Graves disease
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Graves disease
Endocrine system
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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Childbirth
Graves disease and p. 348
Cytokines p. 99, 106
Graves disease and p. 348
Fibroblasts
Graves disease p. 348
Graves disease
autoantibody p. 113
goiter caused by p. 348
HLA-DR3 and p. 98
hyperthyroidism p. 348
type II hypersensitivity p. 110
Hypersensitivity reactions p. 110-111
Graves disease p. 348
IFN- γ (Interferon- γ ) p. 106, 114
Graves disease and p. 348
Thyroid-stimulating hormone (TSH)
Graves disease and p. 348
TNF- α p. 106
Graves disease and p. 348
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Transcript
Content Reviewers
Rishi Desai, MD, MPHContributors
Brittany Norton, MFA
Evan Debevec-McKenney
Jake Ryan
Tanner Marshall, MS
First described by Irish surgeon Robert James Graves, Graves disease is an autoimmune disorder that causes hyperthyroidism.
In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormone, so Graves disease refers to a condition where there’s excess thyroid hormones.
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.
It’s as if the cells are in a bit of 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.
Summary
Graves' disease is an autoimmune disorder in which the body produces thyroid-stimulating antibodies, leading to the overproduction of thyroid hormone. People with Graves' disease present with ophthalmopathy, weight loss, anxiety, tremors, irritability, muscle weakness, and diarrhea.
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)
- "General hyperpigmentation induced by Grave's disease" Medicine (2018)
- "Hyperthyroidism" The Lancet (2016)
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