The cell adapts to increased physiological demands or to pathological stimuli through growth alterations. These changes may take the form of hypertrophy, hyperplasia, atrophy, metaplasia, and dysplasia. If the pathological stimulus persists, the cell may undergo apoptosis (programmed cell death) or cell death.
Hyperplasia is an increase in the number of cells in an organ or tissue. It may be physiologic or pathological.
Physiologic hyperplasia occurs in response to:
Pathological hyperplasia results from continued hormonal stimulation and can lead to conditions such as endometrial and prostatic hyperplasia. However, this type of hyperplasia regresses once the hormonal stimulation ceases.
The mechanism of hyperplasia is an increase in the number of cells due to increased transcription of growth-promoting genes activated by growth factors and hormones.
Hypertrophy is an increase in the size of cells, leading to an increase in the size of an organ. It may accompany hyperplasia.
Typically:
Hypertrophy may be physiologic or pathological.
Physiologic hypertrophy is seen in:
Pathological hypertrophy is seen in the left ventricle in response to long-standing hypertension.
The mechanism of hypertrophy includes:
Some embryonic genes may be re-expressed, e.g. ANP in the heart.
Atrophy is a decrease in the size and weight of a tissue or organ due to loss of cell substance and organelles.
Physiologic atrophy is seen during embryonic development, for example:
It is also seen in the uterus following pregnancy and childbirth, as the uterus reverts back to its previous size.
Pathological atrophy can follow various causes that impair growth and development, and it can lead to cell death if persistent. Causes include:
Ageing is normally accompanied by atrophy, especially in the brain, muscles, and heart.
Atrophic cells:
Cellular components contained in autophagic vacuoles are lysed by lysosomal enzymes.
“Brown atrophy” is a normal part of ageing and is seen in organs such as the heart and liver. It results from deposition of yellow-brown lipofuscin and lipochrome pigments due to autophagy and lipid peroxidation of membranes.
Metaplasia is a reversible change in which one type of adult differentiated cell is replaced by another type of adult differentiated cell. It develops as an adaptation to local stress, and the metaplastic epithelium can better withstand that stress.
Examples include:
Vitamin A deficiency can cause squamous metaplasia of the respiratory tract.
Long-standing metaplasia can predispose to malignancy.
The mechanism of metaplasia is reprogramming of stem cells in response to cytokines, growth factors, and hormones induced by local irritants such as acidity or cigarette smoke. In many cases, reversal is possible once exposure to the irritant is stopped.
Dysplasia is a pre-neoplastic lesion characterised by disorderly cell growth. Some cells show a lack of maturation, and there is irregularity in cell shape and size.
Cytological features of atypia include:
Nuclear features of dysplasia can be differentiated from neoplastic cells by the presence of normal mitotic spindles in dysplasia.
Dysplasia may be reversible if the initiating factor is removed.
Examples include:
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