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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 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...

The Parathyroid Glands

The Parathyroid Glands

The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
Oxyphil cells, whose functions remain elusive, emerge during late puberty, adding a layer of complexity to the parathyroid gland's intricacies. In contrast, principal parathyroid cells undertake a vital role by producing...

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...

Hypothyroidism II: Pathophysiology

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 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...

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Updated: Jun 5, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Papillary thyroid carcinoma variants.

Ricardo V Lloyd¹, Darya Buehler, Elham Khanafshar

¹Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA. rvlloyd@wisc.edu

Head and Neck Pathology

|January 12, 2011

Summary

This summary is machine-generated.

Papillary thyroid carcinoma, the most common thyroid cancer, arises from various factors including radiation and genetic susceptibility. Diagnostic tools like immunohistochemistry and molecular markers aid in identifying its subtypes and differentiating them from benign nodules.

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Area of Science:

Endocrinology
Oncology
Pathology

Background:

Papillary thyroid carcinoma (PTC) represents over 70% of thyroid malignancies.
Radiation exposure is a primary risk factor, alongside genetic predisposition and other contributing elements.
PTC exhibits diverse histological variants, including common types like conventional, follicular, and tall cell, as well as rarer forms such as oncocytic, columnar cell, diffuse sclerosing, and solid variants.

Purpose of the Study:

To review the diagnostic utility of immunohistochemical and molecular markers in papillary thyroid carcinoma.
To highlight key markers for differentiating PTC variants from benign thyroid lesions.
To discuss the role of molecular alterations in PTC diagnosis and classification.

Main Methods:

Review of current literature on papillary thyroid carcinoma diagnosis.
Analysis of immunohistochemical markers including TTF-1, thyroglobulin, HBME-1, and CITED1.
Evaluation of molecular markers such as BRAF V600E, HMGA2, and IGF2/BP3.

Main Results:

Immunohistochemistry for TTF-1 and thyroglobulin is crucial for confirming PTC, particularly in metastatic locations.
HBME-1 and CITED1 assist in distinguishing follicular variants of PTC from follicular adenomas.
The BRAF V600E mutation is prevalent in PTC and anaplastic thyroid carcinomas.
HMGA2 and IGF2/BP3 serve as recent molecular diagnostic tools for differentiating PTC and its variants from benign thyroid nodules.

Conclusions:

Accurate diagnosis of papillary thyroid carcinoma and its variants relies on a combination of histological examination and specific immunohistochemical and molecular markers.
These diagnostic adjuncts are essential for precise classification and effective patient management.
Ongoing research into molecular markers continues to refine diagnostic capabilities for thyroid nodules.