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CHAPTER 10 – ENDOCRINE SYSTEM
🔹 I. Overview
- The endocrine system consists of a network of glands that secrete hormones directly into the bloodstream. These hormones regulate metabolism, growth, reproduction, stress response, and homeostasis.
- Unlike the exocrine system (which secretes into ducts), endocrine glands are ductless , releasing hormones into circulation to act on target organs with specific receptors.
🔹 II. Major Endocrine Glands & Their Functions
Gland Location Major Hormones Function / Target Pituitary gland (“Master gland”) Base of brain in sella turcica
GH, TSH, ACTH, FSH,
LH, Prolactin, ADH (from posterior pituitary), Oxytocin. Controls other endocrine glands; regulates growth, metabolism, reproduction. Thyroid gland Neck, below larynx Thyroxine (T ),₄ Triiodothyronine (T ),₃ Calcitonin. Controls metabolic rate, heat production, calcium balance. Parathyroid glands (4) Posterior thyroid PTH (parathyroid hormone). Regulates calcium & phosphate balance. Adrenal glands Superior to kidneys Cortex: cortisol, aldosterone, androgens; Medulla: epinephrine, norepinephrine. Stress response, electrolyte balance, blood pressure control. Pancreas (Islets of Langerhans) Behind stomach Insulin, Glucagon, Somatostatin. Glucose regulation. Gonads (Testes/Ovaries) Pelvic region. Testosterone, Estrogen, Progesterone Secondary sex characteristics, reproduction.
Gland Location Major Hormones Function / Target Pineal gland Midbrain. Melatonin. Circadian rhythm, puberty regulation. Thymus Mediastinum. Thymosin. Immune system development (T-cell maturation in children). (Growth Hormone (GH), Thyroid-Stimulating Hormone (TSH), Adrenocorticotropic Hormone (ACTH), Follicle-Stimulating Hormone (FSH), Luteinizing Hormone (LH), Prolactin (PRL), Antidiuretic Hormone (ADH) (also known as Vasopressin))
🔹 III. Mechanisms of Hormonal Control
- Humoral stimuli – response to changing blood chemistry (e.g., low calcium → ↑PTH).
- Neural stimuli – nerve fibers stimulate hormone release (e.g., sympathetic stimulation → epinephrine release).
- Hormonal stimuli – one hormone triggers another (e.g., TSH → thyroid hormones). 🔹 IV. Imaging Modalities in Endocrine Evaluation Modality Typical Uses CT Adrenal gland masses, pituitary region, thyroid nodules. MRI Pituitary tumors, hypothalamic lesions, adrenal hyperplasia. Ultrasound Thyroid, parathyroid, testicular, ovarian glands. Nuclear Medicine (Scintigraphy) Thyroid function studies (I-123, Tc-99m), parathyroid adenoma localization. PET/CT Detects functional tumors or metastases (e.g., insulinoma, thyroid carcinoma). DEXA (dual-energy X-ray absorptiometry) Bone density — assesses osteopenia/osteoporosis (secondary to endocrine disorders).
Causes: autoimmune (Hashimoto’s), iodine deficiency, post-surgery. Symptoms: lethargy, weight gain, bradycardia, cold intolerance, myxedema. Imaging: thyroid US shows heterogeneous, hypoechoic gland. c. Goiter Enlargement of thyroid from chronic stimulation (usually iodine deficiency). Imaging: visible neck mass, tracheal deviation on radiograph or CT. d. Thyroid Nodules / Neoplasms Type Description Imaging Adenoma Benign “hot nodule”. Nuclear scan: focal uptake. Carcinoma Papillary (most common), follicular, medullary, anaplastic. Cold nodule, calcifications on US/CT. 🧩 3. Parathyroid Disorders a. Hyperparathyroidism ↑PTH → bone resorption → hypercalcemia. Primary: parathyroid adenoma or hyperplasia. Secondary: chronic renal failure (low calcium → compensatory ↑PTH). Imaging findings: subperiosteal bone resorption, “salt-and-pepper skull,” renal calculi, nephrocalcinosis. Treatment: surgical removal of adenoma. b. Hypoparathyroidism ↓PTH → hypocalcemia → muscle cramps, tetany. Usually postsurgical (after thyroidectomy). 🧩 4. Adrenal Gland Disorders a. Cushing’s Syndrome Excess cortisol from adrenal hyperplasia, adenoma, or exogenous steroids.
Symptoms: “moon face,” “buffalo hump,” truncal obesity, muscle weakness, osteoporosis. Imaging: CT/MRI – enlarged adrenals or adenoma. DEXA: may show osteopenia. b. Addison’s Disease (Adrenal Insufficiency) ↓Cortisol & aldosterone (autoimmune, infection). Symptoms: weakness, hypotension, bronzing of skin, electrolyte imbalance. Imaging: small or calcified adrenals on CT (esp. post-TB). c. Pheochromocytoma Tumor of adrenal medulla → excess epinephrine/norepinephrine. Symptoms: severe hypertension, tachycardia, sweating, palpitations. Imaging: MRI = bright mass (“lightbulb” sign), nuclear MIBG scan confirms. Treatment: surgical removal after blood pressure control. 🧩 5. Pancreatic (Islet Cell) Disorders a. Diabetes Mellitus Type 1: autoimmune destruction of β-cells → insulin deficiency; usually in youth. Type 2: insulin resistance; related to obesity, adults. Chronic complications: Atherosclerosis → CAD, stroke. Diabetic nephropathy (enlarged echogenic kidneys). Retinopathy (vision loss). Neuropathy, infection, poor wound healing. Imaging: IVP/US: nephropathy changes. Angiography: atherosclerosis. DEXA: osteoporosis in long-term diabetics. Treatment: insulin (Type 1), oral hypoglycemics (Type 2), diet, exercise.
Condition Imaging Finding Addison’s disease Small/calcified adrenal glands Graves disease Diffuse thyroid enlargement with ↑ uptake Hashimoto’s thyroiditis Heterogeneous hypoechoic thyroid Hyperparathyroidism Subperiosteal bone resorption, nephrolithiasis Diabetes mellitus Atherosclerosis, nephropathy Pheochromocytoma Intense enhancing adrenal medullary mass Hypoparathyroidism Low calcium → basal ganglia calcifications Pituitary adenoma Enlarged sella on lateral skull radiograph or MRI 🔹 VII. CAMRT-Focused Integration Points
- Metabolic bone changes (osteopenia, bone resorption) = often secondary to endocrine dysfunction (PTH, cortisol, GH imbalance).
- Sella turcica erosion → pituitary tumor (common CAMRT question).
- Hypercalcemia management → key in hyperparathyroidism and metastatic bone disease.
- Adrenal imaging – CT is modality of choice.
- Thyroid scintigraphy differentiates hot vs cold nodules (functioning vs non- functioning).
- MRI pituitary is gold standard for microadenoma detection.
- Pheochromocytoma – think “paroxysmal hypertension” + bright T2 adrenal mass.
- Type 1 vs Type 2 diabetes – immune destruction vs insulin resistance.
- Cushing’s vs Addison’s – opposite cortisol levels, opposite blood pressure effects.
- Osteoporosis secondary to endocrine disease (Cushing’s, menopause, parathyroid) → evaluated by DEXA. 🔹 VIII. Quick Pathology Summary Table Gland Disorder Key Lab / Imaging Finding Pituitary Acromegaly ↑GH, enlarged sella
Gland Disorder Key Lab / Imaging Finding Thyroid Graves ↑T /T , ↑radioiodine uptake₃ ₄ Thyroid Hashimoto’s ↓T /T , heterogeneous gland₃ ₄ Parathyroid Hyperparathyroidism ↑Ca² , bone resorption⁺ Adrenal Cortex Cushing’s ↑Cortisol, truncal obesity Adrenal Cortex Addison’s ↓Cortisol, small adrenals Adrenal Medulla Pheochromocytoma ↑Catecholamines, bright T MRI Pancreas Diabetes Mellitus ↑Glucose, vascular calcifications Gonads PCOS Multiple ovarian cysts Thymus Thymoma Mediastinal mass on chest CT 🔹 CAMRT TIP: Expect applied questions connecting imaging + physiology, e.g.: “Which endocrine disorder results in subperiosteal bone resorption and renal calculi?” → Hyperparathyroidism. Or “A pituitary adenoma causing GH overproduction after epiphyseal closure results in what condition?” → Acromegaly.
Chapter-10: Endocrine System — Full Review Answers and Deep
Explanations
1. Medical treatment designed to lower serum calcium levels is important in the management of: a. Cystitis b. Nephrocalcinosis c. Nephrosclerosis d. Polycystic kidney disease Answer: b. Nephrocalcinosis Explanation: Nephrocalcinosis is deposition of calcium salts in renal parenchyma (usually medulla). It commonly results from hypercalcemia or hypercalciuria (primary hyperparathyroidism, hypervitaminosis D, renal tubular acidosis, immobilization). Lowering serum calcium (and urinary calcium) is central to management because ongoing hypercalcemia drives further deposition and renal damage. Medical measures include hydration, diuretics (e.g., loop diuretics to enhance calcium excretion when appropriate), bisphosphonates (in certain causes), correction of underlying endocrine disorders (parathyroidectomy for primary hyperparathyroidism), and dietary/medication adjustments. Imaging correlation: On radiographs/CT, nephrocalcinosis appears as increased parenchymal calcifications (medullary “nephrocalcinosis” pattern). Sonography may show hyperechoic medullary pyramids. CAMRT tip: Distinguish nephrocalcinosis (parenchymal) from nephrolithiasis (focal stones in collecting system) — imaging and clinical chemistry help. 2. Osteopenia is a term used to describe the radiographic appearance associated with a decrease in bone density and is associated with: a. Craniosynostoses b. Osteopetrosis c. Osteoporosis d. Scoliosis Answer: c. Osteoporosis
5. Corticosteroid production occurs in the: a. Adrenal cortex b. Pancreas c. Pineal gland d. Thyroid gland Answer: a. Adrenal cortex Explanation: The adrenal cortex (outer portion of adrenal gland) produces corticosteroids : glucocorticoids (cortisol), mineralocorticoids (aldosterone), and adrenal androgens. The adrenal medulla produces catecholamines (epinephrine, norepinephrine). Pancreas (endocrine islets) produces insulin/glucagon; pineal produces melatonin; thyroid produces T3/T4 and calcitonin. Clinical relevance: Disorders of adrenal cortical function include Cushing’s syndrome (excess cortisol) and Addison’s disease (insufficiency). 6. α-cells in the pancreas produce: a. Glucagon b. Gonadocorticosteroids c. Insulin d. Thyroxine Answer: a. Glucagon Explanation: Pancreatic islets contain different cell types: α-cells produce glucagon (raises blood glucose by stimulating glycogenolysis and gluconeogenesis), β-cells produce insulin (lowers blood glucose), and δ-cells produce somatostatin (inhibits both). Gonadocorticosteroids are from adrenal cortex; thyroxine from thyroid. Clinical point: In diabetes mellitus, β-cell dysfunction is central; glucagon dysregulation also contributes. 6. Acromegaly is a condition resulting from disorder of the __________ gland. a. Adrenal b. Pineal
c. Pituitary d. Thymus Answer: c. Pituitary Explanation: Acromegaly results from excess growth hormone (GH) secretion after epiphyseal closure (adult), classically due to a pituitary adenoma. It causes soft tissue enlargement, coarse facial features, enlarged hands/feet, and insulin resistance. If GH excess occurs before epiphyseal closure in children, it produces gigantism. Imaging: MRI of the sella turcica detects pituitary adenoma; plain skull films may show enlarged sella.
7. Graves’ disease is associated with: a. Hyperthyroidism b. Hyperparathyroidism c. Hypothyroidism d. Hypoparathyroidism Answer: a. Hyperthyroidism Explanation: Graves’ disease is an autoimmune condition causing thyroid-stimulating immunoglobulins that activate the TSH receptor → diffuse thyroid overactivity and enlargement → hyperthyroidism. Clinical features: weight loss, heat intolerance, tremor, tachycardia, exophthalmos. Imaging/NM: Technetium or iodine thyroid uptake shows diffuse increased uptake in Graves. Contrast with Hashimoto’s (autoimmune destruction) which typically leads to hypothyroidism. 8. Type 1 diabetes mellitus is most common in: a. Adults b. Children Answer: b. Children
