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Graves Disease II: Pathophysiology

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...

Goiter

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

Hyperthyroidism I: Introduction

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: Pathophysiology

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 I: Introduction

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 Hormones

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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Related Experiment Video

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Pathological changes in the thyroid gland in crush asphyxia.

Roger W Byard¹

¹Discipline of Anatomy and Pathology, The University of Adelaide, Frome Road, Level 3 Medical School North Building, Adelaide, SA, 5005, Australia, roger.byard@sa.gov.au.

Forensic Science, Medicine, and Pathology

|August 15, 2013

Summary

Crush asphyxia can cause significant thyroid gland changes, including a dark, "black thyroid" appearance due to intense blood congestion. Histology reveals engorged capillaries and intrafollicular blood, aiding diagnosis in these cases.

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Area of Science:

Forensic Pathology
Toxicology

Background:

Crush asphyxia is a cause of death resulting from chest compression.
Thyroid gland pathology in crush asphyxia is not well-documented.

Observation:

Four male decedents aged 36-65 years died from crush asphyxia.
Autopsies revealed marked congestion of the face, neck, and upper body, petechial hemorrhages, and intense thyroid gland congestion.
The thyroid glands appeared dark/black macroscopically.

Findings:

Microscopic examination showed engorged stromal capillaries and intrafollicular aggregates of erythrocytes within the colloid.
These findings suggest that severe thyroid gland suffusion with blood can occur in crush asphyxia.
The term "black thyroid" is proposed to describe this macroscopic appearance.

Implications:

The "black thyroid" appearance and intrafollicular blood lakes may serve as additional diagnostic indicators for crush asphyxia during forensic autopsies.
This study highlights the importance of examining the thyroid gland in cases of suspected crush asphyxia.