THE PITUITARY GLAND

• Overview:
o Known as the master gland due to its influence on other endocrine glands.
o Located at the brain's inferior aspect, divided into anterior and posterior lobes.
o Controlled by the hypothalamus, connected via the pituitary stalk.
Anterior Pituitary
• Main Hormones:
o FSH, LH, Prolactin, ACTH, TSH, GH (somatotropin).
o Releasing Factors: Controlled by hypothalamus, travel through pituitary portal blood system.
• Functions:
o TSH, ACTH, FSH, LH: Stimulate release of hormones from other endocrine glands.
o Prolactin: Stimulates milk production in breasts.
o GH (Growth Hormone):
▪ Increases protein synthesis and fat breakdown.
▪ Raises blood glucose levels.
▪ Essential for normal growth, requires thyroid hormone and insulin.
▪ Increased by stress, exercise, and low blood glucose.
▪ Half-life of 20-30 minutes, inactivated by liver.
Posterior Pituitary
• Main Hormones:
o Vasopressin (ADH): Regulates water excretion in kidneys.
o Oxytocin: Stimulates milk ejection and uterine contractions during childbirth.
• Regulation:
o Vasopressin: Secretion triggered by increased blood osmolality or decreased blood pressure.
o Oxytocin: Stimulated during pregnancy and labor.
Pathophysiology
• Pituitary Abnormalities:
o Caused by oversecretion or undersecretion of hormones.
o May be due to tumors, trauma, vascular lesions, or hypothalamic disease.
o Hypopituitarism: Insufficient secretion from the pituitary, causing weight loss, organ atrophy,
hair loss, impotence, and hypoglycemia. Coma and death may occur without hormone
replacement.
Anterior Pituitary Disorders
• Hypersecretion:
o ACTH or GH excess leads to Cushing syndrome or acromegaly.
o Acromegaly: Enlarged peripheral body parts in adults (no height increase).
o Gigantism in children (height increases to 7-8 feet).
• Hyposecretion:
o Panhypopituitarism: Decreased secretion of all anterior hormones, causing atrophy of the
thyroid, adrenal cortex, and gonads.
Posterior Pituitary Disorders
• Diabetes Insipidus (DI):
o Caused by deficient vasopressin (ADH) production.
o Leads to large volumes of dilute urine.
o Can occur due to brain tumors, traumatic brain injury, infections, or surgical removal of the
pituitary.
The pituitary gland, the relationship of the brain to pituitary action, and the hormones secreted by the anterior and
posterior pituitary lobes. ADH, antidiuretic hormone; GH, growth hormone; ACTH, adrenocorticotropic hormone;
TSH, thyroid-stimulating hormone; FSH, follicle-stimulating hormone; LH, luteinizing hormone; ICSH, interstitial cell-
stimulating hormone.
Pituitary Tumors:
• Overview:
o 95% of pituitary tumors are benign (NIDDK, 2012).
o Tumors can be primary (originating in the pituitary) or secondary (spread from other areas).
o Tumors can be functional (secreting pituitary hormones) or nonfunctional (not secreting
hormones).
o Tumors affect hormone production, and their location can lead to life-threatening effects.
• Types of Pituitary Tumors:
o Eosinophilic cells: Often secrete growth hormone (GH), leading to conditions like acromegaly.
o Basophilic cells: Can secrete ACTH, causing Cushing's disease.
o Chromophobic cells: These cells do not stain with eosin or basophilic stains, and may not
secrete hormones but can still cause physical problems due to size or pressure on nearby
structures.

Clinical Manifestations of Pituitary Tumors: Summary for Reviewer

• Eosinophilic Tumors (Growth Hormone-Secreting):
o Gigantism: If tumor develops early in life, resulting in height over 7 feet and generalized
enlargement.
o Acromegaly: If tumor occurs in adulthood, resulting in enlargement of hands, feet, nose, chin,
and superciliary ridge.
o Symptoms: Weakness, lethargy, severe headaches, visual disturbances (loss of color
discrimination, diplopia, or partial blindness), decalcification of the skeleton, muscular
weakness, and endocrine issues similar to hyperthyroidism.
• Basophilic Tumors (ACTH-Secreting):
o Cushing Syndrome: Leads to symptoms of hyperadrenalism, including:
▪ Masculinization and amenorrhea in females.
▪ Truncal obesity, hypertension, osteoporosis, and polycythemia.
• Chromophobic Tumors (Nonfunctional):
o Most common (90%) of pituitary tumors.
o Non-hormone producing, but can destroy pituitary tissue, leading to hypopituitarism.
o Symptoms:
▪ Obesity, somnolence (sleepiness), scanty hair, dry/soft skin, pasty complexion,
small bones.
▪ Headaches, loss of libido, visual defects, progressing to blindness.
▪ Polyuria, polyphagia, low basal metabolic rate, and subnormal body temperature.

Assessment and Diagnostic Findings: Summary for Reviewer

• History & Physical Examination:
o Visual acuity and visual fields assessment are crucial for detecting potential optic nerve
pressure from pituitary tumors.
• Diagnostic Imaging:
o CT scans and MRI are used to diagnose the presence and extent of pituitary tumors.
• Hormonal Testing:
o Measurement of serum pituitary hormones and hormones from target organs (e.g., thyroid,
adrenal) helps in confirming diagnosis.

Medical Management and Surgical Treatment of Pituitary Tumors: Summary for Reviewer
• Medical Management:
o Surgical removal (hypophysectomy) via a transsphenoidal approach is the usual treatment.
o Stereotactic radiation therapy targets the tumor with minimal damage to normal tissues.
o Medications such as:
▪ Bromocriptine (Parlodel): A dopamine antagonist.
▪ Octreotide (Sandostatin) & Lanreotide (Somatuline Depot): Synthetic GH analogs that
inhibit GH production and shrink the tumor.
• Surgical Management:
o Hypophysectomy is the treatment of choice for Cushing syndrome and may also be used to
relieve bone pain from metastatic tumors.
o Several surgical approaches include:
▪ Transfrontal, subcranial, and oronasal-transsphenoidal techniques.
o Post-surgery, hormonal replacement therapy (e.g., corticosteroids, thyroid hormone) is
required as the pituitary gland’s functions are compromised.
Diabetes Insipidus (DI)
• Definition: DI is a disorder of the posterior pituitary, characterized by a deficiency of ADH (vasopressin).
• Symptoms:
o Excessive thirst (polydipsia).
o Large volumes of dilute urine.
• Causes:
o Head trauma, brain tumor, or surgical ablation/irradiation of the pituitary.
o Infections: Meningitis, encephalitis, tuberculosis.
o Tumors: Metastatic disease, lymphoma (breast/lung).
o Nephrogenic DI: Failure of renal tubules to respond to ADH, related to:
▪ Hypokalemia, hypercalcemia.
▪ Medications: Lithium, demeclocycline (Declomycin).

Concept Mastery Alert

It is important to distinguish between DI, a disorder of insufficient output of pituitary ADH, and diabetes, a metabolic
disorder characterized by hyperglycemia caused by deficient insulin secretion or action (or both).

Clinical Manifestations of Diabetes Insipidus (DI)

• Excessive Urine Output:
o Output >250 mL/hour of very dilute urine.
o Specific gravity: 1.001 to 1.005 (low).
o No abnormal substances (e.g., glucose, albumin) in urine.
• Intense Thirst (Polydipsia):
o Patient drinks 2 to 20 liters of fluid daily.
o Craves cold water.
• Onset:
o Can be insidious (gradual) or abrupt.
• Inability to Control with Fluid Restriction:
o Limiting fluid intake does not stop high-volume urine loss.
o Hypernatremia (high sodium) and severe dehydration occur if fluid intake is restricted.

Assessment and Diagnostic Findings for Diabetes Insipidus (DI)

• Fluid Deprivation Test:
o Withhold fluids for 8 to 12 hours or until 3-5% body weight is lost.
o Patient is weighed frequently.
o Plasma and urine osmolality studies are performed before and after the test.
o Characteristic findings: inability to increase urine specific gravity or osmolality, large urine
output, weight loss, increased serum osmolality, and elevated serum sodium levels.
o Monitoring: Monitor for tachycardia, excessive weight loss, or hypotension; terminate if these
occur.
• Additional Diagnostic Procedures:
o Measure plasma levels of ADH and plasma/urine osmolality.
o Trial of desmopressin (synthetic vasopressin) therapy and IV hypertonic saline infusion.
o If the cause (e.g., head injury) is not obvious, assess for potential tumors causing DI.
Medical Management of Diabetes Insipidus (DI)
Objectives of Therapy:
1. Replace ADH (typically a long-term therapeutic plan).
2. Ensure adequate fluid replacement.
3. Identify and correct underlying intracranial pathology.
o Nephrogenic DI requires different management approaches.
Pharmacologic Therapy:
• Desmopressin (DDAVP):
o Synthetic vasopressin with no vascular effects.
o Administered intranasally through a flexible calibrated plastic tube.
o One or two administrations daily (every 12 to 24 hours) usually control symptoms.
o Fewer adverse effects and longer duration of action than previous treatments.
o Caution in patients with coronary artery disease due to vasoconstriction.
• Chlorpropamide (Diabinese) and Thiazide Diuretics:
o Used for mild forms of DI.
o They potentiate the action of vasopressin.
o Can cause hyperglycemia.
• Nephrogenic DI:
o Desmopressin is ineffective.
o Treatments: Thiazide diuretics, mild salt depletion, and prostaglandin inhibitors (e.g.,
ibuprofen, indomethacin, aspirin).

Nursing Management for Diabetes Insipidus (DI)

Key Aspects:
1. Physical Assessment:
o Thorough review of the patient’s history.
o Comprehensive physical assessment.
2. Patient Education:
o Educate the patient, family, and caregivers on:
▪ Follow-up care.
▪ Prevention of complications.
▪ Emergency measures.
3. Specific Instructions:
o Provide verbal and written instructions that cover:
▪ Dosage, actions, side effects, and administration of all medications.
▪ Signs and symptoms of hyponatremia.
o Demonstrate and observe the patient during medication administration to ensure proper
technique and dosage.
4. Safety Precautions:
o Advise the patient to wear a medical identification bracelet.
o Ensure the patient carries medication and essential information about DI at all times.
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
Overview:
• Excessive ADH secretion: Despite low serum osmolality, the pituitary releases excess antidiuretic
hormone (ADH), leading to the inability to excrete dilute urine.
• Consequences: Fluid retention and dilutional hyponatremia (low sodium levels due to fluid overload).
Causes:
1. Nonendocrine origins:
o Bronchogenic carcinoma: Malignant lung cells may produce and release ADH.
o Pneumonia, pneumothorax, and other lung disorders.
o Other malignant tumors affecting various organs.
2. Central Nervous System Disorders:
o Head injury, brain surgery, tumors, and infections can directly stimulate the pituitary to release
ADH.
3. Medications and substances:
o Vincristine (Oncovin), phenothiazines, tricyclic antidepressants, thiazide diuretics, and
nicotine: These can either stimulate the pituitary or enhance the renal tubules' sensitivity to ADH.
Implications:
• SIADH results in water retention, leading to dilution of sodium in the blood, which can cause symptoms of
hyponatremia, including confusion, seizures, and muscle cramps.

Medical Management of SIADH

Key Interventions:
1. Eliminate Underlying Cause: If the cause of SIADH (such as a malignancy or CNS disorder) is identified,
treating or removing the cause is the primary step.
2. Fluid Restriction: Limiting fluid intake is essential to prevent further dilution of sodium in the blood, helping
to increase serum sodium levels over time.
3. Diuretic Use:
o Furosemide (Lasix): A loop diuretic may be used in cases of severe hyponatremia to promote fluid
excretion and help restore normal sodium concentrations.

Nursing Management for SIADH

1. Monitoring:
o Fluid Intake and Output (I&O): Carefully track the patient’s fluid intake and urine output to
prevent fluid overload and monitor for signs of fluid retention.
o Daily Weight: Weigh the patient daily to monitor for fluid retention or loss, which can indicate
changes in the patient's condition.
o Urine and Blood Chemistries: Monitor serum sodium levels (to detect hyponatremia), serum
osmolality, and urine osmolality to assess the effectiveness of treatment and fluid balance.
o Neurologic Status: Assess for changes in mental status or signs of cerebral edema (e.g.,
confusion, headaches, seizures) that may result from hyponatremia.