Page 72 - Textbook of Pathology, 6th Edition
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56 hyperplastic growth. Neoplasia differs from hyperplasia in
having hyperplastic growth with loss of growth-regulatory
mechanism due to change in genetic composition of the cell.
Hyperplasia, on the other hand, persists so long as stimulus
is present.
CAUSES. As with other non-neoplastic adaptive disorders
of growth, hyperplasia has also been divided into physiologic
and pathologic.
SECTION I
A. Physiologic hyperplasia. The two most common types
are as follows:
1. Hormonal hyperplasia i.e. hyperplasia occurring under the
influence of hormonal stimulation e.g.
i) Hyperplasia of female breast at puberty, during preg-
nancy and lactation.
ii) Hyperplasia of pregnant uterus.
iii) Proliferative activity of normal endometrium after a
normal menstrual cycle.
iv) Prostatic hyperplasia in old age.
Figure 3.41 Cardiac hypertrophy. The myocardial muscle fibres are
thick with abundance of eosinophilic cytoplasm. Nuclei are also enlarged 2. Compensatory hyperplasia i.e. hyperplasia occurring
with irregular outlines. following removal of part of an organ or a contralateral organ
in paired organ e.g.
iii) Intestinal strictures i) Regeneration of the liver following partial hepatectomy
iv) Muscular arteries in hypertension. ii) Regeneration of epidermis after skin abrasion
3. Hypertrophy of skeletal muscle e.g. hypertrophied muscles iii) Following nephrectomy on one side, there is hyperplasia
in athletes and manual labourers. of nephrons of the other kidney.
4. Compensatory hypertrophy may occur in an organ when B. Pathologic hyperplasia. Most examples of pathologic
the contralateral organ is removed e.g. hyperplasia are due to excessive stimulation of hormones or
i) Following nephrectomy on one side in a young patient, growth factors e.g.
General Pathology and Basic Techniques
there is compensatory hypertrophy as well as hyperplasia i) Endometrial hyperplasia following oestrogen excess.
of the nephrons of the other kidney. ii) In wound healing, there is formation of granulation tissue
ii) Adrenal hyperplasia following removal of one adrenal due to proliferation of fibroblasts and endothelial cells.
gland.
MORPHOLOGIC FEATURES. The affected organ is
enlarged and heavy. For example, a hypertrophied heart
of a patient with systemic hypertension may weigh
700-800 g as compared to average normal adult weight of
350 g. There is enlargement of muscle fibres as well as of
nuclei (Fig. 3.41). At ultrastructural level, there is increased
synthesis of DNA and RNA, increased protein synthesis
and increased number of organelles like mitochondria,
endoplasmic reticulum and myofibrils.
HYPERPLASIA
Hyperplasia is an increase in the number of parenchymal
cells resulting in enlargement of the organ or tissue. Quite
often, both hyperplasia and hypertrophy occur together.
Hyperplasia occurs due to increased recruitment of cells from
G (resting) phase of the cell cycle to undergo mitosis, when
0
stimulated. All body cells do not possess hyperplastic growth
potential (Chapter 6). Labile cells (e.g. epithelial cells of the
skin and mucous membranes, cells of the bone marrow and
lymph nodes) and stable cells (e.g. parenchymal cells of the
liver, pancreas, kidney, adrenal, and thyroid) can undergo Figure 3.42 Pseudocarcinomatous hyperplasia of the skin. The
hyperplasia, while permanent cells (e.g. neurons, cardiac and epidermis shows an increase in the number of layers of the squamous
epithelium. The intervening dermal soft tissue shows moderate chronic
skeletal muscle) have little or no capacity for regenerative inflammation.

