Ectopic Acth
Ectopic Acth - Related Videos
16:19
Localized RNAi and Ectopic Gene Expression in the Medicinal Leech
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Cited by 5 •
2008
In this video, we show a procedure for an accurate biolistic delivery of reagents into live tissue with a novel miniature gene gun. We are knocking down the expression of the axon guidance molecule Netrin in leech embryos by delivering molecules of dsRNA into the ventral body wall and ganglia of single segments.
10:02
An Ectopic Chemokine Expression Model for Testing Macrophage Recruitment In Vivo
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2019
To test the effect of a chemokine on macrophage recruitment in vivo, the whole mount in situ hybridization was used to detect the ectopic expression of the chemokine, and immunostaining was used to label macrophages. Live imaging was used for real-time observation of macrophage migration.
05:40
AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke
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2024
This protocol describes the viral-mediated ectopic expression of Neurod1 following cortical ischemic stroke. Neurod1 is delivered (1) using the Cre-Flex AAV system in wild-type mice during the subacute phase post-stroke (7 days) and (2) using a single AAV vector in conditional reporter mice during the chronic phase post-stroke (21 days).
01:37
Hypothalamic-Pituitary Axis
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2019
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. What Happens During Stress In response to stress, the neurons in the hypothalamus release...
07:01
Direct Mouse Trauma/Burn Model of Heterotopic Ossification
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Cited by 68 •
2015
An Achilles tenotomy and burn injury model of heterotopic ossification allows for the reliable study of trauma induced ectopic bone formation without the application of exogenous factors.
FAQs
In normal endocrine regulation, feedback helps coordinate pituitary ACTH release with adrenal cortisol production. With ectopic ACTH, abnormal cells release the hormone autonomously, so cortisol stimulation continues despite signals that would ordinarily reduce pituitary drive. This loss of normal regulatory control produces ACTH-dependent hypercortisolism and helps explain why the condition differs biologically from ordinary feedback-controlled hormone secretion.
Excess ACTH persistently stimulates the adrenal cortex, causing excessive cortisol production. Elevated cortisol can affect multiple physiological systems, leading to hypertension, muscle weakness, glucose intolerance, and characteristic changes in body composition. These findings reflect the broad effects of sustained cortisol excess rather than an isolated abnormality in the hormone-producing tumor itself.
The distinction depends on combining hormone testing with tumor localization. Both conditions can produce ACTH-dependent Cushing syndrome, but their sources differ: one arises from abnormal cells outside the pituitary, while the other is pituitary-driven. Identifying the hormone pattern and locating a possible tumor helps clinicians determine the underlying source and select an appropriate treatment strategy.
Tumor localization connects the abnormal hormone signal to its biological source. Because ectopic ACTH may arise from neuroendocrine tumors outside the pituitary, locating the responsible lesion supports differentiation from pituitary disease. It also provides essential information for addressing the underlying tumor, rather than treating cortisol excess without investigating the cells that continue to produce ACTH.
Evaluation focuses on recognizing ACTH-dependent cortisol excess, performing hormone testing, and searching for the source of abnormal ACTH production. Testing helps distinguish ectopic from pituitary-driven disease, while tumor localization identifies a possible extra-pituitary source. Together, these steps establish the biological origin of the syndrome and guide management of both hypercortisolism and the underlying tumor.
Recognition has two complementary benefits. Clinically, it guides treatment of excessive cortisol and directs attention toward the underlying tumor. Scientifically, it illustrates how abnormal cells can produce a hormone outside its usual tissue source, bypass normal endocrine regulation, and alter adrenal function. The condition therefore links endocrine physiology, tumor biology, hormone testing, and disease localization.