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Related Concept Videos

The Parathyroid Glands00:59

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...
Cellular Adaptation IV: Dysplasia and Metaplasia01:24

Cellular Adaptation IV: Dysplasia and Metaplasia

DysplasiaDysplasia refers to abnormal changes in the size, shape, and organization of mature cells, characterized by pleomorphism, nuclear abnormalities, and increased mitotic activity. It commonly affects epithelial tissues, including the cervix, gastrointestinal tract, respiratory mucosa, and endometrium. Although it may occur alongside hyperplasia, dysplasia is not a true adaptive response but a preneoplastic change with potential to progress to cancer.When confined above the basement...
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...
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...
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...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...

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Related Experiment Video

Updated: Jul 11, 2026

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
07:13

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation

Published on: March 14, 2017

Hyperparathyroidism and carcinoid tumor.

N A Samaan, R C Hickey, T D Bedner

    Annals of Internal Medicine
    |February 1, 1975
    PubMed
    Summary
    This summary is machine-generated.

    Carcinoid tumors can cause high calcitonin levels, mimicking thyroid issues. This study suggests hyperparathyroidism in these patients is primary, linked to carcinoid tumors as a form of multiple endocrine neoplasia.

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    Last Updated: Jul 11, 2026

    Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
    07:13

    Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation

    Published on: March 14, 2017

    Establishment of a Simple and Effective Rat Model for Intraoperative Parathyroid Gland Imaging
    07:12

    Establishment of a Simple and Effective Rat Model for Intraoperative Parathyroid Gland Imaging

    Published on: August 17, 2022

    Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy
    03:57

    Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

    Published on: July 14, 2023

    Area of Science:

    • Endocrinology
    • Oncology
    • Neoplasia

    Background:

    • Carcinoid tumors are neuroendocrine neoplasms.
    • Hyperparathyroidism is a condition of overactive parathyroid glands.
    • Association between carcinoid tumors and endocrine disorders is known.

    Purpose of the Study:

    • To describe three patients with carcinoid tumor and hyperparathyroidism.
    • To investigate the source of high calcitonin levels in these patients.
    • To explore the relationship between carcinoid tumors and hyperparathyroidism within the context of multiple endocrine tumor formation.

    Main Methods:

    • Clinical case series description.
    • Measurement of circulating immunoreactive calcitonin levels.
    • Neck venous catheterization to assess calcitonin gradients.

    Main Results:

    • All three patients presented with carcinoid tumors and hyperparathyroidism.
    • Elevated circulating immunoreactive calcitonin levels were observed.
    • No differential increase in calcitonin was detected in neck venous catheterization specimens, suggesting a non-thyroidal source.

    Conclusions:

    • The high calcitonin levels likely originated from the carcinoid tumor.
    • Hyperparathyroidism in these cases is presumed to be primary.
    • This association represents a potential manifestation of multiple endocrine tumor syndromes.
    • Investigation for hyperparathyroidism is recommended in patients diagnosed with carcinoid tumors.