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Related Concept Videos

Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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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,...
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Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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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...
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Goiter01:27

Goiter

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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...
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Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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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...
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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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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...
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Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Related Experiment Video

Updated: Apr 25, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
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Subacute thyroiditis masquerading giant cell arteritis.

Upasana Tiwari, Fnu Shailesh, Richa Pandey

    The Journal of the Arkansas Medical Society
    |September 2, 2014
    PubMed
    Summary

    Subacute thyroiditis and giant cell arteritis are rare. This case highlights a rare instance where a patient presented with giant cell arteritis symptoms but was diagnosed with subacute thyroiditis.

    Area of Science:

    • Endocrinology
    • Rheumatology
    • Internal Medicine

    Background:

    • Subacute thyroiditis (SAT) and giant cell arteritis (GCA) are uncommon inflammatory conditions.
    • The simultaneous occurrence or overlapping presentation of SAT and GCA is exceptionally rare in clinical practice.

    Observation:

    • A patient presented with clinical manifestations suggestive of giant cell arteritis.
    • Diagnostic workup revealed findings consistent with subacute thyroiditis, not GCA.

    Findings:

    • The patient's symptoms, initially mimicking GCA, were ultimately attributed to SAT.
    • This case underscores the importance of considering differential diagnoses even with seemingly characteristic presentations.

    Implications:

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  • This rare co-occurrence challenges typical diagnostic pathways for both SAT and GCA.
  • Highlights the need for comprehensive evaluation when symptoms overlap between distinct rare diseases.
  • Contributes to understanding the complex interplay between endocrine and rheumatologic conditions.