Notes on Disorders of the Endocrine System
Overview
Focus on understanding various aspects of endocrine system functions and disorders, including the intricate mechanisms of hormonal regulation, complex feedback loops, and the roles of significant endocrine glands in maintaining homeostasis. The endocrine system plays a crucial role in coordinating bodily functions through chemical messengers.
Key Topics to Review
Endocrine Functions: The system's primary role is to secrete hormones that regulate metabolism, growth and development, tissue function, reproduction, sleep, and mood, among other things.
Hormonal Regulation: Hormones are chemical messengers synthesized and secreted by endocrine glands or specialized cells and transported by the bloodstream to target cells or organs. Regulation ensures appropriate levels are maintained.
Feedback Loops: Essential for maintaining hormone balance. Most hormonal regulation occurs through negative feedback, where a stimulus causes the release of a substance, whose effects then inhibit further release. Positive feedback loops are less common but amplify the initial stimulus.
Nervous System Control: The hypothalamus and pituitary gland form a critical neuroendocrine axis, integrating nervous and endocrine functions to control many bodily processes.
Important Endocrine Glands:
Anterior Pituitary Lobe: Produces and secretes tropic hormones that stimulate other endocrine glands.
Posterior Pituitary Lobe: Stores and releases hormones produced by the hypothalamus.
Hypothalamus: The control center, linking the nervous and endocrine systems.
Adrenal Glands: Involved in stress response, electrolyte balance, and metabolism.
Thyroid: Regulates metabolism, growth, and development.
Parathyroid: Crucial for calcium and phosphate homeostasis.
Important Hormones to Understand
Adrenocorticotropic Hormone (ACTH): Stimulates the adrenal cortex to produce cortisol.
Thyroid-Stimulating Hormone (TSH): Stimulates the thyroid gland to produce thyroid hormones.
Growth Hormone (GH): Promotes growth of body tissues, particularly bone and muscle; also affects metabolism.
Vasopressin (also known as Antidiuretic Hormone, ADH): Regulates water balance by increasing water reabsorption in the kidneys.
Glucocorticoids: A class of steroid hormones that affect metabolism and suppress inflammatory responses.
Cortisol: The primary stress hormone; increases blood glucose, aids in fat, protein, and carbohydrate metabolism, and suppresses the immune system.
Cortisone: A synthetic glucocorticoid used as a drug.
Corticosterone: A minor glucocorticoid in humans, important in rodents.
Mineralocorticoids: A class of corticosteroids that influence salt and water balances.
Aldosterone: The primary mineralocorticoid; regulates blood pressure by controlling sodium and potassium balance.
Androgens: A group of steroid hormones that play a role in male traits and reproductive activity.
Hypothalamus
Serves as the master regulator, acting as a direct extension of the central nervous system and influencing the pituitary gland. It synthesizes and secretes releasing and inhibiting hormones that control the anterior pituitary and also produces ADH and oxytocin, which are stored and released by the posterior pituitary.
Plays a vital role in emotional responses connected to the CNS, including anger, fear, pleasure, pain, and sexual arousal, and regulates basic body functions like temperature, hunger, and thirst.
Pituitary Gland
Positioned under the hypothalamus within the sella turcica, a bony cavity in the sphenoid bone. Often called the "master gland" due to its influential role over other endocrine glands.
Connected Structures:
Anterior Pituitary (Adenohypophysis):
Releases growth hormone (GH), which stimulates body growth and metabolism.
Also secretes various tropic hormones that trigger other glands: TSH (to thyroid), ACTH (to adrenal cortex), FSH and LH (to gonads), and Prolactin (for milk production).
Posterior Pituitary (Neurohypophysis):
Primarily releases ADH (vasopressin), which is vital for water balance regulation by increasing water reabsorption in the renal tubules, and Oxytocin, which stimulates uterine contractions and milk ejection.
Thyroid Gland
Location: Anterior neck, wrapped around the trachea just below the larynx, comprised of two lobes connected by an isthmus.
Associated Hormones:
Thyroxine (T4) and Triiodothyronine (T3):
Require iodine for their synthesis. T4 is the major hormone secreted, but T3 is more potent and often converted from T4 in target tissues.
These hormones regulate metabolic rate, heat production, growth, and development.
Their secretion is stimulated by TSH from the anterior pituitary, forming a classic negative feedback loop.
Calcitonin:
Produced by the parafollicular cells (C cells) of the thyroid gland.
Inhibits the release of calcium from bones into the blood by suppressing osteoclast activity.
Promotes renal excretion of calcium, thus lowering serum calcium levels.
Parathyroid Gland
Typically four small glands located on the posterior surface of the thyroid gland.
Produces Parathyroid Hormone (PTH).
Major Function: Balances serum calcium and phosphate levels. It acts by facilitating the transfer of calcium from bones to blood (through osteoclast activation), increasing calcium reabsorption in the kidneys, and promoting the activation of vitamin D to its active form, 1.25-(OH)2D3 n, which in turn enhances intestinal calcium absorption.
Adrenal Glands
Comprise two main parts, each with distinct functions, located superior to the kidneys:
Adrenal Medulla:
Acts as a modified sympathetic ganglion, secreting catecholamines: Epinephrine (adrenaline), Norepinephrine (noradrenaline), and a small amount of Dopamine.
Critical in the short-term fight or flight stress response, increasing heart rate, blood pressure, and glucose release.
Adrenal Cortex:
Produces three classes of corticosteroids and regulates long-term stress response, metabolism, and fluid/electrolyte balance:
Glucocorticoids (e.g., Cortisol): Influence glucose metabolism, reduce inflammation, and suppress the immune system.
Mineralocorticoids (e.g., Aldosterone): Regulate sodium and potassium balance, thereby affecting blood pressure.
Androgens (e.g., Dehydroepiandrosterone (DHEA)): Contribute to secondary sex characteristics, particularly in females.
Risk Factors for Hormonal Problems
Age: Hormonal production naturally declines or fluctuates with age (e.g., menopause, andropause, decreased GH).
Heredity: Genetic predispositions can lead to conditions like familial hypocalciuric hypercalcemia or multiple endocrine neoplasia.
Congenital factors: Birth defects affecting gland development or hormone synthesis (e.g., congenital hypothyroidism).
Trauma: Injury to endocrine glands (e.g., head trauma affecting the pituitary, neck trauma affecting the thyroid).
Environmental factors: Exposure to endocrine-disrupting chemicals (EDCs), certain toxins, or nutritional deficiencies (e.g., iodine deficiency leading to goiter).
Consequences of other disorders: Autoimmune diseases (e.g., Hashimoto's, Graves', Addison's), infections, tumors (benign or malignant), and chronic systemic illnesses can impair endocrine function.
Children and Hormonal Problems
Careful tracking of their daily activities, growth charts (height, weight, and head circumference for infants), and developmental milestones is crucial. Deviations can signal hormonal imbalances.
Differentiate between normal behavioral variations and those indicating hormonal issues (e.g., extreme lethargy, irritability, or mood swings). Look for signs like precocious or delayed puberty.
Observe dietary habits (e.g., extreme thirst, changes in appetite) and physical development over time (e.g., unusual hair growth, changes in body proportions) as these are key indicators.
Assessment of the Endocrine System
General Considerations
Symptoms of hormonal excess or deficiency can be subtle, diffuse, and mimic other conditions, making diagnosis challenging. A thorough and systematic approach is essential.
Common manifestations include:
Fatigue: Ranging from mild tiredness to debilitating exhaustion.
Depression: Mood disturbances are common due to hormonal influence on neurotransmitters.
Behavioral changes: Irritability, anxiety, altered cognitive function, or severe mood swings.
Changes in energy levels, sleep patterns, weight, and fluid balance.
Subjective Data Collection
Medical History:
Detailed inquiry into the frequency and severity of fatigue or weakness.
Menstrual irregularities (amenorrhea, oligomenorrhea) or changes in libido.
Any unexplained weight changes (gain or loss) without dietary modification.
Appetite changes (increased, decreased, specific cravings).
Emotional state (e.g., instability, anxiety, depression, lethargy, irritability).
Changes in hair, skin, nails, bowel habits, cold/heat intolerance.
Medication Review:
Comprehensive review of all prescription and over-the-counter medications, herbal supplements, and illicit drug use.
Specific inquiry regarding hormone replacements (e.g., thyroid hormones, estrogen/testosterone) and corticosteroid use, as these can significantly impact endocrine function.
Surgical History:
History of growth and development (e.g., birth weight, pubertal timing), any history of trauma (especially head or neck), radiation exposure.
Thorough family health history related to endocrine issues, including diabetes, thyroid disease, and autoimmune conditions.
Objective Data Collection
Systemic assessment, observing for specific signs of endocrine dysfunction:
Integumentary system (skin): Changes in texture, pigmentation (hyperpigmentation, vitiligo), turgor, hair distribution and loss, nail quality.
Head and neck: Facial features (coarsening, moon facies), exophthalmos, goiter (enlarged thyroid), thyroid nodules, venous distention.
Abdomen: Striae, abnormal fat distribution, organomegaly.
Extremities: Finger clubbing, edema, muscle weakness, changes in joint mobility.
Genitalia: Secondary sexual characteristics, changes in pubic or axillary hair.
Thorax: Heart rate and rhythm abnormalities, blood pressure changes.
Diagnostic Studies
Hormonal level assessments are cornerstone for diagnosis and monitoring:
Growth Hormone (GH): Measured to assess pituitary function, especially for suspected acromegaly or dwarfism.
Thyroid Hormones (TSH, T3, T4): TSH is the most sensitive screen for thyroid dysfunction; T3 and T4 directly measure thyroid hormone levels.
Parathyroid Hormone (PTH): Assessed with calcium to evaluate parathyroid function and calcium homeostasis.
Total Calcium: Crucial for assessing bone health, parathyroid function, and kidney function.
Cortisol: Measures adrenal cortex function, often with diurnal variation (higher in morning, lower at night).
Aldosterone: Evaluates mineralocorticoid function, critical for blood pressure and electrolyte balance.
ACTH: Measured to differentiate primary (adrenal) from secondary (pituitary) adrenal insufficiency.
Other tests include glucose levels, electrolyte panels, urine osmolality, imaging studies (MRI/CT), and genetic testing.
Disorders of the Anterior Pituitary: Acromegaly
Pathophysiology:
Caused by excessive secretion of growth hormone (GH) in adulthood, typically after epiphyseal plate closure. This excess GH often results from a benign pituitary tumor (adenoma).
In children, excessive GH leads to gigantism, characterized by proportional overgrowth.
GH promotes growth of soft tissues, cartilage, and bone, leading to characteristic physical changes.
Clinical Manifestations
Insidious onset, often recognized years after it begins.
Physical Changes: Enlargement of hands and feet, changes in facial structure (protruding jaw, enlarged nose, thickened lips, broad forehead), enlarged tongue (macroglossia), joint pain (common and debilitating).
Other Symptoms: Visual disturbances (due to tumor compression on optic chiasm), headaches, sleep apnea, peripheral neuropathy, high blood pressure, glucose intolerance (leading to type 2 diabetes), heart disease, and skin changes (thickening, oily).
Nursing Considerations During Assessment
Patients may express dissatisfaction or distress about their physical changes, which can impact their self-esteem and body image. Assess for anxiety, depression, and social isolation.
Monitor for specific symptoms such as joint pain, visual field deficits, headaches, and signs of cardiac dysfunction. Compare current photos with old ones to note progression of physical changes.
Diagnostic Studies
Insulin-like Growth Factor 1 (IGF-1): Elevated IGF-1 levels are a reliable screening test as GH stimulates IGF-1 production, and its levels fluctuate less than GH.
Oral Glucose Tolerance Test (OGTT): The most accurate diagnostic test. GH levels are measured before and after glucose administration; normally, glucose suppresses GH secretion. In acromegaly, GH levels remain elevated.
Imaging studies (MRI, CT): Identify and localize pituitary tumors.
Nursing Care Post-Operatively (Transsphenoidal Hypophysectomy)
This surgical approach removes the pituitary tumor through the nasal cavity.
Keep head elevated (HOB at 30 degrees) to reduce intracranial pressure and headache, promote venous drainage, and prevent disruption of the surgical site.
Monitor for cerebrospinal fluid (CSF) leaks (clear drainage from nose or postnasal drip, headache, positive glucose test of drainage for CSF). Report immediately.
Monitor for signs of diabetes insipidus (DI) (polyuria, polydipsia), which can occur due to ADH deficiency post-op.
Neurological assessment, pain management, and preventing complications like infection are crucial.
Hormone Replacement Therapy (HRT)
Life-long hormone replacement therapy is necessary if the entire pituitary gland is removed or significantly damaged.
Hormones such as glucocorticoids, thyroid hormones, and sex hormones (estrogen/testosterone) may need to be replaced.
Monitor for risks associated with specific HRT, such as the potential development of polyps and colorectal cancer with long-term GH excess, requiring regular screening if not fully resolved.
Disorders of the Posterior Pituitary:
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Characterized by excess secretion of ADH, leading to increased water reabsorption by the kidneys, resulting in dilutional hyponatremia and fluid overload.
Causes of SIADH
Malignancies: Especially small cell lung cancer, which can produce ectopic ADH.
CNS disorders: Head injuries (trauma, stroke, hemorrhage), infections (meningitis), tumors, surgery.
Infections: Pulmonary infections (pneumonia, tuberculosis) and other systemic infections.
Drug therapies: SSRIs, tricyclic antidepressants, chemotherapy agents (e.g., cyclophosphamide), NSAIDs, certain anesthetics.
Other systemic conditions: Hypothyroidism, adrenal insufficiency.
Clinical Manifestations
Low urine output (oliguria), weight gain (without edema as fluid is intracellular), decreased plasma osmolality (<285 ext{ mOsm/kg}), and dilutional hyponatremia (Na^+ <135 ext{ mEq/L}).
Symptoms of hyponatremia: mild (headache, lethargy, confusion, muscle cramps) to severe (seizures, coma, brain swelling) as sodium levels drop.
Nursing Interventions
Mild Cases (Na^+ >125 ext{ mEq/L}): Fluid restriction to 800-1000 mL/day to promote negative fluid balance. Encourage consumption of foods high in sodium and potassium.
Severe Cases (Na^+ <120 ext{ mEq/L}) or neurological symptoms): Administer hypertonic saline (e.g., 3% NaCl) to slowly raise serum sodium. Use diuretics (e.g., loop diuretics like furosemide) to promote water excretion, especially if severe hyponatremia is accompanied by fluid overload. Strict fluid intake limitation to 500 mL/day or less. Closely monitor neurological status for changes, implement seizure precautions, and observe for signs of rapid sodium correction (e.g., osmotic demyelination syndrome).
May administer vasopressin receptor antagonists (e.g., conivaptan, tolvaptan) to block ADH's effect on renal tubules.
Diabetes Insipidus (DI)
Pathophysiology
A disorder of water metabolism characterized by a deficiency of ADH or a decreased renal response to ADH, leading to excessive urination and thirst.
Can be central (neurogenic): Due to decreased ADH production/release from the hypothalamus/posterior pituitary, often caused by brain injury, tumors, or surgery.
Or nephrogenic: Due to adequate ADH production but the kidneys are unable to respond to ADH (e.g., due to drug toxicity like lithium, renal disease).
Clinical Manifestations
Polyuria: Excretion of large volumes of dilute urine (2-20 L/day, specific gravity <1.005). Patients may void every 30-60 minutes.
Polydipsia: Intense, compensatory thirst, often craving cold water, to prevent dehydration.
Fatigue, weakness, weight loss, and signs of severe dehydration (hypotension, tachycardia, poor skin turgor, dry mucous membranes).
Hypernatremia: Due to water loss, leading to neurological symptoms like irritability, confusion, and coma if severe.
Management of Care
Ensure adequate hydration by providing free access to water and encouraging frequent intake. Intravenous fluid replacement may be necessary for severe dehydration.
Monitor lab values closely, including urine specific gravity, serum and urine osmolality, and electrolytes (Na^+, K^+). Frequent weight monitoring is essential.
Manage electrolyte imbalances promptly. For central DI, desmopressin (DDAVP), an ADH analogue, is the primary treatment, administered orally, intranasally, or parenterally. For nephrogenic DI, management involves treating the underlying cause, low-sodium diet, and sometimes thiazide diuretics.
Promote patient understanding of their condition, medication regimen, and the importance of fluid balance and symptom recognition to prevent complications.
Hyperthyroidism
Disorders of Thyroid Gland
Hyperfunction characterized by the overproduction and release of excessive amounts of thyroid hormones (T3 and T4), leading to accelerated metabolism.
Often results from Graves' disease, an autoimmune disorder where antibodies stimulate the thyroid gland to produce excess hormones.
Case Study of Hyperthyroidism
Assess symptoms such as palpitations, tachycardia, nervousness, anxiety, heat intolerance, unintentional weight loss despite increased appetite, increased bowel movements, and fatigue. Specific signs include exophthalmos (protruding eyeballs) in Graves' disease and sometimes an audible thyroid bruit.
Monitor lab values, including suppressed TSH (due to negative feedback) and elevated free T4 and T3 levels.
Management of Hyperthyroidism
Antithyroid medications: Methimazole (Tapazole) and Propylthiouracil (PTU) inhibit thyroid hormone synthesis. PTU is preferred in pregnancy and for thyroid storm.
Beta-blockers: (e.g., Propranolol) manage symptoms like palpitations, tremors, and anxiety.
Radioactive iodine therapy (^{131}I): Destroys overactive thyroid cells; usually leads to hypothyroidism, requiring lifelong hormone replacement.
Subtotal or total thyroidectomy: Surgical removal of part or all of the thyroid gland.
Surgical Interventions (Thyroidectomy)
Indications include large goiters causing tracheal compression, lack of response to antithyroid medications, or suspected malignancy.
Preoperative care involves achieving a euthyroid state with antithyroid drugs. Postoperative care includes monitoring for airway obstruction, hemorrhage, hypocalcemia (due to parathyroid gland removal/damage), and laryngeal nerve damage.
Risk of thyroid storm (thyrotoxic crisis), a life-threatening hypermetabolic state, which can be precipitated by stressors or surgery.
Hypothyroidism
Case Study
Symptoms include profound fatigue, unexplained weight gain, hair loss (especially outer third of eyebrows), puffy appearance (myxedema), constipation, cold intolerance, slow speech, and bradycardia. Diagnostic tests reveal elevated TSH (primary hypothyroidism) and low free T3/T4 levels.
Myxedema coma: A severe, life-threatening complication characterized by profound hypothermia, hypoventilation, cardiovascular collapse, and impaired consciousness.
Management and Teaching for Patients
Levothyroxine (Synthroid): The primary treatment, a synthetic T4 hormone. Management involves gradual dosage titration based on TSH levels until euthyroid state is achieved.
Encourage a low-sodium, low-cholesterol, high-fiber diet to address constipation and potential cardiovascular risks. Promote regular fluid intake.
Discuss medication adherence: emphasize lifelong therapy, consistent timing of administration (typically early morning on an empty stomach to optimize absorption), and avoidance of interactions with other medications/foods (e.g., calcium, iron supplements, antacids, fiber, coffee).
Considerations for Levothyroxine Therapy
Importance of timing: Take on an empty stomach 30-60 minutes before breakfast for optimal absorption.
Monitoring interactions: Advise patients to inform all healthcare providers about levothyroxine use due to its numerous interactions. Avoid taking concurrently with calcium or iron supplements.
Teach signs of over- and under-dosing. Regular blood tests are crucial to adjust dosage.
Hyperparathyroidism
Overview
Increased PTH secretion leads to elevated serum calcium levels (hypercalcemia) and decreased serum phosphate levels (hypophosphatemia), causing significant bone metabolism issues and affecting other organ systems.
Primary Hyperparathyroidism: Usually caused by a single adenoma in one of the parathyroid glands.
Secondary Hyperparathyroidism: Occurs when a condition (e.g., chronic renal failure, vitamin D deficiency) causes hypocalcemia, leading to compensatory PTH overproduction.
Clinical Manifestations
Often asymptomatic. When symptoms occur, they affect multiple systems: "stones, bones, abdominal groans, and psychiatric overtones."
Stones: Renal calculi (kidney stones) due to hypercalciuria.
Bones: Osteoporosis, bone pain, fractures, demineralization.
Abdominal groans: Anorexia, nausea, vomiting, constipation, peptic ulcers, pancreatitis.
Psychiatric overtones: Fatigue, lethargy, muscle weakness, confusion, memory loss, depression.
Management Approaches
Regular exams and monitoring: For asymptomatic primary hyperparathyroidism, management may involve watchful waiting with regular monitoring of serum calcium, intact PTH, creatinine, and bone density.
Medicinal intervention: Calcimimetics (e.g., cinacalcet) may be used to increase the sensitivity of the calcium-sensing receptor on the parathyroid gland, reducing PTH secretion.
Parathyroidectomy: Surgical removal of the overactive parathyroid gland(s) is the most effective treatment for primary hyperparathyroidism. Pre-operative care includes hydration and mobilization.
Postoperative care focuses on monitoring for hypocalcemia (tetany, tingling, muscle spasms) following sudden reduction in PTH.
Addison's Disease (Primary Adrenocortical Insufficiency)
Pathophysiology
Result of adrenal cortex failure, leading to deficient secretion of all three classes of adrenal corticosteroids (glucocorticoids, mineralocorticoids, and androgens).
Most commonly caused by autoimmune destruction of the adrenal cortex.
Lack of cortisol leads to impaired stress response, hypoglycemia; lack of aldosterone leads to hyperkalemia, hyponatremia, and hypotension.
Clinical Manifestations
Insidious onset, leading to chronic, worsening fatigue, progressive weakness, and unintended weight loss.
Hyperpigmentation: Characteristic bronze-colored skin (especially in sun-exposed areas, pressure points, and mucous membranes) due to increased ACTH.
Gastrointestinal symptoms: Anorexia, nausea, vomiting, diarrhea, abdominal pain.
Cardiovascular: Postural hypotension (orthostatic hypotension), dizziness, tachycardia.
Electrolyte imbalances: Hyponatremia, hyperkalemia, mild acidosis.
Salt craving: Due to aldosterone deficiency.
Complications and Management
Risk for Addisonian crisis (acute adrenal insufficiency): A life-threatening emergency caused by insufficient adrenocortical hormones or a sudden decrease in these hormones (e.g., due to stress, infection, trauma, or abrupt withdrawal of corticosteroid therapy).
Symptoms include severe hypotension, tachycardia, dehydration, hypoglycemia, fever, weakness, confusion, and shock.
Management involves immediate intravenous administration of high-dose corticosteroids (hydrocortisone), large volumes of saline and glucose, and management of electrolyte imbalances.
Long-term management involves lifelong hormone replacement therapy: oral glucocorticoids (e.g., hydrocortisone, prednisone) and oral mineralocorticoids (e.g., fludrocortisone).
Nursing Implementation
Focus on patient education regarding lifelong medication adherence, including instructions on stress dosing (increasing medication during periods of physical or emotional stress, fever, illness, or surgery).
Teach patients to wear a medical alert bracelet/necklace and carry an emergency kit with injectable hydrocortisone and a written protocol for its use.
Educate on signs and symptoms of adrenal insufficiency and crisis, and the importance of regular follow-up with an endocrinologist.