Toxic multinodular goiter
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Toxic multinodular goiter
Pathology
Adrenal gland disorders
Congenital adrenal hyperplasia
Primary adrenal insufficiency
Waterhouse-Friderichsen syndrome
Hyperaldosteronism
Adrenal cortical carcinoma
Cushing syndrome
Conn syndrome
Thyroid gland disorders
Thyroglossal duct cyst
Hyperthyroidism
Graves disease
Thyroid eye disease (NORD)
Toxic multinodular goiter
Thyroid storm
Hypothyroidism
Euthyroid sick syndrome
Hashimoto thyroiditis
Subacute granulomatous thyroiditis
Riedel thyroiditis
Postpartum thyroiditis
Thyroid cancer
Parathyroid gland disorders
Hyperparathyroidism
Hypoparathyroidism
Hypercalcemia
Hypocalcemia
Pancreatic disorders
Diabetes mellitus
Diabetic retinopathy
Diabetic nephropathy
Pituitary gland disorders
Hyperpituitarism
Pituitary adenoma
Hyperprolactinemia
Prolactinoma
Gigantism
Acromegaly
Hypopituitarism
Growth hormone deficiency
Pituitary apoplexy
Sheehan syndrome
Hypoprolactinemia
Constitutional growth delay
Diabetes insipidus
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Gonadal dysfunction
Precocious puberty
Delayed puberty
Premature ovarian failure
Polycystic ovary syndrome
Androgen insensitivity syndrome
Kallmann syndrome
5-alpha-reductase deficiency
Polyglandular syndromes
Autoimmune polyglandular syndrome type 1 (NORD)
Endocrine tumors
Multiple endocrine neoplasia
Pancreatic neuroendocrine neoplasms
Zollinger-Ellison syndrome
Carcinoid syndrome
Pheochromocytoma
Neuroblastoma
Opsoclonus myoclonus syndrome (NORD)
Endocrine system pathology review
Adrenal insufficiency: Pathology review
Adrenal masses: Pathology review
Hyperthyroidism: Pathology review
Hypothyroidism: Pathology review
Thyroid nodules and thyroid cancer: Pathology review
Parathyroid disorders and calcium imbalance: Pathology review
Diabetes mellitus: Pathology review
Cushing syndrome and Cushing disease: Pathology review
Pituitary tumors: Pathology review
Hypopituitarism: Pathology review
Diabetes insipidus and SIADH: Pathology review
Multiple endocrine neoplasia: Pathology review
Neuroendocrine tumors of the gastrointestinal system: Pathology review
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Thyroid hormones p. 342
in toxic multinodular goiter p. 348
Toxic multinodular goiter p. 348
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Transcript
Content Reviewers
Rishi Desai, MD, MPHContributors
Evan Debevec-McKenney
Tanner Marshall, MS
In toxic multinodular goiter, also called Plummer’s disease, ‘toxic’ refers to something harmful, ‘nodular’ refers to little lumps or nodules of tissue, and ‘goiter’ refers to a large thyroid gland.
So toxic multinodular goiter is a condition where the thyroid gland enlarges and is filled with lots of little nodules of tissue - each of which produce so much thyroid hormone that it becomes harmful to the body.
Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.
The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH.
TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.
The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells.
Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.
Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins.
Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.
Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.
So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats.
Summary
Toxic multinodular goiter (TMNG) is a condition characterized by the growth of multiple nodules in the thyroid gland, which can cause the gland to become enlarged and produce too much thyroid hormone. The excess thyroid hormone production can lead to symptoms of hyperthyroidism, including weight loss, rapid heart rate, tremors, and heat intolerance.
TMNG typically develops after prolonged iodine deficiency, which causes hypertrophy and hyperplasia of the thyroid gland. Continued follicular cell division can lead to a genetic mutation of the TSH receptor turning a non-toxic multinodular goiter into a toxic multinodular goiter.
Symptoms include an enlarged thyroid as well as the typical symptoms of hyperthyroidism like weight loss, a rapid heart rate, and hyperactivity. The treatment for TMNG involves medications like beta-blockers and radioactive iodine, or surgery to remove part or all of the thyroid gland.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
- "Harrison's Endocrinology, 4E" McGraw-Hill Education / Medical (2016)
- "Large Multinodular Toxic Goiter: Is Surgery Always Necessary?" Case Reports in Endocrinology (2016)
- "Clinical outcomes after estimated versus calculated activity of radioiodine for the treatment of hyperthyroidism: systematic review and meta-analysis" European Journal of Endocrinology (2009)
- "Molecular Pathogenesis of Euthyroid and Toxic Multinodular Goiter" Endocrine Reviews (2004)
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