Pituitary Gland Hard

• Pituitary gland, or hypophysis, is the "master gland" due to its influence on hormone secretion by other endocrine glands.
• Located on the inferior aspect of the brain, it's a round structure, about 1.27 cm in diameter, divided into anterior and posterior lobes.
• Controlled by the hypothalamus, an adjacent brain area connected by the pituitary stalk.

Anterior Pituitary

• Major hormones include FSH, LH, prolactin (PRL), ACTH, TSH, and GH (somatotropin).
• Hormone secretion is controlled by releasing factors from the hypothalamus, reaching the anterior pituitary via the pituitary portal blood system.
• Other hormones include melanocyte-stimulating hormone and beta-lipotropin (function poorly understood).
• TSH, ACTH, FSH, and LH primarily stimulate hormone release from other endocrine glands.
• Imbalanced ACTH secretion causes Addison’s disease (hypoproduction) or Cushing’s syndrome (hyperproduction).
• Prolactin (PRL) stimulates milk production in the breast.
• GH regulates growth in children, energy, and metabolism in adults.
• GH increases protein synthesis, fatty acid breakdown, and blood glucose levels.
• Thyroid hormone and insulin are required for the GH system to function properly.
• GH secretion increases with deep sleep, stress, exercise, fasting, malnutrition, hypoglycemia, trauma, hypovolemic shock, and sepsis.
• GH secretion decreases in obesity, depression, and hypothyroidism.

Posterior Pituitary

• Secretes vasopressin (ADH) and oxytocin, synthesized in the hypothalamus and stored in the posterior pituitary.
• Vasopressin controls water excretion by the kidney; secretion is stimulated by increased blood osmolality or decreased blood pressure.
• Oxytocin secretion is stimulated during pregnancy and childbirth.
• Oxytocin facilitates milk ejection during lactation and increases uterine contractions during labor and delivery.

Pathophysiology

• Abnormal pituitary function results from over- or undersecretion of hormones.
• Anterior and posterior abnormalities can occur independently.
• Hypopituitarism results from pituitary or hypothalamus disease.
• Hypopituitarism can result from radiation therapy to the head and neck area.
• Total pituitary destruction (trauma, tumor, vascular lesion) removes stimuli to the thyroid, gonads, and adrenal glands.
• Untreated hypopituitarism leads to extreme weight loss, emaciation, endocrine gland atrophy, hair loss, impotence, amenorrhea, hypometabolism, and hypoglycemia; coma and death can occur without hormone replacement.

Anterior Pituitary Abnormalities

• Hypersecretion commonly involves ACTH (Cushing’s syndrome) or GH (acromegaly).
• Acromegaly is caused by excess GH in adults, leading to enlargement of peripheral body parts and soft tissue.
• Oversecretion of GH in children before epiphyseal fusion results in pituitary gigantism.
• Insufficient GH secretion in childhood causes generalized limited growth and pituitary dwarfism.
• Hyposecretion commonly involves all anterior pituitary hormones (panhypopituitarism) causing the thyroid gland, the adrenal cortex, and the gonads to atrophy.

Posterior Pituitary Abnormalities

• Diabetes insipidus (DI) is the most common disorder, characterized by large volumes of dilute urine due to deficient vasopressin.
• DI can occur after brain tumor surgery, with nonsurgical brain tumors, from traumatic brain injury, with nervous system infections, post-hypophysectomy, from renal tubule failure to respond to ADH, and from specific medications.

Pituitary Tumors

• Almost all pituitary tumors are benign and slow-growing.
• Tumors may be primary or secondary, functional or nonfunctional.
• Functional tumors secrete pituitary hormones, nonfunctional tumors do not.
• Tumors cause clinical issues from pressure on adjoining tissues, endocrine dysfunction, or effects on target organs.
• Principal types are overgrowth of eosinophilic, basophilic, or chromophobic cells.

Clinical Manifestations

• Eosinophilic tumors cause gigantism in early life (excessive height, weakness).
• In adults, eosinophilic tumors cause acromegaly (skeletal growth in feet, hands, face), headaches, visual disturbances, decalcification, muscular weakness, and endocrine disturbances.
• Basophilic tumors cause Cushing’s syndrome (hyperadrenalism, masculinization, amenorrhea, truncal obesity, hypertension, osteoporosis, polycythemia).
• Chromophobic tumors (90% of pituitary tumors) usually don't secrete hormones but cause hypopituitarism.
• Chromophobic tumors cause obesity, somnolence, fine hair, dry skin, headaches, loss of libido, visual defects, polyuria, polyphagia, low metabolic rate, and subnormal body temperature.

Assessment and Diagnostic Findings

• Requires careful history and physical examination, including assessment of visual acuity and visual fields.
• CT and MRI scans diagnose the presence and extent of pituitary tumors.
• Serum levels of pituitary and target organ hormones are measured to assist in diagnosis.

Medical Management

• Hypophysectomy (surgical removal of the pituitary gland via transsphenoidal approach) is the usual treatment.
• Stereotactic radiation therapy delivers external-beam radiation precisely to the tumor with minimal effect on normal tissue.
• Other treatments include conventional radiation therapy, bromocriptine, and octreotide.
• Octreotide and lanreotide may be used preoperatively to improve the patient’s clinical condition and to shrink the tumor.

Surgical Management

• Hypophysectomy is the treatment of choice for Cushing’s disease resulting from excessive ACTH production.
• Hypophysectomy may be performed as a palliative measure to relieve bone pain from metastatic breast and prostate lesions.
• Approaches include surgical removal (transfrontal, subcranial, oronasal-transsphenoidal), irradiation, and cryosurgery.
• Transsphenoidal approach and nursing management of cranial surgery are discussed in Chapter 61.
• Acromegaly features are unaffected by surgical tumor removal.
• Pituitary gland absence alters many body systems.
• Menstruation ceases and infertility occurs after pituitary gland ablation so replacement therapy with corticosteroids and thyroid hormone is necessary.

Diabetes Insipidus (DI)

• Rare disorder due to injury to the hypothalamus or pituitary gland with a deficiency of ADH (vasopressin).
• Results in excretion of large volumes of dilute urine and extreme thirst.
• Characterized as central, nephrogenic, dipsogenic, or gestational.
• Primary etiology for central DI is head trauma, surgery, infection, inflammation, brain tumors, or cerebral vascular disease; it may also be idiopathic.
• Nephrogenic DI etiologic factors include kidney injury, medications (lithium), hypokalemia, and hypercalcemia.
• Dipsogenic DI is caused by a defect in the hypothalamus.
• DI must be differentiated from diabetes, which may also cause polydipsia and excessive urination.

DI: Clinical Manifestations

• Enormous daily output (greater than 250 mL per hour) of very dilute urine with a specific gravity of 1.001 to 1.005.
• Urine contains no abnormal substances like glucose or albumin.
• Intense thirst leads to drinking 2 to 20 L of fluid daily, craving cold water.
• Disease cannot be controlled by limiting fluid intake.
• Attempts to restrict fluids cause an insatiable craving for fluid, hypernatremia, and severe dehydration.

DI: Assessment and Diagnostic Findings

• Fluid deprivation test involves withholding fluids for 8 to 12 hours or until 3% to 5% body weight is lost.
• Plasma and urine osmolality studies are performed at the beginning and end of the test.
• Inability to increase the specific gravity and osmolality of the urine is characteristic of DI.
• Patient experiences weight loss, increasing serum osmolality, and elevated serum sodium levels.
• Test is terminated if tachycardia, excessive weight loss, or hypotension develops.
• Other diagnostic procedures include concurrent measurements of plasma levels of ADH and plasma and urine osmolality, a trial of desmopressin therapy, and intravenous (IV) infusion of hypertonic saline solution.

DI: Medical Management

• Objectives of therapy are to replace ADH, ensure adequate fluid replacement, and identify and correct the underlying intracranial pathology.
• Nephrogenic causes require different management approaches.
• Desmopressin, a synthetic vasopressin, is the drug of choice for central DI.
• Vasopressin causes vasoconstriction and must be used cautiously in patients with coronary artery disease.
• Chlorpropamide and thiazide diuretics are also used in mild forms, but with caution due to risk for hypoglycemia.
• If DI is renal in origin, the previously described treatments are ineffective.
• Thiazide diuretics, mild salt depletion, and prostaglandin inhibitors (indomethacin and aspirin) treat the nephrogenic form of DI.

DI: Nursing Management

• Ongoing physical assessment and patient education are crucial.
• Monitor for clinical manifestations of dehydration.
• Severe dehydration can lead to decreased cardiac output and decreased perfusion of the vital organs, specifically the brain and kidneys.
• Ongoing monitoring of vital signs as well as intake and output (I&O) is essential.
• Educate the patient, family, and other caregivers about follow-up care, prevention of complications, and emergency measures.
• Specific verbal and written instructions should include the dose, actions, side effects, and administration of all medications and the signs and symptoms of hyponatremia.
• The patient should be advised to wear a medical identification bracelet and carry required medication and information about DI at all times.

Syndrome of Inappropriate Antidiuretic Hormone Secretion

• Results from a failure of the negative feedback system that regulates ADH release and inhibition.
• Patients cannot excrete dilute urine, retain fluids, and develop dilutional hyponatremia.
• Often of nonendocrine origin, such as bronchogenic carcinoma.
• May occur in patients with severe pneumonia, pneumothorax, and other lung disorders, as well as malignant tumors that affect other organs.
• CNS disorders may produce SIADH by direct stimulation of the pituitary gland.
• Some medications and nicotine either directly stimulate the pituitary gland or increase the sensitivity of renal tubules to circulating ADH.

SIADH: Medical Management

• Generally self-limiting and treatment is focused on eliminating the underlying cause and restricting fluid intake.
• Extracellular fluid volume contracts and serum sodium concentration gradually increases toward normal.
• Diuretic agents such as furosemide may be used along with fluid restriction.
• In severe hyponatremia sometimes a hypertonic NaCl (3%) may be prescribed and administered IV.

SIADH: Nursing Management

• Close monitoring of fluid I&O, daily weight, urine and blood chemistries, and neurologic status is indicated.
• Supportive measures and explanations of procedures and treatments assist the patient in managing this disorder.