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Related Concept Videos

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...
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...
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...
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...
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...

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Related Experiment Video

Updated: May 20, 2026

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

Primary hyperparathyroidism with classic and severe skeletal involvement.

Mark Anthony S Sandoval1, Elizabeth Paz-Pacheco

  • 1Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, Philippine General Hospital, University of the Philippines Manila, Philippines. markanthony_sandoval@yahoo.com

BMJ Case Reports
|July 7, 2012
PubMed
Summary

Primary hyperparathyroidism (PHPT) in a 63-year-old woman caused severe bone fractures, osteoporosis, and kidney stones. Surgical removal of a parathyroid adenoma resolved the condition, though hungry-bone syndrome required treatment.

Related Experiment Videos

Last Updated: May 20, 2026

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
  • Nephrology
  • Orthopedics

Background:

  • Primary hyperparathyroidism (PHPT) is a condition characterized by excessive parathyroid hormone secretion.
  • While historically associated with severe bone disease, PHPT manifestations are often subtler in contemporary clinical practice.

Observation:

  • A 63-year-old woman presented with recurrent fractures, hypercalcemia, and elevated intact parathyroid hormone (iPTH).
  • Radiographic findings indicated severe skeletal involvement, alongside nephrolithiasis and osteoporosis, indicative of advanced PHPT.
  • Imaging confirmed an enlarged parathyroid gland, with functional studies demonstrating hyperfunction.

Findings:

  • Parathyroidectomy successfully removed the parathyroid adenoma.
  • Post-operatively, the patient experienced hungry-bone syndrome, a known complication characterized by rapid calcium shifts.
  • Treatment with calcium and calcitriol effectively managed the hungry-bone syndrome.

Implications:

  • This case highlights that severe skeletal manifestations of PHPT, though rare, can still occur.
  • Early diagnosis and surgical intervention are crucial for managing PHPT and its complications.
  • Understanding and prompt treatment of post-parathyroidectomy hungry-bone syndrome are essential for patient recovery.