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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
Subacute granulomatous thyroiditis
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subacute granulomatous thyroiditis p. 347
Subacute granulomatous thyroiditis, also known as De Quervain’s thyroiditis, belongs to a group of disorders featuring inflammation “-itis” of the thyroid gland.
This inflammation is “granulomatous”, meaning there are aggregations of immune cells, mainly activated macrophages, that form tiny nodules within the thyroid gland.
Subacute implies that it’s somewhere between acute and chronic, typically developing after an acute event, like a viral infection.
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.
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.
So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy.
Subacute granulomatous thyroiditis is a self-limited inflammatory condition of the thyroid gland that commonly occurs after an upper respiratory tract infection. It presents as a transient, painful enlargement of the thyroid gland, which can sometimes press on the esophagus, causing dysphagia. There can also be hyperthyroidism signs, like feeling hot and sweating excessively, diarrhea, and rapidly losing weight even without any change in diet or exercise. In rare cases, there may be progression to a hypothyroid state, with symptoms of a decreased metabolic rate like feeling cold and weak, developing dry and rough skin, having constipation, and rapidly gaining weight without any change in diet or exercise. Subacute granulomatous thyroiditis generally resolves on its own, and treatment is supportive care with pain medications, such as nonsteroidal anti-inflammatory drugs.
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