NR 325 Week 1 Endocrine Disorders – Worksheet

Grace J.
August 12, 2025August 12, 2025
CU BSN, NR-325

Student Name

Chamberlain University

NR-325 Adult Health II

Prof. Name

Date

Diabetes Insipidus (DI) – Posterior Pituitary Disorder

Diabetes insipidus is a disorder characterized by decreased production, secretion, or renal response to antidiuretic hormone (ADH), leading to the excretion of large amounts of dilute urine. There are two primary types:

Central (neurogenic) – caused by damage to the hypothalamus or pituitary gland, impairing ADH secretion.
Nephrogenic – kidneys are unresponsive to ADH despite normal secretion.

Table 6

Diabetes Insipidus: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Central DI: head trauma, neurosurgery, CNS infections, tumors. Nephrogenic DI: renal disease, drug toxicity (lithium). Deficiency or insensitivity to ADH results in inability to concentrate urine.
Clinical Manifestations	Polyuria (5–20 L/day), polydipsia, nocturia, low urine specific gravity (<1.005), dehydration, hypernatremia (confusion, irritability).
Diagnostic Tests	Water deprivation test (failure to concentrate urine confirms DI); serum and urine osmolality; response to desmopressin distinguishes central from nephrogenic DI.
Nursing Interventions	Strict I&O monitoring; daily weights; ensure adequate fluid intake; desmopressin (DDAVP) for central DI; thiazide diuretics and low-sodium diet for nephrogenic DI.
Complications	Severe dehydration, hypovolemic shock, hypernatremia; treat promptly with fluid replacement and ADH analogs.

Hyperthyroidism / Goiter

Hyperthyroidism involves excessive production of thyroid hormones (T3 and T4), resulting in increased metabolic rate and heightened sympathetic nervous system activity. Graves’ disease is the most common cause, often accompanied by goiter and ophthalmopathy (exophthalmos).

Table 7

Hyperthyroidism: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Graves’ disease (autoimmune stimulation of TSH receptors); toxic multinodular goiter; thyroiditis; excess iodine; pituitary adenomas.
Clinical Manifestations	Weight loss despite increased appetite, heat intolerance, tremors, palpitations, tachycardia, goiter, exophthalmos, anxiety, insomnia, brittle hair.
Diagnostic Tests	Low TSH, elevated free T4; radioactive iodine uptake (RAIU) differentiates Graves’ disease from thyroiditis; ECG for arrhythmias.
Nursing Interventions	Antithyroid drugs (methimazole, PTU); beta-blockers for symptom control; radioactive iodine therapy; thyroidectomy in severe cases; eye protection for exophthalmos.
Complications	Thyrotoxic crisis (thyroid storm), heart failure, atrial fibrillation, osteoporosis; treat with supportive care and aggressive antithyroid therapy.

Hypothyroidism

Hypothyroidism results from insufficient thyroid hormone production. It can be primary (thyroid gland dysfunction), secondary (pituitary failure to secrete TSH), or tertiary (hypothalamic dysfunction).

Table 8

Hypothyroidism: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Hashimoto’s thyroiditis (autoimmune destruction), iodine deficiency, thyroid surgery, radioactive iodine therapy, pituitary or hypothalamic disease.
Clinical Manifestations	Fatigue, weight gain, cold intolerance, constipation, dry skin, hair loss, bradycardia, depression, myxedema (severe).
Diagnostic Tests	Primary: elevated TSH, low free T4; Secondary: low TSH and low T4; lipid profile may show hypercholesterolemia.
Nursing Interventions	Lifelong levothyroxine therapy; start low dose in older adults; monitor for cardiac effects; patient education on adherence.
Complications	Myxedema coma (medical emergency) with hypothermia, hypotension, hypoventilation; requires IV thyroid hormone and supportive care.

Hyperparathyroidism

Excess parathyroid hormone (PTH) causes hypercalcemia and hypophosphatemia due to increased bone resorption, renal calcium reabsorption, and intestinal calcium absorption.

Table 9

Hyperparathyroidism: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Primary: parathyroid adenoma. Secondary: chronic kidney disease, vitamin D deficiency.
Clinical Manifestations	Bone pain, muscle weakness, kidney stones, polyuria, constipation, depression.
Diagnostic Tests	Elevated serum calcium, low phosphate, elevated PTH; bone density scan.
Nursing Interventions	Hydration to prevent stones; bisphosphonates to inhibit bone resorption; parathyroidectomy for primary disease; monitor calcium post-op.
Complications	Osteoporosis, fractures, nephrolithiasis, cardiac dysrhythmias.

Hypoparathyroidism

Deficient PTH secretion results in hypocalcemia and hyperphosphatemia, often after thyroid or parathyroid surgery.

Table 10

Hypoparathyroidism: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Surgical removal or damage to parathyroid glands; autoimmune destruction; genetic syndromes.
Clinical Manifestations	Tetany, muscle cramps, paresthesia, positive Chvostek’s and Trousseau’s signs, laryngospasm.
Diagnostic Tests	Low calcium, high phosphate, low PTH; ECG may show prolonged QT interval.
Nursing Interventions	Administer IV calcium gluconate for acute hypocalcemia; oral calcium and vitamin D supplementation; seizure precautions.
Complications	Laryngospasm, seizures, cardiac arrhythmias.

Cushing’s Syndrome

Cushing’s syndrome results from chronic exposure to excess corticosteroids, most commonly glucocorticoids.

Table 11

Cushing’s Syndrome: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Exogenous corticosteroid use; ACTH-secreting pituitary adenoma (Cushing’s disease); adrenal tumors; ectopic ACTH production.
Clinical Manifestations	Central obesity, moon face, buffalo hump, purple striae, muscle weakness, osteoporosis, hyperglycemia, mood changes.
Diagnostic Tests	24-hour urinary cortisol; dexamethasone suppression test; CT/MRI of pituitary/adrenals.
Nursing Interventions	Taper corticosteroids if drug-induced; surgery or radiation for tumors; monitor glucose, electrolytes, infection signs.
Complications	Hypertension, diabetes mellitus, infections, fractures.

Addison’s Disease (Adrenocortical Insufficiency)

Addison’s disease is a chronic deficiency of adrenal cortex hormones (glucocorticoids, mineralocorticoids, and androgens).

Table 12

Addison’s Disease: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Autoimmune destruction (most common in developed countries); infections (TB, HIV); metastatic cancer; abrupt withdrawal of corticosteroids.
Clinical Manifestations	Fatigue, weight loss, hyperpigmentation, hypotension, hyponatremia, hyperkalemia, hypoglycemia.
Diagnostic Tests	Low cortisol levels; ACTH stimulation test; electrolyte imbalances; CT/MRI of adrenal glands.
Nursing Interventions	Lifelong corticosteroid and mineralocorticoid replacement; stress-dose steroids during illness; carry medical alert bracelet.
Complications	Addisonian crisis (shock, severe hypotension, electrolyte imbalance); treat with IV hydrocortisone and fluids.

Hyperaldosteronism

Excess aldosterone secretion causes sodium retention, potassium loss, and metabolic alkalosis.

Table 13

Hyperaldosteronism: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Primary: adrenal adenoma. Secondary: renal artery stenosis, heart failure, cirrhosis.
Clinical Manifestations	Hypertension, hypokalemia (muscle weakness, arrhythmias), metabolic alkalosis.
Diagnostic Tests	Elevated aldosterone, low renin levels; CT/MRI of adrenals.
Nursing Interventions	Adrenalectomy for adenomas; spironolactone to block aldosterone; BP monitoring.
Complications	Stroke, myocardial infarction, arrhythmias.

Pheochromocytoma

A rare tumor of the adrenal medulla producing excess catecholamines (epinephrine and norepinephrine).

Table 14

Pheochromocytoma: Summary of Key Points

Aspect	Details
Etiology / Pathophysiology	Adrenal medullary tumor; may be part of genetic syndromes (MEN type 2).
Clinical Manifestations	Episodic hypertension, severe headaches, palpitations, sweating, tremors, anxiety.
Diagnostic Tests	Elevated plasma and urinary metanephrines; CT/MRI for tumor localization.
Nursing Interventions	Alpha-adrenergic blockade pre-surgery; beta-blockers after alpha-blockade; adrenalectomy; avoid palpating tumor.
Complications	Hypertensive crisis, stroke, arrhythmias, death.

References

Ross, D. S., & Burch, H. B. (2022). Evaluation and management of thyrotoxicosis. The New England Journal of Medicine, 387(10), 893–906. https://doi.org/10.1056/NEJMra2032456

American Diabetes Association. (2024). Standards of medical care in diabetes—2024. Diabetes Care, 47(Supplement_1), S1–S154. https://doi.org/10.2337/dc24-SINT