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NR203 Test 4 Endocrine 10 Final Test Questions

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Cancer of the Thyroid
• Rare, approximately 2000 deaths annually.
• Usually results from exposure to ionizing radiation to head and neck during childhood:
– Many adults treated for colds and sinus infections in the 50’s and 60’s with x-ray treatments.
• Treatment: Surgery, radioactive iodine therapy, and chemotherapy
• Nonmetastasized: Survival is 96% for 5 years
Hyperparathyroidism
Result of...
Result of an increase in the secretion of the parathyroid hormone. This hormone regulates normal serum levels of
Calcium and phosphorus.
Hyperparathyroidism

pathophysiologic changes:
An increase in PTH affects the kidneys and bones resulting in the following pathophysiologic changes:
• Increased absorption of calcium and increased excretion of phosphate-may result in hypercalcemia and hypophosphatemia
• Increased bicarbonate excretion and decreased acid excretion – may lead to metabolic acidosis and hypokalemia
• Increased release of calcium and phosphorus by bones, resulting in increased bone decalcification
• Deposits of calcium in soft tissue and kidney stones
Hyperparathyroidism

⬢ 3 Types
⬢ More common in women
⬢ 3 Types
⬢ Primary: Hyperplasia or adenoma in one of the parathyroid glands
⬢ Secondary: Compensatory response by the parathyroid glands to chronic hypocalcemia
⬢ Tertiary: Hyperplasia of the parathyroid glands and a loss of response to serum calcium levels, often seen in patients with chronic renal failure
Hyperparathyroidism
Symptomatology:
Hyperparathyroidism
Symptomatology:
⬢ Symptoms related to hypercalcemia
⬢ Musculoskeletal, renal and gastric symptoms
GI: abdominal pain, constipation, anorexia, peptic ulcer formation
⬢ Cardiac: arrhythmias, hypertension, increased sensitivity to cardiotonic glycosides (Digoxin)
Hyperparathyroidism
– Manifestation of body systems
Hyperparathyroidism
– Manifestation of body systems
– Bone pain, pathologic fractures, muscle weakness muscle atrophy, renal calculi, polyuria, polydipsia, abd. pain, peptic ulcers, pancreatitis, nausea, constipation, arrhythmias, hypertension, paresthesias, depression, psychosis, acidosis, wt. Loss.
• Patients with persistently elevated calcium levels due to overproduction of parathyroid hormone also can have complaints of bone pain.. In the severe form, bones can give up so much of their calcium that the bones become brittle and break.
Hyperparathyroidism
what tests are done to diagnose
Hyperparathyroidism
⬢ Diagnosis made after all other possible causes of hypercalcemia are ruled out, 6 month history of symptoms, lab analysis of calcium, phosphorus, magnesium, bicarbonate, and chloride, and bone x-ray studies and scans
Treatment for Hyperparathyroidism
Treatment for Hyperparathyroidism
• Decrease serum calcium levels
– Large amounts of saline fluids
– Diuretics
– Calcitonin
– Fosamax / Aredia
• Surgery: For primary hyperparathyroidism surgery is performed removing the parathyroid glands affected by the hyperplasia or adenoma.

• Promote fluid intake
• Maintain dilute urine
– Prune/ cranberry juice
• Observe for S&S of Digitalis Toxicity
– Vision changes, anorexia, change in HR/Rhythm
Nursing Care for Clients with Hyperparathyroidism
⬢ Surgical clients require essentially the same care postoperative as that of a client having a thyroidectomy
⬢ Risk for Injury
⬢ Pain related to effects of increased parathyroid hormones
⬢ Impaired Physical Mobility
⬢ Risk for Altered Urinary Elimination
⬢ Fluid Volume Excess
HYPOparathyroidism
⬢ Results from abnormally low levels of PTH.
⬢ Most commonly caused from damage or removal of the parathyroid glands during a thyroidectomy.
⬢ The lack of circulating PTH causes hypocalcemia
and an elevated phosphorus level.
Hypoparathyroidism
⬢ Reduced levels of PTH result in ...
Hypoparathyroidism
• Reduced levels of PTH result in impaired renal tubular regulation of calcium and phosphate.
• The low calcium levels results in a decreased threshold for nerve and muscle excitability:
– Tetany: a continuous spasm of the muscles.
• Chvostek’s sign
• Trousseau’s sign
Hypoparathyroidism
Lab and Diagnostics
Lab and Diagnostics
• Lab: diagnosed by low levels of serum calcium levels and high phosphate levels
• Treatment: Increase calcium levels
– IV calcium for immediate need
– Supplemental calcium
– Increased dietary consumption of calcium
– Vitamin D therapy
Nursing Care for the Client with Hypoparathyroidism
Nursing Care for the Client with Hypoparathyroidism
• Risk for Injury Muscle Tetany re: low levels of calcium and risk of tetany
– Outcomes: Client will be free of injury evidenced by calcium levels returning to normal range

• Knowledge deficit re: lack of knowledge about a diet that is high in calcium and low in phosphorus
– Outcomes: Client will verbalize appropriate food selections that will enhance desired calcium and phosphorus levels

• Breathing patterns, ineffective R/T laryngeal spasms and stridor
– Outcomes: Client will demonstrate normal respiratory
Adrenal Gland Disorders
Adrenal Cortex Hyperfunction
Adrenal Gland Disorders
Adrenal Cortex Hyperfunction
• Cushing’s Syndrome: Chronic disorder in which hyperfunction of the adrenal cortex produces excessive amounts of circulating cortisol due to an excessive amount of ACTH
– May be primary, secondary, iatrogenic
Cushing’s Syndrome
3 TYPES
• Primary: Benign or malignant adrenal tumor
• Secondary: Results from one of the following:
– Pituitary or hypothalamic disorder
– Ectopic disorder that produces ACTH (bronchogenic or pancreatic carcinoma
• Iatrogenic: Long term glucocorticoid therapy and excess cortisol levels. Most common
cause.
Cushing’s Syndrome Pathophysiology
⬢ Most common in Women
⬢ Age 30 to 50 years old
⬢ For clients taking long term steroids may develop syndrome at any age.
Cushing’s Syndrome
Signs and Symptoms
Cushing’s Syndrome
Signs and Symptoms
• Changes in fat metabolism in the abdomen, fat pads under the clavicle, “buffalo hump” over the upper back, and a round “moon” face
• Changes in protein metabolism results in muscle weakness and wasting
• As thin skin stretches over abdomen and buttocks purple striae (stretch marks) are common
• Glucose metabolism is altered, often resulting in diabetes mellitus.
• Electrolyte imbalances
• Inhibited immune response
• Emotional changes
• Women: hirsutism, acne, irregular cycles
• Increase gastric secretions may result in increase risk of peptic ulcers
Cushing’s Syndrome
Complications if not treated:
• Complications if not treated:
– Electrolyte imbalances
– Hypertension
– Emotional disturbances
Cushing’s Syndrome
Treatment:
Surgery:
• Treatment: pharmacologic, radiation or surgery:
– Surgery: Bilateral adrenalectomy to treat syndrome may result in an acute deficit of cortisol (addisonian crisis)
Surgery: Bilateral adrenalectomy
Surgery: Unilateral adrenalectomy
⬢ Bilateral adrenalectomy: requires LIFETIME hormonal replacement therapy.

⬢ Unilateral adrenalectomy: may need cortisol replacement on a temporary basis (remaining adrenal gland will usually begin functioning for surgically removed gland)
⬢
Cushing’s Syndrome
– Surgery:
POST OP MONITORING
Monitor patient post operatively for signs and symptoms of infection related to higher circulating steroids
Cushing’s Syndrome
Lab and Diagnostics
Lab and Diagnostics
• Measurement of cortisol levels
– If Cushing’s disease is present there will be a loss of normal diurnal variations of higher levels of cortisol in the morning and lower levels in the evening
• Measurement of plasma ACTH levels
– Distinguishes origin of syndrome (primary or secondary)
• 24 hour urine tests
• Measurement of serum potassium, calcium, and glucose levels
Cushing’s Syndrome
Plasma ACTH Levels
Secondary Cushing’s Syndrome: ACTH INCREASES


Primary Cushing’s Syndrome:
ACTH DECRESES
⬢ Measurement of plasma ACTH levels
• ACTH suppression test
– Given to identify the cause of the disorder
• Synthetic cortisol is given to suppress the production of ACTH and plasma cortisol levels. If an extremely high dose of cortisol is necessary to suppress ACTH the primary disorder is adrenal cortex hyperplasia. If ACTH is not suppressed with the synthetic cortisol, the cause may be an adrenal tumor
Treatment of Cushing’s Syndrome
• Pharmacology
– Cytadren and Nizoral
• Radiation Therapy
– If gland completely destroyed will require lifelong replacement therapy
• Surgery
– Transphenoidal approach
Nursing Care of the Client with Cushing’s Syndrome
⬢ Fluid Volume Excess
⬢ Risk for Injury
⬢ Risk for Infection
⬢ Body Image Disturbance
⬢ Activity Intolerance
⬢ Risk for Impaired Skin Integrity
⬢ Altered thought processes
⬢ Risk for Decreased Cardiac Output
⬢ Anxiety
⬢ Altered sexuality patterns
Cushing’s Syndrome
• Expected Outcomes
Cushing’s Syndrome
• Expected Outcomes
– Regain normal body fluid balance
– Remain free of injury.
– Remain free of infection.
– Verbalize understanding of the physical effects of the disease process & realistic expectations of desired changes in appearance.
Adrenal Cortex Hypofunction
⬢ May be primary or secondary:
Adrenal Cortex Hypofunction
• May be primary or secondary:
– Primary: Results from the destruction of the layers of the adrenal cortex
• Autoimmune disorder
• Most common form of adrenal cortex insufficiency is
Addisons disease.
• Other causes: TB, Septicemia, Bilateral Adrenalectomy and infiltrative diseases, anticoagulants, major trauma
– Secondary: Caused from an ACTH deficit resulting from pituitary tumors, pituitary surgery or irradiation and the use of exogenous steroids.
Addison’s Disease
• Results from:
Addison’s Disease
• Results from failure of the adrenal cortex function:
– Deficits of glucocorticoids, mineralocorticoids, and androgens
– Most common in who??
• May occur when long-term, high dose steroid therapy is withdrawn.
• Anticoagulant Drugs:
Addison’s Disease
• Onset is:
_____ ACTH levels, _________aldosterone and cortisol
Addison’s Disease
• Onset is slow, client will exhibit symptoms after about 90% of the gland is lost.
• Elevated ACTH levels, decreased aldosterone and cortisol
– Aldosterone deficiency impacts the distal tubules of the nephrons to conserve sodium.
• Sodium is lost, potassium retained, extracellular fluid is depleted and blood volume is decreased.
• Postural hypotension, syncope common
• Hypovolemic shock may occur.
Addison’s Disease
Aldosterone Deficiency
Addison’s Disease
Aldosterone Deficiency
• Hyponatremia:
– Dizziness
– Confusion
– Neuromuscular irritability
• Hyperkalemia
– Cardiac arrhythmias
Addison’s Disease
Cortisol Insufficiency
Addison’s Disease
Cortisol Insufficiency
• Decreased Hepatic Glyconeogenesis with Hypoglycemia
• Difficulty handling stress
• Lethargy
• Weakness
• Anorexia
• Nausea/Vomiting
• Increased ACTH stimulates hyperpigmentation (98%)
•
Addisonian Crisis
Addisonian Crisis
• Serious, life-threatening condition
• Commonly precipitated by major stressors
• Occurs with abrupt withdrawal from glucocorticoid therapy or from hemorrhage into the adrenal glands
• Primary complications include:
– Severe hypotension, circulatory collapse, shock, coma
Treatment for Addisonian Crisis
Treatment for Addisonian Crisis
• Treatment: rapid IV replacement of fluids and glucocorticoids
– NS & 5% dextrose 1st liter over 30 minutes
– Fluid deficit usually corrects over 12
hours
– Monitor temperature
– Vasopressor Amines if hypotension perists.
Lab and Diagnostics
Addison’s Disease
Lab and Diagnostics
Addison’s Disease • Lab: Decreased levels of cortisol, aldosterone and urinary 17-ketosteroids.
– Dehydration: Elevated BUN and Hematocrit
– Blood Glucose decreased
– Potassium increased
• ACTH stimulation test:
– Cortisol levels rise with pituitary deficiency; does not rise in primary adrenal insufficiency.
Pharmacology
Addison’s Disease •
Pharmacology
Addison’s Disease • Replacement of corticosteroids and mineralocorticoids
• Increased sodium in diet.
• Hydrocortisone given orally to replace cortisol.
• Fludrocortisone (Florinef) given orally to replace mineralocorticoids.
Pharmacology
Teaching
Addison’s Disease
• 2/3rd’s of the dose is generally given when patient gets up in the a.m.; 1/3rd of the dose around 4 p.m. (different for shift workers). Attempting to mimic natural circadian cycle.
• NEVER stop oral glucocorticoids independently. Wear medic alert device, reduce stress, report signs of infection immediately.
• ANY INDUCED STRESS such as surgery, dental work, childbirth, vacations, weddings, etc. will require 2 to 3 times normal dose of glucocorticoids.
Nursing Care for the Client with Addison’s Disease
⬢ Fluid Volume Deficit
⬢ Risk for Ineffective Management of Therapeutic Regimen
⬢ Ineffective Individual Coping
⬢ Activity Intolerance
⬢ Altered Tissue Perfusion
⬢ Anxiety
⬢ Risk for Injury
Nursing Care for the Client with Addison’s Disease
Expected Outcomes
⬢ Regain normal fluid balance.
⬢ Remain free of injury.
⬢ Regain normal peripheral perfusion with blood pressure within normal range.
⬢ Verbalize knowledge of the causes and effects of adrenal insufficiency and ability to self manage at home.
⬢
Hyperfunction of the Adrenal Medulla
Hyperfunction of the Adrenal Medulla
• Extremely Rare
– Pheochromocytomas: Tumor of the chromaffin tissues in the adrenal medulla
• Blood Pressure Concerns:
• Attacks precipitated by physical, emotional, or environmental stimuli
Anterior Pituitary Disorders
• Hyperfunction: Generally caused by a pituitary tumor or hyperplasia
• Hypofunction: Results in a deficiency of one or more of the gland’s hormones.
• Gigantism: Growth hormone oversecretion
– Begins before puberty (Height may exceed 7ft)
• Acromegaly: Enlarged extremities: Sustained growth hormone during adulthood. Client continues to grow.
• Panhypopituitarism
Nursing Care of Clients with Anterior Pituitary Disorders
⬢ Sexual Dysfunction
⬢ Activity Intolerance
⬢ Body Image Disturbance
⬢ Anxiety
⬢ Anticipating Grieving
Posterior Pituitary Gland Disorders
⬢ Results from either excessive or deficiencies in secretion of the antidiuretic hormone (ADH).
⬢ Syndrome of Inappropriate ADH Secretion
⬢ Diabetes Insipidus⬢
Syndrome of Inappropriate ADH Secretion
• High levels of ADH in the absence of serum hypoosmolality.
– Malignant Tumors
– Head Injury
– Pituitary Surgery
– Medications
• Hyponatremia and Water Intoxication
– Brain cells swell
SIADH
SYNDROME OF INAPPROPRIATE ADH

Etiology Of: neoplasm, pulmonary disease, CNS disease, endocrine disorders, and medication. Primary Cause: small cell or oat cell Ca of the lung.
Pathophysiology of: Increase in total body water and extracellular fluid volume due to small amounts of hyperosmolar urine and increased ADH
Manifestations of ADH on body systems
– Decreased plasma Na (hyponatremia) and plasma osmolality (hypotonic), increased urinary Na and urinary osmolality, decreased urinary volume , increased weight, absence of edema
– Neurologic changes: lethargy, headache,mild disorientation that progresses to seizures, emotional/behavioral changes, anxiety, irritability, uncooperativeness, hostility, GI changes, anorexia, nausea, vomiting.
SIADH
NANDA Diagnoses:
SIADH
NANDA Diagnoses:
– Fluid volume excess
– Alteration in nutrition
– Alteration in thought processes
SIADH
Expected Outcomes:
SIADH
Expected Outcomes:
– Demonstrate hyponatremia is reversed
– Fluid volume excess will be excreted
– Acknowledge the cause of the disorder and its management
– Urinary output will be >30 cc/hr.
SIADH
Nursing Care
Nursing Care
Monitor daily weights, daily I & O, and VS & neuro q 4 hrs
Identify clients at risk
Pharmacological agents & nursing implications
3% hypertonic saline and loop diuretic (Lasix)
Correct carefully, NS may be sufficient.
– Diagnostic procedures & nursing implications
Daily serum and urinary sodium levels and osmolality
– Unique nutritional needs
Water restriction is the first priority of management, 800mL/d
Oral salt intake is increased
– Health teaching: Usually resolve in 3 days.
Diabetes Insipidus
Diabetes Insipidus
• Results from ADH Insufficiency
– Neurogenic Diabetes Insipidus
• Hypothalamus or Pituitary Disorder
• Trauma/ Surgery
– Nephrogenic Diabetes
• Renal tubules are not receptive to ADH
• Familial Link
• Lack of ADH or ineffective kidney response to ADH results in insufficient reabsorption of fluids
• Polyuria: up to 20L / day
• If caused by cerebral injury symptoms occur 3-6 days after injury; lasting 7-10 days.
• When ICP decreases, generally the DI is resolved.
• Desmopressin acetate: Administered intranasally, single dose in the evening
• Administer hypotonic fluids
• Increase fluids
• Replace ADH hormone•
Nursing Care of the Client with Posterior Pituitary Gland Disorders
⬢ Fluid Volume Excess related to effects of SIADH
⬢ Fluid Volume Deficient related to the effects of diabetes insipidus secondary to closed-head injury
⬢ Risk for Injury
⬢ Risk for Altered Health Maintenance
⬢ Sleep Pattern Disturbance
⬢ Altered Urinary Elimination⬢
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