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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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autoantibody p. 113
cholangitis association p. 404
goiter causes p. 348
HLA subtypes with p. 98
lymphoma association p. 349
Hashimoto thyroiditis and p. 347
Pauline Rowsome, BSc (Hons)
Tanner Marshall, MS
Hashimoto’s thyroiditis, named after the Japanese physician Hakaru Hashimoto who first described it, belongs to a group of disorders where there’s some form of inflammation “-itis” of the thyroid gland.
It’s basically an autoimmune destruction of the thyroid gland, which typically progresses gradually to hypothyroidism, or state of too low “hypo-“ thyroid hormones.
In fact, Hashimoto’s thyroiditis is the most common cause of hypothyroidism in areas of the world where dietary iodine, the basic structural element of thyroid hormones, is sufficient.
Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, or ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.
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.
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.
Hashimoto thyroiditis is a type of autoimmune disease that attacks and destroys the thyroid gland. This can cause hypothyroidism, which can lead to a wide range of symptoms, such as tiredness, weight gain, depression, and changes in your menstrual cycle. The cause of hashimoto's thyroiditis is unknown, but it's thought to be caused by a combination of genetic and environmental factors.
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