CELLULAR ADAPTATIONS OF GOWTH AND DIFFERRENTIATION.ppt

CELLULAR ADAPTATIONS OF
GOWTH AND
DIFFERRENTIATION
•Hypertrophy
•Hyperplasia
•Atrophy
•Metaplasia
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Cellular Adaptation - V.Mythily, JCE/BME

Cellular Adaptation
– When a cell in homeostasis is subjected to stress,
there is a functional and a structural response
from the cell
– It consists of hypertrophy, hyperplasia, atrophy or
metaplasia
– Due to this it achieves a new steady state
– It is a reversible response
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Cellular Adaptation - V.Mythily, JCE/BME 3
3/14/2024
Cellular Adaptation

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HYPERTROPHY
• Hypertrophy is an increase in the size of cells
resulting in increase in the size of the organ.
• In pure hypertrophy, there are no new cells, just
bigger cells containing increased amounts of
structural proteins and organelles
• Hypertrophy occurs when cells have a limited
capacity to divide
• Hypertrophy can be physiologic or pathologic
• Cause : 1. increased functional demand , 2.
growth factor or hormonal stimulation
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Physiologic cellular Hypertrophy
• The massive physiologic enlargement of the
uterus during pregnancy occurs as a consequence of
estrogen stimulated smooth muscle hypertrophy
and smooth muscle hyperplasia
Pathologic cellular Hypertrophy
• An example of pathologic cellular hypertrophy is
the cardiac enlargement that occurs with
hypertension or aortic valve disease
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Physiological Hypertrophy
Mechanism
• Due to cell growth in response to estrogen
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PHYSIOLOGIC HYPERTROPHY: UTERUS ENLARGEMENT DURING
PREGNANCY
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Normal Myocytes Myocytes showing hypertrophy
Pathologic hypertrophy: Cardiac Enlargement
The mechanisms driving cardiac hypertrophy involve at least
two types of signals:
mechanical triggers, such as stretch
trophic triggers, which typically are soluble mediators that
stimulate cell growth, such as growth factors and
adrenergic hormones. These stimuli turn on signal
transduction pathways that lead to the induction of number
of genes, which in turn stimulate synthesis of many cellular
proteins, including growth factors and structural proteins.
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• If stress (Hypertension / cardiac valve disease
)is not removed, several “degenerative”
changes occur in the myocardial fibers, of
which the most important are fragmentation and
loss of myofibrillar contractile elements
• Net result of these changes is ventricular
dilation and ultimately cardiac failure, a
sequence of events that illustrates how an
adaptation to stress can progress to functionally
significant cell injury if the stress is not relieved
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Pathological Hypertrophy
Mechanism
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HYPERPLASIA:
• characterized by an increase in cell number because of proliferation of
differentiated cells and replacement by tissue stem cells.
• Hyperplasia is an adaptive response in cells capable of replication
• Hypertrophy and hyperplasia also can occur together, and obviously both
result in an enlarged hypertrophic organ.
Hyperplasia
Physiologic
Hormonal
Compensatory
Pathologic
Hormonal
Growth factor
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Molecular mechnism
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Examples
• Physiologic hyperplasia
– Hormonal
• Glandular epithelium of the breast during puberty and
pregnancy
– Compensatory
• Liver regeneration
• Pathologic hyperplasia
– Hyperplasia of endometrium due to excess estrogen
– Benign prostatic hypertrophy
– Skin warts (papilloma virus)
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HYPERPLASIA
• HORMONAL HYPERPLASIA (Physiologic): Proliferation of the
glandular epithelium of the female breast at puberty and during pregnancy
• COMPENSATORY HYPERPLASIA (Physiologic): 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 weight.
• HORMONAL HYPERPLASIA (Pathologic): Disturbed balance between
estrogen and progesterone causes endometrial hyperplasia, which is a
common cause of abnormal menstrual bleeding.
• GROWTH FACTOR INDUCED HYPERPLASIA: eg. Response of
connective tissue cells in wound healing, in which proliferating fibroblasts
and blood vessels aid in repair. In this process, growth factors are produced
by white blood cells (leukocytes) responding to the injury and by cells in
the extracellular matrix.
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HYPERPLASIA
• The hyperplastic process remains
controlled; if the signals that initiate it
abate, the hyperplasia disappears.
• In cancer, the growth control mechanisms
become dysregulated or ineffective
• 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

ATROPHY
• Shrinkage in the size of the cell by the loss of cell substance
• When a sufficient number of cells are involved, the entire
tissue or organ diminishes in size, becoming atrophic.
Although atrophic cells may have diminished function, they
are not dead.
• CAUSES OF ATROPHY:
 Physiologic: loss of innervation, diminished blood supply,
inadequate nutrition, loss of endocrine stimulation, and aging
(senile atrophy),
 Pathologic: the loss of hormone stimulation in menopause
• The mechanisms of atrophy consist of a combination of
decreased protein synthesis and increased protein
degradation in cells.

ATROPHY
• Protein synthesis decreases because of reduced metabolic
activity.
• The degradation of cellular proteins occurs mainly by the
ubiquitin-proteasome pathway.
• Nutrient deficiency and disuse may activate ubiquitin
ligases, which attach multiple copies of the small peptide
ubiquitin to cellular proteins and target them for
degradation in proteasomes.
• In many situations, atrophy is also accompanied by
increased autophagy, with resulting increases in the
number of autophagic vacuoles. Autophagy (“self-eating”) is
the process in which the starved cell eats its own components in an
attempt to survive.

ATROPHY OF BRAIN
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Atrophy
Examples
• Physiologic atrophy
– Fetal organs – like notochord and thyroglossal duct
– Uterus after parturition
• Pathologic atrophy
– Disuse atrophy after immobilization in fracture cast
– Denervation atrophy
– Ischemic atrophy
– Senile atrophy – heart
– Inadequate nutrition – marasmus, cachexia
– Loss of endocrine stimulation – vaginal, endometrial and breast
atrophy after menopause
– Pressure atrophy – in areas surrounding the tumor
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Molecular Mechanism
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METAPLASIA
• Metaplasia is a reversible change in which one adult cell type
(epithelial or mesenchymal) is replaced by another adult cell
type.
• In this type of cellular adaptation, a cell type sensitive to a
particular stress is replaced by another cell type better able to
withstand the adverse environment
• In habitual cigarette smokers: The normal ciliated
columnar epithelial cells of the trachea and bronchi are
focally or widely replaced by stratified squamous epithelial
cells.
• The rugged stratified squamous epithelium may be able to
survive the noxious chemicals in cigarette smoke that the
more fragile specialized epithelium would not tolerate.

METAPLASIA
• Although the metaplastic squamous epithelium has
survival advantages, important protective mechanisms are
lost, such as mucus secretion and ciliary clearance of
particulate matter.
• Moreover, the influences that induce metaplastic change, if
persistent, may predispose to malignant transformation of
the epithelium.
• It is thought that cigarette smoking initially causes
squamous metaplasia, and cancers arise later in some of
these altered foci.
• Since vitamin A is essential for normal epithelial
differentiation, its deficiency may also induce squamous
metaplasia in the respiratory epithelium

Examples
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METAPLASIA
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