Assess eyes for risk for injury caused by exophthalmos, and note degree of muscle weakness.

f. Never palpate the thyroid gland of a patient with hyperthyroidism because palpation can stimulate release of thyroid hormone and precipitate a thyrotoxic crisis.

iii. Goiter

1. Pathophysiology

a. Enlargement of the thyroid gland is called a goiter.

b. The thyroid gland may enlarge in response to increased TSH levels or sometimes in response to the autoimmune process that occurs in Graves disease.

c. TSH is elevated in response to low TH, iodine deficiency, pregnancy, or viral, genetic, or other conditions.

d. When a goiter is caused by iodine deficiency or other environmental factors, it is called an endemic goiter.

e. Some medications are goitrogens. 

i. These substances interfere with the body’s use of iodine.

ii. Some goitrogenic  medications include propylthiouracil, sulfonamides, lithium, and salicylates (aspirin).

f. A goiter can be associated with a hyperthyroid, hypothyroid, or euthyroid state.

11

i. A goiter that occurs with hyperthyroidism is sometimes called a toxic goiter.

ii. Once the cause of the goiter is removed, the gland usually returns to normal size.

2. Nursing Care

a. Be careful to assess the effect of the goiter on breathing and swallowing.

b. Stridor, a whistling sound, may be heard if the airway is obstructed.

i. Stridor is an ominous sign and should be reported to the HCP immediately.

c. If the patient experiences difficulty swallowing, notify the HCP and collaborate with the dietitian to provide soft foods that are easy to swallow.

i. A swallowing study might be ordered.

ii. This will assist a speech pathologist or other expert in making specific recommendations for safe swallowing.

C. What are the disorders that effect the parathyroid, how do you care for clients with these disorders?

i. Hypoparathyroidism

1. Pathophysiology

a. A decrease in PTH causes a decrease in bone resorption of calcium, a decrease in calcium absorption by the gastrointestinal tract, and decreased resorption in the kidneys.

i. This means that calcium stays in the bones instead of being moved into the blood, and more calcium is excreted from the body.

ii. The result is a decreased serum calcium level, called hypocalcemia.

iii. As calcium levels fall, phosphate levels rise.

2. Nursing Care

a. Closely monitored for symptoms of tetany.

b. If you suspect tetany, check for Chvostek and Trousseau signs.

c. Monitor respirations closely for stridor, a sign of laryngospasm.

ii. Hyperparathyroidism

1. Pathophysiology

a. Overactivity of one or more of the parathyroid glands causes an increase in PTH, with a subsequent increase in the serum calcium level (hypercalcemia).

12

i. This is achieved through movement of calcium out of the bones and into the blood, absorption in the small intestine, and reabsorption by the kidneys.

ii. PTH also promotes phosphorus excretion by the kidneys.

2. Nursing Care

a. Assess the patient for symptoms related to hypercalcemia, including muscle weakness, lethargy, bone pain, anorexia, nausea, vomiting, behavioral changes, and renal insufficiency.

b. Monitor serum calcium levels as ordered.

D. What are the disorders that effect the adrenal glands, how do you care for clients with these disorders?

i. Pheochromocytoma

1. Pathophysiology

a. A pheochromocytoma is a rare tumor of the adrenal medulla that secretes excess catecholamines (epinephrine and norepinephrine).

b. Most pheochromocytomas are benign.

ii. Adrenocortical Insufficiency/Addison Disease

1. Pathophysiology

a. AI is associated with reduced levels of cortisol, aldosterone, or both hormones.

i. A deficiency in androgens may also exist.

b. In primary disease, adrenocorticotropic hormone (ACTH) levels from the pituitary gland can be elevated in an attempt to stimulate the adrenal cortex to synthesize more hormone.

c. In secondary disease, deficient ACTH fails to stimulate adrenal steroid synthesis.

d. In most cases, the adrenal glands are atrophied, small, and misshapen and are unable to produce adequate amounts of hormone.

2. Nursing Care

a. The patient with Addison disease should be assessed for understanding of and adherence to the treatment regimen.

b. Monitor vital signs and daily weights or I&O to track fluid status.

c. Monitor serum glucose levels and symptoms of hyperkalemia and hyponatremia.

d. Report changes in mental status.

e. If the patient is in crisis, monitor vital signs closely and report any signs of fluid volume deficit such as orthostatic hypotension or poor skin turgor to the HCP immediately.

iii. Cushing Syndrome

13

1. Pathophysiology

a. Cortisol is hypersecreted without regard to stress or time of day.

i. When levels of cortisol are very high, effects related to excess aldosterone and androgens are also seen.

2. Nursing Care

a. Assess the patient’s medication history.

b. Monitor vital signs and complications related to fluid and sodium excess.

c. Auscultate the lungs for crackles and assess extremities for edema.

d. Assess skin integrity, and monitor capillary glucose as ordered by the HCP.

e. Watch for signs of infection.

E. Know s/s of each disorder of each gland

i. Diabetes Insipidus

1. Signs and Symptoms

a. Urinates Frequently (polyuria), and night time urination (nocturia) is present.

i. This results in high serum osmolality and low urine osmolality.

ii. Urine specific gravity is decreased, making the urine dilute and light in color.

b. The patient experiences extreme thirst (polydipsia), and consumes large volumes of water.

i. Often patients crave ice-cold water.

c. If urine output exceeds fluid intake, dehydration occurs, with characteristic symptoms of hypotension, poor skin turgor, and weakness.

i. Hypovolemic shock occurs if fluid balance is not restored.

d. Dehydration and electrolyte imbalances result in a decrease in level of consciousness and death if the problem is not corrected.

ii. Syndrome of Inappropriate Antidiuretic Hormone

1. Signs and Symptoms

a. Fluid overload, such as weight gain (usually without edema) and dilutional hyponatremia.

i. The actual amount of sodium in the blood may be normal, but it appears to be low because of the diluting effect of the extra fluid.

b. Serum osmolality is less than 275 mOsm/kg.

c. The urine is concentrated because water is not being excreted.

14

d. Electrolyte imbalance can cause muscle cramps and weakness.

e. Because the osmolality of the blood is low, fluid can leak out of the vessels and cause brain swelling.

f. If untreated, this results in lethargy, confusion, seizures, coma, and death.

iii. Growth Hormone Deficiency

1. Children may grow to only 3 to 4 feet in height but have normal body proportions.

2. Sexual maturation may be slowed, related to involvement of additional pituitary hormones.

3. Short stature in children is sometimes accompanied by mental retardation.

4. In adults, symptoms of GH deficiency include fatigue, weakness, excess body fat, decreased muscle and bone mass, sexual dysfunction, high cholesterol, and increased risk for cardiovascular and cerebrovascular disease.

5. Headaches, mental slowness, and psychological disturbances may also occur.

6. All of these signs and symptoms can lead to decreased quality of life.

iv. Acromegaly

1. Symptoms develop very slowly, and the disorder may be present for years before it is recognized.

2. Often the first symptom noticed is a change in ring or shoe size.

3. The nose, jaw, brow, hands, and feet enlarge

4. The teeth may be displaced, causing difficulty chewing, or dentures may no longer fit.

5. The tongue becomes thick, causing difficulty in speaking and swallowing (dysphagia).

6. The patient may develop sleep apnea.

7. Visual disturbances can occur because of tumor pressure on the optic nerve.

8. Headaches result from tumor pressure on the brain.

9. Diabetes mellitus may develop because GH increases blood glucose and causes an increased workload for the pancreas

10. With treatment, soft tissues reduce in size, but bone growth is permanent.

v. Hypothyroidism

1. Manifestations are related to the reduced metabolic rate and include fatigue, weight gain, bradycardia, constipation, mental dullness, feeling cold, shortness of breath, decreased sweating, and dry skin and hair

15

2. Heart failure may occur because of decreased pumping strength of the heart.

3. Altered fat metabolism causes hyperlipidemia, which can lead to cardiovascular disease.

4. In advanced disease, myxedema develops, which is a nonpitting edema of the face, hands, and feet.

vi. Hyperthyroidism

1. Many signs and symptoms are related to the hypermetabolic state, such as heat intolerance, increased appetite with weight loss, and increased frequency of bowel movements.

2. Nervousness, tremor, tachycardia, and palpitations are caused by the increase in sympathetic nervous system activity and may be more common in younger patients.

3. Heart failure can occur because of tachycardia and the resulting inefficient pumping of the heart.

4. If treatment is not begun, the patient can become manic or psychotic.

5. Additional signs that occur only with Graves disease include thickening of the skin on the anterior legs and exophthalmos (bulging of the eye) caused by swelling of the tissues behind the eyes.

6. Other eye changes include photophobia and blurred or double vision.

7. Older adult patients may not have the typical signs and symptoms of hyperthyroidism, so be especially alert for this.

8. These patients may present with heart failure, atrial fibrillation, fatigue, apathy, and depression.

vii. Goiter

1. The thyroid gland is enlarged, and swelling may be apparent at the base of the neck.

2. Alternatively, the gland may enlarge posteriorly, which can interfere with swallowing or breathing.

3. The patient may have a full sensation in the neck.

4. Symptoms of hypothyroidism or hyperthyroidism may be present.

viii. Hypoparathyroidism

1. Calcium plays an important role in nerve cell stability.

2. Hypocalcemia causes neuromuscular irritability.

3. In acute cases, tetany can occur, with numbness and tingling of the fingers, tongue, and lips; muscle spasms; and twitching.

4. Positive Chvostek and Trousseau signs are early indications of tetany.

5. Chronic hypocalcemia can lead to lethargy; calcifications in the brain, leading to psychosis; cataracts; and convulsions.

6. Bone changes may be evident on x-ray examination.

16

7. Electrocardiogram (ECG) changes and heart failure can develop because of the importance of calcium to cardiac function.

8. Death can result from laryngospasm if treatment is not effective.

ix. Hyperparathyroidism

1. Signs and symptoms of hyperparathyroidism are caused primarily by the increase in the serum calcium level, although many patients are asymptomatic.

2. Symptoms include fatigue, depression, confusion, increased urination, anorexia, nausea, vomiting, kidney stones, and cardiac arrhythmias.

3. The increased serum calcium level also causes gastrin secretion, resulting in abdominal pain and peptic ulcers.

a. Because calcium is being removed from bones, bone and joint pain and pathological fractures can occur.

b. Severe hypercalcemia can result in coma and cardiac arrest.

x. Pheochromocytoma

1. Because norepinephrine is the fight-or-flight hormone, patients with a pheochromocytoma have exaggerated fight-or-flight symptoms.

2. Manifestations include hypertension, tachycardia (with heart rate greater than 100 beats per minute), palpitations, tremor, diaphoresis, feeling of apprehension, and severe pounding headache.

3. The most prominent characteristic is intermittent unstable hypertension.

4. Diastolic pressure may be greater than 115 mm Hg.

5. If hypertension and tachycardia are not controlled, the patient is at risk for stroke, heart attack and heart failure, vision changes, seizures, psychosis, and organ damage.

xi. Adrenocortical Insufficiency/Addison Disease

1. The most significant sign of Addison disease is hypotension.

a. This is related to the lack of aldosterone.

2. Remember that aldosterone causes sodium and water retention in the kidney and potassium loss.

3. If aldosterone is deficient, sodium and water are lost and hypotension and tachycardia result.

4. Low cortisol levels cause hypoglycemia, weakness, fatigue, weight loss, confusion, and psychosis.

5. In primary AI, increased ACTH may produce hyperpigmentation of the skin, causing the patient to have a tanned or bronze appearance.

6. Anorexia, nausea, and vomiting may also occur, possibly as the result of electrolyte imbalances.

7. Women may have decreased body hair because of low androgen levels.

17

8. Patients may report craving salt.

xii. Cushing Syndrome

1. Most signs and symptoms of Cushing syndrome are related to excess cortisol levels.

2. Weight gain, central obesity with thin arms and legs, fat pads on the upper back (buffalo hump), and a round, moon-shaped face result from deposits of adipose tissue at these sites

3. Cortisol also causes insulin resistance and stimulates gluconeogenesis, which results in glucose intolerance.

a. Some patients develop secondary diabetes mellitus

4. Muscle wasting and thin skin with purple striae occur as a result of cortisol’s catabolic effect on tissues.

5. Catabolic effects on bone lead to osteoporosis, pathological fractures, and back pain from compression fractures of the vertebrae.

6. Because cortisol has anti-inflammatory and immunosuppressive actions, the patient is at risk for infection.

7. Hyperpigmentation of the skin may occur.

8. About half of patients develop mental status changes, from irritability to psychosis (sometimes referred to as steroid psychosis).

9. Sodium and water retention are related to the mineralocorticoid effect.

10. As sodium is retained, potassium is lost in the urine, causing hypokalemia.

11. Androgen effects include acne, growth of facial hair, and amenorrhea (absence of menses) in women.

F. Know therapeutic measure to care for each disorder of each gland

i. Diabetes Insipidus

1. Hypotonic intravenous (IV) fluids such as 0.45% saline solution may be ordered to replace intravascular volume without adding extra sodium.

2. IV fluids are especially important if the patient is unable to take oral fluids.

3. Medical treatment of DI involves replacement of ADH.

4. In acute cases, vasopressin, a synthetic form of ADH, is given via the IV or subcutaneous route, along with IV fluid replacement.

5. In patients who require long-term therapy, synthetic ADH (desmopressin, or DDAVP) can be administered orally, subcutaneously, or intranasally.

6. Thiazide diuretics may decrease urine flow in the absence of ADH (even though they usually are used to increase urine output).

7. If a pituitary tumor is involved, treatment usually involves removal of the pituitary gland (hypophysectomy).

18

ii. Syndrome of Inappropriate Antidiuretic Hormone

1. Treatment is aimed at the underlying cause.

2. If a tumor is secreting ADH, surgical removal may be indicated.

3. Symptoms can be alleviated by restricting fluids to 800 to 1000 mL per 24 hours.

4. Hypertonic saline fluids may be administered via IV, and an oral sodium tablet may be prescribed to maintain the serum sodium level.

5. A loop diuretic such as furosemide (Lasix) increases water excretion.

6. A vasopressin receptor antagonist such as conivaptan (Vaprisol) may be used to block the action of ADH in the kidney.

iii. Growth Hormone Deficiency

1. Treatment of GH deficiency is administration of GH.

2. In the past, GH was derived from human pituitary glands, so treatment was expensive and risky.

3. Now GH, or somatropin (Humatrope), can be made in a laboratory using recombinant DNA technology, so it is more readily available to those who need it.

4. It is administered by subcutaneous injection.

5. Surgery may be indicated if a tumor is the cause.

iv. Acromegaly

1. Treatment may include medications to block GH or hypophysectomy.

2. Radiation may be indicated if a tumor is the cause.

v. Hypothyroidism

1. Primary hypothyroidism is easily treated with oral thyroid replacement hormone.

2. Most patients now take synthetic thyroid hormone (levothyroxine [Synthroid]).

3. Doses are started low and slowly increased to prevent symptoms of hyperthyroidism or cardiac complications.

vi. Hyperthyroidism

1. Methimazole (Tapazole) inhibits the synthesis of TH, but it may take several months to be effective and must be continued for 12 to 18 months.

2. Beta blockers relieve sympathetic nervous system symptoms.

3. Calcium and vitamin D are given to protect bones.

4. Radioactive iodine (131I, or RAI) may be used to destroy a portion of the thyroid gland.

a. The patient takes one oral dose of RAI.

19

b. Dietary iodine normally goes to the thyroid gland, where it is used to make TH.

c. When RAI is given, the radioactivity destroys some of the cells that make TH.

d. Sometimes medications or RAI alone can control hyperthyroidism.

e. If this does not occur, surgery is planned.

5. Prior to surgery, antithyroid medications are prescribed to calm the thyroid.

a. They help slow the heart rate and reduce other symptoms, making surgery safer.

6. Oral iodine reduces the vascularity of the thyroid gland, decreasing the risk of bleeding during surgery.

7. Adequate preparation of the patient is important because a euthyroid state helps prevent a postoperative thyrotoxic crisis.

8. Thyroidectomy can be done with a traditional, open approach or with newer minimally invasive techniques that use a combination of a tiny incision and an endoscope.

a. Patients can usually go home the same day and have a faster recovery time with minimally invasive surgery.

b. The surgeon may choose to leave some of the thyroid gland intact, to continue to secrete some hormone.

c. Following surgery, the patient will likely be hypothyroid and will require thyroid replacement hormone (levothyroxine [Synthroid]).

d. Nursing care of the patient undergoing a thyroidectomy is discussed later in this chapter.

9. If vision is impaired from exophthalmos, surgical orbital decompression can be done. Current endoscopic techniques have made this a safer option than in the past.

vii. Goiter

1. Treatment is aimed at the cause.

2. Consult the HCP if goitrogenic medications are being used.

3. If iodine deficiency is a problem, it is added to the diet with supplements or iodized salt.

4. Hypothyroidism or hyperthyroidism is treated if indicated.

5. Levothyroxine (Synthroid) may be given to reduce TSH levels via negative feedback.

6. RAI therapy or thyroidectomy may be needed to treat hyperthyroid symptoms or if the enlarged gland is interfering with breathing or swallowing.

20

viii. Hypoparathyroidism

1. Acute cases of hypoparathyroidism are treated with IV calcium gluconate.

2. Long-term treatment includes a high-calcium diet , with oral calcium and vitamin D supplements.

3. Magnesium is given if hypomagnesemia is present.

ix. Pheochromocytoma

1. Treatment for pheochromocytoma is surgical removal of one or both adrenal glands.

2. Calcium channel blockers, alpha blockers, and beta blockers are used to control symptoms.

3. Teach the patient to avoid caffeine and other stimulants prior to surgery.

4. After surgery, the patient is at risk for hypotension, hypertension, and hypoglycemia.

5. Monitor vital signs and blood glucose, and report variations from normal.

6. If both adrenal glands have been entirely removed, the patient will require lifelong replacement hormones. 

x. Addison Disease

1. Long-term treatment consists of replacement of glucocorticoids (hydrocortisone) and mineralocorticoids (fludrocortisone [Florinef]). Some patients also receive androgen therapy.

2. Patients will need hormone replacement therapy for the rest of their lives.

3. Hormones are given in divided doses, with two-thirds of the daily dose given in the morning and one-third in the evening to mimic the body’s own diurnal rhythm.

4. Remember that steroid hormones are our natural stress hormones and so are naturally elevated during times of stress.

5. Therefore, during times of stress or illness, doses need to be increased to two to three times normal.

6. The patient may also be placed on a high-sodium diet.

7. If the patient is ill and can’t tolerate oral medication, hormones must be injected.

xi. Cushing Syndrome

1. If a pituitary or ACTH-secreting tumor is present, surgical removal or radiation therapy to the pituitary gland may be employed.

2. If the adrenal glands are the primary cause of the problem, radiation or removal of the adrenal gland or glands may be performed.

21

3. Drugs such as ketoconazole can be used to block production of adrenal steroids.

4. If the cause of Cushing syndrome is administration of steroid medication, a lower dose, an every-other-day schedule, or once-a-day dosing in the morning may reduce side effects.

5. Usually steroids are prescribed as a last resort for chronic disorders that are unresponsive to other treatment.

6. The patient and HCP must weigh the risks and benefits of continuing the medication.

7. The HCP may order a high-potassium, low-sodium, high-protein diet.

8. Potassium supplements may be ordered.

9. If the patient has high blood sugar, appropriate therapy for diabetes is instituted

G. How will you know if your care is effective or working?

i. Diabetes Insipidus

1. If treatment has been effective, signs of dehydration will be absent, and weight and vital signs will be stable.

ii. Inappropriate Antidiuretic Hormone

1. Weight should stabilize at the pre-illness level once treatment is begun.

2. Serum sodium level should be within normal limits.

iii. Growth Hormone Deficiency

1. Nursing care has been effective if the patient is able to demonstrate self-administration of GH and describe plans for related self-care activities.

iv. Hyperthyroidism

1. If the plan of care is effective, the patient will remain free from complications and injury.

2. Vital signs will be within normal limits.

3. Diarrhea will be controlled, and complications of diarrhea such as skin breakdown and dehydration will be avoided.

4. The patient’s weight should remain stable.

5. The patient should report that he or she is rested on awakening and that anxiety is controlled.

v. Hypoparathyroidism

1. If the plan is effective, symptoms of hypercalcemia will be recognized and reported quickly, and complications and injury will be prevented.

vi. Addison’s

22

1. If nursing care is effective, the patient’s fluid status will be stable, and the patient and family will be able to carry out proper self-care of Addison disease.

vii. Cushing’s

1. If care has been effective, complications of fluid overload will be recognized and treated early.

2. The patient will have intact skin and be free from signs of infection.

3. The patient will demonstrate skill in self-care of diabetes if indicated and will verbalize acceptance of self despite changes in appearance.

H. Know key terms, learning tips, tables, and charts

i. Amenorrhea : the absence or suppression of menstruation. Amenorrhea is normal before puberty, after menopause, and during pregnancy and lactation.

ii. Ectopic: Out of normal position. For example, ectopic hormones are secreted from sites other than the gland where they would normally be found.

iii. Euthyroid : normal thyroid function

iv. Goitrogens: Foods or medications that cause a goiter

v. Hyperplasia: Excessive increase in the number of normal cells.

vi. Hypophysectomy : Surgical removal of the pituitary gland.

vii. Myxedema: Condition resulting from hypofunction of the thyroid gland.

viii. Nocturia: Excessive urination at night.

ix. Osmolality : Osmotic concentration; ionic concentration of the dissolved substances per unit of solvent.

x. Pheochromocytoma: Rare tumor of the adrenal system that secretes catecholamines.

xi. Polydipsia: Excessive thirst.

xii. Polyuria : Excessive urination.

xiii. Tetany : Muscle spasms, numbness, and tingling caused by changes in pH and low serum calcium.

3. CHAPTER 40

A. What is the cause of Type 1 DM

i. Is caused by destruction of the beta cells in the islets of Langerhans of the pancreas. 

B. What is the cause of Type 2 DM

i. In type 2 diabetes, tissues are resistant to insulin.

ii. Insulin is still made by the pancreas but in inadequate amounts.

iii. Sometimes, the amount of insulin is normal or even high, but because the tissues are resistant to it, hyperglycemia results.

23

iv. As the disease advances, the pancreas eventually wears out, leading to little or no insulin secretion.

C. Know the risk factors for Type 1 & Type 2

i. Heredity

ii. Obesity is a major contributing factor.

iii. Often the patient with a new diagnosis of type 2 diabetes is obese, relates a family history of diabetes, and has had a recent life stressor, such as the death of a family member, illness, or loss of a job

D. What are the s/s of DM (both types)

i. Classic symptoms of diabetes include polydipsia (excessive thirst), polyuria (excessive urination), and polyphagia (excessive hunger).

ii. The excess glucose in the blood causes an increase in serum concentration, or osmolality.

iii. The renal tubules are unable to reabsorb all the extra glucose that is filtered by the glomeruli, and glycosuria results.

iv. Large amounts of body water are required to excrete this glucose, causing polyuria, nocturia (nighttime urination), and dehydration.

v. Increased osmolality and dehydration cause polydipsia.

vi. Because glucose is unable to enter the cells, the cells starve, causing polyphagia.

vii. High BG can also cause fatigue, blurred vision, abdominal pain, and headaches.

viii. Ketones (acidic by-products of fat breakdown) can build up in the blood and urine of patients with type 1 diabetes or late in the course of type 2 diabetes (ketoacidosis).

E. How do you treat hypoglycemia & hyperglycemia

i. Hyperglycemia:

1. Confirm hyperglycemia with glucose meter; if patient is at risk, check urine for ketones and increase fluid intake.

2. Assess cause of hyperglycemia, and teach prevention.

3. Return to prescribed treatment plan if applicable.

4. Call health care provider (HCP) for medication adjustment if indicated or if blood glucose exceeds 180 mg/dL for 2 days.

5. Call HCP if patient is ill or vomiting.

ii. Hypoglycemia :

1. Confirm hypoglycemia with glucose meter (if able).

2. Administer 15 g fast-acting carbohydrate.

3. Recheck glucose in 15 minutes. If still low, readminister carbohydrate.

4. Continue cycle of checking glucose and administering fast sugar until hypoglycemia subsides. If symptoms worsen, call HCP or emergency help.

24

5. Administer glucagon subcutaneously or dextrose 50% via intravenous route if ordered.

6. Assess cause of hypoglycemia, and teach prevention.

F. What are the risk associated with DM both types

i. Listed previously.

G. Know values for HgA1C, blood sugar (random, fasting, etc)

i. Random Blood Glucose

1. Sometimes it is not feasible to check a fasting BG.

2. A random BG (RPG) is checked without regard to the last meal.

3. Diabetes is diagnosed if the RPG is 200 mg/dL or greater, with symptoms of diabetes.

ii. Fasting Blood Glucose Level

1. Diagnosis of diabetes is based on BG levels measured by a laboratory.

2. A normal BG level is less than 100 mg/dL.

3. When the fasting BG (drawn after at least 8 hours without eating) is 126 mg/dL or higher, diabetes is diagnosed.

4. A second test may be required if the first test is not clearly diagnostic.

5. If the fasting BG is between 100 and 125 mg/dL, the patient has impaired fasting glucose (IFG) and prediabetes

HbA1c (%) Fasting Blood Glucose (mg/dL)6 1267 1548 1839 21210 24011 26912 298

H. Know your insulins

Very short-acting

Insulin lispro(Humalog) Insulin aspart(NovoLog) Insulin glulisine (Apidra)Inhaled insulin (Afrezza)

Short-acting Insulin regular (Humulin R, Novolin R)Intermediate-

actingInsulin neutral protamine Hagedorn

(NPH) (Humulin N, Novolin N)Basal Insulin glargine (Lantus AE)

25

Insulin detemir (Levemir)

i.

I. Know oral hypoglycemics

i. The patient with type 2 diabetes may be able to control BG levels with nutrition therapy and exercise alone.

ii. If needed, oral hypoglycemic medication or insulin will also be prescribed.

iii. Oral hypoglycemic agents are not insulin pills but work to produce more insulin (e.g., by stimulating the pancreas) or make the tissues more sensitive to insulin.

iv. Because many oral hypoglycemic agents depend on at least a partially functioning pancreas, they are not useful for patients with type 1 diabetes.

v. Most oral hypoglycemic agents should be administered before meals.

vi. Care should be taken to prevent passage of more than 30 minutes between medication administration and the meal because this may result in a hypoglycemic episode.

vii. Check individual drugs for specific timing.

viii. If the BG level is not controlled with an oral hypoglycemic agent, insulin may be needed for the person with type 2 diabetes.

ix. However, the goal of insulin use is different than for the person with type 1 diabetes:

x. While insulin may be needed to control BG, insulin is not needed to sustain life as is the case for the person with type 1 diabetes.

J. How will you keep your diabetics safe? *what will you be TEACHING*

i. The individual with diabetes must receive diabetes self-management education if at all possible.

ii. No amount of care from an HCP or nurse can replace the self-care required of the person with diabetes.

iii. The involvement of family or significant others is also important for the successful treatment and well-being of the person with diabetes.

iv. If the patient is hospitalized at diagnosis, initial instruction is done in the hospital.

v. However, hospital stays are so short, you cannot waste any time.

vi. Begin assessing baseline knowledge and teaching as soon as the patient is feeling physically well enough to learn.

vii. Depending on your state nurse practice act, this may be the responsibility of the primary or registered nurse, although aspects of the instruction may be delegated to the LPN/LVN.

viii. Some hospitals have a certified diabetes educator who provides classroom or bedside instruction.

ix. The dietitian should be contacted to provide nutrition instruction.

26

x. Most hospitals have policies or management plans describing the instruction to be provided by the nurse.

xi. Generally, this encompasses survival skills, which include the basic information the patient needs initially to survive at home.

xii. Survival skills include medication administration, glucose monitoring, meal plan basics, and what to do if high or low BG levels occur.

xiii. A variety of helpful aids, such as pamphlets and videos, is available.

xiv. Diabetes equipment suppliers provide kits that are full of samples and information.

xv. These are a significant help when you are teaching a patient.

xvi. Also advise the patient to purchase a medical alert bracelet or necklace.

xvii. It is difficult to know how to operate and teach glucose monitoring with the variety of glucose monitors available.

xviii. Many drugstores and medical supply stores not only sell the monitors but also provide training for the patient and family.

xix. You can obtain this information by calling local medical suppliers or by contacting the certified diabetes educator or discharge planner at your institution.

xx. After discharge, the patient should be referred to outpatient diabetes classes for further instruction.

xxi. If classes are unavailable or if the patient is unable to leave home, a referral to a visiting nurse should be made.

xxii. It is usually advisable to have a nurse present for the patient’s first insulin injection at home.

xxiii. The American Association of Diabetes Educators recommends that diabetes self-management education include information about the following

1. Diabetes pathophysiology and treatment options

2. Healthy eating

3. Physical activity

4. Medications usage

5. Monitoring and using patient-generated health data (such as BG)

6. Preventing, detecting, and treating acute and chronic complications

7. Healthy coping with psychosocial issues and concerns

8. Problem-solving

K. Know key terms, learning tips, tables, and charts

27

i. diabetes mellitus : A chronic disease characterized by impaired production or use of insulin and high blood glucose levels.

ii. endogenous: Produced or originating from within a cell or organism.

iii. gastroparesis : Paralysis of the stomach, resulting in poor emptying.

iv. glycosuria: Abnormal amount of glucose in the urine, often associated with diabetes mellitus.

v. hyperglycemia : Excess glucose in the blood.

vi. hypoglycemia: Below-normal amount of glucose in the blood.

vii. ketoacidosis: A condition in which fat breakdown produces ketones, which cause an acidic state in the body; may be associated with weight loss or diabetes mellitus.

viii. Kussmaul respirations : Term describing deep respirations of an individual with ketoacidosis. Also called Kussmaul’s respirations.

ix. nephropathy: Any disease of the kidney.

x. neuropathy: A general term denoting functional disturbances and pathological changes in the peripheral nervous system.

xi. nocturia : Excessive urination at night.

xii. polydipsia:  Excessive thirst.

xiii. polyphagia : Excessive eating.

xiv. polyuria:  Excessive urination.

xv. postprandial: After a meal.

xvi. preprandial:  Before a meal.

xvii. retinopathy: Disease of the retina of the eye.

28