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Related Concept Videos

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...
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 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...
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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Semi-Automated Analysis of Peak Amplitude and Latency for Auditory Brainstem Response Waveforms Using R
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Auditory brainstem response findings in hypothyroid and hyperthyroid disease.

A R D Thornton1, S J Jarvis

  • 1MRC Institute of Hearing Research, Royal South Hants Hospital, Southampton SO14 0YG, UK. ardt@soton.ac.uk

Clinical Neurophysiology : Official Journal of the International Federation of Clinical Neurophysiology
|February 20, 2008
PubMed
Summary

Hypothyroidism may cause hearing loss, but auditory brainstem response abnormalities in hypothyroid patients are likely due to low body temperature, not direct retrocochlear issues. Treatment normalized auditory brainstem response findings.

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Area of Science:

  • Otolaryngology
  • Endocrinology
  • Neuroscience

Background:

  • Retrocochlear sensorineural hearing loss has been anecdotally linked to hypothyroidism.
  • Auditory Brainstem Response (ABR) is a key diagnostic tool for evaluating retrocochlear function.

Purpose of the Study:

  • To investigate the association between hypothyroidism and retrocochlear sensorineural hearing loss.
  • To differentiate between direct effects of hypothyroidism and confounding factors like body temperature on ABR measures.

Main Methods:

  • Audiometric testing and Auditory Brainstem Response (ABR) measurements were performed on patients with hyperthyroidism and hypothyroidism.
  • Data analysis included stratification by body temperature to assess its influence on ABR findings.

Main Results:

  • Hyperthyroid patients showed no significant differences from controls in audiometric or ABR results.
  • Hypothyroid patients exhibited a higher prevalence of hearing threshold abnormalities (36% > 25dB).
  • ABR in hypothyroid patients revealed reduced wave amplitudes and prolonged I-V intervals, but these were explained by lower body temperatures.

Conclusions:

  • The study found no significant auditory differences in hyperthyroid patients compared to controls.
  • While hypothyroid patients showed some hearing and ABR differences, these abnormalities were attributable to low body temperature, not direct retrocochlear damage.
  • Thyroxine treatment normalized ABR findings, supporting the role of body temperature in the observed abnormalities.