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Related Concept Videos

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...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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...
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...
Hypothalamic-Pituitary Axis01:37

Hypothalamic-Pituitary Axis

The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
Cushing Syndrome I: Introduction01:26

Cushing Syndrome I: Introduction

Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...

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Related Experiment Video

Updated: Jul 4, 2026

Laparoscopic Oocyte Retrieval and Cryopreservation during Vaginoplasty for Treatment of Mayer-Rokitansky-Kuster-Hauser Syndrome
11:53

Laparoscopic Oocyte Retrieval and Cryopreservation during Vaginoplasty for Treatment of Mayer-Rokitansky-Kuster-Hauser Syndrome

Published on: May 10, 2022

Mayer-Rokitansky-Kuster-Hauser syndrome with hyperprolactinemia.

Dania H Al-Jaroudi1, Ayda M Nasser

  • 1Department of Reproductive Medicine Unit, Minimally Invasive Gynecologic Surgery, Reproductive Medicine Unit, Women's Specialized Hospital, King Fahad Medical City, PO Box 59046, Riyadh 11525, Kingdom of Saudi Arabia. daljaroudi@kfmc.med.sa

Saudi Medical Journal
|June 4, 2008
PubMed
Summary

Mayer-Rokitansky-Kuster-Hauser Syndrome (MRKH) with hyperprolactinemia is exceptionally rare. This case highlights a unique co-occurrence in an 18-year-old Saudi female with absent menses and Müllerian hypoplasia.

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A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
08:20

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome

Published on: October 2, 2018

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Last Updated: Jul 4, 2026

Laparoscopic Oocyte Retrieval and Cryopreservation during Vaginoplasty for Treatment of Mayer-Rokitansky-Kuster-Hauser Syndrome
11:53

Laparoscopic Oocyte Retrieval and Cryopreservation during Vaginoplasty for Treatment of Mayer-Rokitansky-Kuster-Hauser Syndrome

Published on: May 10, 2022

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
08:20

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome

Published on: October 2, 2018

Area of Science:

  • Reproductive Endocrinology
  • Gynecology
  • Medical Imaging

Background:

  • Mayer-Rokitansky-Kuster-Hauser Syndrome (MRKH) is a congenital disorder characterized by uterine and vaginal hypoplasia or aplasia.
  • Hyperprolactinemia is a condition of elevated prolactin levels, often associated with pituitary dysfunction.
  • The simultaneous occurrence of MRKH and hyperprolactinemia is exceedingly rare in medical literature.

Observation:

  • An 18-year-old Saudi female presented with primary amenorrhea.
  • Physical examination revealed normal secondary sexual characteristics but a rudimentary vagina (2 cm length).
  • Pelvic MRI confirmed Müllerian hypoplasia (Class I American Fertility Society), with a small uterus and cervix, and normal ovaries.

Findings:

  • Serum prolactin levels were significantly elevated at 1,517 mIU/L.
  • Cranial MRI ruled out a pituitary tumor or other structural abnormalities.
  • The patient was diagnosed with concomitant MRKH syndrome and hyperprolactinemia.

Implications:

  • This case underscores the importance of considering rare endocrine associations in patients with congenital anomalies.
  • Further research may elucidate potential shared etiologies or mechanisms between MRKH and hyperprolactinemia.
  • Management strategies may need to address both the reproductive tract anomaly and the hormonal imbalance.