What hormones are secreted by the Anterior Pituitary?
TSH (Thyroid Stimulating Hormone), ACTH (Adrenocorticotropic Hormone), FSH (follicle Stimulating Hormone), LH (Lutenizing Hormone), and GH (Growth Hormone).
What hormones are stored in the Posterior Pituitary?
ADH (Antidiurectic Hormone), Oxytocin.
What is Acromegaly?
Rare condition resulting from excess secretion of growth hormone (GH).
What are the clinical manifestations of Acromegaly?
Enlargement of the hands and feet, thickening and enlargement of face and head body and soft tissue, deepening of the voice, enlargement of the tongue, visual changes, thick leathery skin, sleep apnea, signs of diabetes mellitus, cardiomegaly, and hypertension.
What diagnostic studies are done for Acromegaly?
H & P, evaluation of plasma insulin like growth factor (IGF-1), IGF binding proteins (IGFBP-3), and GH response to an oral glucose challenge. MRI and CT scan.
How is an Oral Glucose Tolerance Test performed?
GH secretion is inhibited by glucose. Two baseline GH levels are obtained before ingestion of 75 - 100 g of oral glucose, and additional GH measurements are made at 30, 60, 90 and 120 minutes following oral glucose load. Normally GH concentrations fall during an OGTT. In acromegaly, GH levels do not fall below 3 ng/mL2.
What is Nursing Management following a Hypophysectomy with a Acromegaly patient?
Avoidance of virgorous coughing, sneezing and straining at stool to prevent CSF leakage from where sella turcica was entered. Head of bed elevated 30 degrees at all times. Neurological status and monitor. Mild analgesia is used for headache. Teeth brushing is avoided for ten days.
What is treatment for Acromegaly?
Goal is to return GH levels to normal through surgery, radioation, and drug therapy. Prognosis is dependent on age of onset, when treatment was initiated and tumor size.
What are the surgical options for Acromegaly?
Hypophysectomy - removal of the entire pituitary gland.
What does a patient need after a Hypophysectomy or pituitary damage?
ADH, cortisol and thyroid replacement for life.
When is radiation therapy used for Acromegaly?
When surgery has failed to complete remission, and those considered high risk for surgery. Used in combination of drugs and can also reduce the size of the tumor before surgery.
When is the drug therapy for Acromegay used?
Used in patients who have inadequate response to or cannot be treated with radiation therapy.
What is drug therapy for Acromegaly?
Octrotide (Sandostatin) - a somatostatin analog that reduces GH levels to within normal range in many patients. Given subcutaneously three times a week. Long acting analogs are available, injections given every 2 - 4 weeks.
What is Syndrome of Inappropriate Antidiuretic Hormone (SIADH)?
Results from abnormal production or sustained secretionof ADH.
What is the most common cause of SIADH?
What can cause SIADH besides lung cancer?
Head injury or head trauma.
What are the clinical manifestations of SIADH?
Hypoosmolality, hyponatremia, muscle cramps, weakness, increased vascular volume -> hypertension, edema, low U/O, seizure/coma/death.
What diagnostic procedures are positive for SIADH?
Serum osmolality less than 275, increased urine osmolality, all normal serum electrolyte levels except serum sodium.
What is Nursing Management for SIADH?
Assess VS. Monitor I & O. Monitor cardiovascular and pulmonary status. Seizure precautions. Lowest bed position possible. Good oral hygiene. Skin care - monitor breakdowns and edema. Safety.
What is Treatment for SIADH?
Directed at underlying cause with a goal to restore normal fluid volume and osmolality. Fluid restriction, and self management.
What is Diabetes Insipidus (DI)?
Associated with deficiency of production or secretion of ADH or decreased renal response to ADH. May be transient or life-long.
What are the Clinical Manifestations of DI?
Polydipsia, polyuria, decreased urine osmolality, hypernatremia, increased serum osmolality, fatigue, constipation, poor skin turgor, hypotension, tachycardia.
What happens if oral fluid intake cannot keep up with urinary losses?
Severe fluid volume deficit results as manifested by weight loss, constipation, poor skin turgor, hypotension and shock. Increased urinary output and plasma osmolality can cause severe fluid and electrolyte balance.
What Diagnostic Tests are done for DI?
Water Restriction/Deprivation Test.
How is a Water Restriction/Deprivation Test done?
Basline weight, pulse, urine/plasma osmolalities, urine specific gravity and BP. Instruct pt to with-hold all fluids for 8 - 16 hours before testing. Reassure testing will be stopped if fluid volume deficit symptoms become severe. Observe the patient throughout the test because of craving to drink. During the test assess patients BP, weight and urine osmolality. Test continues until urine osmolality stabilizes, or body weight declines 3%. Vasopressin is given, and urinary osmolality is measured 1 hour later.
What indicates positive DI with a Water Restriction/Deprivation Test?
Urine osmolality after vasopressin exceeding 9%.
What is Nursing Management for DI?
Early detection, maintenance of adequate hydration and patient teaching for long term management.
What is collaborative care for DI?
Hypotonic IV fluids, desmopression (ADH), low sodium diet, thiazide diuretics, monitor U/O, daily weights and I & O.
What is treatment for DI?
Treating the primary cause central to management. Therapeutic goal is maintenance of fluid and electrolyte balance.
What is Goiter?
an enlarged thyroid gland.
What happens in the formation of a Goiter?
Thyroid cells are stimulated to grow, which may result in an overactive thyroid (hyperthyroidism) or underactive one (hypothyroidism).
What diagnostic data is measure to determine Thyroid Function?
TSH and T4 levels.
What surgical procedure is used for Goiters?
Surgical removal of large goiters may be performed.
What is Hyperthyroidism?
Thyroid gland hyperactivity with sustained increase in synthesis and release of thyroid hormone.
Who is more likely to have Hyperthyroidism?
Women ages 20 - 40.
What is Thyrotoxicosis?
Physiologic effects or clinical syndrome of hypermetabolsim that results from excess circulating levels of T4, T3 or both.
What is Graves Disease?
An autoimmune disease of unknow etiology marked by diffused thyroid enlargement and excessive hormone secretion. 75% of hyperthyroidism cases.
What are the clinical manifestations of Hyperthyroidism?
Related to the effect of excess thyroid hormone. Increases metabolism and increases tissue sensitivity to stimulation by the SNS. Goiter, opthalamopathy - exophtalamos, weight loss, intolerance to heat, tachycardia, insomnia tremors, hypertension.
What are the diagnostic values for Hyperthyroidism?
Decreased TSH and elevated free thyroxine (free T4 levels).
What other testing besides TSH and T4 levels can be done for hyperthyroidism?
Radioactive Iodine Uptake (RAIU).
What is treatment for hyperthyroidism?
Antithyroidmedication, Radioactive Iodine Therapy (usual choice), and subtotal thyroidectomy.
What is the overall goal with treatment of Hyperthyroidism?
Patient will experience a relief of symptoms, have no serious complications related to the disease or treatment, maintain nutritional balance and cooperate with the therapeutic plan.
What is Collaborative Management for Hyperthyroidism?
Medication, antithyroid drugs, iodine, beta adrenergic blockers, radioactive iodine therapy, surgery, nutrition, quiet calm environment, cardiac monitoring, artificial tears.
What is management after Surgery of a Thyroidectomy?
Airway management, semi to high fowlers, monitor for hypercalcemia, laryngeal strider.
What two things do you keep at the side of the bed post Thyroidectomy?
Trachesotomy kit and calcium.
What is a Thyrotoxic Crisis (Thyroid Storm)?
Acute, rare condition in which all hyperthyroid manifestations are heightened.
What are the manifestations of a Thyroid Crisis?
Tachycardia, shock, hyperthermia, seizures, abdominal pain, diarrhea, delirium and coma.
What is treatment for Thyrotoxic Crisis?
Focuses on reducing circulating thyroid hormone levels by drug therapy.
What is Hypothyroidism?
Common medical disorder resulting from insufficient circulating thyroid hormone.
What are the causes of Hypothyroidism?
Primary from destruction of thyroid tissue or defective hormone synthesis, or secondary related to pituitary disease with decreased TSH secretion or hypothalamic dysfunction with decrease thyrotropin-releasing hormone secretion.
What is the most common cause of hypothyroidism?
What are the clinical manifestations of Hypothyroidism?
Characterized by slow body proesses. Fatique, lethargy, personality and mental changes, decreased cardiac output, anemia, constipation, cold intolerance, hair loss, flaky skin or nails, weight gain.
What are possible complications of Hypothyroidism?
Myxedema, Myxedema coma.
What is Myxedema?
Accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues.
What does Myxedema cause?
Facies of hypothyroidism (puffiness, periorbital edema and masklike affect).
What is Myxedema Coma precipitated by?
Infection, drugs (especially opiods, tranquilizers and barbiturates), exposure to cold and trauma.
What is Myxedema Coma characterized by?
Subnormal temperature, hypotension and hypoventilation.
What is supportive therapy for Myxedema Coma?
VS functions are support and IV thyroid hormone replacement is administered.
What are the diagnostic levels for Hypothyroidism?
TSH levels increased, decreased T4 levels.
What is the goal of treatment with Hypothyroidism?
Restoration of euthyroid state as safely and rapidly as possible with hormone replacement therapy. Levothyroxine is drug of choice.
What is Collaborative Management for Hypothyroidism?
Levothyroxine, weight loss, monitor bowel function, skin care, acute care of myxedemas coma client. Teach client s/s of hyperthyroidism and monitor weights. Life long therapy.
What is Hyperparathyroidism?
Involves increased secretion of parathyroid hormone (PTH) that leads to hypercalcemia and hypophosphatemia.
What are the clinical manifestations of Hyperparathyroidism?
Weakness, loss of appetite, constipation, sleepiness, emotional disorders, decreased attention span, osteoporosis/fracture, and kidney stones.
What Diagnostic Studies are indicative of hyperparahytoidism?
Elevated PTH levels, serum calcium levels exceed 10 mg/DL, serum phosphorus levels less than 3 mg/DL. Elevation in urine calcium, serum chloride, uric acid, creatinine, amylase (pancreatitis), and alkaline phosphatase (bone disease).
What other diagnostic studies are useful for hyperparathyroidism?
Bone density. Dual energy x-ray asorptimetry (DEXA) tested for hypocalcemia. MRI, CT and ultrasound for adenoma.
What is the surgical treatment for hyperparathyroidism?
What are the non-surgical treatments for hyperparathyroidism?
Avoidance of immobility, high fluid intake, moderate calcium intake. Drug therapy agents that lower calcium such as biphosphates, estrogens, oral phosphates, diuretics and calcimemetics.
What is Nursing Care post-operatively for a Parathyroidectomy?
Watch for edema, laryngospasms, tetany, semi-fowlers, tracheostomy tray close to bed, foods high in calcium, watch phytic acid. Monitor I & O. Asses calcium potassium phosphate, and magnesium levels. Chvosteks and Trousseaus sign. Encourage mobility.
What is Hypoparathyroidism?
Results from inadequate circulating PTH that results in hypocalcemia.
What is the most common cause of hypoparathyroidism?
Iatogenic from accidental removal of parathyroid galnds or damage to these glands during neck surgery.
What are the clinical Manifestations of hypoparathyroidism?
Positive chvosteks and trousseaus sign, tetany (tingling of lips, fingertips and increased muscle tension with paraesthesia and stiffness). Cardiac arrhytmias, laryngospasms, muscle cramps and irritability.
What is the emergency treatment of Tetany?
Give IV calcium chlorde, calcium gluconate, calcium gluceptate slowly. Monitoring is needed during administration because hypotension, serium cardiac dysrythmias or arrest can occur.
What is Collaborative Management for Hypoparathyroidism?
EKG monitoring, respiratory monitoring, VS monitor, calcium supplementation. Vitamin D supplementation. Meal high in calcium, Avoidance of Oxalic acid, phytic acid and phosphorus.
What are foods high in calcium?
Dark green vegetables, soybeans and tofu.
What are foods that contain Oxalic Acid?
What are foods that contain phytic acid?
Bran and whole grains.
What does the patient with hypoparathyroidism need to be taught?
Instructions on lifelong treatment, including drug therapy, nutrition, and monitoring calcium levels.
What is Cushings Syndrome?
Spectrum of clinical abnormalities by excessive corticosteroids, particularly glucocorticoids.
What is the most common cause of Cushings Syndrome?
Administration of exogenous corticosteroids such as prednisone.
What is the endogenous cause of Cushings Syndrome?
Adrenocoriticotropic hormone secreting pituitary tumor.
What are the clinical manifestations of Cushings Syndrome?
Weight gain, moon face, buffalo hump, hyperglycemia, muscle wasting, loss of bone, thin fragile skin that bruises easily, excess body hair, hypertension, hypokalemia, menstrual irregularity, poor wound healing, purple striae below the skin surfaces.
What diagnostics are used with Cushings Syndrome?
24 hour collection of urine cortisol, dexamethasone suppression test, CT or MRI of adrenal glands or pituitary for tumor.
What is treatment for Cushings Syndrome?
Dependent on underlying cause and include surgery and drug therapy to normalize hormone levels. Ween off corticosteroids if not contraindicated, drugs that inhibit adrenal function (very toxic).
When is an Adrenalectomy indicated?
When cushings is caused by tumors or hyperplasia.
What is Nursing Care for Cushings Syndrome?
Around the clock diagnosis for risk of infection, imbalanced nutrition, disturbed self esteem, and impaired skin integrity. Care instructions are based on patients inability to react on stressors physiologically.
What is Collaborative Management for Cushings Syndrome?
Medication to suppress adrenal function, Vs, monitor glucose, monitor potassium, daily weights, pre and post op management, skin care, and psychosocial support.Lifelong therapy is required by many patients.
What is Addisons Disease?
Primary hypofunction of the adrenal cortex that results in reduction of all three classes of adrenal corticosteroids. Secondary diseases result from pituitary dysfunction.
What is the most common cause of Addisons Disease?
Autoimmune when the adrenal cortex is destroyed by autoantibodies.
What are the clinical manifestations of Addisons Disease?
Weakness, fatigue, weight loss, anorexia, hyperpigmentation of the skin, orthostatic hypotension, hyponatremia, hyperkalemia, N & V, diarrhea, hypoglycemia.
What is a possible complication of Addisons Disease?
What is an Addisonian Crisis?
Life threatening emergency caused by insufficient adrenocorticol hormones or a sudden sharp decrease in these hormones.
What is Addisonian Crises triggered by?
Stress (infection, surgery, trauma, hemorrhage, or psychological distress), the sudden withdrawal of corticosteroids hormone replacement therapy, or after adrenal surgery or following sudden pituitary gland destruction.
What are the manifestations of Addisonian Crisis?
Hypotension (mainly postural), tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness and confusion. May lead to shock. Severe vomiting, diarrhea and pain in abdomen.
What is treatment of an Addisonian Crisis?
Shock management and high dose hydrocortisone replacement. Large volume of 0.9% saline solutions and 5% dextrose are given to reverse hypotension and electrolyte imbalance until BP normalizes.
What diagnosic tests are used for Addisons disease?
Plasma cortisol levels, hyperkalemia, hypoglycemia, anemia, CT scans and MRI to localize tumors or adrenal calcifications/enlargement.
What is treatment for Addisons Disease?
Replacement therapy. Hydrocortisone. Increased dosage during times of stress to prevent addisonian crisis. Mineralcorticoid replacement with fludrocortisone acetate with increased dietary salt.
What is nursing management for Addisons disease?
When hospitalized frequent nursing assessments are necessary. Daily weights, diligent corticosteroid administration, protection against exposure to infection and assistance with daily hygiene. Lifelong therapy is needed.
What is Pheochromocytoma?
A rare condition characterized by an adrenal medulla tumor that produces excessive caecholamines (epinephrine, norepinephrine) resulting in severe hypertension.
What are the clinical manifestations of Pheochromocytoma?
Severe episodic hypertension accompanied by classic triaf of severe pounding headache, tachycardia with palpitations and profuse sweating, and unexplained abdominal or chest pain.
What can Pheochromocytoma attacks be provoked by?
Many medications including antihypertensives, opiods, radiologic contrast media, and tricyclic antidepressants.
What can Pheochromocytoma lead to if left undiagnosed?
Diabetes mellitus, cardiomyopathy, and death.
What are the Diagnostic Procedures for Pheochromocytoma?
Urinary fractionated meanphrines and fractionated catecholamines and creatinine usually done in 24 hour urine collection. CT Scans and MRIs for tumors.
What is treatment for Pheochromocytoma?
Surgical removal of the tumor.
What is pre-operative treatment for Pheochromocytoma?
a-adrenergic receptor blockers and b-adrenergic receptor blockers are required to control BP and prevent intraoperative hypertensive crisis. Given 7 - 10 days preoperatively. Advise patient about orthostatic hypotension.
What is Nursing management for Pheochromocytoma post-operatively?
Make patient as comfortable as possible, monitor blood glucose levels to assess for DM. Rest, nourishing food, and emotional support. Follow up and routine monitoring.
What can long term corticosteroid use lead too?
Serious complications and side effects.
Who is corticosteroid therapy reserved too?
Disease in which there is a risk of death or permanent loss of function and condition in which short therm therapy is likely to produce remission or recovery. Treatment must be weight against risks.
Why should corticosteroid therapy never be abruptly stopped?
May lead to addisonian crisis and possible death.
What is needed during times of stress with corticosteroid therapy?
Increased amount of medication.
What should a diet contain for someone on corticosteroid therapy?
Diet high in protein, calcium potassium but low in fat and concentrated simple carbohydrates.
What should patients with DM do with corticosteroid therapy?
Monitor blood glucose closer.
What happens when corticosteroids are taken longer than 1 week?
Adrenal production is suppressed, oral corticosteroids should be tapered.
What are side effects of Corticosteroids?
Hypokalemia, peptic ulcer disease, skeletal muscle atrophy and weakness, mood and behavior changes, fat redistribution, delayed healing, susceptibility to infection is increased, suppression of pituitary ACTH, increased blood pressure, protein depletion.