Endocrine System

Endocrine System

• Review of Anatomy and Physiology

Function of the Endocrine System

• Endocrine glands continuously secrete products called hormones, which are chemical messengers that deliver stimulatory or inhibitory signals to target cells as a result of a feedback mechanism

Structures of the Endocrine System

Thyroid Gland

• Overlies thyroid cartilage below the larynx

• Thyroid hormones: accelerate cellular reactions in most body cells

• Thyroxine: stimulates metabolic rate; essential for normal physical and mental development

• Triiodothyronine: inhibits anterior pituitary secretion of thyroid stimulating hormone

• Calcitonin (thyrocalcitonin): decreases loss of calcium from bone; promotes hypocalcemia; action opposite that of parathormone

Parathyroid Glands

• Small glands (2-12) embedded in the posterior part of the thyroid

• Parathyroid hormone (parathormone)

• Increases blood calcium concentration

• Breakdown of bone to release of calcium into blood (requires the active form of vitamin D)

• Calcium absorption from intestine into blood

• Kidney tubule reabsorption of calcium

• Decreases blood phosphate concentration by slowing its reabsorption from the kidneys, thereby decreasing calcium loss in urine

Testes and Ovaries

• Structures of the Male and Female Reproductive Systems

Adrenal Glands

• Two closely associated structures, adrenal medulla and adrenal cortex, positioned at each kidney’s superior border

• Adrenal hormones:

• Adrenal medulla produces two catecholamines, epinephrine and norepinephrine

• Stimulate liver and skeletal muscle to breakdown glycogen

• Increase oxygen use and carbon dioxide production

• Increase blood concentration of free fatty acids through stimulation of lipolysis in adipose tissue

• Cause constriction of nearly all blood vessels of body, thereby greatly increasing total peripheral resistance and arterial pressure

• Increase heart rate and force of contraction and thereby raise cardiac output

• Inhibit contractions of gastrointestinal and uterine smooth muscle


• Epinephrine significantly dilates bronchial smooth muscle

• Adrenal cortex: secretes the mineralocorticoid aldosterone and the glucocorticoids cortisol and corticosterone

Aldosterone

• Markedly accelerates sodium and water reabsorption by kidney tubules

• Markedly accelerates potassium excretion by kidney tubules

• Aldosterone secretion increases as sodium ions decrease or potassium ions increase

Cortisol and Corticosterone

• Accelerate mobilization and catabolism of tissue protein and fats

• Accelerate liver gluconeogenesis (formation of glucose from mobilized proteins, a hyperglycemic effect)

• Decreased antibody formation (immunosuppressive, anti-allergy effect)

• Slow the proliferation of fibroblasts characteristic of inflammation (anti-inflammatory effect)

• Decrease ACTH secretion

• Mildly accelerate sodium and water reabsorption and potassium excretion by kidney tubules

Pancreas

• Retroperitoneal in abdominal cavity

• Pancreatic hormones: regulate glucose homeostasis through the action of insulin and glucagon

Insulin

• Secreted by beta cells of islets of langerhans

• Promote the cellular uptake of glucose

• Stimulates intracellular macromolecular synthesis, such as glycogen synthesis (glycogenesis), fat synthesis (lipogenesis), and protein synthesis

• Stimulates cellular uptake of sodium and potassium (latter is significant in the treatment of diabetic coma with insulin)

Glucagon

• Secreted by alpha cells of islets of Langerhans

• Induces liver glycogenolysis; antagonizes the glycogen synthesis stimulated by insulin

• Inhibits hepatic protein synthesis; this makes amino acids available for gluconeogenesis and also increases urea production

• Stimulates hepatic ketogenesis and release of glycerol and fatty acids from adipose tissue

Thymus Gland

• Located at root of neck and anterior thorax

• Thymic hormone (thymosin)

• Regulates immunologic processes

• Just after birth produces T lymphocytes that migrate to the lymph nodes and spleen to provide immunologic potential

• Synthesizes hormones that regulate the rate of development of lymphoid cells, particularly T cells

Pineal Gland

• Located in midbrain attached to third ventricle

• Pineal hormone (melatonin)

• May regulate diurnal fluctuations of hypothalamic hypophyseal hormones

• Inhibits numerous endocrine functions, particularly gonadotropic hormones

Pituitary Gland

• Located in cranial cavity in sella turcica of sphenoid bone; near optic chiasm

• Composed of an anterior lobe (adenohypophysis) and a posterior lobe (neurohypophysis)

• Pituitary hormones

• Hormones secreted by the anterior lobe:

• Growth hormone (GH): (1) promotes protein anabolism (2) promotes fat mobilization and catabolism (3) slows carboydrate metabolism


• Thyroid stimulating hormone (TSH): stimulates synthesis and secretion of thyroid hormones

• Adrenocorticotropic hormone (ACTH): (1) stimulates growth of adrenal cortex (2) stimulates the secretion of glucocorticoids ; slightly stimulates mineralocorticoid secretion


• Follicle stimulating hormone (FSH): (1) stimulates primary graafian follicle to grow and develop (2) stimulates follicle cells to secrete estrogen (3) stimulates development of seminiferous tubules and spermatogenesis


• Luteinizing hormone (LH): (1) stimulates maturation of follicle and ovum; required for ovulation (2) forms corpus luteum in ruptured follicle following ovulation; stimulates corpus luteum to secrete progesterone (3) in males, LH is called interstitial cell stimulating hormone (ICSH); stimulates testes to secrete testosterone

• Prolactin: (1) promotes breast development during pregnancy (2) initiates milk production after delivery (3) stimulates progesterone secretion by corpus luteum


• Hormones secreted by the posterior lobe:

• Anti diuretic hormone (ADH); vasopressin: (1) increases water reabsorption by distal and collecting tubules of kidneys (2) stimulates vasoconstriction, raising blood pressure

• Oxytocin: (1) stimulates contractions by pregnant uterus (2) stimulates milk ejection from alveoli of lactating breasts into ducts

• Melanocyte stimulating hormone (MSH): stimulates synthesis and dispersion of melanin in skin, causing darkening

Summary…

Anterior lobe

1. Growth Hormone

2. Thyroid stim H.

3. Follicle stimulating H.

4. Luteinizing H.

5. Prolactin

6. Melanocyte stim H.

7. adrenocorticotropic H.

Posterior lobe

1. Anti diuretic H.

2. Oxytocin

Major Disorders of the Endocrine System:

• Hyperpituitarism/ Hypopituitarism

• Diabetes Insipidus/ SIADH Syndrome

• Hyperthyroidism/ Hypothyroidism

• Hyper- & Hypo- parathyroidism

• Diabetes Mellitus

• Cushing’s disease/ Addison’s disease

Hyperthyroidism (Graves’ disease, thyrotoxicosis)

• Excessive concentration of thyroid hormones in the blood as a result of thyroid disease or increased TSH; leads to hypermetabolic state

• Etiology of Graves’ disease is believed to be involved with an autoimmune process of impaired regulation; secondary to other autoimmune disorders

• The gland may also enlarge (goiter) as a result of decrease iodine intake; no increase in secretion of thyroid is present


• Clinical findings:

• Subjective : polyphagia; emotional lability; apprehension; heat intolerance

• Objective: weight loss; loose stools; tremors; hyperactive reflexes; diaphoresis; insomnia; exophthalmos; corneal ulceration; increased systolic blood pressure, temperature, pulse and respiration

• Decreased TSH levels if thyroid disorder; increased TSH levels if secondary to a pituitary disorder


• Increased triiodothyronine (T3), thyroxine (T4), protein bound iodine (PBI), long acting thyroid stimulator (LATS), and radioactive iodine uptake

• Thyrotoxic crisis (thyroid storm): a state of hypermetabolism that may lead to heart failure; usually precipitated by a period of severe physiologic or psychologic stress, thyroid surgery, or radioactive iodine therapy


• Therapeutic interventions:

• Anti thyroid medications such as propylthiouracil (PTU) and methimazole (Tapazole) to block the synthesis of thyroid hormone

• Anti thyroid medications such as iodine (Lugol’s solution or SSKI) to reduce the vascularity of the thyroid gland

• Radio active iodine to destroy thyroid gland cells, thereby decreasing the production of thyroid hormone

• Medications to relieve the symptoms related to the increased metabolic rate (e.g., digitalis, propranolol [Inderal], phenobarbital)

• Well balanced, high calorie diet with vitamin and mineral supplements

• Surgical intervention involves a subtotal or total thyroidectomy

Nursing Care of Clients with Hyperthyroidism

Assessment:

• History of weight loss, diarrhea, insomnia, emotional lability, palpitations and heat intolerance

• Eyes for exophthalmos, tearing and sensitivity to light

• Neck palpation for enlarged thyroid gland

• Weight and vital signs to establish baseline

Analysis/ Nursing Diagnoses:

• Ineffective individual coping related to emotional lability

• Altered nutrition, less than body requirements, related to increased metabolic needs

Planning/ Implementation:

• Use measures such as decreased stimulation, medications, and back rub to establish a climate for uninterrupted rest

• Protect the client from stress producing situations

• Keep the room cool


• Provide diet high in calories, proteins and carbohydrates with supplemental feedings between meals and at bedtime; vitamin and mineral supplements should be given as prescribed

• Understand that the client is upset by lability of mood and exaggerated response to environmental stimuli; take time to explain disease processes involved

• Provide eye drops or patches as needed

Care for the client before a thyroidectomy:

• Administer prescribed anti thyroid medications to achieve euthyroid state

• Teach breathing exercises and use of hands to support neck and to avoid strain on suture line

Care for the client following a thyroidectomy:

• Observe for signs of respiratory distress and laryngeal stridor caused by tracheal edema (keep tracheotomy set available)

• Provide humidity with cold steam nebulizer to keep secretions moist when at home

• Keep the bed in a semi Fowler’s position

• Observe dressings at the operative site and back of the neck and shoulders for signs of hemorrhage

• Observe for signs of thyroid storm such as high fever, tachycardia, irritability, delirium, coma; may result from manipulation of the gland during surgery, which releases thyroid hormone into bloodstream

• Notify the physician immediately if signs of thyroid storm occur; administer propranolol (Inderal), iodides, propylthiouracil, and steroids as ordered


• Observe for signs of tetany such as numbness or twitching of extremities, spasm of the glottis; hypocalcemia can occur after accidental trauma or removal of the parathyroid glands; if tetany occurs, give calcium gluconate or calcium chloride (IV) as prescribed

• assess for hoarseness; may result from endotracheal intubation or laryngeal nerve damage

Teach signs and symptoms of:

• Hypothyroidism as a result of treatment

• Hyperthyroidism as a result of thyroid storm or overmedication with thyroid hormone replacement therapy

• Teach the importance of taking anti thyroid medications regularly and to observe for adverse effects

Evaluation/ Outcomes:

• Maintains ideal body weight

• Establishes regular routine of activity and rest

Hypothyroidism

• Absence or decreased production of thyroid hormone because of primary thyroid disease, response to decreased TSH, or effect of thyroid surgery or radioactive iodine (RAI) treatment; most common cause is Hashimoto’s thyroiditis, an autoimmune disorder

• Classified according to the time of life in which it occurs:

• Cretinism: hypothyroidism in infants and young children

• Lymphocytic thyroiditis most frequently appears after 6 years of age and peaks during adolescence; generally self limiting

• Hypothyroidism without myxedema: mild degree of thyroid failure in older children and adults

• Hypothyroidism with myxedema: severe degree of thyroid failure in older individuals

• Myxedema coma is the most severe degree of hypothyroidism, representing a potentially fatal endocrine emergency; precipitated by a severe physiologic stress, myxedema coma involves hypothermia, bradycardia, hypoventilation and progressive loss of consciousness

• Decreased levels of thyroid hormones may interfere with erythropoiesis and lipid metabolism

Clinical findings

• Subjective: dull mental processes; apathy; lethargy; loss of libido; intolerance to cold; anorexia

• Objective:

• Lack of facial expression; increase in weight; constipation; subnormal temperature and pulse; dry, brittle hair and nails; pale, dry, coarse skin; enlarged tongue ; drooling; hoarseness; thinning of lateral eyebrows; scalp, axilla and pubic hair loss; diminished hearing; anemia; periorbital edema

• Decreased basal metabolic rate (BMR)

• Decreased thyroxine (T4), triiodothyronine (T3), and radioactive iodine uptake; delayed or poor response to TSH stimulation test in secondary hypothyroidism, increased in TSH in primary hypothyroidism

• Therapeutic Interventions:

• Administer thyroid hormones; maintain vital functions

Nursing Care of Clients with Hypothyroidism

• Assessment:

• History that may have contributed to condition

• Activity tolerance, bowel elimination, sleeping patterns, sexual function, and intolerance to cold

• Skin and hair for characteristic changes

• Weight and vital signs to establish baseline

• Signs of anemia, atherosclerosis, or arthritis

• Analysis/ Nursing Diagnoses:

• Activity intolerance related to decreased metabolic rate

• Constipation related to decreased gastrointestinal activity

Planning/ Implementation:

• Have patience with a lethargic client; activity tolerance and mental functioning will improve with therapy

• Teach the client and family to be alert for signs of complications

• Angina pectoris: chest pain, indigestion

• Cardiac failure: dyspnea, palpitations

• Myxedema coma: weakness, syncope, slow pulse rate, subnormal temperature, slow respirations, lethargy

• Teach the client to seek medical supervision regularly and when signs of illness develop

• Explain the importance of continued hormone replacement throughout life

• Review the signs of hypothyroidism and hyperthyroidism to help client recognize signs of under medication or overmedication

• Explain that increased sensitivity to narcotic analgesics and tranquilizers necessitates dosage adjustment; OTC drugs should be avoided unless approved by the physician

• Help the client and family recognize that the client’s inability to adapt to cold temperature requires additional protection and modification of outdoor activity in cold weather

• Teach the client to avoid constipation by the use of adequate hydration and roughage in the diet

• Apply moisturizers to skin

• Teach the need to restrict calories, cholesterol and fats in the diet

Evaluation/ Outcomes:

• Completes activities of daily living (ADL) without fatigue

• Complies with dietary, exercise, and medication regimen

• Establishes regular pattern of bowel elimination

Diabetes Mellitus

• Occurs when there is insufficient supply of insulin and/ or cells become insulin resistant ; may result from:

• Failure in body’s production

• Blockage of insulin supply

• Autoimmune response wherein the insulin may bind to an immune serum globulin fraction, preventing use

• Excess body fat, which alters glucose metabolism

• Glucose level in the blood remains high

• Body attempts to rid itself of excess glucose by excreting some via kidneys

• Osmotic force is created within the kidneys because of glucose excretion, and body fluid is lost

• Body is unable to use carbohydrates properly, and fat is oxidized as a compensatory mechanism; oxidation of fats gives off ketone bodies

Risk factors: obesity, age, heredity

• Classification:

Type 1: insulin dependent diabetes mellitus (IDDM) has rapid onset; requires insulin administration because of minimal or absence of beta cell function

Type 2: non insulin dependent diabetes mellitus (NIDDM) accounts for 90% of all diabetes; has gradual onset and often can be controlled with diet and exercise; caused by decreased sensitivity of insulin receptors (insulin resistance) and decreased insulin secretion; often associated with obesity

Gestational: onset during 2nd or 3rd trimester of pregnancy; may or may not resolve after pregnancy

• Secondary: associated with syndromes such as Cushing’s disease, pancreatic disease, and glucocorticoid medications

• Impaired glucose tolerance: high serum glucose levels but not diagnostic for diabetes mellitus

• Acute increases in serum glucose levels: diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic (HHNK) syndrome

• Causes: insufficient insulin, major stresses ( e.g., infection, surgery, trauma, pregnancy, emotional turmoil, nausea and vomiting), or drugs (steroids)

Pathophysiology:

• DKA is associated with IDDM; with inadequate insulin to support basal needs, proteins and fats are used; ketones are excreted via urine and breathing; dehydration and electrolyte imbalances occur

• HHNK is associated with NIDDM; hyperglycemia increases intravascular osmotic pressure, leading to polyuria and cellular dehydration

Acute decrease in serum glucose: insulin shock or reaction

• Causes: excess insulin or oral anti diabetic medications; too little food or too much exercise when receiving anti diabetic medications

• Pathophysiology: excessive insulin lowers serum glucose as glucose is carried into cells; decreased food intake in relation to prescribed anti diabetic medications results in hypoglycemia; excessive exercise uses glucose for metabolism decreasing serum glucose

Long term complications of diabetes include microangiopathy (retinopathy, nephropathy), macroangiopathy (peripheral vascular diseases, arterio-atherosclerosis, coronary artery disease), neuropathy

Clinical findings:

• Subjective: polydipsia; polyphagia; fatigue, blurred vision (retinopathy; osmotic changes); peripheral neuropathy

• Objective: polyuria; weight loss; glycosuria; peripheral vascular changes; ulcers; gangrene

• Hyperglycemia: detected by fasting blood sugar, glucose tolerance test, 2 hour post-prandial glucose, and glycosylated hemoglobin (provides measure of average glucose level over preceding 2-3 months

DKA and HHNK

• Hyperglycemia, glycosuria, polyuria

• Dehydration: flushed, hot, dry skin, decreased skin turgor (tenting), hypotension, tachycardia, thirst, headache confusion, drowsiness

• Metabolic acidosis (DKA only): Kussmaul respirations as body attempts to blow off carbon dioxide; ketonuria, sweet breath odor, anorexia, nausea, vomiting, decreased serum pH, decreased pCO2

Hypoglycemia (Insulin shock or reaction)

• Occurs as a result of sympathetic nervous system stimulation or reduced cerebral glucose supply

• CNS effects: mental confusion, blurred vision, diplopia, slurred speech, fatigue, seizures

• SNS (adrenergic) effects: nervousness, weakness, pallor, diaphoresis, tremor, tachcardia, hunger

Therapeutic interventions:

• Lifestyle changes:

• Weight control: obesity leads to insulin resistance; this can be reversed by weight loss

• Exercise: increases insulin sensitivity but must be regular; brisk walking, swimming and bicycling are recommended

Diet: current recommendations include:

• Caloric control to maintain ideal body weight

• 50-60% of caloric intake should be from carbohydrates with emphasis on complex carbohydrates, high fiber foods rich in water soluble fiber (oat bran, peas, all forms of beans, pectin rich fruits and vegetables); foods with a high glycemic index should be avoided; glycemic index refers to effect of particular foods on blood glucose

• Protein: intake should be consistent with the dietary guidelines, usually between 60 and 85 grams; should be 12% to 20% of daily calories

• Fat intake not to exceed 30% of daily calories (70-90 grams/day); keep saturated fat intake low; emphasize mono- and polyunsaturated fats

• Dietary ratio: carbohydrate to protein to fat usually about 5:1:2

• Distribute food fairly evenly throughout the day in three or 4 meals, with snacks added between and at bedtime as needed in accordance with total food allowance and therapy (insulin or oral hypoglycemics)

• Basic tools for planning diet: food composition tables showing nutrient content of foods; glycemic index of foods

Insulin administration:

• Adjusted after considering the client’s physical and emotional stresses; a specific type of insulin and schedule is prescribed

• Somogyi effect: insulin-induced hypoglycemia rebounds to hyperglycemia:

• Epinephrine and glucagon are released in response to hypoglycemia

• These reactions cause mobilization of the liver’s stored glucose and iatrogenically induce hyperglycemia

Somogyi phenomenon is treated by gradually lowering insulin dosage while monitoring blood glucose, particularly during the night (when hypoglycemia is most likely to occur)

• Insulin pump

• External battery-operated device that delivers insulin through a needle inserted into subcutaneous tissue

• Small (basal) doses of regular insulin are programmed into computer to be delivered every few minutes; bolus doses (extra preset amounts) are delivered before meals

• Improves glucose control for clients with wide variations in insulin need as a result of irregular schedules, pregnancy, or growth requirements

• A prescribed amount of insulin for 24 hours plus priming is drawn into syringe

• The administration set is primed and needle inserted aseptically, usually into subcutaneous tissue of abdomen

• Oral anti diabetics for certain clients with NIDDM who cannot be managed with lifestyle changes alone; must have some functioning beta cells in the islets of Langerhans

• Other therapies include pancreatic islet cell grafts, pancreas transplants, implantable insulin pumps that continually monitor blood glucose and release insulin accordingly, cyclosporin therapy to prevent beta cell destruction in insulin dependent (type 1) diabetes

Management of DKA and HHNK:

• IV to provide fluid replacement and direct access to the circulatory system, and a Foley catheter to monitor urine output

• Rapid acting insulin based on serum glucose levels

• Replacement of lost electrolytes, particularly sodium and potassium, using blood studies to determine dosage; when insulin is administered potassium reenters the cell resulting in hypokalemia

• Cardiac monitoring if circulatory collapse is imminent or dysrhythmias associated with electrolyte imbalance occur

• Treat acidosis according to cause

• Management of hypoglycemia (Insulin shock or reaction):

• 10 to 15 grams of simple sugar (e.g., glucose tablets, 4 to 6 ounces of juice or soda, hard candy) followed by complex carbohydrate and protein (e.g., cheese and crackers)

• Establish an intravenous line for circulatory access

• Administration of 50% dextrose solution

• If unconscious, glucagon injection to stimulate glycogenolysis

Nursing Care of Clients with Diabetes Mellitus

• Assessment:

• Family history of diabetes mellitus

• Cardinal signs of polyuria, polydipsia, and polyphagia

• History of fatigue, visual changes, impaired wound healing, urinary tract infections, fungal infections, and altered sensation

• Blood glucose levels

• Visual acuity and retinal changes

• Vital signs and weight for baseline data

• Urine for acetone

• Renal function

• Dietary and exercise patterns

Analysis/ Nursing Diagnoses:

• Individual ineffective management of therapeutic regimen related to complexity of therapies and chronicity of the illness

• Altered nutrition, less than body requirements related to impaired carbohydrate, fat and protein metabolism

Planning/ Implementation:

• Assist the client and family to understand the disease process

• Encourage the client to express feelings about illness and the necessary changes in life style and self image

• Help the client with the administration of medication until self administration is both physically and psychologically possible

• Assist the client in recognizing the need for activities and diet that promote and maintain normal body weight

• Monitor serum glucose with routine finger sticks

• Test urine for ketones when glucose is high; obtain double voided specimen or specimen from port of retention catheter if in place

Teach client and family to:

• Use blood glucose monitoring system to test blood glucose

• Test urine for ketones when blood glucose is high

• Avoid infection

• Care for the legs, feet and toe nails properly; inspect, bathe, dry, lubricate feet except between toes; avoid exposure of feet to heat sources

• Administer insulin by using sterile technique, rotating injection sites, measuring dosage, noting types, strengths of insulin, and peak action periods; using insulin pump, need to carry carbohydrate source

• Use ADA dietary exchange list

• Avoid tight shoes and smoking, which will constrict circulation

• Recognize signs of impending hypoglycemia (insulin shock, reaction)

• Recognize signs of impending hyperglycemia (DKA, HHNK)

• Encourage the client to continue medical supervision and follow up care, including visits to an eye care specialist and podiatrist

• Encourage follow up nutritional counseling

Evaluation/ Outcomes:

• Complies with medical regimen of diet, exercise, and medications

• Maintains blood glucose levels with an acceptable range

Hyperparathyroidism

• Hyperfunction of the parathyroid glands; usually caused by adenoma; hypertrophy and hyperplasia of the glands may also be responsible

• As the result the absorption of calcium and excretion of phosphorus by the kidneys is increased

• If dietary intake is not enough to meet calcium levels demanded by high levels of parathormonre, demineralization of the bone occurs

Clinical findings:

• Subjective: apathy, fatigue; muscular weakness; anorexia; nausea; emotional irritability; deep bone pain (if demineralization occurs)

• Objective: bone cysts, pathologic fractures; renal calculi composed of calcium; pyelonephritis; renal damage; polyuria; vomiting, constipation

• Elevated serum calcium and parathormone

• Decreased serum phosphorus

• Cardiac dysrhythmias

Therapeutic interventions:

• Surgical excision of a parathyroid hormone

• Calcium intake restricted

• Administration of furosemide (Lasix) to increase renal excretion of calcium

• Administration of galium nitrate, calcitonin, or plicamycin with glucocorticoid to lower calcium level

Nursing Care of Clients with Hyperparathyroidism

• Assessment:

• presence of Gi disturbance or bone pain

• History of renal calculi or fractures

• Signs of renal calculi such as hematuria or flank pain

• Use of thiazide diuretics or vitamin D, which can increase serum calcium

• Serum calcium and phosphorus levels

• Baseline vital signs, particularly heart rate and rhythm

Analysis/ Nursing Diagnoses:

• Risk for injury related to bone demineralization

• Altered urinary elimination related to obstruction by calculi

Planning/ Implementation:

• Strain the urine, observing for calculi

• Encourage fluid intake

• Assist the client with ambulating to help prevent demineralization; avoid high impact activites

• Monitor intake and output

• Encourage foods with fiber to limit constipation


• Instruct the client to limit intake of foods high in calcium, especially milk products

• Provide cardiac monitoring if hypercalcemia is severe

• If surgery is performed provide post operative care the same as for clients undergoing thyroidectomy

Evaluation/ Outcomes:

• Maintains skeletal integrity

• Remains free of urinary complications

Hypoparathyroidism

• Parathyroid glands may not secrete a sufficient amount of parathormone after thyroid surgery, parathyroid surgery, or radiation therapy of the neck ; idiopathic hypoparathyroidism rare

• As levels of parathormone drop, the serum calcium also drops, causing signs of tetany; a concomittant rise in serum phosphate occurs

Clinical findings:

• Subjective: photophobia; muscle cramps; irritability; dyspnea; tingling of extremities

• Objective:

• Trousseau’s sign (carpopedal spasm)

• Chvostek’s sign (contraction of the facial muscle in response to tapping near the angle of the jaw)

• Decreased serum calcium and parathormone; elevated serum phosphate

• Stridor, wheezing from laryngeal spasm; tremors; convulsions

• X-ray examination reveals increased bone density

• Cardiac dysrhythmias; alkalosis; cataracts if the disease is chronic

Therapeutic Interventions:

• Calcium chloride or calcium gluconate given IV for emergency treatment of overt tetany

• Calcium salts administered orally (calcium carbonate, calcium gluconate)

• Vitamin D (dihydrotachysterol, ergocalciferol) to increase absorption of calcium from the GI tract


• Parathormone injections

• High calcium, low phosphate diet

• Aluminum hydroxide to decrease absorption of phosphorus from the GI tract

Nursing Care of Clients with Hypoparathyroidism

Assessment:

• History of muscle spasms, numbness or tingling of extremities, visual disturbances, or convulsions

• Presence of neuromuscular irritability

• Status of respiratory functioning

• Heart rate and rhythm

• Serum calcium and phosphate levels

Analysis/ Nursing Diagnoses:

• Ineffective airway clearance related to laryngeal spasm

• Risk for injury related to neuromuscular irritability

Planning/ Implementation:

• Observe for respiratory distress and have emergency equipment available for tracheostomy and mechanical ventilation

• Maintain seizure precautions

• Reduce environmental stimuli

• Provide drug and dietary instruction including elimination of milk, cheese and egg yolks because of high phosphorus content


• Teach symptoms of hypocalcemia and hypercalcemia; instruct client to contact physician immediately if either should occur

Evaluation/ Outcomes:

• Remains free from neuromuscular irritability

• Maintains respiratory functioning within normal limits

Cushing’s Syndrome

• Results from excess secretion of adrenocortical hormones

• Caused by hyperplasia or by a tumor of the adrenal cotrtex; however, the primary lesion may occur in the pituitary gland, causing excess production of ACTH

• Administration of excess glucocorticoids or ACTH will also cause Cushing’s syndrome

Clinical findings:

• Subjective: weakness; decreased libido; mood swings; psychosis

• Objective:

• Obese trunk, thin arms and legs; moon face; buffalo hump; acne; hirsutism; ecchymotic areas; purple striae on breast and abdomen; amenorrhea; increased susceptibility to infections


• Hypertension

• Hyperglycemia; hypokalemia; elevated plasma cortisol level

• Elevated 17-hydroxycorticosteroids and 17-ketosteroids in urine

• Osteoporosis may be evident on X-ray examination

Therapeutic interventions:

• Reduce dosage of externally administered corticoids

• If lesion on pituitary is causing hypersecretion of ACTH, a hypophysectomy or irradiation of the pituitary may be done

• Surgical excision of the adrenal tumors (adrenalectomy)


• Adrenal enzyme inhibitors

• Potassium supplements

• High protein diet with sodium restriction

Nursing Care of Clients with Cushing’s Syndrome

Assessment:

• Baseline vital signs, weight, blood glucose and electrolytes

• Urine specimens for diagnostic purposes

• Physical appearance

• Changes in coping and sexuality from history

Analysis/ Nursing Diagnoses:

• Body image disturbance related to altered appearance

• Fluid volume excess related to sodium excess

• Risk for infection related to altered immune response

Planning/ Implementation:

• Monitor vital signs, daily weight, intake and output, blood glucose, and electrolytes

• Protect the client from exposure to infections

• Encourage ventilation of feelings by the client and spouse because changes in body image and sex drive can altermarital support

• Attempt to minimize stress in the environment by measures such as limiting visitors and explaining procedures carefully

• Instruct client regarding diet and supplementation; encourage diet rich in nutrient dense foods such as fruits, vegetables, whole grains, and legumes to improve and maintain nutritional status and prevent any possible drug induced nutrient deficiencies


• Care for the client following bilateral adrenalectomy

• Care for the client following a hypophysectomy

Evaluation/ Outcomes:

• Maintains fluid balance

• Remains free of infection

• Discusses feelings regarding physical changes

Addison’s disease

• Hyposecretion of adrenocortical hormones

• Generally caused by autoimmune destruction of the cortex or by idiopathic atrophy

• Addisonian crisis (acute adrenal insufficiency) can be precipitated by stresses such as pregnancy, surgery, infection, dehydration, emotional turmoil; fatal if not treated

Clinical findings:

• Subjective: weakness, fatigue; anorexia, nausea

• Objective: increased bronze pigmentation of skin; vomiting; diarrhea; hypotension; decreased serum cortisol, 17-ketosteroids, and 17-hydroxysteroids; increased plasma ACTH; hyponatremia; hypoglycemia; hyperkalemia

Therapeutic interventions:

• Replacement of hormones: glucocorticoids to correct metabolic imbalance and hypotension

• Correction of fluid, electrolyte, and glucose imbalances

• High carbohydrate, high protein diet

Nursing Care on Clients with Addison’s disease

Assessment:

• Basal vital signs, weight, electrolytes, and serum glucose

• 24 hour urine specimens for diagnostic purposes (17-hydroxycorticosteroids and 17-ketosteroids)

• Appearance of skin

• Changes in energy or activity from history

Analysis/ Nursing Diagnoses:

• Fluid volume deficit related to excess sodium loss

• Decreased cardiac output related to electrolyte imbalances

Planning/ Implementation:

• Monitor vital signs four times a day; be alert for elevation in temperature (infection, dehydration), alterations in pulse rate and rhythm (hyperkalemia), and alterations in blood pressure

• Observe for signs of sodium and potassium imbalance

• Monitor intake and output and weigh daily

• Administer steroids as ordered; give with milk or an antacid to limit ulcerogenic factor of the drug

• Put the client in a private room to prevent contact with clients having infectious diseases

• Limit the number of visitors

• Advise the client to avoid physical and emotional stress

• Teach client need for lifelong hormone replacement with increased dosage during stress

• Review signs of adrenal hypofunction or hyperfunction so client can recognize need for adjustment of steroid dose

• Instruct client to wear medical alert band

• Encourage diet consistent with the dietary goals with emphasis on diet high in nutrient dense foods and adequate sodium

• Administer anti-emetics to prevent fluid and electrolyte loss by vomiting

Evaluation/ Outcomes:

• Maintains fluid balance

• Maintains electrolyte balance

Diabetes Insipidus

• A deficient production or secretion of the anti diuretic hormone (ADH) by the posterior pituitary gland decreasing reabsorption of water in nephron tubules; may be familial, idiopathic, secondary to trauma, surgery, tumors, infections, or autoimmune disorders

Neurogenic diabetes insipidus, a renal tubular defect resulting in decreased water absorption, may be familial, or result from renal disorders, primary aldosteronism, or excessive water intake (primary polydipsia); results in impaired renal concentrating ability

Clinical findings:

• Subjective: polydipsia; craving for cold water

• Objective: polyuria (5-25 liters/24 hours); dilute urine; specific gravity, 1.001 to 1.005; osmolality 50-200 mOsm/kg; increased serum sodium and plasma osmolality

• Signs of dehydration (poor skin turgor, dry mucous membranes, elevated temperature

Therapeutic interventions:

• Anti diuretic hormone replacement: vasopressin, lypressin (Diapid), desmopressin (DDAVP), vasopressin tannate (Pitressin Tannate)

• Treatment of underlying cause

Nursing care of Clients with Diabetes Insipidus

Assessment:

• Intake and output, weight and specific gravity of urine to establish baseline data

• Results of serum electrolyte evaluation

• Dryness of skin and mucous membranes

Analysis/ Nursing Diagnoses:

• Fluid volume deficit related to polyuria

• Ineffective management of therapeutic regimen (individual) related to chronicity of problem

Planning/ Implementation:

• Monitor fluid and electrolyte status: intake and output, daily weight, skin turgor, electrolyte levels

• Replace fluid by mouth or parenterally

• Monitor response to ADH replacement

• Teach client on long term vasopressin therapy the need for daily weight records, recognition of polyuria, and wearing a medical alert bracelet; overdosage may cause syndrome of inappropriate anti diuretic hormone (SIADH), leading to water retention and hyponatremia

• Advise client to avoid alcohol because it suppresses ADH secretion

Evaluation/ Outcomes:

• Maintains fluid balance

• States sign of overmedication and undermedication with ADH replacement

Syndrome of Inappropriate Anti Diuretic Hormone Secretion

• Excessive ADH secretion leads to fluid retention and dilutional hyponatremia

• May be caused by head trauma, tumors, or infection; malignant tumor cells may produce ADH

Clinical findings:

• Subjective: anorexia; nausea; fatigue; headache

• Objective: reduced urine output; decreased deep tendon reflexes; change in mental status, seizures, coma

• Signs of fluid retention such as weight gain, crackles, jugular vein distention

• Decrease serum sodium and osmolality

Therapeutic interventions:

• Fluid restriction

• Hypertonic parenteral fluids

Nursing Care of Clients with Syndrome of Inappropriate Anti Diuretic Hormone

Assessment:

• History of malignancy, infection, or increased intra cranial pressure

• Intake and output, daily weight, vital signs

• Serum and urine for sodium and osmolality

• Neurologic evaluations

Analysis/ Nursing Diagnoses:

• Fluid volume excess related to fluid retention

• Risk for injury related to altered neurologic function

Planning/ Implementation:

• Monitor fluid and electrolyte status

• Restrict fluid intake; administer hypertonic intravenous solutions as ordered

• Institute seizure precautions

• Provide supportive measures for related disorders

Evaluation/ Outcomes:

• Maintains fluid balance

• Remains seizure free

Hyperpituitarism

• May result from overactivity of gland or from an adenoma

• Characterized by an excessive concentration of pituitary hormones (GH, ACTH, PRL) in the blood, overactivity, and changes in the anterior lobe of the pituitary gland

Two classifications of GH overproduction:

• Giantism: generalized increase in size, especially in children; involves the long bones

• Acromegaly: occurs after epiphyseal closing, with subsequent enlargement of cartilage, bone, and soft tissue of body

• ACTH overproduction leads to Cushing’s disease

Clinical findings:

• Subjective: headaches; depression; weakness

• Objective: increased soft tissue and bone thickness; facial features become hoarse and heavy, with enlargment of lower jaw, lips and tongue; enlarged hand and feet; increased growth hormone (GH), corticotrophic hormone (ACTH), or PRL

• X ray examination of long bones, skull (sella turcica area), and jaw demonstrates change in structure; amenorrhea; signs of increased intracranial pressure such as vomiting, papilledema, focal neurologic deficits; diabetes and hyperthroidism may also occur

Therapeutic interventions:

• Medications: somatostatin analog octreotide (Sandostatin); Dopamine agonist bromocriptine (Parlodel)

• Medications to relieve symptoms of other endocrine imbalances resulting from pituitary hyperfunctioning

• Surgical intervention (hypophysectomy) or irradiation of the pituitary

Nursing Care of Clients with Hyperpituitarism

Assessment:

• Changes in energy level, sexual function and menstrual patterns

• Face, hands, and feet for thickening, enlargement; and changes in the sizes of hat, gloves, rings, or shoes

• Presence of dysphagia or voice changes

• Presence of hypogonadism as a result of hyperprolactinemia

• Reaction to changes in physical appearance and sexual function

Analysis/ Nursing Diagnoses:

• Body image disturbance related to altered appearance

• Sensory/ Perceptual alterations related to neurologic deficits

• Sexual dysfunction related to hormonal imbalance

Planning/ Implementation:

• Help the client accept the altered body image that is irreversible

• Assist family to understand what the client is experiencing

• Help the client recognize that medical supervision will be required for life


• Assist the client in expressing feelings

• Help the client understand the basis for the change in sexual functioning

• Care for the client following a hypophysectomy:

• Encourage following an established medical regimen

• Protect from stress situations

• Protect from infection

• Follow and maintain an established schedule for hormone replacement

Care for the client undergoing intracranial surgery:

• Perform neurologic assessments

• Measure specific gravity of urine, monitor intake and output , and check daily weight to identify complication of diabetes insipidus

• Check clear nasal drainage for glucose to determine presence of CSF

• Encourage deep breathing, but not coughing

• Institute measures to prevent constipation because straining increases intracranial pressure

Evaluation/ Outcomes:

• Verbalizes an improved body image

• Report satisfying sexual relationship

• Continues medical supervision

Hypopituitarism

• Deficiency of one or more anterior pituitary hormones

• Total absence of pituitary hormones referred to as panhypopituitarism (Simmond’s disease)

• Occurs when there is destruction of the anterior lobe of the gland by trauma , tumor, or hemorrhage

• Clinical findings vary with target organs affected

Clinical findings:

• Subjective: lethargy; loss of strength and libido; decreased tolerance for cold

• Objective: decreased temperature; postural hypotension; hypoglycemia; decreased levels of GH, ACTH, TSH, FSH, and LH

• Sterility; loss of secondary sexual characteristics

• Visual disturbances if tumor impinges on optic nerve

Therapeutic interventions:

• Replace hormones

• Intervene surgically if tumor is present

Nursing Care of Clients with Hypopituitarism

Assessment:

• Baseline vital signs

• Sexual patterns: loss of libido; painful intercourse; inability to maintain an erection

• Past and present menstrual patterns

• Visual acuity

• Loss of secondary sexual characteristics

• Activity tolerance

Analysis/ Nursing Diagnoses:

• Activity intolerance related to decreased serum glucose

• Body image disturbance related to loss of secondary sexual characteristics

• Sexual dysfunction related to loss of libido

Planning/ Implementation:

• Monitor effects of hormone replacement

• Discuss the importance of adhering to medical regimen on a long term basis

• Allow the client ample time to verbalize feelings regarding the long term nature of the disease and impact on daily life

• Provide adequate rest periods

Evaluation/ Outcomes:

• Complies with medical regimen

• Expresses positive feelings of body image

• Establishes satisfying sexual relationship