• The two types of physiologic hyperplasia are (1) hormonal hyperplasia, exemplified by the proliferation of the glandular epithelium of the female breast at puberty and during pregnancy, and (2) compensatory hyperplasia, in which residual tissue grows after removal or loss of part of an organ. For example, when part of a liver is resected, mitotic activity in the remaining cells begins as early as 12 hours later, eventually restoring the liver to its normal size. The stimuli for hyperplasia in this setting are polypeptide growth factors produced by uninjured hepatocytes as well as nonparenchymal cells in the liver (Chapter 3). After restoration of the liver mass, various growth inhibitors turn off cell proliferation.
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Fig. 2.22 Atrophyasseeninthebrain.(A)Normalbrainofayoungadult.(B)Atrophyofthebraininan82-year-oldmanwithatheroscleroticdisease.Atrophyofthebrainiscausedbyagingandreducedbloodsupply.Notethatlossofbrainsubstancenarrowsthegyriandwidensthesulci.Themeningeshavebeenstrippedfromthebottomhalfofeachspecimentoshowthesurfaceofthebrain.
• Most forms of pathologic hyperplasia are caused by excessive hormonal or growth factor stimulation. For example, after a normal menstrual period there is a burst of uterine epithelial proliferation that is normally tightly regulated by the stimulatory effects of pituitary hormones and ovarian estrogen and the inhibitory effects of progesterone. A disturbance in this balance leading to increased estrogenic stimulation causes endometrial hyperplasia, which is a common cause of abnormal menstrual bleeding. Benign prostatic hyperplasia is another common example of pathologic hyperplasia induced in responses to hormonal stimulation by androgens. Stimulation by growth factors also is involved in the hyperplasia that is associated with certain viral infections; for example, papillomaviruses cause skin warts and mucosal lesions that are composed of masses of hyperplastic epithelium. Here the growth factors may be encoded by viral genes or by the genes of the infected host cells.
An important point is that in all of these situations, the hyperplastic process remains controlled; if the signals that initiate it abate, the hyperplasia disappears. It is this responsiveness to normal regulatory control mechanisms that distinguishes pathologic hyperplasias from cancer, in which the growth control mechanisms become permanently dysregulated or ineffective (Chapter 6). Nevertheless, in many cases, pathologic hyperplasia constitutes a fertile soil in which cancers may eventually arise. For example, patients with hyperplasia of the endometrium are at increased risk of developing endometrial cancer (Chapter 19).
Atrophy is shrinkage in the size of cells by the loss of cell substance. When a sufficient number of cells are involved, the entire tissue or organ is reduced in size, or atrophic (
Fig. 2.22 ). Although atrophic cells may have diminished function, they are not dead.
Causes of atrophy include a decreased workload (e.g., immobilization of a limb to permit healing of a fracture), loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging (senile atrophy). Although some of these stimuli are physiologic (e.g., the loss of hormone stimulation in menopause) and others are pathologic (e.g., denervation), the fundamental cellular changes are similar. They represent a retreat by the cell to a smaller size at which survival is still possible; a new equilibrium is achieved between cell size and diminished blood supply, nutrition, or trophic stimulation.
Cellular atrophy results from a combination of decreased protein synthesis and increased protein degradation.
Protein synthesis decreases because of reduced metabolic activity.