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ANTERIOR PITUITARY DISORDERS

Disorders of the pituitary gland occur most frequently in the anterior lobe. Major causes of pituitary disease Include functioning tumors, nonfunctioning tumors, pituitary infarction, genetic disorders and trauma. The three (3) principal pathologic consequences of pituitary disorders are: (1) Hyperpituitarism (2) Hypopituitarism (3) Local compression of brain tissue by expanding tumor masses

DISEASE
Hyperpituitarism and Hyperprolactinemia -defined as oversecretion of one or more of the hormones secreted by the pituitary gland

ETIOLOGY AND RISK FACTORS


-Caused primarily by a hormone-secreting pituitary tumor, typically benign adenoma.

PATHOPHYSIO
- Prolactin and growth hormone are commonly overproduced by adenomas. They lead to hyperprolactinemia and acromegaly. Increased amounts of GH lead to rapid growth of all body tissue which leads to gigantism. This occurs before closure of epiphysis and acromegaly if it occurs after epiphyseal closure.

CLINICAL MANIFESTATIONS
-produce both systemic and local effects. -Systemic effects include : Excessive growth pattern Galactorrhea Overstimulation of one or more of the target glands, resulting in excess thyroid, sex or adrenocortical hormones. -Local manifestations visual field abnormalities Headaches

DISEASE Hyperpituitarism and Hyperprolactinemia -

MANAGEMENT
-Surgical *tumor resection, usually transsphenoid hypophysectomy -Nursing Assessment Assess reaction to the diagnosis, expectations for the surgery, educational needs and available support network after disharge Baseline VS, weight and neurologic (eyes, hand grip, LOC, orientation to time, place , person and location, response to stimul and visual acuity and fields Preop eye examination

DIAGNOSIS -Risk for injury r/t


postoperative complications. Interventions Prevent adrenal insufficiency ( IV injection of cortisol or glucocorticoids) Monitor intracranial pressure (wof : elevated BP, widened pulse pressure,low PR, pupil changes, altered respiratory pattern, decreasing LOC) Monitor for hormonal insufficiencies (wof: adrenal insufficiency and hypothyroidism, DI; maintain strict I/O Provide oral hygiene (gauze sponge only, should not brush the teeth for 2 weeks)

EVALUATION -Absence of postoperative complications and the clients ability to manage lifetime hormone replacement.

DISEASE Hypopituitarism -deficiency of one or more of the hormones produced by the anterior lobe of the pituitary

ETIOLOGY AND RISK FACTORS Nine Is -Invasion -infarction -infiltration -injury -immunologic -iatrogenic -infectious -idiopathic -isolated

PATHOPHY - Manifestations depend on age of onset as well as the hormones that are deficient. Classic course is an initial loss of GH and gonadotropin, followed by deficiencies of TSH, ACTH and prolactin.

CLINICAL MANIFESTATIONS
-Short stature -Sexual and reproductive: sterility, diminished sex drive, decreased secondary sex characteristics, infertility, amenorrhea, diminished spermatogenesis and testicular atrophy - hypothyoidism - secondary adrenocortical insufficiency -Absence of lactation in the postpartum women Diagnostic test results : -low cortisol levels -high or low ACTH depending if primary or secondary hypopituitarism -low thyroid hormone and TSH levels -low levels of sex steroids -enlargement of sella turcica, erosion of sphenoid bone or calcification of suprasellar mass

DISEASE Hypopituitarism -deficiency of one or more of the hormones produced by the anterior lobe of the pituitary

ETIOLOGY AND RISK FACTORS Nine Is -Invasion -infarction -infiltration -injury -immunologic -iatrogenic -infectious -idiopathic -isolated

PATHOPHY - Manifestations depend on age of onset as well as the hormones that are deficient. Classic course is an initial loss of GH and gonadotropin, followed by deficiencies of TSH, ACTH and prolactin.

CLINICAL MANIFESTATIONS
-Short stature -Sexual and reproductive: sterility, diminished sex drive, decreased secondary sex characteristics, infertility, amenorrhea, diminished spermatogenesis and testicular atrophy - hypothyoidism - secondary adrenocortical insufficiency -Absence of lactation in the postpartum women Diagnostic test results : -low cortisol levels -high or low ACTH depending if primary or secondary hypopituitarism -low thyroid hormone and TSH levels -low levels of sex steroids -enlargement of sella turcica, erosion of sphenoid bone or calcification of suprasellar mass

Surgical Management -Treatment involves removal of the causative factor and permanent replacement of the hormones secreted by the target organs
Medical Management of Hypopituitarism -Injections of human growth hormone successfully treat growth hormone deficiency. -Medications prescribed to replace hormones include corticosteroids to correct secondary adrenocortical deficiency, thyroid hormone to treat myxedema and sex hormones to correct hypogonadism. -Assessment and nursing interventions of clients with hypopituitarism are directed at problems resulting from deficiency at the target organs.

POSTERIOR PITUITARY (NEUROHYPOPHYSEAL) DISORDERS

Diabetes Insipidus

Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)


- excessive amounts of ADH secreted from posterior pituitary and other ectopic sources Approximately 80% with small cell carcinoma have evidence of impaired ability to excrete water secondary to ectopic production of vasopressin

Definition

-deficiency of Antidiuretic hormone (ADH, vasopressin) results in inability to conserve water Unknown, Idiopathic in 30% of all clients, tumor in 25%, head injury in 10%, cranial surgery in 20% of DI cases.

Incidence

Etiology

-central or neurogenic: : CNS


interruption of anatomic integrity of posterior pituitary, generalized or localized edema from head trauma, vascular lesions, centrally acting drugs, CNS infections -complete : disruption of hypophyseal tract and complete absence of ADH -nephrogenic : rare hereditary d/o -idiopathic

-ectopic production of
vasopressin by malignancy is most common cause

Diabetes Insipidus Risk Factors


-head injury, neurosurgery,hypothalamic tumors, pituitary tumors,brain infections or inflammation, drugs that inhibit vasopressin release;ethanol, glucocorticoids, adrenergic agents, phenytoin, narcotic antagonists, lithium.

SIADH
- Vasopressin overuse, malignant conditions, bronchogenic carcinoma, duodenal, brain and bladder lymphoma, pancreatic cancer, prostate cancer, increased ICP, viral or bacterial pneumonia, drugs that mat stimulate vasopressin release, endocrine disorders, adrenal nsufficiency, myxedema, anterior pituitary insuffciency, analgesics and vomiting. -Key features of ADH excess : (1) Water retention (2) Hyponatremia- suppresses renin and aldosterone secretions causing decrease in proximal tubule reabsorption of Na+ (3) Hypo-osmolality; a contnual release of ADH causes water retention from renal tubules and collecting ducts; extracellular fluid volume increases with dilutional hyponatremia

Pathophysiology

-With ADH deficiency, permeability of water is diminished, resulting in large volumes of hypotonic fluid. 3 patterns may develop : (1) Transient: abrupt onset w/in few days after surgery; resolves w/in few days (2) Permanent: persists for several weeks or forever, usually occurs after damage to hypothalamus or neurohypophyseal stalk (3) Triphasic : immediate post injury increase in urine volume w/ decrease in urine osmolality lasting 4-5 days; interphase occurs over next 5-7 days when urine decreases to normal and is

Diabetes Insipidus Physical Examination


-Integumentary; dry, cool skin, dry mucous membranes -Cardiovascular: tachycardia -Physical manifestations related to specific electrolyte imbalance

SIADH
-Decreased deep tendon reflexes, fatigue, headache,a anorexia, nausea, decreased mental status, seizures,coma (related to hyponatremia) -weight gain w/o edema; jugular venous distention,tachycardia, tachypnea, rales (related to fluid volume excess) -Related to degree of hyponatremia: confusion, lethargy, irritablity, seizures, coma -Gastrointestinal : decreased motility with anorexia, nausea, vomiting, abrupt weight gain without edema of 5-10%

Clinical Manifestations

-Genitourinary polyuria : a few liters to 18L/day; clear urine; urinary frequency; nocturia -Gastrointestinal: weight loss, polydipsia -Integumentary : dry skin and mucous membranes -Neurologic: mentation changes as electrolyte imabalance and hypotension worsen Electrolyte imbalance; hypovolemia; hypotension; shock

Complications

Seizures, coma, permanent brain damage; disease processes already in progress may be complicated.

Diabetes Insipidus Diagnosis -Urine output- a few liters to 18L/day; spec gravity 1.005; osmolality: <200 mOsm/kg H2O -Plasma osmolalty : increase 2 to hypovolemia and dehydration -Serum Na+ : increase 2 to hypovolemia and dehydration -Serum osmolality : >290 mOsm/kg H2O -Serum Na+ : decrease 2 to volume depletion -Water deprivation study : + -Hypertonic saline test: + for DI if there is little or no increase in plasma ADH levels - Hypophysectomy to remove posterior pituitary tumor

SIADH -Serum Na+: decrease -Urine Na+: increase -BUN : increase -Serum osmolality: decrease - urine osmolalty : increase -Absence of hypotension -Hypovolemia -Water load: (+) -Abnormal water excretion -Serum Na+: remains decrease -Serum osmolality : remains decrease; urine osmolality: remains increase

Surgical Management

-none

Diabetes Insipidus Medical Management


- IV fluids; ADH replacement with desmopressin IV, subcutaneous or intranasal, nasal solution bid is drug of choice, Pitressin tannate n oil is given IM; aqueous Pitressin is used for acute, transient form of DI -Know which clients are at risk -Monitor I/O -Monitor for thirst and excessive urination -Assess serum and urine values: decrease SG, increase urine osmolality; increase serum osmolality are early indicators of DI -Observe effects of DI on concurrent medical and surgical disorders -Client and family teaching

SIADH
-Hypertonic IV fluids to correct hyponatremia; sodium restriction ; diuretics to correct low plasma osmolality; monitor urne electrolyte loss; replace electrolyte loss; demeclocycline to facilitate free water clearance; treat underlying cause. -Know which clients are at risk -Monitor appropriate urine and serum lab tests -Assess for manifestations of hyponatremia -Monitor daily weights and I/O -Observe for changes in concurrent disorders -Administer demeclocycline as ordered -Monitor for hypernatremia with fluid over correction -Client and family teaching

Nursing Management

Prognosis

-Excellent if there is compliance -Depends on cause and sodium


with vasopressin therapy level and serum osmolality; poor for client w/ broncho Ca

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