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Related Concept Videos

Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Published on: March 17, 2023

EXPERIMENTAL THYROIDISM.

R H Cunningham1

  • 1Department of Physiology of Columbia University at the College of Physicians and Surgeons, New York.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary
This summary is machine-generated.

Fresh thyroid tissue is not toxic when ingested. However, decomposed thyroid material causes intoxication, and other animal tissues can induce similar symptoms. Thyroid extracts can palliate cachexia in thyroidless dogs but do not sustain life.

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Area of Science:

  • Physiology
  • Endocrinology
  • Toxicology

Background:

  • Induced thyroidism symptoms arise from ingesting decomposed thyroid material.
  • Similar intoxication symptoms can result from ingesting various animal tissues.
  • The function of internal secretions during life is not necessarily indicated by injection effects.

Purpose of the Study:

  • To investigate the toxicity of fresh and decomposed thyroid gland material.
  • To determine the effects of animal tissue extracts on induced thyroidism.
  • To evaluate the palliative effects of thyroid and thymus extracts on cachexia in thyroidless dogs.

Main Methods:

  • Ingestion and injection of fresh and decomposed thyroid gland material.
  • Administration of various animal tissue extracts.
  • Observation of symptoms and survival rates in totally thyroidless dogs and monkeys.

Main Results:

  • Fresh thyroid is not toxic when ingested; decomposed material causes intoxication.
  • Intoxication symptoms are not specific to the thyroid and can be induced by other animal tissues.
  • Thyroid and thymus extracts can palliate cachexia in thyroidless dogs but do not prolong survival significantly.

Conclusions:

  • Symptoms of experimental thyroidism result from intoxication by decomposed material, not thyroid function itself.
  • Thyroid and thymus tissues yield substances that can palliate cachexia, but these are not enzymes or iodine-containing.
  • The pathology of exophthalmic goiter may be explained by deficient thyroid activity as plausibly as by augmented function.