Hashimoto thyroiditis
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Hashimoto thyroiditis
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
Assessments
Hashimoto thyroiditis
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Hashimoto thyroiditis
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Questions
USMLE® Step 1 style questions USMLE
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Radioactive iodine uptake test is performed and reveals diffusely decreased uptake. Which of the following is most likely involved in the pathogenesis of this patient’s condition?
Memory Anchors and Partner Content
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First Aid
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2016
Hashimoto thyroiditis p. 347
autoantibody p. 113
cholangitis association p. 404
goiter causes p. 348
HLA subtypes with p. 98
lymphoma association p. 349
Non-Hodgkin lymphoma p. 436, 437
Hashimoto thyroiditis and p. 347
External Links
Transcript
Contributors
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.
Summary
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.
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)
- "Immune Disorders in Hashimoto’s Thyroiditis: What Do We Know So Far?" Journal of Immunology Research (2015)
- "Hashimoto’s Thyroiditis: History and Future Outlook" Hormones (2013)
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