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While an organ may respond to hormonal signals or increased demands by increasing the size of individual cells, it can also increase function by increasing the number of cells, a process known as hyperplasia. Hypertrophy and hyperplasia are often seen concurrently. Hormonal signals can induce a physiologic hyperplastic effect. For example, the normal increase in estrogen levels at puberty and during the early phase of the menstrual cycle leads to an increased number of both endometrial and uterine stromal cells. A similar hyperplastic response is commonly produced by the administration of exogenous estrogen in postmenopausal women. Estrogens also produce hyperplasia in men. Gynecomastia, an enlargement of the male breast characterized by hyperplasia and hypertrophy of breast lobules, occurs after the treatment of prostatic carcinoma with exogenous estrogens. Similarly, gynecomastia is seen in patients with chronic liver disease, a disease in which circulating estrogen levels are raised because of diminished hepatic inactivation. Hormones produced by tumours can also lead to hyperplasia. For example, secretion of erythropoietin by cancer of the kidney leads to an increase in the number of red blood cell precursors in the bone marrow. Hyperplasia, like hypertrophy, may also follow increased physiologic demand. Residence at high altitude, where the oxygen content of the air is relatively low, leads to compensatory hyperplasia of red blood cell precursors in the bone marrow and an increased number of circulating red blood cells (secondary polycythemia). The decrease in the amount of oxygen carried in each red blood cell is balanced by an increase in the number of cells. Upon return to sea level, the number of red blood cells promptly falls to normal. Similarly, chronic blood loss, as in abnormal uterine bleeding, causes hyperplasia of erythocytic elements. The immune system's response to many antigens ( a vital mechanism for protection from foreign invaders )constitute another example of demand-induced hyperplasia. Morphologically, lymphocyte hyperplasia is conspicuous in chronic inflammation caused by conditions such as bacterial infection or transplant rejection. An increased demand for parathyroid hormone results in hyperplasia of the parathyroid glands, a sequence seen in some cases of chronic renal disease. In such cases, decreased calcium absorption from the small intestine results in mobilization of calcium from the bones to maintain appropriate blood calcium levels. This demand is mediated by parathyroid hormone, and the gland responds with an increase in the number of cells. Persistent cell injury may lead to hyperplasia. Hyperplasia should be viewed as either a compensatory response to decreased function or simply as a manifestation of mitotic signals generated by injury. In the skin and the lining epithelium of some viscera, chronic inflammation or chronic exposure to physical or chemical injury results in a hyperplastic response. For instance, pressure from ill-fitting shoes causes hyperplasia of the skin of the foot, so-called corns or calluses. The primary function of the skin is to protect the underlying structures. In this perspective such hyperplasia, with resultant thickening of the skin serves to enhance functional capacity. Chronic inflammation of the bladder (chronic cystitis) commonly causes hyperplasia of the bladder epithelium, a condition easily viewed grossly by endoscopy as whitish plaques of the bladder lining. Abnormal hyperplasia can itself be harmful - Example: Psoriasis, a disease of unknown etiology, characterized by conspicuous hyperplasia of the skin. Summary: Increase in the number of cells in an organ or tissue. Example: (i) Compensatory hyperplasia of one kidney after removal of other kidney (ii) Hormonal hyperplasia- breast, uterus during pregnancy; senile enlargement of prostate. Hypertrophy and hyperplasia are closely related and often develop together in the involved organ.
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