▪ DISORDERS OF THE PITUITARY GLAND

▪ PATHOPHYSIOLOGY

 Abnormalities of the pituitary function are caused by OVERSECRETION or UNDERSECRETION OF

ANY HORMONES PRODUCEED OR RELEASED by the gland.

 Abnormalities of the anterior and posterior pituitary portions of the gland may occur
INDEPENDENTLY.

a. HYPOPITUITARISM- hypofunction of the pituitary gland

▪ The results of the total destruction of the pituitary gland can lead to:

 extreme weight loss

 Emaciation

 Atrophy of all the endocrine glands and organs

 Hair loss

 Impotence

 Amenorrhea

 Hypometabolism

 Hypoglycemia

▪ DISORDERS OF THE ANTERIOR PITUITARY GLAND

▪ GROWTH HORMONE

A. GIGANTISM-hypersecretion of GH in children (before epiphysial closure). This is characterized by

exaggerated growth in height and weight.

B. ACROMEGALY– Hypersecretion of GH in adults (after epiphyseal closure).

- primarily cause by pituitary tumors.

- Clinical Manifestations:

1. LARGE HANDS AND FEET

2. THICKENING AND PROTRUSION OF THE JAW

3. ORGANOMEGALY

4. VISUAL DISTURBANCES

5. ARTHRITIC CHANGES

6. DIAPHORESIS

7. OILY ROUGH SKIN

8, HYPERTENSION

9. DYSPHAGIA

10. DEEPENING OF VOICE

C. DWARFISM- characterized by failure to grow in height.

▪ PROLACTIN

A. GALACTORRHEA- hypersecretion of prolactin; characterized by excessive milk production

B. Absence of milk production during lactation results from hyposecretion of prolactin.

▪ ADRENOCORTICOTROPIC HORMONE ( ACTH )

▪ THYROID-STIMULATING HORMONE

▪ GONADOTROPINS (FSH AND LH)

▪ HYPERSECRETION of hormones results to precocious puberty

▪ HYPOSECRETION of hormones results to failure of secondary sex characteristics. The

manifestations are as follows:

▪ MELANOCYTE – STIMULATING HORMONE

▪ HYPERSECRETION – results to hyperpigmentation of the skin ( eternal tan) or BRONZE

appearance

▪ HYPOSECRETION – ALBINISM ( Hypopigmentation of the skin)

• Nursing Management of DI and SIADH

• Objectives

• Describe the normal function of ADH in water and electrolyte regulation.

• Compare and contrast the etiologies of SIADH and DI.

• Describe the assessment findings of SIADH and DI.

• Evaluate the management and treatment of SIADH and DI.

• Evaluate the possible complications of SIADH and DI.

• Brain Regulation

• Disorder of sodium and water balance is a common complication following neurosurgery

 • Neuroscience patients must be continually assessed and monitored for their response to
therapy

• Early detection is critical to the protection and integrity of the brain

• Normal Brain Regulation

• TBW accounts for 60% of body weight

– 20% ECF

– 40% ICF

– Fluid shifts can occur depending on concentrations of solutes in ICF and ECF

• Na and K are principle determinants in fluid shifts

• Osmolarity: amount of solute in fluid (urine, blood)

Normal Serum Osmolarity: 280-295 mOsm/L

• Serum Osmo above 295 mOsm/L = water deficit

– Concentration is too great OR

– Water concentration is too little

– Serum Osmo below 280 mOsm/L = water excess

– Amount of particles or solute is too small in proportion to the amount of water OR

– Too much water for the amount of solute

To maintain plasma or serum osmo within range, free water intake and excretion must balance

• Antidiuretic Hormone (ADH): balances Na and water in body and controls water conservation

• Changes in pressure of ECF triggers release of ADH from pituitary gland

• Release is coordinated with activity of the thirst center- regulates intake

• ADH binds with receptor sites of the collecting duct in kidney resulting in increased free-water
resorption

• ADH causes vasoconstriction

Presence of ADH- renal tubule permeability to water is increased and water is reabsorbed

Absence of ADH- renal tubule permeability to water is decreased – renal excretion to fluids

• Plasma osmolality = Primary regulatory mechanism for the release of ADH

• Receptors in the brain are sensative to changes in osmolality

• Receptors that trigger thirst mechanism are close to those that control ADH release
• Serum osmo greater than 290 mOsm/L triggers thirst

• ADH Feedback Loop

• Syndrome of Inappropriate Antidiuretic Hormone

• SIADH: Persistent abnormally high (inappropriate) levels of ADH in the absence of stimuli with
normal renal function

– No longer regulated by plasma osmo and volume

– Imbalance of fluid and electrolytes

– Feedback system is impaired and posterior pituitary continues to release ADH

• Renal tubules continue to reabsorb free water regardless of the serum osmolality

• Excessive activity of the neurohypophyseal system r/t brain disease

• At Risk Patients for SIADH

• Post-Operative with pituitary surgery

• Acute head injury

• Pulmonary infections (Pneumonia)

• Psychoses

• Drugs

• Nervous system infections (meningitis)

• Investigate the following conditions for SIADH

• Thirst and fluid status with accurate I&O

• Confusion

• Dyspnea

• Headache

• Fatigue

• Weakness

• Increased weight w/o edema

• Change in LOC

• Lethargy

• Vomiting
 • Muscle weakness and cramping

• Muscle twitching

• Seizures

• Labs to Diagnose SIADH

Serum Na

Urine Na

Urine Osmolality

Serum Osmolality

BUN/Creatinine

Urine Specific Gravity

Serum Potassium

• Lab Results for SIADH

• Treatment of SIADH

• Correct underlying cause

• Fluid restriction 500-1000 ml/day

• Severe hyponatremia:

– 3% NS may be given

– Lasix may be given (watch K level)

• Nursing Management of SIADH

• Frequent Neuro assessment

– Mental status and LOC

– Pulmonary assessment

– s/s fluid overload

– Cardiac assessment

– Dysrhythmias and BP abnormalities

– Monitor for seizure activity

– Seizure precautions

– Accurate I&O

• Daily Weights
 – Same time each day, same scale, same clothes

– Oral hygiene

• Reduce stress, pain, discomfort

• Correlation of Decreasing Sodium Levels and Symptoms

• Diabetes Insipidus

Disordered regulation of water balance due to impaired urinary concentrating ability secondary to
inadequate secretion of ADH or resistance to ADH.

Four Types of DI:

Central/Neurogenic (CDI)

Nephrogenic (NDI)

Dipsogenic

Gestational

• Pathophysiology of DI

• Central/Neurogenic

Inadequate secretion of

ADH due to loss or malfunction of neurosecretory neurons that make up the posterior pituitary.

Vasopressin Sensitive

• Nephrogenic

Inadequate response by the kidneys to ADH.

A disorder of renal tubular function resulting in the inability to respond to ADH in absorption of water.

Vasopressin Resistant

• Diabetes Insipidus (DI) Clinical Signs!

• Dehydration! Excessive loss of water from body tissue and imbalance of essential electrolytes
(Ns, K, Cl)

• Polydipsia (excessive thirst)

• Polyuria (excessive amount of urine)

• Low specific gravity (1.001 to 1.005)

• Serum hyperosmolality and hypernatremia

• Causes of DI
 • Head Trauma

• Post-operative (hypophysectomy, pituitary tumor)

• Brain Tumors

• CNS Infection (meningitis, abcess)

• Increased ICP

• Idiopathic

• ICH

• Stroke

• Hypoxia

• Medications (Dilantin, clonidine, alcohol)

• Damage to hypothalamus or posterior pituitary

• Investigate the following for DI

• Unquenchable thirst

• Polydipsia

• Polyuria

(hourly urine output > 200 mls)

• Unexplained weight loss

• Urinary frequency

• Nocturia

• Dry skin/poor skin turgor

• Tachycardia and hypotension

• Inability to respond to the increased thirst stimulus and compensate for the excessive polyuria

• Hypernatremia that becomes severe and is manifested by- confusion, irritability, stupor, coma
and neuromuscular hyperactivity progressing to seizures.

• Elderly

• Unconscious/intubated

• Labs and Diagnostics for DI

Serum calcium

Glucose
Creatinine

Potassium

Urea level

• The following may also be indicated:

– 24hr urine collection to quantitative polyuria

– CT/MRI

• rule out pituitary causes, metastases, hemorrhage, neuronal damage, cerebral

tumors.

– Radioimmunoassy: to measure circulating ADH concentrations

• Lab Results for diagnosis of DI

• Water Deprivation Test

– After baseline measurement of: weight, ADH, plasma sodium, and urine/plasma
osmolality, the patient is deprived of fluids under strict medical supervision

– Frequent (q2h) monitoring of plasma and urine osmolality follows.

– The test is generally terminated when plasma osmolality is >295 mOsm/kg or the
patient loses ≥3.5% of initial body weight.

– DI is confirmed if the plasma osmolality is >295 mOsm/kg and the urine osmolality is
<500 mOsm/kg.

• Nephrogenic DI vs Neurogenic DI

• DDAVP Challenge

– Check urine osmolality 1-2hrs after 1mcg SQ DDAVP

• If little or no change: likely NDI or dipsogenic DI

• If significant increase in urine osmolality, likely CDI

• 5 units vasopressin IV

– Measure osmolality

– A significant increase (>50%) in urine osmolality after administration of ADH is indicative

of CDI

• Treatment of DI

Correct the underlying cause and maintain adequate fluid replacement.

• DI Therapy varies with the degree and type of DI present or suspected.

 • IVF may be necessary to correct hypernatremia; avoid rapid replacement

• Free water restriction

• After assessing fluid status and serum sodium level, treat both dehydration and hypernatremia

• For chronic neurogenic DI- require hormonal replacement therapy: DDAVP (nasal vasopressin)

• Consultation with an endocrinologist is strongly recommended

• Treatment for Nephrogenic DI

Removal of the underlying cause/offending drug

• DDAVP usually ineffective

• Thiazide diuretic (HCTZ) is first line treatment

• Adequate hydration

• Low-sodium diet + thiazide diuretics to induce mild sodium depletion.

• Indomethacin may also be useful to reduce urine volume.

• Nursing Management of DI

• Hourly Neuro Checks

• Frequent Vital Signs

• Evaluate for s/s of hypovolemic shock

• Strict I&O

• Rehydrate for symptoms of extreme thirst

• Measure and record weight using the same scales at the same time and with the patient
wearing the same clothing

• Assess mucous membranes and skin turgor and monitor for symptoms of dehydration

• Provide rest

• Safety measures to prevent injury secondary to dizziness and fatigue

• Alert the health care team of problems of urinary frequency and extreme thirst that interferes
with sleep and activities.

• SIADH vs DI Lab Values

• Complications to treatments of DI and SIADH

• Cerebral Edema!

• Central Pontine Myelinolysis: brain cell dysfunction caused by destruction of the myelin sheath
covering nerve cells in brainstem
• Na levels rise too fast or corrected too quickly

• s/s: (not necessarily immediate)

– Acute paralysis

– Dyschagia

– Dysarthria

• Most Important Nursing Intervention for DI and SIADH

• Frequent Labs

– We have severe electrolyte abnormalities

– Careful not to correct too quickly!!

– Na should not rise more than 0.5mEq/L/hr and 10 mmol/L/24 hrs

• Frequent neuro assessment

– The nurse can pick up abnormal behavior and signs and symptoms first

– Note any changes from baseline