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Related Concept Videos

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...
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...
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...
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...
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...
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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Cochlear dysfunction in patients with acute hypothyroidism.

Vassilis Psaltakos1, Dimitrios G Balatsouras, Ioannis Sengas

  • 1Ear, Nose and Throat Department, Tzanion General Hospital, Piraeus, Greece.

European Archives of Oto-Rhino-Laryngology : Official Journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : Affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
|December 26, 2012
PubMed
Summary
This summary is machine-generated.

Acute hypothyroidism, induced by thyroidectomy, temporarily impairs hearing thresholds and causes subclinical cochlear damage in patients. This study highlights the significant impact of thyroid hormone levels on auditory function.

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A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function
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Area of Science:

  • Otolaryngology
  • Endocrinology
  • Auditory Neuroscience

Background:

  • Thyroid hormones are crucial for maintaining normal physiological functions, including those of the inner ear.
  • The effects of acute, temporary hypothyroidism on cochlear function in humans are not fully understood.

Purpose of the Study:

  • To prospectively investigate the impact of acute hypothyroidism on cochlear function in patients undergoing total thyroidectomy.
  • To assess changes in hearing thresholds and otoacoustic emissions during a period of induced hypothyroidism.

Main Methods:

  • A prospective study involving 52 patients with thyroid carcinoma undergoing total thyroidectomy without immediate levothyroxine replacement.
  • Pure-tone audiometry, tympanometry, and transiently evoked otoacoustic emissions (TEOAEs) were performed preoperatively and 6-8 weeks postoperatively.
  • Comparison with a control group of healthy volunteers.

Main Results:

  • Postoperative audiometry revealed elevated hearing thresholds across all frequencies, with significant variations.
  • Transiently evoked otoacoustic emissions showed reduced signal-to-noise ratios at all measured frequencies in the hypothyroid state.
  • Otoacoustic emission testing indicated subclinical cochlear involvement in more ears than pure-tone audiometry.

Conclusions:

  • Acute hypothyroidism leads to elevated hearing thresholds in humans.
  • Subclinical damage to cochlear function is a significant consequence of acute hypothyroidism.
  • Thyroid hormone levels play a critical role in maintaining normal cochlear function.