Disorders of the Pituitary and Adrenal Glands Notes

Disorders of the Posterior Pituitary Gland

Learning Objectives

• Understand the role of ADH, Glucocorticoids, Mineralocorticoids, and Adrenal Androgens within the body.

• Identify the pathophysiology, clinical manifestations, diagnostic tests, and treatment options for a patient with SIADH.

• Differentiate between different causes of Diabetes Insipidus (DI).

• Recognize clinical manifestations, diagnostic tests, and treatment options for a patient with Diabetes Insipidus.

• Understand the difference between Cushing Syndrome, adrenal insufficiency, and Addison disease.

• Anticipate clinical manifestations, diagnostic testing, and nursing care of a patient with Cushing Syndrome.

• Identify signs and symptoms, testing options, and interprofessional care for a patient with adrenal insufficiency.

• Weigh risks versus benefits of corticosteroid treatment for chronic illness.

Key Terms

• Addison Disease

• Addisonian Crisis (“acute adrenal insufficiency”)

• Adrenal Insufficiency

• Antidiuretic Hormone (ADH)

• Cushing Disease

• Cushing Syndrome

• Diabetes Insipidus (DI)

• Hyperaldosteronism

• Serum Osmolality

• Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Hormone of the Posterior Pituitary Gland

• Antidiuretic hormone/ADH (biggest) / Arginine vasopressin (AVP)

  • Helps body balance water and maintain stable blood concentration (serum osmolality).

    • Controls how much water the kidneys save or release.

    • ADH retains water.

• Problems arise when there is:w

  • Overproduction

    • Over secretion of ADH

    • Syndrome of Inappropriate ADH (SIADH)

      • Retention of water

  • Underproduction

    • Under secretion of ADH

    • Diabetes Insipidus (DI)

      • Excess fluid loss

Normal Feedback Mechanism of ADH

• Increased serum osmolality (blood too concentrated → body wants to dilute with more water to compensate)

  • Stimulates secretion of ADH

    • Increased water reabsorption in the kidney tubules

      • more concentrated urine

      • less concentrated serum (water moves from urine back into the blood)

      ↑ Serum osmolality (concentrated blood/less water)

      ↑ ADH

      Reabsorb water → dilute the blood

• Decreased serum osmolality (blood too dilute → need less water reabsorbed into blood)

  • Suppresses secretion of ADH

    • Decreased water reabsorption in the kidney tubules

      • less concentrated urine (more dilute)

      • more concentrated serum (kidneys excrete more water to prevent reabsorption into blood)

    ↓ Serum osmolality (diluted blood/too much water)

    ↓ ADH

    Excrete water → concentrate the blood

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Etiology

• Overproduction of ADH → retains water

  • Too much ADH tells kidneys to reabsorb water and dilutes the blood.

• Abnormally high production or secretion of ADH

• ADH is released despite normal or low serum osmolarity

• More common in older adults

• Causes:

  • Most common – malignancy

    • Small cell lung cancer, lymphoma, prostate cancer, pancreatic cancer (paraneoplastic syndrome → body’s reaction to cancer either from release of cytokines that caused SIADH to happen or due to an autoimmune reaction)

  • Self limiting (resolves by itself or after removing offending agent)

    • Drugs

    • Head Trauma or Infection (meningitis/encephalitis)

  • Chronic

    • Tumors or Metabolic Disease (how body reacts to it)

Pathophysiology

• Impaired water excretion due to the inability to suppress ADH secretion

  • Fluid retention even if kidneys are healthy due to hormone telling them to do the wrong thing.

  • Too much water in the blood.

• Hyponatremia from excess water, not a sodium deficiency.

  • The nonphysiological secretion of ADH results in enhanced water reabsorption, leading to dilutional hyponatremia (blood too diluted).

  • Inappropriate thirst sensation, which leads to an intake of water that is in excess of water excreted.

  • Hyponatremia and hypo-osmolality lead to acute edema of the brain cells.

    • Pt will present with ALOC.

  • Rapid increase in brain water leads to severe cerebral edema, herniation (note: Cushing’s triad before → widened pulse pressure, bradycardia, irregular respirations) and death.

Clinical Manifestations

• Thirst

• Dyspnea on exertion

• Fatigue

• Weight gain

• Low urine output

• Hyponatremia

  • mild = muscle cramps, weakness, headache

  • moderate (<120) = vomiting, abdominal cramps, muscle twitching

  • severe = lethargy, confusion, seizures, coma

Diagnosis

• Urine osmolality/specific gravity

  • >1.030

• Serum Osmolality

  • <280 mOsm/kg

• Sodium

  • <134 mEq/L

• Condition

  • Well hydrated

    • Urine specific gravity value <1.010

  • Minimal dehydration

    • Urine specific gravity value 1.010-1.020

  • Significant dehydration

    • Urine specific gravity value 1.021-1.030

  • Serious dehydration

    • Urine specific gravity value >1.030

Medication Therapy

• Vasopressin receptor antagonist (VRAs or “Vaptans”)

  • MOA selectively antagonizes V2 receptors in the collecting tubules increasing free water excretion. Ex. conivaptan, tolvaptan.

• Diuretics (if Na >125 mEq/L)

  • Furosemide (Lasix)

    • MOA loop diuretic

    • Monitor electrolytes (K, Na, Ca, Mag)

• Demeclocycline

  • Tetracycline Antibiotic - “off label use”

  • MOA causes diuresis by inhibiting water re-absorption in tubules

Interprofessional Care

• Treat underlying cause

• Fluid restriction

  • 800-1000 cc/24 hrs

• Assess: heart/lungs, neuro checks, daily weight, strict I&O

• HOB flat or no higher than 30 degrees

• BMP

• Na <120 hypertonic (3%) saline infusion

• Na > 125 fluid restriction w/ or w/o lasix

• Seizure and fall precautions

• Manage thirst

  • Ice chips, chewing gum, lozenge-type candy, mouth swabs

• Increase dietary Na and K

• High K foods = leafy greens, nuts, dairy, bananas, oranges

Diabetes Insipidus (DI)

Etiology

• Inadequate ADH (“vasopressin”)

  • deficiency in production/secretion, or

  • decreased renal response

• Causes

  • Central DI (neurogenic) - most common

    • Brain tumor, head injury or surgery, CNS infection

  • Nephrogenic DI

    • Renal disease/damage, lithium toxicity

  • Primary DI

    • Excessive water intake – psychological or lesion in thirst center

Pathophysiology

• Decreased water reabsorption in the kidney tubules leads to decreased intravascular volume

  • Dehydration → Hypotension, tachycardia, skin turgor tenting, dry mucous membranes, and urinary output reduction.

• Increased serum osmolarity leads to hypernatremia

  • Rapid excretion of water → concentrated blood (less water) → sodium stays in blood

• Excessive urine output

• Neurogenic

  • Interference in ADH synthesis, transport, & release

    • Following trauma or surgery to the region of the pituitary and hypothalamus

• Nephrogenic

  • Inadequate renal response to ADH in V2 receptor

    • Decrease in ADH, decreased water reabsorption in the tubules, decreased intravascular fluid volume → increased serum osmolality (concentrated blood/less water) with excessive urine output.

Clinical Manifestations

• Polydipsia

• Polyuria = 2-20 L/day of dilute urine (specific gravity <1.005)

• Nocturia

• Dehydration

  • Poor skin turgor, hypotention, tachycardia, hypovolemic shock

• Hypernatremia

  • irritability

  • mental dullness

  • Coma

• High serum osmolality if dehydration not corrected (>295 mOsm/kg)

Diagnosis

• Urine Osmolality/specific gravity

  • <1.005 mOsm/kg

• Water deprivation test

  • Measure body weight, urine osmolality, specific gravity, and volume

  • Withhold water for 8-12 hrs and administer desmopressin (synthetic ADH)

    • If decrease in urine volume and increase in urine osmolality = + for (central) neurogenic DI

    • If no increase in urine osmolality = + for nephrogenic DI

• ADH levels

  • Measure levels with administration of desmopressin (DDAVP)

  • Differentiates between neurogenic & nephrogenic

Interprofessional Care

• Early recognition

• Adequate hydration

  • Acute DI - IV hypotonic (.45%) saline or D5W titrate to uo

• Nephrogenic DI

  • Low Na diet, 3 gm/day

• Maintenance of fluid and electrolyte balance

  • daily weights, strict I&O

  • IV or oral fluids depending on ability to maintain adequate intake v. output

• Monitor heart rate, B/P

• BMP

• Na >146, neuro checks/LOC

Medications

• Central DI

  • Desmopressin (DDAVP) – ADH analog

    • Desmopressin MOA- increases permeability of collecting tubules to water

    • SQ, IV, PO

    • Assess patient response to drug, lung sounds, skin turgor, water intoxication

• Nephrogenic DI

  • Thiazide diuretics

    • Hydrochlorothiazide MOA- acts on distal tubule to decrease NA reabsorption

    • (may reduce flow to the ADH sensitive distal nephron – paradoxical effect)

  • NSAID

    • Indomethacin MOA- inhibits prostaglandin synthesis, decreasing inflammation

    • (increases renal responsiveness to ADH)

Adrenal Gland Physiology

• Endocrine Function

Anatomy & Physiology

• Adrenal Gland

  • Adrenal Medulla

    • Synthesizes Catecholamines → most prevalent is epinephrine and norepinephrine

  • Adrenal Cortex

    • Steroidogenesis = where corticosteroid creation happens

      • Glucocorticoids (Cortisol) → released during stress

      • Mineralocorticoids (Aldosterone)

        • Helps regulate blood pressure and fluid balance by controlling how much sodium and potassium your kidneys keep or get rid of.

        • Increases sodium reabsorption in the kidneys → water follows sodium → increases blood volume and blood pressure.

      • Adrenal Androgens

        • Male sex hormones

HPA Axis (normal feedback mechanism to secrete cortisol and androgen)

• HPA Axis controls cortisol & androgens

  • A negative feedback loop will reduce secretion of cortisol and androgen.

• Hypothalamus releases corticotrophin-Releasing Hormone (CRH).

• CRH triggers the anterior pituitary and releases Adrenocorticotropic Hormone (ACTH) into the bloodstream.

• ACTH travels through blood to reach adrenal gland to release cortisol and androgens.

RAAS (helps release blood pressure and fluid balance)

• RAAS -> Mineralocorticoids (aldosterone)

  • Blood pressure ↓ → Renin (kidney) ↑ → Angiotensin II ↑ → Adrenal gland releases Aldosterone → Kidneys retain salt & water → Blood volume & pressure ↑

• Triggered by blood pressure fall.

• Kidneys release Renin.

• Renin converts angiotensinogen (a protein produced by the liver) into angiotensin I.

• ACE converts angiotensin I into Angiotensin II.

• Angiotensin II stimulates adrenal cortex to secrete aldosterone → increases sodium and water reabsorption to hold onto→ increases blood volume and raises blood pressure.

• The blood vessels vasoconstrict to increase blood pressure.

Cushing Syndrome

Etiology and Pathophysiology

• Caused by chronic exposure to excess corticosteroids, especially glucocorticoids.

• Common causes:

  • Iatrogenic administration of exogenous corticosteroids (most common)

    • Long-term use puts pt at huge risk.

  • ACTH-secreting pituitary adenoma (Cushing disease)

  • Adrenal tumors

  • Ectopic ACTH production by tumors

    • Usually lung or pancreatic tumor trigger excess release.

Clinical Manifestations

• Most manifestations are related to glucocorticoid excess.

• S/s of excess glucocorticoids:

  • Profound physical changes

    • Weight gain (truncal obesity, moon face, buffalo hump)

    • Purplish red striae (stretch marks)

  • Muscle wasting causes weakness

  • Loss of bone matrix causes osteoporosis and back pain

  • Loss of collagen causes thin skin, easily bruises

  • Delay in wound healing

  • Hyperglycemia related to glucose intolerance and increased gluconeogenesis

  • Emotional lability (euphoria, irritability, depression, insomnia, anxiety)

• Mineralocorticoid (aldosterone) excess may cause:

  • Hypokalemia

  • Hypertension

• Adrenal androgen excess may cause:

  • Severe acne

  • Male characteristics in women (hirsutism)

  • Feminization in men (gynecomastia, testicular atrophy)

Diagnostic Studies

• Confirmation of increased plasma cortisol levels (3 options)

  • Midnight or late-night salivary cortisol

  • Low-dose dexamethasone suppression test

  • 24-hour urine cortisol

• CT or MRI to look for pituitary or adrenal tumors

• Plasma ACTH levels

  • High or normal with Cushing disease (pituitary etiology)

  • Low or undetectable indicate adrenal or medication cause

• Hypokalemia and alkalosis

  • With ectopic ACTH syndrome (lung/pancreatic CA) or adrenal cancer

• Other findings may include: ↑ WBC, ↑ glucose, glucosuria, osteoporosis

Interprofessional Care

• Goal: normalize hormone secretion

• Treatment depends on cause

  • Surgical removal or irradiation of pituitary adenoma

  • Adrenalectomy for adrenal tumors or hyperplasia

  • Removal of ACTH-secreting tumors

  • If surgery is not an option, can treat with meds (“medical adrenalectomy”)

    • Ketoconazole and mitotane

• If cause is iatrogenic (prolonged use of exogenous corticosteroids)

  • Gradually discontinue therapy

    • Decrease dose

    • Convert to an alternate-day dosing

  • Dose must be tapered gradually → risk for adrenal insufficiency

  • Examples of exogenous corticosteroids: prednisone, hydrocortisone (cortisol), dexamethasone, methylprednisolone.

Nursing Implementation

• Health promotion

  • Identify patients at risk for Cushing syndrome

  • Long-term exogenous cortisol therapy is major risk factor

  • Teach patients about medication use and to monitor for side effects

• Emotional support

  • Patient may feel unattractive or unwanted

  • Be sensitive to patient’s feelings and be respectful

  • Reassure patient that physical changes and emotional lability will resolve when hormone levels return to normal

• Acute Care: Monitor

  • Vital signs (may be hypertensive)

  • Daily weight

  • Blood glucose and potassium levels

  • Assess for signs and symptoms of

    • Inflammation/infection

    • VTE

  • Implement

    • High protein diet

• Postoperative care

  • Increased risk of bleeding

  • Large release of hormones into circulation can cause instabilities in BP, fluid balance, and electrolyte levels.

    • most pronounced in first 24-48 hours post-op

  • High doses of corticosteroids are given IV during and for several days after surgery

    • monitor blood glucose

    • monitor for Infection and delayed wound healing

    • Daily morning urine sample to assess cortisol levels

  • Monitor for acute adrenal insufficiency (severe/sudden lack of glucocorticoid)

    • Vomiting

    • Weakness

    • Dehydration

    • Hypotension

    • Also may experience painful joints, pruritus, peeling skin, severe emotional problems

• Ambulatory care, post-surgery

  • Always wear Medic Alert bracelet

  • Lack of endogenous corticosteroids reduces ability to respond to stress

    • Avoid exposure to extremes temperatures, infection, and psychologic stress

    • Teach how to adjust medication and when to call HCP

  • Lifetime replacement therapy

Adrenal Insufficiency and Addison Disease

Etiology and Pathophysiology

• Primary (“Addison Disease”)

  • Problem with adrenal cortex

  • Causes a reduction of glucocorticoids, mineralocorticoids, and androgens

• Secondary

  • Caused by pituitary disease or suppression from exogenous corticosteroid use

  • Lack of pituitary ACTH

  • Lack of glucocorticoids and androgens

• Addison Disease (primary adrenal insufficiency)

  • 80% of cases caused by an autoimmune response

    • Autoimmune adrenalitis

      • Antibodies destroy adrenal cortex

    • Autoimmune polyglandular syndrome

      • Co-occurring endocrine conditions, such as:

        • Type 1 diabetes

        • Autoimmune thyroid disease (Graves or Hashimotos)

        • Pernicious anemia

          • caused by lack of vitamin B12 (can be autoimmune)

        • Celiac disease

          • Most common in white females

  • Less Common Causes

    • TB (not a common cause in United States)

    • Amyloidosis, Fungal infections, AIDS, Metastatic cancer

  • Iatrogenic Addison’s disease

    • Adrenal hemorrhage (pts on anticoagulant therapy)

      • Glands are vascular, so is thyroid and adrenal glands (more likely to hemorrhage)

        • Hemorrhage → decrease blood flow to tissue and causes necrosis

    • Chemotherapy

    • Bilateral adrenalectomy

      • may need due to tumors

Clinical Manifestations

• Insidious onset (>90% gland destroyed before specific symptoms appear)

• Anorexia

• Nausea

• Progressive weakness

• Fatigue

• Weight loss

• Disease often advanced before diagnosed

• Hyperpigmentation

  • only in Addison Disease

  • sun-exposed areas

  • joints, creases

• Abdominal pain

• Diarrhea

• Headache

• Orthostatic hypotension

• Salt craving

• Joint pain

• Irritability, depression

Complications

• Addisonian Crisis

  • “Acute adrenal insufficiency”

  • Insufficient or sudden, sharp decrease in hormones

  • Life-threatening emergency

  • Potential triggers:

    • Stress- infections, surgery

    • Sudden withdrawal of corticosteroids

    • Adrenal surgery

    • Sudden pituitary gland destruction

  • Manifestations of glucocorticoid and mineralocorticoid deficiencies:

    • Hypotension, tachycardia

    • Dehydration

    • Decreased sodium, increased potassium, increased glucose

    • Fever, weakness, confusion

    • Severe vomiting, diarrhea, pain

  • Shock may cause circulatory collapse

  • Often unresponsive initially to usual treatments – fluids, vasopressors

  • Administer high-dose IV hydrocortisone (Solu-Cortef)

Diagnostic Studies

• ACTH stimulation test

  • First - Baseline levels of cortisol and ACTH drawn

  • Second - IV injection of synthetic ACTH (cosyntropin) given

  • Third - Levels rechecked after 30 and 60 minutes

    • Elevated blood cortisol level = normal

    • Little or no increase in cortisol levels with high ACTH = adrenal insufficiency

• CRH stimulation test

  • Ordered if abnormal ACTH test response. Helps determine if disease is primary (Addison) or secondary adrenal insufficiency.

  • First - IV injection of synthetic CRH

  • Second - Blood drawn after 30 and 60 minutes

    • High ACTH levels with no cortisol = Addison disease

    • Absence of ACTH or delayed response = secondary adrenal insufficiency

• Other Diagnostic Studies

  • High potassium

  • Low chloride, sodium, glucose

  • Anemia

  • Increased BUN

  • ECG changes r/t hyperkalemia

  • CT scan, MRI

Nursing Implementation

• Acute care

  • Frequent VS and neurologic assessment

  • Correct fluid and electrolyte imbalance

    • Daily weight

    • Accurate I and O

    • Monitor daily labs

    • Assess for s/s of electrolyte and glucose abnormalities

  • Obtain complete medication history

    • Some medications interact with corticosteroids – anticoagulants, NSAIDs, oral anti-diabetics, digoxin

  • Watch for signs of Cushing syndrome

  • Minimize additional stress (noise, light, temperature)

  • Protect against hospital acquired infection

Medications

• Lifelong hormone therapy

  • Hydrocortisone (Cortef)

    • Acts as both glucocorticoid and mineralocorticoid

    • Divide doses = take 2/3rd in the morning, 1/3rd in the afternoon

    • Increased dpses needed during periods of stress

  • Fludrocortisone (Florinef)

    • Mineralocorticoid replacement; give one daily in the AM

    • Monitor BP, increase salt intake

  • Dehydroepiandrosterone (DHEA)

    • Androgen replacement – for women only

• Patient teaching

  • Report signs and symptoms of corticosteroid deficiency or excess to HCP

  • Increase steroid doses during infection, hospitalization, other stress

  • Gastroenteritis may require hospitalization

  • Increase dietary salt intake

    • Additional salt r/t excessive heat or humidity

  • Emergency kit

    • How to administer IM hydrocortisone

    • Written instructions

    • Safety alert bracelet and/or Wallet ID card

Chronic Corticosteroid Therapy

• Medication class usually ends in “-sone” or “-one”

• Many possible routes: PO, IV, IM, intranasal, inhaled, topical

• Beneficial Effects: anti-inflammatory, immunosuppressive, BP maintenance

• Examples:

  • Prednisone

  • Methylprednisolone

  • Dexamethasone (Decadron)

  • Hydrocortisone (Cortef and Solu-cortef)

  • Fluticasone

  • Triamcinolone

  • Budesonide

• Complications and side effects with long-term use

  • potential benefits must be weighed against risks

  • Effective in treating many diseases and disorders

    • Deficiency states (adrenal insufficiency)

    • Allergic reactions (anaphylaxis, contact dermatitis, drug reactions)

    • Autoimmune disease (RA, SLE, Hashimotos, IBD)

    • Neurologic conditions (cerebral edema, head trauma)

    • Pulmonary disorders (COPD, asthma, PNA)

    • Cancer

    • Organ Transplant

• Side Effects

  • Decreased potassium and calcium

  • Increased glucose and BP

  • Delayed healing, increased risk of wound dehiscence

  • Susceptibility to infection

  • Suppressed immune response

  • Peptic ulcer disease

  • Muscle atrophy/weakness; osteoporosis

  • Mood and behavior changes

  • Weight gain - moon face, truncal obesity

  • Risk for acute adrenal crisis if therapy is stopped abruptly

• Patient Teaching

  • Nonreplacement steroids – take in the morning with food

    • Notify HCP if epigastric pain develops

  • Do not stop abruptly if taken >1 week; must be tapered

  • Need to monitor for hyperglycemia

  • Need to prevent injury/infection

  • Therapies to reduce osteoporosis

    • ↑ Ca2+, Vit D intake

    • Concurrent bisphosphonate therapy (ex. alendronate)

    • Low-impact exercise program