Hyperplasia
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maria Fernanda Villarreal, M.D. [2]
Synonyms and keywords: Physiologic hyperplasia; Pathologic hyperplasia; Hypergenesis
Overview
Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue. Hyperplasia may result in the gross enlargement of an organ, the formation of a benign tumor. Hyperplasia is considered to be a physiological response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasia (the process underlying cancer and some benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.[1]
Classification
- Hyperplasia may be classified into 2 groups:[2]
Physiologic hyperplasia
- Normal stressor (eg. pregnancy)
Pathologic hyperplasia
- Abnormal stressor (eg. pituitary adenoma)
Pathophysiology
- The pathogenesis of hyperplasia is characterized by an increase in the number of cells.[2]
- Hyperplasia is the result of growth factor driven proliferation of mature cells.[1]
- The pathogenesis of hyperplasia is limited to cells that have the capability of reproduction, excluding primarily myocytes and neurons.
- On gross pathology, findings of hyperplasia will depend on the anatomical site.
Causes
- Hyperplasia may be caused by either increased metabolic demand, chronic inflammatory response, or compensation for damage.
Differentiating Hyperplasia from other Diseases
- Hyperplasia must be differentiated from other diseases that cause abnormal tissue growth such as:[2]
- Some examples of hyperplasia, include:
- Congenital adrenal hyperplasia
- Endometrial hyperplasia
- Benign prostatic hyperplasia
- Hyperplasia of the breast
- Focal epithelial hyperplasia
- Sebaceous hyperplasia
- Compensatory liver hyperplasia
Risk Factors
- Common risk factors in the development of hyperplasia are genetic mutations, chronic inflammation, increased metabolic demand, and hormonal stimulation.[2]
References
- ↑ 1.0 1.1 Ramzi Cotran, Vinay Kumar, Tucker Collins (1999). Robbins Pathologic Basis of Disease, Sixth Edition. W.B. Saunders. ISBN 072167335X.
- ↑ 2.0 2.1 2.2 2.3 Hyperplasia. Wikipedia. https://en.wikipedia.org/wiki/Hyperplasia Accessed on April 7, 2016