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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...

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Related Experiment Video

Updated: Jun 4, 2026

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models
08:57

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Published on: May 17, 2024

Multiple endocrine neoplasia: types 1 and 2.

Deborah J Marsh, Oliver Gimm

    Advances in Oto-Rhino-Laryngology
    |March 2, 2011
    PubMed
    Summary

    Multiple endocrine neoplasia (MEN) types 1 and 2 are inherited conditions causing hormone-secreting cell tumors. MEN 2 management benefits from genetic testing and prophylactic surgery, unlike MEN 1.

    Area of Science:

    • Endocrinology
    • Genetics
    • Oncology

    Background:

    • Multiple endocrine neoplasia types 1 (MEN 1) and 2 (MEN 2) are autosomal dominant inherited syndromes.
    • Germline mutations in MEN1 (loss-of-function) or RET proto-oncogene (gain-of-function) predispose to tumors in hormone-secreting cells.
    • MEN 1 is associated with pituitary, parathyroid, pancreatic tumors, and thymic carcinoids. MEN 2 is linked to medullary thyroid carcinoma, pheochromocytoma, and parathyroid tumors.

    Purpose of the Study:

    • To review current knowledge of MEN 1 and MEN 2.
    • To emphasize aspects relevant to otorhinolaryngologists.
    • To compare genetic testing and management strategies for MEN 1 and MEN 2.

    Main Methods:

    • Literature review of MEN 1 and MEN 2.

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    Last Updated: Jun 4, 2026

    Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models
    08:57

    Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

    Published on: May 17, 2024

  • Analysis of genetic mutations and associated clinical manifestations.
  • Comparison of diagnostic and therapeutic approaches.
  • Main Results:

    • MEN 2 management is guided by RET testing and allows for prophylactic thyroidectomy, preventing malignancy.
    • Genetic testing for MEN 1 is complex due to a lack of hotspots and less straightforward patient benefit.
    • Genotype-phenotype correlations are established for MEN 2 but absent for MEN 1.

    Conclusions:

    • MEN 2 serves as a model for integrating molecular medicine into patient care.
    • Prophylactic interventions are possible for MEN 2 but not for MEN 1.
    • Understanding these genetic syndromes is crucial for targeted clinical management and research.