Hashimoto's thyroiditis

(noun)

An autoimmune disease resulting in a malfunction of the endocrine system associated with low thyroid hormone levels.

Related Terms

Examples of Hashimoto's thyroiditis in the following topics:

  • Thyroid Gland Disorders

    • Hypothyroid disorders may occur as a result of congenital thyroid abnormalities, autoimmune disorders such as Hashimoto's thyroiditis, iodine deficiency (more likely in poorer countries), or the removal of the thyroid following surgery to treat severe hyperthyroidism or thyroid cancer.
    • Hashimoto's thyroiditis or Hashimoto's disease is an autoimmune disorder whereby the body's own immune system reacts with the thyroid tissues in an attempt to destroy it.
    • Hashimoto's disease is more common in females than males, usually appearing after the age of 30, and tends to run in families.
    • Also more common in individuals with Hashimoto's thyroiditis are type 1 diabetes and celiac disease.
    • The etiology is not always known, but can sometimes be attributed to autoimmunity, such as Hashimoto's thyroiditis or Graves' disease.

  • Type IV (Delayed Cell-Mediated) Reactions

    • Other examples include: temporal arteritis, Hashimoto's thyroiditis, symptoms of leprosy, symptoms of tuberculosis, coeliac disease, graft-versus-host disease and chronic transplant rejection.

  • Cytotoxic Autoimmune Reactions

    • The X-inactivation skew theory, suggesting the female-high tendency, and proposed by Princeton University's Jeff Stewart, has recently been confirmed experimentally in scleroderma and autoimmune thyroiditis.
    • Prominent examples include Coeliac disease, diabetes mellitus type 1 (IDDM), Sarcoidosis, systemic lupus erythematosus (SLE), Sjögren's syndrome, Churg-Strauss Syndrome, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, Addison's Disease, rheumatoid arthritis (RA) and allergies.
    • The X-inactivation skew theory, proposed by Princeton University's Jeff Stewart, has recently been confirmed experimentally in scleroderma and autoimmune thyroiditis.

  • Primary and Secondary Antibody Responses

    • Common autoimmune diseases include Hashimoto's thyroiditis, rheumatoid arthritis, diabetes mellitus type 1, and systemic lupus erythematosus.

  • The Roles of Genetics and Gender in Autoimmune Disease

    • Prominent examples include Coeliac disease, diabetes mellitus type 1 (IDDM), Sarcoidosis, systemic lupus erythematosus (SLE), Sjögren's syndrome, Churg-Strauss Syndrome, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, Addison's Disease, rheumatoid arthritis (RA), and allergies.

  • Adrenal Gland Disorders

    • Autoimmune adrenalitis may be part of Type 2 autoimmune polyglandular syndrome, (which can include type 1 diabetes), hyperthyroidism, autoimmune thyroid disease (also known as autoimmune thyroiditis and Hashimoto's disease).

  • Formation, Storage, and Release of Thyroid Hormones

    • Thyroid hormones (T4 and T3) are produced by the follicular cells of the thyroid gland and regulated by thyroid-stimulating hormone (TSH).
    • The thyroid hormones thyroxine (T4) and triiodothyronine (T3) are produced from thyroid follicular cells within the thyroid gland, a process regulated by the thyroid-stimulating hormone secreted by the anterior pituitary gland.
    • If there is a deficiency of dietary iodine, the thyroid will not be able to make thyroid hormone.
    • A lack of thyroid hormone will lead to decreased negative feedback on the pituitary, which in turn, will lead to increased production of thyroid-stimulating hormone, which causes the thyroid to enlarge (goiter).
    • This enlarged endemic colloid goiter has the effect of increasing the thyroid's ability to trap more iodide, compensating for the iodine deficiency and allowing it to produce adequate amounts of thyroid hormone.

  • Control of Thyroid Hormone Release

    • The production of thyroxine and triiodothyronine is regulated by thyroid-stimulating hormone (TSH) that is released from the anterior pituitary.
    • Thyroid hormones also provide negative feedback to the hypothalamus and anterior pituitary gland.
    • When thyroid levels in the blood are elevated TSH and TRH production is reduced.
    • Thyroid hormones are produced from the thyroid under the influence of thyroid-stimulating hormone (TSH) from the anterior pituitary gland, which is itself under the control of thyroptropin-releasing hormone (TRH) secreted by the hypothalamus.
    • Thyroid hormones provide negative feedback, inhibiting secretion of TRH and TSH when blood levels are high.

  • Action of Thyroid Hormones

    • The primary function of the thyroid is to produce the hormones triiodothyronine (T3), thyroxine (T4), and calcitonin.
    • Triiodothyronine (T3) and thyroxine (T4) are enzymes produced by the thyroid gland.
    • The main activity of the thyroid hormones T3 and T4 is to boost the basal metabolic rates of proteins, fats, and carbohydrates as well as vitamins.
    • Thyroid hormones affect the dilation of blood vessels, which in turn affects the rate at which heat can escape the body.
    • A person who suffers from hyperthyroidism (an over-active thyroid) will experience a fever; conversely, a person who suffers from hypothyroidism (a less active thyroid) will experience a decrease in body temperature.

  • Thyroid Gland

    • When the thyroid swells due to dysfunction, it can be felt under the skin of the neck.
    • The thyroid gland is made up of many spherical thyroid follicles which are lined with a simple cuboidal epithelium.
    • This glycoprotein is the precursor to the thyroid hormones.
    • The thyroid gland produces the hormones T3 (triiodothyronine) and T4 (thyroxine).
    • These thyroid hormones increase the rates of mitochondrial ATP production.