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Congenital adrenal hyperplasia
Primary adrenal insufficiency
Adrenal cortical carcinoma
Thyroglossal duct cyst
Thyroid eye disease (NORD)
Toxic multinodular goiter
Euthyroid sick syndrome
Subacute granulomatous thyroiditis
Growth hormone deficiency
Constitutional growth delay
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Premature ovarian failure
Polycystic ovary syndrome
Androgen insensitivity syndrome
Autoimmune polyglandular syndrome type 1 (NORD)
Multiple endocrine neoplasia
Pancreatic neuroendocrine neoplasms
Opsoclonus myoclonus syndrome (NORD)
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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Brittany Norton, MFA
Jahnavi Narayanan, MBBS
With Riedel’s thyroiditis, thyroid- refers to the thyroid gland, and -itis means inflammation. So, Riedel’s thyroiditis is a condition where there is inflammation of the thyroid gland, which slowly causes fibrous tissue to replace the normal thyroid tissue. The condition is named after the German surgeon - Dr. Bernhard Moritz Carl Ludwig Riedel - who first described it.
Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, known as ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary gland. The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, 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”. If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small, hollow spheres whose walls are lined with follicular cells and are separated by a small amount of connective tissue. 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, but 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 then 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 fats and sugars. It’s as if the cells are in a bit of a frenzy.
T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.
Riedel's thyroiditis (RT) is a form of chronic inflammation of the thyroid gland, characterized by fibrosis (scarring) and thickening of the thyroid gland, which can result in the gland becoming stone-hard and fixed to adjacent structures. This loss of normal thyroid tissue can eventually lead to hypothyroidism, with symptoms like cold intolerance, lack of energy, constipation, or dry skin. Treatment of Riedel's thyroiditis includes corticosteroids to suppress the immune system, and thyroid hormone replacement to correct hypothyroidism. Surgery may be done to remove a goiter, but it can be difficult if it's spread to nearby structures.
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